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Nurses
Quick
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Diseases
Second Edition
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STAFF The clinical treatments described and recommended in

this publication are based on research and consultation
Executive Publisher with nursing, medical, and legal authorities. To the best
Judith A. Schilling McCann, RN, MSN of our knowledge, these procedures reflect currently
Editorial Director accepted practice. Nevertheless, they cant be considered
H. Nancy Holmes absolute and universal recommendations. For individual
applications, all recommendations must be considered in
Clinical Director light of the patients clinical condition and, before
Joan M. Robinson, RN, MSN administration of new or infrequently used drugs, in light
of the latest package-insert information. The authors and
Art Director publisher disclaim any responsibility for any adverse
Elaine Kasmer effects resulting from the suggested procedures, from any
Editorial Project Manager undetected errors, or from the readers misunderstanding
Ann E. Houska of the text.

Clinical Project Manager 2009 by Lippincott Williams & Wilkins. All rights
Janet Rader Clark, RN, BSN reserved. This book is protected by copyright. No part of
it may be reproduced, stored in a retrieval system, or
Editor transmitted, in any form or by any meanselectronic,
Kimberly A.J. Bilotta mechanical, photocopy, recording, or otherwise
Clinical Editors without prior written permission of the publisher, except
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Anita Lockhart, RN, MSN; Dorothy P. Terry, RN reviews and testing and evaluation materials provided by
the publisher to instructors whose schools have adopted
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Diane Paluba (manager), Joyce Rossi Biletz, Library of Congress Cataloging-in-Publication Data
Donald G. Knauss, Donna S. Morris Nurses quick check. Diseases. 2nd ed.
p. ; cm.
Associate Manufacturing Manager Includes bibliographical references and index.
Beth J. Welsh 1. DiseasesHandbooks, manuals, etc. 2. Nursing
Editorial Assistants Handbooks, manuals, etc. I. Lippincott Williams & Wilkins.
Karen J. Kirk, Jeri OShea, Linda K. Ruhf [DNLM: 1. DiseaseHandbooks. 2. Nursing Care
Handbooks. 3. TherapeuticsHandbooks.
Indexer WY 49 N9742 2008]
Dianne Schneider RT65.N78 2008
616dc22
ISBN-13: 978-0-7817-8940-0 (alk. paper)
ISBN-10: 0-7817-8940-0 (alk. paper) 2007049036
9400 FM.qxd 8/2/12 4:16 PM Page v

Contents

Contributors and consultants vii

Diseases (in alphabetical order) 1

Less common diseases 922

Selected references 933
Web resources 935
Index 937

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Contributors
and consultants

Beverly Anderson, RN, MSN, MOT Kendra S. Seiler, RN, MSN

Associate Professor Nursing Instructor
Malcolm X College Rio Hondo College
Chicago Whittier, Calif.

Elizabeth A. Archer, RN, EdD LaDelle Smothers, RN, BSN, MS

Associate Professor RN Consultant (traveling)
Baptist College of Health Sciences Britthaven, Inc.
Memphis Kinston, N.C.

Julie A. Calvery, RN, MS Rita M. Wick, RN, BSN

Instructor Education Specialist
University of Arkansas Berkshire Health Systems
Fort Smith Pittsfield, Mass.

Kim Cooper, RN, MSN

Nursing Department Chair
Ivy Tech Community College
Terre Haute, Ind.

Lillian Craig, RN, MSN, FNP-C

Adjunct Faculty
Oklahoma Panhandle State University
Goodwell

Shelley Yerger Hawkins, APRN-BC, DSN, FNP, GNP,

FAANP
Post Doctoral Fellow
University of North Carolina
Chapel Hill

Elizaveta House, RN, BSN

Procurement Coordinator
LifeChoice Donor Services, Inc.
Windsor, Conn.

Angela R. Irvin, RN, MSN, ARNP, NP-C

Nurse Practitioner
University of Louisville (Ky.) Family & Geriatric Medicine

Vanessa Kramasz, RN, MSN, FNP

Lead Faculty & Nurse Practitioner
Gateway Technical College
Burlington, Wis.

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Nurses
Quick
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Diseases
Second edition
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A
Abortion, spontaneous
Overview
Description
H Also known as miscarriage
H Expelled products of conception from the uterus be-
fore fetal viability (see Types of spontaneous abor-
tion)
Pathophysiology
H Abortion may result from fetal, placental, or maternal
factors.
Common characteristics
H Pink discharge for several days before cramping
H Scant brown discharge for several weeks before
cramping
H Abdominal cramps
H Vaginal bleeding

Complications
H Infection
H Hemorrhage
H Anemia
H Coagulation defects
H Disseminated intravascular coagulation
H Psychological issues of loss and failure

Fetal factors
H Fetal factors usually cause abortion to occur between Assessment
9 and 12 weeks gestation.
H Spontaneous abortion may result from defective em- History
bryologic development. H Pink discharge for several days or scant brown dis-
H Faulty implantation of a fertilized ovum may cause charge for several weeks before onset of cramps and
the ovum to be rejected. increased vaginal bleeding
H Abortion may also result from failure of the en- H Cramps that appear for a few hours, intensify, then
dometrium to accept the fertilized ovum. occur more frequently
Placental factors H Continued cramps and bleeding if any uterine con-
H Placental factors usually cause abortion to occur tents remain (cramps and bleeding may subside if
around 14 weeks gestation when the placenta takes entire contents expelled)
over the hormone production necessary to maintain
pregnancy. These factors include: Physical findings
premature separation of a normally implanted H Vaginal bleeding
placenta H Cervical dilation
abnormal placental implantation H Passage of nonviable products of conception
abnormal platelet function.
Maternal factors Test results
H Maternal factors usually cause abortion to occur Laboratory
between 11 and 19 weeks gestation. H Serum human chorionic gonadotropin levels are
decreased, suggesting spontaneous abortion.
Causes H Cytologic analysis shows evidence of products of
Spontaneous abortion conception.
H Fetal factors H Serum hemoglobin level and hematocrit are de-
H Placental factors creased due to blood loss.
H Maternal infection Imaging
H Severe malnutrition H Presence or absence of fetal heart tones or empty
H Abnormalities of the reproductive organs amniotic sac is revealed by ultrasound examination.
H Thyroid gland dysfunction
H Lowered estriol secretion
H Diabetes mellitus Treatment
H Trauma
H Surgery that necessitates manipulation of the pelvic General
organs H Accurate evaluation of uterine contents before plan-
H Blood group incompatibility and Rh isoimmunization ning treatment
H Illicit drug use H Progression of spontaneous abortion unpreventable,
H Environmental toxins except in cases caused by an incompetent cervix
H Incompetent cervix H Hospitalization to control severe hemorrhage
H Possible bed rest
Incidence
H Percentage of all pregnancies that end in miscar-
riage: up to 15%
H First pregnancies that end in miscarriage: about 30%
H Miscarriages that occur during the first trimester: at
least 75%

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Medications
H Transfusion with packed red blood cells or whole
blood (severe bleeding)
H I.V. oxytocin (stimulates uterine contractions)
H Rho(D) immune globulin for an Rh-negative female
with a negative indirect Coombs test
Surgery
H Dilatation and curettage or dilatation and evacuation,
if remnants remain in the uterus
H Surgical reinforcement of the cervix (cerclage) to
prevent abortion
Nursing considerations
Key outcomes
The patient will:
H exhibit no signs and symptoms of infection
H communicate feelings about the current situation
H express feelings of having greater control over the
current situation
H use available support systems, such as family and
friends, to aid in coping.
Nursing interventions
H Do not allow bathroom privileges because the pa-
tient may expel uterine contents without knowing it.
H Inspect bedpan contents carefully for intrauterine
material.
H Save all sanitary pads for evaluation.
H Give prescribed drugs.
H Provide perineal care.
H Provide emotional support and counseling.
H Encourage expression of feelings.
H Help the patient develop effective coping strategies.
Monitoring
H Amount, color, and odor of vaginal bleeding
H Vital signs
H Intake and output
Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H vaginal bleeding or spotting
H bleeding that lasts longer than 8 days or excessive
bleeding
H importance of reporting signs of bright red blood
immediately
H signs of infection, such as fever and foul-smelling
vaginal discharge
H gradual increase of daily activities
H schedule for returning to work (normally within 1
to 4 weeks)
H abstinence from intercourse for 1 to 2 weeks
H prevention of spontaneous abortion
Types of spontaneous abortion
Depending on clinical findings, a spontaneous abortion
(miscarriage) may be threatened or inevitable, incomplete
or complete, or missed, habitual, or septic. Heres how the
seven types compare.
Threatened abortion
Bloody vaginal discharge occurs during the first half of
pregnancy. About 20% of pregnant women have vaginal
spotting or actual bleeding early in pregnancy; of these,
about 50% abort.
Inevitable abortion
The membranes rupture and the cervix dilates. As labor
continues, the uterus expels the products of conception.
Incomplete abortion
The uterus retains part or all of the placenta. Before 10
weeks gestation, the fetus and placenta are usually ex-
pelled together; after the 10th week, theyre expelled sepa-
rately. Because part of the placenta may adhere to the
uterine wall, bleeding continues. Hemorrhage is possible
because the uterus doesnt contract and seal the large
vessels that feed the placenta.
Complete abortion
The uterus passes all the products of conception. Minimal
bleeding usually accompanies complete abortion because
the uterus contracts and compresses the maternal blood
vessels that feed the placenta.
Missed abortion
The uterus retains the products of conception for 2
months or more after the death of the fetus. Uterine
growth ceases; uterine size may even seem to decrease.
Prolonged retention of the dead products of conception
may cause coagulation defects such as disseminated in-
travascular coagulation.
Habitual abortion
Spontaneous loss of three or more consecutive pregnan-
cies constitutes habitual abortion.
Septic abortion
Infection accompanies abortion. This may occur with
spontaneous abortion, but usually results from an illegal
abortion or from the presence of an intrauterine device.
H contraceptive information
H avoidance of tampons for 1 to 2 weeks
H follow-up examination.
Discharge planning
H Refer the patient for professional counseling, if
indicated.
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Abruptio placentae H Disseminated intravascular coagulation (DIC)

H Maternal death
H Fetal death

Overview
Description
H Premature separation of the placenta from the uter-
ine wall
H Usually occurs after 20 weeks gestation, most com-
monly during the third trimester
H Common cause of bleeding during the second half of
pregnancy
H Fetal prognosis depending on gestational age and
amount of blood lost
H Good maternal prognosis if hemorrhage can be con-
trolled
H Classified according to degree of placental separation
and severity of maternal and fetal symptoms (see De-
grees of placental separation in abruptio placen-
tae)
H Also called placental abruption
Assessment
History
Mild abruptio placentae (marginal
separation)
H Mild to moderate vaginal bleeding
H Vague lower abdominal discomfort
H Mild to moderate abdominal tenderness
Moderate abruptio placentae (about 50%
placental separation)
H Continuous abdominal pain
H Moderate dark red vaginal bleeding
H Severe or abrupt onset of symptoms
Severe abruptio placentae (70% placental
separation)
H Abrupt onset of agonizing, unremitting uterine pain
H Moderate vaginal bleeding

Pathophysiology Physical findings

H Spontaneous rupture of blood vessels at the placental Mild abruptio placentae
bed may be due to lack of resiliency or to abnormal H Fetal monitoring possibly indicating uterine ir-
changes in uterine vasculature. ritability
H State may be complicated by hypertension or by an H Strong and regular fetal heart tones
enlarged uterus that cant contract sufficiently to seal Moderate abruptio placentae
off the torn vessels. H Vital signs possibly indicating impending shock
H Bleeding continues unchecked, possibly shearing off H Tender uterus remaining firm between contractions
the placenta partially or completely. H Barely audible or irregular and bradycardic fetal
heart tones
Causes H Labor that usually starts within 2 hours and proceeds
H Exact cause unknown rapidly
H Traumatic injury Severe abruptio placentae
H Amniocentesis H Vital signs that indicate rapidly progressive shock
H Chronic or gestational hypertension H Absence of fetal heart tones
H Multiparity H Tender uterus with boardlike rigidity
H Short umbilical cord H Possible increased uterine size in severe concealed
H Dietary deficiency abruptions
H Smoking
H Advanced maternal age Test results
H Pressure on the vena cava from an enlarged uterus Laboratory
H Diabetes mellitus H Serum hemoglobin level and platelet counts are de-
creased.
Incidence H Progression of abruptio placentae and detection of
H Most common in multigravida women older than DIC is shown by fibrin split products.
age 35, women with gestational hypertension, and Imaging
women who use cocaine H Pelvic examination under double setup (preparations
for an emergency cesarean delivery) and ultrasonog-
Common characteristics raphy may rule out placenta previa.
H Vaginal bleeding
H Abdominal discomfort
H Abdominal tenderness Treatment
Complications General
H Hemorrhage H Blood loss evaluated and controlled
H Shock H Viable infant delivered
H Renal failure H Coagulation disorders prevented

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Degrees of placental separation in abruptio placentae

Mild separation Moderate separation Severe separation
Internal bleeding between the placenta In moderate separation, external hem- External hemorrhage is also character-
and uterine wall characterizes mild orrhage occurs through the vagina. istic in severe separation.
separation.

H For severe placental separation with no signs of fetal H Obtain blood samples for hemoglobin level and
life, vaginal delivery unless contraindicated by un- hematocrit, coagulation studies, and type and cross-
controlled hemorrhage or other complications matching, as ordered.
H Provide emotional support during labor.
H Provide information of progress and condition of
ALERT
fetus during labor.
Because of possible fetal blood loss through the pla- H Encourage verbalization of feelings.
centa, a pediatric team should be ready at delivery H Help develop effective coping strategies.
to assess and treat the neonate for shock, blood H Administer I.V. fluids and blood products.
loss, and hypoxia.
Monitoring
ALERT H Maternal vital signs
H Central venous pressure
Complications of abruptio placentae require H Intake and output
prompt appropriate treatment. With a complica- H Vaginal bleeding
tion such as DIC, the patient needs immediate in- H Fetal heart rate (electronically)
tervention with platelets and whole blood, as or- H Progression of labor
dered, to prevent exsanguination.

H Nothing to eat or drink until delivery of the fetus Patient teaching

H Bed rest until delivery of the fetus
Be sure to cover:
Medications H the disorder, diagnosis, and treatment
H I.V. fluid infusion (by large-bore catheter) as H signs of placental abruption
ordered H possibility of an emergency cesarean delivery
H possibility of the delivery of a premature neonate
Surgery H changes to expect in the postpartum period
H Cesarean delivery if the fetus is in distress H possibility of neonatal death
H factors affecting survival of the neonate
H importance of frequent monitoring and prompt
Nursing considerations management to reduce the risk of death.
Key outcomes Discharge planning
The patient will: H Refer the patient for professional counseling, if
H maintain stable vital signs indicated.
H maintain balanced fluid volume
H express feelings of increased comfort
H communicate feelings about the situation
H use available support systems to aid in coping.

Nursing interventions
H Insert an indwelling urinary catheter.

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Physical findings
Acceleration- H Neck muscle asymmetry

deceleration injuries H Reduced neck mobility

H Gait disturbances
H Rigidity or numbness in the arms
H Tenderness at the exact location of the injury
Overview H Decreased active and passive range of motion

Description Test results

H Injury resulting from sharp hyperextension and flex- Imaging
ion of the neck that damages muscles, ligaments, H Full cervical spine X-rays rule out cervical fracture.
disks, and nerve tissue
H Excellent prognosis; symptoms usually subside with
symptomatic treatment Treatment
H Also called whiplash
General
Pathophysiology H Soft cervical collar (see Applying a cervical collar)
H Unexpected force causes the head to jerk back and H Ice packs
then forward. H Physical therapy
H The neck bones snap out of position, causing injury. H Limited activity during the first 72 hours after the in-
H Irritated nerves can interfere with blood flow and jury
transmission of nerve impulses. H Limited neck movement
H Pinched nerves can affect certain body part func- H Limited strenuous activities, such as lifting and con-
tions. tact sports, until full recovery has been established
(which may take more than 2 years)
Causes
H Motor vehicle accident Medications
H Sports accident H Oral analgesics, such as acetaminophen, non-
H Fall steroidal anti-inflammatory drugs, and opioids
H Assault, including shaking a child H Muscle relaxants, such as baclofen, carisoprodol,
and cyclobenzaprine
Risk factors H Corticosteroids
H Absence of head restraint in automobile
H Osteoporosis Surgery
H Driving under the influence of alcohol or drugs H Surgical stabilization possible in severe cervical
acceleration-deceleration injuries
Incidence
H 1,000,000 cases each year in the United States
H Average age of patient with acceleration-deceleration Nursing considerations
injury: the late 40s
Key outcomes
Common characteristics The patient will:
H Nuchal rigidity H identify factors that intensify pain
H Neck muscle asymmetry H modify behavior to limit movement and avoid extend-
ed injury
Complications H develop effective coping mechanisms
H Temporomandibular disorder H attain the highest degree of mobility possible
H state feelings and fears about the injury.

Assessment Nursing interventions

H Provide protection of the spine during all care.
History H Give prescribed drugs.
H Mechanism of injury H Apply a soft cervical collar.
H Pain initially minimal, but increases 12 to 72 hours
after the accident Monitoring
H Dizziness H Pain control
H Headache H Response to medications
H Back pain H Complications
H Shoulder pain H Neurologic status
H Vision disturbances
H Tinnitus

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Applying a cervical collar

Cervical collars are used to support an injured or weak-
ened cervical spine and to maintain alignment during
healing.The soft cervical collar, made of spongy foam,
provides gentler support and reminds the patient to avoid
cervical spine motion.

Patient teaching
Be sure to cover:
H activity restrictions
H proper application of soft cervical collar
H medication administration, dosage, and possible
adverse effects
H instructions regarding driving and the use of alcohol
while taking opioids.

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Acne vulgaris H Lithium

H Halothane

Incidence
Overview H Affects nearly 75% of adolescents, although lesions
can appear as young as age 8
Description H Affects males more commonly and more severely
H Inflammatory disorder of the sebaceous gland con- H Occurs in females at an earlier age and tends to
tiguous with a hair follicle (pilosebaceous follicle) affect them for a longer time, sometimes into adult-
H Possibly developing in distinctive pilosebaceous units hood
(sebaceous follicles) H Tends to be familial
H Acne lesions: inflammatory (pustules, papules, and
nodules) and noninflammatory (closed and open Common characteristics
comedones) lesions H Pustules, papules, nodules
H Good prognosis with treatment H Closed and open comedones
H Follicles located primarily on face and upper parts of
Pathophysiology chest and back
H Acne begins with sebum accumulation that obstructs
the pilosebaceous unit. Complications
H The mass of accumulated keratinous sebaceous ma- H Deep cystic process
terial and bacteria within the pilosebaceous follicle H Gross inflammation
causes inflammation when its exposed to the dermis H Abscess formation
with rupture of a follicle. H Secondary bacterial infection
H The Propionibacterium acnes bacteria produce H Acne scars
substances that promote inflammation.
H In noninflammatory acne, the comedones are open,
called blackheads, or closed, called whiteheads; ac- Assessment
cumulated material causes distention of the follicle
and thinning of follicular canal walls. History
H Inflammatory acne develops in closed comedones H Presence of one or more predisposing factors
when the follicular wall ruptures, expelling sebum H Seasonal or monthly eruption patterns
into the surrounding dermis and initiating inflamma- H Pain and tenderness around area of infected follicle
tion.
H Pustules form when the inflammation is close to the Physical findings
surface; papules and cystic nodules can develop H Acne lesions, typically located on the face, neck,
when the inflammation is deeper, causing mild to shoulders, chest, and upper back
severe scarring. H Red, swollen area around the infected follicle
H Acne plugs that appear as closed or open comedones
Causes H Oily and thickened skin
H Exact cause unknown H Visible scars
H Follicular hyperkeratinization
H Excessive sebum production Test results
H Proliferation of P. acnes Laboratory
H Hormonal dysfunction H Culture and sensitivity of pustules or abscesses shows
Causes of acne flare-ups causative organism of secondary bacterial infection.
H Menstrual cycle
H Stress
H Trauma Treatment
H Tropical climates
H Rubbing from tight clothing General
H Environmental exposure to coal tar derivatives, cer- H Treatment of causative factors
tain chemicals, cosmetics, or hair pomades H Well-balanced diet
H Hormonal contraceptives containing norethindrone H Regular exercise
and norgestrel; testosterone
H Anabolic agents Medications
H Corticotropin, gonadotropins, corticosteroids (pro- H Topical
longed use) Antibiotics, including erythromycin, clindamycin,
H Iodine- or bromine-containing drugs and sodium sulfacetamide
H Trimethadione Keratolytics, including benzoyl peroxide, azelaic
H Phenytoin acid, and salicylic acid
H Isoniazid

8 Acne vulgaris
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Retinoids, including adapalene, tretinoin, and H Sensitivity reactions

tazarotene H GI disturbances
H Systemic H Liver dysfunction
Antibiotics, such as tetracycline, erythromycin, and H Response to treatment
clindamycin H Skin and mucous membranes
Diuretics such as spironolactone
Oral hormonal contraceptives
Retinoids, including isotretinoin Patient teaching
Surgery Be sure to cover:
H Comedo extraction H the disorder and treatment
H Intralesional steroids such as triamcinolone H medications and possible adverse reactions
H Cryosurgery H when to notify the physician
H Dermabrasion H signs and symptoms of infection
H causative factors associated with acne flare-up
H well-balanced diet
Special populations
H adequate rest
Tetracycline is contraindicated during pregnancy H stress management.
and childhood because it may cause permanent
discoloration of teeth (in children younger than
age 8), enamel defects, and bone growth retar-
dation. Erythromycin is an alternative for these pa-
tients.

ALERT
Because oral tretinoin is known to cause birth de-
fects, the manufacturer, with Food and Drug Ad-
ministration approval, recommends pregnancy
testing before dispensing, dispensing only a 30-day
supply, repeat pregnancy testing throughout the
treatment period, effective contraception during
treatment, and informed consent of the patient or
parents regarding the danger of the drug.

Nursing considerations
Key outcomes
The patient will:
H exhibit improved or healed wounds or lesions
H demonstrate the recommended skin care regimen
H verbalize feelings about body image
H verbalize understanding of the condition and treat-
ment.
Nursing interventions
H Give prescribed drugs.
H Assist the patient in identifying and eliminating pre-
disposing factors.
H Encourage good personal hygiene and the use of oil-
free skin care products.
H Discourage picking or squeezing the lesions.
H Encourage the patient to verbalize his feelings.
H Encourage patient to develop interests that support a
positive self-image and de-emphasize appearance.
Monitoring
H Liver function studies, serum triglyceride levels, and
pregnancy testing with tretinoin use
H Complications

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Acquired Assessment
immunodeficiency History
syndrome and human H Mononucleosis-like syndrome after high-risk expo-
sure and inoculation; then may remain asymptomatic
immunodeficiency virus for years
H Laboratory evidence of seroconversion only sign in
latent stage
Overview Physical findings
H Persistent generalized adenopathy
Description H Nonspecific symptoms (weight loss, fatigue, night
H Human immunodeficiency virus (HIV) type 1; retro- sweats, fevers)
virus causing acquired immunodeficiency syndrome H Neurologic symptoms resulting from HIV encepha-
(AIDS) lopathy
H Causes patients to become susceptible to opportunis- H Opportunistic infection or cancer (Kaposis sarco-
tic infections, unusual cancers, and other abnormali- ma)
ties
H Marked by progressive failure of the immune system Special populations
H Transmitted by contact with infected blood or body
fluids and associated with identifiable high-risk be- Children show a higher incidence of bacterial
haviors infections.
Pathophysiology
H HIV strikes helper T cells bearing the CD4 antigen. Test results
H The antigen serves as a receptor for the retrovirus Laboratory
and lets it enter the cell. H CD4+ T-cell count of at least 200 cells/ml confirms
H After invading a cell, HIV replicates, leading to cell HIV infection.
death, or becomes latent. H Screening test enzyme-linked immunosorbent assay
H HIV infection leads to profound pathology, either and confirmatory test (Western blot) detect the pres-
directly, through destruction of CD4+ cells, other ence of HIV antibodies, which indicate HIV infection.
immune cells, and neuroglial cells, or indirectly,
through the secondary effects of CD4+ T-cell dys-
function and resultant immunosuppression. Treatment
Causes General
H Infection with HIV, a retrovirus H Variety of therapeutic options for opportunistic infec-
tions (the leading cause of morbidity and mortality in
Risk factors patients infected with HIV)
H I.V. drug users who share needles or syringes H Disease-specific therapy for a variety of neoplastic
H Unprotected sexual intercourse and premalignant diseases and organ-specific syn-
H Placental transmission dromes
H History of sexually transmitted disease H Symptom management (fatigue and anemia)
H Homosexual lifestyle H Well-balanced diet
H Contact with infected blood H Regular exercise, as tolerated, with adequate rest
periods
Incidence
H Average time between exposure to the virus and diag- Medications
nosis of AIDS: 8 to 10 years, but can be shorter and H Immunomodulatory agents
longer H Anti-infectives, as appropriate
H Antineoplastics
Common characteristics H Highly active antiretroviral therapy (HAART)
H May produce no symptoms for years Primary therapy
H Flulike symptoms H Protease inhibitors, such as ritonavir, amprenavir,
and nelfinavir
Complications H Nucleoside reverse transcriptase inhibitors, such as
H Repeated opportunistic infections zidovudine and lamivudine
H Neoplasms H Nonnucleoside reverse transcriptase inhibitors, such
H Premalignant diseases as delavirdine and nevirapine
H Organ-specific syndrome

10 Acquired immunodeficiency syndrome and human immunodeficiency virus

9400A.qxd 8/2/12 4:21 PM Page 11

Preventing HIV transmission

H Use precautions in all situations that risk exposure to
blood, body fluids, and secretions. Diligently practicing
standard precautions can prevent the inadvertent
transmission of human immunodeficiency virus (HIV),
hepatitis B, and other infectious diseases that are
transmitted by similar routes.
H Teach the patient, his family, sexual partners, and friends
about disease transmission and prevention of extending
the disease to others.
H Tell the patient not to donate blood, blood products,
organs, tissue, or sperm.
H If the patient uses I.V. drugs, caution him not to share
needles.
H Inform the patient that high-risk sexual practices for HIV
transmission are those that exchange body fluids, such
as vaginal or anal intercourse without a condom.
H Discuss safer sexual practices, such as hugging, petting,
mutual masturbation, and protected sexual intercourse.
Abstinence is the most effective method to prevent
transmission.
H Advise the female patient of childbearing age to avoid
pregnancy. Explain that an infant may become infected
before birth, during delivery, or during breast-feeding.

Nursing considerations Patient teaching

Key outcomes Be sure to cover:
The patient will: H medication regimens
H achieve management of symptoms of illness H importance of informing potential sexual partners,
H demonstrate use of protective measures, including caregivers, and health care workers of HIV infection
conservation of energy, maintenance of well- (see Preventing HIV transmission)
balanced diet, and getting adequate rest H signs of impending infection and the importance of
H follow safer sex practices seeking immediate medical attention
H use available support systems to help with coping H symptoms of AIDS dementia and its stages and
H express feelings about changes in sexual identity and progression.
social response to disease
H develop no complications of illness Discharge planning
H comply with the treatment regimen. H Refer the patient to a local support group.
H Refer the patient to hospice care, as indicated.
Nursing interventions
H Help the patient cope with an altered body image, the
emotional burden of serious illness, and the threat of
death.
H Avoid glycerin swabs for mucous membranes. Use
normal saline or bicarbonate mouthwash for daily
oral rinsing.
H Ensure adequate fluid intake during episodes of
diarrhea.
H Provide meticulous skin care, especially in the debili-
tated patient.
H Encourage the patient to maintain as much physical
activity as he can tolerate. Make sure his schedule
includes time for exercise and rest.
Monitoring
H Fever, noting any pattern
H Skin integrity
H Signs of illness, such as cough, sore throat, and
diarrhea
H Swollen, tender lymph nodes
H Laboratory values
H Calorie intake
H Progression of lesions in Kaposis sarcoma
H Opportunistic infections or signs of disease
progression
H Compliance with medication regimen

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Acute poststreptococcal Assessment

glomerulonephritis History
H Untreated respiratory streptococcal infection 1 to
3 weeks before
Overview H Decreased urination
H Smoky or coffee-colored urine
Description H Fatigue
H Renal disease in which the glomeruli become H Dyspnea and orthopnea
inflamed
H Usually associated with a postinfectious state, com- Physical findings
monly a streptococcal infection of the respiratory H Oliguria
tract or, less commonly, a skin infection such as H Mild to moderate periorbital edema
impetigo H Mild to severe hypertension
H Up to 95% recovery in children and 70% in adults H Bibasilar crackles (with heart failure)
H Possible chronic renal failure within months in el-
derly patients Test results
H Relatively common Laboratory
H Also called acute glomerulonephritis H Electrolyte imbalances are evident.
H Blood urea nitrogen (BUN) and creatinine levels are
Pathophysiology elevated.
H Antigen-antibody complexes are produced in re- H Serum protein levels are decreased.
sponse to group A beta-hemolytic streptococcus H The presence of RBCs, white blood cells, mixed cell
infection. casts, and protein in the urine indicates renal failure.
H Entrapment and collection of antigen-antibody com- H Fibrin-degradation products and C3 protein levels
plexes occurs in the glomerular capillary mem- are high.
branes.
H Inflammatory damage results, impeding glomerular Special populations
function.
H Immune complement may further damage the glo- Proteinuria in an elderly patient usually isnt as
merular membrane. pronounced.
H Damaged and inflamed glomeruli lose the ability to
be selectively permeable. H Antistreptolysin-O titers (in 80% of patients), strep-
H Red blood cells (RBCs) and proteins then filter tozyme, and anti-DNase B titers are elevated; serum
through as the glomerular filtration rate decreases. complement levels, which verify recent streptococcal
H Uremic poisoning may result. infection, are low.
H Group A beta-hemolytic streptococci is revealed by
Causes throat culture.
H Untreated group A beta-hemolytic streptococcus in- Imaging
fection, especially of the respiratory tract H Kidney-ureter-bladder radiography reveals bilateral
kidney enlargement.
Risk factors Diagnostic procedures
H Streptococcal infection H Renal biopsy or assessment of renal tissue confirms
H Impetigo diagnosis.
Incidence
H Occurs most commonly in boys ages 3 to 7; can oc- Treatment
cur at any age
General
Common characteristics H Correction of electrolyte imbalances (possible dialy-
H Oliguria sis)
H Fluid overload H Fluid restriction
H Periorbital edema H High-calorie, low-protein, low-sodium, low-
potassium diet
Complications H Bed rest
H Progressive deterioration of renal function
Medications
H Antibiotics if appropriate
H Loop diuretics, such as metolazone and furosemide

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Nursing considerations
Key outcomes
The patient will:
H avoid or minimize complications
H maintain fluid balance
H maintain urine specific gravity within the designated
limits
H report increased comfort
H identify risk factors that exacerbate the condition and
modify lifestyle accordingly.
Nursing interventions
H Give prescribed drugs.
H Encourage verbalization.
H Provide support.

Monitoring
H Vital signs
H Electrolyte values and serum creatinine and BUN
levels
H Urine creatinine clearance test results
H Intake and output
H Daily weight

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H importance of follow-up examinations to monitor
renal function
H medication administration, dosage, and possible
adverse effects.
Discharge planning
H Refer the patient to appropriate resources for infor-
mation and support.

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Acute pyelonephritis Assessment

History
Overview H Pain over one or both kidneys
H Urinary urgency and frequency
Description H Burning during urination
H Inflammation of the kidney occurring mainly in the H Dysuria, nocturia, hematuria
interstitial tissue and renal pelvis and occasionally in H Anorexia, vomiting, diarrhea
the renal tubules H Fatigue
H Affecting one or both kidneys H Symptoms that develop rapidly over a few hours or a
H Good prognosis; extensive permanent damage rarely few days
occurs
H Also called acute infective tubulointerstitial Physical findings
nephritis H Pain on flank palpation
H Cloudy urine
Pathophysiology H Ammonia-like or fishy odor to urine
H Infection spreads from the bladder to the ureters to H Fever of 102 F (38.9 C) or higher
the kidneys, commonly through vesicoureteral reflux. H Shaking chills
H Vesicoureteral reflux may result from congenital
weakness at the junction of the ureter and bladder. Test results
H Bacteria refluxed to intrarenal tissues may create Laboratory
colonies of infection within 24 to 48 hours. H Urinalysis and culture and sensitivity testing reveal
H Female anatomy allows for higher incidence of pyuria, significant bacteriuria, low specific gravity
infection. and osmolality, slightly alkaline urine pH, or protein-
uria, glycosuria, and ketonuria (less frequent).
Causes H White blood cell count, neutrophil count, and ery-
H Bacterial infection of the kidneys throcyte sedimentation rate are elevated.
Imaging
Risk factors H Kidney-ureter-bladder radiography reveals calculi,
H Renal procedures that involve instrumentation such tumors, or cysts in the kidneys or urinary tract.
as cystoscopy H Excretory urography shows asymmetrical kidneys,
H Hematogenic infection such as septicemia possibly indicating a high frequency of infection.
H Sexually active women
H Pregnant women
H Neurogenic bladder Treatment
H Obstructive disease
H Renal diseases General
H Identification and correction of predisposing factors
Incidence to infection, such as obstruction or calculi
H More common in females than in males H Short courses of therapy for uncomplicated infec-
H Community-acquired cases in 15 per 100,000 tions
annually H Increased fluid intake
H Hospital-acquired cases in 7 per 10,000 annually
Medications
Common characteristics H Antibiotics, as appropriate
H Pain over one or both kidneys H Urinary analgesics such as phenazopyridine
H Urinary urgency and frequency
H Dysuria
H Nocturia Nursing considerations
Complications Key outcomes
H Renal calculi The patient will:
H Renal failure H maintain fluid balance
H Renal abscess H maintain urine specific gravity within the designated
H Multisystem infection limits
H Septic shock H identify risk factors that exacerbate decreased tissue
H Chronic pyelonephritis perfusion and modify lifestyle appropriately
H report increased comfort.

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Nursing interventions
H Give prescribed drugs.

Monitoring
H Vital signs
H Intake and output
H Characteristics of urine
H Pattern of urination
H Daily weight
H Renal function studies

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H avoidance of bacterial contamination by following hy-
gienic toileting practices (wiping the perineum from
front to back after bowel movements for women)
H proper technique for collecting a clean-catch urine
specimen
H medication administration, dosage, and possible
adverse effects
H routine checkup with a history of urinary tract
infections
H signs and symptoms of recurrent infection.

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Incidence
Life-threatening disorder H Patients with three concurrent causes: 85% probabil-
ity of developing ARDS
Acute respiratory Common characteristics
distress syndrome H Shortness of breath
H Dry cough with thick, frothy sputum
H Bloody, sticky secretions

Overview Complications
H Metabolic acidosis
Description H Respiratory acidosis
H Severe form of alveolar injury or acute lung injury H Cardiac arrest
H A form of pulmonary edema; may be difficult to H Multiple organ dysfunction syndrome
recognize
H Hallmark sign: hypoxemia despite increased supple-
mental oxygen Assessment
H A four-stage syndrome; can rapidly progress to in-
tractable and fatal hypoxemia History
H Little or no permanent lung damage in patients who H Causative factor (one or more)
recover H Dyspnea, especially on exertion
H May coexist with disseminated intravascular coagula-
tion (DIC) Physical findings
H Also known as ARDS, adult respiratory distress syn- Stage I
drome and shock, stiff, white, wet, or Da Nang H Shortness of breath, especially on exertion
lung H Normal to increased respiratory and pulse rates
H Diminished breath sounds
Pathophysiology Stage II
H Increased permeability of the alveolocapillary mem- H Respiratory distress
branes allows fluid to accumulate in the lung intersti- H Use of accessory muscles for respiration
tium, alveolar spaces, and small airways, causing the H Pallor, anxiety, and restlessness
lung to stiffen. H Dry cough with thick, frothy sputum
H Ventilation is impaired, reducing oxygenation of pul- H Bloody, sticky secretions
monary capillary blood. H Cool, clammy skin
H Elevated capillary pressure increases interstitial and H Tachycardia and tachypnea
alveolar edema. H Elevated blood pressure
H Alveolar closing pressure then exceeds pulmonary H Basilar crackles
pressures. Stage III
H Closure and collapse of the alveoli occurs. H Respiratory rate greater than 30 breaths/minute
H Tachycardia with arrhythmias
Causes H Labile blood pressure
H Indirect or direct lung trauma (most common) H Productive cough
H Anaphylaxis H Pale, cyanotic skin
H Aspiration of gastric contents H Crackles and rhonchi possible
H Diffuse pneumonia (especially viral) Stage IV
H Drug overdose H Acute respiratory failure with severe hypoxia
H Idiosyncratic drug reaction H Deteriorating mental status (may become comatose)
H Inhalation of noxious gases H Pale, cyanotic skin
H Near-drowning H Lack of spontaneous respirations
H Oxygen toxicity H Bradycardia with arrhythmias
H Coronary artery bypass grafting H Hypotension
H Hemodialysis H Metabolic and respiratory acidosis
H Leukemia
H Acute miliary tuberculosis Test results
H Pancreatitis Laboratory
H Thrombotic thrombocytopenic purpura H Arterial blood gas (ABG) analysis initially shows a
H Uremia reduced partial pressure of arterial oxygen (PaO2)
H Venous air embolism (less than 60 mm Hg) and a decreased partial pres-
sure of arterial carbon dioxide (PaCO2) (less than
35 mm Hg).

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H ABG analysis later shows increased PaCO2 (more than
45 mm Hg) and decreased bicarbonate levels (less
than 22 mEq/L) and decreased PaO2 despite oxygen
therapy.
H Gram stain and sputum culture and sensitivity show
infectious organism.
H Blood cultures reveal infectious organisms.
H Toxicology tests show drug ingestion in overdose.
H Serum amylase levels are increased in pancreatitis.
Imaging
H Chest X-rays may show early bilateral infiltrates; in
later stages, a ground-glass appearance and, eventu-
ally, whiteouts of both lung fields.
Diagnostic procedures
H Pulmonary artery catheterization may show a pulmo-
nary artery wedge pressure of 12 to 18 mm Hg.
Nursing interventions
H Give prescribed drugs.
H Maintain a patent airway.
H Perform tracheal suctioning, as necessary.
H Ensure adequate humidification.
H Reposition the patient often.
H Consider prone positioning for alveolar recruitment.
H Administer tube feedings or parenteral nutrition, as
ordered.
H Allow periods of uninterrupted sleep.
H Perform passive range-of-motion exercises.
H Provide meticulous skin care.
H Reposition the endotracheal (ET) tube per facility
policy.
H Provide emotional support.
H Provide alternative communication means.

Monitoring
Treatment H Vital signs and pulse oximetry
H Hemodynamics
General H Intake and output
H Treatment of the underlying cause H Respiratory status (breath sounds, ABG results)
H Correction of electrolyte and acid-base imbalances H Mechanical ventilator settings
For mechanical ventilation H Sputum characteristics
H Target low tidal volumes; use of increased respiratory H Level of consciousness
rates H Daily weight
H Target plateau pressures less than or equal to H Laboratory studies
40 cm H2O H Response to treatment
H Positive end-expiratory pressure (PEEP) as necessary H Complications, such as cardiac arrhythmias, DIC, GI
H Fluid restriction bleeding, infection, malnutrition, or pneumothorax
H Tube feedings or parenteral nutrition H Nutritional status
H Bed rest

Medications ALERT
H Humidified oxygen Because PEEP may lower cardiac output, check for
H Bronchodilators, such as albuterol and theophylline hypotension, tachycardia, and decreased urine
H Diuretics, such as furosemide and torsemide output. To maintain PEEP, suction only as needed.
For mechanical ventilation
H Sedatives If the patient requires mechanical
H Opioids ventilation
H Neuromuscular blockers H Ventilator settings
H Short course of high-dose corticosteroids if fatty H Cuff pressure
emboli or chemical injury H Complications of mechanical ventilation
H Sodium bicarbonate if severe metabolic acidosis H ET tube position and patency
H Fluids and vasopressors if hypotensive H Signs and symptoms of stress ulcer
H Antimicrobials, as appropriate, for nonviral infection

Surgery Patient teaching

H Possible tracheostomy
Be sure to cover:
H the disorder, diagnosis, and treatment
Nursing considerations H medications and possible adverse reactions
H when to notify the physician
Key outcomes H complications, such as GI bleeding, infection, and
The patient will: malnutrition
H maintain adequate ventilation H recovery time.
H maintain a patent airway
H use effective coping strategies Discharge planning
H maintain skin integrity H Refer the patient to a pulmonary rehabilitation
H report feelings of increased comfort. program, if indicated.

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H Metabolic alkalosis
Life-threatening disorder H Respiratory and cardiac arrest

Acute respiratory Assessment

failure History
Precipitating events
H Infection
Overview H Accumulated pulmonary secretions secondary to
cough suppression
Description H Trauma
H Inadequate ventilation resulting from the inability of H MI
the lungs to adequately maintain arterial oxygenation H Heart failure
or eliminate carbon dioxide H Pulmonary emboli
H Exposure to irritants (smoke or fumes)
Pathophysiology H Myxedema
H If respiratory failure is primarily hypercapnic, its the H Metabolic acidosis
result of inadequate alveolar ventilation.
H If respiratory failure is primarily hypoxemic, its the Physical findings
result of inadequate exchange of oxygen between the H Cyanosis of the oral mucosa, lips, and nail beds
alveoli and capillaries. H Yawning and use of accessory muscles
H Many people have a combined hypercapnic and H Pursed-lip breathing
hypoxemic respiratory failure. H Nasal flaring
H Ashen skin
Causes H Rapid breathing
H Any condition that increases the work of breathing H Cold, clammy skin
and decreases the respiratory drive of patients with H Asymmetrical chest movement
chronic obstructive pulmonary disease H Decreased tactile fremitus over an obstructed
H Respiratory tract infection bronchi or pleural effusion
H Bronchospasm H Increased tactile fremitus over consolidated lung
H Accumulated secretions secondary to cough suppres- tissue
sion H Hyperresonance
H Ventilatory failure H Diminished or absent breath sounds
H Gas exchange failure H Wheezes (in asthma)
H Central nervous system depression H Rhonchi (in bronchitis)
H Myocardial infarction (MI) H Crackles (in pulmonary edema)
H Heart failure
H Pulmonary emboli Test results
H Airway irritants Laboratory
H Endocrine or metabolic disorders H ABG analysis reveals hypercapnia and hypoxemia.
H Thoracic abnormalities H Serum white blood cell count is increased in bacteri-
al infections.
Incidence H Serum hemoglobin level and hematocrit show de-
H Occurs in patients with hypercapnia and hypoxemia creased oxygen-carrying capacity.
H Occurs in patients who have an acute deterioration in H Serum electrolyte results reveal hypokalemia and
arterial blood gas (ABG) values hypochloremia.
H Blood cultures, Gram stain, and sputum cultures
Common characteristics show the pathogen. (See Identifying respiratory
H Rapid breathing failure.)
H Restlessness Imaging
H Anxiety H Chest X-rays may show underlying pulmonary dis-
H Depression eases or conditions, such as emphysema, atelectasis,
H Lethargy lesions, pneumothorax, infiltrates, and effusions.
H Agitation Diagnostic procedures
H Confusion H Electrocardiography may show arrhythmias, cor pul-
monale, and myocardial ischemia.
Complications H Pulse oximetry may show decreased arterial oxygen
H Tissue hypoxia saturation.
H Chronic respiratory acidosis

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H Pulmonary artery catheterization may show pulmo-
nary or cardiovascular causes of acute respiratory
failure.
Treatment
General
H Mechanical ventilation with an endotracheal (ET) or
a tracheostomy tube
H High-frequency ventilation, if the patient doesnt
respond to conventional mechanical ventilation
H Fluid restriction with heart failure
H Activity as tolerated
Medications
H Cautious oxygen therapy to increase partial pressure
of arterial oxygen
H Antacids
H Histamine-receptor antagonists, such as cimetidine
and ranitidine
H Antibiotics, as appropriate
H Bronchodilators, such as albuterol and theophylline
H Corticosteroids
H Positive inotropics, such as digoxin and milrinone
H Vasopressors, such as dopamine and dobutamine
H Diuretics, such as furosemide and torsemide
Surgery
H Possible tracheostomy
Nursing considerations
Key outcomes
The patient will:
H maintain a patent airway
H maintain adequate ventilation
H use a support system to assist with coping
H maintain skin integrity
H express feelings of increased comfort
H modify lifestyle to minimize the risk of decreased
tissue perfusion.
Nursing interventions
H Give prescribed drugs.
H Orient the patient frequently.
H Administer oxygen, as ordered.
H Maintain a patent airway.
H Encourage pursed-lip breathing.
H Encourage the use of an incentive spirometer.
H Reposition the patient every 1 to 2 hours.
H Help clear the patients secretions with postural
drainage and chest physiotherapy.
H Assist with or perform oral hygiene.
H Position the patient for comfort and optimal gas
exchange.
H Maintain normothermia.
H Schedule care to provide frequent rest periods.
Identifying respiratory failure
Use these measurements to identify respiratory failure:
H vital capacity less than 15 cc/kg
H tidal volume less than 3 cc/kg
H negative inspiratory force less than 25 cm H2O
H respiratory rate more than twice the normal rate
H diminished partial pressure of arterial oxygen despite
increased fraction of inspired oxygen
H elevated partial pressure of arterial carbon dioxide with
pH lower than 7.25.
If the patient requires mechanical
ventilation
H Obtain blood samples for ABG analysis, as ordered.
H Suction the trachea after hyperoxygenation, as
needed.
H Provide humidification.
H Secure the ET tube per facility policy.
H Prevent infection.
H Prevent tracheal erosion.
H Maintain skin integrity.
H Provide alternative communication means.
H Provide sedation, as necessary.
Monitoring
H Vital signs and pulse oximetry
H Intake and output
H Laboratory studies
H Daily weight
H Cardiac rate and rhythm
H Respiratory status (breath sounds and ABG results)
H Chest X-ray results
H Complications
H Sputum quality, consistency, and color
H Signs and symptoms of infection
If the patient requires mechanical
ventilation
H Ventilator settings
H Cuff pressures
H Complications of mechanical ventilation
H ET tube position and patency
H Signs and symptoms of stress ulcers
Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medications and possible adverse reactions
H when to notify the physician
H smoking cessation, if appropriate
H communication techniques, if intubated
H signs and symptoms of respiratory infection.
Discharge planning
H Refer the patient to a smoking-cessation program, if
applicable.
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Physical findings
Acute tubular necrosis H Acute tubular necrosis usually in advanced stage
when diagnosis made
H Evidence of bleeding abnormalities, such as petechi-
Overview ae and ecchymosis
H Dry, pruritic skin
Description H Dry mucous membranes
H Injury to the nephrons tubular segment resulting H Uremic breath
from ischemic or nephrotoxic injury and causing H Cardiac arrhythmia, if hyperkalemic
renal failure and uremic syndrome H Muscle weakness
H Also known as acute tubulointerstitial nephritis
Test results
Pathophysiology Laboratory
H In ischemic injury, circulatory collapse, severe hy- H Urinary sediment contains red blood cells (RBCs)
potension, trauma, hemorrhage, dehydration, car- and casts.
diogenic or septic shock, surgery, anesthetics, and H Urine specific gravity is low (1.010).
reactions to transfusions may cause disruption of H Urine osmolality is low (less than 400 mOsm/kg).
blood flow to the kidneys. H Urine sodium level is high(40 to 60 mEq/L).
H Nephrotoxic injury may follow ingestion of certain H Potassium, blood urea nitrogen, and serum creati-
chemical agents, such as contrast medium or antibi- nine levels are elevated.
otics, or result from a hypersensitive reaction of the H Complete blood count shows decreased RBC count,
kidneys. hemoglobin level, and hematocrit.
H Metabolic acidosis is evident from blood gas and
Causes electrolyte study results.
H Diseased tubular epithelium Diagnostic procedures
H Obstructed urine flow H Electrocardiography may show arrhythmias and, with
H Ischemic injury to glomerular epithelial cells or vas- hyperkalemia, a widening QRS complex, disappear-
cular endothelium ing P waves, and tall, peaked T waves.
Incidence
H Accounts for about 75% of acute renal failure cases Treatment
H Most common cause of acute renal failure in critical-
ly ill patients General
Acute phase
Common characteristics H Vigorous supportive measures until normal kidney
H Decreased urine output function resumes
H Hyperkalemia Long-term management
H Uremic syndrome with oliguria or, rarely, anuria H Daily replacement of projected and calculated fluid
loss (including insensible loss)
Complications H Peritoneal dialysis or hemodialysis if the patient is
H Heart failure catabolic or if hyperkalemia and fluid volume over-
H Uremic pericarditis load arent controlled by other measures
H Pulmonary edema H Fluid restriction
H Uremic lung H Low-sodium, low-potassium diet
H Anemia H Rest periods when fatigued
H Anorexia, intractable vomiting
H Poor wound healing due to debilitation Medications
H Diuretics
H Transfusion of packed RBCs
ALERT
H Epoetin alfa
Fever and chills may signal the onset of an infec- H Antibiotics, as appropriate
tion, the leading cause of death in acute tubular H Emergency I.V. administration of 50% glucose, regu-
necrosis. lar insulin, and sodium bicarbonate (with hyper-
kalemia)
H Sodium polystyrene sulfonate with sorbitol by mouth
Assessment or enema (with hyperkalemia)
History
H Ischemic or nephrotoxic injury
H Low urine output (less than 400 ml/24 hours)
H Fever and chills

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Nursing considerations
Key outcomes
The patient will:
H maintain fluid balance
H maintain hemodynamic stability
H maintain urine specific gravity within the designated
limits
H have improved kidney function.

Nursing interventions
H Give prescribed drugs and blood products.
H Restrict foods containing high sodium and potassium
levels.
H Use aseptic technique, particularly when handling
catheters.
H Perform passive range-of-motion exercises.
H Provide good skin care.

Monitoring
H Intake and output
H Vital signs
H Laboratory studies
H Complications

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H signs of infection and when to report them to the
physician
H dietary restrictions
H how to set goals that are realistic for the patients
prognosis.
Discharge planning
H Refer the patient to appropriate supportive services
or social service.

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Adrenal hypofunction H Family history of autoimmune disease (may predis-

pose the patient to Addisons disease and other
endocrinopathies)
Secondary hypofunction
Overview H Hypopituitarism
H Abrupt withdrawal of long-term corticosteroid
Description therapy
H Primary adrenal hypofunction or insufficiency (Addi- H Removal of a corticotropin-secreting tumor
sons disease) originating within the adrenal gland Adrenal crisis
and characterized by the decreased secretion of min- H Exhausted body stores of glucocorticoids in a patient
eralocorticoids, glucocorticoids, and androgens with adrenal hypofunction after trauma, surgery, or
H Secondary adrenal hypofunction due to a disorder other physiologic stress
outside the gland such as impaired pituitary secre-
tion of corticotropin; characterized by decreased glu- Incidence
cocorticoid secretion Primary hypofunction
H Adrenal crisis (addisonian crisis), a critical deficien- H Relatively uncommon
cy of mineralocorticoids and glucocorticoids gener- H Can occur at any age and in both sexes
ally following acute stress, sepsis, trauma, surgery, or Autoimmune Addisons disease
the omission of steroid therapy in patients who have H Most common in white females (genetic predisposi-
chronic adrenal insufficiency; adrenal crisis, a med- tion likely)
ical emergency that needs immediate, vigorous treat- H More common in patients with a familial predisposi-
ment tion to autoimmune endocrine diseases
Pathophysiology
Special populations
H Dysfunction of the adrenal gland results from the
partial or complete destruction of the adrenal cortex. Most people with Addisons disease are diagnosed
H It manifests as a clinical syndrome in which the in their 20s to 40s.
symptoms are associated with deficient production of
the adrenocortical hormones cortisol, aldosterone,
and androgen. Common characteristics
H High levels of corticotropin and corticotropin- Primary hypofunction
releasing hormone are produced. H Conspicuous bronze color of the skin
H Addisons disease involves all zones of the cortex, H Darkening of scars, areas of vitiligo (absence of pig-
causing deficiencies of the adrenocortical secretions, mentation), and increased pigmentation of the mu-
glucocorticoids, androgens, and mineralocorticoids. cous membranes, especially the buccal mucosa
H Cortisol deficiency causes decreased liver gluconeo- H Decreased tolerance for even minor stress
genesis (the formation of glucose from molecules H Fasting hypoglycemia
that arent carbohydrates); resulting low blood glu- H Craving for salty food
cose levels can become dangerously low in patients Secondary hypofunction
who take insulin routinely. H Similar to primary hypofunction, but without hyper-
H An aldosterone deficiency causes increased renal pigmentation
sodium loss and enhances potassium reabsorption. Addisonian crisis
H Hypotension then develops due to sodium excretion. H Profound weakness and fatigue
H Angiotensin II production increases due to the low H Nausea, vomiting, and dehydration
plasma volume and decreased arteriolar pressure. H Hypotension
H Androgen deficiency may decrease hair growth in H High fever followed by hypothermia (occasionally)
axillary and pubic areas (less noticeable in men)
as well as on the extremities of women. Complications
H Hyperpyrexia
Causes H Psychotic reactions
Primary hypofunction H Deficient or excessive steroid treatment
H Autoimmune process in which circulating antibodies H Shock
react specifically against the adrenal tissue H Profound hypoglycemia
H Tuberculosis (once the chief cause, now responsible H Ultimate vascular collapse, renal shutdown, coma,
for less than 20% of adult cases) and death (if untreated)
H Bilateral adrenalectomy
H Hemorrhage into the adrenal gland
H Neoplasms
H Infections (histoplasmosis, cytomegalovirus)

22 Adrenal hypofunction
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Assessment Nursing considerations

History Key outcomes
H Synthetic steroid use, adrenal surgery, or recent The patient will:
infection H maintain stable vital signs
H Muscle weakness H maintain an adequate fluid balance
H Fatigue H remain free from signs and symptoms of infection
H Weight loss H develop adequate coping skills.
H Craving for salty food
H Decreased tolerance for stress Nursing interventions
H GI disturbances H Until onset of mineralocorticoid effect, encourage
H Dehydration fluids to replace excessive fluid loss.
H Amenorrhea (in females) H Arrange for a diet that maintains sodium and potassi-
H Impotence (in males) um balances; if the patient is anorexic, suggest six
small meals per day to increase caloric intake.
Physical findings H Observe for cushingoid signs such as fluid retention
H Poor coordination around the eyes and face.
H Decreased axillary and pubic hair (in females) H Check for petechiae.
H Bronze coloration of the skin, darkening of scars H If the patient receives glucocorticoids alone, observe
H Areas of vitiligo for orthostatic hypotension or electrolyte abnormali-
H Increased pigmentation of mucous membranes ties.
H Weak, irregular pulse
H Hypotension Monitoring
H Vital signs
Test results H Signs of shock (decreased level of consciousness and
Laboratory urine output)
H Rapid corticotropin stimulation test: low corticotro- H Hyperkalemia before treatment; hypokalemia after
pin level indicates a secondary disorder; elevated treatment
level indicates a primary disorder. H Cardiac rhythm
H Plasma cortisol level is decreased (less than 10 H Blood glucose levels
mcg/dl in the morning; less in the evening). H Daily weight
H Serum sodium and fasting blood glucose levels are H Intake and output
decreased.
H Serum potassium, calcium, and blood urea nitrogen
levels are increased. Patient teaching
H Hematocrit is elevated and lymphocyte and eosino-
phil counts are increased. Be sure to cover:
Imaging H lifelong steroid therapy requirement
H Chest X-ray shows small heart. H symptoms of steroid overdose (swelling, weight gain)
H Computed tomography scan of the abdomen shows and steroid underdose (lethargy, weakness)
adrenal calcification (if the cause is infectious). H risk for developing diabetes
H dosage may need to be increased during times of
stress or illness (when the patient has a cold, for
Treatment example)
H infection, injury, or profuse sweating in hot weather
General may precipitate adrenal crisis
H I.V. fluids H importance of carrying a medical identification card
H Periods of rest that states the patient is on steroid therapy (name of
H Small, frequent, high-protein meals the drug and its dosage should be included on the
card)
Medications H how to give a hydrocortisone injection and to keep
H Lifelong corticosteroid replacement, usually with an emergency kit containing hydrocortisone in a pre-
cortisone or hydrocortisone pared syringe available for use in times of stress
H Oral fludrocortisone H stress-management techniques.
H Hydrocortisone
H I.V. saline and glucose solutions (for adrenal crisis) Discharge planning
H Refer the patient to the National Adrenal Diseases
Foundation for support and information.

Adrenal hypofunction 23
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Adrenogenital fusion and an enlarged clitoris with a urethral open-

ing at its base.)
syndrome Salt-losing CAH
FEMALES
H More complete virilization than the simple form
H Results in development of male external genitalia
Overview without testes
MALES
Description H No external genital abnormalities
H A group of disorders resulting from hyperplasia of H Difficult immediate neonatal diagnosis; commonly
the adrenal cortex delayed until the infant develops severe systemic
H May be inherited (congenital adrenal hyperplasia symptoms
[CAH]) or acquired, usually as a result of an adrenal
tumor (adrenal virilism) Complications
H May cause fatal adrenal crisis in neonates (salt-losing H Hypertension
CAH) H Hyperkalemic infertility
H Adrenal tumor
Pathophysiology H Adrenal crisis
H Deficiencies occur in the enzymes needed for adre- H Altered growth, external genitalia, and sexual
nocortical secretion of cortisol and, possibly, aldo- maturity
sterone. Salt-losing CAH
H Compensatory secretion of corticotropin produces H Cardiovascular collapse
varying degrees of adrenal hyperplasia. H Cardiac arrest
Simple virilizing CAH
H Deficiency of the enzyme 21-hydroxylase results in
underproduction of cortisol. Assessment
H This cortisol deficiency stimulates increased secre-
tion of corticotropin, producing large amounts of History
cortisol precursors and androgens that dont require Simple virilizing CAH
21-hydroxylase for synthesis. H Failure to begin menstruation
Salt-losing CAH H Frequent erections at an early age
H 21-hydroxylase is almost completely absent. Salt-losing CAH
H Corticotropin secretion increases, causing excessive H Apathy, failure to eat, and diarrhea (in infants)
production of cortisol precursors, including salt- H Symptoms of adrenal crisis in the first week of life
wasting compounds. (vomiting, dehydration from hyponatremia, hyper-
H Plasma cortisol and aldosterone levels both de- kalemia)
pendent on 21-hydroxylase fall precipitously and,
in combination with the excessive production of salt- Physical findings
wasting compounds, precipitate acute adrenal crisis. H In CAH, pseudohermaphroditism in females or pre-
H Corticotropin hypersecretion stimulates adrenal an- cocious puberty in both sexes
drogens and produces masculinization. Salt-losing CAH
H Signs of progressive virilization at an early age: early
Causes appearance of pubic and axillary hair, deep voice,
H Transmitted as an autosomal recessive trait acne, facial hair
H Small testes
Incidence H Possible greater height than other children of the
H Acquired adrenal virilism: rare and affects twice as same age
many females as males
Test results
Special populations Laboratory
H Plasma 17-ketosteroid (17-KS) levels , which can be
CAH is the most prevalent adrenal disorder in in- suppressed by administering oral dexamethasone,
fants and children; simple virilizing CAH and salt- are elevated.
losing CAH are the most common forms. H Urine levels of hormone metabolites, particularly
pregnanetriol, are elevated.
H Plasma 17-hydroxyprogesterone level is elevated.
Common characteristics H Urine levels of 17-hydroxycorticosteroids are normal
Simple virilizing CAH or decreased.
H Ambiguous genitalia but normal genital tract and go- H Plasma aldosterone and cortisol levels are de-
nads (Female neonates may present with labioscrotal creased.
H Serum DHEA sulfate levels are high.

24 Adrenogenital syndrome
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Special populations Monitoring

H Body weight
Adrenal hypofunction or adrenal crisis in the first H Blood pressure
week of life suggests salt-losing CAH. Hyperkale- H Serum electrolyte levels
mia, hyponatremia, and hypochloremia with ex- H Edema, weakness, and hypertension for the patient
cessive urinary 17-KS and pregnanetriol and de- receiving desoxycorticosterone or fludrocortisone
creased urinary aldosterone levels confirm it.

Diagnostic procedures Patient teaching

H Gonadal biopsy and chromosomal studies confirm
hermaphrodism.
Other
H Sex chromatin and karyotype studies determine the
genetic sex of patients with ambiguous external geni-
talia.
H X-ray evaluates accelerated bone aging.
Treatment
General
H Well-balanced diet
H No activity restriction
Medications
Simple virilizing CAH
H Daily administration of cortisone or hydrocortisone
Salt-losing CAH with patient in adrenal crisis
H Immediate I.V. sodium chloride and glucose infusion
H Desoxycorticosterone I.M. and hydrocortisone I.V.
H Maintenance includes mineralocorticoid (desoxycor-
ticosterone, fludrocortisone, or both) and glucocor-
ticoid (cortisone or hydrocortisone) replacement
Surgery
H Reconstructive surgery based on the determined sex
and external genitalia
Be sure to cover:
H possible adverse effects (cushingoid symptoms) of
long-term therapy (lifelong maintenance therapy with
hydrocortisone, cortisone, or the mineralocorticoid
fludrocortisone is essential)
H importance of not withdrawing therapeutic drugs
suddenly because potentially fatal adrenal hypofunc-
tion will result
H need to report stress and infection, which require in-
creased steroid dosages
H importance of carrying a medical identification card
that states the patient is on steroid therapy (name of
the drug and its dosage should be included on the
card)
H risk of developing diabetes due to long-term
cortisone therapy.
Discharge planning
H Refer the patient for psychological counseling to help
accept this disorder.

Nursing considerations
Key outcomes
The patient will:
H maintain stable vital signs
H maintain adequate fluid balance
H have normal laboratory test results
H express understanding of the disorder and treatment
modality, as will his family.
Nursing interventions
H Maintain I.V. access, infuse fluids, and give steroids,
as ordered.
H Watch for cyanosis, hypotension, tachycardia, tachyp-
nea, and signs of shock.
H Minimize external stressors.
H If a child is receiving maintenance therapy with
steroid injections, rotate I.M. injection sites to
prevent atrophy; tell the parents to do the same.

Adrenogenital syndrome 25
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Causes
Age-related macular H Unknown

degeneration H Genetic in origin

Risk factors
H Smoking
Overview H Age
H Race
Description H High blood pressure
H Deterioration of the macular portion of the retina, H Vascular disease
which is responsible for detailed vision H High intake of saturated fat and cholesterol
H May be atrophic, also called involutional or dry H Farsightedness
H May be exudative, also called hemorrhagic or wet H Exposure to sunlight
H No cure for atrophic form
H Commonly affects both eyes Incidence
H Also known as AMD H Affects as many as 15 million Americans
H Leading cause of vision loss in people older than age
Pathophysiology 60 in the United States
H Pathologic changes occur primarily in the retinal pig- H Irreversible central vision loss in at least 10% of
ment epithelium, Bruchs membrane, and choriocap- elderly people
illaries in the macular region that result from the H Atrophic form in about 85% of patients
hardening and obstruction of retinal arteries. H More common in whites, but affects all races
H Formation of new blood vessels in the macular area
obscures central vision. Common characteristics
H Vision loss occurs as the retinal pigment epithelium H Decreased central vision, for near and distance (see
detaches and becomes atrophic. How AMD affects central vision)
H Exudative macular degeneration develops as new H Progressive worsening
blood vessels in the choroid project through abnor- H Blind spots
malities in Bruchs membrane, invading the potential
space underneath the retinal pigment epithelium. Complications
H The vessels leak, and fluid in the retinal pigment ep- H Blindness
ithelium increases, resulting in blurry vision. H Nystagmus

How AMD affects central vision

Central vision occurs in the macula and involves the ability
to perceive sharp, detailed images. At the center of the mac-
ula is the fovea containing the highest concentration of
rods and cones and the most light-sensitive portion of
the macula.
Light entering the cornea and lens are focused on the
fovea. If any part of the macula deteriorates, the eye must
rely on the less-sensitive, outer portion of the retina, which
is responsible for peripheral vision.
With age-related macular degeneration (AMD), grayness,
haziness, or a blind spot may appear in the area of central
vision. Words may be blurred on a page; straight lines may
appear to have kinks in them; colors may seem dimmer.

Lens

Visual
axis

Cornea

Iris

Macula
Fovea
Optic nerve

26 Age-related macular degeneration

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Monitoring
Assessment H Visual acuity
H Environment (for safety purposes)
History
H Blank spot seen in the center of a page (scotoma)
while reading Patient teaching
H Central vision that blurs intermittently and has gradu-
ally worsened Be sure to cover:
H Straight lines appearing distorted H ways to modify the home environment for safety
H Letters appearing fragmented H effects on peripheral vision.

Physical findings Discharge planning

H Tiny yellowish spots (drusen) beneath retina H Refer the patient to the American Foundation for
the Blind or Associated Services for the Blind, as
Test results indicated.
Diagnostic procedures H Refer the patient to a local support group.
H Indirect ophthalmoscopy may show changes in the
macular region of the fundus.
H Fluorescein angiography may show leaking vessels in
subretinal neovascular net.
H Amsler grid test may detect visual distortion.

Treatment
General
H Laser treatment, if leaking blood vessels have devel-
oped away from the fovea
H Diet high in vitamins A, C, and E; beta-carotene; and
zinc
H Activity restrictions based on visual acuity

Medications
H Copper and zinc supplements
H Lutein, vitamins C and E, and beta-carotene

Surgery
H In exudative form, argon laser photocoagulation
(may slow the progression of severe visual loss)

Nursing considerations
Key outcomes
The patient will:
H express feelings and concerns over diminishing eye-
sight
H sustain no harm or injury
H verbalize understanding of the condition and treat-
ment
H maintain optimal visual function or adapt as neces-
sary.
Nursing interventions
H Help the patient obtain optical aids such as magni-
fiers.
H Offer the patient emotional support.
H Encourage expression of fears and concerns.

Age-related macular degeneration 27

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Alcoholism of 12- to 17-year-olds have serious drinking prob-

lems. Research also suggests that alcoholism affects
2% to 10% of adults older than age 60.
Overview
Common characteristics
Description H Hide or deny addiction
H Chronic disorder of uncontrolled intake of alcoholic H May temporarily manage to maintain a functional
beverages lifestyle
H Interferes with physical and mental health, social and
familial relationships, and occupational responsibili- Complications
ties H Cardiomyopathy
H Pneumonia
Pathophysiology H Cirrhosis
H Alcohol is soluble in water and lipids and permeates H Esophageal varices
all body tissues. H Pancreatitis
H Liver metabolizes 90% of alcohol absorbed and is the H Alcoholic dementia
most severely affected organ; hepatic steatosis fol- H Wernickes encephalopathy
lowed by hepatic fibrosis is evident days after heavy H Seizure disorder
drinking. H Depression
H Laennecs cirrhosis may develop after inflammatory H Multiple substance abuse
response (alcoholic hepatitis) or in absence of in- H Hypoglycemia
flammation, as a consequence of direct activation of H Leg and foot ulcers
lipocytes (Ito cells). H Suicide and homicide
H Lactic acidosis and excess uric acid is promoted; glu- H Death
coneogenesis, B-oxidation of fatty acids, and the
Krebs cycle are opposed; and hypoglycemia and hy-
perlipidemia develop. Assessment
H Toxicity of cells occurs through reduction of mito-
chondrial oxygenation utilization, depletion of de- History
oxyribonucleic acid, and other actions. H Need for daily or episodic alcohol use for adequate
function
Causes H Inability to discontinue or reduce alcohol intake
H Biological factors H Episodes of anesthesia or amnesia during intoxica-
H Psychological factors tion
H Sociocultural factors H Episodes of violence during intoxication
H Interference with social and familial relationships
Risk factors and occupational responsibilities
H Male gender H Malaise, dyspepsia, mood swings or depression, and
H Low socioeconomic status an increased incidence of infection
H Family history H Secretive behavior
H Depression
H Anxiety Physical findings
H History of other substance abuse disorders H Poor personal hygiene
H Unusually high tolerance for sedatives and opioids
Incidence H Signs of nutritional deficiency
H Affects all social and economic groups H Signs of injury
H 10% of the population accounts for 50% of all alco- H Withdrawal signs and symptoms
hol consumed H Major motor seizures
H About 13% of all adults older than age 18 have suf-
fered from alcohol abuse or dependence DSM-IV-TR criteria
H Males are two to five times more likely to abuse alco- A diagnosis is confirmed when the patient meets at least
hol than females three of these signs and symptoms:
H Occurs at all stages of the life cycle, beginning as H more alcohol ingested than intended
early as elementary school age H persistent desire or efforts to diminish alcohol use
H Prevalent in 20% of adult hospital inpatients H excessive time spent obtaining alcohol
H frequent intoxication or withdrawal symptoms
H impairment of social, occupational, or recreational
Special populations
activities
Prevalence of drinking is highest between ages 21
and 34, but current statistics show that up to 19%

28 Alcoholism
9400A.qxd 8/2/12 4:21 PM Page 29

H continued alcohol consumption despite knowledge

of a social, psychological, or physical problem thats
caused or exacerbated by alcohol use
H marked tolerance
H characteristic withdrawal symptoms
H alcohol used to relieve or avoid withdrawal symp-
toms
H persistent symptoms for at least 1 month or recur-
rence over a longer time.
Test results
Laboratory
H Blood alcohol tests show levels of at least 0.10%
weight/volume (200 mg/dl).
H Serum electrolyte levels are abnormal.
H Serum ammonia levels are increased.
H Serum amylase levels are increased.
H Urine toxicology may show abuses of other drugs.
H Liver function study results are abnormal.
Other
H CAGE screening test: two affirmative responses make
patient 7 times more likely to be alcohol dependent.
H Alcohol disorders identification test (AUDIT): score
greater than 8 indicates alcohol dependency.
H Michigan alcohol screening test (MAST): score
greater than 5 indicates alcohol dependency.
Treatment
General
Immediate
H Support for respiration
H Prevention of aspiration of vomitus
H Replacement of fluids
H Administration of I.V. glucose
H Correction of hypothermia or acidosis
H Treatment of trauma, infection, or GI bleeding
Long-term
H Total abstinence
H Detoxification, rehabilitation, and aftercare program
H Supportive counseling
H Individual, group, or family psychotherapy
H Ongoing support groups
H Well-balanced diet
H Safety precautions, including preventing aspiration
of vomitus
H Seizure precautions
Nursing considerations
Key outcomes
The patient (or family) will:
H report feeling safe in hospital environment
H join gradually in self-care and the decision-making
process
H engage in appropriate social interaction with others
H demonstrate a decrease in negative self-evaluation
verbally and behaviorally
H identify support systems to assist them and partici-
pate in mobilizing these systems.
Nursing interventions
H Institute seizure precautions.
H Give prescribed drugs.
H Orient the patient to reality.
H Maintain a calm environment, minimizing noise and
shadows.
H Avoid restraints, unless necessary for protection.
H Use a nonthreatening approach.
Monitoring
H Mental status
H Vital signs
H Safety measures
H Nutritional and hydration status
H Intake and output
Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H alcohol abstinence
H plan for relapse
H medication administration, dosage, and possible
adverse effects
H effects of disorder on significant others.
Discharge planning
H Refer the patient to a rehabilitation program.
H Refer the patient to social services.
H Refer the patient to support services.
H Refer the patient to personal and family counseling.

Medications
H Anticonvulsants
H Antiemetics
H Antidiarrheals
H Tranquilizers, particularly benzodiazepines
H Naltrexone
H Antipsychotics
H Daily oral disulfiram
H Vitamin supplements

Alcoholism 29
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Allergic purpura Henoch-Schnlein syndrome

H Transient or severe colic
H Tenesmus (spasmodic contraction of the anal
sphincter)
Overview H GI bleeding
H Rheumatoid pains and periarticular effusions, usually
Description affecting the legs and feet
H An acute or chronic vascular inflammation affecting
the skin, joints, and GI and genitourinary (GU) Complications
tracts, in association with allergy symptoms H Renal disease (renal failure and acute glomeru-
H Purpura associated with other conditions such as lonephritis)
erythema nodosum H Hypertension
H A nonthrombocytopenic purpura
H Known as Henoch-Schnlein syndrome or anaphy-
lactoid purpura when it primarily affects the GI tract Assessment
and is accompanied by joint pain
History
Pathophysiology H Bacterial infection or exposure to allergen
H An autoimmune reaction triggered by a bacterial in- H Moderate and irregular fever
fection is directed against vascular walls. H Headache
H Inflammation of the veins and capillaries disrupts the H Anorexia
vascular wall, resulting in loss of red blood cells and H Pruritus and paresthesia in areas of lesions
bleeding and leakage into the skin and mucous
membranes. Physical findings
H Characteristic lesions that usually appear in symmet-
Causes rical patterns on the arms, legs, and buttocks
H Bacterial infection (particularly streptococcal infec- H In children, urticarial skin lesions that expand and
tion) become hemorrhagic
H Allergic reactions to some drugs and vaccines, insect H Possibly scattered petechiae on the legs, buttocks,
bites, and foods (such as wheat, eggs, milk, and and perineum
chocolate) H Localized edema of the hands, feet, or scalp

Incidence Test results

H Affects more males than females
H Most prevalent in children ages 3 to 7
Common characteristics
H Skin lesions that are purple, macular, ecchymotic,
and of varying size and are caused by vascular leak-
age into the skin and mucous membranes (see Iden-
tifying purpuric lesions)
Identifying purpuric lesions
Lesions of allergic purpura, such as those pictured on the
foot and leg below, characteristically vary in size.
Laboratory
H Results of tests for blood in the urine and stool may
be positive.
H Increased blood urea nitrogen and creatinine levels
may indicate renal involvement.
ALERT
No laboratory test clearly identifies allergic purpu-
ra (although white blood cell count and erythrocyte
sedimentation rate are elevated).
Imaging
H Small-bowel X-rays may reveal areas of transient
edema.

Treatment
General
H Symptomatic

Medications
H Steroids
H Analgesics

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Nursing considerations
Key outcomes
The patient will:
H express feelings of comfort and relief of pain
H exhibit improved or healed lesions
H identify precipitating factors with appropriate skin
care regimen.
Nursing interventions
H Encourage maintenance of an elimination diet to
help identify specific allergenic foods.
H Provide analgesics, as needed.
H Provide passive range-of-motion exercises, if appro-
priate.
H Provide emotional support and reassurance, espe-
cially if the patient is temporarily disfigured by florid
skin lesions.
Monitoring
H Condition and number of skin lesions
H Level of pain
H GI and GU complications

Patient teaching
Be sure to cover:
H need for the patient to immediately report recur-
rence of symptoms (most common about 6 weeks
after initial symptoms)
H importance of returning for follow-up urinalysis as
scheduled.

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Allergic rhinitis Perennial allergic rhinitis

H Chronic and extensive nasal obstruction or stuffiness

Physical findings
Overview Seasonal allergic rhinitis
H Pale, cyanotic, edematous nasal mucosa
Description H Red and edematous eyelids and conjunctivae
H An immune response of the upper airways triggered H Excessive lacrimation
by inhaled airborne allergens Perennial allergic rhinitis
H Seasonal allergic rhinitis: an immunoglobulin (Ig) E- H Nasal polyps
mediated type I hypersensitivity response to an envi- H Dark circles under the eyes (allergic shiners)
ronmental antigen (allergen) in a genetically suscep-
tible person Test results
H Perennial rhinitis: inhaled allergens provoke antigen Laboratory
responses that produce signs and symptoms H Sputum and nasal secretions show a high number of
year-round eosinophils.
H IgE levels are normal or elevated, possibly linked to
Pathophysiology seasonal overproduction of interleukin-4 and -5
H The bodys immune system overresponds to common (involved in the allergic inflammatory process).
allergens in the nose.
H Antibodies attach to mast cells, which release several
chemicals, including histamine, which cause dilation Treatment
of blood vessels, skin redness, and swollen mem-
branes in the nose. General
H Elimination of environmental antigens, if possible
Causes H Increased fluid intake to loosen secretions
Seasonal allergic rhinitis H Restriction of activities in areas of allergen exposure
H Tree pollens (in spring)
H Grass and weed pollens (in summer) Medications
H Weed pollens (in fall) H Antihistamines, such as cetirizine, diphenhydramine,
H Mold spores (occasionally, in summer and fall) and loratadine
Perennial allergic rhinitis H Intranasal corticosteroids, such as budesonide and
H House dust and dust mites triamcinolone
H Molds H Leukotriene receptor antagonists such as mon-
H Animal dander telukast
H Tobacco smoke H Nasal decongestants, such as oxymetazoline and
H Processed materials or industrial chemicals pseudoephedrine
Long-term management
Incidence H Immunotherapy or desensitization with injections of
H Affects more than 20 million Americans allergen extracts administered before or during the
H Can affect anyone at any age allergy season or perennially
H Most prevalent in young children and adolescents

Common characteristics Nursing considerations

H Swollen nasal membranes
Key outcomes
Complications The patient (or family) will:
H Secondary sinus and middle ear infections H maintain current health status
H Nasal polyps H verbalize feelings and concerns
H express feelings of increased comfort.

Assessment Nursing interventions

History
Seasonal allergic rhinitis
H Paroxysmal sneezing, profuse watery rhinorrhea
H Nasal obstruction or congestion
H Pruritus of the nose and eyes
H Headache or sinus pain
H Itchy throat, malaise, and fever
H Implement measures to relieve signs and symptoms
and increase the patients comfort.
H Encourage increased fluid intake to loosen secre-
tions.
H Elevate the head of the bed and provide humidifica-
tion to ease breathing.

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ALERT
Before giving a desensitization injection, assess the
patients symptoms. After giving the injection, ob-
serve him for 30 minutes to detect adverse reac-
tions, including anaphylaxis and severe localized
erythema. Make sure epinephrine and emergency
resuscitation equipment are available.

Monitoring
H Compliance with the prescribed drug regimen
H Changes in control of signs and symptoms
H Indications of drug misuse

Patient teaching
Be sure to cover:
H importance of calling the physician if the patient ex-
periences a delayed reaction to the desensitizing in-
jections
H reduction of environmental exposure to airborne al-
lergens
H skin protectant applications
H possible lifestyle changes, such as relocation to a
pollen-free area either seasonally or year-round, in
severe and resistant allergic rhinitis
H medication administration, dosage, and possible
adverse effects.

Allergic rhinitis 33
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Alopecia H Follicular lichen planus

H Severe bacterial or viral infections

Incidence
Overview H Affects males more than females
H Occurs most commonly in males older than age 50
Description in male-pattern alopecia
H More commonly known as hair loss, typically occurs H Rises with increasing age in male-pattern alopecia
on the scalp; less common and conspicuous else- H Occurs to some degree in 37% of postmenopausal
where on the body women
H Can be irreversible because scarring alopecia usually
destroys hair follicle Common characteristics
H Nonscarring form (noncicatricial alopecia): hair H Hair loss
generally regrows
H Most common form of nonscarring alopecia known Complications
as male-pattern alopecia or androcentric alopecia H Impaired self-image
H Telogen effluvium: a diffuse alopecia in which nu-
merous hair follicles simultaneously change from the
growing anagen phase to the resting telogen phase of Assessment
the hair growth cycle
H Alopecia areata (idiopathic form): a generally re- History
versible and self-limiting disorder most prevalent in Male-pattern alopecia
young and middle-aged adults of both sexes H Presence of predisposing factors
H Time of onset, degree of baldness, speed with which H Family history of hair loss
it spreads, and pattern of hair loss dependent on ge- H Gradual onset of hair loss
netic predisposition H Typically describes hairline as receding and his
H Poor prognosis for regrowth with hair loss that per- crown becoming bald
sists for more than 1 year Female-pattern alopecia
H Typically describes a widening of her part and in-
Pathophysiology creasing visibility of her front scalp or crown
H In male-pattern alopecia, a genetically predisposed Telogen effluvium
response to androgens causes transformation of the H Loss of about 400 hairs per day, which is four to five
androgen-sensitive follicles into vellus follicles; nor- times greater than the normal daily hair loss
mal hair is shed and replaced by fine, light, short Alopecia areata
hair. H Sudden loss of hair
H In female-pattern alopecia, theres usually an eleva-
tion in serum adrenal androgen dehydroepian- Physical findings
drosterone sulfate. H Small patches of visible scalp or entire scalp visible
(alopecia totalis); may involve the entire body
Causes (alopecia universalis)
Nonscarring alopecia H Generally, normal scalp appearance
H Genetic predisposition H Exclamation point hairs (loose hairs with dark,
H Androgen response rough, brushlike tips on narrow, less pigmented
H Aging shafts) at the periphery of new patches
H Radiation H Regrowth initially as fine, white, downy hair; re-
H Chemotherapy placed by normal hair
H Drugs (see Cancer drugs that cause alopecia)
H Bacterial and fungal infections Test results
H Psoriasis Laboratory
H Seborrhea H Direct microscopic examination shows structural
H Endocrine disorders abnormalities or signs of infection.
H Excess vitamin A Diagnostic procedures
Scarring alopecia TELOGEN EFFLUVIUM
H Physical or chemical trauma H Pluck or pull test reveals positive results if more than
H Radiation four hairs come out.
H Chemotherapy H Woods lamp examination shows presence of fungal
H Chronic tension on a hair shaft infection.
H Destructive skin tumors H Trichogram shows abnormal ratio of anagen to
H Granulomas telogen hairs.
H Lupus erythematosus H Scalp biopsy shows hair phase and the extent of
H Scleroderma structural damage.

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Cancer drugs that cause alopecia

Certain cancer drugs can cause hair loss ranging from sporadic thinning to complete baldness. Some drugs damage hair fol-
licles and cause hair roots to atrophy.
Mild alopecia Moderate alopecia Severe alopecia
H bleomycin H busulfan H cyclophosphamide
H carmustine H etoposide H daunorubicin
H fluorouracil H floxuridine H doxorubicin
H hydroxyurea H methotrexate H vinblastine
H melphalan H mitomycin H vincristine

Treatment H For the patient undergoing radiation therapy or

chemotherapy with drugs that cause alopecia, sug-
General gest selecting a hair replacement before treatment.
H Encourage the patient to express his feelings. Help
H Identification and treatment of underlying cause him develop interests that contribute to a positive
H Cosmetic interventions, such as hairpieces, weaving, self-image.
or bonding
H Occlusive dressing that promotes normal hair growth Monitoring
by protecting the site of hair loss (in trichotilloma- H Complications
nia) H Response to treatment
H Cold cap application and scalp tourniquet that re-
duce the blood supply to the scalp and thereby pre-
serve more hair structure Patient teaching
Medications Be sure to cover:
H Topical application of minoxidil H the disorder, diagnosis, and treatment
H Oral finasteride H medications and possible adverse reactions
H when to notify the physician
H familial link in male-pattern alopecia
ALERT
H well-balanced diet with adequate protein
Finasteride is contraindicated in women of child- H avoidance of excess vitamin A
bearing age. H myths concerning commercial preparations
H signs and symptoms of skin infection
H Corticosteroids H possibility that hair may grow back in a different col-
H Photochemotherapy with methoxsalen and ultraviolet or or type, such as curly or straight.
light
H Dermatomucosal agents
H Antibiotics
H Antifungal agents

Surgery
H Surgical redistribution of hair follicles by auto-
grafting
H Hair transplantation and tunnel grafting

Nursing considerations
Key outcomes
The patient will:
H express concerns about his condition or treatment
H avoid complications
H verbalize feelings about changed body image.

Nursing interventions
H Give prescribed drugs.
H Reassure the patient with female-pattern alopecia
that hair thinning doesnt lead to total baldness. Sug-
gest that she wear a wig or hairpiece.

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Alzheimers disease H Pneumonia and other infections

H Malnutrition and dehydration

Overview Assessment
Description History
H Degenerative disorder of the cerebral cortex (espe- H History obtained from a family member or caregiver
cially the frontal lobe), which accounts for more H Insidious onset
than 50% of all cases of dementia H Initial changes almost imperceptible
H Poor prognosis H Forgetfulness and subtle memory loss
H No cure or definitive treatment H Recent memory loss
H Difficulty learning and remembering new information
Pathophysiology H General deterioration in personal hygiene
H Alzheimers disease is a genetic abnormality on chro- H Inability to concentrate
mosome 21. H Tendency to perform repetitive actions and experi-
H Brain damage is caused by a genetic substance (amy- ence restlessness
loid). H Negative personality changes (irritability, depression,
H There are three distinguishing features of brain tis- paranoia, hostility)
sue: neuro-fibrillary tangles, neuritic plaques, and H Nocturnal awakening
granulovascular degeneration. H Disorientation
H Suspicious and fearful of imaginary people and situa-
Causes tions
H Unknown H Misperceives own environment
H Misidentifies objects and people
Risk factors H Complains of stolen or misplaced objects
Neurochemical H Emotions may be described as labile
H Deficiencies of the neurotransmitters H Mood swings, sudden angry outbursts, and sleep dis-
Environmental turbances
H Aluminum and manganese
H Trauma Physical findings
H Genetic abnormality on chromosome 21 H Impaired sense of smell (usually an early symptom)
H Slow-growing central nervous system viruses H Impaired stereognosis
H Gait disorders
Incidence H Tremors
H Severe form in patients older than age 65 H Positive snout reflex
H May affect 5 million Americans H Organic brain disease in adults
H Affects 13% or 1 in 8 people older than age 65 and H Urinary or fecal incontinence
nearly 50% of those older than age 85 H Seizures

Common characteristics Test results

H Gradual loss of recent and remote memory H Diagnosed by exclusion; tests are performed to rule
H Loss of sense of smell out other diseases.
H Flattening of affect and personality H Positive diagnosis is made on autopsy.
H Difficulty with learning new information Imaging
H Deterioration in personal hygiene H Position-emission tomography reveals metabolic
H Inability to concentrate activity of the cerebral cortex.
H Increasing difficulty with abstraction and judgment H Computed tomography scan shows excessive and
H Impaired communication progressive brain atrophy.
H Loss of coordination H Magnetic resonance imaging rules out intracranial
H Inability to write or speak lesions.
H Nocturnal awakenings H Cerebral blood flow studies reveal abnormalities in
H Signs of anxiety blood flow to the brain.
H Loss of eye contact and fearful look Diagnostic procedures
H Acute confusion, agitation, obsessive-compulsive H Cerebrospinal fluid analysis shows chronic neuro-
behavior logic infection.
H EEG evaluates the brains electrical activity and may
Complications show slowing of the brain waves in late stages of the
H Injury from violent behavior, wandering, or unsuper- disease.
vised activity

36 Alzheimers disease
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Other Monitoring
H Neuropsychologic tests may show impaired cognitive H Response to medications
ability and reasoning. H Fluid intake and nutrition status
H Environment (for safety purposes)

Treatment
Patient teaching
General
H Behavioral interventions (patient-centered or care- Be sure to cover:
giver training) focused on managing cognitive and H the disease process
behavioral changes H exercise regimen
H Well-balanced diet (may need to be monitored) H importance of cutting food and providing finger
H Safe activities as tolerated (may need to be foods, if indicated
monitored) H use of plates with rim guards, built-up utensils, and
cups with lids
Medications H independence.
H Psychostimulators
H Antidepressants, such as paroxetine, sertraline, and Discharge planning
fluoxetine H Refer the patient to the Alzheimers Association.
H Anxiolytics, such as alprazolam and diazepam H Refer the patient to a local support group.
H Antipsychotics, such as haloperidol, risperidone, and H Refer the patient to social services for additional sup-
quetiapine port.
H Anticonvulsants, such as valproic acid, gabapentin,
and lamotrigine
H Anti-inflammatories (experimental)
H Anticholinesterase agents, such as donepezil, rivastig-
mine, and galantamine
H Vitamin E (experimental)
H N-methyl-D-aspartate receptor antagonists such as
memantine

Nursing considerations
Key outcomes
The patient will:
H perform activities of daily living
H maintain daily calorie requirements
H remain free from signs and symptoms of infection
H perform self-care needs
H use support systems and develop adequate coping
behaviors.
Nursing interventions
H Provide an effective communication system.
H Use soft tones and a slow, calm manner when speak-
ing to the patient.
H Allow the patient sufficient time to answer questions.
H Protect the patient from injury.
H Provide rest periods.
H Provide an exercise program.
H Encourage independence.
H Offer frequent toileting.
H Assist with hygiene and dressing.
H Give prescribed drugs.
H Provide familiar objects to help with orientation and
behavior control.

Alzheimers disease 37
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Amebiasis Assessment
History
Overview Acute amebic dysentery
H Fever, chills
Description H Abdominal cramping
H An acute or chronic protozoal infection caused by H Profuse, bloody, mucoid diarrhea
Entamoeba histolytica Chronic amebic dysentery
H Produces varying degrees of illness, from no symp- H Multiple (4 to 18) foul-smelling mucus- and blood-
toms to mild diarrhea to fulminant dysentery tinged stools daily
H Extraintestinal type: may induce hepatic abscess and H Mild fever
infections of the lungs, pleural cavity, pericardium, H Vague abdominal cramps
peritoneum and, rarely, the brain H Possible weight loss
H Also known as amebic dysentery
Physical findings
Pathophysiology Acute amebic dysentery
H E. histolytica exists in two forms, as a cyst (which H Diffuse abdominal tenderness
can survive outside the body) and a trophozoite Chronic amebic dysentery
(which cant survive outside the body). H Tenderness over the cecum and ascending colon
H The ingested cysts pass through the intestine, where H Hepatomegaly (occasionally)
digestive secretions break them down and liberate
the motile trophozoites within. Test results
H The trophozoites multiply and either invade and ul- Laboratory
cerate the mucosa of the large intestine or simply H Stool or aspirates from abscesses, ulcers, or tissue
feed on intestinal bacteria. show E. histolytica.
H As the trophozoites are carried slowly toward the H Indirect hemagglutination test with current or previ-
rectum, theyre encysted and then excreted in feces. ous infection is positive.
H Complement fixation is positive (usually only during
Causes active disease).
H Ingestion of feces-contaminated food or water Imaging
H Barium studies rule out nonamebic causes of diar-
Incidence rhea, such as polyps and cancer.
H Occurs worldwide: most common in the tropics, sub- Diagnostic procedures
tropics, and other areas with poor sanitation and H Sigmoidoscopy detects rectosigmoid ulceration.
health practices
H In the United States: overall incidence between 1%
and 3% but may be higher among homosexuals and Treatment
institutionalized people, in whom fecal-oral contami-
nation is more common and in immigrants from de- General
veloping countries H Small, frequent meals
H Increased fluid intake
Common characteristics H Frequent rest periods
H The clinical effects of amebiasis varying with the H Avoidance of enemas
severity of the infestation
Acute amebic dysentery Medications
H Sudden high temperature of 104 to 105 F (40 to H Metronidazole
40.6 C) H Emetine hydrochloride
H Profuse, bloody, mucoid diarrhea with tenesmus H Iodoquinol (diiodohydroxyquin)
Chronic amebic dysentery H Chloroquine
H Intermittent diarrhea that lasts for 1 to 4 weeks and H Tetracycline (in combination with emetine hydro-
recurs several times per year chloride, metronidazole, or paromomycin)
Amebic granuloma
H Blood and mucus in the stool Surgery
H Partial or complete bowel obstruction H Exploratory surgery hazardous; can lead to peritoni-
tis, perforation, and pericecal abscess
Complications
H Subacute appendicitis
H Perforation of the intestinal wall with spread to the
liver, lungs, pleural cavity, peritoneum, and brain.

38 Amebiasis
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Nursing considerations
Key outcomes
The patient will:
H maintain or improve weight
H maintain skin integrity
H return to a normal elimination pattern
H express feelings of increased comfort and relief from
pain.
Nursing interventions
H Encourage adequate fluid intake.
H Give prescribed drugs.
H Apply perirectal protective cream to prevent excoria-
tion and skin breakdown.
Monitoring
H Vital signs, especially temperature
H Fluid and electrolyte balance
H Daily weight
H Frequency, amount, and character of stools
H Skin integrity

Patient teaching
Be sure to cover:
H need for avoiding alcohol ingestion when taking
metronidazole, which can cause nausea, vomiting,
and headache
H importance of returning for follow-up appointments
H advising family and sexual partners to seek medical
attention for amebiasis
H how to handle infectious material and perform
proper hand washing
H safer sex practices
H boiling untreated or contaminated water when travel-
ing to endemic areas.

Amebiasis 39
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Amenorrhea H Absence of menstruation for 3 months in a previously

established menstrual pattern
H Change in menstrual pattern
H Dependent on cause: may include headaches, hot
Overview flashes, nausea, weight gain or loss, emotional upset,
trauma, extreme exercise, prolonged use of hor-
Description monal contraceptives
H The abnormal absence or suppression of menstrua-
tion Physical findings
H Primary amenorrhea: the absence of menarche in an H Based on cause of amenorrhea: may include hir-
adolescent (age 16 and older) sutism, acne, abdominal mass, signs of malnutrition
H Secondary amenorrhea: the failure of menstruation
for at least 3 months after the normal onset of Test results
menarche Laboratory
H Pregnancy test is positive (when pregnancy is the
Pathophysiology cause).
Primary amenorrhea H Pituitary gonadotropin levels are either elevated or
H The hypothalamic-pituitary-ovarian axis is dysfunc- low.
tional. H Thyroid levels are abnormal.
H Anatomic defects of the central nervous system cause H Serum progesterone levels are abnormal.
the ovary not to receive the hormonal signals that H Serum androgen levels are abnormal.
normally initiate the development of secondary sex H Urine 17-ketosteroid levels are elevated with exces-
characteristics and the beginning of menstruation. sive androgen secretions.
Secondary amenorrhea H Plasma follicle-stimulating hormone (FSH) level is
H The endometrium is sufficiently scarred and no func- greater than 50 International Units/L, depending on
tional endometrium exists. the laboratory; this suggests primary ovarian failure.
H FSH level is either normal or low; this suggests possi-
Causes ble hypothalamic or pituitary abnormality, depending
H Pregnancy on the clinical situation.
H Hormonal abnormalities Imaging
H Lack of ovarian response to gonadotropins H X-rays identify ovarian, adrenal, and pituitary tumors.
H Constant presence of progesterone or other en- Diagnostic procedures
docrine abnormalities H Microscopic examination shows ferning of cervical
H Absence of a uterus mucus (an estrogen effect).
H Endometrial damage H Vaginal cytologic examination and endometrial biop-
H Ovarian, adrenal, or pituitary tumors sy evaluate hormone levels.
H Emotional disorders Other
H Malnutrition and intense exercise H Pelvic examination reveals anatomic abnormalities.

Incidence
H Primary amenorrhea: 0.3% of women Treatment
H Secondary amenorrhea: 5% of women
General
Common characteristics H Based on cause
H Absence of menstruation H Well-balanced diet
H Vasomotor flushes, vaginal atrophy, hirsutism (ab- H Moderate exercise routine
normal hairiness), and acne (secondary amenor-
rhea) Medications
H Progestational agents (to stimulate menstruation)
Complications H Calcium supplement (if cause is hypoestrogenism)
H Infertility H Clomiphene citrate (may induce ovulation in women
H Endometrial adenocarcinoma with amenorrhea caused by gonadotropin deficiency,
H Estrogen deficiency syndrome polycystic ovary syndrome, or excessive weight loss
H Osteoporosis or gain)
H FSH and human menopausal gonadotropins for
women with pituitary disease
Assessment
Surgery
History H Removal of tumor or obstruction
H Failure to menstruate in females age 16 and older

40 Amenorrhea
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Nursing considerations
Key outcomes
The patient will:
H maintain adequate nutrition
H express understanding of disorder
H communicate feelings about the situation.

Nursing interventions
H Provide reassurance and emotional support.
H Give prescribed drugs.

Monitoring
H Signs and symptoms
H Intake and output
H Laboratory test results

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H how to keep an accurate record of menstrual cycles
to aid early detection of recurrent amenorrhea.
Discharge planning
H Refer the patient for psychological counseling, if
appropriate.

Amenorrhea 41
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Amyotrophic lateral H Easy fatigue and easy cramping in the affected mus-
cles
sclerosis Physical findings
H Location of the affected motor neurons
H Severity of the disease
Overview H Fasciculations in the affected muscles
H Progressive weakness in muscles of the arms, legs,
Description and trunk
H Most common motor neuron disease of muscular H Brisk and overactive stretch reflexes
atrophy H Difficulty talking, chewing, swallowing, and breathing
H Chronic, progressive, and debilitating disease thats H Shortness of breath and occasional drooling
invariably fatal
H Also known as Lou Gehrig disease Test results
Laboratory
Pathophysiology H Cerebrospinal fluid analysis shows increased protein
H An excitatory neurotransmitter accumulates to toxic levels.
levels. Imaging
H Motor units no longer innervate. H Computed tomography scan rules out other disor-
H Progressive degeneration of axons cause loss of ders.
myelin. Diagnostic procedures
H Progressive degeneration of upper and lower motor H Muscle biopsy discloses atrophic fibers.
neurons occurs. Other
H Progressive degeneration of motor nuclei in the cere- H EEG rules out other disorders.
bral cortex and corticospinal tracts occurs. H Electromyography shows the electrical abnormalities
of involved muscles.
Causes H Nerve conduction studies appear normal.
H Exact cause unknown
H 10% of patients inherit as an autosomal dominant
trait Treatment
H Virus that creates metabolic disturbances in motor
neurons General
H Immune complexes such as those formed in autoim- H Rehabilitative measures
mune disorders H May need tube feedings
Precipitating factors that cause acute H Activity as tolerated
deterioration
H Severe stress such as myocardial infarction Medications
H Traumatic injury H Muscle relaxants or antispasmodics such as dantro-
H Viral infections lene and baclofen
H Physical exhaustion H I.V. or intrathecal administration of thyrotropin-
releasing hormone
Incidence H Riluzole to slow progression
H Three times more common in males than in females
H Affects people ages 40 to 70
Nursing considerations
Common characteristics
H Muscle weakness Key outcomes
H Atrophy The patient will:
H Fasciculations H maintain a patent airway and adequate ventilation
H maintain joint mobility and range of motion (ROM)
Complications H maintain daily calorie requirements
H Respiratory tract infections H seek support systems and exhibit adequate coping
H Complications of physical immobility behaviors
H remain free from infection.

Assessment Nursing interventions

History
H Mental function intact
H Family history of amyotrophic lateral sclerosis (ALS)
H Asymmetrical weakness first noticed in one limb
H Provide emotional and psychological support.
H Promote independence.
H Turn and reposition the patient frequently.
H Give prescribed drugs.
H Provide airway and respiratory management.

42 Amyotrophic lateral sclerosis

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Modifying the home for a patient with ALS

To help the patient with amyotrophic lateral sclerosis (ALS) H Recommend devices to ease the patients and caregivers
live safely at home, follow these guidelines: work, such as extra pillows or a wedge pillow to help the
patient sit up, a draw sheet to help him move up in bed,
H Explain basic safety precautions, such as keeping stairs
a lap tray for eating, or a bell for calling the caregiver.
and pathways free from clutter; using nonskid mats in
H Help the patient adjust to changes in the environment.
the bathroom and in place of loose throw rugs; keeping
Encourage independence.
stairs well lit; installing handrails in stairwells and the
H Advise the patient to keep a suction machine handy to
shower, tub, and toilet areas; and removing electrical and
reduce the fear of choking due to secretion accumulation
telephone cords from traffic areas.
and dysphagia. Teach him how to suction himself when
H Discuss the need for rearranging the furniture, moving
necessary.
items in or out of the patients care area, and obtaining a
hospital bed, a commode, or oxygen equipment.

H Promote nutrition.
H Maintain aspiration precautions.

Monitoring
H Muscle weakness
H Respiratory status
H Speech
H Swallowing ability
H Skin integrity
H Nutritional status
H Environment (for safety purposes)
H Response to treatment
H Complications
H Signs and symptoms of infection

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H swallowing therapy regimen
H medications and adverse effects
H skin care
H ROM exercises
H deep-breathing and coughing exercises
H safety in the home. (See Modifying the home for a
patient with ALS.)
Discharge planning
H Refer the patient to a local ALS support group.
H Refer the patient to hospice, as appropriate.

Amyotrophic lateral sclerosis 43

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H A lump in the patients throat caused by angioedema

Life-threatening disorder H Dyspnea and complaints of chest tightness

Physical findings
Anaphylaxis H Hives
H Hoarseness or stridor, wheezing
H Severe abdominal cramps, nausea, diarrhea
Overview H Urinary urgency and incontinence
H Dizziness, drowsiness, headache, restlessness, and
Description seizures
H Dramatic, acute atopic reaction to an allergen H Hypotension, shock; sometimes, angina and cardiac
H Marked by sudden onset of rapidly progressive ur- arrhythmias
ticaria and respiratory distress H Angioedema
H More severe the sooner signs and symptoms appear
after exposure to the antigen Test results
H Vascular collapse, leading to systemic shock and, H No tests are required to identify anaphylaxis. The pa-
possibly, death from severe reaction tients history and signs and symptoms establish the
diagnosis.
Pathophysiology Laboratory
H After initial exposure to an antigen, the immune sys- H Skin testing may help identify a specific allergen.
tem produces specific immunoglobulin (Ig) antibod-
ies in the lymph nodes. Helper T cells enhance the
process. Treatment
H The antibodies (IgE) then bind to membrane recep-
tors located on mast cells and basophils. General
H After the body re-encounters the antigen, the IgE an- H Patent airway (establish and maintain)
tibodies, or cross-linked IgE receptors, recognize the H Cardiopulmonary resuscitation, if cardiac arrest oc-
antigen as foreign; this activates the release of power curs
chemical mediators. H Nothing by mouth, until stable
H IgG or IgM enters into the reaction and activates the H Bed rest, until stable
release of complement factors.
Medications
Causes H Immediate injection of epinephrine 1:1,000 aque-
H Systemic exposure to sensitizing drugs, foods, insect ous solution, 0.1 to 0.5 ml subcutaneously or I.V.
venom, or other specific antigens H Corticosteroids
H Diphenhydramine I.V.
Incidence H Volume expander infusions, as needed
H Most common anaphylaxis-causing antigen is peni- H Vasopressors, such as norepinephrine and dopamine
cillin, which induces a reaction in 1 to 4 of every H Aminophylline I.V.
10,000 patients treated H Antihistamines

Common characteristics
H Apprehension and anxiety Nursing considerations
H Dyspnea
H Hoarseness Key outcomes
H Angioedema The patient will:
H maintain a patent airway
Complications H maintain adequate ventilation
H Respiratory obstruction H express feelings of increased comfort and decreased
H Systemic vascular collapse pain
H Death H maintain normal cardiac output and normal heart
rate
H identify causative allergen.
Assessment
Nursing interventions
History H Provide supplemental oxygen and prepare to assist
H Immediately after exposure, complaints of a feeling with insertion of an endotracheal tube, if necessary.
of impending doom or fright and exhibiting appre- H Insert a peripheral I.V. line
hension, restlessness, cyanosis, cool and clammy H Administer medications as prescribed.
skin, erythema, edema, tachypnea, weakness, sweat- H Continually reassure the patient, and explain all tests
ing, sneezing, dyspnea, nasal pruritus, and urticaria and treatments.

44 Anaphylaxis
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H If the patient undergoes skin or scratch testing, mon-

itor for signs of a serious allergic reaction. Keep
emergency resuscitation equipment readily available.

ALERT
If a patient must receive a drug to which hes aller-
gic, prevent a severe reaction by making sure he
receives careful desensitization with gradually in-
creasing doses of the antigen or with advance ad-
ministration of corticosteroids. Closely monitor the
patient during testing and have resuscitation
equipment and epinephrine readily available.

Monitoring
H Vital signs
H Adverse reactions from radiographic contrast media
H Respiratory status
H Serious allergic response after skin or scratch testing
H Neurologic status
H Response to treatment
H Complications
H Degree of edema

Patient teaching
Be sure to cover:
H risk for delayed symptoms and importance of report-
ing them immediately
H avoidance of exposure to known allergens
H importance of carrying and becoming familiar with
an anaphylaxis kit and learning to use it before the
need arises
H need for medical identification jewelry to identify al-
lergy.

Anaphylaxis 45
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Anemia, aplastic H Bibasilar crackles, tachycardia, and a gallop murmur

H Fever, oral and rectal ulcers, and sore throat
H Nausea
H Decreased hair and skin quality
Overview H Petechial rash

Description Test results

H Potentially fatal marrow failure syndrome resulting
from injury to or destruction of stem cells in bone
marrow or the bone marrow matrix
H Causes pancytopenia (anemia, leukopenia, thrombo-
cytopenia) and bone marrow hypoplasia
Pathophysiology
H Aplastic anemia usually develops when damaged or
destroyed stem cells inhibit red blood cell (RBC)
production.
H Less commonly, this disease develops when damaged
bone marrow microvasculature creates an unfavor-
able environment for cell growth and maturation.
Causes
H Result of adverse drug reaction
H Immunologic factors; severe disease, especially hep-
atitis; viral infection, especially in children; and pre-
leukemic and neoplastic infiltration of bone marrow
H Congenital hypoplastic anemia, also known as
Diamond-Blackfan anemia, which develops
between ages 2 and 3 months and Fanconis
syndrome, between birth and age 10
H May be idiopathic
Incidence
H More common in children and young adults
Common characteristics
H Pallor and ecchymoses
Laboratory
H RBC count is 1 million/mm3 or less, usually with nor-
mochromic and normocytic cells; absolute reticulo-
cyte count is very low.
H Serum iron levels are elevated (unless bleeding
occurs), but total iron-binding capacity is normal or
slightly reduced.
H Serum platelet and white blood cell counts are de-
creased.
Diagnostic procedures
H Bone marrow biopsies performed at several sites
may yield a dry tap or show severely hypocellular or
aplastic marrow, with a varying amount of fat, fibrous
tissue, or gelatinous replacement; absence of tagged
iron and megakaryocytes; and depression of ery-
throid elements.
Treatment
General
H Elimination of identifiable cause
H Vigorous supportive measures, such as packed
RBCs, platelets, and experimental histocompatibility
antigen-matched leukocyte transfusions
H Respiratory support with oxygen
H Prevention of infection ranging from frequent hand
washing to filtered airflow
H Well-balanced diet
H Neutropenic precautions, if appropriate

Complications Medications
H Hemorrhage H Antibiotics
H Infection H Marrow-stimulating agents, such as erythropoietin,
H Heart failure and colony-stimulating factors, such as filgrastim and
sargramostim
H Immunosuppressants
Assessment Corticosteroids such as methylprednisolone
Antithymocyte globulin
History Cyclosporine
H Fatigue
H Weakness Surgery
H Weight loss H Bone marrow transplantation (for severe aplasia and
H Dizziness patients who need constant RBC transfusions)
H Syncope
H Bruising
H Nosebleeds Nursing considerations
H Shortness of breath
Key outcomes
Physical findings The patient will:
H Pallor, ecchymosis, petechiae, or retinal hemorrhage H state the need to increase activity level gradually
H Alterations in level of consciousness, weakness, fa- H maintain vital signs within prescribed limits during
tigue activity

46 Anemia, aplastic
9400A.qxd 8/2/12 4:21 PM Page 47

H maintain normal cardiac output

H exhibit adequate ventilation
H express feelings of increased comfort and decreased
pain.
Nursing interventions
H Help the patient to prevent or manage hemorrhage,
infection, adverse effects of drug therapy, and blood
transfusion reaction.
H If the patients platelet count is low (less than
20,000/mm3), prevent hemorrhage by avoiding I.M.
injections, and suggesting the use of an electric razor
and a soft toothbrush. Apply pressure to venipunc-
ture sites until bleeding stops.
H Follow neutropenic precautions.
H Make sure throat, urine, nasal, stool, and blood cul-
tures are done regularly and correctly to check for
infection.
H Schedule frequent rest periods.
H Administer oxygen therapy.
H Ensure a comfortable environmental temperature.
H If blood transfusions are necessary, administer ac-
cording to facility policy and assess for transfusion
reactions.
Monitoring
H Blood studies in patients receiving anemia-inducing
drugs
H Early detection of bleeding

Patient teaching
Be sure to cover:
H avoidance of contact with potential sources of infec-
tion, such as crowds, soil, and standing water that
can harbor organisms
H the disorder and its treatment
H prescribed drugs and possible adverse reactions and
when to report them
H normal lifestyle with appropriate restrictions until re-
mission occurs (for the patient who doesnt require
hospitalization).
Discharge planning
H Refer the patient to the Aplastic Anemia Foundation
of America for additional information, assistance,
and support.

Anemia, aplastic 47
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Anemia, folic acid H Palpitations

H Weakness and light-headedness

(folate) deficiency H Numbness or tingling in hands and feet

Overview
Description
H A common, slowly progressive megaloblastic anemia
H Caused by a deficiency of the vitamin folate
Pathophysiology
H When folic acid stores in the body are low or diet is
deficient in folic acid, the bone marrow produces
large red blood cells or megaloblasts resulting in
anemia.
Causes
H Alcohol abuse
H Poor diet
H Impaired absorption from small intestine
H Bacteria competing for available folic acid
H Excessive cooking of foods, which destroys the avail-
able nutrient
H Limited storage capacity in infants
H Prolonged drug therapy with such drugs as anticon-
vulsants, estrogens, and methotrexate
H Increased folic acid requirements during pregnancy,
rapid growth periods in infancy, childhood and ado-
lescence, and in patients with neoplastic diseases or
some skin diseases such as exfoliative dermatitis
Physical findings
H Generalized pallor and jaundice
H Weight loss
H Wasted or malnourished appearance
H Possible reddened lips with fissures (cheilosis)
H Red, swollen, smooth, shiny, and tender tongue
(glossitis)
H Reduced sense of taste
H Tachycardia
Test results
Laboratory
H Folic acid deficiency anemia and pernicious anemia
can be distinguished by the Schilling test and a thera-
peutic trial of vitamin B12 injections.
H Blood studies show macrocythemia, decreased retic-
ulocyte count, increased mean corpuscular volume,
abnormal platelets, and serum folate levels less than
4 mg/ml.
Treatment
General
H Elimination of contributing causes
H Well-balanced diet high in folic acid (see Foods high
in folic acid)
H Frequent rest periods during activity, as needed

Incidence Medications
H Most prevalent in infants, adolescents, pregnant and H Folic acid supplements
lactating women, alcoholics, elderly people, and peo- H Vitamin supplementation (should begin at least 3
ple with malignant or intestinal diseases months before conception in women trying to be-
come pregnant)
Common characteristics H Blood transfusions in severe cases
H Progressive fatigue
H Systemic signs of anemia
Nursing considerations
Complications
H Pregnant women deficient in folic acid have an in- Key outcomes
creased risk for giving birth to a neonate with a neur- The patient will:
al tube defect. H state the need to increase activity level gradually
H maintain vital signs within prescribed limits during
activity
Assessment H remain hemodynamically stable
H have normal bowel movements
History H experience no further weight loss.
H Severe, progressive fatigue, the hallmark of
folic acid deficiency Nursing interventions
H Diarrhea H Plan activities, rest periods, and necessary diagnostic
H Nausea tests to conserve energy.
H Anorexia H Advise the patient to report signs and symptoms of
H Headaches decreased perfusion to vital organs (dyspnea, chest
H Forgetfulness pain, dizziness).
H Irritability H If the patient has glossitis, emphasize the importance
H Chest pain of good oral hygiene.
H Shortness of breath

48 Anemia, folic acid (folate) deficiency

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Foods high in folic acid

The body needs folic acid to develop healthy red blood cells Food mcg/100 g
and synthesize deoxyribonucleic acid. Although body stores
Asparagus spears 109
are comparatively small (about 70 mg), this vitamin is plen-
Beef liver 294
tiful in most well-balanced diets. But because folic acid is
Broccoli spears 54
water-soluble and heat-labile, its easily destroyed by cook-
Collards (cooked) 102
ing. Also, about 20% of folic acid intake is excreted unab-
Mushrooms 24
sorbed. Daily folic acid intake less than 50 mcg/day usually
Oatmeal 33
induces folic acid deficiency within 4 months. Heres a list of
Peanut butter 57
foods high in folic acid.
Red beans 180
Wheat germ 305

H Ask the dietitian to give the patient nonirritating

foods because a sore mouth and tongue make eating
painful. If these symptoms make talking difficult,
supply a pad and pencil or some other aid to facili-
tate communication.
H To ensure accurate Schilling test results, make sure
that all urine excreted over a 24-hour period is col-
lected and that the specimens remain uncontaminat-
ed by bacteria.
H Provide a well-balanced diet, including foods high in
folate, such as dark green leafy vegetables, organ
meats, eggs, milk, oranges, bananas, dry beans, and
whole-grain breads.
Monitoring
H Vital signs
H Fluid and electrolyte balance

Patient teaching
Be sure to cover:
H importance of a well-balanced diet high in folic acid
H use of commercially prepared formulas for mothers
who arent breast-feeding
H daily folic acid requirements and the need to keep
taking the supplements even when he begins to feel
better
H importance of guarding against infections and re-
porting signs of infection promptly.

Anemia, folic acid (folate) deficiency 49

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Common characteristics
Anemia, iron deficiency H Fatigue
H Systemic signs of anemia

Overview Complications
H Infection
Description H Pneumonia
H Decreased total iron body content diminishing ery- H Overreplacement of oral or I.M. iron supplements,
thropoiesis which can affect the liver, heart, pituitary glands, and
H Produces smaller (microcytic) cells with less color joints
on staining (hypochromia)
Pathophysiology Special populations
H Body stores of iron, including plasma iron, decrease. In a child, iron deficiency anemia can cause pica,
H Transferrin, which binds with and transports iron, which may lead to eating lead-based paint result-
also decreases. ing in lead poisoning.
H Insufficient body stores of iron lead to a depleted red
blood cell mass and to a decreased hemoglobin con-
centration.
H Anemic state results in decreased oxygen-carrying Assessment
capacity of the blood. (See Iron absorption and
storage.) History
H Can persist for years without signs and symptoms
Causes H Fatigue
H Inadequate dietary intake of iron H Inability to concentrate
H Iron malabsorption H Headache, shortness of breath (especially on exer-
H Blood loss secondary to drug-induced GI bleeding or tion)
due to heavy menses, hemorrhage from trauma, GI H Increased frequency of infections
ulcers, malignant tumors, and varices H Pica, an uncontrollable urge to eat strange things,
H Pregnancy such as clay, starch, ice and, in children, lead
H Intravascular hemolysis-induced hemoglobinuria or H Menorrhagia
paroxysmal nocturnal hemoglobinuria H Dysphagia
H Mechanical erythrocyte trauma caused by a prosthet- H Vasomotor disturbances
ic heart valve or vena cava filter H Numbness and tingling of the extremities
H Can be related to lead poisoning in children H Neuralgic pain

Incidence Physical findings

H Common worldwide H Red, swollen, smooth, shiny, and tender tongue
H Affects 10% to 30% of the adult population of the (glossitis)
United States H Corners of the mouth may be eroded, tender, and
H Most prevalent among premenopausal women, in- swollen (angular stomatitis)
fants, children, adolescents, alcoholics, and elderly H Spoon-shaped, brittle nails
people H Tachycardia

Iron absorption and storage
Found in abundance throughout the body, iron is needed
for erythropoiesis. Two-thirds of total-body iron is found
in hemoglobin; the other third, mostly in the reticuloen-
dothelial system (liver, spleen, and bone marrow), with
small amounts in muscle, serum, and body cells.
Adequate iron in the diet and recirculation of iron re-
leased from disintegrating red blood cells maintain iron
supplies. The duodenum and upper part of the small intes-
tine absorb dietary iron. Such absorption depends on gas-
tric acid content, the amount of reducing substances
(ascorbic acid, for example) present in the alimentary
canal, and amount of iron intake. If iron intake is deficient,
the body gradually depletes its iron stores, causing de-
creased hemoglobin levels and, eventually, signs and
symptoms of iron deficiency anemia.
Test results
Laboratory
H Serum hemoglobin levels are decreased (males, less
than 12 g/dl; females, less than 10 g/dl) or, in severe
anemia, decreased mean corpuscular hemoglobin
level.
H Serum hematocrit is decreased (males, less than
47 ml/dl; females, less than 42 ml/dl).
H Serum iron levels are decreased with high binding
capacity.
H Serum ferritin levels are decreased.
H Serum red blood cell (RBC) count is decreased with
microcytic and hypochromic cells (in early stages,
RBC count may be normal, except in infants and chil-
dren).

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Diagnostic procedures Recognizing iron overdose

H Bone marrow studies reveal depleted or absent iron
stores (done by staining) as well as normoblastic
hyperplasia.
H GI studies, such as guaiac stool tests, barium swallow
and enema, endoscopy, and sigmoidoscopy, rule out
or confirm the diagnosis of bleeding causing the iron
deficiency.
Excessive iron replacement may produce signs and symp-
toms, such as diarrhea, fever, severe stomach pain, nau-
sea, and vomiting.
When these signs and symptoms occur, notify the
physician and give prescribed treatment, which may in-
clude chelation therapy, vigorous I.V. fluid replacement,
gastric lavage, whole-bowel irrigation, and supplemental
oxygen.

Treatment
General Monitoring
H Determination of underlying cause H Vital signs
H Nutritious, nonirritating foods H Compliance with prescribed iron supplement therapy
H Planned rest periods during activity H Iron replacement overdose (see Recognizing iron
overdose)
Medications
H Oral preparation of iron or a combination of iron
and ascorbic acid Patient teaching
H I.M. iron in rare cases
H Total-dose I.V. infusions of supplemental iron for Be sure to cover:
pregnant and elderly patients with severe disease H the disorder, diagnosis, and treatment
H dangers of lead poisoning, especially if the patient
reports pica
Nursing considerations H importance of continuing therapy, even after the pa-
tient begins to feel better
Key outcomes H absorption interference with milk or antacid of iron
The patient will: supplementation
H maintain weight without further loss H increased absorption with vitamin C
H maintain vital signs within prescribed limits during H avoidance of staining teeth by drinking liquid supple-
activity mental iron through a straw
H express feelings of increased energy H when to report adverse effects of iron therapy
H express feelings of increased comfort and decreased H basics of a nutritionally balanced diet
pain. H importance of avoiding infection and when to report
signs of infection
Nursing interventions H need for regular checkups
H Note the patients signs or symptoms of decreased H compliance with prescribed treatment.
perfusion to vital organs.
H Provide oxygen therapy, as necessary.
H Assess the familys dietary habits for iron intake, not-
ing the influence of childhood eating patterns, cultur-
al food preferences, and family income on adequate
nutrition.
H Ask the dietitian to give the patient nonirritating
foods.
H Give prescribed analgesics for headache and other
discomfort.
H Evaluate the patients drug history. Certain drugs,
such as pancreatic enzymes and vitamin E, can inter-
fere with iron metabolism and absorption; aspirin,
steroids, and other drugs can cause GI bleeding.
H Provide frequent rest periods.
H If the patient receives iron I.V., monitor the infusion
rate carefully and observe for an allergic reaction.
H Use the Z-track injection method when administering
iron I.M. to prevent skin discoloration, scarring, and
irritating iron deposits in the skin.
H Provide good nutrition and meticulous care of I.V.
sites.

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Anemia, pernicious Assessment

Overview
Description
H Deficiency of vitamin B12 causing serious neurologic,
psychological, gastric, and intestinal abnormalities
H Characterized by decreased gastric production of hy-
drochloric acid and deficiency of intrinsic factor, es-
sential for vitamin B12 absorption
H Also known as Addisons anemia
Pathophysiology
H An inherited autoimmune response may cause gastric
mucosal atrophy and resultant decreased hydrochlo-
ric acid and intrinsic factor production, a substance
normally secreted by the parietal cells of the gastric
mucosa.
H Intrinsic factor deficiency impairs vitamin B12 ab-
sorption.
H Vitamin B12 deficiency inhibits the growth of all
cells, particularly red blood cells (RBCs), leading to
insufficient and deformed RBCs with poor oxygen-
carrying capacity.
Causes
H Genetic predisposition
H Secondary pernicious anemia results from partial
removal of the stomach
H Chronic gastric inflammation
Incidence
H In the United States, most common in New England
and the Great Lakes region because of ethnic con-
centration
H Common in Northern Europeans of fair complexion
H Rare in children, Blacks, and Asians
H Onset typically between ages 50 and 60; incidence
increases with advancing age
Common characteristics
H Weakness
H Beefy red, sore tongue
H Systemic signs of anemia
Complications
H Heart failure with severe anemia
H Myocardial ischemia
H Paralysis
H Psychotic behavior
H Loss of sphincter control of bowel and bladder
H Peptic ulcer disease
History
H Characteristic triad of symptoms: weakness; a beefy
red, sore tongue; and numbness and tingling in the
extremities
H GI disturbance: nausea, vomiting, anorexia, weight
loss, flatulence, diarrhea, and constipation
H Peripheral numbness and paresthesia
H Light-headedness
H Headache
H Diplopia and blurred vision
H Loss of taste
H Tinnitus
Physical findings
H Smooth, beefy red, painful tongue
H Slightly jaundiced sclera and pale to bright yellow
skin
H Tachycardia
H Systolic murmur
H Enlarged liver and spleen
H Weakness in the extremities
H Disturbed position sense
H Lack of coordination
H Impaired fine finger movement
H Loss of bowel and bladder control
H Impotence (in males)
H Irritable, depressed, delirious, and ataxic
H Memory loss
H Positive Babinskis and Rombergs signs
H Optic muscle atrophy
Test results
Laboratory
H Hemoglobin level is decreased.
H RBC count is decreased.
H Mean corpuscular volume is increased (less than
120 mm3); mean corpuscular hemoglobin concen-
tration is also increased.
H White blood cell and platelet counts may be de-
creased, and the platelets are large and malformed.
H Serum vitamin B12 tests may show levels less than
0.1 mcg/ml.
H Serum lactate dehydrogenase levels are elevated.
Diagnostic procedures
H Bone marrow studies reveal erythroid hyperplasia
with increased numbers of megaloblasts but few nor-
mally developing RBCs.
H Gastric analysis shows an absence of free hydrochlo-
ric acid after histamine or pentagastrin injection.
H The Schilling test may reveal a urinary excretion of
less than 3% in the first 24 hours in patients with
pernicious anemia; may reveal normal excretion of
vitamin B12 when repeated with intrinsic factor
added.

52 Anemia, pernicious
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Dietary sources of vitamin B12

Treatment
The following foods are good sources of vitamin B12:
H Meat, especially organ meats
General H Poultry, fresh fish, and seafood
H Based on underlying cause H Eggs
H Well-balanced diet, including foods high in vitamin H Dairy products
B12 H Fortified cereals and flours
H Sodium and fluid restriction for heart failure
H If anemia causes extreme fatigue, bed rest until
hemoglobin level increases
H observance of and when to report confusion and irri-
Medications tability
H Early I.M. vitamin B12 replacement H prevention of pernicious anemia, by taking vitamin
H Maintenance levels (monthly) of vitamin B12 doses, B12 supplements, in patients who have had extensive
after the patients condition improves gastric resections or who follow strict vegetarian
diets.
Nursing considerations
Key outcomes
The patient will:
H state his understanding of the need to increase activi-
ty level gradually
H modify lifestyle to minimize risk for decreased tissue
perfusion
H maintain normal hemoglobin level and hematocrit
H maintain normal coagulation profile.

Nursing interventions
H If the patient has severe anemia, plan activities, rest
periods, and necessary diagnostic tests to conserve
his energy.
H To ensure accurate Schilling test results, make sure
that all urine excreted over a 24-hour period is col-
lected.
H Provide a well-balanced diet, including foods high in
vitamin B12. (See Dietary sources of vitamin B12.)
H Institute safety precautions to prevent falls.

Monitoring
H Vital signs
H Mental and neurologic status
H Environment (for safety purposes)

Patient teaching
Be sure to cover:
H protection against infections and when to report
signs of infection
H when to report signs and symptoms of decreased
perfusion to vital organs and symptoms of neurop-
athy
H avoidance of irritating foods
H avoidance of exposure to extreme heat or cold on the
extremities
H continuation of vitamin B12 replacement even after
symptoms subside
H proper injection techniques

Anemia, pernicious 53
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Anemia, sickle cell
Overview
Description
H Congenital hemolytic disease that results from a de-
fective hemoglobin (Hb) molecule, HbS, that causes
red blood cells (RBCs) to become sickle-shaped
H Impaired circulation caused by sickle cells resulting
in chronic ill health (fatigue, dyspnea on exertion,
swollen joints), periodic crises, long-term complica-
tions, and premature death
H No cure
Pathophysiology
H The abnormal HbS found in the patients RBCs be-
comes insoluble whenever hypoxia occurs.
H The RBCs become rigid, rough, and elongated, form-
ing a crescent or sickle shape.
H Sickling can produce hemolysis (cell destruction).
H The altered cells accumulate in capillaries and small-
er blood vessels, making the blood more viscous.
H Normal circulation is impaired, causing pain, tissue
infarctions, and swelling.
Causes
H Homozygous inheritance of the HbS-producing gene
(defective Hb gene from each parent)
Incidence
H Most common in tropical Africans and in people of
African descent
H Abnormal gene about 1 in 10 blacks (if two such
carriers have offspring, each child has a 1-in-4
chance of developing the disease)
H Found in one in every 500 blacks in the United States
H Also occurs in Puerto Rico, Turkey, India, the Middle
East, and the Mediterranean area
Common characteristics
H Chronic fatigue
H Intense pain due to vascular occlusion in a sickling
episode
H Frequent bacterial infections due to involvement of
spleen
H Systemic signs of anemia
Complications
H Chronic obstructive pulmonary disease
H Heart failure
H Retinopathy
H Nephropathy
54 Anemia, sickle cell
Assessment
History
H Signs and symptoms usually dont develop until after
age 6 months
H Chronic fatigue
H Unexplained dyspnea or dyspnea on exertion
H Joint swelling
H Aching bones
H Chest pain
H Ischemic leg ulcers
H Increased susceptibility to infection
H Pulmonary infarctions and cardiomegaly
Physical findings
H Jaundice or pallor
H May appear small in stature for age
H Delayed growth and puberty
H Spiderlike body build (narrow shoulders and hips,
long extremities, curved spine, and barrel chest) in
adult
H Tachycardia
H Hepatomegaly and, in children, splenomegaly
H Systolic and diastolic murmurs
H Sleepiness with difficulty awakening
H Hematuria
H Pale lips, tongue, palms, and nail beds
H Body temperature greater than 104 F (40 C) or a
temperature of 100 F (37.8 C) that persists for 2
or more days
In painful crisis
H Most common crisis and the hallmark of the disease,
usually appears periodically after age 5, character-
ized by severe abdominal, thoracic, muscle, or bone
pain and, possibly, increased jaundice, dark urine,
and a low-grade fever
In aplastic crisis
H Pallor, lethargy, sleepiness, dyspnea, possible coma,
markedly decreased bone marrow activity, and RBC
hemolysis
In acute sequestration crisis
H Occurs in infants between ages 8 months and 2
years, causes lethargy and pallor and, if untreated,
progresses to hypovolemic shock and death
In hemolytic crisis
H Liver congestion and hepatomegaly
Test results
Laboratory
H Stained blood smear shows sickle cells and Hb elec-
trophoresis shows HbS. (Electrophoresis should be
done on umbilical cord blood samples at birth to
provide sickle cell disease screening for all neonates
at risk.)
H RBC counts and erythrocyte sedimentation rate are
decreased; white blood cell and platelet counts are
elevated; and serum iron levels are increased.
H RBC survival is decreased and reticulocytosis is pre-
sent; Hb levels are normal or low.
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Imaging
H A lateral chest X-ray detects the characteristic Lin-
coln log deformity. (This spinal abnormality devel-
ops in many adults and some adolescents with sickle
cell anemia, leaving the vertebrae resembling logs
that form the corner of a cabin.)
Diagnostic procedures
H Ophthalmoscopic examination reveals corkscrew or
comma-shaped vessels in the conjunctivae.
Treatment
General
H Avoidance of extreme temperatures
H Avoidance of stress
H Well-balanced diet
H Adequate amounts of folic acidrich foods
H Adequate fluid intake
H Bed rest during crises
H Activity as tolerated
Medications
H Vaccines, such as polyvalent pneumococcal vaccine
and Haemophilus influenzae B vaccine
H Anti-infectives, as appropriate
H Analgesics
H Iron supplements
H Transfusion of packed RBCs, if Hb level decreases
suddenly or if condition deteriorates rapidly
H Sedation and administration of analgesics, blood
transfusion, oxygen therapy, and large amounts of
oral or I.V. fluids, in an acute sequestration crisis
Nursing considerations
Key outcomes
The patient will:
H demonstrate age-appropriate skills and behaviors to
the extent possible
H exhibit adequate ventilation
H maintain collateral circulation
H maintain balanced fluid volume where input will
equal output
H express feelings of increased comfort and decreased
pain
H maintain normal peripheral pulses
H maintain normal skin color and temperature.
Nursing interventions
H Encourage the patient to talk about his fears and
concerns.
H If a male patient develops sudden, painful priapism,
reassure him that such episodes are common and
have no permanent harmful effects.
H Make sure that the patient receives adequate
amounts of folic acidrich foods such as green,
leafy vegetables.
H Encourage adequate fluid intake.
H Apply warm compresses, warmed thermal blankets,
and warming pads or mattresses to painful areas of
the patients body, unless he has neuropathy.
H Administer analgesics and antipyretics, as needed.
H When cultures demonstrate the presence of infection,
administer prescribed antibiotics.
H Administer prescribed prophylactic antibiotics.
H Use strict sterile technique when performing treat-
ments.
H Encourage bed rest with the head of the bed elevated
to decrease tissue oxygen demand.
H Administer oxygen, as needed.
H Administer blood transfusions.
H If the patient requires general anesthesia for surgery,
help ensure that he receives adequate ventilation to
prevent hypoxic crisis.
Monitoring
H Vital signs
H Intake and output
H Complete blood count and other laboratory study
results
Patient teaching
Be sure to cover:
H avoidance of tight clothing that restricts circulation
H conditions that provoke hypoxia, such as strenuous
exercise, vasoconstricting medications, cold temper-
atures, unpressurized aircraft, and high altitude
H importance of normal childhood immunizations,
meticulous wound care, good oral hygiene, regular
dental checkups, and a balanced diet as safeguards
against infection
H need for prompt treatment of infection
H need to increase fluid intake to prevent dehydration,
which can cause increased blood viscosity
H symptoms of vaso-occlusive crisis
H need for hospitalization in a vaso-occlusive crisis in
which I.V. fluids, parenteral analgesics, oxygen thera-
py, and blood transfusions may be necessary
H need to inform all health care providers that the pa-
tient has this disease before undergoing any treat-
ment, especially major surgery
H pregnancy and the disease
H balanced diet, including folic acid supplements dur-
ing pregnancy.
Discharge planning
H Refer parents of children with sickle cell anemia for
genetic counseling to answer their questions about
the risk to future offspring.
H Refer other family members for genetic counseling to
determine if theyre heterozygote carriers.
H If necessary, refer the patient for psychological coun-
seling to help him cope.
H Refer women with sickle cell anemia for birth con-
trol counseling.
Anemia, sickle cell 55
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Physical findings
Anemia, sideroblastic H Pale skin and oral mucous membranes
H Slight jaundice
H Petechiae or bruises
Overview H Enlarged lymph nodes
H Hepatosplenomegaly
Description
H A group of heterogenous disorders with a common Test results
defect that causes failure to use iron in hemoglobin Laboratory
synthesis despite the availability of adequate iron H Red blood cell (RBC) indices that are revealed by
stores microscopic examination of blood show erythrocytes
H Can be acquired or hereditary; the acquired form, in to be hypochromic or normochromic and slightly
turn, can be primary or secondary macrocytic; RBC precursors may be megaloblastic,
with anisocytosis (abnormal variation in RBC size)
Pathophysiology and poikilocytosis (abnormal variation in RBC
H Normoblasts fail to use iron to synthesize hemoglo- shape).
bin. H Vitamin B12 and folic acid levels are normal unless
H Iron is deposited in the mitochondria of normo- combined anemias are present.
blasts, rather than in the hemoglobin molecules. H Serum reticulocyte count is low because young cells
H Iron toxicity can cause organ damage. die in the marrow.
Diagnostic procedures
Causes H Ringed sideroblasts on microscopic examination of
H Hereditary; may be due to a rare genetic defect on bone marrow aspirate stained with Prussian blue dye
the X chromosome confirms the diagnosis. (See Ringed sideroblast.)
H Acquired form may be secondary to ingestion of or
exposure to toxins, such as alcohol and lead, or to
drugs such as isoniazid and chloramphenicol Treatment
H Complication of neoplastic and inflammatory dis-
eases, such as lymphoma, rheumatoid arthritis, lupus General
erythematosus, multiple myeloma, tuberculosis, and H Underlying cause determines the course of treatment
severe infections (for example, in acquired secondary form, the caus-
H Primary acquired form cause unknown ative drug or toxin is removed)
H Nutritious diet
Incidence H Frequent rest periods
H Most prevalent in young males H Chelation therapy to decrease iron overload from
H Appears to be transmitted by X-linked inheritance; fe- repeated transfusions
males are carriers and usually show no signs of this
disorder Medications
H Primary acquired form most common in elderly peo- In hereditary sideroblastic anemia
ple but occasionally found in young people H High doses of pyridoxine
In primary acquired anemia
Common characteristics H Transfusion or high doses of androgens
H Anorexia and fatigue In chronic iron overload
H Systemic signs of anemia H Deferoxamine

Complications
H Severe cardiac, hepatic, splenic, and pancreatic Nursing considerations
disease
H Acute myelogenous leukemia Key outcomes
The patient will:
H express feelings of increased energy
Assessment H maintain skin integrity
H not develop infection
History H show improvement or healing in his lesions or
H Anorexia wounds
H Fatigue H express feelings of increased comfort and decreased
H Weakness pain.
H Dizziness
H Dyspnea

56 Anemia, sideroblastic
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Nursing interventions Ringed sideroblast

H Provide frequent rest periods. Plan activities and di-
Electron microscopy shows large iron deposits in the mi-
agnostic tests so the patient can rest in between. tochondria that surround the nucleus, forming the charac-
H Institute safety measures to prevent falls. teristic ringed sideroblast.
H Give prescribed drugs.
H Provide comfort measures; have the patient perform
relaxation techniques to facilitate coping.
H Administer blood transfusions. Notify the physician if
signs of a transfusion reaction occur.
H If the patient has jaundice or pruritus, provide metic-
ulous skin care.
H Ask about possible exposure to lead in the home
(especially for children) or on the job.
Monitoring
H Vital signs
H Complications
H Response to treatment
H Signs and symptoms of neuropathy
H Signs and symptoms of decreased perfusion

Patient teaching
Be sure to cover:
H prescribed treatment and possible complications
H importance of continuing prescribed therapy, even
after the patient begins to feel better
H precautions for parents about house paint and not al-
lowing children to eat paint chips because of the pos-
sibility of lead
H recognition of and when to report adrenergic ad-
verse effects, if androgens are used as part of the
treatment
H recognition of and when to report signs and symp-
toms of heart failure
H need for proper hygiene and other measures to
guard against infections and when to report signs
and symptoms of infection.
Discharge planning
H Identify patients who abuse alcohol and refer them
for appropriate therapy.

Anemia, sideroblastic 57
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Aneurysm, H Lower back pain unaffected by movement

H Gastric or abdominal fullness

abdominal aortic H Sudden onset of severe abdominal pain or lumbar

pain with radiation to flank and groin
H May note a pulsating mass in the periumbilical area:
dont palpate
Overview Ruptured aneurysm
H Into the peritoneal cavity, severe, persistent abdomi-
Description nal and back pain
H Abnormal dilation in the arterial wall of the aorta, H Into the duodenum, GI bleeding with massive he-
commonly between the renal arteries and iliac matemesis and melena
branches H Mottled skin; poor distal perfusion
H Can be fusiform (spindle-shaped), saccular (pouch- H Absent peripheral pulses distally
like), or dissecting H Decreased level of consciousness
H Diaphoresis
Pathophysiology H Hypotension
H Focal weakness in the tunica media layer of the aorta H Tachycardia
due to degenerative changes allows the tunica intima H Oliguria
and tunica adventitia layers to stretch outward. H Distended abdomen
H Blood pressure within the aorta progressively weak- H Ecchymosis or hematoma in the abdominal, flank, or
ens vessel walls and enlarges the aneurysm. groin area
H Paraplegia if aneurysm rupture reduces blood flow to
Causes the spine
H Arteriosclerosis or atherosclerosis (95%) H Systolic bruit over the aorta
H Trauma H Tenderness over affected area
H Syphilis; other infections
Test results
Risk factors Imaging
H Hypertension H Abdominal ultrasonography or echocardiography
H Smoking determines the size, shape, and location of the
H Hypercholesterolemia aneurysm.
H Obesity H Anteroposterior and lateral abdominal X-rays detect
aortic calcification, which outlines the mass, at least
Incidence 75% of the time.
H Seven times more common in hypertensive males H Computed tomography scan can visualize the aneu-
than in females rysms effect on nearby organs.
H Most common in whites ages 50 to 80 H Aortography shows the condition of vessels proximal
and distal to the aneurysm and the extent of the
Common characteristics aeurysm; aneurysm diameter may be underestimated
H Located in the infrarenal aorta (98%) because it shows only the flow channel and not the
H Most develop at bifurcations in the vessels surrounding clot.
Complications
H Hemorrhage Treatment
H Shock
H Dissection General
H Delayed surgery if aneurysm is small and produces
no symptoms
Assessment H Careful control of hypertension
H Fluid and blood replacement
History H Weight reduction, if appropriate
H Asymptomatic until the aneurysm enlarges and com- H Low-fat diet
presses surrounding tissue H Activity as tolerated
H Syncope when aneurysm ruptures
H Asymptomatic when clot forms and bleeding stops or Medications
abdominal pain when bleeding continues into the H Beta-adrenergic blockers such as metoprolol
peritoneum H Antihypertensives
H Analgesics
Physical findings H Antibiotics, as appropriate
Intact aneurysm
H Gnawing, generalized, steady abdominal pain

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Endovascular grafting for repair of AAA

Endovascular grafting is a minimally invasive procedure for the patient who
requires repair of an abdominal aortic aneurysm (AAA). Endovascular
grafting reinforces the walls of the aorta to prevent rupture and expansion
of the size of the aneurysm.
The procedure is performed with fluoroscopic guidance, whereby a de-
livery catheter with an attached compressed graft is inserted through a
small incision into the femoral or iliac artery over a guidewire. The delivery
catheter is advanced into the aorta, where its positioned across the
aneurysm. A balloon on the catheter expands the graft and affixes it to the
vessel wall. The procedure usually takes 2 to 3 hours to perform. Patients
are instructed to walk the first day after surgery and are discharged from
the hospital in 1 to 3 days.

Surgery H Watch for signs of bleeding retroperitoneally from

H Endovascular grafting or resection of large aneu- the graft site.
rysms or those that produce symptoms (see Endo- H Maintain blood pressure in prescribed range with
vascular grafting for repair of AAA) fluids and medications.
H Bypass procedures for poor perfusion distal to
aneurysm ALERT
H Repair of ruptured aneurysm with a graft replacement
Assess the patient for severe back pain, which can
indicate that the graft is tearing.
Nursing considerations
H Have the patient cough, or suction the endotracheal
Key outcomes tube, as needed.
The patient will: H Provide frequent turning, and assist with ambulation
H maintain adequate cardiac output as soon as the patient is able.
H maintain hemodynamic stability
H maintain palpable pulses distal to the aneurysm site Monitoring
H maintain adequate urine output (output equivalent to H Cardiac rhythm and hemodynamics
intake) H Vital signs, intake and output hourly, neurologic sta-
H express feelings of increased comfort and decreased tus, and pulse oximetry
pain. H Respirations and breath sounds at least every hour
H Arterial blood gas values as ordered
Nursing interventions H Daily weight
In a nonacute situation H Fluid status
H Allow the patient to express his fears and concerns H Nasogastric intubation for patency, amount, and type
and identify effective coping strategies. of drainage
H Offer the patient and his family psychological sup- H Laboratory studies
port. H Abdominal dressings
H Give prescribed drugs. H Wound site for infection
In an acute situation
H Insert an I.V. line with at least a 14G needle to facili-
tate blood replacement. Patient teaching
H Obtain blood samples for laboratory tests as ordered.
H Give prescribed drugs. Be sure to cover:
H surgical procedure and expected postoperative care
H importance of taking all medications as prescribed
ALERT
and carrying a list of medications at all times, in case
Be alert for signs of rupture, which may be imme- of an emergency
diately fatal. If rupture does occur, surgery needs to H physical activity restrictions until medically cleared
be immediate. Medical antishock trousers may be by the physician
used while transporting the patient to surgery. H need for regular examination and ultrasound checks
to monitor progression of the aneurysm, if surgery
After surgery wasnt performed.
H Assess peripheral pulses for graft failure or occlusion.

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Aneurysm, Treatment
femoral and popliteal General
H Nothing by mouth before surgery
H Limited movement of the affected extremity
Overview
Medications
Description H Analgesics
H Progressive atherosclerotic changes occurring in the H Antibiotics (before surgery), as appropriate
walls (medial layer) of the femoral and popliteal H Anticoagulants, such as warfarin and heparin
arteries resulting in a dilation or outpouching (see
Arteries of the leg) Surgery
H May be fusiform (spindle-shaped) or saccular H Surgical bypass and reconstruction of the artery, usu-
(pouchlike) ally with an autogenous saphenous vein graft replace-
H Usually progressive, eventually ending in thrombosis, ment
embolization, and gangrene H Leg amputation if arterial occlusion causes severe
ischemia and gangrene
Pathophysiology
H Atherosclerotic plaque formation or loss of elastin
and collagen in the vessel wall causes localized out- Nursing considerations
pouching or dilation of a weakened arterial wall.
Key outcomes
Causes The patient will:
H Atherosclerosis H maintain pulses and adequate circulation to damaged
H Congenital weakness in the arterial wall (rare) aneurysm site
H Trauma (blunt or penetrating) H express feelings of increased comfort and decreased
H Bacterial infection pain
H Peripheral vascular reconstructive surgery (which H carry out activities of daily living without excess fa-
causes suture line or false aneurysms, whereby a tigue or exhaustion.
blood clot forms a second lumen)
Nursing interventions
Incidence Before corrective surgery
H Most common in males older than age 50 H Evaluate the patients circulatory status, noting the lo-
cation and quality of peripheral pulses in the affected
Common characteristics arm or leg.
H Pain H Administer a prophylactic antibiotic or anticoagulant,
H Edema and venous distention as needed.
H Symptoms of severe ischemia in the leg or foot H Discuss expected postoperative procedures with the
patient, and review the surgical procedure.
Complications After arterial surgery
H Gangrene H Correlate condition of extremity with preoperative
circulatory assessment. Mark the sites on the pa-
tients skin where pulses are palpable, to facilitate re-
Assessment peated checks.
H Help the patient walk soon after surgery, to prevent
History venostasis and thrombus formation.
H Pain in affected extremity
Monitoring
Physical findings H Neurovascular condition of affected extremity (pulse,
H Loss of pulse and color, coldness in the affected leg temperature, sensation, color)
or foot H Vital signs
H Distal petechial hemorrhages (from aneurysmal em- H Pain control
boli)
H Pulsating mass above or below the inguinal ligament
H Firm, nonpulsating mass above or below the inguinal Patient teaching
ligament when thrombosis has occurred
Be sure to cover:
Test results H importance of immediately informing the physician
Diagnostic procedures of any recurrence of symptoms
H Arteriography or ultrasonography reveals aneurysm.

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Arteries of the leg

Front view Back view

Abdominal
aorta

Common
iliac artery

Internal
iliac artery
External
iliac artery

Deep femoral
Deep femoral artery
artery

Superficial
femoral artery Superficial
femoral artery

Popliteal artery

Popliteal artery

Anterior tibial
artery

Anterior
tibial artery Posterior tibial
artery

Dorsalis pedis
Medial plantar
artery

Lateral plantar
artery

H how to apply antiembolism stockings (Warn the pa- H importance of follow-up blood studies to monitor an-
tient against wearing constrictive clothing.) ticoagulant therapy.
H measures to prevent bleeding (if an anticoagulant is
prescribed) such as using an electric razor
H importance of reporting signs of bleeding immediate-
ly (bleeding gums, easy bruising, or black, tarry
stools)

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Life-threatening disorder Assessment

History
Aneurysm, intracranial H Headache
H Intermittent nausea
H Seizure
Overview H Photophobia
H Blurred vision
Description
H Weakness in the wall of a cerebral artery that causes Physical findings
localized dilation Typically, the severity of a ruptured intracranial
H Most common form is the berry aneurysm, a saclike aneurysm is graded according to the patients signs and
outpouching in a cerebral artery symptoms. (See Determining severity of an intracra-
H Usually occurs at an arterial junction in the Circle of nial aneurysm rupture.)
Willis, the circular anastomosis forming the major H Nuchal rigidity
cerebral arteries at the base of the brain H Back and leg pain
H Commonly ruptures and causes subarachnoid hem- H Fever
orrhage H Restlessness
H Irritability
Pathophysiology H Hemiparesis
H Blood flow exerts pressure against a congenitally H Hemisensory defects
weak arterial wall, stretching it like an overblown H Dysphagia
balloon and making it likely to rupture. H Visual defects (diplopia, ptosis, dilated pupil, and in-
H Such a rupture is followed by a subarachnoid hemor- ability to rotate the eye caused by compression on
rhage, in which blood spills into the space normally the oculomotor nerve if aneurysm is near the internal
occupied by cerebrospinal fluid. carotid artery)
H Blood spills into brain tissue, where a clot can cause
potentially fatal increased intracranial pressure and Test results
brain tissue damage. Imaging
H Computed tomography scan reveals subarachnoid or
Causes ventricular bleeding with blood in subarachnoid
H Congenital defect space and displaced midline structures.
H Degenerative process H Magnetic resonance imaging shows a cerebral blood
H Combination of congenital defect and degenerative flow void.
process H Skull X-rays may reveal calcified wall of the aneurysm
H Trauma and areas of bone erosion.
Diagnostic procedures
Incidence H Cerebral angiography reveals altered cerebral blood
H Slightly higher in females than in males, especially flow, vessel lumen dilation, and differences in arterial
those in their late 40s or early- to mid-50s filling.
H May occur at any age in either sex

Common characteristics Treatment

H Headache
H Nuchal rigidity General
H Stiff back and legs H Bed rest in a quiet, darkened room with minimal
With rupture stimulation
H Sudden severe headache H Avoidance of coffee, other stimulants, and aspirin
H Altered level of consciousness (LOC)
Medications
Complications H Analgesics
H Neurologic deficits H Antihypertensive agents
H Recurrent bleeding H Sedatives
H Vasospasm H Calcium channel blockers, such as nicardipine and
H Death diltiazem for vasodilation
H Corticosteroids
H Anticonvulsants
H Aminocaproic acid to control bleeding

62 Aneurysm, intracranial
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Determining severity of an intracranial aneurysm rupture

The severity of symptoms varies from patient to patient, de-
pending on the site and amount of bleeding. Five grades
characterize a ruptured cerebral aneurysm:
H Grade I: minimal bleeding The patient is alert with no
neurologic deficit; he may have a slight headache and
nuchal rigidity.
H Grade II: mild bleeding The patient is alert, with a mild
to severe headache and nuchal rigidity; he may have
third-nerve palsy.
H Grade III: moderate bleeding The patient is confused
or drowsy, with nuchal rigidity and, possibly, a mild focal
deficit.
H Grade IV: severe bleeding The patient is stuporous,
with nuchal rigidity and, possibly, mild to severe
hemiparesis.
H Grade V: moribund (usually fatal) If the rupture is
nonfatal, the patient is in a deep coma or decerebrate.

Surgery Patient teaching

H Surgical repair by clipping, ligation, or wrapping
(before or after rupture) Be sure to cover:
H the disorder, diagnosis, and treatment
H how to recognize signs of rebleeding.
Nursing considerations
Discharge planning
Key outcomes H Refer the patient to a visiting nurse or a rehabilita-
The patient will: tion center when necessary.
H maintain adequate ventilation
H maintain or improve LOC
H maintain hemodynamic stability.

Nursing interventions
H Establish and maintain a patent airway.
H Position the patient to promote pulmonary drainage
and prevent upper airway obstruction.
H Impose aneurysm precautions (bed rest in a quiet,
darkened room, keeping the head of the bed flat or
less than 30 degrees, as ordered; limited visitation;
avoidance of strenuous physical activity and straining
with bowel movements; and restricted fluid intake).
H Assist with active range-of-motion (ROM) exercises;
if the patient is paralyzed, perform regular passive
ROM exercises.
H If the patient has facial weakness, assess the gag re-
flex and assist him during meals, placing food in the
unaffected side of his mouth. If he cant swallow, in-
sert a nasogastric tube, as ordered, and administer
tube feedings.
H If the patient cant speak, establish a simple means of
communication or use cards or a notepad. Encour-
age his family to speak to him in a normal tone, even
if he doesnt seem to respond.
H Provide emotional support, and include the patients
family in his care as much as possible. Encourage
family members to adopt a realistic attitude, but
dont discourage hope.
Monitoring
H Vital signs
H Neurologic status
H Arterial blood gas levels
H Intake and output

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Aneurysm, thoracic H Dyspnea

H Cyanosis

aortic H Leg weakness

H Transient paralysis
H Abrupt onset of intermittent neurologic deficits
H Abrupt loss of radial and femoral pulses and right
Overview and left carotid pulses
H Increasing area of flatness over the heart, suggesting
Description cardiac tamponade and hemopericardium
H Abnormal widening of the ascending, transverse, or In dissecting ascending aneurysm
descending part of the thoracic aorta H Pain with a boring, tearing, or ripping sensation in
H May be saccular (outpouching), fusiform (spindle- the thorax or the right anterior chest; may extend to
shaped), or dissecting the neck, shoulders, lower back, and abdomen
H Pain most intense at onset
Pathophysiology H Murmur of aortic insufficiency, a diastolic murmur
H Thoracic aortic aneurysm is caused by a circumfer- H Pericardial friction rub (if hemopericardium pre-
ential or transverse tear of the aortic wall intima, sent)
usually within the medial layer. H Blood pressure may be normal or significantly elevat-
H This occurs in about 60% of patients; its usually an ed, with a large difference in systolic blood pressure
emergency with poor prognosis. between the right and left arms
In dissecting descending aneurysm
Causes H Sharp, tearing pain located between the shoulder
H Atherosclerosis blades that usually radiates to the chest
H Blunt chest trauma H Carotid and radial pulses present and equal
H Bacterial infections, usually at an atherosclerotic bilaterally
plaque H Systolic blood pressure equal
H Coarctation of the aorta H May detect bilateral crackles and rhonchi if pulmo-
H Syphilis infection nary edema present
H Rheumatic vasculitis In dissecting transverse aneurysm
H Marfan syndrome H Sharp, boring, and tearing pain that radiates to the
shoulders
Risk factors H Hoarseness
H Cigarette smoking H Dyspnea
H Hypertension H Throat pain
H Dysphagia
Incidence H Dry cough
H Ascending thoracic aorta most common site
H Occurs predominantly in males younger than age 60 Test results
who have coexisting hypertension Laboratory
H Descending thoracic aortic aneurysms most common H Hemoglobin levels are normal or decreased due to
in younger patients who have had chest trauma blood loss caused by a leaking aneurysm.
Imaging
Common characteristics H Posteroanterior and oblique chest X-rays show
H Asymptomatic until dissection widening of the aorta and mediastinum.
H Aortography shows lumen of the aneurysm and its
Complications size and location.
H Cardiac tamponade H Magnetic resonance imaging and computed tomogra-
H Dissection phy scan help confirm and locate the presence of
aortic dissection.
Diagnostic procedures
Assessment H Electrocardiography helps rule out the presence of
myocardial infarction.
History H Echocardiography may help identify dissecting
H Without signs and symptoms until aneurysm expands aneurysm of the aortic root.
and begins to dissect H Transesophageal echocardiography can be used to
H Sudden pain and possibly syncope measure the aneurysm in the ascending and de-
scending aorta.
Physical findings
H Pallor
H Diaphoresis

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ALERT
Treatment
After surgical repair, monitor for signs that resem-
General ble those of the initial dissecting aneurysm, sug-
H I.V. fluids and whole blood transfusions, if needed gesting a tear at the graft site.
H Weight reduction, if appropriate
H Low-fat diet
H No activity restrictions unless surgery Patient teaching
Medications Be sure to cover:
H Antihypertensives H the diagnosis
H Analgesics H procedure and expected postoperative care, if
H Antibiotics, as appropriate surgery is scheduled
H compliance with antihypertensive therapy, including
Surgery the need for such drugs and the expected adverse
H Surgical resection with a Dacron or Teflon graft effects
replacement H monitoring of blood pressure
H when to call the physician if the patient has any sharp
pain in the chest or back of the neck.
Nursing considerations
Discharge planning
Key outcomes H Refer the patient to a smoking-cessation program, if
The patient will: indicated.
H maintain adequate cardiac output and hemodynamic
stability
H maintain adequate ventilation
H express feelings of increased comfort and decreased
pain
H show no signs or symptoms of infection
H maintain adequate fluid volume.

Nursing interventions
H In a nonemergency situation, allow the patient to ex-
press his fears and concerns and identify and use ef-
fective coping strategies.
H Offer the patient and his family psychological sup-
port.
H Give prescribed analgesics to relieve pain.
After repair of thoracic aneurysm
H Maintain blood pressure in prescribed range with
fluids and medications.
H Give prescribed analgesics.
H After stabilization of vital signs, encourage and assist
the patient in turning, coughing, and deep breathing.
H Help the patient walk as soon as hes able.
H Assist the patient with range-of-motion exercises.

Monitoring
H Vital signs and hemodynamics
H Chest tube drainage
H Heart and lung sounds
H Laboratory results
H Distal pulses
H Level of consciousness and pain
H Signs of infection
H I.V. therapy and intake and output

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Aneurysm, ventricular H Double, diffuse, or displaced apical impulse

H Gallop rhythm
H Crackles and rhonchi

Overview Test results

Description
H An outpouching, almost always of the left ventricle,
that produces ventricular wall dysfunction
H May develop within days to weeks after myocardial
infarction (MI) or may be delayed for years
Pathophysiology
H When MI destroys a large muscular section of the left
ventricle, necrosis reduces the ventricular wall to a
thin sheath of fibrous tissue.
H Under intracardiac pressure, the thin sheath stretch-
es and forms a separate noncontractile sac (aneu-
rysm).
H Abnormal muscle wall movement accompanies ven-
tricular aneurysm.
H During systolic ejection, the abnormal muscle wall
movements cause the remaining normally function-
ing myocardial fibers to increase the force of con-
traction to maintain stroke volume and cardiac
output.
H At the same time, a portion of the stroke volume is
lost to passive distention of the noncontractile sac.
Causes
H MI
Incidence
H Occurs in about 20% of patients after MI
Common characteristics
H Occurs after MI
Complications
H Ventricular arrhythmias
H Cerebral embolization
H Heart failure
Imaging
H Two-dimensional echocardiography demonstrates
abnormal motion in the left ventricular wall.
H Left ventriculography reveals left ventricular enlarge-
ment, with an area of akinesia or dyskinesia (during
cineangiography) and diminished cardiac function.
H Chest X-rays may disclose an abnormal bulge distort-
ing the hearts contour if the aneurysm is large;
X-rays may be normal if the aneurysm is small.
H Noninvasive nuclear cardiology scan may indicate the
site of infarction and suggest the area of aneurysm.
Diagnostic procedures
H Electrocardiography may show persistent ST-T wave
elevations.
Treatment
General
H Depends on the size of the aneurysm and the pres-
ence of complications
H May require only routine medical examination to fol-
low the patients condition
H May require aggressive measures, such as cardiover-
sion, defibrillation, and endotracheal intubation
H Weight reduction, if appropriate
H Low-fat diet
H No activity restrictions, unless surgery
Medications
H Antiarrhythmics, such as lidocaine and procainamide
H Cardiac glycosides such as digoxin
H Diuretics, such as furosemide and torsemide
H Fluid and electrolyte replacement
H Analgesics
H Antihypertensives, as appropriate
H Nitrates
H Anticoagulants, such as heparin and warfarin

Assessment Surgery
H Embolectomy
History H Aneurysmectomy with myocardial revascularization
H Previous MI
H Dyspnea
H Fatigue Nursing considerations
Physical findings Key outcomes
H Edema The patient will:
H Visible or palpable systolic precordial bulge H maintain adequate cardiac output
H Distended jugular veins, if heart failure is present H maintain hemodynamic stability
H Irregular peripheral pulse rhythm H maintain adequate fluid balance
H Arrhythmias such as premature ventricular contrac- H express feelings of increased energy and decreased
tions fatigue
H Pulsus alternans H express feelings of decreased anxiety.

66 Aneurysm, ventricular
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Nursing interventions
H Give prescribed drugs.
H Prepare for surgery, if indicated.

ALERT
Be alert for sudden changes in sensorium that may
indicate cerebral embolization and for any signs
that suggest renal failure or MI.

H Provide psychological support for the patient and his

family.
Monitoring
Heart failure
H Vital signs and heart sounds
H Cardiac rhythm, especially for ventricular arrhyth-
mias
H Intake and output; and fluid and electrolyte balance
H Blood urea nitrogen and serum creatinine levels
After surgery
H Pulmonary artery catheter pressures
H Signs and symptoms of infection
H Type and amount of chest tube drainage

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medications and possible adverse reactions
H when to notify the physician
H expected postoperative care, if the patient is sched-
uled to undergo resection
H monitoring pulse irregularity and rate changes.

Discharge planning
H Refer family or caregiver to a community-based car-
diopulmonary resuscitation training program.
H Refer the patient to a weight-reduction program, if
indicated.
H Refer the patient to a smoking-cessation program, if
indicated.

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Ankylosing spondylitis
Overview
Description
H Rheumatoid disease primarily affecting sacroiliac,
apophyseal, and costocervical joints and adjacent lig-
amentous or tendinous attachments to bone
H Usually occurs as a primary disorder; may occur sec-
ondary to Reiters syndrome, psoriatic arthritis, or
inflammatory bowel disease
H Also called rheumatoid spondylitis or Marie-
Strmpell disease
Pathophysiology
H Disease begins in the sacroiliac; gradually progresses
to the lumbar, thoracic, and cervical spine.
H Bone and cartilage deterioration leads to fibrous
tissue formation and eventual fusion of the spine
or peripheral joints.
Causes
H Unknown
H Familial tendency
H Initial inflammation may result from immune system
activation by bacterial infection
Incidence
H Affects males two to three times more commonly
than females
H Well-recognized in males but commonly overlooked
or missed in females
H More peripheral joint involvement in females
Common characteristics
H Symptoms can unpredictably remit, exacerbate, or
arrest at any stage
Complications
H Atlantoaxial subluxation of cervical vertebrae
H Deposits of amyloid material in the kidneys, which
may lead to renal impairment or failure
Detecting ankylosing spondylitis
in women
Ankylosing spondylitis seldom occurs in women, which is
why if a womans symptoms include pelvic pain diagnosti-
cians typically overlook ankylosing spondylitis and sus-
pect pelvic imflammatory disease. However, its important
to assess a female patient with apparent pelvic disease
carefully especially if culture results identify no appar-
ent cause of her discomfort. Otherwise, misdiagnosis can
lead to unwarranted invasive tests and treatments and
cause the patient needless anxiety related to contracting a
sexually transmitted disease. Asking the patient if theres a
family history of ankylosing spondylitis and the perfor-
mance of a thorough health and social history is advisable.
68 Ankylosing spondylitis
Assessment
History
H Intermittent lower back pain most severe in the
morning or after inactivity and relieved by exercise
H Mild fatigue, fever, anorexia, and weight loss
H May describe pain in shoulders, hips, knees, and an-
kles
H Pain over the symphysis pubis, which may lead to its
being mistaken for pelvic inflammatory disease (see
Detecting ankylosing spondylitis in women)
Physical findings
H Stiffness or limited motion of the lumbar spine
H Pain and limited chest expansion
H Kyphosis
H Iritis
H Warmth, swelling, or tenderness of affected joints
H Sausage shape to small joints such as toes
H Aortic murmur caused by insufficiency
H Cardiomegaly
H Upper lobe pulmonary fibrosis, which mimics tuber-
culosis, that may reduce vital capacity to 70% or less
of predicted volume
Test results
H Diagnosis of primary ankylosing spondylitis requires
meeting established criteria. (See Diagnosing pri-
mary ankylosing spondylitis.)
Laboratory
H HLA antigen typing test shows serum findings that in-
clude HLA-B27 in about 95% of patients with primary
ankylosing spondylitis and up to 80% of patients with
secondary disease.
H Serum rheumatoid factor tests show the absence of
rheumatoid factor, which helps rule out rheumatoid
arthritis, which has similar symptoms.
H Serum alkaline phosphate and creatine kinase tests
show slightly elevated erythrocyte sedimentation rate,
serum alkaline phosphate levels, and creatine kinase
levels in active disease.
H Serum immunoglobulin (Ig) profile shows elevated
serum IgA levels.
Imaging
H X-ray studies define characteristic changes, such as
bilateral sacroiliac involvement (the hallmark of the
disease); blurring of the joints bony margins in early
disease; patchy sclerosis with superficial bony ero-
sions; eventual squaring of vertebral bodies; and
bamboo spine with complete ankylosis.
Treatment
General
H Good posture; stretching and deep-breathing
exercises
H Braces and lightweight supports, if appropriate
H Heat, warm showers, baths, and ice
9400A.qxd 8/2/12 4:21 PM Page 69

H Nerve stimulation Diagnosing primary ankylosing

H Nutritious diet spondylitis
H Encourage activity as tolerated
For a reliable diagnosis, the patient must meet:
H criterion 7 and any one of criteria 1 through 5, or
Medications H any five of criteria 1 through 6 if he doesnt have
H Nonsteroidal anti-inflammatory drugs such as criterion 7.
ibuprofen Seven criteria
H Sulfasaline 1. Axial skeleton stiffness for at least 3 months thats
H Methotrexate relieved by exercise
H Corticosteroids 2. Lumbar pain that persists at rest
H Tumor-necrosis-factor alpha inhibitors 3. Thoracic cage pain of at least 3 months duration that
persists at rest
Surgery 4. Past or current iritis
5. Decreased lumbar range of motion
H Hip replacement surgery with severe hip involvement
6. Decreased chest expansion (age-related)
H Spinal wedge osteotomy with severe spinal involve-
7. Bilateral, symmetrical sacroiliitis demonstrated by
ment radiographic studies

Nursing considerations
H avoidance of prolonged walking, standing, sitting, or
Key outcomes driving
The patient will: H regular stretching and deep-breathing exercises;
H express feelings of increased comfort and decreased swimming on a regular basis, if possible
pain H measurement of patients height every 3 to 4 months
H express feelings of increased energy to detect kyphosis
H recognize limitations imposed by illness and express H nutrition and weight maintenance.
feelings about these limitations
H identify factors that increase the risk for injury. Discharge planning
H Refer the patient to physical therapy, as needed.
Nursing interventions H Refer the patient to the Spondylitis Association of
H Keep in mind the patients limited range of motion America or the Arthritis Foundation for additional
(ROM) when planning self-care tasks and activities. support and information.
H Offer support and reassurance.
H Give prescribed analgesics.
H Apply heat locally and massage, as indicated.
H Have the patient perform active ROM exercises.
H Pace periods of exercise and rest to help the patient
achieve comfortable energy levels and lung oxygena-
tion.
H If treatment includes surgery, ensure proper body
alignment and positioning.
H Involve other caregivers, such as a social worker, vis-
iting nurse, and dietitian.
Monitoring
H Mobility and comfort level
H Respiratory status
H Heart sounds

Patient teaching
Be sure to cover:
H avoidance of physical activity that places stress on the
back such as lifting heavy objects
H importance of standing upright; sitting upright in a
high, straight-back chair; and avoiding leaning over a
desk
H importance of sleeping in a prone position on a hard
mattress and avoiding using pillows under the neck
or knees

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Anorexia nervosa H Limits or restricts food intake; eats small portions

(see Criteria for hospitalizing a patient with
anorexia nervosa)
Overview Complications
H Suicide
Description H Electrolyte imbalances
H Psychological disorder of self-imposed starvation re- H Malnutrition
sulting from a distorted body image and an intense H Dehydration
and irrational fear of gaining weight H Esophageal erosion, ulcers, tears, and bleeding
H Actual loss of appetite, which is rare H Tooth and gum erosion and dental caries
H May occur simultaneously with bulimia nervosa H Decreased left ventricular muscle mass and chamber
size
Pathophysiology H Decreased cardiac output
H Decreased calorie intake depletes body fat and pro- H Hypotension
tein stores. H Electrocardiogram (ECG) changes
H Estrogen deficiency occurs (in females) due to lack H Heart failure
of lipid substrate for synthesis, causing amenorrhea. H Increased susceptibility to infection
H Testosterone levels fluctuate (in males), and de- H Amenorrhea
creased erectile function and sperm count occurs. H Anemia
H Ketoacidosis occurs from increased use of fat as en- H Death
ergy fuel.
Causes Assessment
H Exact cause unknown
H Social attitudes that equate slimness with beauty History
H Subconscious effort to exert personal control over H 15% or greater weight loss for no organic reason
life or to protect oneself from dealing with issues H Morbid fear of being fat
surrounding sexuality H Compulsion to be thin
H Elaborate food preparation and eating rituals H Angry disposition
H Achievement pressure H Tendency to minimize weight loss
H Dependence and independence issues H Ritualistic
H Stress caused by multiple responsibilities H Amenorrhea
H History of sexual abuse H Infertility
H Loss of libido
Risk factors H Fatigue
H Low self-esteem H Sleep alterations
H Compulsive personality H Intolerance to cold
H High achievement goals H Constipation or diarrhea

Incidence Physical findings

H 5% to 10% of the population; more than 90% of H Hypotension
those affected are females H Bradycardia
H Emaciated appearance
H Skeletal muscle atrophy
Special populations
H Loss of fatty tissue
Anorexia nervosa occurs primarily in adolescents H Atrophy of breast tissue
and young adults but may also affect older females H Blotchy or sallow skin
and, occasionally, males. H Lanugo on the face and body
H Dryness or loss of scalp hair
H Calluses of the knuckles
Common characteristics H Abrasions and scars on the dorsum of the hand
H Preoccupation with body size H Dental caries
H Tendency to describe self as fat H Oral or pharyngeal abrasions
H Dissatisfaction with a particular aspect of physical H Painless salivary gland enlargement
appearance H Bowel distention
H Compulsive exercising H Slowed reflexes
H Self-induced vomiting
H Laxative or diuretic abuse

70 Anorexia nervosa
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DSM-IV-TR criteria
These criteria must be documented:
H Refusal to maintain or achieve normal weight for age
and height
H Intense fear of gaining weight or becoming fat, even
though underweight
H Disturbance in perception of body weight, size, or
shape
H Absence of at least three consecutive menstrual cy-
cles when otherwise expected to occur (in females)
Test results
Laboratory
H Hemoglobin level, platelet count, and white blood
cell count are decreased.
H Bleeding time is prolonged.
H Erythrocyte sedimentation rate is decreased.
H Serum creatinine, blood urea nitrogen, uric acid,
cholesterol, total protein, albumin, sodium, potassi-
um, chloride, calcium, and fasting blood glucose
levels are decreased.
H Alanine aminotransferase and aspartate aminotrans-
ferase levels are elevated in severe starvation states.
H Serum amylase levels are elevated.
H In females, serum luteinizing hormone and follicle-
stimulating hormone levels are decreased.
H Triiodothyronine levels are decreased.
H Urinalysis shows dilute urine.
Diagnostic procedures
H ECG may show nonspecific ST interval, T-wave
changes, and prolonged PR interval; ventricular
arrhythmias may also be present.
Treatment
General
H Behavior modification
H Curtailed activity for cardiac arrhythmias
H Group, family, or individual psychotherapy
H Balanced diet with a normal eating pattern
H Parenteral nutrition, if necessary
H Gradual increase in physical activity when weight
gain and stabilization occur
Medications
H Vitamin and mineral supplements
H Electrolyte replacement
H Serotonin reuptake inhibitors, such as citalopram,
fluoxetine, and sertraline, after weight gain is estab-
lished
Nursing considerations
Key outcomes
The patient will:
H acknowledge change in body image
H express positive feelings about self
H achieve and maintain expected body weight
H achieve expected state of wellness.
Criteria for hospitalizing a patient
with anorexia nervosa
A patient with anorexia nervosa can be successfully treat-
ed on an outpatient basis. However, if the patient displays
any of the signs listed here, hospitalization is mandatory:
H rapid weight loss equal to 15% or more of normal body
mass
H persistent bradycardia (50 beats/minute or less)
H hypotension with a systolic reading less than or equal
to 90 mm Hg
H hypothermia (core body temperature less than or equal
to 97 F (36.1 C)
H presence of medical complications, suicidal ideation
H persistent sabotage or disruption of outpatient
treatment resolute denial of condition and the need
for treatment.
Nursing interventions
H Support the patients efforts to achieve target weight.
H Negotiate an adequate food intake with the patient.
H Supervise the patient one-on-one during meals and
for 1 hour afterward.
Monitoring
H Vital signs
H Intake and output
H Electrolyte and complete blood count levels
H Weight on a regular schedule
H Activity for compulsive exercise
ALERT
Monitor the patient for 1 hour after meals to en-
sure no self-induced vomiting.
Patient teaching
Be sure to cover:
H nutrition
H importance of keeping a food journal
H avoidance of discussions about food between the
patient and her family.
Discharge planning
H Refer the patient to support services.
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Incidence
Life-threatening disorder H Occurs worldwide
H Most common in developing countries

Anthrax H Most common in domestic herbivores, including

sheep, cattle, horses, and goats, and wild herbivores
H Estimates of 20,000 to 100,000 cases per year (Ap-
proximately 95% of human anthrax are the cuta-
Overview neous form; about 5% are the inhalation form; GI an-
thrax is rare.)
Description
H An acute bacterial infection occurring most com- Common characteristics
monly in herbivorous animals; the natural resistance H History of exposure to B. anthracis spores
of humans to anthrax greater than that of these H Clinical manifestation will depend on the form of
animals anthrax
H Also known as a potential agent for use in bioterror-
ism and biological warfare; classified as a Category A Complications
biological disease H Septicemia
H Three forms of anthrax in humans, depending on the H Hemorrhagic mediastinitis
mode of transmission: cutaneous, inhalation (wool- H Pneumonia
sorters disease), and GI H Respiratory failure
H Cutaneous anthrax: the most common form H Hemorrhagic thoracic lymphadenitis
H Without treatment, mortality rate from cutaneous an- H Meningitis
thrax, 20%; mortality rate less than 1% with treat- H Death
ment
H Even with treatment, inhalation anthrax usually fatal
H With treatment, death in 25% to 60% of cases of GI Assessment
anthrax
H No screening test for anthrax History
Cutaneous anthrax
Pathophysiology H Painless ulcer
H Bacillus anthracis is an encapsulated, aerobic, H Mild or no constitutional symptoms
chain-forming, gram-positive rod that forms oval Inhalation anthrax
spores; spores are hardy and can survive for years H Initial prodromal flulike symptoms:
under adverse conditions. Malaise; dry cough
H B. anthracis, an extracellular pathogen, evades Mild fever; chills
phagocytosis, invades the bloodstream, and multi- Headache; myalgia
plies rapidly. Severe respiratory distress
H In cutaneous anthrax, spores enter the body through Chest pain
abraded or broken skin or by biting flies; the spores GI anthrax
germinate within hours, the vegetative cells multiply, H Nausea; vomiting
and anthrax toxin is produced. H Decreased appetite
H In inhalation anthrax, spores are deposited directly H Fever
into the alveoli and phagocytized by macrophages; H Abdominal pain
some are carried to and germinate in mediastinal H Vomiting blood
nodes. This may result in overwhelming bacteremia, H Severe bloody diarrhea
hemorrhagic mediastinitis, and secondary pneumo-
nia. Physical findings
H In GI anthrax, primary infection can occur in the in- Cutaneous anthrax
testine by organisms that survive passage through the H Initially, a small, papular, pruritic lesion that resem-
stomach; acute inflammation of the intestinal tract bles an insect bite
results. H Lesion that develops into a vesicle in 1 to 2 days
H Lesion that finally becomes a small, painless ulcer
Causes with a necrotic center, surrounded by nonpitting
H Bacterial infection with B. anthracis edema
H Smaller secondary vesicles that may surround some
Risk factors lesions
H Laboratory and industrial workers at risk for occupa- H Lesions that are generally located on exposed areas
tional exposure of the skin
H Painful, regional, nonspecific lymphadenitis

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Inhalational anthrax H Encourage verbalization of fears and concerns.

H Increasing fever H Provide adequate hydration.
H Dyspnea, stridor H Provide a well-balanced diet.
H Hypoxia; cyanosis H Assist the patient in the development of effective cop-
H Hypotension; shock ing mechanisms.
GI anthrax H Provide adequate rest periods.
H Fever
H Rapidly developing ascites Monitoring
H Vital signs
Test results H Intake and output
Laboratory H Respiratory status
H Gram stain, direct fluorescent antibody staining, and H Neurologic status
culture show presence of B. anthracis. H Cardiovascular status
H Blood cultures show presence of B. anthracis. H Skin lesions
H Cerebrospinal fluid analysis reveals presence of H GI status
B. anthracis. H Complications
H Complete blood count shows polymorphonuclear H Response to treatment
leukocytosis in severe disease. H Progression of infection
H Serum antibody tests reveal the presence of the
specific antibody to B. anthracis.
Imaging Patient teaching
H Chest X-ray show symmetrical mediastinal widening
in hemorrhagic mediastinitis. Be sure to cover:
H the disorder, diagnosis, and treatment
H medications and possible adverse reactions
Treatment H when to notify the physician
H anthrax prevention.
General
H Treatment initiated as soon as exposure to anthrax is
suspected (essential to preventing anthrax infection;
may also help prevent death)
H No dietary restrictions
H Adequate fluid intake
H Physical activity as tolerated

Medications
H Antibiotics, such as ciprofloxacin, doxycycline, and
amoxicillin
H Oxygen, as needed

Surgery
H May be necessary for complications such as hemor-
rhagic mediastinitis

Nursing considerations
Key outcomes
The patient will:
H maintain adequate nutrition and hydration
H verbalize feelings of fear and anxiety
H demonstrate effective coping mechanisms
H maintain tissue perfusion and cellular oxygenation
H maintain effective ventilation.

Nursing interventions
H Give prescribed drugs.
H Maintain patent airway and adequate ventilation.
H Report any case of anthrax in either livestock or hu-
mans to the local board of health.
H Maintain standard precautions.

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Aortic insufficiency H Palpitations, head pounding

H Symptoms of heart failure, in late stages

Physical findings
Overview H Corrigans pulse
H Pulsus bisferiens
Description H Pulsating nail beds and Quinckes sign
H A heart condition in which blood flows back into the H Wide pulse pressure
left ventricle, causing excess fluid volume H Diffuse, hyperdynamic apical impulse, displaced lat-
H Also called aortic regurgitation erally and inferiorly
H Systolic thrill at base or suprasternal notch
Pathophysiology H S3 gallop with increased left ventricular end-diastolic
H Blood flows back into the left ventricle during dias- pressure
tole, causing increased left ventricular diastolic pres- H High frequency, blowing early-peaking, diastolic de-
sure. crescendo murmur best heard with the patient sitting
H This results in volume overload, dilation and, eventu- leaning forward and in deep fixed expiration (see
ally, hypertrophy of the left ventricle. Identifying the murmur of aortic insufficiency)
H Excess fluid volume also eventually results in in- H Austin Flint murmur
creased left atrial pressure and increased pulmonary H Head bobbing with each heartbeat
vascular pressure. H Tachycardia, peripheral vasoconstriction, and pul-
monary edema if severe aortic insufficiency
Causes
H Rheumatic fever Test results
H Primary disease of the aortic valve leaflets, the wall Imaging
or the aortic root, or both H Chest X-rays may show left ventricular enlargement
H Hypertension and pulmonary vein congestion.
H Infective endocarditis H Echocardiography may show left ventricular enlarge-
H Trauma ment, increased motion of the septum and posterior
H Idiopathic valve calcification wall, thickening of valve cusps, prolapse of the valve,
H Aortic dissection flail leaflet, vegetations, or dilation of the aortic root.
H Aortic aneurysm Diagnostic procedures
H Connective tissue diseases H Electrocardiography shows sinus tachycardia, left
axis deviation, left ventricular hypertrophy, and left
Incidence atrial hypertrophy in severe disease.
H Occurs most commonly in males H Cardiac catheterization shows presence and degree
H When associated with mitral valve disease: more of aortic insufficiency, left ventricular dilation and
common in females function, and coexisting coronary artery disease.
Common characteristics
H Typically asymptomatic until the fourth or fifth Treatment
decade of life
H Orthopnea General
H Paroxysmal nocturnal dyspnea H Periodic noninvasive monitoring of aortic insufficien-
H Exertional dyspnea cy and left ventricular function with echocardiogram
H Medical control of hypertension
Complications H Low-sodium diet
H Left-sided heart failure H Planned periodic rest periods to avoid fatigue
H Pulmonary edema
H Myocardial ischemia Medications
H Cardiac glycosides such as digoxin
H Diuretics, such as furosemide and torsemide
Assessment H Vasodilators such as nitrates
H Antihypertensives
History H Antiarrhythmics, such as amiodarone and
H Exertional dyspnea, orthopnea, paroxysmal noctur- propafenone
nal dyspnea H Infective endocarditis prophylaxis, as appropriate
H Sensation of a forceful heartbeat, especially in supine H Anticoagulants such as warfarin
position H Antiplatelets, such as clopidogrel and ticlopidine
H Angina, especially nocturnal
H Fatigue

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ALERT Identifying the murmur of aortic

insufficiency
Avoid using beta-adrenergic blockers due to their A high-pitched, blowing decrescendo murmur that radi-
negative inotropic effects. ates from the aortic valve area to the left sternal border
characterizes aortic insufficiency.
Surgery
SYSTOLE DIASTOLE SYSTOLE
H Valve replacement S1 S2 S1 S2

Nursing considerations
Key outcomes
The patient will:
H carry out activities of daily living without excess fa-
tigue or decreased energy
H maintain cardiac output, demonstrate hemodynamic
stability, and not develop arrhythmias Patient teaching
H maintain adequate fluid balance
H maintain adequate ventilation. Be sure to cover:
H the disorder, diagnosis, and treatment
Nursing interventions H medications and possible adverse reactions
H Give prescribed drugs. H when to notify the physician
H If the patient needs bed rest, stress its importance; H periodic rest periods in the patients daily routine
provide a bedside commode. H leg elevation whenever the patient sits
H Alternate periods of activity and rest. H dietary restrictions
H Allow the patient to express his concerns about the H signs and symptoms of heart failure
effects of activity restrictions on his responsibilities H importance of consistent follow-up care
and routines. H monitoring of pulse rate and rhythm
H Keep the patients legs elevated while he sits in a H blood pressure control.
chair.
H Place the patient in an upright position, if necessary, Discharge planning
and administer oxygen. H Refer the patient to an outpatient cardiac rehabilita-
H Keep the patient on a low-sodium diet. Consult a di- tion program, if indicated.
etitian. H Refer the patient to a smoking-cessation program, if
H Following surgery, watch for hypotension, arrhyth- indicated.
mias, and thrombus formation. H Refer the patient to a weight-reduction program, if
indicated.
Monitoring
H Signs and symptoms of heart failure
H Pulmonary edema
H Adverse reactions to drug therapy
H Complications
After surgery
H Vital signs and cardiac rhythm
H Heart sounds
H Chest tube drainage
H Neurologic status
H Arterial blood gas levels
H Intake and output; daily weight
H Blood chemistry studies, prothrombin time, and
International Normalized Ratio values
H Chest X-ray results
H Pulmonary artery catheter pressures

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Physical findings
Aortic stenosis H Small, sustained arterial pulses that rise slowly
H Distinct lag between carotid artery pulse and apical
pulse
Overview H Orthopnea
H Prominent jugular vein a waves
Description H Peripheral edema
H Narrowing of the aortic valve that affects blood flow H Diminished carotid pulses with delayed upstroke
in the heart H Apex of the heart may be displaced inferiorly and lat-
H Classified as either acquired or rheumatic erally
H Suprasternal thrill
Pathophysiology
H Stenosis of the aortic valve results in impedance to Special populations
forward blood flow.
H The left ventricle requires greater pressure to open An early systolic ejection murmur may be present
the aortic valve. in children and adolescents who have noncalcified
H Added workload increases myocardial oxygen de- valves. The murmur is low-pitched, rough, and
mands. rasping and is loudest at the base in the second in-
H Diminished cardiac output reduces coronary artery tercostal space.
blood flow.
H Left ventricular hypertrophy and failure result. H Split S2 develops as stenosis becomes more severe
H Prominent S4
Causes H Harsh, rasping, mid- to late-peaking systolic murmur
H Idiopathic fibrosis and calcification thats best heard at the base and commonly radiates
H Congenital aortic bicuspid valve to carotids and apex (see Identifying the murmur
H Rheumatic fever of aortic stenosis)
H Atherosclerosis
Test results
Risk factors Imaging
H Diabetes mellitus H Chest X-ray shows valvular calcification, left ventricu-
H Hypercholesterolemia lar enlargement, pulmonary vein congestion and, in
later stages, left atrial, pulmonary artery, right atrial,
Incidence and right ventricular enlargement.
H Possibly asymptomatic until ages 50 to 70, even H Echocardiography shows decreased valve area, in-
though stenosis present since childhood creased gradient, and increased left ventricular wall
H About 80% of patients: male thickness.
Diagnostic procedures
Common characteristics H Cardiac catheterization shows increased pressure
H Long latent period gradient across the aortic valve, increased left ven-
H Classic triad of angina pectoris, syncope, and tricular pressures, and presence of coronary artery
dyspnea disease.
H Electrocardiography may show left ventricular hyper-
Complications trophy, atrial fibrillation, or other arrhythmia.
H Left-sided heart failure
H Right-sided heart failure
H Infective endocarditis Treatment
H Cardiac arrhythmias, especially atrial fibrillation
H Sudden death General
H Left ventricular hypertrophy H Periodic noninvasive evaluation of the severity of
valve narrowing
H Lifelong treatment and management of congenital
Assessment aortic stenosis
H Low-sodium, low-fat, low-cholesterol diet
History H Planned rest periods
H May be asymptomatic
H Dyspnea on exertion Medications
H Angina H Cardiac glycosides such as digoxin
H Exertional syncope H Antibiotic infective endocarditis prophylaxis
H Fatigue H Anticoagulants, such as warfarin
H Palpitations H Antiplatelets such as clopidogrel and ticlopidine
H Paroxysmal nocturnal dyspnea

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ALERT Identifying the murmur of aortic stenosis

A low-pitched, harsh crescendo-decrescendo murmur that
The use of diuretics and vasodilators may lead to radiates from the aortic valve area to the carotid artery
hypotension and inadequate stroke volume. characterizes aortic stenosis.

Surgery SYSTOLE DIASTOLE SYSTOLE

S1 S2 S1 S2
H In adults, valve replacement after they become symp-
tomatic with hemodynamic evidence of severe ob-
struction
H Percutaneous balloon aortic valvuloplasty
H In children without calcified valves, simple commis-
surotomy under direct visualization
H Ross procedure in patients younger than age 5

Nursing considerations Patient teaching

Key outcomes
The patient will:
H perform activities of daily living without excess fa-
tigue or exhaustion
H avoid complications
H maintain cardiac output
H demonstrate hemodynamic stability
H maintain balanced fluid status
H maintain joint mobility and range of motion
H develop and demonstrate adequate coping skills.
Nursing interventions
H Give prescribed drugs.
H Maintain a low-sodium diet. Consult with a dietitian.
H If the patient requires bed rest, stress its importance.
Provide a bedside commode.
H Alternate periods of activity and rest.
H Allow the patient to voice concerns about the effects
of activity restrictions.
H Keep the patients legs elevated while he sits in a
chair.
H Place the patient in an upright position, and adminis-
ter oxygen, as needed.
H Allow the patient to express his fears and concerns.
Be sure to cover:
H the disorder, diagnosis, and treatment
H medications and possible adverse reactions
H when to notify the physician
H periodic rest in the patients daily routine
H leg elevation whenever the patient sits
H dietary and fluid restrictions
H importance of consistent follow-up care
H signs and symptoms of heart failure
H infective endocarditis prophylaxis
H pulse rate and rhythm
H monitoring for atrial fibrillation and other arrhyth-
mias.
Discharge planning
H Refer the patient to a weight-reduction program, if
indicated.
H Refer the patient to a smoking-cessation program, if
indicated.

Monitoring
H Vital signs
H Intake and output
H Signs and symptoms of heart failure
H Signs and symptoms of progressive aortic stenosis
H Daily weight
H Arrhythmias
H Respiratory status
H Prothrombin time and International Normalized
Ratio
If the patient has surgery
H Signs and symptoms of thrombus formation
H Hemodynamics
H Arterial blood gas results
H Blood chemistry results
H Chest X-ray results

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Appendicitis H Anorexia
H Nausea, vomiting

Physical findings
Overview H Low-grade fever, tachycardia
H Adjusts posture to decrease pain
Description H Guarding
H Inflammation of the vermiform appendix H Normoactive bowel sounds, with possible constipa-
H Most common major abdominal surgical disease tion or diarrhea
H Fatal if left untreated; gangrene and perforation de- H Rebound tenderness and spasm of the abdominal
velop within 36 hours muscles
H Rovsings sign (pain in right lower quadrant that oc-
Pathophysiology curs with palpation of left lower quadrant)
H Mucosal ulceration triggers inflammation, which H Psoas sign (abdominal pain that occurs when the pa-
temporarily obstructs the appendix. tient flexes his hip with pressure applied to his knee)
H Obstruction causes mucus outflow, increasing pres- H Obturator sign (abdominal pain that occurs when the
sure in the distended appendix; the appendix then hip is rotated)
contracts. H Absent abdominal tenderness or flank tenderness
H Bacteria multiply and inflammation and pressure in- with retrocele or pelvic appendix
crease, restricting blood flow and causing thrombus
and abdominal pain. Test results
Laboratory
Causes H White blood cell count is moderately elevated, with
H Foreign body an increased numbers of immature cells.
H Neoplasm Imaging
H Mucosal ulceration H Abdominal or transvaginal ultrasound shows appen-
H Fecal mass diceal inflammation.
H Stricture H Barium enema reveals nonfilling appendix.
H Barium ingestion H Abdominal computed tomography scan demonstrates
H Viral infection suspected perforation or abscess.
Risk factors
H Adolescent male Treatment
Incidence General
H Can occur at any age; however, the majority of cases H Delaying surgery until antibiotic therapy has been ini-
occur between ages 11 and 20 tiated, if an abscess suspected
H Affects both sexes; however, between puberty and age H Nothing by mouth until after surgery, then gradual re-
25, more prevalent in men turn to regular diet
H Early postoperative ambulation
Common characteristics H Incentive spirometry
H Abdominal pain
H Anorexia Medications
H Vomiting H I.V. fluids
H Analgesics
Complications H Antibiotics preoperatively and if peritonitis develops
H Wound infection
H Intra-abdominal infection Surgery
H Fecal fistula H Appendectomy
H Intestinal obstruction
H Incisional hernia
H Peritonitis (most common) Nursing considerations
H Death
Key outcomes
The patient will:
Assessment H express feelings of increased comfort
H avoid complications
History H exhibit no signs of infection
H Abdominal pain thats initially generalized, then lo- H maintain calorie requirement
calizes in the right lower abdomen (McBurneys H maintain normal fluid volume.
point)

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Nursing interventions
H Maintain nothing-by-mouth status until surgery is
performed.
H Administer I.V. fluids
H Avoid administering analgesics until the diagnosis is
confirmed.
H Avoid administering cathartics or enemas that may
rupture the appendix.
H Place the patient in Fowlers position to decrease
pain.
H Give prescribed drugs.

ALERT
Never apply heat to the right lower abdomen; this
can cause the appendix to rupture.

Monitoring
After surgery
H Vital signs
H Intake and output
H Pain control
H Bowel sounds, passing of flatus, or bowel movements
H Wound healing

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H preoperative teaching
H possible complications
H appropriate wound care
H medication administration, dosage, and possible
adverse reactions
H postoperative activity limitations.

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Arterial occlusive Assessment

disease History
H One or more risk factors
H Family history of vascular disease
Overview H Intermittent claudication
H Rest pain
Description H Poor healing wounds or ulcers
H An obstruction or narrowing of the lumen of the aor- H Impotence
ta and its major branches H Dizziness or near syncope
H May affect arteries, including the carotid, vertebral, H Transient ischemic attack symptoms
innominate, subclavian, femoral, iliac, renal, mesen-
teric, and celiac Physical findings
H Prognosis dependent on location of the occlusion H Trophic changes of involved arm or leg
and development of collateral circulation that coun- H Diminished or absent pulses in arm or leg
teracts reduced blood flow H Presence of ischemic ulcers
H Pallor with elevation of arm or leg
Pathophysiology H Dependent rubor
H Narrowing of vessel leads to interrupted blood flow, H Arterial bruit
usually to the legs and feet. H Hypertension
H During times of increased activity or exercise, blood H Pain
flow to surrounding muscles cant meet the metabol- H Pulselessness distal to the occlusion
ic demand. H Paralysis and paresthesia occurring in the affected
H This results in pain in affected areas. arm or leg
H Cool extremities
Causes
H Atherosclerosis Test results
H Immune arteritis Imaging
H Embolism H Arteriography shows type, location, and degree of
H Thrombosis obstruction, and the establishment of collateral cir-
H Thromboangiitis obliterans culation.
H Raynauds disease H Ultrasonography and plethysmography show de-
H Fibromuscular disease creased blood flow distal to the occlusion.
H Atheromatous debris (plaques) H Doppler ultrasonography shows a relatively
H Indwelling arterial catheter low-pitched sound and a monophasic waveform.
H Direct blunt or penetrating trauma H EEG and computed tomography scan may show the
presence of brain lesions.
Risk factors Other
H Smoking H Segmental limb pressures and pulse volume mea-
H Hypertension surements show the location and extent of the occlu-
H Dyslipidemia sion.
H Diabetes mellitus H Ophthalmodynamometry shows the degree of ob-
H Advanced age struction in the internal carotid artery.
H Electrocardiography may show presence of cardio-
Incidence vascular disease.
H More common in males than in females
H Usually occurs in people older than age 50
H Higher incidence in patients with diabetes Treatment
H Arteries in the legs more commonly affected
General
Common characteristics H Smoking cessation
H Intermittent claudication H Hypertension, diabetes, and dyslipidemia control
H Decreased temperature in arms and legs H Foot and leg care
H Numbness or paresthesia H Weight control
H Low-fat, low-cholesterol, high-fiber diet
Complications H Regular walking program
H Severe ischemia
H Skin ulceration Medications
H Gangrene H Antiplatelets, such as clopidogrel and ticlopidine
H Limb loss H Lipid-lowering agents

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H Hypoglycemics Monitoring
H Antihypertensives H Signs and symptoms of fluid or electrolyte imbalance
H Thrombolytics, such as alteplase and streptokinase or renal failure
H Anticoagulants, such as warfarin and heparin H Signs and symptoms of stroke
H Niacin or vitamin B complex H Vital signs
H Intake and output
Surgery H Distal pulses
H Embolectomy H Neurologic status
H Endarterectomy H Bowel sounds
H Atherectomy H Prothrombin time and International Normalized
H Laser angioplasty Ratio
H Endovascular stent placement
H Percutaneous transluminal angioplasty
H Laser surgery Patient teaching
H Patch grafting
H Bypass graft Be sure to cover:
H Lumbar sympathectomy H the disorder, diagnosis, and treatment
H Amputation H medications and possible adverse reactions
H Bowel resection H when to notify the physician
H dietary restrictions
H regular exercise program
Nursing considerations H foot care
H signs and symptoms of graft occlusion
Key outcomes H signs and symptoms of arterial insufficiency and
The patient will: occlusion
H report increased comfort and decreased pain H avoidance of wearing constrictive clothing, crossing
H maintain palpable pulses and collateral circulation legs, or wearing garters
H maintain skin integrity H risk factor modification
H maintain joint mobility and range of motion H avoidance of temperature extremes.
H develop no signs or symptoms of infection.
Discharge planning
Nursing interventions H Refer the patient to a physical and occupational ther-
For chronic arterial occlusive disease apist, as indicated.
H Use preventive measures, such as minimal pressure H Refer the patient to a podiatrist for foot care, as
mattresses, heel protectors, a foot cradle, or a foot- needed.
board. H Refer the patient to an endocrinologist for glucose
H Avoid using restrictive clothing such as antiembolism control, as indicated.
stockings. H Refer the patient to a smoking-cessation program,
H Give prescribed drugs. as indicated.
H Allow the patient to express fears and concerns.
For preoperative care during an acute episode
H Assess the patients circulatory status.
H Give prescribed analgesics.
H Give prescribed heparin or thrombolytics.
H Wrap the patients affected foot in soft cotton batting,
and reposition it frequently to prevent pressure on
any one area.
H Strictly avoid elevating or applying heat to the affect-
ed leg.
For postoperative care
H Watch the patient closely for signs of hemorrhage.
H In mesenteric artery occlusion, connect a nasogastric
tube to low intermittent suction.
H Give prescribed analgesics.
H Assist with early ambulation, but dont allow the pa-
tient to sit for an extended period.
H If amputation has occurred, check the stump careful-
ly for drainage, and note and record its color and
amount and the time.
H Elevate the stump as ordered.

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Arteriovenous H Symptoms of intracranial (intracerebral, subarach-

noid, or subdural) hemorrhage, including sudden
malformations severe headache, seizures, confusion, lethargy, and
meningeal irritation
H Hydrocephalus

Overview Complications
H Aneurysm development and subsequent rupture
Description H Hemorrhage (intracerebral, subarachnoid, or sub-
H Tangled masses of thin-walled, dilated blood vessels dural, depending on the location of the AVM)
between arteries and veins that dont connect by cap- H Hydrocephalus
illaries
H Common in the brain, primarily in the posterior por-
tion of the cerebral hemispheres Assessment
H Adequate perfusion of brain tissue prevented due to
abnormal channels between arterial and venous sys- History
tem mixing oxygenated and unoxygenated blood H Chronic headache
H Range in size from a few millimeters to large malfor- H Seizures
mations extending from the cerebral cortex to the H Change in mental status
ventricles
H Commonly more than one arteriovenous malforma- Physical findings
tion (AVM) present H Systolic carotid bruit
H Neurologic deficits
Pathophysiology
H Typical structural characteristics of the blood vessels Test results
arent present. Diagnostic procedures
H Vessels of an AVM are very thin. (One or more arter- H Cerebral arteriogram confirms the presence of AVMs
ies feed into the AVM, causing it to appear dilated and evaluates blood flow.
and torturous.) H Doppler ultrasonography of cerebrovascular system
H Typically, high-pressured arterial flow moves into the indicates abnormal, turbulent blood flow.
venous system through the connecting channels to
increase venous pressure, engorging and dilating the
venous structures. Treatment
H If the AVM is large enough, the shunting can deprive
the surrounding tissue of adequate blood flow. General
H Thin-walled vessels may ooze small amounts of blood H Support measures, including aneurysm precautions
or actually rupture, causing hemorrhage into the to prevent possible rupture
brain or subarachnoid space. H Nothing by mouth, if scheduled for surgery
H Limited activity
Causes H Quiet atmosphere
H Congenital (hereditary)
H Penetrating injuries such as trauma Medications
H I.V. fluid
Incidence H Analgesics
H Males and females equally affected H Sedatives
H AVMs possibly familial H Stool softener
H Most AVMs present at birth; however, typically asymp-
tomatic until ages 10 to 20 Surgery
H Block dissection, laser, or ligation to repair the com-
Common characteristics municating channels and remove the feeding vessels
H Chronic mild headache and confusion H Embolization or radiation therapy, if surgery isnt
H Seizures possible, to close the communicating channels and
H Systolic bruit over carotid artery, mastoid process, or feeder vessels and thus reduce the blood flow to the
orbit AVM
H Focal neurologic deficits (depending on the location
of the AVM) resulting from compression and dimin-
ished perfusion

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Nursing considerations
Key outcomes
The patient will:
H maintain stable vital signs
H maintain stable neurologic status
H express an understanding of the disorder and treat-
ment.
Nursing interventions
H Control hypertension and seizure activity.
H Maintain a quiet atmosphere and provide relaxation
techniques.
H If the AVM has ruptured, work to control elevated in-
tracranial pressure and intracranial hemorrhage.
Monitoring
H Vital signs
H Neurologic status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H importance of reporting signs of intracranial bleed-
ing immediately (sudden severe headache, vision
changes, decreased movement in extremities, change
in level of consciousness).
Discharge planning
H Refer the patient to social service for support ser-
vices if neurologic deficits have occurred due to a
ruptured AVM.

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Asbestosis
Overview
Description
H Lung disease characterized by diffuse interstitial pul-
monary fibrosis resulting from prolonged exposure
to airborne asbestos particles
H May develop many years (about 15 to 20) after regu-
lar exposure to asbestos ceases
H Pleural plaques and mesotheliomas of the pleura and
the peritoneum formed by exposure
H A form of pneumoconiosis
H Also known as mesothelioma
Pathophysiology
H Inhaled asbestos fibers travel down the airway and
penetrate respiratory bronchioles and alveolar walls.
H Mucus production and goblet cells are stimulated to
protect the airway and aid in expectoration.
H Fibers become encased in a brown, iron-rich, pro-
teinlike sheath, called asbestosis bodies.
H Chronic irritation by the fibers continues, causing
edema of the airways.
H Fibrosis develops in response to the chronic irrita-
tion.
Causes
H Prolonged inhalation of asbestos fibers from indus-
tries, such as mining and milling, construction, fire-
proofing, and textile
H Production of paints, plastics, and brake and clutch
linings
H Exposure to fibrous dust shaken off workers cloth-
ing
H Exposure to fibrous dust or waste piles from nearby
asbestos plants
Incidence
H Commonly occurring between ages 40 and 75
H Affects males more commonly than females
Assessment
History
H Exposure to asbestos fibers
H Exertional or rest dyspnea
H Cough
H Chest pain
H Recurrent respiratory tract infections
Physical findings
H Tachypnea
H Clubbing of the fingers
H Characteristic dry crackles in the lung bases
Test results
Laboratory
H Arterial blood gas (ABG) analysis shows decreased
partial pressures of arterial oxygen and carbon diox-
ide.
Imaging
H Chest X-rays may show fine, irregular, and linear dif-
fuse infiltrates; a honeycomb or ground-glass ap-
pearance to lungs; and pleural thickening and pleur-
al calcification, bilateral obliteration of costophrenic
angles, and an enlarged heart with shaggy border.
Other
H Pulmonary function tests may show decreased vital
capacity, forced vital capacity (FVC), and total lung
capacity; decreased or normal forced expiratory vol-
ume in 1 second (FEV1) a normal ratio of FEV1 to
FVC; and reduced diffusing capacity for carbon
monoxide.
Treatment
General
H Controlled coughing and postural drainage with
chest percussion and vibration
H At least 3 qt (3 L) of fluids daily
H High-calorie, high-protein, low-sodium diet
H Activity as tolerated

Common characteristics Medications

H Exposure to asbestos fibers H Inhaled mucolytics such as acetylcysteine
H Exertional or rest dyspnea H Supplemental oxygen
H Dry cough H Diuretics, such as furosemide and torsemide
H Chest pain H Cardiac glycosides such as digoxin
H Recurrent respiratory tract infections H Antibiotics, as appropriate

Complications Surgery
H Pulmonary fibrosis H Lung transplantation, in severe cases
H Respiratory failure
H Pulmonary hypertension
H Cor pulmonale

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Nursing considerations
Key outcomes
The patient will:
H maintain adequate ventilation
H maintain adequate caloric intake
H express understanding of the illness
H identify measures to prevent or reduce fatigue.

Nursing interventions
H Give prescribed drugs and provide oxygen therapy.
H Provide supportive care.
H Provide chest physiotherapy.
H Provide high-calorie, high-protein, low-sodium foods
in small, frequent meals.
H Encourage oral fluid intake.
H Provide frequent rest periods.

Monitoring
H Vital signs
H Intake and output
H Daily weight
H Respiratory status (breath sounds, ABG results)
H Sputum production
H Mentation
H Complications

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medications and possible adverse reactions
H transtracheal catheter care, if applicable
H prevention of infection
H signs and symptoms of infection
H influenza and pneumococcus immunizations
H home oxygen therapy, if required
H importance of follow-up care
H chest physiotherapy
H high-calorie, high-protein, low-sodium diet
H adequate oral fluid intake
H energy conservation techniques.

Discharge planning
H Refer the patient to a smoking-cessation program, if
indicated.

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Test results
Ascariasis Laboratory
H Microscopic studies show ova in the stool, or adult
worm is observed in emesis.
Overview H Complete blood count: shows eosinophilia
Imaging
Description H Abdominal X-rays show whirlpool pattern of intralu-
H Intestinal infection caused by the parasitic worm As- minal worms. (Intestinal obstruction may be noted.)
caris lumbricoides, a large roundworm resembling H Chest X-rays show characteristic bronchovascular
an earthworm markings infiltrates, patchy areas of pneumonitis,
H Never passes directly from person to person and widening of hilar shadows (if migrated to lungs).
H Also known as roundworm infection

Pathophysiology
H After ingestion, A. lumbricoides ova hatch and re-
lease larvae, which penetrate the intestinal wall and
reach the lungs through the bloodstream.
H After about 10 days in pulmonary capillaries and
alveoli, the larvae migrate to the bronchioles,
bronchi, trachea, and epiglottis.
H From the epiglottis, the larvae are swallowed and
return to the intestine to mature into worms.
Causes
H Ingestion of food, drink, or soil contaminated with
A. lumbricoides ova
Incidence
H Occurs worldwide but most common in tropical ar-
eas with poor sanitation and in Asia, where farmers
use human stool as fertilizer
H In the United States, more prevalent in the South,
particularly among younger children
Common characteristics
H Stomach discomfort
H Vomiting
Treatment
General
H Nasogastric (NG) suctioning (with intestinal obstruc-
tion)
H Nothing by mouth until stable
H Rest as needed
Medications
H I.V. fluids
H Mebendazole and albendazole
H Anthelmintic therapy (pyrantel or piperazine) (avoid
use if intestinal obstruction is present)
ALERT
Piperazine is contraindicated in patients with
seizure disorder and may cause stomach upset,
dizziness, and urticaria. Pyrantel produces red
stool and vomitus and may cause stomach upset,
headache, dizziness, and rash. Albendazole and
mebendazole may cause abdominal pain and diar-
rhea.

Complications Surgery
H Intestinal obstruction H Intestinal surgery to relieve obstruction, if necessary
H Pneumonitis

Nursing considerations
Assessment
Key outcomes
History The patient will:
H Stomach discomfort or pain H maintain adequate fluid balance
H Nausea and vomiting H regain normal intestinal function
H Recent travel to endemic area H express understanding of proper sanitation of food
H Restlessness and hands.
H Disturbed sleep
Nursing interventions
Physical findings H Isolation is unnecessary; proper disposal of stool and
H Abdominal tenderness soiled linen, using standard precautions, should be
H Dehydration adequate.
H Crackles, wheezing, and tachypnea (if migrated to H If the patient is receiving NG suctioning, provide
the lungs) good mouth care.

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Monitoring
H Vital signs
H Intake and output
H Appearance of stools (for worms)

Patient teaching
Be sure to cover:
H proper hand washing, especially before eating and
after defecating
H bathing and changing underwear and bed linens
daily
H adverse effects of medications prescribed for the
patient.
Discharge planning
H Refer the patient to social services if living conditions
are questionable regarding cleanliness.

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H Organ transplants
Life-threatening disorder H TB or another cavitary lung disease (in asper-
gilloma)
Aspergillosis Incidence
H Aspergillus: found worldwide, commonly in ferment-
ing compost piles and damp hay
Overview
Common characteristics
Description Aspergilloma
H An opportunistic, sometimes life-threatening infec- H May produce no symptoms
tion, growth, or allergic response caused by fungi of H Mimics TB, causing a productive cough and purulent
the genus Aspergillus, usually A. fumigatus, A. or blood-tinged sputum, dyspnea, empyema, and
flavus, or A. niger, occurring in: lung abscesses
Aspergilloma: produces a fungus ball in the lungs Allergic aspergillosis
(called a mycetoma) H Wheezing
Allergic aspergillosis: a hypersensitive asthmatic H Dyspnea
reaction to Aspergillus antigens H Cough with some sputum production
Aspergillosis endophthalmitis: an infection of the H Pleural pain
anterior and posterior chambers of the eye that H Fever
can lead to blindness Aspergillosis endophthalmitis
Invasive aspergillosis: an acute infection that pro- H Usually appears 2 to 3 weeks after an eye injury or
duces septicemia, thrombosis, and infarction of surgery
virtually any organ, especially the heart, lungs, H Clouded vision
brain, and kidneys H Eye pain
H Variable prognosis according to each form (as- H Reddened conjunctivae
pergilloma possibly causing fatal hemoptysis) Invasive aspergillosis
H Thrombosis
Pathophysiology H Infarctions
H Conidia (asexual spores) travel into the alveoli via in- H Sepsis
halation or, in aspergillosis endophthalmitis, through
a wound or other tissue injury. Complications
H Pulmonary macrophages may be able to kill the coni- H Infection of the ear (otomycosis), cornea (mycotic
dia. keratitis), or prosthetic heart valve (endocarditis)
H The alternative complement pathway is activated, re- H Pneumonia (especially in those receiving an im-
sulting in recruitment of neutrophils and monocytes. munosuppressant such as an antineoplastic drug or
H The disease may be accompanied by hyphal invasion high-dose steroid therapy)
of the blood vessels in the involved tissues. H Sinusitis
H In aspergilloma, colonization of the bronchial tree H Brain abscesses
with Aspergillus produces plugs and atelectasis and H Life-threatening hemoptysis
forms a tangled ball of hyphae (fungal filaments), H Septicemia
fibrin, and exudate in a cavity left by a previous ill-
ness such as tuberculosis (TB).
Assessment
Causes
H Contact with Aspergillus, commonly found growing History
on dry leaves, stored grain, compost piles, or decay- Aspergilloma and allergic aspergillosis
ing vegetation H Immunosuppression
H Dyspnea
Risk factors H Cough with sputum production
H Excessive or prolonged use of antibiotics, glucocorti- Aspergillosis endophthalmitis
coids, or other immunosuppressants H Eye pain
H Radiation therapy H Vision changes
H Acquired immunodeficiency syndrome H Recent eye injury or surgery
H Hodgkins disease Invasive aspergillosis
H Leukemia H History based on infected organ
H Azotemia
H Alcoholism
H Sarcoidosis
H Bronchitis and bronchiectasis

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Physical findings Nursing interventions

Aspergilloma and allergic aspergillosis H Perform chest physiotherapy every 2 hours.
H Diminished breath sounds H Encourage coughing and deep breathing every hour.
H Adventitious breath sounds
H Cough with sputum production Monitoring
Aspergillosis endophthalmitis H Vital signs
H Reddened conjunctivae H Sputum production, amount, color, and character
H Blurred vision
Invasive aspergillosis
H Findings based on infected organ Patient teaching
Test results Be sure to cover:
Laboratory H the disorder, diagnosis, and treatment
ASPERGILLOMA H adverse effects of medications.
H Serum is positive for anti-Aspergillus antibodies.
ALLERGIC ASPERGILLOSIS
H Sputum culture reveals hyphae that grow Aspergillus
and eosinophils.
H Serum is positive for immunoglobulin (Ig) E and IgG
anti-Aspergillus antibodies.
ASPERGILLOSIS ENDOPHTHALMITIS
H Eye culture or exudate shows Aspergillus.
Diagnostic procedures
INVASIVE ASPERGILLOSIS
H Bronchoscopy and open lung biopsy are performed
to obtain a tissue sample that confirms diagnosis.
Imaging
ASPERGILLOMA
H Chest X-ray shows a round to oval mass with a radi-
olucent crescent over the upper portion of the mass
(Monods sign).

Treatment
General
H Supportive therapy

Medications
Allergic aspergillosis
H Desensitization
H Steroids
Aspergillosis endophthalmitis
H Amphotericin B
Invasive aspergillosis
H Antifungal therapy

Surgery
Aspergilloma
H Local excision of the lesion
H Lobectomy

Nursing considerations
Key outcomes
The patient will:
H maintain adequate ventilation
H maintain stable vital signs
H express understanding of the disorder and treatment.

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H Altered respiratory rate

Life-threatening disorder H Little or no air movement
H Intercostal rib retractions

Asphyxia H Pale skin

H Cyanosis in mucous membranes, lips, and nail beds
H Erythema and petechiae on the upper chest (trauma)
H Cherry-red mucous membranes (carbon monoxide
Overview poisoning)
H Decreased or absent breath sounds
Description
H A condition of insufficient oxygen and accumulating Test results
carbon dioxide in the blood and tissues Laboratory
H Leads to cardiopulmonary arrest; fatal without H Decreased partial pressure of arterial oxygen (less
prompt treatment than 60 mm Hg) and increased partial pressure of
arterial carbon dioxide (more than 50 mm Hg) are
Pathophysiology indicated by arterial blood gas (ABG) analysis.
H An interference with respiration causes insufficient H Toxicology tests show drugs, chemicals, or abnormal
oxygen intake and hypoxemia. hemoglobin level.
H Carbon dioxide accumulates due to the lack of gas Imaging
exchange in the lungs. H Chest X-rays may detect a foreign body, pulmonary
H This leads to inadequate tissue perfusion and cell edema, or atelectasis.
death. H Pulmonary function tests may indicate respiratory
muscle weakness.
Causes H Bronchoscopy can locate foreign body.
H Opioid abuse
H Respiratory muscle paralysis
H Airway obstruction Treatment
H Aspiration
H Pulmonary edema General
H Near drowning H Establish airway and ventilation
H Tumor H Treat the underlying cause
H Strangulation H Nothing by mouth until able to protect airway
H Trauma to airway H Activity based on outcome of interventions
H Carbon monoxide poisoning
H Smoke inhalation Medications
H Oxygen
Incidence H Narcan (if caused by opioid abuse)
H Can occur at any age
Surgery
Common characteristics H Tumor removal
H Altered respirations
H Changes in level of consciousness
H Cardiac arrest Nursing considerations
Complications Key outcomes
H Neurologic damage The patient will:
H Death H maintain a patent airway
H maintain adequate ventilation
H maintain acceptable cardiac output
Assessment H demonstrate knowledge of safety measures to prevent
suffocation.
History
H Cause of the asphyxia possibly apparent Nursing interventions
H Causes of signs and symptoms varying H Perform abdominal thrust, if obstruction is present.
H Maintain patent airway.
Physical findings H Begin cardiopulmonary resuscitation, if necessary.
H Anxiousness or agitation H Insert a nasogastric tube or an Ewald tube for lavage
H Confusion (for opioid abuse).
H Dyspnea H Give prescribed drugs.
H Prominent neck muscles H Reassure the patient and his family.
H Wheezing and stridor H Ensure I.V. access.

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Monitoring
H ABG levels, pulse oximetry
H Respiratory status
H Cardiac status
H Vital signs
H Neurologic status

Patient teaching
Be sure to cover:
H cause of asphyxia (with patient and family members,
discuss measures to prevent recurrence, if appropri-
ate)
H safety measures if the victim is a child.

Discharge planning
H Refer the patient to the proper authorities, if criminal
intent was involved.
H Refer the patient to resource and support services, if
appropriate.

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H Psychological stress
Life-threatening disorder H Cold air
H Exercise

Asthma
Overview
Description
H A chronic reactive airway disorder involving episod-
ic, reversible airway obstruction resulting from bron-
chospasms, increased mucus secretions, and mucos-
al edema
H Signs and symptoms that range from mild wheezing
and dyspnea to life-threatening respiratory failure
H Signs and symptoms of bronchial airway obstruction
that may persist between acute episodes
Pathophysiology
H Tracheal and bronchial linings overreact to various
stimuli, causing episodic smooth-muscle spasms that
severely constrict the airways.
H Mucosal edema and thickened secretions further
block the airways.
H Immunoglobulin (Ig) E antibodies, attached to
histamine-containing mast cells and receptors on cell
membranes, initiate intrinsic asthma attacks.
H When exposed to an antigen such as pollen, the IgE
antibody combines with the antigen. On subsequent
exposure to the antigen, mast cells degranulate and
release mediators.
H The mediators cause the bronchoconstriction and
edema of an asthma attack.
H During an asthma attack, expiratory airflow decreas-
es, trapping gas in the airways causing alveolar hy-
perinflation.
H Atelectasis may develop in some lung regions.
H The increased airway resistance initiates labored
breathing.
Causes
H Sensitivity to specific external allergens or from in-
ternal, nonallergenic factors
Extrinsic causes
H Pollen
H Animal dander
H House dust or mold
H Kapok or feather pillows
H Food additives containing sulfites and any other sen-
sitizing substance
Intrinsic causes
H Emotional stress
H Genetic factors
Bronchoconstriction
H Hereditary predisposition
H Sensitivity to allergens or irritants such as pollutants
H Viral infections
H Drugs, such as aspirin, beta-adrenergic blockers,
and nonsteroidal anti-inflammatory drugs
H Tartrazine
Incidence
H Can occur at any age; about 50% of all patients with
asthma are younger than age 10; affects twice as
many boys as girls
H In about one-third of patients, onset between ages 10
and 30
H In about one-third of patients, two or more patients
in same immediate family
H Coexistence of intrinsic and extrinsic causes in many
patients
Common characteristics
H Wheezing
H Shortness of breath, feelings of suffocation
H Tightness in chest
H Extrinsic asthma in children; commonly accompa-
nied by other manifestations of atopy
Complications
H Status asthmaticus
H Respiratory failure
H Death
Assessment
History
H Often preceded by severe respiratory tract infections,
especially in adults
H Irritants, emotional stress, fatigue, endocrine
changes, temperature and humidity variations, and
exposure to noxious fumes possibly aggravating in-
trinsic asthma attacks
H An asthma attack possibly beginning dramatically,
with simultaneous onset of severe, multiple symp-
toms, or insidiously, with gradually increasing respi-
ratory distress
H Exposure to a particular allergen then followed by a
sudden onset of dyspnea and wheezing and by tight-
ness in the chest also accompanied by a cough that
produces thick, clear, or yellow sputum
Physical findings
H Visibly dyspneic
H Ability to speak only a few words before pausing for
breath
H Use of accessory respiratory muscles
H Diaphoresis
H Increased anteroposterior thoracic diameter
H Hyperresonance
H Tachycardia; tachypnea; mild systolic hypertension
H Inspiratory and expiratory wheezes
H Prolonged expiratory phase of respiration
H Diminished breath sounds
H Cyanosis, confusion, and lethargy indicating the onset
of life-threatening status asthmaticus and respiratory
failure

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Test results H use effective coping strategies

Laboratory H report feelings of comfort
H Arterial blood gas (ABG) analysis reveals hypoxemia. H maintain skin integrity.
H Serum IgE levels are increased due to an allergic re-
action. Nursing interventions
H Complete blood count with differential shows in- H Give prescribed drugs.
creased eosinophil count. H Place the patient in high Fowlers position.
Imaging H Encourage pursed-lip and diaphragmatic breathing.
H Chest X-rays may show hyperinflation with areas of H Administer prescribed humidified oxygen.
focal atelectasis. H Adjust oxygen according to the patients vital signs
Diagnostic procedures and ABG values.
H Pulmonary function tests (PFTs) may show decreased H Assist with intubation and mechanical ventilation, if
peak flows and forced expiratory volume in 1 sec- appropriate.
ond, low-normal or decreased vital capacity, and in- H Perform postural drainage and chest percussion, if
creased total lung and residual capacities. tolerated.
H Skin testing may identify specific allergens. H Suction an intubated patient, as needed.
H Bronchial challenge testing shows the clinical signifi- H Treat the patients dehydration with I.V. or oral fluids
cance of allergens identified by skin testing. as tolerated.
Other H Anticipate bronchoscopy or bronchial lavage.
H Pulse oximetry measurements may show decreased H Keep the room temperature comfortable.
oxygen saturation. H Advise the patient to use an air conditioner or a fan
in hot, humid weather.
Treatment Monitoring
H Vital signs
General H Intake and output
H Identification and avoidance of precipitating factors H Response to treatment
H Desensitization to specific antigens H Signs and symptoms of theophylline toxicity
H Establishment and maintenance of patent airway H Breath sounds
H Fluid replacement H ABG results
H Activity as tolerated H PFT results
H Pulse oximetry
Medications H Complications of corticosteroids
H Bronchodilators, such as albuterol, pirbuterol, sal- H Level of anxiety
meterol, and theophylline
H Corticosteroids
H Histamine antagonists, such as cetirizine and diphen- Patient teaching
hydramine
H Leukotriene antagonists, such as montelukast, zafir- Be sure to cover:
lukast, and zileuton H the disorder, diagnosis, and treatment
H Anti-inflammatories, such as cromolyn and ne- H medications and possible adverse reactions
docromil H when to notify the physician
H Low-flow oxygen H avoidance of known allergens and irritants
H Antibiotics, as appropriate H metered-dose inhaler or dry powder inhaler use
H pursed-lip and diaphragmatic breathing
H use of peak flow meter
ALERT
H effective coughing techniques
The patient with increasingly severe asthma that H maintaining adequate hydration.
doesnt respond to drug therapy is usually admitted
for treatment with corticosteroids, epinephrine, Discharge planning
and sympathomimetic aerosol sprays. He may re- H Refer the patient to a local asthma support group.
quire endotracheal intubation and mechanical
ventilation.

Nursing considerations
Key outcomes
The patient will:
H maintain adequate ventilation
H maintain a patent airway

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Atelectasis Assessment
History
Overview H Recent abdominal or other major surgery
H Prolonged immobility
Description H Mechanical ventilation
H Incomplete expansion of alveolar clusters or lung H CNS depression
segments leading to partial or complete lung collapse H Smoking
H May be chronic or acute H COPD
H Good prognosis with prompt removal of any airway H Rib fractures, tight chest dressings
obstruction, relief of hypoxia, and re-expansion of
the collapsed lung Physical findings
H Decreased chest wall movement
Pathophysiology H Cyanosis
H Due to incomplete expansion, certain regions of the H Diaphoresis
lung are removed from gas exchange. H Substernal or intercostal retractions
H Unoxygenated blood passes unchanged through these H Anxiety
regions and produces hypoxia. H Decreased fremitus
H Alveolar surfactant causes increased surface tension, H Mediastinal shift to the affected side
permitting complete alveolar deflation. H Dullness or flatness over lung fields
H End-inspiration crackles
Causes H Decreased (or absent) breath sounds
H Bronchial occlusion H Tachycardia
H Bronchiectasis
H Cystic fibrosis Test results
H Bed rest in a supine position Laboratory
H General anesthesia H Arterial blood gas analysis shows hypoxia.
H Pleural effusion Imaging
H Pulmonary embolism H Chest X-rays show characteristic horizontal lines in
H Sarcoidosis the lower lung zones and characteristic dense shad-
H Bronchogenic carcinoma ows.
H Inflammatory lung disease Diagnostic procedures
H Idiopathic respiratory distress syndrome of the H Bronchoscopy may show an obstructing neoplasm,
neonate foreign body, or pneumonia.
H Oxygen toxicity H Pulse oximetry shows decreased oxygen saturation.
H Pulmonary edema
H External compression
Treatment
Incidence
H Common in patients after upper abdominal or tho- General
racic surgery H Incentive spirometry
H More common in patients with prolonged immobility, H Chest percussion
on mechanical ventilation, or with central nervous H Postural drainage
system (CNS) depression H Frequent coughing and deep-breathing exercises
H Increased predisposition in patients who smoke and H Bronchoscopy if above measures fail
those with chronic obstructive pulmonary disease H Humidity
(COPD) H Intermittent positive-pressure breathing therapy
H Radiation possibly required for obstructing neoplasm
Common characteristics H Diet based on patients condition as tolerated
H Shortness of breath H Increased fluids
H Chest pain H Activity as tolerated; discourage bed rest
H Anxiety
Medications
Complications H Bronchodilators, such as albuterol, pirbuterol, and
H Hypoxemia salmeterol
H Acute respiratory failure H Analgesics after surgery
H Pneumonia
Surgery
H May be required if obstructing neoplasm present

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Nursing considerations
Key outcomes
The patient will:
H maintain a patent airway
H maintain adequate ventilation
H report feelings of increased comfort
H use support systems to assist with anxiety and fear.

Nursing interventions
H Give prescribed drugs and provide oxygen therapy.
H Encourage coughing and deep breathing.
H Reposition the patient often.
H Encourage and assist with ambulation as soon as
possible.
H Help the patient use an incentive spirometer.
H Humidify inspired air.
H Encourage adequate fluid intake.
H Loosen secretions with postural drainage and chest
percussion.
H Provide suctioning, as needed.
H Offer the patient reassurance and emotional support.

Monitoring
H Vital signs
H Intake and output
H Pulse oximetry
H Respiratory status (breath sounds, arterial blood gas
results)

Patient teaching
Be sure to cover:
H use of incentive spirometer
H postural drainage and percussion
H coughing and deep-breathing exercises
H importance of splinting incisions
H energy-conservation techniques
H stress-reduction strategies
H importance of mobilization.

Discharge planning
H Refer the patient to a smoking-cessation program, if
indicated.
H Refer the patient to a weight-reduction program, if
indicated.

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Atopic dermatitis
Overview
Description
H A chronic skin disorder characterized by superficial
skin inflammation and intense itching
Pathophysiology
H The allergic mechanism of hypersensitivity results in
a release of inflammatory mediators through sensi-
tized antibodies of the immunoglobulin (Ig) E class.
H Histamine and other cytokines induce acute inflam-
mation.
H Abnormally dry skin and a decreased threshold for
itching set up the itch-scratch-itch cycle, which
eventually causes lesions (excoriations, lichenifica-
tion).
Causes
H The exact etiology of atopic dermatitis unknown;
however, genetic predisposition likely
H Possible contributing factors:
Food allergy
Infection
Chemical irritants
Extremes of temperature and humidity
Psychological stress or strong emotions
Special populations
About 10% of juvenile cases of atopic dermatitis
are caused by allergic reactions to certain foods,
especially eggs, peanuts, milk, and wheat.
Factors contributing to atopy
H Changes associated with industrialization, such as
exposure to new chemicals like diesel fumes, have
proven to increase the antigenicity of common pollens.
H Increased exposure to antigens, such as dust mites (in
wall-to-wall carpets), especially at an early age,
contributes to a predisposition to developing allergies.
H Dietary changes, such as increased fat intake and an
earlier weaning from human breast milk, may be
contributing factors.
H Vaccination may cause a shift in T-cell function away
from the normal helper T cell (Th1) response to the
Th2 allergic response by limiting early bacterial and
viral infections.
H Lack of exposure to intestinal parasites may contribute
to a similar shift in T-cell functioning.
H Frequent use of antibiotics, especially in early
childhood, may decrease normal intestinal flora and
further contribute to the shift.
96 Atopic dermatitis
Incidence
H May appear at any age but typically begins during in-
fancy or early childhood (may then subside sponta-
neously, followed by exacerbations in late childhood,
adolescence, or early adulthood)
H Affects less than 1% of the population
Common characteristics
H Erythematous, weeping lesions, usually located in ar-
eas of flexion and extension, such as the neck, ante-
cubital fossa, popliteal folds, and behind the ears
In children with atopic dermatitis
H Pink pigmentation and swelling of the upper eyelid
and a double fold under the lower lid (Morgans line
or Dennies sign)
Complications
H Scarring
H Severe viral infections
H Bacterial and fungal skin infections
H Ocular disorders
H Allergic contact dermatitis
Assessment
History
H Atopy, such as asthma, hay fever, or urticaria (or
similar family history)(see Factors contributing to
atopy)
H Exposure to allergen
H Pruritus
Physical findings
H Erythematous, weeping lesions (see Signs of atopic
dermatitis)
H Pink pigmentation and swelling of the upper eyelid
and a double fold under the lower lid
Test results
Laboratory
H Complete blood count shows eosinophilia.
H Serum IgE levels are elevated.
Other
H Skin testing shows specific allergen.
Treatment
General
H Meticulous skin care
H Environmental control of offending allergens
H Nonirritating topical lubricants
Medications
H Corticosteroids
H Antipruritics such as hydroxyzine
H Antihistamines, such as diphenhydramine and fexofe-
nadine
H Antibiotics if secondary infection develops
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Signs of atopic dermatitis

Nursing considerations
This illustration shows the typical lesions involved in
Key outcomes atopic dermatitis.

The patient will:

H express relief from itching and pain Edema, crusting,
H demonstrate improved skin condition and scaling
H remain free from infection.

Nursing interventions
Erythematous
H Offer support to help the patient and his family cope areas on dry
with this chronic disorder. skin
H Dissuade the patient from scratching during urticaria
to help prevent infection.
H Apply prescribed topical medications.
H Give prescribed drugs.

Monitoring
H Compliance with drug therapy
H Treatment of lesions
H Nutritional status

Patient teaching
Be sure to cover:
H when and how to apply topical corticosteroids
H importance of regular personal hygiene using only
water with little soap
H signs and symptoms of secondary infection
H avoidance of laundry additives, such as fragrances
and dyes
H avoidance of allergens.

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Complications
Atrial fibrillation H Transient ischemic attack
H Stroke
H Heart failure
Overview H Thromboembolism

Description
H Rhythm disturbance of the atria Assessment
H Characterized by an irregularly irregular cardiac rate
and rhythm (see Recognizing atrial fibrillation) History
H Palpitations
Pathophysiology H Fatigue
H Rapid discharges from numerous ectopic foci in the H Dyspnea
atria occur. H Chest pain
H This leads to erratic and uncoordinated atrial H Syncope
rhythm.
Physical findings
Causes H Irregular pulse
H Hypertension H Possible tachycardia
H Myocardial infarction (MI) H Hypotension
H Pulmonary embolism H Signs of heart failure
H Heart failure H Respiratory distress
H Cardiomyopathy
H Hypersympathetic state associated with acute alcohol Test results
ingestion Laboratory
H Pericarditis H Cardiac enzymes show myocardial damage (with MI).
H Hyperthyroidism H Thyroid function studies reveal hyperthyroidism.
H Valvular disease H Complete blood count checks for anemia, if the pa-
H Cardiothoracic surgery tient has a history of recent blood loss.
H Atrial fibrosis Imaging
H Chest X-ray may determine if pulmonary edema is
Incidence present.
H Seen more commonly in patients older than age 70 H Echocardiogram or transesophageal echocardiogra-
H Males affected more than females phy may help identify valvular disease, left ventricular
dysfunction, or atrial clots.
Common characteristics Diagnostic procedures
H Cardiac rhythm: irregularly irregular H Electrocardiography may indicate irregular rhythm.
H Holter monitor may diagnose paroxysmal atrial fibril-
lation.

Recognizing atrial fibrillation

The following rhythm strip shows atrial fibrillation.

H Rhythm: Irregular H P wave: Absent; replaced by fine H T wave: Indiscernible

H Rate: Atrial indiscernible; fibrillatory waves H QT interval: Unmeasurable
ventricular 130 beats/minute H PR interval: Indiscernible H Other: None
H QRS complex: 0.08 second

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Discharge planning
Treatment H Refer the patient to programs such as Coumadin
Clinic to monitor anticoagulant therapy.
General
H Possible electrical cardioversion
H Atrial fibrillation suppression pacemaker
H Ablation
H Surgical maze procedure
H Low-fat, low-sodium diet
H Fluid restriction, if indicated
H Planned rest periods, as needed

Medications
H Calcium channel blockers, such as cardizem and am-
lodipine
H Beta-adrenergic blockers, such as metoprolol and
atenolol
H Antiarrhythmics, such as amiodarone, propafenone,
and sotalol
H Cardiac glycosides such as digoxin
H Anticoagulants such as warfarin

Nursing considerations
Key outcomes
The patient will:
H report ways to reduce activity intolerance
H identify effective coping mechanisms to manage
anxiety
H discuss the causes of fatigue
H verbalize understanding of medication regimen.

Nursing interventions
H Give prescribed drugs.
H Encourage the patient and his family to talk about
feelings and concerns.
H Plan rest periods.

Monitoring
H Vital signs at rest and after physical activity
H Signs and symptoms of embolism
H Intake and output
H Daily weight
H Abnormal bleeding
H Prothrombin time and International Normalized
Ratio

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medications and possible adverse reactions
H when to notify the physician
H instructions on how to monitor pulse
H anticoagulation precautions
H abnormal bleeding
H signs and symptoms of embolic events.

Atrial fibrillation 99
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Common characteristics
Atrial septal defect H Fatigue after exertion
H Early to midsystolic murmur at the second or third
left intercostal space
Overview H Low-pitched diastolic murmur at the left lower ster-
nal border; more pronounced on inspiration
Description H Fixed, widely split S2
H An acyanotic congenital heart defect featuring an H Systolic click or late systolic murmur at the apex
opening between the left and right atria that allows H Clubbing and cyanosis, if a right-to-left shunt
blood to flow from left to right, resulting in ineffec- develops
tive pumping of the heart, thus increasing the risk of
heart failure ALERT
H Three types:
Ostium secundum defect, the most common type: An infant may be cyanotic because he has a car-
occurs in the region of the fossa ovalis and, occa- diac or pulmonary disorder. Cyanosis that worsens
sionally, extends inferiorly, close to the vena cava with crying most likely has a cardiac cause because
Sinus venosus defect: occurs in the superior- crying increases pulmonary resistance to blood
posterior portion of the atrial septum, sometimes flow, resulting in an increased right-to-left shunt.
extending into the vena cava, and almost always Cyanosis that improves with crying most likely has
associated with abnormal drainage of pulmonary a pulmonary cause because deep breathing im-
veins into the right atrium proves tidal volume.
Ostium primum defect: occurs in the inferior por-
tion of the septum primum and usually associated
with atrioventricular valve abnormalities (cleft mi- Complications
tral valve) and conduction defects H Physical underdevelopment
H Respiratory infections
Pathophysiology H Heart failure
H Blood shunts from the left atrium to the right atrium H Atrial arrhythmias
because the left atrial pressure is normally slightly H Mitral valve prolapse
higher than the right atrial pressure.
H This pressure difference forces large amounts of
blood through a defect. Assessment
H This shunt results in right heart volume overload,
affecting the right atrium, right ventricle, and pulmo- History
nary arteries. H Increasing fatigue
H Eventually, the right atrium enlarges, and the right H Chest pain
ventricle dilates to accommodate the increased blood H Dyspnea
volume. H Coughing
H If pulmonary artery hypertension develops, increased H Dizziness or syncope
pulmonary vascular resistance and right ventricular
hypertrophy follow. Physical findings
H Irreversible pulmonary artery hypertension causes H Early to midsystolic murmur at the second or third
reversal of the shunt direction in some adults, which left intercostal space
results in unoxygenated blood entering the systemic H Low-pitched diastolic murmur at the left lower ster-
circulation, causing cyanosis. nal border, more pronounced on inspiration
H Fixed, widely split S2
Causes H Systolic click or late systolic murmur at the apex
H No known cause H Peripheral edema
H Ostium primum defects commonly occurring in H Cyanosis
patients with Down syndrome H Distended jugular veins

Incidence Test results

H Accounts for about 10% of congenital heart defects
H Appears almost twice as often in females than in
males, with a strong familial tendency
H Usually benign defect during infancy and childhood
(Delayed development of symptoms and complica-
tions makes it one of the most common congenital
heart defects diagnosed in adults.)
Imaging
H Chest X-ray shows an enlarged right atrium and right
ventricle, a prominent pulmonary artery, and in-
creased pulmonary vascular markings.
Diagnostic procedures
H Electrocardiography results may be normal, but
commonly show right axis deviation, a prolonged
PR interval, varying degrees of right bundle-branch

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block, right ventricular hypertrophy, atrial fibrillation

(particularly in severe cases in patients older than
age 30) and, in ostium primum defect, left axis devi-
ation.
H Echocardiography measures right ventricular en-
largement, may locate the defect, and shows volume
overload in the right side of the heart. It may reveal
right ventricular and pulmonary artery dilation.
H Two-dimensional echocardiography with color
Doppler flow, contrast echocardiography, or both has
supplanted cardiac catheterization as the confirming
test for atrial septal defects (ASDs). Cardiac catheter-
ization is used if inconsistencies exist in the clinical
data or if significant pulmonary hypertension is sus-
pected.
Patient teaching
Be sure to cover:
H pretest and posttest procedures to the child and his
parents (If possible, use drawings or other visual
aids to explain it to the child.)
H postoperative procedures, tubes, dressings, and
monitoring equipment
H antibiotic prophylaxis to prevent infective endo-
carditis.

Treatment
General
H Activity as tolerated
H Low-fat, low-cholesterol diet

Medications
H Diuretics, such as furosemide and torsemide
H Antibiotics, as appropriate
H Analgesics

Surgery
H Minimally invasive heart surgery may be required for
the patient with an uncomplicated ASD with evidence
of significant left-to-right shunting.
H A large defect may need immediate surgical closure
with sutures or a patch graft.
H Cardiac catheterization closure the insertion of an
umbrella-like patch or septal occluder through a
cardiac catheter may be performed.

Nursing considerations
Key outcomes
The patient will:
H maintain an optimal cardiac output
H maintain hemodynamic stability
H experience no cardiac arrhythmias.

Nursing interventions
H Encourage the child to engage in any activity he can
tolerate.
H Give prescribed drugs.

Monitoring
H Vital signs
H Central venous and intra-arterial pressures
H Intake and output
H Cardiac rhythm
H Oxygenation

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Physical findings
Attention deficit Symptoms of inattention
hyperactivity disorder H Makes careless mistakes
H Struggles to sustain attention
H Fails to finish activities
H Difficulty with organization
Overview H Avoids tasks that require sustained mental effort
H Distracted or forgetful
Description Symptoms of hyperactivity
H A behavioral problem characterized by difficulty with H Fidgets
inattention, impulsivity, hyperactivity, and boredom H Cant sit still for sustained period
H Also called ADHD and ADD H Difficulty playing quietly
H Talks excessively
Pathophysiology Symptoms of impulsivity
H Alleles of dopamine genes may alter dopamine, sero- H Interrupts
tonin, and adrenalin transmission in the neural net- H Cant wait patiently
works.
H During fetal development, bouts of hypoxia and hy- DSM-IV-TR criteria
potension could selectively damage neurons located These criteria confirm a diagnosis:
in some of the critical regions of the anatomical net- H six symptoms or more from the inattention or hyper-
works. activity-impulsivity categories
H symptoms present for at least 6 months
Causes H symptoms evident before age 7
H Underlying cause unknown H impairment present in two or more settings
H Limited evidence of a genetic component H symptoms arent accounted for by another mental
H May result from altered neurotransmitter levels in the disorder.
brain
Test results
Risk factors H Complete psychological, medical, and neurologic
H Family history evaluations rule out other problems; specific tests in-
H History of learning disability clude continuous performance test, behavior rating
H Mood or conduct disorder scales, and learning disability.
Incidence
H Present at birth, but diagnosis before age 4 or 5 is Treatment
difficult; some patients undiagnosed until adulthood
H Occurs in 3% to 5% of school-age children General
H Affects males three times more than females H Education regarding the nature and effect of the dis-
order
Common characteristics H Behavior modification
H Impulsive behavior H External structure
H Inattentiveness H Supportive psychotherapy
H Disorganization in school H Elimination of sugar, dyes, and additives from diet
H Tendency to jump quickly from one partly completed H Monitor activity (for safety purposes)
project, thought, or task to another
H Difficulty meeting deadlines and keeping track of Medications
school or work tools and materials H Stimulants, such as methylphenidate, dextroampheta-
mine, and pemoline
Complications H Tricyclic antidepressants, such as desipramine and
H Emotional and social complications imipramine
H Poor nutrition H Mood stabilizers such as bupropion
H Beta-adrenergic blockers such as propranolol
H Selective norepinephrine reuptake inhibitors such as
Assessment atomoxetine
H Alpha2-agonists such as clonidine
History
H Characterized as a fidgeter and a daydreamer
H Appears inattentive and lazy
H Performs sporadically at school or work

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Nursing considerations
Key outcomes
The patient (or family) will:
H demonstrate effective social interaction skills in one-
on-one and group settings
H report improvement in family and social interactions
H demonstrate effective coping behavior.

Nursing interventions
H Set realistic expectations and limits to avoid frustrat-
ing the patient.
H Maintain a calm and consistent manner.
H Keep all instructions short and simple make one-
step requests.
H Provide praise, rewards, and positive feedback when-
ever possible.
H Provide diversional activities suited to a short atten-
tion span.
Monitoring
H Activity level
H Nutritional status
H Adverse drug reactions
H Response to treatment
H Complications
H Activity (for safety purposes)

Patient teaching
Be sure to cover:
H behavior therapy
H reinforcement of good behavior
H realistic expectations
H medications and possible adverse reactions
H nutrition.

Discharge planning
H Refer the patient to family therapy.

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Autistic disorder H Pronoun reversal

H Bizarre or self-destructive behavior
H Extreme compulsion for sameness
H Abnormal reaction to sensory stimuli
Overview H Cognitive impairment
H Eating, drinking, and sleeping problems
Description H Mood disorders
H A severe, pervasive developmental disorder
H Degree of impairment varies DSM-IV-TR criteria
H Usually apparent before age 3 At least 6 of these 12 characteristics must be present,
H Poor prognosis including at least 2 items from the first section, 1 from
H Sometimes called Kanners autism the second, and 1 from the third.
H Qualitative impairment in social interaction:
Pathophysiology Impaired nonverbal behavior
H Defects in the central nervous system (CNS) may Absence of peer relationships
arise from prenatal complications. Failure to seek or share enjoyment, interests, or
achievements
Causes Lack of social or emotional reciprocity
H Exact cause unknown H Qualitative impairment in communication:
H Defects in CNS from prenatal complications such as Delay or lack of language development
rubella Inability to initiate or sustain conversation
H Nutritional deficiency Idiosyncratic or repetitive language
H Disease caused or triggered by immunizations Lack of appropriate imaginative play
H Restricted repetitive and stereotyped patterns of be-
Risk factors havior, interests, and activities:
H High-risk pregnancy Abnormal preoccupation with a restricted pattern
of interest
Incidence Inflexible routines or rituals
H Affects an estimated 1 in 1,000 children Repetitive motor mannerisms
H Three to four times more likely in males than in Preoccupation with parts of objects
females, usually the firstborn male H The diagnostic criteria also include delays or abnor-
mal functioning in at least one of these areas before
Common characteristics age 3:
H Unresponsive to social contact Social interaction and language skills
H Gross deficit in intelligence and language develop- Symbolic or imaginative play
ment
H Ritualistic and compulsive behavior
H Restricted capacity for developmentally appropriate Treatment
activities and interests
H Bizarre response to the environment General
H Structured treatment plan
Complications H Behavioral techniques
H Epileptic seizures H Pleasurable sensory and motor stimulation
H Depression H Monitor activities (for safety purposes)
During stress
H Catatonic phenomena Medications
H Undifferentiated psychotic state H Serotonin receptor reuptake inhibitors, such as flu-
voxamine and sertratine
H Antidepressants, such as doxepin, imipramine, and
Assessment clomipramine
H Antipsychotics, such as haloperidol, thioridazine, and
History risperidone
H Becomes rigid or flaccid when held H Stimulants, such as dextroamphetamine and
H Cries when touched methylphenidate
H Shows little or no interest in human contact H Alpha2-agonists such as clonidine
H Bet-adrenergic blockers such as propranolol
Physical findings
H Delayed smiling response
H Severe language impairment
H Lack of socialization and imaginative play
H Echolalia

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Nursing considerations
Key outcomes
The patient (or family) will:
H identify and contact available resources, as needed
H openly share feelings about the present situation
H as much as possible, demonstrate age-appropriate
skills and behaviors
H practice safety measures and take safety precautions
in the home
H interact with family or friends.

Nursing interventions
H Institute safety measures when appropriate.
H Provide positive reinforcement.
H Encourage development of self-esteem.
H Encourage self-care.
H Prepare the child for change by telling him about it.
H Help family members develop strong one-on-one
relationships with the patient.
Monitoring
H Response to treatment
H Complications
H Adverse drug reactions
H Patterns of behavior
H Nutritional status
H Social interaction
H Communication skills
H Activity

Patient teaching
Be sure to cover:
H physical care for the childs needs
H importance of identifying signs of excessive stress
and coping skills.
Discharge planning
H Refer the parents to resource and support services.

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Avian influenza H Shortness of breath

H Eye infections
H Cytokine storm
Hypotension
Overview Tachycardia
Dyspnea
Description Fever
H Extremely virulent virus occurring naturally in birds Uncontrollable hemmorrhage
H Rapidly mutating and has been transmitted from Signs of multisystem organ failure from ischemia
birds to mammals, including humans or insufficient tissue perfusion
H Risk of pandemic as the virus evolves and more hu-
man cases occur each year Test results
H International concern because virus spreads by mi- Laboratory
gratory birds H Oropharyngeal, nasal, nasopharyngeal, or lower res-
piratory tract specimen culture shows causative or-
Pathophysiology ganism.
H The virus invades the epithelium of the respiratory H Serology for influenza H5N1-specific antibody shows
tract, causing inflammation. causative organism.
H The immune system releases inflammatory mediators
(cytokines, oxygen free radicals and coagulation fac-
tors). Treatment
H Cytokine storm, an inappropriate and exaggerated
immune response, is caused by rapidly proliferating General
and active T-cells. H Supportive measures
H If the immune response isnt limited, the lungs are
permanently damaged. Medications
H Patients develop acute respiratory distress syndrome, H Antibiotics as appropriate
sepsis, and multisystem organ failure. H Anti-viral medications (effectiveness under study)
H Angiotensin-converting enzyme inhibitors, such as
Causes captopril, enalapril and lisinopril and angiotensin II
H Influenza A, H5N1 virus strain receptor blockers, such as candesartan, valsartan
and irbesartan to treat cytokine storm
Incidence H Corticosteroids
H Few hundred cases per year world-wide H Vaccine produced and approved for distribution by
H No recent cases in the United States public-health officials if needed (Further vaccine re-
H Affects all age-groups and both sexes search is underway.)
H Primarily in those with exposure to infected poultry
H Greater than 50% mortality
Nursing considerations
Common characteristics
H Influenza-like symptoms Key outcomes
The patient will:
Complications H develop no complications
H Acute respiratory distress H maintain stable vital signs
H Viral pneumonia H express understanding of the disorder and treatment
H Multisystem organ failure regimen
Nursing interventions
Assessment H Observe standard and respiratory precautions to pre-
vent transmission of the disease.
History H Give prescribed drugs.
H Close contact with infected poultry or contaminated H Provide supportive care and emotional support.
surfaces
H Rarely, close contact with infected human Monitoring
H Vital signs
Physical findings H Respiratory status
H Influenza-like symptoms H Cardiovascular status
Fever H Response to treatment
Cough H Complications
Sore throat
Muscle aches

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Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H measures to prevent the spread of disease
H medication administration, dosage, and possible ad-
verse effects
H importance of continuing the prescribed antibiotic
until the entire prescription is finished
H disposal of secretions and the use of proper hand-
washing technique
H fact that seasonal influenza vaccine doesnt protect
against avian flu
Discharge planning
H Refer the patient to an infectious disease specialist, if
necessary.

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BBasal cell carcinoma

Overview
Description
H Nonmelanoma skin cancer
H Slow-growing, destructive cancerous skin tumor
H Two major types: noduloulcerative and superficial
H Most common malignant tumor that affects whites
(see Identifying basal cell carcinoma)
Pathophysiology
H Although the pathogenesis is uncertain, some experts




A reddish patch
A shiny bump
A pink growth
A scarlike area
Complications
H Disfiguring lesions of the eyes, nose, and cheeks

Assessment
History
H Odd-looking skin lesion
H Prolonged exposure to the sun
H Nonhealing sore of varying duration
hypothesize that it originates when undifferentiated
basal cells become carcinomatous instead of differ- Physical findings
entiating into sweat glands, sebum, and hair. H Lesions characterized as small, smooth, pinkish, and
translucent papules (early-stage noduloulcerative)
Causes H Telangiectatic vessels across surface and lesions may
H Prolonged sun exposure (90% of tumors occur on be pigmented
sun-exposed areas of the body) H Lesions enlarge with depressed centers and firm and
elevated borders (also called rodent ulcers)
Risk factors H Multiple oval or irregularly shaped, lightly pigmented
H Arsenic ingestion plaques on chest or back
H Radiation exposure H Head and neck possibly showing waxy, sclerotic, yel-
H Burns low to white plaques without distinct borders
H Immunosuppression
H Vaccinations (rare) Test results
H History of previous nonmelanoma skin cancer Diagnostic procedures
H Incisional or excisional biopsy and histologic study
Incidence may help determine the tumor type and histologic
H Usually occurs in people older than age 40 subtype.
H Most prevalent in blond, fair-skinned males Other
H All types of basal cell carcinomas are diagnosed by
Common characteristics clinical appearance.
H Lesion found on face, head, neck, and back
H Five warning signs
An open sore Treatment
General
Identifying basal cell carcinoma H Depends on the size, location, and depth of the le-
This illustration shows an enlarged nasal nodule in basal sion
cell carcinoma. Note its depressed center and firm, elevat- H Irradiation, if the tumor location requires it; pre-
ed border. ferred for elderly or debilitated patients who might
not tolerate surgery
H Cryotherapy (liquid nitrogen that freezes the cells
and kills them)
H Well-balanced diet; no restrictions
H Avoidance of sun exposure

Medications
H Chemotherapy such as topical fluorouracil
H Immune response modifier such as topical
imiquimod
Surgery
H Curettage and electrodesiccation

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H Microscopically controlled surgical excision, known

as Mohs surgery, that carefully removes recurrent
lesions until a tumor-free plane is achieved (after
removal of large lesions, skin grafting may be re-
quired)
H Simple excision
H Chemosurgery

Nursing considerations
Key outcomes
The patient will:
H express positive feelings about self
H express feelings of increased comfort
H exhibit healing lesions or wounds
H demonstrate effective coping mechanisms.

Nursing interventions
H Encourage verbalization and provide support.
H Provide appropriate wound care.

Monitoring
H Complications of treatment
H Response to treatment
H Signs and symptoms of infection
H Wound healing
H Skin surveillance for additional lesions

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H appropriate wound care
H importance of avoiding excessive sun exposure,
wearing protective clothing, and using a strong sun-
screen or sunshade to protect the skin.
Discharge planning
H Refer the patient to resource and support services, as
needed.

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Bells palsy H Local traumatic injury

H Autoimmune disease
H Lyme disease
H Tumor
Overview H Bacterial infections such as meningitis

Description Incidence
H Condition in which the impulses from the seventh H Affects all age-groups
cranial nerve are blocked, causing muscle weakness H Most common between ages 20 and 60
or paralysis H Affects males and females equally
H Rapid onset
H Subsides spontaneously in 80% to 90% of patients Common characteristics
H Complete recovery in 1 to 8 weeks H Unilateral facial weakness
H Delayed recovery in elderly people H Aching at jaw angle
H Partial recovery: contractures may develop on the H Drooping mouth
paralyzed side of the face H Distorted and loss of taste
H May recur on same or opposite side of the face H Impaired ability to fully close eye on affected side
H Tinnitus
Pathophysiology
H An inflammatory reaction occurs around the seventh Complications
cranial nerve (motor innervation of the facial mus- H Corneal ulceration and blindness
cles). H Impaired nutrition secondary to paralysis of the low-
H Inflammation is usually at the internal auditory er face
meatus. H Long-term psychosocial problems
H Unilateral facial weakness or paralysis results.

Causes Assessment
H Unknown
H Ischemia History
H Viral disease, such as herpes simplex or herpes H Pain on the affected side around the angle of the jaw
zoster or behind the ear for a few hours or days before on-
set of weakness
Facial paralysis in Bells palsy H Difficulty chewing on the affected side
H Difficulty speaking clearly
Unilateral facial paralysis characterizes Bells palsy. The
paralysis produces a distorted appearance and an inability Physical findings
to wrinkle the forehead, close the eyelid, smile, show the H Mouth droops on the affected side (see Facial paral-
teeth, or puff out the cheek on the affected side.
ysis in Bells palsy)
H Smooth forehead
H Distorted taste perception
H Inability to raise eyebrow, smile, show teeth, or puff
out cheek
H Impaired ability to close eye on the weak side
H Eye rolls upward (Bells phenomenon) when at-
tempting to close the eye
H Excessive tearing

Test results
H Diagnosis is based on clinical presentation.
Imaging
H Magnetic resonance imaging rules out tumor.

Treatment
General
H Eliminating the source of damage to the nerve imme-
diately
SMILING

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H Oral hygiene maintenance

H Eye protection such as sunglasses
H Hearing protection
H Moist heat
H Diet, as tolerated
H Activity, as tolerated

Medications
H Oral corticosteroids, such as prednisone and
hydrocortisone
H Analgesic such as ibuprofen
H Antiviral such as acyclovir

Surgery
H Exploration of the facial nerve (possibly)
H Facial reanimation, such as direct facial nerve repair
or facial nerve grafting

Nursing considerations
Key outcomes
The patient will:
H experience increased comfort and relief from pain
H consume an adequate amount of calories daily
H express positive feelings about self
H express understanding of the condition and treat-
ment regimen
H exhibit improvement in facial muscle movement.

Nursing interventions
H Provide psychological support.
H Apply moist heat to the affected side of the face.
H Massage the patients face with a gentle upward
motion.
H Provide a facial sling.
H If the patient had surgery, provide preoperative and
postoperative care.
H Administer medication, as ordered.

Monitoring
H Neurologic function
H Response to medications
H Signs and symptoms of peptic ulceration, pancreati-
tis, or other GI adverse effects of prednisone and
hydrocortisone
H Nutritional status
H Facial muscle movement

Patient teaching
Be sure to cover:
H the disorder
H medication and adverse effects
H protection of affected eye
H exercises of the facial muscles
H nutritional management program.

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Benign prostatic H Urinary hesitancy and frequency

H Difficulty initiating urination

hyperplasia H Nocturia, hematuria

H Dribbling, incontinence
H Urine retention

Overview Physical findings

H Visible midline mass above the symphysis pubis from
Description distended bladder
H Enlargement of prostate gland enough to compress H Enlarged prostate on digital rectal examination
urethra, causing overt urinary obstruction
H May be treated surgically or symptomatically, de- Test results
pending on the size of prostate, age and health of Laboratory
patient, and extent of obstruction H Elevated blood urea nitrogen and serum creatinine
H Referred to as BPH levels suggest impaired renal function.
H Bacterial count that exceeds 100,000/mm3 reveals
Pathophysiology hematuria, pyuria, and UTI.
H Changes occur in periurethral glandular tissue. Imaging
H Prostate enlarges and may extend into the bladder. H Excretory urography may indicate urinary tract ob-
H Compression or distortion of prostatic urethra struction, hydronephrosis, calculi or tumors, and
obstructs urine outflow. bladder filling and emptying defects.
H BPH may cause diverticulum through the muscula- Diagnostic procedures
ture leading to urinary retention. H Cystourethroscopy determines the best surgical inter-
vention and shows prostate enlargement, bladder
Causes wall changes, calculi, and raised bladder.
H Unknown Other
H Possible link with hormonal activity H International Prostate Symptom Score classifies
disorders severity.
Risk factors
H Age
H Intact testes Treatment
Incidence General
H Prostatic massage
Special populations H Short-term fluid restriction (prevents bladder disten-
tion)
BPH occurs in 80% of all males older than age 40, H Avoidance of lifting, performing strenuous exercises,
and in 95% of all males older than age 80. and taking long automobile rides for at least 1 month
after surgery
H No sexual intercourse for several weeks after surgery
Common characteristics
H Changes in voiding patterns and urine stream Medications
H Antibiotics, such as cefepime and levofloxacin, if
Complications infection present
H Urinary stasis, urinary tract infection (UTI), or renal H Alpha-1-adrenergic blockers, such as doxazosin and
calculi terazosin
H Bladder wall trabeculation H 5-Alpha-reductase inhibitors such as dutasteride and
H Detrusor muscle hypertrophy finasteride
H Bladder diverticula and saccules
H Urethral stenosis Surgery
H Hydronephrosis H For relief of acute urine retention, hydronephrosis,
H Paradoxical (overflow) incontinence severe hematuria, and recurrent UTI or for palliative
H Acute or chronic renal failure relief of intolerable symptoms
H Acute postobstructive diuresis H Suprapubic (transvesical) prostatectomy
H Perineal prostatectomy
H Retropubic (extravesical) prostatectomy
Assessment H Transurethral resection of the prostate
H Balloon dilatation, ultrasound needle ablation, and
History use of stents
H Decreased urine stream caliber and force
H Interrupted urinary stream

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Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort
H express understanding of disorder and treatment
H demonstrate skill in managing urinary elimination
H express feelings about potential or actual changes in
sexual activity.
Nursing interventions
H Give prescribed drugs.
H Avoid giving sedatives, alcohol, antidepressants, or
anticholinergics (which can worsen the obstruction).
H Provide I.V. therapy, as ordered.
H Administer continuous bladder irrigation, as pre-
scribed.
H Keep the head of the bed elevated at least 30 degrees
to prevent pneumonia.
H Encourage coughing, deep breathing, and incentive
spirometer use.
Monitoring
H Vital signs
H Intake and output
H Daily weight

ALERT
Watch for signs of postobstructive diuresis, charac-
terized by polyuria exceeding 2 L in 8 hours and
excessive electrolyte losses. Although usually self-
limiting, it can result in vascular collapse and
death if not promptly treated.

After prostatic surgery

H Pain control
H Catheter function and drainage
H Continuous bladder irrigation function
H Signs of infection

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H signs of UTI that should be reported
H when to seek medical care (fever, unable to void, or
passing bloody urine).

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Common characteristics
Bipolar disorder Manic phase
H Accelerated speech
H Frequent changes of topic
Overview H Flight of ideas
Depressive phase
Description H Loss of self-esteem
H An affective disorder marked by severe pathologic H Overwhelming inertia
mood swings from hyperactivity and euphoria to H Social withdrawal
sadness and depression H Feelings of hopelessness
H In cyclothymia, a variant of bipolar disorder: numer- H Apathy or self-reproach
ous episodes of hypomania and depressive symptoms H Suicidal thoughts
too mild to meet the criteria for major depression or Bipolar II disorder
bipolar disorder (see Cyclothymic disorder) H Meets all the diagnostic criteria for a manic episode
H Manic episodes that emerge over a period of days to H May experience recurrent depressions, separated by
weeks, but onset possible within hours periods of mild activation and increased energy
H Untreated episodes that can last weeks or as long as
8 to 12 months, with some having an unremitting Complications
course H Emotional and social consequences
H Found in 15% of patients, mostly female, rapid cy- H Sexually transmitted disease
cling, in which four or more episodes of either de- H Exhaustion
pression or mania occur in 1 year H Nutritional deficits
H Difficulties in work performance and psychosocial H Sleep disturbances
functioning in about half of all patients with this dis- H Suicide
order
Pathophysiology Assessment
H Bipolar disorder may be an effect of neurotransmit-
ter imbalance. History
H Mood swings may involve membrane changes in H Sleeping and eating disturbances
sodium- and potassium-activated adenosine triphos- H Exhibits expansive, grandiose, sometimes irritable
phatase involving disordered intracellular signals. mood alternating with symptoms of depression
Causes Physical findings
H Exact cause unclear Mania
H Autosomal dominant inheritance found in genetic H Increased psychomotor activity
studies H Excessive social extroversion
H Some evidence that links to an X chromosome H Impulsive actions
disorder H Impaired judgment
H May be triggered by death, separation, or divorce H Delusions
H Imbalances in the biochemistry that controls food H Paranoid thinking
(biochemical) imbalances H Limited attention span
H Inflated sense of self-esteem
Risk factors H Rapid responses to external stimuli
H Family history Depression
H Substance abuse H Slow speech and response
H No obvious disorientation or intellectual impairment
Incidence H Psychomotor retardation
H Affects over 5 million people in the United States H Lethargy
H Equally common in females and males H Low muscle tone
H Females: likely to have more depressive episodes H Weight loss
H Males: likely to have more manic episodes H Slowed gait
H Higher among relatives of affected patients than in
the general population DSM-IV-TR criteria
Diagnosis is confirmed when the patient meets the cri-
Special populations teria established for a manic or hypomanic episode:
H experiences a distinct period of abnormally and per-
Age of onset is usually between ages 20 and 35, but sistently elevated, expansive, or irritable mood
35% of patients experience onset between ages 35 H during the mood disturbance, at least three of these
and 60. symptoms must persist (four, if the mood is only irri-
table) and be present to a significant degree:

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inflated self-esteem or grandiosity Cyclothymic disorder

decreased need for sleep
A chronic mood disturbance of at least 2 years duration,
excessive talking
cyclothymic disorder involves numerous episodes of hy-
flight of ideas pomania or depressive symptoms that arent of sufficient
easily distracted severity or duration to qualify as a major depressive
psychomotor agitation episode.
excessive involvement in dangerous activities In the hypomanic phase, the patient may experience in-
symptoms dont meet criteria for a mixed episode somnia; hyperactivity; inflated self-esteem; increased pro-
impairment in occupational function, usual social ductivity and creativity; overinvolvement in pleasurable
activities, or relations with others severe enough activities, including an increased sexual drive; physical
to require hospitalization to prevent harm to self restlessness; and rapid speech. Depressive symptoms
or others may include insomnia, feelings of inadequacy, decreased
substance use or other causative medical condi- productivity, social withdrawal, loss of libido, loss of inter-
tions not present. est in pleasurable activities, lethargy, depressed speech,
and crying.
A number of medical disorders (for example, endocri-
Treatment nopathies, such as Cushings disease, stroke, brain tu-
mors, head trauma, and drug overdose) can produce a
similar pattern of mood alteration. These organic causes
General must be ruled out before making a diagnosis of cyclo-
H Group and individual therapy thymic disorder.
H Monitoring of activity when in manic phase
H No dietary restrictions

Medications H Encourage verbalization; provide support.

H Anticonvulsants, such as carbamazepine and valproic H Institute safety measures.
acid H Encourage physical activity.
H Antimanic such as lithium
H Antipsychotics, such as aripiprazole, olanzapine, Monitoring
quetiapine, risperidone, and ziprasidone H Patterns of behavior
H Antidepressant such as fluoxetine H Response to treatment
H Social interaction
H Complications
Nursing considerations H Adverse drug reactions
H Nutritional status
Key outcomes
The patient will:
H identify effective coping techniques Patient teaching
H recognize symptoms and comply with medication
regimen Be sure to cover:
H express feelings related to self-esteem H the disorder, diagnosis, and treatment
H join gradually in self-care and the decision-making H medication administration, dosage, and possible ad-
processes. verse effects
H importance of continuing the prescribed medication
Nursing interventions regimen.
For the manic patient
H Encourage activities that require gross motor move- Discharge planning
ments. H Refer the patient for psychological counseling.
H Assist with personal hygiene; encourage responsibili- H Refer the patient to support services.
ty for personal care.
H Protect from overstimulation.
H Set realistic goals and limits for the patients behav-
ior.
H Provide diversional activities suited to a short atten-
tion span.
H Reorient to reality.
H Avoid power struggles.
For the depressed patient
H Avoid overwhelming expectations.
H Allow increased time for activities and responses.
H Provide a structured routine.
H Promote interaction with others.

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Bladder cancer Assessment

History
Overview H Gross, painless, intermittent hematuria, usually with
clots
Description H Suprapubic pain after voiding suggesting invasive
H Malignant tumor that develops on the bladder wall lesions
surface or grows within the wall and quickly invades H Bladder irritability, urinary frequency, nocturia, and
underlying muscles dribbling
H Less common bladder tumors: adenocarcinomas, H Flank pain possibly indicating an obstructed ureter
epidermoid carcinomas, squamous cell carcinomas,
sarcomas, tumors in bladder diverticula, and carci- Physical findings
noma in situ H Gross hematuria
H Most common cancer of the urinary tract H Flank tenderness if ureteral obstruction present

Pathophysiology Test results

H About 90% of bladder cancers are transitional cell
carcinomas, arising from the transitional epithelium
of mucous membranes. (They may result from malig-
nant transformation of benign papillomas.)
Causes
H Exact cause unknown
H Associated with chronic bladder irritation and infec-
tion in people with renal calculi, indwelling urinary
catheters, chemical cystitis caused by cyclophospha-
mide, or pelvic irradiation
Risk factors
H Certain environmental carcinogens, such as
2-naphthylamine, tobacco, nitrates, and coffee
H Occupational exposure to carcinogens
Incidence
H Bladder tumors most prevalent in people older than
age 50
H More common in males than in females
H Occurs more commonly in densely populated indus-
trial areas
Common characteristics
H Asymptomatic in early stages for 25% of patients
H First sign: gross, painless, intermittent hematuria,
with or without clots
H Suprapubic pain after voiding most commonly
associated with invasive lesions
H Bladder irritability
H Urinary frequency
H Nocturia
H Dribbling
Complications
H Bone metastasis
H Problems resulting from tumor invasion of contigu-
ous viscera
Laboratory
H Complete blood count helps detect anemia.
H Urinalysis detects blood and malignant cells in the
urine.
Imaging
H Excretory urography can identify a large, early-stage
tumor or an infiltrating tumor; delineate functional
problems in the upper urinary tract; assess hydro-
nephrosis; and detect rigid deformity of the bladder
wall.
H Retrograde cystography evaluates bladder structure
and integrity; it also helps confirm a bladder cancer
diagnosis.
H Bone scan can detect metastasis.
H Computed tomography scan defines the thickness of
the involved bladder wall and discloses enlarged
retroperitoneal lymph nodes.
H Ultrasonography reveals metastasis in tissues beyond
the bladder and can distinguish a bladder cyst from a
bladder tumor.
Diagnostic procedures
H Cystoscopy and biopsy confirm bladder cancer diag-
nosis; if the test results show cancer cells, further
studies will determine the cancer stage and treat-
ment.
Other
H Bimanual examination may be performed during a
cystoscopy if the patient has received an anesthetic;
this helps to determine whether the bladder is fixed
to the pelvic wall.
Treatment
General
H Cancers stage, patients lifestyle, other health prob-
lems, and mental outlook influencing selection of
therapy
H Initially postoperatively, avoidance of heavy lifting
and contact sports
H After recovery, no activity restrictions

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Medications Discharge planning

H Intravesical chemotherapy, such as thiotepa and H Refer the patient to resource and support services.
mitomycin H Before discharge, arrange for follow-up home nurs-
H Attenuated live bacille Calmette-Gurin vaccine ing care.
H Chemotherapy, such as cisplatin and doxorubicin H Refer the patient to an enterostomal therapist and for
services provided by the therapist.
Surgery
H Transurethral resection (cystoscopic approach) and
fulguration (electrically)
H Segmental bladder resection
H Radical cystectomy
H Ureterostomy, nephrostomy, continent vesicostomy
(Kock pouch), ileal bladder, and ureterosigmoidos-
tomy

Nursing considerations
Key outcomes
The patient will:
H maintain adequate fluid balance
H express feelings of increased comfort and decreased
pain
H exhibit adequate coping mechanisms
H express feelings about potential or actual changes in
sexual activity.
Nursing interventions
H Provide support and encourage verbalization.
H Give prescribed drugs.
H Provide preoperative teaching; discuss procedure
and postoperative course.
H Keep the head of the bed elevated at least 30 degrees
to prevent pneumonia.
H Encourage coughing, deep breathing, and incentive
spirometer use.
H Provide skin care.
H Provide stoma care.

Monitoring
H Vital signs
H Wound site
H Postoperative complications, such as pneumonia,
deep vein thrombosis, and infection
H Intake and output
H Pain control
H Respiratory status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H stoma care
H skin care and evaluation
H avoidance of heavy lifting and contact sports (post-
operatively with a urinary stoma)
H encouragement of participation in usual athletic and
physical activities.

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Physical findings
Blastomycosis H Thick sputum (may contain blood)
H Bronchial breath sounds; dullness on chest percus-
sion
Overview H Decreased breath sounds
H Tachypnea
Description H Decreased pulse oximetry
H Fungal infection that usually affects the lungs and H Raised and reddened lesions
produces bronchopneumonia H Chest pain
H May develop into extrapulmonary disease H Dyspnea
H Also called Gilchrists disease Extrapulmonary findings
H Skin lesions
Pathophysiology H Osteolytic lesions
H Blastomycosis is generally contracted by inhalation of H Joint swelling
aerosolized conidial forms of the fungus from its nat-
ural soil habitat. Test results
H The conidia then transforms to the yeast phase at Laboratory
body temperature (thermal dimorphism). H Culture from skin lesions, pus, sputum, or pulmo-
H Inflammatory response is evoked by multiplication nary secretions shows presence of B. dermatitidis.
of organism. H White blood cell count and erythrocyte sedimentation
H Dissemination is possible through the blood and rate are increased.
lymphatics to other organs. H Serum globulin levels are slightly increased, and mild
normochromic anemia occurs.
Causes H Alkaline phosphatase level is increased (with bone
H Inhalation of the yeastlike fungus Blastomyces lesions).
dermatitidis Imaging
H Chest X-ray may show pulmonary infiltrates.
Incidence Diagnostic procedures
H Generally found in North America, where B. der- H Biopsy of tissue from the skin or lungs or of bron-
matitidis normally inhabits the soil chial washings, sputum, or pus shows infecting
H Endemic to the southeastern United States organism.
H More common in males than females Other
H Onset most common between ages 30 and 50, but H Immunodiffusion testing detects antibodies for the A
can occur at any age and B antigens of blastomycosis.
Common characteristics
H Signs and symptoms of a viral upper respiratory tract Treatment
infection
H Small, painless, nonpruritic, and nondistinctive mac- General
ules or papules on exposed body parts H Increased fluid intake
H Respiratory treatments
Complications H Rest periods, as needed
H Osteomyelitis
H Central nervous system, skin, and genital disorders Medications
H Addisons disease (adrenal insufficiency) H Antifungals, such as amphotericin B, itraconazole,
H Pericarditis and ketoconazole
H Arthritis H Antipyretic such as acetaminophen

Assessment Nursing considerations

History Key outcomes
H Fever, chills The patient will:
H Dry, hacking, productive cough H maintain adequate oxygenation
H Weight loss H improve skin integrity
H Night sweats H report increased comfort and decreased pain.
H Pleuritic chest pain
H Malaise
H Myalgia

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Nursing interventions
H Provide a cool room; if the patient is feverish, admin-
ister a tepid sponge bath.
H Elevate painful joints and apply heat.
H Provide appropriate skin care.
H Give prescribed drugs.

Monitoring
H Vital signs
H Pulse oximetry
H Laboratory tests
H Sputum production for hemoptysis
H Level of consciousness and pupil response
H Hematuria
H Lesion healing
H Respiratory status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H proper administration of medications
H skin care.

Discharge planning
H Stress appropriate follow-up care.

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Blepharitis Ulcerative blepharitis

H Flaky scales on eyelashes, especially in morning
H Missing eyelashes
H Ulcerations on eyelid margins
Overview
Test results
Description Laboratory
H Common inflammation of eyelash follicles and H Culture of the ulcerated eyelid margin reveals
meibomian glands of the upper or lower eyelids S. aureus in ulcerative blepharitis.
H May affect both eyes
H May affect upper and lower eyelids
H Ulcerative type: may coexist with seborrheic bleph- Treatment
aritis
General
Pathophysiology H Early treatment to prevent recurrence or complica-
H Inflammatory responses of the eyelids to bacteria or tions
seborrheic dermatitis occurs. H Daily cleansing (using diluted baby-shampoo on a
cotton-tipped applicator or washcloth) to remove
Causes scales from eyelid margins
Seborrheic blepharitis H Warm eye compresses
H Generally results from seborrhea of the scalp, eye- H Removal of nits with forceps for blepharitis caused
brows, and ears by pediculosis
Ulcerative blepharitis H Avoidance of eye makeup
H Generally results from a Staphylococcus aureus in- H Avoidance of contact lens use until resolved
fection
H Pediculosis Medications
H Antibiotic eye ointment such as gentamicin
Incidence H Ophthalmic physostigmine or other insecticidal
H More common in elderly people ointment for blepharitis caused by pediculosis
H Most common ocular disease

Common characteristics Nursing considerations

H Eye drainage
H Burning, itching, and swelling of eyes Key outcomes
H Tends to recur The patient will:
H May become chronic H sustain no harm or injury
H verbalize feelings and concerns
Complications H identify available health resources
H Ocular involvement H demonstrate appropriate coping skills
H Keratitis H maintain current visual acuity.
H Excess tearing or dry eye
Nursing interventions
H Provide eyelid care at least twice daily.
Assessment H Apply warm compresses, four times daily.
H Give prescribed drugs.
History H Apply ointments, as ordered. (See Applying an
H Eyelids itch or burn ophthalmic ointment.)
H Feeling of foreign body H Maintain infection-control techniques.
H Crusty eyelids, which stick together when awakening
H Loss of eyelashes Monitoring
H Response to treatment
Physical findings H Adverse reactions to medication
H Continual blinking H Complications
H Red-rimmed appearance to the eyelid margins
H Swelling of eyelids
Seborrheic blepharitis
H Scales along eyelids, especially upon awakening
H Dandruff on scalp and eyebrows

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Applying an ophthalmic ointment

Follow these directions to apply an ophthalmic ointment
cleanly and quickly:
H Tilt the patients head back, and ask him to look toward
the ceiling.
H Gently pull the lower eyelid down, and squeeze a small
ribbon of ointment along the edge of the conjunctival
sac from the inner to the outer canthus.
H Take care to avoid touching the eye with the tip of the
ointment tube.
H Repeat this procedure for the other eye, if ordered.

Patient teaching
Be sure to cover:
H the disorder and treatment
H daily eyelid care
H removal of scales from eyelids
H application of warm compresses
H medications and possible adverse effects
H infection control
H potential complications
H importance of keeping follow-up appointments.

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Risk factors
Life-threatening disorder H Multiple transfusions
H Rare blood type

Blood transfusion Incidence

reaction H Mild reactions in 1% to 2% of transfusions

Common characteristics
H Mild to severe fever within the first 15 minutes of
Overview transfusion or within 2 hours after its completion
H Chills
Description H Urticaria
H A hemolytic reaction following the transfusion of mis- H Shortness of breath
matched blood
H Accompanies or follows I.V. administration of blood Complications
components H Bronchospasm
H Mediated by immune or nonimmune factors H Acute tubular necrosis leading to acute renal failure
H From mild to severe H Anaphylactic shock
H Vascular collapse
Pathophysiology H Disseminated intravascular coagulation
H Recipients antibodies, immunoglobulin (Ig) G or
IgM, attach to donor red blood cells (RBCs), leading
to widespread clumping and destruction of recipi- Assessment
ents RBCs.
H Transfusion with Rh-incompatible blood triggers a History
less serious reaction, known as Rh isoimmuniza- H Transfusion of blood product
tion, within several days to 2 weeks. (See Under- H Chills, nausea, vomiting, chest tightness, or chest and
standing the Rh system.) back pain
H A febrile nonhemolytic reaction the most common
type of reaction develops when cytotoxic or agglu- Physical findings
tinating antibodies in the recipients plasma attack H Fever, tachycardia, and hypotension
antigens on transfused lymphocytes, granulocytes, or H Dyspnea, anxiety, and restlessness
plasma cells. H Urticaria and angioedema
H Wheezing
Causes H In a surgical patient, blood oozing from mucous
H Transfusion with incompatible blood membranes or the incision site
H In a hemolytic reaction: fever, an unexpected de-
crease in serum hemoglobin level, frank blood in
urine, and jaundice
Understanding the Rh system
Test results
The Rh system contains more than 30 antibodies and
antigens. Of the worlds population, about 85% are Rh
Laboratory
H Serum hemoglobin levels are decreased.
positive, which means that their red blood cells carry the
D or Rh antigen. The rest of the population are Rh nega- H Serum bilirubin levels and indirect bilirubin levels
tive and dont have this antigen. are elevated.
Effects of sensitization H Urinalysis reveals hemoglobinuria.
When an Rh-negative person receives Rh-positive blood H Indirect Coombs test or serum antibody screen is
for the first time, he becomes sensitized to the D antigen positive for serum anti-A or anti-B antibodies.
but shows no immediate reaction to it. If he receives Rh- H Prothrombin time is increased and fibrinogen level is
positive blood a second time, he experiences a massive decreased.
hemolytic reaction. H Blood urea nitrogen and serum creatinine levels are
For example, an Rh-negative mother who delivers an
increased.
Rh-positive baby is sensitized by the babys Rh-positive
blood. During her next Rh-positive pregnancy, her sensi-
tized blood will cause a hemolytic reaction in the fetal cir-
culation.
Treatment
Preventing sensitization
To prevent the formation of antibodies against Rh-positive
General
blood, an Rh-negative mother should receive Rho(D) im- H Immediate halt of transfusion
mune globulin (human) (RhoGAM) I.M. within 72 hours H Dialysis (may be necessary if acute tubular necrosis
after delivering an Rh-positive baby. occurs)

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H Diet, as tolerated
H Bed rest Patient teaching
Medications Be sure to cover:
H Osmotic or loop diuretics, such as mannitol and H signs and symptoms of transfusion reaction (before
furosemide transfusion begins)
H I.V. normal saline solution H importance of notifying health care providers of
H I.V. vasopressors, such as dopamine and phenyl- history of reaction
ephrine H wearing or carrying rare blood type identification.
H Adrenergic such as epinephrine
H Antihistamine such as diphenhydramine
H Corticosteroid such as dexamethasone
H Antipyretic such as acetaminophen

Nursing considerations
Key outcomes
The patient will:
H maintain hemodynamic stability
H show no signs of active bleeding
H maintain adequate ventilation
H express understanding of disorder.

Nursing interventions
H Stop the blood transfusion.
H Maintain a patent I.V. line with normal saline
solution.
H Insert an indwelling urinary catheter.
H Report early signs of complications.
H Cover the patient with blankets to ease chills.
H Administer supplemental oxygen, as needed.
H Document the transfusion reaction on the patients
chart, noting the duration of the transfusion and the
amount of blood absorbed.
H Follow your facilitys blood transfusion policy and
procedure.

ALERT
Double-check the patients name, identification
number, blood type, and Rh status before adminis-
tering blood. If you find any discrepancy, dont ad-
minister the blood. Notify the blood bank immedi-
ately and return the unopened unit.

Monitoring
H Vital signs
H Intake and output
H Signs of shock
H Laboratory results
H Respiratory status
H Cardiac status
H Pulse oximetry

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Bone tumors, primary H Hemorrhage

H Local recurrence

malignant H Pathologic fractures

Assessment
Overview
History
Description H Localized, dull bone pain
H Rare type of bone cancer (less than 1% of all malig- H Weight loss
nant tumors) H Impaired mobility
H Also known as osteoblastoma or osteosarcoma H Pathologic fracture

Pathophysiology Physical findings

H Proliferation of cancerous cells clump together to H Palpable mass
form a tumor, which is able to spread beyond the H Cachectic appearance
original site. H Abnormal gait
H Osseous bone tumors arise from the bony structure H Swelling and redness at the site
itself and include osteogenic sarcoma (most com-
mon), parosteal osteogenic sarcoma, chondrosarco- Test results
ma (chondroblastic), and malignant giant cell tumor. Laboratory
H Nonosseous bone tumors arise from hematopoietic, H Serum alkaline phosphatase levels are elevated (with
vascular, and neural tissues and include Ewings sar- sarcoma).
coma, fibrosarcoma (fibroblastic), and chordoma. Imaging
H Bone X-rays and radioisotope bone and computed
Causes tomography (CT) scans show tumor size.
H No immediately apparent cause in most cases H Bone scans and CT scans of the lungs reveal meta-
H Genetic abnormalities (retinoblastoma, Rothmund- static disease.
Thomson syndrome) Diagnostic procedures
H Exposure to carcinogens H Incision or aspiration biopsy confirms primary
H Heredity, trauma, and excessive radiation therapy, malignancy.
according to theories
Incidence Treatment
H Account for less than 0.2% of all cancers
H More common in males than females General
H Higher incidence in children and adolescents, al- H High-protein, high-calorie diet
though some types occurring in patients between H Rest periods, as needed
ages 35 and 60 (see Types of primary malignant H Physical therapy
bone tumors) H Radiation therapy

Special populations
Osteogenic and Ewings sarcomas are the most
common bone tumors in children.
Common characteristics
H Localized, dull bone pain
H Usually more intense at night
H Presence of a mass or tumor
Medications
H Chemotherapy, such as gemcitabine and docetaxel
H Analgesics, such as morphine, oxycodone, hydro-
codone, and fentanyl
Surgery
H Excision of the tumor
H Radical surgery, such as hemipelvectomy or inter-
scapulothoracic or limb amputation

Special populations
Nursing considerations
Limb pain, refusal to walk, and limited range of Key outcomes
motion (ROM) are common findings in children The patient will:
with bone tumors. H maintain weight within an acceptable range
H maintain joint mobility and ROM
H express feelings of comfort and decreased pain
Complications H express feelings and fears.
H Infection

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Types of primary malignant bone tumors

Type Clinical features Treatment

OSSEOUS ORIGIN

Chondrosarcoma Develops from cartilage Hemipelvectomy, surgical resec-

Painless; grows slowly; locally recurrent and invasive tion (ribs)
Occurs most commonly in pelvis, proximal femur, ribs, and Radiation (palliative)
shoulder girdle Chemotherapy
Usually in males ages 30 to 50

Malignant Arises from benign giant cell tumor Curettage

giant cell tumor Found most commonly in long bones, especially in the knee Total excision
area Radiation for recurrent disease
Usually in females ages 18 to 50

Osteogenic Osteoid tumor present in specimen Surgery (tumor resection, high

sarcoma Tumor arises from bone-forming osteoblast and bone- thigh amputation, hemipelvec-
digesting osteoclast tomy, interscapulothoracic
Occurs most commonly in femur, but also tibia and humer- surgery)
us; occasionally, in fibula, ileum, vertebra, or mandible Chemotherapy
Usually in males ages 10 to 30

Parosteal Develops on surface of bone instead of interior Surgery (tumor resection, possi-
osteogenic Progresses slowly ble amputation, interscapulotho-
sarcoma Occurs most commonly in distal femur, but also in tibia, racic surgery, hemipelvectomy)
humerus, and ulna Chemotherapy
Usually in females ages 30 to 40 Combination of the above

NONOSSEOUS ORIGIN

Chordoma Derived from embryonic remnants of notochord Surgical resection (commonly

Progresses slowly resulting in neural defects)
Usually found at end of spinal column and in spheno- Radiation (palliative, or when
occipital, sacrococcygeal, and vertebral areas surgery not applicable, as in
Characterized by constipation and visual disturbances occipital area)
Usually in males ages 50 to 60

Ewings sarcoma Originates in bone marrow and invades shafts of long and High-voltage radiation (tumor is
flat bones radiosensitive)
Usually affects lower extremities, most commonly femur, Chemotherapy to slow growth
innominate bones, ribs, tibia, humerus, vertebra, and fibula; Amputation only if theres no evi-
may metastasize to lungs dence of metastasis
Pain increasingly severe and persistent
Usually in males ages 10 to 20
Prognosis poor

Fibrosarcoma Relatively rare Amputation

Originates in fibrous tissue of bone Radiation
Invades long or flat bones (femur, tibia, mandible) but also Chemotherapy
involves periosteum and overlying muscle Bone grafts (with low-grade fibro-
Usually in males ages 30 to 40 sarcoma)

Nursing interventions H Cardiovascular status

H Encourage communication, and help the patient set
realistic goals.
H Administer prescribed I.V. infusions and drugs. Patient teaching
H Postoperative care, including coughing, deep breath-
ing, incentive spirometer use, and turning. Be sure to cover:
H Keep the head of the bed elevated at least 30 degrees. H use of assistive devices
H Elevate the foot of the bed or place the affected H wound care
stump on a pillow for the first 24 hours. (Be care- H reporting new pain or masses
ful not to leave the stump elevated for more than H the need for antibiotic prophylaxis when undergoing
48 hours because this may lead to contractures.) dental procedures (with bone grafts or prosthetic
implants).
Monitoring
H Vital signs Discharge planning
H Circulation to the affected extremity H Refer the patient to the American Cancer Society for
H Wound dressings information and support.
H Respiratory status

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Common characteristics
Life-threatening disorder H Symptoms 18 to 30 hours after ingestion of con-
taminated food; may be delay of up to 10 days before
Botulism symptoms appear
H Range in severity and can mimic other illnesses,
especially neurologic disorders
Overview Complications
H Respiratory failure
Description H Paralytic ileus
H Life-threatening paralytic illness H Death
H Results from an exotoxin produced by the gram-
positive, anaerobic bacillus Clostridium botulinum
H Occurs as botulism food poisoning, wound botulism, Assessment
and infant botulism (see Infant botulism)
H Mortality about 25%, with death most commonly History
caused by respiratory failure during the first week of H Consumption of home-canned food 18 to 30 hours
illness before onset of symptoms
H Critical and potentially fatal illness signaled by onset H Vertigo
within 24 hours H Sore throat
H Weakness
Pathophysiology H Nausea and vomiting
H Endotoxin acts at the neuromuscular junction of H Constipation or diarrhea
skeletal muscle, preventing acetylcholine release and H Diplopia
blocking neural transmission, eventually resulting in H Blurred vision
paralysis. H Dysarthria
H Dysphagia
Causes H Dyspnea
H Clostridium botulinum bacteria H Heroin use

Risk factors Physical findings

H Eating improperly preserved foods H Ptosis
H Use of injectable street drugs H Dilated, nonreactive pupils
H Appearance of dry, red, and crusted oral mucous
Incidence membranes
H Occurs worldwide H Abdominal distention with absent bowel sounds
H Average yearly occurrence of about 110 cases in the H Descending weakness or paralysis of muscles in the
United States extremities or trunk
H Affects adults more than children H Deep tendon reflexes may be intact, diminished, or
absent
H Unexplained orthostatic hypotension
H Urine retention
H Photophobia
H Slurred speech
Infant botulism
Infant botulism, which usually afflicts neonates and in-
Test results
fants between 3 and 20 weeks old, is commonly caused Laboratory
by ingesting the spores of botulinum bacteria, which then H Mouse bioassay detects toxin thats found in the pa-
grow in the intestines and release toxin. This disorder can tients serum, stool, or gastric contents.
produce floppy infant syndrome, characterized by consti- Diagnostic procedures
pation, a feeble cry, a depressed gag reflex, and an inabili- H Electromyography shows diminished muscle action
ty to suck. The infant also exhibits a flaccid facial expres- potential after a single supramaximal nerve stimulus.
sion, ptosis, and ophthalmoplegia the result of cranial
nerve deficits.
As the disease progresses, the infant develops general-
ized weakness, hypotonia, areflexia, and sometimes a
Treatment
striking loss of head control. Almost 50% of affected in-
fants develop respiratory arrest.
General
Intensive supportive care allows most infants to recover H Supportive measures
completely. Antitoxin therapy isnt recommended because H Early tracheotomy and ventilatory assistance in respi-
of the risk of anaphylaxis. ratory failure
H Nasogastric (NG) suctioning

126 Botulism
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H Total parenteral nutrition

H Bed rest

Medications
H I.V. or I.M. botulinum antitoxin

Surgery
H Debridement of wounds to remove source of toxin-
producing bacteria

Nursing considerations
Key outcomes
The patient will:
H maintain tissue perfusion and cellular oxygenation
H maintain adequate ventilation
H maintain stable neurologic status.

Nursing interventions
H Administer I.V. fluids, as ordered.
H Administer oxygen as needed.
H Perform NG suctioning as needed.

ALERT
Immediately report all cases of botulism to the
local board of health.

Monitoring
H Neurologic status
H Cardiac and respiratory function
H Cough and gag reflexes
H Intake and output
H Arterial blood gas analysis
H Pulse oximetry

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H proper techniques in processing and preserving
foods
H never tasting food from a bulging can or one with a
peculiar odor
H sterilizing utensils by boiling what came in contact
with suspected contaminated food
H not feeding honey to infants (can be fatal if contami-
nated).
Discharge planning
H If botulism exposure appears to be related to adverse
socioeconomic conditions, refer the patient to the
appropriate community agency.

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Brain tumor Life-threatening complications from

increased ICP
H Coma
H Respiratory or cardiac arrest
Overview H Brain herniation

Description
H Abnormal growth among cells within the intracranial Assessment
space
H May affect brain tissue, meninges, pituitary gland, History
and blood vessels H Insidious onset
H In adults, most common tumor types: gliomas and H Headache
meningiomas (usually benign), which usually occur H Nausea and vomiting
above the covering of the cerebellum, and supraten-
torial tumors Physical findings
H In children, most common tumor types: astrocyto- H May vary according to size and location of tumor
mas, medulloblastomas, ependymomas, and brain Signs and symptoms of increased ICP
stem gliomas H Vision disturbances
H Weakness, paralysis
Pathophysiology H Aphasia, dysphagia
H Tumor is classified based on histology or grade of H Ataxia, incoordination
cell malignancy. H Seizure
H Central nervous system changes occur due to cancer H Decreased level of consciousness
cells invading and destroying tissues and by secon-
dary effect mainly compression of the brain, cra- Test results
nial nerves, and cerebral vessels; cerebral edema; Imaging
and increased intracranial pressure (ICP). H Skull X-rays confirm presence of tumor.
H Brain scan confirms presence of tumor.
Causes H Computed tomography scan confirms presence of
H Unknown tumor.
H Magnetic resonance imaging confirms presence of
Risk factors tumor.
H Preexisting cancer H Cerebral angiography confirms presence of tumor.
H Positron-emission tomography confirms presence of
Incidence tumor.
H Slightly more common in males than in females Diagnostic procedures
H Gliomas, meningiomas, and schwannomas: overall H Tissue biopsy confirms type of tumor.
incidence of 4.5 per 100,000 Other
H Can occur at any age, but most in children before age H Lumbar puncture shows increased cerebrospinal
1 or between ages 2 and 12 fluid (CSF) pressure, which reflects ICP, increased
H In adults, incidence highest between ages 40 and 60 protein levels, decreased glucose levels and, occa-
sionally, tumor cells in CSF.
Common characteristics
H Increased ICP
H Headache Treatment
H Decreased motor strength and coordination
H Seizures General
H Altered vital signs H Specific treatments varying with the tumors histolog-
H Nausea and vomiting ic type, radiosensitivity, and location
H Papilledema H No dietary restrictions unless swallowing impaired
H Possibly altered physical ability based on neurologic
Complications status
H Radiation encephalopathy
Medications
H Chemotherapy, such as carmustine, cisplatin, and
Special populations
lomustine
Brain tumors are the most common cause of can- H Steroid such as dexamethasone
cer death in children. H Histamine-receptor antagonists, such as cimetidine,
famotidine, and ranitidine
H Anticonvulsants, such as phenytoin and fosphenytoin
H Analgesic such as codeine

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Surgery
For glioma Patient teaching
H Resection by craniotomy
H Radiation therapy and chemotherapy follow resection Be sure to cover:
For low-grade cystic cerebellar astrocytoma H the disease process, diagnosis, and treatment
H Surgical resection H signs of infection or bleeding that may result from
For astrocytoma chemotherapy
H Repeated surgeries, radiation therapy, and shunting H adverse effects of chemotherapy and other treatments
of fluid from obstructed CSF pathways and actions that may alleviate them
For oligodendroglioma and ependymoma H early signs of tumor recurrence.
H Surgical resection and radiation therapy
For medulloblastoma Discharge planning
H Surgical resection H Consult with occupational and physical therapy staff
H Possibly, intrathecal infusion of methotrexate or for postdischarge care plan.
another antineoplastic drug H Refer the patient to resource and support services.
For meningioma
H Surgical resection, including dura mater and bone
For schwannoma
H Microsurgical technique

Nursing considerations
Key outcomes
The patient will:
H recognize limitations imposed by illness and express
feelings about them
H continue to function in usual roles as much as
possible
H enlist support from available sources
H express feelings of increased comfort.

Nursing interventions
H Maintain a patent airway.
H Take steps to protect the patients safety.
H Give prescribed drugs.
H After supratentorial craniotomy, elevate the head of
the bed about 30 degrees.
H After infratentorial craniotomy, keep the patient flat
for 48 hours.
H As appropriate, instruct the patient to avoid Valsalvas
maneuver and isometric muscle contractions when
moving or sitting up in bed.
H Provide postoperative care.
H Encourage incentive spirometer use.
H Consult with occupational, speech, and physical
therapists.
H Provide emotional support.

Monitoring
H Neurologic status
H Vital signs
H Wound site
H Postoperative complications
H Pulse oximetry
H Respiratory status
H Pain level, location, and effectiveness of treatment
H Cardiovascular status

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Breast cancer H Estrogen therapy

H Antihypertensive therapy
H Alcohol and tobacco use
H Preexisting fibrocystic disease
Overview
Incidence
Description H A female living in the United States to age 80 a
H Malignant proliferation of epithelial cells lining the 1-in-8 chance of developing invasive breast cancer
ducts or lobules of the breast sometime during her life
H Early detection and treatment influencing the prog- H The second-leading cause of cancer death in females
nosis considerably after lung cancer
H Most common after age 50; but may develop anytime
ALERT after puberty
H Seldom occurs in males
The most reliable detection method of breast can-
cer is regular breast self-examination, followed by Special populations
an immediate professional evaluation of any ab-
normality. (Theoretically, slow-growing breast can- Breast cancer is the leading cause of cancer deaths
cer may take up to 8 years to become palpable at among females ages 35 to 54.
1 cm.)

H With adjunctive therapy, 10-year (or longer) 70% to Common characteristics

75% survival in females with negative nodes, com- H Lump or mass in the breast (see Breast tumor
pared to 20% to 25% survival in females with positive sources and sites)
nodes H Breast pain
H Change in symmetry or size of breast
Pathophysiology H Change in skin, such as thickening, scaly skin around
H Breast cancer spreads by way of the lymphatic system the nipple, dimpling, edema, or ulceration
and the bloodstream through the right side of the H Nipple discharge
heart to the lungs and to the other breast, chest wall,
liver, bone, and brain. Complications
Classification H Distant metastasis
H Adenocarcinoma (ductal) arises from the epithelium. H Infection
H Intraductal cancer develops within the ducts (in- H Central nervous system effects
cludes Pagets disease). H Respiratory effects
H Infiltrating cancer occurs in the breasts parenchymal
tissue.
H Inflammatory cancer (rare) grows rapidly and caus- Assessment
es overlying skin to become edematous, inflamed,
and indurated. History
H Lobular carcinoma in situ involves the lobes of glan- H Detection of a painless lump or mass in the breast
dular tissue. H Change in breast tissue
H Medullary or circumscribed cancer is an enlarged tu- H History of risk factors
mor with a rapid growth rate.
Physical findings
Causes H Clear, milky, or bloody discharge from the nipple,
H Unknown nipple retraction, scaly skin around the nipple, and
skin changes, such as dimpling or inflammation
Risk factors H Arm edema
H Family history of breast cancer, particularly first- H Hard lump, mass, or thickening of breast tissue
degree relatives, including mother, sister, maternal H Lymphadenopathy
grandmother, and maternal aunt
H Positive tests for genetic mutations (BRCA1) Test results
H A female older than age 45 and premenopausal Laboratory
H Long menstrual cycles H Hormonal receptor assay determines whether the
H Early onset of menses, late menopause tumor is estrogen- or progesterone-dependent; also
H Nulliparous or first pregnancy after age 30 guides decisions to use therapy that blocks the action
H High-fat diet of the estrogen hormone that supports tumor growth.
H Endometrial or ovarian cancer H In Vitro Diagnostic Multivariate Index Assay predicts
H History of unilateral breast cancer the odds that an early-stage breast cancer will metas-
H Radiation exposure tasize in 5 to 10 years.

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Imaging Breast tumor sources and sites

H Mammography can reveal a tumor thats too small to
palpate.
H Ultrasonography can distinguish between a
fluid-filled cyst and solid mass.
H Chest X-rays can pinpoint metastasis in the chest.
H Scans of the bone, brain, liver, and other organs can
detect distant metastasis.
Diagnostic procedures
H Fine-needle aspiration and excisional biopsy provide
cells for histologic examination that may confirm the
diagnosis.
About 90% of all breast tumors arise from the epithelial
cells lining the ducts. About half of all breast cancers de-
velop in the breasts upper outer quadrant the section
containing the most glandular tissue.
The second most common cancer site is the nipple,
where all the breast ducts converge.
The next most common site is the upper inner quadrant,
followed by the lower outer quadrant and, finally, the low-
er inner quadrant.

Treatment
General 50%

H The choice of treatment usually depends on: stage 15%

and type of disease, age, menopausal status, and any 18%

disfiguring effects of surgery 11%
H Therapy may include: any combination of surgery, 6%
radiation, chemotherapy, and hormone therapy
H Arm motion and exercises possibly needed after
surgery
H Primary radiation therapy
H Preoperative breast irradiation

Medications
H Chemotherapy, such as a combination of drugs, in-
cluding anastrozole, capecitabine, cyclophospha-
mide, docetaxel, epirubicin, ememestane, fluo- H Provide emotional support.
rouracil, methotrexate, doxorubicin, vincristine, H Provide postoperative care, such as turning, cough-
paclitaxel, prednisone, and trastuzumab ing, deep breathing, and incentive spirometer use.
H Regimen of cyclophosphamide, methotrexate, and H Keep the head of the bed elevated at least 30 degrees
fluorouracil (used in premenopausal and post- to prevent pneumonia.
menopausal females) H Encourage early ambulation.
H Antiestrogen therapy such as tamoxifen
H Hormonal therapy, including estrogen, progesterone, Monitoring
androgen, or antiandrogen aminoglutethimide H Wound site
therapy H Postoperative complications
H Vital signs
Surgery H Intake and output
H Lumpectomy H White blood cell count
H Partial, total, or modified radical mastectomy H Pain control
H Psychological status
H Respiratory status
Nursing considerations
Key outcomes Patient teaching
The patient will:
H recognize limitations imposed by illness and express Be sure to cover:
feelings about these limitations H all procedures and treatments
H express positive feelings about self H activities or exercises that promote healing
H report feelings of comfort H breast self-examination
H express increased sense of well-being H risks and signs and symptoms of recurrence
H use situational supports to reduce fear. H avoidance of venipuncture or blood pressure moni-
toring on the affected arm.
Nursing interventions
H Provide information about the disease process, diag- Discharge planning
nostic tests, and treatment. H Refer the patient to local and national support
H Give prescribed drugs. groups.

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Bronchiectasis H Dramatically decreased incidence over the past 20

years due to the availability of antibiotics to treat
acute respiratory infections
H Highest among Inuit populations in the northern
Overview hemisphere and the Maoris of New Zealand
Description Common characteristics
H Lung disease characterized by abnormal dilation of H Chronic cough productive for copious, foul-smelling,
the bronchi and destruction of the bronchial walls mucopurulent secretions
H Results from conditions associated with repeated H Dyspnea
damage to bronchial walls and with abnormal mu- H Weight loss
cociliary clearance, causing a breakdown of support- H Malaise
ing tissue adjacent to the airways
H Can occur throughout the tracheobronchial tree, or Complications
may be confined to one segment or lobe H Chronic malnutrition
H Usually bilateral and involves the basilar segments of H Amyloidosis
the lower lobes H Right-sided heart failure
H Occurs in three forms: cylindrical (fusiform), vari- H Cor pulmonale
cose, and saccular (cystic) H Respiratory failure

Pathophysiology
H Hyperplastic squamous epithelium, denuded of cilia, Assessment
replaces ulcerated columnar epithelia.
H Abscess formation occurs, involving all layers of the History
bronchial walls, which produces inflammatory cells H Frequent bouts of pneumonia
and fibrous tissues, resulting in dilation and narrow- H Coughing up of blood or blood-tinged sputum
ing of the airways. H Chronic cough that produces copious, foul-smelling,
H Sputum stagnates in the dilated bronchi and leads to mucopurulent secretions
secondary infection, characterized by inflammation H Dyspnea
and leukocytic accumulations. H Weight loss
H Additional debris collects in the bronchi and oc- H Malaise
cludes them.
H Building pressure from the retained secretions in- Physical findings
duces mucosal injury. H Sputum that may show a cloudy top layer, a central
H Extensive vascular proliferation of bronchial circula- layer of clear saliva, and a heavy, thick, purulent bot-
tion occurs and produces frequent hemoptysis. tom layer upon settling
H Clubbed fingers and toes
Causes H Cyanotic nail beds
H Cystic fibrosis H Dullness over affected lung fields, if pneumonia or
H Mucoviscidosis atelectasis present
H Immune disorders H Diminished breath sounds
H Recurrent bacterial respiratory tract infections H Crackles during inspiration over affected area
H Complications of measles, pneumonia, pertussis, or H Occasional wheezes
influenza
H Obstruction with recurrent infection Test results
H Inhalation of corrosive gas Laboratory
H Repeated aspiration of gastric juices H Sputum culture and Gram stain show predominant
H Congenital anomalies (rare) such as bronchomalacia pathogens.
H Various rare disorders such as immotile cilia syn- H Complete blood count reveals anemia and leuko-
drome cytosis.
Imaging
Risk factors H Computed tomography scan shows bronchiectasis.
H Occupational exposure to damaging inhalants H Bronchography shows location and extent of disease.
H Risky behaviors that lead to immunodeficiency disor- H Chest X-rays show peribronchial thickening, atelec-
ders, such as human immunodeficiency virus and ac- tatic areas, and scattered cystic changes.
quired immunodeficiency syndrome Diagnostic procedures
H Bronchoscopy may show the source of secretions or
Incidence the bleeding site in hemoptysis.
H Affects people of both sexes and of all ages H Pulmonary function studies show decreased vital
capacity, expiratory flow, and hypoxemia.

132 Bronchiectasis
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Other H Arterial blood gas results

H A sweat electrolyte test may show cystic fibrosis as H Complications
the underlying cause. H Chest tube drainage after surgery
H Pain control

Treatment
Patient teaching
General
H Postural drainage and chest percussion Be sure to cover:
H Bronchoscopy to remove secretions H the disorder, diagnosis, and treatment
H Well-balanced, high-calorie diet H medications and possible adverse effects
H Adequate hydration H when to notify the physician
H Activity, as tolerated H proper disposal of secretions
H infection control techniques
Medications H frequent rest periods
H Antibiotics, such as cefdinir, cefpodoxime, and H preoperative and postoperative instructions, if
levofloxacin surgery is required
H Bronchodilators, such as albuterol and aformoterol H postural drainage and percussion
H Oxygen H coughing and deep-breathing techniques
H Mucolytic such as acetylcysteine H avoidance of air pollutants and people with known
upper respiratory tract infections
Surgery H immunizations
For poor pulmonary function H balanced, high-protein diet
H Segmental resection H avoidance of milk products
H Bronchial artery embolization H adequate hydration.
H Lobectomy
Discharge planning
H Refer the patient to a smoking-cessation program, if
Nursing considerations indicated.
Key outcomes
The patient will:
H maintain a patent airway
H maintain adequate ventilation
H utilize energy conservation techniques
H demonstrate effective coping mechanisms.

Nursing interventions
H Perform preoperative and postoperative teaching.
H Give prescribed drugs.
H Provide supportive care.
H Administer oxygen, as needed.
H Perform chest physiotherapy.
H Provide a warm, quiet, comfortable environment.
H Alternate rest and activity periods.
H Provide well-balanced, high-calorie meals.
H Offer small, frequent meals.
H Provide adequate hydration.
H Provide frequent mouth care.
H Encourage incentive spirometer use, coughing, and
deep breathing.
H Provide postoperative care.
H Keep the head of the bed elevated at least 30 degrees.

Monitoring
H Vital signs
H Intake and output
H Respiratory status
H Cardiac status
H Sputum production
H Pulse oximetry

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Bronchitis, chronic Assessment

History
Overview H Longtime smoker
H Frequent upper respiratory tract infections
Description H Productive cough
H An inflammation of the lining of the bronchial tubes H Exertional dyspnea
H Form of chronic obstructive pulmonary disease H Cough, initially prevalent in winter, but gradually
H Characterized by excessive production of tracheo- becoming year-round
bronchial mucus with a cough for at least 3 months H Increasingly severe coughing episodes
each year for 2 consecutive years H Worsening dyspnea
H Severity linked to the amount of cigarette smoke or
other pollutants inhaled and inhalation duration Physical findings
H Respiratory tract infections that typically exacerbate H Cough producing copious gray, white, or yellow
the cough and related symptoms sputum
H Development of significant airway obstruction seen in H Cyanosis
few patients with chronic bronchitis H Accessory respiratory muscle use
H Tachypnea
Pathophysiology H Substantial weight gain
H Hypertrophy and hyperplasia of the bronchial mu- H Pedal edema
cous glands, increased goblet cells, ciliary damage, H Jugular vein distention
squamous metaplasia of the columnar epithelium, H Wheezing
and chronic leukocytic and lymphocytic infiltration H Prolonged expiratory phase
of bronchial walls results. H Rhonchi
H Additional effects include widespread inflammation,
airway narrowing, and mucus within the airways Test results
all producing resistance in the small airways and, in Laboratory
turn, a severe ventilation-perfusion imbalance. (See H Arterial blood gas analysis shows decreased partial
What happens in chronic bronchitis.) pressure of oxygen and normal or increased partial
pressure of carbon dioxide.
Causes H Sputum culture reveals microorganisms and neu-
H Cigarette smoking trophils.
H Possible genetic predisposition Imaging
H Environmental pollution H Chest X-ray may show hyperinflation and increased
H Organic or inorganic dusts and noxious gas exposure bronchovascular markings.
Diagnostic procedures
Incidence H Pulmonary function tests show increased residual
H About 20% of males affected volume, decreased vital capacity and forced expirato-
H More than 8.8 million people in the United States di- ry flow, and normal static compliance and diffusing
agnosed annually capacity.
H More prevalent in females than in males H Electrocardiography may show atrial arrhythmias;
H Children of parents who smoke: higher risk for con- peaked P waves in leads II, III, and aVF; and right
tracting chronic bronchitis than children of parents ventricular hypertrophy.
who dont smoke
Common characteristics Treatment
H Long-time smoker
H Frequent upper respiratory tract infections General
H Productive cough H Smoking cessation
H Exertional dyspnea H Avoidance of air pollutants
H Chest physiotherapy
Complications H Ultrasonic or mechanical nebulizer treatments
H Cor pulmonale H Adequate fluid intake
H Pulmonary hypertension H High-calorie, protein-rich diet
H Right ventricular hypertrophy H Activity, as tolerated with frequent rest periods
H Acute respiratory failure
Medications
H Oxygen
H Antibiotics, such as cefdinir, cefpodoxime, and
levofloxacin

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What happens in chronic bronchitis

In chronic bronchitis, irritants inhaled
CROSS SECTION OF THE NORMAL NARROWED BRONCHIAL TUBE IN
for a prolonged period inflame the tra-
BRONCHIAL TREE CHRONIC BRONCHITIS
cheobronchial tree. The inflammation
leads to increased mucus production
and a narrowed or blocked airway. Cilia
Cilia
As inflammation continues, the
mucus-producing goblet cells undergo
hypertrophy, as do the ciliated epithe-
lial cells that line the respiratory tract.
Hypersecretion from the goblet cells
blocks the free movement of the cilia,
which normally sweep dust, irritants,
and mucus from the airways.
Goblet cell Epithelial cell Goblet cell Epithelial cell
As a result, the airway stays
blocked, and mucus and debris accu-
mulate in the respiratory tract.

H Bronchodilators, such as aformoterol, salmeterol, H Daily weight

and tiotropium H Edema
H Corticosteroids, such as fluticasone, hydrocortisone, H Response to treatment
methylprednisolone, and prednisone H Cardiovascular status
H Diuretics such as furosemide

Surgery Patient teaching

H Tracheostomy in advanced disease
Be sure to cover:
H the disorder, diagnosis, and treatment
Nursing considerations H medications and possible adverse effects
H when to notify the physician
Key outcomes H infection control practices
The patient will: H influenza and pneumococcus immunizations
H maintain adequate ventilation H home oxygen therapy, if required
H identify measures to prevent or reduce fatigue H postural drainage and chest percussion
H express understanding of the illness H coughing and deep-breathing exercises
H maintain a patent airway. H inhaler use
H high-calorie, protein-rich meals
Nursing interventions H adequate hydration
H Give prescribed drugs. H avoidance of inhaled irritants
H Encourage expression of fears and concerns. H prevention of bronchospasm
H Include the patient and his family in care decisions. H respiratory hygiene and cough etiquette.
H Perform chest physiotherapy.
H Provide a high-calorie, protein-rich diet. Discharge planning
H Offer small, frequent meals. H Refer the patient to a smoking-cessation program, if
H Encourage energy-conservation techniques. indicated.
H Ensure adequate oral fluid intake. H Refer the patient to the American Lung Association
H Provide frequent mouth care. for information and support.
H Encourage daily activity. H Refer the patient to support services for respiratory
H Provide diversional activities, as appropriate. care equipment and supplies.
H Provide frequent rest periods.
H Encourage coughing, deep breathing, and incentive
spirometer use.
H Keep the head of the bed elevated at least 30 degrees.

Monitoring
H Vital signs
H Intake and output
H Sputum production
H Respiratory status, including breath sounds and
pulse oximetry

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Brucellosis H Hepatosplenomegaly
H Enlarged lymph nodes

Complications
Overview H Abscesses in the testes, ovaries, kidneys, and brain
(meningitis and encephalitis)
Description H Osteomyelitis
H An acute febrile illness transmitted to humans from H Orchitis
animals H Subacute bacterial endocarditis
H Also known as undulant fever, Malta fever, or H Pleural effusions
Bangs disease H Pneumothorax
H Eczematous rashes, petechiae, purpura
Pathophysiology
H Brucellosis is transmitted through the consumption
of unpasteurized dairy products or uncooked or un- Assessment
dercooked contaminated meat, and through contact
with infected animals or their secretions or excre- History
tions. H Direct exposure to animals
H Ingestion of unpasteurized dairy products
Causes H Recent travel to an endemic area
H The nonmotile, nonspore-forming, gram-negative H Fatigue
coccobacilli of the genus Brucella, notably B. suis H Headache
(found in swine), B. melitensis (in goats), B. abor- H Intermittent fever
tus (in cattle), and B. canis (in dogs) H Profuse sweating
H Anxiety
Risk factors H General aching
H Occupational exposure to animals
Physical findings
Incidence H Excessive perspiration
H Most common among farmers, stock handlers, H Chills
butchers, and veterinarians H Weakness
H Six times more common in males than in females H Lymphadenopathy
H Less common in children H Hepatosplenomegaly
H People with chlorhydria particularly susceptible be- H Tenderness in the right upper quadrant
cause hydrochloric acid in gastric juices kills Bru-
cella bacteria Test results
H Most prevalent in the Middle East, Africa, Russia, In- Laboratory
dia, South America, and Europe; uncommon in the H Agglutinin titers are 1:160 or higher.
United States H Definitive diagnosis is provided by three to six
cultures of blood and bone marrow and biopsies
Common characteristics of infected tissue (for example, the spleen).
Acute phase H Erythrocyte sedimentation rate is increased.
H Fever H White blood cell count is either normal or reduced.
H Chills
H Profuse sweating
H Fatigue Treatment
H Headache
H Backache General
H Enlarged lymph nodes H Bed rest during the acute phase
H Hepatosplenomegaly H High-calorie, high-protein diet
H Weight loss H Secretion precautions until lesions stop draining
H Abscess and granuloma formulation in subcutaneous
tissues, lymph nodes, liver, and spleen Medications
Chronic phase H Antibiotic such as tetracycline
H Recurrent depression H Antipyretic such as acetaminophen
H Sleep disturbances H Corticosteroids, such as hydrocortisone, methylpred-
H Fatigue nisolone, and prednisone
H Headache
H Sweating
H Sexual impotence

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Nursing considerations
Key outcomes
The patient will:
H be free from signs and symptoms of infection
H attain relief from immediate symptoms
H experience feelings of comfort or absence of pain
H regain or maintain skin integrity.

Nursing interventions
H Keep suppurative granulomas and abscesses dry.
H Maintain contact precautions: double-bag and prop-
erly dispose of all secretions and soiled dressings.
H Reassure the patient that this infection is curable.
H Keep the head of the bed elevated at least 30 degrees.

Monitoring
H Vital signs
H Complications
H Depression and disturbed sleep pattern
H Lesion healing
H Neurologic status

Patient teaching
Be sure to cover:
H continuing medication for the prescribed duration
H preventing recurrence by cooking meat thoroughly
and avoiding unpasteurized milk
H advice to meat packers and other people at risk for
occupational exposure to wear rubber gloves and
goggles.

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Buergers disease H Digital ischemia

H Trophic nail changes
H Absent or diminished radial, ulnar, or tibial pulses
H Ischemic ulcers on the toes, feet, or fingers
Overview H Superficial thrombophlebitis

Description Test results

H An inflammatory, nonatheromatous occlusive condi- Imaging
tion that impairs circulation to the legs, feet and, oc- H Doppler ultrasonography shows diminished circula-
casionally, hands tion in the peripheral vessels.
H Sometimes called thromboangiitis obliterans H Arteriography locates lesions and rules out athero-
sclerosis.
Pathophysiology Diagnostic procedures
H Polymorphonuclear leukocytes infiltrate the walls of H Plethysmography helps detect decreased circulation
small and medium-sized arteries and veins. in the peripheral vessels.
H Thrombus develops in the vascular lumen, eventually Other
occluding and obliterating portions of the small ves- H Allens test results are abnormal. (See Performing
sels, resulting in decreased blood flow to the feet and Allens test.)
legs.
H This diminished blood flow may produce ulceration
and, eventually, gangrene. Treatment
Causes General
H Unknown H Smoking cessation
H Linked to smoking (suggesting a hypersensitivity H Nothing by mouth, if surgery is needed
reaction to nicotine) H Exercise program that uses gravity to fill and drain
the blood vessels
Incidence
H More common in males than females Medications
H Most patients ages 20 to 45 H Antibiotics, such as cefuroxime, gentamicin, and
H Affects natives of India, Japan, and Korea and Ashke- tobramycin, for secondary infection
nazic Jews H Analgesics, such as morphine, hydromorphone, and
ketarolac
Common characteristics
H Intermittent claudication of the instep, aggravated by Surgery
exercise and relieved by rest H In severe disease, a lumbar sympathectomy to in-
H Initially, coldness, cyanosis, and numbness in feet crease blood supply to the skin
during exposure to low temperature; later, redness, H Amputation for nonhealing ulcers, intractable pain,
heat, and tingling or gangrene
H Impaired peripheral pulses and migratory superficial
thrombophlebitis
Nursing considerations
Complications
H Ulceration Key outcomes
H Muscle atrophy The patient will:
H Gangrene H express feelings of increased comfort and decreased
pain
H maintain tissue integrity
Assessment H carry out previous roles without the limitations of the
disease process
History H develop adequate coping mechanisms.
H Exposure to secondhand smoke
H Use of nicotine patch Nursing interventions
H Use of chewing tobacco H Position the patient for comfort with the head of the
H Smoking bed elevated at least 30 degrees.
H Painful, intermittent claudication of the instep, aggra- H Provide a padded footboard or bed cradle to prevent
vated by exercise and relieved by rest pressure from bed linens.
H Protect the feet with soft padding.
Physical findings H Provide emotional support.
H Feet that are cold, numb, and cyanotic when exposed H Administer medications, as ordered.
to low temperatures

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Performing Allens test

Dont obtain an arterial blood gas specimen from the radial artery until you assess collateral arterial blood supply using the
Allens test.
Direct the patient to close his hand Tell the patient to open his hand. Release pressure on the ulnar artery.
while you occlude his radial and ulnar Color should return to the patients
arteries for 10 to 30 seconds, watch- hand in 15 seconds. If the color
ing for the hand to blanch. doesnt return, select another site
for an arterial puncture.

Monitoring
H Skin integrity
H Peripheral circulation
H Infection
H Pain control

Patient teaching
Be sure to cover:
H avoiding precipitating factors, such as emotional
stress, exposure to extreme temperatures, and
trauma
H proper foot care, especially the importance of wear-
ing well-fitting shoes and cotton or wool socks.
Discharge planning
H Refer the patient to a self-help group to help him
stop smoking.
H Refer the patient for psychological counseling, if
needed.
H If the patient has undergone amputation, refer him
to physical therapists, occupational therapists, and
social service agencies, as needed.

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Bulimia nervosa H Distinguished for participation in competitive activi-

ties
Complications
Overview H Dental caries
H Erosion of tooth enamel
Description H Parotitis
H Behavioral disorder characterized by eating binges H Gum infections
followed by feelings of guilt, humiliation, and H Electrolyte imbalances
self-deprecation H Dehydration
H Self-induced vomiting, the use of laxatives or diuret- H Arrhythmias
ics, or strict dieting or fasting to overcome the effects H Cardiac failure
of the binges H Sudden death
H Seldom incapacitating H Esophageal tears
H Gastric ruptures
Pathophysiology H Mucosal damage to intestine
H Decreased caloric intake depletes body fat and pro- H Suicide
tein stores.
H Estrogen deficiency occurs in women due to lack of
lipid substrate for synthesis, causing amenorrhea. Assessment
H Testosterone levels fluctuate in men, causing de-
creased erectile function and sperm count. History
H Ketoacidosis occurs from increased use of fat as en- H Episodic binge eating
ergy fuel. H Continues eating until abdominal pain, sleep, or the
presence of another person interrupts it
Causes H Preferred food usually sweet, soft, and high in calo-
H Exact cause unknown ries and carbohydrate content
H Exaggerated sense of guilt
Risk factors H Depression
H Family disturbance or conflict H Childhood trauma
H Sexual abuse H Parental obesity
H Maladaptive learned behavior H Unsatisfactory sexual relationships
H Struggle for control or self-identity
H Cultural overemphasis on physical appearance Physical findings
H Parental obesity H Thin or slightly overweight
H Female gender H Use of diuretics, laxatives, vomiting, and exercise
H Adolescent or young adult H Abdominal and epigastric pain
H Amenorrhea
Incidence H Painless swelling of the salivary glands
H Affects nine females for every one male H Unusual swelling of cheeks or jaw area
H Between 1% and 3% of adolescent and young fe- H Hoarseness
males meeting the diagnostic criteria; 5% to 15% H Throat irritation or lacerations
having some symptoms of the disorder H Calluses of the knuckles or abrasions and scars on
the dorsum of the hand
Special populations DSM-IV-TR criteria
Bulimia has been found to begin in adolescence or Diagnosis of bulimia nervosa can be confirmed when
early adulthood. these criteria are met, on average, twice per week for
3 months:
H recurrent episodes of binge eating
Common characteristics H repeated inappropriate behaviors to prevent weight
H Strongly associated with depression gain.
H Can occur simultaneously with anorexia nervosa
H More prone to psychoactive substance abuse Test results
H Hyperactivity Laboratory
H Peculiar eating habits or rituals H Serum electrolyte studies show elevated bicarbonate,
H Frequent weighing decreased potassium, and decreased sodium levels.
H Perceived by others as a perfect student, mother, Other
or career woman H The Beck Depression Inventory may identify coexist-
ing depression.

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Treatment
General
H Inpatient or outpatient psychotherapy
H Self-help groups
H Drug rehabilitation
H Balanced diet
H Monitoring of eating pattern
H Monitoring of activity

Medications
H Antidepressant such as fluoxetine

Nursing considerations
Key outcomes
The patient will:
H acknowledge change in body image
H participate in decision-making about her case
H express positive feelings about self
H achieve expected state of wellness.

Nursing interventions
H Supervise mealtime and for a specified period after
meals, usually up to 1 hour.
H Set a time limit for each meal.
H Provide a pleasant, relaxed environment for eating.
H Use behavior modification techniques.
H Establish a food contract, specifying the amount and
type of food to be eaten at each meal.
H Encourage verbalization and provide support.

Monitoring
H Suicide potential
H Elimination patterns
H Eating patterns
H Complications
H Response to treatment
H Activity

Patient teaching
Be sure to cover:
H importance of keeping a food journal
H risks of laxative, emetic, and diuretic abuse
H assertiveness training
H medication administration, dosage, and possible
adverse effects.
Discharge planning
H Refer the patient to support services or specialized
inpatient care.
H Refer the patient for psychological counseling.

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Burns H Nausea and vomiting

Deep, partial-thickness burns
H Thin-walled, fluid-filled blisters
H Mild to moderate pain
Overview H White, waxy appearance of damaged area
Full-thickness burns
Description H Pale, white, brown, or black leathery tissue
H Heat or chemical injury to tissue H Visible thrombosed vessels
H May be permanently disfiguring and incapacitating H No blister formation
H May be partial thickness or full thickness H Painless
Electrical burns
Pathophysiology H Silver-colored, raised area at contact site
Superficial, partial-thickness burns H Smoke inhalation and pulmonary damage
H These burns cause localized injury to the epidermis H Singed nasal hair
that isnt life-threatening. Mucosal burns
Deep, partial-thickness burns H Sores in mouth or nose
H These burns cause destruction of the epidermis and H Voice changes
some dermis resulting in thin-walled and fluid-filled H Coughing, wheezing
blisters. H Darkened sputum
H Nerve endings are exposed to air as blisters break.
H Pain develops when blisters are exposed to air. Complications
H Barrier function of the skin is lost. H Respiratory complications
Full-thickness burns H Sepsis
H These burns affect every body system and organ and H Hypovolemic shock
extend into the subcutaneous tissue layer damaging H Anemia
muscle, bone, and interstitial tissues. H Malnutrition
H Interstitial fluids result in edema and an immediate H Multiple organ dysfunction syndrome
immunologic response occurs.
H These burns carry a threat of wound sepsis.
H Depending on the level of nerve damage, the patient Assessment
may have no pain.
History
Causes H Cause of the burn revealed
H Residential fires H Preexisting medical conditions
H Motor vehicle accidents
H Improper use or handling of matches Physical findings
H Improperly stored gasoline H Depth and size of the burn assessed
H Space heater or electrical malfunctions H Severity of the burn estimated
H Improper handling of firecrackers H Major more than 10% of the patients body sur-
H Scalding accidents face area (BSA); more than 20% of a childs BSA
H Child or elder abuse H Moderate 3% to 10% of a patients BSA; 10% to
H Contact, ingestion, inhalation, or injection of acids, 20% of a childs BSA
alkali, or vesicants H Minor less than 3% of a patients BSA; less than
H Contact with faulty electrical wiring 10% of a childs BSA
H Contact with high-voltage power lines H Respiratory distress and cyanosis
H Chewing electric cords H Edema
H Friction or abrasion H Alteration in pulse rate, strength, and regularity
H Sun exposure H Stridor, wheezing, crackles, and rhonchi
H S3 or S4
Incidence H Hypotension
H Affects more than 2 million people each year
H 70,000 hospitalizations Test results
H 20,000 specialized burn unit admissions Laboratory
H Arterial blood gas levels show hypoxia.
Common characteristics H Complete blood count shows decreased hemoglobin
Superficial, partial-thickness burns level and hematocrit, if blood loss has occurred.
H Localized pain H Electrolyte levels are abnormal due to fluid losses
H Erythema and shifts.
H Blanching H Blood urea nitrogen levels are increased with fluid
H Chills losses.
H Headache

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H Glucose level is decreased in children due to limited H Remove constricting items. F

glycogen storage. H Encourage coughing, deep breathing, and incentive
H Urinalysis shows myoglobinuria and hemoglobinuria. spirometer use. T
H Carboxyhemoglobin level is increased. H Perform appropriate wound care. f
Diagnostic procedures H Keep the head of the bed elevated at least 30 degrees. F
H Electrocardiography may show myocardial ischemia, H Provide adequate hydration. E
injury, or arrhythmias, especially in electrical burns. H Weigh the patient daily.
H Fiber-optic bronchoscopy may show airway edema. H Encourage verbalization and provide support.
H Perform range-of-motion exercises.

Treatment Monitoring B

H Wound healing
General H Vital signs

H Burn source cessation H Respiratory status, including pulse oximetry
H Airway secured H Signs of infection P
H Hypoxia prevention H Intake and output
H Giving I.V. fluids through a large-bore I.V. line H Hydration and nutritional status
Adult: maintain urine output of 30 to 50 ml/hour. H Pain control
Child less than 66 lb (30 kg): maintain urine out- H Cardiac status
S
put of 1 ml/kg/hour. E
H Nasogastric tube and urinary catheter insertion
H Wound care Patient teaching
H Nothing by mouth until severity of burn established,
then high-protein, high-calorie diet Be sure to cover: B
H Increased hydration with high-calorie, high-protein H the injury, diagnosis, and treatment
drinks, not free water H appropriate wound care
H Total parenteral nutrition if unable to take food by H medication administration, dosage, and possible
mouth adverse effects P

H Activity limitation based on extent and location of H developing a dietary plan
burn H signs and symptoms of complications.

H Physical therapy
Discharge planning
Medications H Refer the patient to rehabilitation, if appropriate.
H Booster of tetanus toxoid H Refer the patient to psychological counseling, if
H Analgesic such as morphine needed.
H Antibiotics, such as gentamicin, tobramycin, and H Refer the patient to resource and support services.
vancomycin
H Antianxiety agent such as lorazepam

Surgery
H Loose tissue and blister debridement
H Escharotomy
H Skin grafting

Nursing considerations
Key outcomes
The patient will:
H report increased comfort and decreased pain
H attain the highest degree of mobility
H maintain fluid balance within the acceptable range
H maintain a patent airway
H demonstrate effective coping techniques.

Nursing interventions
H Apply immediate, aggressive burn treatment.
H Use strict sterile technique.
H Remove clothing thats still smoldering; soak first
with normal saline solution if its stuck to patients
skin.

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C Campylobacteriosis
Overview
Description
H In humans and animals, intestinal infection caused
by the Campylobacter organism, a spiral-shaped
bacteria
H Signs and symptoms developing 2 to 5 days after ex-
posure to Campylobacter
H May spread to the bloodstream in persons with com-
promised immune systems, causing a life-threatening
infection
H More common in the summer months

Common characteristics
H Mild or severe diarrhea
H Abdominal cramps
H Malaise

Complications
H Bacteremia
H Severe dehydration and electrolyte disturbances
H Guillain-Barr syndrome
H Reiters syndrome

Assessment
Pathophysiology History
H The organism invades and destroys the epithelial H Exposure to contaminated food or water
cells of the jejunum, ileum, and colon. H Acute onset of diarrhea
H This produces an increase in motility and secretions H Recent close contact with a person who has diarrhea
that results in diarrhea.
Physical findings
Causes H Cramping abdominal pain
H Ingestion of contaminated food or water or unpas- H Nausea and vomiting
teurized milk H Fever
H Occasionally from infected pets or wild animals H Traces of blood in the stool
H Contact with an infected persons stool
Test results
Risk factors Laboratory
H Occupational exposure to cattle, sheep, and other H Stool culture identifies Campylobacter.
farm animals
H Laboratory worker
H Homosexual men Treatment
Incidence General
H Most common bacterial cause of diarrheal illness in H Contact precautions (see Contact precautions)
the United States H Correction of fluid and electrolyte imbalances
H Increased fluid intake
H Activity as tolerated
Contact precautions
Medications
In addition to standard precautions, follow these precau-
H Oral antibiotics, such as doxycycline, minocycline,
tions:
H Place the patient in a private room. If a private room and tetracycline
isnt available, consult with infection control personnel.
As an alternative, he may be placed in a room with a
patient who has an active infection with the same mi-
Nursing considerations
croorganism.
H Wear gloves whenever you enter the patients room. Al- Key outcomes
ways change them after contact with infected material. The patient will:
Remove them before leaving the room. Wash your H regain or maintain normal fluid and electrolyte bal-
hands immediately with an antimicrobial soap, or rub ance
them with a waterless antiseptic. Then avoid touching H have an elimination pattern that returns to normal.
contaminated surfaces.
H Wear a gown when entering the patients room if you Nursing interventions
think your clothing will have extensive contact with him
H Follow contact precautions for those with active diar-
or anything in his room or if he has diarrhea or is in-
continent. Remove the gown before leaving the room. rhea.
H Limit the patients movement from the room, and H Isolate a patient who cant practice good hygiene.
check with infection control personnel whenever he H Give prescribed drugs.
must leave it. H Replace lost fluids and electrolytes through diet or
I.V. fluids.

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Monitoring
H Intake and output
H Vital signs
H Signs of dehydration
H Electrolytes
H Amount and characteristics of stool
H Abdominal status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H proper hand-washing technique
H proper food-handling practices
H medications and possible adverse effects
H complications and when to notify the physician
H preventive measures.

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Candidiasis H Total parenteral nutrition

H Surgery
H Use of antibiotic agents

Overview
Description
H Mild, superficial fungal infection
H Can lead to severe disseminated infections and
fungemia in immunocompromised patient, transplant
recipient, burn patient, low-birth-weight neonate, or
patient on hyperalimentation
H Prognosis variable, depending on patients resistance
H Also known as candidosis and moniliasis
Pathophysiology
H Change in the patients resistance to infection, his im-
munocompromised state, and antibiotic use permit
the sudden proliferation of Candida albicans.
Causes
H In most cases, infection with C. albicans or C. tropi-
calis
Risk factors
H Maternal vaginitis present during vaginal delivery
H Preexisting diabetes mellitus, cancer, or immunosup-
pressant illness
H Immunosuppressant drug use
H Radiation
H Aging
H Irritation from dentures
H I.V. or urinary catheterization
H Drug abuse
Identifying thrush
Candidiasis of the oropharyngeal mucosa (thrush) causes
cream-colored or bluish white pseudomembranous patch-
es on the tongue, mouth, or pharynx (as shown). Fungal
invasion may extend to circumoral tissues.
Incidence
H Affects 14% of immunocompromised patients
H Affects males and females equally
H Can occur at any age
Common characteristics
H Causative fungi infecting the nails (paronychia), skin
(diaper rash), or mucous membranes, especially the
oropharynx (thrush), vagina (vaginitis), esophagus,
and GI tract (see Identifying thrush)
H Systemic infection predominating among drug
abusers and diabetic and immunosuppressed
patients
Complications
H Dissemination with organ failure of the kidneys,
brain, GI tract, eyes, lungs, and heart
Assessment
History
H Underlying illness
H Recent course of antibiotic or antineoplastic therapy
H Drug abuse
H Hyperalimentation
Physical findings
H Scaly, erythematous, papular rash, possibly covered
with exudate and erupting in breast folds, between
fingers, and at the axillae, groin, and umbilicus
H Red, swollen, darkened nailbeds; occasionally, puru-
lent discharge; possibly nail separation from the
nailbed
H Scales in the mouth and throat
H White or yellow vaginal discharge, with local excoria-
tion; white or gray raised patches on vaginal walls,
with local inflammation
H Cream-colored or bluish white lacelike patches of
exudate on the tongue, mouth, or pharynx revealing
bloody engorgement when scraped
H Hemoptysis, cough; coarse breath sounds in the
infected lung fields
H Flank pain, dysuria, hematuria, cloudy urine with
casts
H Headache, nuchal rigidity, seizures, focal neurologic
deficits
H Blurred vision, orbital or periorbital pain, eye exu-
date, floating scotomata, and lesions with a white,
cotton-ball appearance seen during ophthalmoscopy
H Chest pain and arrhythmias
H Septic shock

Test results
Laboratory
H Fungal serological panel shows the presence of the
candidal organism.

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Treatment
General
H Treatment of predisposing condition
H No dietary restrictions unless oral infection
H With oral infection, spicy food only as tolerated
H Activity as tolerated

Medications
H Antifungals, such as amphotericin B, anidulafungin,
clotrimazole, and nystatin
Surgery
H Abscess drainage; surgically or percutaneously

Nursing considerations
Key outcomes
The patient will:
H express increased comfort
H avoid or have minimal complications
H maintain skin integrity
H express understanding of disorder and treatment.

Nursing interventions
H Follow standard precautions.
H Give prescribed drugs.
H Provide a nonirritating mouthwash to loosen tena-
cious secretions and a soft toothbrush to avoid irrita-
tion.
H Observe high-risk patients daily for patchy areas, irri-
tation, sore throat, oral and gingival bleeding, and
other signs of superinfection.
H Assess the patient for underlying systemic causes.

Monitoring
H Vital signs
H Intake and output
H Blood urea nitrogen, serum creatinine, and urine
blood and protein levels
H Potassium levels

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H good oral hygiene practices
H (for a woman in her third trimester of pregnancy)
the need for examination for vaginitis to protect her
neonate from thrush infection at birth.

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Physical findings
Life-threatening disorder H Vary with volume of fluid and speed of fluid accumu-
lation
Cardiac tamponade H Diaphoresis
H Anxiety and restlessness
H Pallor or cyanosis
H Jugular vein distention
Overview H Edema
H Rapid, weak pulses
Description H Hepatomegaly
H Rapid increase in intrapericardial pressure caused H Decreased arterial blood pressure
by fluid accumulation in the pericardial sac H Increased central venous pressure
H Impaired diastolic filling of the heart H Pulsus paradoxus
H Narrow pulse pressure
Pathophysiology H Muffled heart sounds
H Progressive accumulation of fluid in the pericardial
sac causes compression of the heart chambers. Test results
H Compression of the heart chambers obstructs blood Imaging
flow into the ventricles and reduces the amount of H Chest X-rays show slightly widened mediastinum and
blood pumped out with each contraction. enlargement of the cardiac silhouette.
H With each contraction, more fluid accumulates, Diagnostic procedures
decreasing cardiac output. (See Understanding H Electrocardiography may show low voltage complex-
cardiac tamponade.) es in the precordial leads.
H Hemodynamic monitoring shows equalization of
Causes mean right atrial, right ventricular diastolic, pulmo-
H May be idiopathic nary artery wedge, and left ventricular diastolic pres-
H Effusion in cancer, bacterial infections, tuberculosis sures.
and, rarely, acute rheumatic fever H Echocardiography may show an echo-free space, in-
H Trauma dicating fluid accumulation in the pericardial sac.
H Hemorrhage from nontraumatic cause
H Viral, postirradiation, or idiopathic pericarditis
H Acute myocardial infarction Treatment
H Chronic renal failure
H Drug reaction General
H Connective tissue disorders H Pericardiocentesis, if necessary
H Cardiac catheterization H Diet, as tolerated
H Cardiac surgery H Bed rest with the head of the bed elevated at least 30
degrees
Incidence
H More common in males than in females Medications
H Occurs with 2% of penetrating chest traumas H Intravascular volume expansion
H Inotropic agents, such as digoxin, milrinon, and
Common characteristics inamrinone
H Systemic hypotension H Oxygen
H Muffled heart sounds
H Jugular vein distention Surgery
H Pericardial window
Complications H Subxiphoid pericardiotomy
H Cardiogenic shock H Complete pericardectomy
H Death H Thoracotomy

Assessment Nursing considerations

History Key outcomes
H Presence of one or more causes The patient will:
H Dyspnea H maintain hemodynamic stability
H Shortness of breath H maintain adequate cardiac output
H Chest pain H not develop arrhythmias
H express understanding of disorder and treatment.

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Understanding cardiac tamponade

The pericardial sac, which surrounds NORMAL HEART AND PERICARDIUM

and protects the heart, is composed of
several layers. The fibrous pericardium
Aorta
is the tough outermost membrane; the
inner membrane, called the serous Superior vena cava
membrane, consists of the visceral and
parietal layers. The visceral layer clings Parietal pericardium
to the heart and is also known as the
Visceral pericardium
epicardial layer of the heart. The pari-
etal layer lies between the visceral layer Fibrous pericardium
and the fibrous pericardium. The peri-
cardial space between the visceral Pericardial space
and parietal layers contains 10 to Attachment of fibrous
30 ml of pericardial fluid. This fluid pericardium to diaphragm
lubricates the layers and minimizes
friction when the heart contracts.

Diaphragm

In cardiac tamponade, blood or fluid CARDIAC TAMPONADE

fills the pericardial space, compressing
the heart chambers, increasing intracar- Aorta
diac pressure, and obstructing venous
return. As blood flow into the ventricles Superior vena cava
falls, so does cardiac output. Without
prompt treatment, low cardiac output Fibrous pericardium
can be fatal.
Parietal pericardium

Visceral pericardium

Pericardial space filled

with excess fluid

Compressed heart

Diaphragm

Nursing interventions H Pulse oximetry

H Give prescribed drugs. H Jugular vein distention
H Provide reassurance. H Chest tube drainage
H Assist with pericardiocentesis, if necessary.
H Infuse I.V. solutions, as ordered.
H Administer oxygen therapy, as needed. Patient teaching
H Maintain the chest drainage system, if used.
Be sure to cover:
Monitoring H the disorder, diagnosis, and treatment
H Vital signs H medications and possible adverse effects
H Intake and output H when to notify the physician
H Signs and symptoms of increasing tamponade H preoperative and postoperative care
H Cardiovascular status, including cardiac rhythm H emergency procedures.
H Hemodynamics
H Arterial blood gas levels
H Respiratory status
H Complications

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Cardiomyopathy, dilated H Dry cough at night

H Shortness of breath
H Fatigue
H Weight gain
Overview
Complications
Description H Intractable heart failure
H Disease of the heart muscle fibers H Arrhythmias
H Also called congestive cardiomyopathy H Emboli

Pathophysiology
H Extensively damaged myocardial muscle fibers re- Assessment
duce contractility of left ventricle.
H The hearts pumping ability is reduced. History
H As systolic function declines, cardiac output falls. H Possible history of a disorder that can cause cardio-
H The sympathetic nervous system is stimulated to in- myopathy
crease heart rate and contractility. H Gradual onset of shortness of breath, orthopnea,
H When compensatory mechanisms can no longer dyspnea on exertion, paroxysmal nocturnal dyspnea,
maintain cardiac output, the heart begins to fail. fatigue, dry cough at night, palpitations, and vague
(See Understanding dilated cardiomyopathy.) chest pain
Causes Physical findings
H Viral or bacterial infections H Peripheral edema
H Hypertension H Jugular vein distention
H Peripartum syndrome related to toxemia H Ascites
H Ischemic heart disease H Peripheral cyanosis
H Valvular disease H Tachycardia even at rest and pulsus alternans in late
H Drug hypersensitivity stages
H Chemotherapy H Hepatomegaly and splenomegaly
H Cardiotoxic effects of drugs or alcohol H Narrow pulse pressure
H Irregular rhythms, diffuse apical impulses, pansys-
Incidence tolic murmur
H Most commonly affects middle-aged males but can H S3 and S4 gallop rhythms
occur in any age-group and females H Pulmonary crackles

Common characteristics
ALERT
H Dyspnea on exertion
Dilated cardiomyopathy may need to be differenti-
Understanding dilated cardiomyopathy ated from other types of cardiomyopathy. (See As-
sessment findings in cardiomyopathies.)

H Greatly increased chamber size
H Thinning of left ventricular muscle
H Increased atrial chamber size
H Increased myocardial mass
H Normal ventricular inflow resistance
H Decreased contractility
Test results
Imaging
H Chest X-rays demonstrate moderate to marked car-
diomegaly and possible pulmonary edema.
H Echocardiography may reveal ventricular thrombi,
global hypokinesis, and the degrees of left ventricular
dilation and systolic dysfunction.
H Gallium scans may identify patients with dilated car-
diomyopathy and myocarditis.
Diagnostic procedures
H Cardiac catheterization evaluates heart structure and
function.
H Transvenous endomyocardial biopsy may be useful in
determining underlying disorder in some patients.
H Electrocardiography evaluates ischemic heart disease
and identifies arrhythmias and intraventricular con-
duction defects.

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Assessment findings in cardiomyopathies

Type Assessment findings

Dilated cardiomyopathy Generalized weakness, fatigue

Chest pain, palpitations
Syncope
Tachycardia
Narrow pulse pressure
Pulmonary congestion, pleural effusions
Jugular vein distention, peripheral edema
Paroxysmal nocturnal dyspnea, orthopnea, dyspnea on exertion

Hypertrophic cardiomyopathy Angina, palpitations

Syncope
Orthopnea, dyspnea on exertion
Pulmonary congestion
Loud systolic murmur
Life-threatening arrhythmias
Sudden cardiac arrest

Restrictive cardiomyopathy Generalized weakness, fatigue

Bradycardia
Dyspnea
Jugular vein distention, peripheral edema
Liver congestion, abdominal ascites

H develop no complications of excess fluid volume

Treatment
General
H No ingestion of alcohol if cardiomyopathy caused by
alcoholism
H Low-sodium diet supplemented by vitamin therapy
H Rest periods
Special populations
A woman of childbearing age with dilated cardio-
myopathy should avoid pregnancy.
Medications
H Cardiac glycoside such as digoxin
H Diuretic such as furosemide
H Angiotensin-converting enzyme inhibitors, such as
benazepril and captopril
H Oxygen
H Anticoagulant such as warfarin
H Vasodilator such as isosorbide
H Antiarrhythmic such as esmolol
H Beta-adrenergic blocker such as metoprolol
H recognize and accept limitations of chronic illness
H express feelings of increased energy and decreased
fatigue.
Nursing interventions
H Administer prescribed medications.
H Alternate periods of rest with required activities of
daily living.
H Consult with dietitian to provide a low-sodium diet.
H Administer oxygen, as needed.
H Check serum potassium levels for hypokalemia, es-
pecially if therapy includes a cardiac glycoside.
H Offer support and let the patient express his feelings.
H Allow patient and family to express fears and con-
cerns; help them identify effective coping strategies.
Monitoring
H Vital signs and hemodynamics
H Cardiac rhythm
H Intake and output
H Daily weights
H Cardiovascular status
H Respiratory status

Surgery Patient teaching

H Heart transplantation
H Possible cardiomyoplasty Be sure to cover:
H the disorder, diagnosis, and treatment
H medications and possible adverse effects
Nursing considerations H when to notify the physician
H sodium and fluid restrictions
Key outcomes H signs and symptoms of worsening heart failure.
The patient will:
H maintain adequate cardiac output and hemodynamic Discharge planning
stability H Refer family members to community cardiopul-
H maintain adequate ventilation monary resuscitation classes.

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Common characteristics
Cardiomyopathy, H Dyspnea

hypertrophic H Fatigue
H Signs of heart failure

Complications
Overview H Pulmonary hypertension
H Heart failure
Description H Ventricular arrhythmias
H Primary disease of cardiac muscle characterized by
left ventricular hypertrophy
H Also known as idiopathic hypertrophic subaortic Assessment
stenosis, hypertrophic obstructive cardiomyopa-
thy, and muscular aortic stenosis History
H Generally, no visible clinical features until disease
Pathophysiology well advanced
H The hypertrophied ventricle becomes stiff, noncom- H Atrial fibrillation
pliant, and unable to relax during ventricular filling. H Possible family history of hypertrophic cardiomyop-
H Ventricular filling time is reduced as compensation athy
to tachycardia. H Orthopnea
H Reduced ventricular filling leads to low cardiac out- H Dyspnea on exertion
put. (See Understanding hypertrophic cardiomy- H Anginal pain
opathy.) H Fatigue
H Syncope, even at rest
Causes
H Transmission by autosomal dominant trait (about Physical findings
one-half of all cases) H Rapidly rising carotid arterial pulse possible
H Associated with hypertension H Pulsus bisferiens
H Double or triple apical impulse, possibly displaced
Incidence laterally
H More common in males than females H Bibasilar crackles if heart failure present
H Affects 5 to 8 people per 100,000 in the United States H Harsh systolic murmur heard after S1 at the apex
H More common in blacks near the left sternal border
H Possible S4

Understanding hypertrophic
cardiomyopathy ALERT
Hypertrophic cardiomyopathy may need to be dif-
ferentiated from other types of cardiomyopathy.
(See Assessment findings in cardiomyopathies, page
151.)

H Normal right and decreased left chamber size
H Left ventricular hypertrophy
H Thickened interventricular septum (hypertrophic
obstructive cardiomyopathy)
H Atrial chamber size increased on left
H Increased myocardial mass
H Increased ventricular inflow resistance
H Increased or decreased contractility
Test results
Imaging
H Chest X-rays may show a mild to moderate increase
in heart size.
H Thallium scan usually reveals myocardial perfusion
defects.
H Angiography reveals a dilated, diffusely hypokinetic
left ventricle.
Diagnostic procedures
H Echocardiography shows left ventricular hypertrophy
and a thick, asymmetrical intraventricular septum in
obstructive hypertrophic cardiomyopathy, whereas
hypertrophy affects various ventricular areas in
nonobstructive hypertrophic cardiomyopathy.
H Cardiac catheterization reveals elevated left ventricu-
lar end-diastolic pressure and, possibly, mitral insuf-
ficiency.

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H Electrocardiography usually shows left ventricular ALERT

hypertrophy, ST-segment and T-wave abnormalities,
Q waves in leads II, III, aVF, and in V4 to V6 (because
of hypertrophy, not infarction), left anterior hemi-
block, left axis deviation, and ventricular and atrial
arrhythmias.
If beta-adrenergic blockers will be discontinued,
dont stop the drug abruptly; doing so may cause
rebound effects, resulting in myocardial infarction
or sudden death.

H Offer support and let the patient express his feelings.

Treatment H Allow the patient and his family to express their fears
and concerns and identify effective coping strategies.
General
H Cardioversion for atrial fibrillation Monitoring
H Low-fat, low-sodium diet H Vital signs
H Fluid restrictions H Cardiac rhythm
H Avoidance of alcohol H Hemodynamics
H Activity limitations individualized H Intake and output
H Bed rest, if necessary H Cardiovascular status
H Respiratory status (amiodarone may cause lung
Medications toxicity)
H Beta-adrenergic blocker such as propranolol H Emotional status
H Calcium channel blocker such as diltiazam
H Antiarrhythmic such as amiodarone (if atrioventricu-
lar block isnt present) Patient teaching
H Antibiotic prophylaxis such as amoxicillin
Be sure to cover:
H that propranolol can cause depression and the need
ALERT
to notify the physician if symptoms occur
Angiotensin-converting enzyme inhibitors, ni- H instructions to take medication as ordered
trates, other beta-adrenergic blockers, and digoxin H the need to notify any physician caring for the patient
are contraindicated in hypertrophic cardiomyop- that he shouldnt be given nitroglycerin, digoxin, or
athy. diuretics because they can worsen the obstruction
H the need for antibiotic prophylaxis before dental
work or surgery to prevent infective endocarditis
Surgery H warnings against strenuous activity, which may pre-
H Ventricular myotomy alone or combined with mitral cipitate syncope or sudden death
valve replacement H the need to avoid Valsalvas maneuver or sudden
H Heart transplantation position changes.
Discharge planning
Nursing considerations H Refer family members to community cardiopulmo-
nary resuscitation classes.
Key outcomes
The patient will:
H maintain adequate cardiac output and hemodynamic
stability
H develop no complications of excess fluid volume
H carry out activities of daily living (ADLs) without ex-
cess fatigue or decreased energy
H express feelings of comfort and decreased pain
H develop adequate coping mechanisms.

Nursing interventions
H Alternate periods of rest with required ADLs and
treatments.
H Provide personal care, as needed, to prevent fatigue.
H Provide active or passive range-of-motion exercises.
H Obtain daily weight.
H Administer prescribed medications.

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Common characteristics
Cardiomyopathy, H Fatigue

restrictive H Dyspnea
H Orthopnea
H Chest pain
H Edema
Overview H Systolic murmurs

Description Complications
H Disease of the heart muscle fibers resulting in re- H Heart failure
strictive filling and reduced diastolic volume of one H Arrhythmias
or both ventricles H Systemic or pulmonary embolization
H Irreversible if severe H Sudden death

Pathophysiology
H Stiffness of the ventricle is caused by left ventricular Assessment
hypertrophy and endocardial fibrosis and thickening,
thus reducing the ventricles ability to relax and fill History
during diastole. H Fatigue
H Failure of the rigid myocardium to contract com- H Viral infection
pletely during systole causes decreased cardiac out- H Dyspnea
put. (See Understanding restrictive cardiomyop- H Chest pain
athy.)
Physical findings
Causes H Peripheral edema
H Idiopathic or associated with other disease (for ex- H Liver engorgement
ample, amyloidosis or endomyocardial fibrosis) H Peripheral cyanosis
H Heart transplant H Pallor
H Mediastinal radiation H S3 or S4 gallop rhythms (due to heart failure)
H Carcinoid heart disease H Systolic murmurs

Incidence
ALERT
H Rare; accounts for 5% of all cases of primary heart
disease Restricted cardiomyopathy may need to be differ-
H Occurs equally in males and females entiated from other types of cardiomyopathy. (See
Assessment findings in cardiomyopathies, page 151.)

Understanding restrictive
cardiomyopathy Test results
Laboratory
H Complete blood count reveals eosinophilia.
Imaging
H Chest X-ray may reveal cardiomegaly.
H Echocardiography may reveal left ventricular muscle
mass, normal or reduced left ventricular cavity size,
and decreased systolic function.
Diagnostic procedures
H Electrocardiography may reveal low-voltage hyper-
trophy, arterioventricular conduction defects, and ar-
rhythmias.
H Cardiac catheterization shows reduced systolic func-
tion and increased left ventricular end-diastolic pres-
sures.

H Decreased ventricular chamber size

H Left ventricular hypertrophy
Treatment
H Increased atrial chamber size
H Normal myocardial mass
General
H Increased ventricular inflow resistance H Treatment of underlying cause
H Decreased contractility H Low-sodium diet
H Initially, bed rest, then activity, as tolerated

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Medications
H Cardiac glycoside such as digoxin
H Diuretic such as furosemide
H Vasodilator such as isosorbide
H Angiotensin-converting enzyme inhibitor such as
captopril
H Anticoagulant such as warfarin
H Corticosteroid such as prednisone

Surgery
H Permanent pacemaker
H Heart transplantation

Nursing considerations
Key outcomes
The patient will:
H maintain adequate cardiac output and hemodynamic
stability
H express understanding of the disorder
H recognize and accept limitations of chronic illness
H seek support and establish coping mechanisms.

Nursing interventions
H Give prescribed drugs.
H Provide psychological support.
H Provide appropriate diversionary activities for the pa-
tient restricted to prolonged bed rest.
Monitoring
H Cardiac rhythm
H Vital signs
H Intake and output
H Hemodynamics
H Daily weight
H Cardiovascular status
H Respiratory status

Patient teaching
Be sure to cover:
H signs of digoxin toxicity
H importance of recording daily weight and reporting
weight gain of 2 lb (0.9 kg) or more
H dietary restrictions.

Discharge planning
H Refer for psychosocial counseling, as necessary, for
assistance in coping with restricted lifestyle.

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Pathophysiology
Carpal tunnel syndrome H Space-occupying lesion or direct pressure within the
carpal canal increases pressure on the median nerve,
resulting in compression.
Overview H Compression of the median nerve interrupts normal
function. (See The carpal tunnel.)
Description
H Compression of the median nerve in the wrist Causes
H Most common nerve entrapment syndrome H Exact cause unknown
H May pose a serious occupational health problem H Repetitive wrist motions involving excessive flexion
or extension
H Dislocation
H Acute sprain that may damage the median nerve
H Tumors
The carpal tunnel H Gout
H Amyloidosis
The carpal tunnel is clearly visible in this palmar view and
H Edema-producing conditions
cross section of a right hand. Note the median nerve, flex-
or tendons of fingers, and blood vessels passing through
the tunnel on their way from the forearm to the hand.
Risk factors
H Diabetes
H Pregnancy
H Alcoholism
H Hypothyroidism
H Renal failure

Flexor Incidence
tendons
Radial nerve H Most common in females ages 30 to 60
of fingers
Median nerve
H Occurs in people who move their wrists continually

CARPAL
Ulnar nerve Common characteristics
TUNNEL H Weakness, pain, burning, numbness, tingling in the
hand
H Thumb, forefinger, middle finger, and half of fourth
finger affected by paresthesia
H Inability to clench fist
H Atrophic nails
H Dry and shiny skin

Complications
H Tendon inflammation
H Compression
H Neural ischemia
H Permanent nerve damage with loss of movement and
sensation

Assessment
History
H Occupation or hobby requiring strenuous or repeti-
tive use of the hands
H Condition that causes swelling in carpal tunnel struc-
tures
H Weakness, pain, burning, numbness, or tingling that
occurs in one or both hands
H Paresthesia that worsens at night and in the morning
Flexor tendons Transverse
H Pain that spreads to the forearm and, in severe cases,
of fingers carpal ligament
as far as the shoulder
H Pain can be relieved by:
shaking hands vigorously
dangling the arms at sides

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Physical findings H the prescribed medication regimen

H Inability to make a fist H adverse reactions to drugs
H Fingernails may be atrophied, with surrounding dry, H avoidance of NSAIDs in pregnancy.
shiny skin
Discharge planning
Test results H Refer the patient for occupational counseling if a job
Imaging change is necessary.
H Electromyography shows a median nerve motor con-
duction delay of more than 5 milliseconds.
H Digital electrical stimulation shows median nerve
compression by measuring the length and intensity of
stimulation from the fingers to the median nerve in
the wrist.
Other
H Compression test result supports the diagnosis.

Treatment
General
H Conservative initially:
Splinting the wrist for 1 to 2 weeks
Possible occupational changes
Correction of any underlying disorder
H Activity, as tolerated

Medications
H Nonsteroidal anti-inflammatory drug (NSAID) such
as ibuprofen
H Corticosteroid such as prednisone
H Vitamin supplement such as vitamin B complex

Surgery
H Decompression of the nerve
H Neurolysis

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort and pain relief
H maintain muscle strength
H maintain joint mobility and range of motion
H perform activities of daily living.

Nursing interventions
H Promote self-care.
H Give prescribed analgesics.

Monitoring
H Response to analgesia
H After surgery, vital signs
H Color, sensation, and motion of the affected hand

Patient teaching
Be sure to cover:
H splint application
H hand exercises in warm water

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Cataract H Hyphema
H Pupillary block glaucoma
H Retinal detachment
H Infection
Overview
Description Assessment
H Opacity of the lens or lens capsule of the eye
H Common cause of gradual vision loss History
H Commonly affects both eyes H Painless, gradual vision loss
H Traumatic cataracts usually unilateral H Blinding glare from headlights with night driving
H Poor reading vision
Pathophysiology H Annoying glare
H The clouded lens blocks light shining through the H Poor vision in bright sunlight
cornea. H Better vision in dim light than in bright light (central
H Images cast onto the retina are blurred. opacity)
H A hazy image is interpreted by the brain.
Physical findings
Causes H Milky white pupil on inspection with a penlight
H Classified according to cause H Grayish white area behind the pupil (advanced
Senile cataracts cataract)
H Chemical changes in lens proteins in elderly patients H Red reflex lost (mature cataract)
Congenital cataracts
H Inborn errors of metabolism Test results
H Maternal rubella infection during the first trimester Diagnostic procedures
H Congenital anomaly H Indirect ophthalmoscopy reveals a dark area in the
H Genetic causes (usually autosomal dominant) normally homogeneous red reflex.
H Recessive cataracts may be sex-linked H Slit-lamp examination confirms lens opacity.
Traumatic cataracts H Visual acuity test establishes the degree of vision loss.
H Foreign bodies causing aqueous or vitreous humor
to enter lens capsule
Complicated cataracts Treatment
H Uveitis
H Glaucoma General
H Retinitis pigmentosa H Before surgery, eyeglasses and contact lenses that
H Retinal detachment may help to improve vision
H Diabetes H Sunglasses in bright light and lamps that provide re-
H Hypoparathyroidism flected lighting rather than direct lighting, decreasing
H Atopic dermatitis glare and aiding vision
H Ionizing radiation or infrared rays H Restricted activity according to vision loss
Toxic cataracts
H Drug or chemical toxicity: Medications
ergot For cataract removal
dinitrophenol H Nonsteroidal anti-inflammatory drugs, such as
naphthalene ketorolac and bromfenac
phenothiazines
Surgery
Incidence H Lens extraction and implantation of intraocular lens
H Most prevalent in people older than age 70 (see Comparing methods of cataract removal)
H Extracapsular cataract extraction
Common characteristics H Intracapsular cataract extraction
H Painless, gradual vision loss H Phacoemulsification
H Glare
H Milky white pupil
Nursing considerations
Complications
H Complete vision loss Key outcomes
Possible complications of surgery The patient will:
H Loss of vitreous H maintain current health status
H Wound dehiscence H sustain no harm or injury

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Comparing methods of cataract removal

Cataracts can be removed by intracapsular or extracapsular techniques.

Intracapsular cataract extraction Lens Cryoprobe

In this technique, the surgeon makes a partial incision at
the superior limbus arc. He then removes the lens using Cornea
specially designed forceps or a cryoprobe, which freezes
and adheres to the lens to facilitate its removal.

Extracapsular cataract extraction

In this technique, the surgeon may use irrigation and aspiration or phacoemulsification. In the former approach, the sur-
geon makes an incision at the limbus, opens the anterior lens capsule with a cystotome, and exerts pressure from below
to express the lens. He then irrigates and suctions the remaining lens cortex.
In phacoemulsification, he uses an ultrasonic probe to break the lens into minute particles, which are aspirated by the
probe.

IRRIGATION AND ASPIRATION PHACOEMULSIFICATION

Cortical and nuclear cataract Cystotome Nucleus and cortex fragmented

material aspirated through and aspirated by probe
needle
Lens
Lens Ultrasonic probe

H voice feelings and concerns

H regain visual function.
Patient teaching
Be sure to cover:
Nursing interventions H the need to avoid activities that increase intraocular
H Perform routine postoperative care. pressure, such as straining with coughing, bowel
H Assist with early ambulation. movements, or lifting
H Apply an eye shield or eye patch postoperatively, as H the need to abstain from sexual intercourse until the
ordered. patient receives physicians approval
H proper instillation of ophthalmic ointment or drops.
Monitoring
H Vital signs ALERT
H Visual acuity
H Complications of surgery If the patient has increased eye discharge, sharp
eye pain thats unrelieved by analgesics, or deterio-
ration in vision, instruct him to notify his physi-
cian immediately.

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Celiac disease H Pancreatic insufficiency

H Skin disorders (dermatitis herpetiformis)
H Unexplained infertility or miscarriage
H Vitamin K deficiency with risk of hemorrhage
Overview H Vitamin and mineral deficiencies

Description
H A multisystem intestinal intramucosal enzyme defect Assessment
H Characterized by poor food absorption and inability
to digest gluten, a protein found in wheat and wheat History
products, rye, barley and, possibly, oats H GI symptoms, including chronic diarrhea or consti-
H Also known as idiopathic steatorrhea, nontropical pation (or both) and recurrent attacks of steatorrhea
sprue, gluten enteropathy, celiac sprue (pale, foul-smelling, or fatty stool)
H Abdominal pain
Pathophysiology H Anorexia or increased appetite without weight gain
H A toxic reaction in response to the ingestion of gluten H Fatigue
causes damage to the small intestines mucosal sur- H Bone or joint pain (especially in lower back, rib
face. cage, and pelvis)
H Villi in the small intestine atrophy. H Muscle cramps
H Activity and amount of enzymes in the surface of the H Mood changes and irritability
epithelium decrease. H Tingling or numbness in the legs
H Interference with nutrient absorption results. H Seizures
H Amenorrhea
Causes H Itchy skin rash
H Exact mechanism unknown
H Environmental factors Physical findings
H Genetic predisposition (associated with a group of H Abdominal distention
genes on chromosome 6) H Muscle wasting
H May be autoimmune in nature H Compression fractures
H Strongly associated with two human leukocyte anti- H Unexplained short stature
gen haplotypes, DR3 and DQw2 H Peripheral neuropathy
H Can appear at any time in a persons life H Dry skin, eczema, psoriasis, dermatitis herpetiformis,
H Triggers include surgery, infection, severe emotional or acne rosacea
stress, and childbirth H Generalized fine, sparse, prematurely gray hair
H Brittle nails
Risk factors H Localized hyperpigmentation on the face, lips, and
H Family history mucosa
H Pale sores inside the mouth, called aphthous ulcers
Incidence H Tooth discoloration or loss of enamel
H Affects 1 in every 133 persons in United States
H Affects twice as many females as males Special populations
H Primarily affects whites and those of European ances-
try Infants, toddlers, and children are commonly
H Commonly associated with type 1 diabetes mellitus, found to have delayed growth, failure to thrive,
lactose intolerance, thyroid disease, Down syndrome, rickets, vomiting, a bloated abdomen, and behav-
liver disease, and autoimmune disorders, such as ioral changes.
rheumatoid arthritis and systemic lupus erythemato-
sus
Test results
Common characteristics Laboratory
H Varying significantly from person to person H Alkaline phosphatase level is elevated possibly due to
H Some people asymptomatic bone loss.
H Cholesterol, albumen, and serum carotene levels are
Complications decreased and may reflect malabsorption and malnu-
Prognosis usually good with treatment compliance trition.
Without treatment: H Unexplained decrease in hemoglobin level and
H Anemia hematocrit is noted; white blood cell and platelet
H Central and peripheral nervous system disorders counts are reduced.
H Intestinal lymphomas H Liver enzyme levels are mildly elevated.
H Neurologic changes H Prothrombin time is decreased.
H Osteoporosis or osteopenia

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H Antibody blood testscombined are sensitive and

specific indicator. Patient teaching
H Total serum immunoglobulin A (IgA), IgA anti-
endomysium antibodies (AEA), anti-tissue transgluta- Be sure to cover:
minase (tTGA), and antigliadin (IgA and IgG) levels H the disorder and its treatment
are elevated. H the reasons for not beginning a gluten-free diet be-
Diagnostic procedures fore a diagnosis is made
H Small-bowel biopsy specimens obtained by esopha- H foods that are allowed on a gluten-free diet
gogastroduodenoscopy show histologic changes that H food product labels and how to identify ingredients
confirm the diagnosis. that may contain hidden gluten
H that gluten may be used as a binder in some medica-
tions and vitamins as well as stamp and envelope ad-
Treatment hesives
H importance of contacting a dietitian
General H testing of family members.
H Life-long gluten-free dietfull return to normal in
months or may never occur
H Eliminate all wheat, barley, rye, and oat products as
well as foods made from these grains, such as breads
and baked goods
Medications
H Corticosteroids for short-term use
H Supportive treatment with vitamin B12, iron, folic
acid, and vitamin K

Nursing considerations
Key outcomes
The patient will:
H express understanding of the disease and treatment
regimen
H consume an adequate number of calories daily
H express feelings of comfort and decreased pain
H develop a normal bowel elimination pattern
H demonstrate adaptive coping behaviors.

Nursing interventions
H Assess the patients acceptance and understanding of
the disease and treatment regimen.
H Observe the patients nutritional status and progress
by daily calorie counts and weight checks.
H Assess the patients pain and administer pain medica-
tion as ordered.
H Provide fluid replacement as ordered, and observe
for signs and symptoms of dehydration and elec-
trolyte imbalance.
H Encourage the patient to use support systems to as-
sist with coping.
Monitoring
H Signs and symptoms of complications
H Compliance with dietary restrictions
H Nutritional status
H Frequency and characteristics of stools

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Complications
Cellulitis H Sepsis
H Deep vein thrombosis (DVT)
H Progression of cellulitis
Overview H Local abscesses
H Thrombophlebitis
Description H Lymphangitis
H Acute infection of the dermis and subcutaneous tis- H Amputation
sue causing inflammation of the cells
H May follow damage to the skin, such as a bite or
wound Assessment
H Prognosis usually good with timely treatment
H With other comorbidities, such as diabetes, in- History
creased risk of developing or spreading cellulitis H Presence of one or more risk factors
H Tenderness
Pathophysiology H Pain at the site and possibly surrounding area
H A break in skin integrity almost always precedes in- H Erythema and warmth
fection. H Edema
H As the offending organism invades the compromised H Possible fever, chills, malaise
area, it overwhelms the defensive cells, including the
neutrophils, eosinophils, basophils, and mast cells, Physical findings
that normally contain and localize the inflammation. H Erythema with indistinct margins
H As cellulitis progresses, the organism invades tissue H Fever
around the initial wound site. H Warmth and tenderness of the skin
H Regional lymph node enlargement and tenderness
Causes H Red streaking visible in skin proximal to area of cel-
H Bacterial infections, usually by Staphylococcus au- lulitis
reus and group A beta-hemolytic streptococci
H Fungal infections Test results
H Extension of a skin wound or ulcer Laboratory
H Furuncles or carbuncles H White blood cell count shows mild leukocytosis.
H Erythrocyte sedimentation rate shows mild elevation.
Risk factors H Culture and Gram stain may show the causative
H Venous and lymphatic compromise organism.
H Edema
H Diabetes mellitus
H Underlying skin lesion Treatment
H Prior trauma
General
H Immobilization and elevation of the affected
Special populations
extremity
Cellulitis of the lower extremity is more likely to H Moist heat
develop into thrombophlebitis in an elderly patient. H Well-balanced diet
H Bed rest, with the head of bed elevated at least
30 degrees, possibly necessary in severe infection
Incidence
H Occurs most commonly in the lower extremities Medications
H Affects males and females equally H Antibiotics, such as cefuroxime and cephalexin
H Topical antifungal such as mupirocin
H Analgesics, such as ibuprofen and acetaminophen
Special populations
Perianal cellulitis occurs more commonly in chil- Surgery
dren, especially boys. H Tracheostomy possibly needed for severe cellulitis of
head and neck
H Possible abscess drainage
Common characteristics H Amputation (with gas-forming cellulitis [gangrene])
H Tenderness
H Pain
H Erythema
H Warmth
H Edema

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Nursing considerations
Key outcomes
The patient will:
H avoid injury
H express feelings of increased comfort
H remain free from signs and symptoms of infection
H verbalize feelings and concerns.

Nursing interventions
H Give prescribed drugs.
H Elevate affected extremity.
H Apply moist heat, as ordered.
H Encourage a well-balanced diet.
H Encourage adequate fluid intake.
H Encourage verbalization of feelings and concerns.
H Institute safety precautions.
H Institute contact precautions if a draining wound is
present.
Monitoring
H Vital signs
H Pain control
H Edema
H Laboratory results
H Signs and symptoms of infection
H Complications
H Cellulitis progression

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medications and possible adverse effects
H when to notify the physician
H use of warm compresses
H signs and symptoms of infection
H prevention of injury and trauma
H infection control
H signs and symptoms of DVT.

Discharge planning
H Refer the patient for management of diabetes melli-
tus, as indicated.

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Test results
Cerebral contusion Imaging
H Computed tomography scan shows contusion.

Overview
Treatment
Description
H Ecchymosis of brain tissue resulting from injury to General
the head H Establishment of a patent airway
H Administration of oxygen as needed
Pathophysiology H Administration of I.V. fluids
H Trauma to the head causes tearing or twisting of the H Minimization of environmental stimuli
structures and blood vessels of the brain. H Activity based on neurologic status
H Scattered hemorrhages form over the surface. H Initially, bed rest with the head of bed elevated at
H Functional disruption occurs and may be prolonged. least 30 degrees
H Avoidance of contact sports
Causes
H Acceleration-deceleration or coup-contrecoup Medications
injuries H Analgesics, such as codeine and acetaminophen
H Head trauma
Surgery
Risk factors H Craniotomy
H Unsteady gait
H Participation in contact sports
H Receiving anticoagulant therapy Nursing considerations
Incidence Key outcomes
H Occurs at any age The patient will:
H use support systems to assist with coping
Common characteristics H maintain a stable neurologic state
H Change in level of consciousness H express feelings of comfort and pain relief
H Hypertension H maintain adequate fluid volume.
H Dizziness
H Headache Nursing interventions
H Nausea and vomiting H Perform neurologic examinations.
H Pupil changes H Maintain a patent airway.
H Hemiparesis H Give prescribed drugs (no aspirin).
H Memory loss or forgetfulness H Protect from injury.
H Seizure H Institute seizure precautions.

Complications Monitoring
H Intracranial hemorrhage H Vital signs
H Hematoma H Neurologic and respiratory status
H Tentorial herniation H Check for cerebrospinal fluid (CSF) leakage
H Increased intracranial pressure (see What happens H Pain control
with increased ICP)
Patient teaching
Assessment
Be sure to cover:
History H the need to avoid coughing, sneezing, or blowing the
H Head injury or motor vehicle accident nose until after recovery
H Loss of consciousness H observation for CSF drainage
H how to detect and report mental status changes
Physical findings H signs and symptoms of infection.
H Unconscious patient: pale and motionless; altered
vital signs Discharge planning
H Conscious patient: drowsy or easily disturbed H Refer the patient to a neurologist for follow-up, as
H Scalp wound indicated.
H Possible involuntary evacuation of bowel and bladder H Refer the patient for rehabilitation, as needed.
H Hemiparesis

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What happens with increased ICP

Intracranial pressure (ICP) is the pressure exerted within the intact skull by the intracranial volume, which is comprised of
about 10% blood, 10% cerebrospinal fluid (CSF), and 80% brain tissue. The rigid skull allows very little space for expansion
of these substances. When ICP increases to pathologic levels, brain damage can result.
The brain compensates for increases in ICP by regulating the volumes of the three substances in the following ways:
H limiting blood flow to the head
H displacing CSF into the spinal canal
H increasing absorption or decreasing production of CSF withdrawing water from brain tissue into the blood and excret-
ing it through the kidneys.
When compensatory mechanisms become overworked, small changes in volume lead to large changes in pressure.

Brain insult
Trauma (contusion, laceration, intracranial hemorrhage)
Cerebral edema (following surgery, stroke, infection, hypoxia)
Hydrocephalus
Space-occupying lesion (tumor, abscess)

Slight increase in ICP

Attempt at normal regulation of ICP by decreased blood flow to head

Slight decrease in cerebral perfusion pressure (CPP)

Loss of autoregulatory mechanism of constriction or dilation

of cerebral blood vessels if increased ICP persists

Passive dilation

Increased cerebral blood flow; venous congestion

Further increase in ICP

Cellular hypoxia

Uncal or central herniation Further decrease in CPP

BRAIN DEATH

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Cerebral palsy H Poisoning

H Any condition resulting in cerebral thrombus or em-
bolus
Overview Incidence
H Highest in premature neonates and in those who are
Description small for gestational age
H Most common crippling neuromuscular disease in H Slightly more common in boys than in girls
children H More common in whites
H Comprises several neuromuscular disorders
H Results from prenatal, perinatal, or postnatal central Common characteristics
nervous system (CNS) damage H Excessive lethargy or irritability
H Three types (sometimes occur in mixed forms): H High-pitched cry
spastic (affecting about 70% of children with cere- H Poor head control
bral palsy) H Weak sucking reflex
athetoid (affecting about 20%) H Delayed motor development
ataxic (affecting about 10%) H Abnormal head circumference
H Motor impairment may be minimal or severely dis- H Abnormal postures
abling H Abnormal reflexes
H Associated defects: H Abnormal muscle tone and performance
seizures
speech disorders Complications
mental retardation H Seizure disorders
H Prognosis varies H Speech, vision, and hearing problems
H Language and perceptual deficits
Pathophysiology H Mental retardation (in up to 40% of patients)
H A lesion or an abnormality occurs in the early stages H Dental problems
of brain development. H Respiratory difficulties
H Structural and functional defects occur, impairing H Poor swallowing and gag reflexes
motor or cognitive function.
H Defects may not be distinguishable until months after
birth. Assessment
Causes History
H Conditions that result in cerebral anoxia, hemor- H Maternal or patient history revealing possible cause
rhage, or other CNS damage (see When to suspect cerebral palsy)
Prenatal causes
H Rh factor incompatibility Physical findings
H ABO blood type incompatibility H Child with retarded growth and development
H Maternal infection (especially rubella in the first H Difficulty chewing and swallowing
trimester) Spastic cerebral palsy
H Maternal diabetes H Underdevelopment of affected limbs
H Irradiation H Characteristic scissors gait
H Anoxia H Walks on toes
H Toxemia H Crosses one foot in front of the other
H Malnutrition H Hyperactive deep tendon reflexes
H Abnormal placental attachment H Increased stretch reflexes
H Isoimmunization H Rapid alternating muscle contraction and relaxation
Parturition causes H Muscle weakness
H Trauma during delivery H Impaired fine and gross motor skills
H Depressed maternal vital signs from general or spinal H Contractures in response to manipulation of muscles
anesthesia Athetoid cerebral palsy
H Asphyxia from the cord wrapping around the neck H Involuntary movements
H Prematurity H Grimacing
H Prolonged or unusually rapid labor H Wormlike writhing
H Multiple births (neonates born last in a multiple H Dystonia
birth have an especially high rate of cerebral palsy) H Sharp jerks that impair voluntary movement
Postnatal causes H Involuntary facial movements (speech difficult)
H Infections, such as meningitis and encephalitis H Drooling
H Head trauma

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Ataxic cerebral palsy When to suspect cerebral palsy

H Lack of leg movement during infancy
H Wide gait when child begins to walk
H Disturbed balance
H Incoordination (especially of the arms)
H Hypoactive reflexes
H Nystagmus
H Muscle weakness
H Tremors
Test results
Imaging
H Computed tomography scan and magnetic resonance
imaging of the brain may show structural abnormali-
ties of the brain such as cerebral atrophy.
H EEG may show the source of seizure activity.
Early detection of cerebral palsy is essential for effective
treatment and requires careful clinical observation during
infancy and precise neurologic assessment. Suspect cere-
bral palsy whenever a neonate:
H has difficulty sucking or keeping the nipple or food in
his mouth
H seldom moves voluntarily or has arm or leg tremors
with voluntary movement
H crosses his legs when lifted from behind rather than
pulling them up or bicycling like a normal neonate
H has legs that are hard to separate, making diaper
changing difficult
H persistently uses only one hand or, as he gets older,
uses his hands well but not his legs.

H Provide a safe physical environment.

Treatment H Keep the head of the bed elevated at least 30 degrees.

General Monitoring
H Braces or splints H Pain control
H Special appliances, such as adapted eating utensils H Seizure activity
and low toilet seat with arms H Speech
H Range-of-motion (ROM) exercises H Visual and auditory acuity
H Prescribed exercises to maintain muscle tone H Respiratory status
H Swallowing function
Medications H Neurologic status
H Anticonvulsant such as phenytoin H Nutritional status
H Muscle relaxant such as dantrolene H Skin integrity
H Antianxiety agent such as lorazepam H Motor development
H Muscle strength
Surgery
H Orthopedic surgery
H Neurosurgery Patient teaching
Be sure to cover:
Nursing considerations H the prescribed medication regimen
H adverse drug reactions
Key outcomes H daily skin inspection and massage
The patient will: H the need to place food far back in patients mouth to
H consume calorie requirements daily facilitate swallowing
H express positive feelings about self H the need to chew food thoroughly
H maintain joint mobility and ROM H drinking through a straw
H develop adequate coping mechanisms H sucking lollipops to develop muscle control
H develop effective communication skills. H proper nutrition
H opportunities for learning, such as summer camps or
Nursing interventions Special Olympics
H Speak slowly and distinctly. H correct use of assistive devices.
H Give all care in an unhurried manner.
H Allow participation in care decisions. Discharge planning
H Provide a diet with adequate calories. Stroking the H Refer family members to community support groups
throat may aid swallowing. such as the local chapter of the United Cerebral Palsy
H Provide frequent mouth and dental care. Association.
H Provide skin care.
H Perform prescribed exercises to maintain muscle
tone.
H Care for associated hearing and vision disturbances,
as necessary.
H Postoperatively, give analgesics, as ordered.

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Incidence
Cervical cancer H Typically occurs between ages 30 and 45; rarely,
before age 20
Overview Common characteristics
H Abnormal vaginal bleeding
Description
H Proliferation of cancer cells in the cervix Complications
H Third most common cancer of the female reproduc- H Renal failure
tive system H Distant metastasis
H Classified as either preinvasive (curable in 75% to H Vaginal stenosis
90% of patients with early detection and proper H Ureterovaginal or vesicovaginal fistula
treatment) or invasive H Proctitis
H Cystitis
Pathophysiology H Bowel obstruction
Preinvasive cancer
H Preinvasive cancer ranges from minimal cervical dys-
plasia, in which the lower third of the epithelium Assessment
contains abnormal cells, to carcinoma in situ, in
which the full thickness of the epithelium contains History
abnormally proliferating cells. H One or more risk factors present
Invasive cancer Preinvasive cancer
H Cancer cells penetrate the basement membrane and H No symptoms or other clinical changes
can spread directly to contiguous pelvic structures or Invasive cancer
disseminate to distant sites by way of lymphatic H Abnormal vaginal bleeding or discharge
routes. H Gradually increasing flank pain
H Most (95%) cases are squamous cell carcinoma; 5%
of cases are adenocarcinomas. Physical findings
H Vaginal discharge
Causes H Postcoital bleeding
H Unknown H Irregular bleeding

Risk factors Test results

H Frequent intercourse at a young age (younger than
age 16)
H Multiple sexual partners
H Multiple pregnancies
H Human papillomavirus (HPV) infection
H Bacterial or viral venereal infections
H Exposure to diethylstilbestrol in utero
H Human immunodeficiency virus
H Smoking (see Preventing cervical cancer)
Imaging
H Lymphangiography can show metastasis.
H Cystography can show metastasis.
H Organ and bone scans can show metastasis.
Diagnostic procedures
H Papanicolaou (Pap) test shows abnormal cells, and
colposcopy shows the source of the abnormal cells
seen on the Pap test. (See Testing for cervical can-
cer.)
H Cone or punch biopsy is performed if endocervical
curettage is positive.
H Vira Pap test permits examination of the specimens
deoxyribonucleic acid structure to detect HPV.

Prevention
Preventing cervical cancer
Treatment
Cervical cancer can be prevented by following these General
guidelines: H Accurate clinical staging used to determine type of
H Delay sexual intercourse.
treatment
H Limit the number of sexual partners.
H Well-balanced diet, as tolerated
H Avoid sexual activity with people who have had many
other sexual partners. Medications
H Use barrier protection.
H Dont smoke. H Chemotherapy, such as bleomycin, cisplatin, ifos-
H Receive the human papilloma virus vaccine. famide, and topotecan

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Testing for cervical cancer

To analyze cervical cells, the ThinPrep may be collected in
the same manner as a Papanicolaou (Pap) test using a cyto-
brush and plastic spatula. The specimens are deposited in
a bottle provided with a fixative and sent to the laboratory.
A filter is then inserted into the bottle and excess mucus,
blood, and inflammatory cells are filtered out by centrifuge.
Remaining cells are then placed on a slide in a uniform, thin
layer and read as a Pap test. This causes fewer slides to be
classified as unreadable, significantly reducing the incidence
of false negatives and the need for repeat tests.
When the ThinPrep test is used, screening can also be
easily done for the human papillomavirus (HPV), of which
certain strains have been identified as the primary cause of
cervical cancer. The Digene hc2 HPV deoxyribonucleic acid
(DNA) test has been approved by the Food and Drug Admin-
istration to determine if those identified as high risk for de-
veloping cervical cancer have been exposed to HPV. The
specimen is collected as a Pap smear but is dispersed with
ThinPrep solution. Separate aliquots are used for each test,
from brushings of the endocervix. The brush is then inserted
into the specialized tube and snapped off at the shaft, cap-
ping securely. The target solution in the tube disrupts the
virus and releases target DNA, which combines with specific
ribonucleic acid (RNA) probes creating RNA:DNA hybrids.
The hybrids are captured, bound, and able to be magnified
and measured using a luminometer.
If a patient is positive for HPV, it means she had been in-
fected with the virus. Depending on the type of HPV found
through DNA testing, those harboring high-risk HPV strains
have a high risk of developing cervical cancer. These pa-
tients should have a colposcopy in which the cervix is
viewed under microscope and a biopsy taken from the tissue
sample.

Surgery Patient teaching

Preinvasive lesions
H Total excisional biopsy Be sure to cover:
H Cryosurgery H the disease process, diagnosis, and treatment
H Laser destruction H importance of follow-up care
H Conization, followed by frequent Pap test follow-ups H how treatment wont radically alter the patients
H Hysterectomy (rare) lifestyle or prohibit sexual intimacy
Invasive squamous cell carcinoma H medication administration, dosage, and possible
H Radical hysterectomy and radiation therapy (internal, adverse effects.
external, or both)
H Pelvic exenteration (rare; may be performed for re- Discharge planning
current cervical cancer) H Refer the patient to resource and support services.

Nursing considerations
Key outcomes
The patient will:
H express increased comfort and decreased pain
H express feelings and perceptions about changes in
sexual activity
H maintain joint mobility and range of motion
H experience no signs or symptoms of infection
H use support systems and develop coping strategies.

Nursing interventions
H Encourage verbalization and provide support.
H Give prescribed drugs.

Monitoring
H Vital signs
H Complications
H Pain control
H Vaginal discharge
H Renal status
H Response to treatment

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Chalazion H Infection
H Vision disturbance

Overview Assessment
Description History
H Painless, slowly growing nodule on the eyelid H Nodule on eyelid
H Common disorder of the sebaceous gland in the H Rosacea or blepharitis
eyelid
H May become large enough to press on the eyeball, Physical findings
producing astigmatism H Palpable small lump in the eyelid
H May be chronic H Red, elevated area on the conjunctival surface (see
Recognizing chalazion)
Pathophysiology
H Granulomatous inflammation in the upper or lower Test results
eyelid is the result of an obstruction of the meibomi- Other
an (sebaceous) gland duct. H Visual examination and palpation of the eyelid
H Edema is usually contained on the conjunctival por- reveals chalazion.
tion of the eyelid. H Biopsy rules out meibomian cancer.

Causes
H Rosacea Treatment
H Chronic blepharitis
H Seborrhea General
H Meibomian cancer H Warm compresses to the affected eyelid

Incidence
H Higher incidence in fair-skinned males than in other
groups, possibly because of that groups higher inci-
dence of rosacea and blepharitis
H More common in adults ages 30 to 50
Common characteristics
H Painless, hard lump that usually points toward the
conjunctival side of the eyelid
Complications
H Cosmetic deformity
H Bleeding after surgery
Recognizing chalazion
A chalazion is a nontender granulomatous inflammation of
a meibomian gland on the upper or lower eyelid.
Medications
H Antibiotic such as sulfacetamide
H Corticosteroid such as dexamethasone
Surgery
H Incision and curettage of the chalazion under local
anesthetic (possibly)
Nursing considerations
Key outcomes
The patient will:
H report improvement of condition of eyelid
H maintain positive outlook regarding body image
H remain free from signs of bleeding or infection.
Nursing interventions
H Apply warm compress after surgery.
H Apply eye patch to the affected eye for 24 hours. (See
Applying an eye patch.)
H Instill eyedrops, as ordered.

Monitoring
H Bleeding (after surgery)

Patient teaching
Be sure to cover:
H proper instillation of eyedrops
H signs and symptoms of infection
H reporting recurrence.

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Applying an eye patch

You may apply an eye patch for various reasons: to protect the eye after injury or surgery, to prevent accidental damage to
an anesthetized eye, to promote healing, to absorb secretions, to protect the eye from drying when the patient is comatose
or unable to close the eye as in Bells palsy, or to prevent the patient from touching or rubbing his eye.
A thicker patch, called a pressure patch, may be used to help corneal abrasions heal, compress postoperative edema, or
control hemorrhage from traumatic injury. Application requires an ophthalmologists prescription and supervision.

To apply a patch, choose a gauze pad of appropriate size

for the patients face, place it gently over the closed eye (as
shown), and secure it with two or three strips of tape. Ex-
tend the tape from midforehead across the eye to below
the earlobe.

A pressure patch, which is markedly thicker than a single-

thickness gauze patch, exerts extra tension against the
closed eye. After placing the initial gauze pad, build it up
with additional gauze pieces. Tape it firmly so that the
patch exerts even pressure against the closed eye (as
shown).

For increased protection of an injured eye, place a plastic

or metal shield (as shown) on top of the gauze pads and
apply tape over the shield.
Occasionally, you may use a head dressing to secure a
pressure patch. The dressing applies additional pressure
or, in burn patients, holds the patch in place without tape.

ALERT
Tell the patient to start applying warm compresses
at the first sign of lid irritation to increase the
blood supply and keep the lumen open.

Discharge planning
H Encourage follow-up care, as ordered.

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Chancroid H More common in males than in females

H Occurs at any age but is most common among young,
sexually active people
Overview Common characteristics
H Multiple papules that ulcerate
Description H Lesions possibly healing spontaneously and usually
H Sexually transmitted disease responding well to treatment when no secondary
H Characterized by painful genital ulcers and inguinal infections present
adenitis
H Common cause of genital ulcers in patients in devel- Complications
oping countries H Phimosis and urethral fistulas in males
H Secondary infection
Pathophysiology H Abscess formation
H Organisms are carried from the site of entry through H Inguinal adenitis and formation of buboes
the lymphatics to regional lymph nodes, resulting in
node swelling.
H The initial lesion is a papule that ulcerates within Assessment
24 hours. (See Chancroidal lesion.)
H Untreated infections disseminate to other organs, History
causing systemic inflammation and specific organ H May report unprotected sexual contact with an infect-
dysfunction. ed person or with unknown or multiple partners
H Pain from ulcers and lymphadenopathy
Causes H Headaches and malaise
H Haemophilus ducreyi, a short, nonmotile, gram-
negative bacillus Physical findings
H Genital area initially with single or multiple papules
Risk factors surrounded by redness that rapidly become pustular
H Poor personal hygiene and then ulcerate
H Unprotected sex H Ulcers nonindurated with ragged edges, a base of
H Multiple sex partners granulation tissue, and bleed easily; range from 1 to
H Uncircumcised males 2 mm in diameter
H Lesions on the tongue, lip, or breast
Incidence H Suppuration with bubo formation in the untreated
H Increasing in the United States patient; rupture of abscess may follow
H Tender, fluctuant inguinal nodes

Chancroidal lesion Test results

Chancroid produces a soft, painful chancre, similar to that
of syphilis. Without treatment, it may progress to inguinal
adenitis and formation of buboes (enlarged, inflamed
lymph nodes).
Laboratory
H Cultures from the lesion show H. ducreyi.
Treatment
General
H Aspiration of fluid-filled nodes
H Good personal hygiene
H Abstinence from sexual activity (until genital lesions
are healed)
H Evaluation of patient for syphilis, herpes simplex
virus, and human immunodeficiency virus (HIV)
Medications
H Antibiotics, such as azithromycin, doxycycline,
erythromycin, minocylcine, and tetracycline
Surgery
H Surgical drainage for large abscess

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Nursing considerations
Key outcomes
The patient will:
H communicate feelings about changes in body image
H regain skin integrity with decrease in size of chan-
croids
H state infection risk factors
H voice feelings about changes in sexual activity.

Nursing interventions
H Follow standard precautions.
H Give prescribed drugs.
H Wash the affected area with soap and water, followed
by a bactericidal agent.
H Dry the affected area thoroughly.
H Report all cases of chancroid to the local board of
health.
Monitoring
H Response to treatment
H Adverse effects of medications
H Compliance with treatment regimen
H Complications

Patient teaching
Be sure to cover:
H need to avoid applying creams, lotions, or oils on or
near genitalia or on other lesion sites
H abstaining from sexual contact until follow-up shows
that healing is complete
H proper washing techniques of the genitalia
H HIV infection and recommend testing
H following safer sex practices.

Discharge planning
H Refer the patient and affected sexual partners for
treatment.

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Chlamydial infections H Urethral and rectal strictures

H Perihepatitis
H Cervical cancer
H Trachoma
Overview H Urethritis and epididymitis (in males)
H Sterility
Description H Stillbirth, neonatal death, premature labor (with in-
H Infection that results in urethritis in males, cervicitis fected pregnant females)
in females, and lymphogranuloma venereum in both
sexes
H Trachoma inclusion conjunctivitis: seldom occurs in Assessment
United States, but is leading cause of blindness in de-
veloping countries History
H Most common sexually transmitted disease (STD) in H Unprotected sexual contact with an infected person
the United States H Previous STD

Pathophysiology Physical findings

H Chlamydial infections are transmitted by direct con- H Two-thirds of patients asymptomatic
tact (such as sexual). Female
H Infection produces local inflammation. H Pelvic or abdominal pain
H Endometritis and salpingitis occur as the organism H Dyspareunia
ascends the genitourinary tract. H Cervical erosion
H Mucopurulent discharge
Causes H Dysuria
H Transmission of Chlamydia trachomatis, by sexual H Urinary frequency
contact (oral, anal, or vaginal) Male
H Neonate infection caused by transport through the H Dysuria
infected mothers birth canal H Urinary frequency
H Pruritus
Risk factors H Urethral discharge (copious and purulent)
H Multiple sex partners or new sex partner H Meatal erythema
H Unprotected sex H Severe scrotal pain
H Coinfection with another STD Lymphogranuloma venereum
H Painless vesicle or nonindurated ulcer, 2 to 3 mm in
Incidence diameter, on the glans or shaft of the penis; on the
H About 4 million cases annually labia, vagina, or cervix; or in the rectum
H Affects primarily the Native American population of H Enlarged inguinal lymph nodes
the southwest United States H Regional nodes appearing as series of bilateral
H Occurs more commonly among minorities and lower buboes
socioeconomic groups and people living in urban H Untreated buboes possibly rupturing and forming
areas sinus tracts that discharge thick, yellow, granular
secretion
Special populations Test results
Chlamydial infections have a 10% incidence Laboratory
among sexually active adolescent girls. H Swab culture of the infection site shows C. tra-
chomatis. (See Chlamydia trachomatis.)
H Culture of aspirated blood, pus, or cerebrospinal
Common characteristics fluid establishes epididymitis, prostatitis, and
H Primarily occurring after vaginal or rectal inter- lymphogranuloma venereum.
course or oral-genital contact with an infected per- H Serologic studies reveal previous exposure.
son H Enzyme-linked immunosorbent assay shows C. tra-
H Late appearance of signs and symptoms during the chomatis antibody.
course of the disease
H No symptoms in 75% of females, 50% of males
H Sexual transmission of organism that occurs un- Treatment
knowingly
General
Complications H Symptomatic treatment (sex partners also treated)
H Infertility H Abstinence from sexual activity until infection re-
H Pelvic inflammatory disease solved

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Medications Chlamydia trachomatis

H Antibiotics, such as azithromycin, doxycycline,
In chlamydial infections, microscopic examination reveals
erythromycin, levofloxacin, and tetracycline Chlamydia trachomatis, a unicellular parasite with a rigid
cell wall.
Nursing considerations
Key outcomes
The patient will:
H voice feelings about changes in sexuality
H express concern about self-concept, self-esteem, and
body image
H exhibit improved or healed lesions or wounds
H express relief from pain.

Nursing interventions
H Follow standard precautions.
H Check the neonate of an infected mother for signs of
infection.
H Give prescribed drugs.
H Provide appropriate skin care.
H Report cases of chlamydial infection to the local
board of health.
Monitoring
H Response to treatment
H Adverse effects of medication
H Complications

Patient teaching
Be sure to cover:
H the disorder, signs and symptoms, and treatment
H proper hand-washing technique
H abstinence from intercourse or use of condoms
H importance of getting tested for the human immuno-
deficiency virus
H dealing with long-term risks and complications from
infection
H transmission of infection
H prevention of STDs by following safer sex practices
H follow-up care
H complications.

Discharge planning
H Refer the patient to support services.
H Advise rescreenings at 3 to 4 months and annual
screenings for sexually active teens and females ages
20 to 25.

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Cholelithiasis, immobility, chronic dieting, adhesions, prolonged

anesthesia, and opioid abuse)
cholecystitis, Risk factors
and related disorders H High-calorie, high-cholesterol diet
H Obesity
H Elevated estrogen levels due to hormonal contracep-
tive use, postmenopausal hormone-replacement
Overview therapy, or pregnancy
H Diabetes mellitus, ileal disease, hemolytic disorders,
Description hepatic disease (cirrhosis), or pancreatitis
Cholelithiasis H Rapid weight loss
H Leading biliary tract disease
H Formation of calculi (gallstones) in the gallbladder Incidence
Cholecystitis H Six times more common in females ages 20 to 50
H Related disorder that arises from formation of gall- H Males and females equal after age 50; increases with
stones each succeeding decade
H Acute or chronic inflammation of gallbladder
H Usually caused by a gallstone lodged in the cystic Common characteristics
duct H Epigastric or right upper quadrant abdominal pain
H Acute form most common during middle age H Nausea, vomiting
H Chronic form most common among elderly persons H Low-grade fever
Choledocholithiasis H Abdominal distention
H Related disorder arising from formation of gallstones
H Partial or complete biliary obstruction due to gall- Complications
stones lodged in the common bile duct Cholelithiasis
Cholangitis H Cholangitis
H Related disorder that arises from formation of gall- H Cholecystitis
stones H Choledocholithiasis
H Infected bile duct H Gallstone ileus
H Commonly linked to choledocholithiasis Cholecystitis
H Rapid response of nonsuppurative type to antibiotic H Gallbladder complications, such as empyema,
treatment hydrops or mucocele, and gangrene
H Poor prognosis of suppurative type unless surgery to H Chronic cholecystitis and cholangitis
correct obstruction and drain infected bile per- Choledocholithiasis
formed promptly H Cholangitis
Gallstone ileus H Obstructive jaundice
H Related disorder that arises from obstruction of the H Pancreatitis
small bowel by a gallstone H Secondary biliary cirrhosis
H Most common in elderly persons Cholangitis
H Septic shock
Pathophysiology H Death
H Calculi formation in the biliary system causes ob- Gallstone ileus
struction. H Bowel obstruction
H Obstruction of hepatic duct leads to intrahepatic re-
tention of bile; increased release of bilirubin into the
bloodstream occurs. Assessment
H Obstruction of cystic duct leads to inflammation of
the gallbladder; increased gallbladder contraction History
and peristalsis occurs. H Gallbladder disease possibly producing no symptoms
H Obstruction of bile causes impairment of digestion (even when X-rays reveal gallstones)
and absorption of lipids. Acute cholecystitis
H Sudden onset of severe steady or aching pain in the
Causes midepigastric region or the right upper abdominal
H Calculi formation; type of disorder that develops de- quadrant
pendent on where in the gallbladder or biliary tract H Pain radiating to the back, between the shoulder
the calculi collect blades or over the right shoulder blade, or just to the
H Acute cholecystitis also a result of conditions that al- shoulder area
ter gallbladders ability to fill or empty (trauma, re- H Attack occurring after eating a fatty meal or a large
duced blood supply to the gallbladder, prolonged meal after fasting for an extended time
H Attack occurring in the middle of the night

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H Nausea, vomiting, and chills H Bile salts

H Low-grade fever H Analgesics
H History of milder GI symptoms that preceded the H Antispasmodics
acute attack; indigestion, vague abdominal discom- H Anticholinergics
fort, belching, and flatulence after eating meals or H Antiemetics
snacks rich in fats H Antibiotics

Physical findings Surgery

H Severe pain H Cholecystectomy (laparoscopic or abdominal), cho-
H Pallor lecystectomy with operative cholangiography, chole-
H Diaphoresis dochostomy, or exploration of the common bile duct
H Low-grade fever (high in cholangitis)
H Exhaustion Other
H Jaundice (chronic) H Endoscopic retrograde cholangiopancreatography to
H Dark-colored urine and clay-colored stools visualize and remove calculi
H Tachycardia H Lithotripsy
H Tenderness over the gallbladder, which increases on
inspiration (Murphys sign)
H Palpable, painless, sausagelike mass (calculus-filled Nursing considerations
gallbladder without ductal obstruction)
H Hypoactive bowel sounds Key outcomes
The patient will:
Test results H express feelings of increased comfort
Laboratory H show no signs of infection
H Blood studies may reveal elevated levels of serum al- H have laboratory values that return to within normal
kaline phosphatase, lactate dehydrogenase, aspartate parameters
aminotransferase, icteric index, and total bilirubin; H avoid complications.
white blood cell count is slightly elevated during
cholecystitis attack. Nursing interventions
Imaging H Position the patient for comfort and reposition at
H Plain abdominal X-rays show gallstones if they con- least every 2 hours.
tain enough calcium to be radiopaque. X-rays are H Keep the head of the bed elevated at least 30 degrees.
also helpful in identifying porcelain gallbladder, limy H Give prescribed drugs.
bile, and gallstone ileus. H Encourage coughing, deep breathing, and incentive
H Ultrasonography of the gallbladder confirms spirometer use.
cholelithiasis in most patients and distinguishes be- H Encourage early ambulation postoperatively.
tween obstructive and nonobstructive jaundice; cal- H Maintain nothing-by-mouth status.
culi as small as 2 mm can be detected.
H Oral cholecystography confirms the presence of gall- Monitoring
stones, although this test is gradually being replaced H Vital signs
by ultrasonography. H Intake and output
H Technetium-labeled iminodiacetic acid scan of the H Pain control
gallbladder indicates cystic duct obstruction and H Abdominal status
acute or chronic cholecystitis if the gallbladder cant H Respiratory status
be seen. After surgery
Diagnostic procedures H T tube patency and drainage
H Percutaneous transhepatic cholangiography, imaging H Cardiac status
performed under fluoroscopic guidance, supports H Postoperative complications
the diagnosis of obstructive jaundice and is used to
visualize calculi in the ducts.
Patient teaching
Treatment Be sure to cover:
H the disease, diagnosis, and treatment
General H how to breathe deeply, cough, expectorate, and per-
H Low-fat diet form leg exercises that are necessary after surgery
H Nothing by mouth if surgery required H dietary modifications
H Activity, as tolerated H medication administration, dosage, and possible
adverse effects
Medications H wound care.
H Gallstone dissolution therapy

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Incidence
Cholera H Most common in Africa, Southern and Southeast
Asia, and the Middle East, although outbreaks have
occurred in Japan, Australia, and Europe
Overview H Occurs during the warmer months; most prevalent
among lower socioeconomic groups
Description H Common among children ages 1 to 5 in India, but
H Acute enterotoxin-mediated GI infection equally distributed among all age-groups in other
H Transmitted through food and water contaminated endemic areas
with fecal material from carriers or people with ac-
tive infections Common characteristics
H Food poisoning caused by Vibrio parahaemolyticus, H Acute, painless, profuse, watery diarrhea
a similar bacterium (see Vibrio parahaemolyticus H Effortless vomiting (without preceding nausea)
food poisoning)
H Also known as Asiatic cholera or epidemic cholera Complications
H Dehydration
Pathophysiology H Hypovolemic shock
H Humans are the only hosts and victims of V. choler- H Metabolic acidosis
ae, a motile, aerobic organism. H Uremia
H The incubation period is several hours to 5 days. H Coma and death
H Enterotoxins cause profuse watery diarrhea and vom-
iting without nausea.
H Massive fluid and electrolyte loss occurs and, if not Assessment
corrected, leads to metabolic acidosis, uremia, and
possibly coma and death. History
H Infection doesnt confer permanent immunity. H Profuse, watery diarrhea
H Vomiting
Causes H Intense thirst
H Gram-negative bacillus V. cholerae H Weakness
H Muscle cramps (especially in the extremities)
Risk factors
H Deficiency or absence of hydrochloric acid Physical findings
H Stools containing white flecks of mucus (rice-water
stools)
H Loss of skin turgor, wrinkled skin, sunken eyes
H Pinched facial expression
H Cyanosis
H Tachycardia
Vibrio parahaemolyticus food poisoning H Tachypnea
H Thready or absent peripheral pulses
Vibrio parahaemolyticus is a common cause of gastroen- H Hypotension
teritis in Japan. Outbreaks also occur on American cruise
H Fever
ships and in the eastern and southeastern coastal areas of
H Inaudible, hypoactive bowel sounds
the United States, especially during the summer.
V. parahaemolyticus, which thrives in a salty environ- Test results
ment, is transmitted through the ingestion of uncooked or
undercooked contaminated shellfish, particularly crab and Laboratory
shrimp. After an incubation period of 2 to 48 hours, H A culture of V. cholerae from feces or vomitus indi-
V. parahaemolyticus causes watery diarrhea, moderately cates cholera.
severe cramps, nausea, vomiting, headache, weakness, H Microscopic examination of fresh feces shows rapid-
chills, and fever. Food poisoning is usually self-limiting ly moving bacilli (like shooting stars).
and subsides spontaneously within 2 days. Occasionally, H Agglutination reveals reactions to group- and type-
however, its more severe and may even be fatal in debili- specific antisera.
tated or elderly persons.
Other
Diagnosis requires bacteriologic examination of vomi-
H In endemic areas or during epidemics, typical clini-
tus, blood, stool smears, or fecal specimens collected by
rectal swab. Diagnosis must rule out not only other caus-
cal features strongly suggest cholera.
es of food poisoning but also other acute GI disorders.
Treatment is supportive, consisting primarily of bed rest
and oral fluid replacement. I.V. replacement therapy is sel-
dom necessary, but oral tetracycline may be prescribed.
Thorough cooking of seafood prevents this infection.

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Treatment
General
H Standard precautions
H Supportive care
H Increased fluid intake

Medications
H Rapid I.V. infusion of large amounts (50 to 100 ml/
minute) of isotonic saline solution, alternating with
sodium bicarbonate or sodium lactate
H Antibiotic such as tetracycline

Nursing considerations
Key outcomes
The patient will:
H regain and maintain adequate fluid and electrolyte
balance
H have normal elimination patterns
H have stable vital signs
H produce adequate urine volume.

Nursing interventions
H Maintain standard precautions.
H Carefully observe jugular veins.
H Administer prescribed medications.

Monitoring
H Vital signs
H Intake and output
H Laboratory values
H I.V. infusion
H Jugular veins
H Respiratory status
H GI status

Patient teaching
Be sure to cover:
H administration of cholera vaccine to travelers in
endemic areas
H proper hand-washing technique
H need for increased fluid intake.

Discharge planning
H Explain the use of oral tetracycline to family mem-
bers.
H If the physician orders a cholera vaccine, tell the
patient that hell need a booster 3 to 6 months later
for continuing protection.

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Incidence
Chronic fatigue and H Affects people of all ages, occupations, and income

immune dysfunction levels

H More common in females than in males or children,

syndrome especially females younger than age 45

Overview
Description
H Characterized by prolonged overwhelming fatigue
H Also called chronic fatigue syndrome, chronic
Epstein-Barr virus, myalgic encephalomyelitis,
and Yuppie flu
Pathophysiology
H Infectious agents or environmental factors trigger
an abnormal immune response and hormonal al-
terations.
Causes
H Exact cause unknown
H Possibly cytomegalovirus, herpes simplex virus types
1 and 2, human herpesvirus 6, Inoue-Melnick virus,
human adenovirus 2, enteroviruses, measles virus, or
a retrovirus that resembles human T-cell lymphotro-
pic virus type II
H May result from overactive immune system
H Sporadic incidence and epidemic clusters
H Estimated to affect about 200 out of every 100,000
persons in the United States
Special populations
Chronic fatigue and immune dysfunction syn-
drome is most prevalent among professionals in
their 20s and 30s.
Common characteristics
H Suggests viral illness in some cases
H Characterized by incapacitating fatigue
H Waxing and waning symptoms
H Severely debilitating; can last for months or years
H Depression and anxiety after the syndromes onset
H Fever
H Pharyngitis
H Lymphadenopathy
Complications
H Social and occupational impairment

Risk factors Assessment

H Genetic predisposition
H Hormonal balance History
H Neuropsychiatric factors H Characteristic complaints of prolonged, overwhelm-
H Gender ing fatigue (see Diagnosing chronic fatigue syn-
H Previous illness drome)
H Stressful environment
Physical findings
H Myalgia
H Cognitive dysfunction
Diagnosing chronic fatigue syndrome
Chronic fatigue and immune dysfunction syndrome is de-
Test results
fined by: Laboratory
H New or relapsing fatigue that isnt the result of ongoing H Lymphocyte differential reveals reduced natural killer
exertion or alleviated by rest and reduces occupational, cell cytotoxicity, abnormal CD4+:CD8+ T-cell ratios,
educational, social, or personal activities or efforts. and mild lymphocytosis.
H Four or more of the following symptoms, occurring for H Immunoglobulin profile shows decreased immuno-
6 months or more:
globulin subclasses.
self-reported impairment in short-term memory or
H Immune complex profile reveals circulating immune
concentration
sore throat complexes.
tender cervical or axillary nodes H Antimicrosomal antibody testing reveals increased
muscle pain levels of antimicrosomal antibodies.
multiple joint pain without redness or swelling
headaches of a new pattern or severity
nonrefreshing sleep
postexertional malaise lasting 24 hours or longer.

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Treatment
General
H Focus on supportive care
H Psychiatric evaluation
H Behavioral therapy
H Well-balanced diet high in vitamins and minerals
H Physical therapy
H Frequent rest periods, as needed
H Avoidance of strenuous activities

Medications
H Nonsteroidal anti-inflammatory drug such as ibu-
profen
H Antidepressants, such as sertraline and paroxetine
H Antihistamines, such as loratidine and fexofenidine

Nursing considerations
Key outcomes
The patient will:
H verbally report having an increased energy level
H express feelings about diminished capacity to
perform usual roles
H recognize limitations imposed by illness
H make decisions regarding the course of treatment
and management of the illness
H voice feelings related to self-esteem.

Nursing interventions
H Provide emotional support.
H Begin a graded exercise program.
H Administer prescribed medications.

Monitoring
H Response to treatment
H Adverse effects of medication
H Complications

Patient teaching
Be sure to cover:
H the need to decrease activities when fatigue is
greatest
H the need to avoid bed rest, which has no proven
therapeutic value
H medication administration, dosage, and possible
adverse effects
H appropriate activity planning.

Discharge planning
H Refer the patient to support services.

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Cirrhosis Assessment
History
Overview H Chronic alcoholism
H Malnutrition
Description H Viral hepatitis
H Chronic hepatic disease H Exposure to liver toxins such as arsenic and certain
H Several types medications
H Prolonged biliary tract obstruction or inflammation
Pathophysiology Early stage
H Diffuse destruction and fibrotic regeneration of H Vague signs and symptoms
hepatic cells occurs. H Abdominal pain
H Necrotic tissue yields to fibrosis. H Diarrhea, constipation
H Liver structure and normal vasculature are altered. H Fatigue
H Blood and lymph flow are impaired. H Nausea, vomiting
H Hepatic insufficiency occurs. H Muscle cramps
Later stage
Causes H Chronic dyspepsia
Lannecs or micronodular cirrhosis H Constipation
(alcoholic or portal cirrhosis) H Pruritus
H Chronic alcoholism H Weight loss
H Malnutrition H Bleeding tendency, such as frequent nosebleeds, easy
Postnecrotic or macronodular cirrhosis bruising, and bleeding gums
H Complication of viral hepatitis
H Possible after exposure to such liver toxins as Physical findings
arsenic, carbon tetrachloride, and phosphorus H Telangiectasis on the cheeks
Biliary cirrhosis H Spider angiomas on the face, neck, arms, and trunk
H Prolonged biliary tract obstruction or inflammation H Gynecomastia
Idiopathic cirrhosis (cryptogenic) H Umbilical hernia
H No known cause H Distended abdominal blood vessels
H Sarcoidosis H Ascites
H Chronic inflammatory bowel disease H Testicular atrophy
H Menstrual irregularities
Risk factors H Palmar erythema
H Alcoholism H Clubbed fingers
H Toxins H Thigh and leg edema
H Biliary obstruction H Ecchymosis
H Hepatitis H Jaundice
H Metabolic disorders H Palpable, large, firm liver with a sharp edge (early
finding)
Incidence H Enlarged spleen
H Tenth most common cause of death in the United H Asterixis
States H Slurred speech, paranoia, hallucinations
H Most common among those ages 45 to 75
H Occurs in twice as many males as females Test results
Laboratory
Common characteristics H Liver enzyme levels, such as alanine aminotrans-
H Abdominal pain ferase, aspartate aminotransferase, total serum bili-
H Pruritus rubin, and indirect bilirubin are elevated.
H Jaundice H Total serum albumin and protein levels are de-
H Ascites creased.
H Indigestion H Prothrombin time is prolonged.
H Anemia H Hemoglobin, hematocrit, and serum electrolyte levels
are decreased.
Complications H Vitamins A, C, and K are deficient.
H Portal hypertension H Urine levels of bilirubin and urobilinogen are in-
H Bleeding esophageal varices creased; fecal urobilinogen levels are decreased.
H Hepatic encephalopathy
H Hepatorenal syndrome
H Death

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Imaging H Provide appropriate skin care.

H Abdominal X-rays show an enlarged liver and spleen H Maintain patient safety.
and cysts or gas in the biliary tract or liver; liver cal-
cification; and massive ascites. Monitoring
H Computed tomography and liver scans determine H Vital signs
liver size, identify liver masses, and visualize hepatic H Laboratory values
blood flow and obstruction. H Hydration and nutritional status
H Radioisotope liver scans show liver size, blood flow, H GI status
or obstruction. H Cardiovascular status
Diagnostic procedures H Hemodynamic status
H Liver biopsy is the definitive test for cirrhosis, reveal- H Respiratory status
ing hepatic tissue destruction and fibrosis. H Abdominal girth
H Esophagogastroduodenoscopy reveals bleeding H Weight
esophageal varices, stomach irritation or ulceration, H Bleeding tendencies
and duodenal bleeding and irritation. H Skin integrity
H Changes in mentation, behavior
H Neurologic status
Treatment
General Patient teaching
H Removal or alleviation of underlying cause
H I.V. fluids Be sure to cover:
H Blood transfusion H the disorder, diagnosis, and treatment
H Restricted sodium consumption H over-the-counter medications that may increase
H Restricted fluid intake bleeding tendencies
H No alcohol intake H dietary modifications
H High-calorie diet H the need to avoid infections and abstain from alcohol
H Frequent rest periods, as needed H the need to avoid sedatives and acetaminophen (he-
H Paracentesis patotoxic)
H Esophageal balloon tamponade H high-calorie diet and small, frequent meals.
H Sclerotherapy
Discharge planning
Medications H Refer the patient to Alcoholics Anonymous, if appro-
H Vitamin supplementation such as thiamine priate.
H Posterior pituitary hormone such as vasopressin H Refer the patient for psychological counseling, if
H Potassium-sparing diuretic such as spirolactone needed.
H Ammonia detoxicant such as lactoluse
H Antiemetic such as metoclopramide
H Antidiarrheal such as octreotide

Surgery
H May be required to divert ascites into venous circula-
tion; if so, peritoneovenous shunt used
H Portal-systemic shunts
H Transjugular intrahepatic portosystemic shunt

Nursing considerations
Key outcomes
The patient will:
H maintain caloric intake, as required
H maintain normal fluid volume
H incur no injuries
H exhibit no bleeding.

Nursing interventions
H Give prescribed I.V. fluids and blood products.
H Give prescribed drugs.
H Encourage verbalization and provide support.

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Cleft lip and cleft palate
Overview
Description
H Imperfect fusion of front and sides of the face and
the palatine shelves during pregnancy
H May occur separately or in combination
H Can occur unilaterally, bilaterally or, rarely, in the
midline
H May affect just the lip or extend into the upper jaw or
nasal cavity (see Types of cleft deformities)
Pathophysiology
H Chromosomal abnormality, exposure to teratogens,
genetic abnormality, or environmental factors cause
the lip or palate to fuse imperfectly during the sec-
ond month of pregnancy.
H A complete cleft includes the soft palate, the bones of
the maxilla, and the alveolus on one or both sides of
the premaxilla.
H A double cleft runs from the soft palate forward to ei-
ther side of the nose, separating the maxilla and pre-
maxilla into freely moving segments. The tongue and
other muscles can displace the segments, enlarging
the cleft.
ALERT
Isolated cleft palate occurs more commonly with
congenital defects other than isolated cleft lip. The
constellation of U-shaped cleft palate, mandibular
hypoplasia, and glossoptosis known as Robin se-
quence can occur as an isolated defect or one fea-
ture of many different syndromes.These infants
should have comprehensive genetic evaluation. Be-
cause of their mandibular hypoplasia and glossop-
tosis, the airway in infants with Robin sequence
must be carefully evaluated and managed.
Causes
H Chromosomal or Mendelian syndrome (cleft defects
caused by more than 300 syndromes)
H Exposure to teratogens during fetal development
H Combined genetic and environmental factors
Incidence
H Twice as common in males than in females
H More common in children with a family history of
cleft defects
H Cleft lip with or without cleft palate occurs in about 1
in 1,000 births among Whites; incidence higher in
Asians (1.7 in 1,000) and Native Americans (more
than 3.6 in 1,000), but lower in Blacks (1 in 2,500)
184 Cleft lip and cleft palate
Common characteristics
H Obvious cleft lip or cleft palate
H Feeding difficulties from incomplete fusion of the
palate
Complications
H Malnutrition
H Hearing impairment
H Permanent speech impediment
Assessment
History
H Family history of cleft defects
H Maternal exposure to teratogens during pregnancy
H Clinical presentation obvious at birth
Physical findings
H Cleft that runs from the soft palate forward to either
side of the nose
Test results
Imaging
H Prenatal targeted ultrasound reveals abnormality.
Treatment
General
H Orthodontic prosthesis to improve sucking
H Use of a contoured speech bulb attached to the pos-
terior of a denture to occlude the nasopharynx when
a wide horseshoe defect makes surgery impossible
(to help the child develop intelligible speech)
H Use of a large, soft nipple with large holes, such as a
lambs nipple, to improve feeding patterns and pro-
mote adequate nutrition
Medications
ALERT
Daily use of folic acid before conception decreases
the risk for isolated (not associated with another
genetic or congenital malformation) cleft lip or
palate by up to 25%. Women of childbearing age
should be encouraged to take a daily multivitamin
containing folic acid until menopause or until
theyre no longer fertile.
Surgery
H Surgical correction of cleft lip in the first few days of
life and again at 12 to 18 months, after the infant
gains weight and is infection-free
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Types of cleft deformities

Nursing considerations
These illustrations show variations of cleft lip and cleft
Key outcomes palate.

The patient will: NOTCH IN THE VERMILLION BORDER

H exhibit normal growth and development patterns (JUNCTION OF THE LIP AND SURROUNDING SKIN)
within the confines of the disorder
H not aspirate feedings.
The family will:
H express an understanding of the condition and
treatment
H seek appropriate resources to assist with coping.

Nursing interventions
H Encourage the mother of an infant with cleft lip to
breast-feed if the cleft doesnt prevent effective
sucking.
H Suction, as necessary. UNILATERAL CLEFT LIP AND PALATE
H Help the parents deal with their feelings about the
childs deformity.

ALERT
Never place a child with Robin sequence on his
back because his tongue could fall back and ob-
struct his airway. Place the infant on his side for
sleeping. Most other infants with a cleft palate can
sleep on their backs without difficulty.

Monitoring BILATERAL CLEFT LIP AND PALATE

H Swallowing ability
H Weight gain
H Intake and output

Patient teaching
Be sure to cover:
H treatment plan
H how to best feed the infant
H burping the infant frequently
H gently cleaning the palatal cleft with a cotton-tipped CLEFT PALATE
applicator dipped in half-strength hydrogen peroxide
or water after each feeding.
Discharge planning
H Refer the patient to speech therapy to correct speech
patterns.
H Refer the parents to a social worker who can guide
them to community resources, if needed, and to a
genetic counselor to determine the recurrence risk.

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Clostridium difficile H Hemorrhage

H Pseudomembranous colitis

infection
Assessment
Overview History
H Recent antibiotic therapy
Description H Abdominal pain
H A gram-positive anaerobic bacterium commonly H Cramping
resulting in antibiotic-associated diarrhea
H Symptoms ranging from asymptomatic carrier states Physical findings
to severe pseudomembranous colitis caused by H Soft, unformed, or watery diarrhea (more than three
exotoxins (Toxin A is an enterotoxin and toxin B stools in a 24-hour period) that may be foul smelling
is a cytotoxin.) or grossly bloody
H Within 14 to 30 days of treatment, recurrence with H Abdominal tenderness
the same organism possible in 10% to 20% of H Fever
patients
Test results
Pathophysiology Laboratory
H Antibiotics may trigger toxin production. H Cell cytotoxin test shows toxins A and B.
H Toxin A mediates alteration in fluid secretion, en- H Enzyme immunoassay identifies C. difficile; its
hances inflammation, and causes leakage of albumin slightly less sensitive than cell cytotoxin test but
from the postcapillary venules. has a turnaround time of only a few hours.
H Toxin B causes damage and exfoliation to the superfi- H Stool culture identifies C. difficile.
cial epithelial cells and inhibits adenosine diphos-
phate ribosylation of Rho proteins.
H Both toxins cause electrophysiologic alterations of Treatment
colonic tissue.
General
Causes H Withdrawal of causative antibiotic
H Antibiotics that disrupt the bowel flora H Avoidance of antimotility agents
H Enemas and intestinal stimulants H Good skin care
H Transmission from infected person H Well-balanced diet
H Some antifungal and antiviral agents H Increased fluid intake, if appropriate
H Rest periods, if fatigued
Risk factors
H Contaminated equipment and surfaces Medications
H Antibiotics H Antibiotics, such as vancomycin and metronidazole
H Abdominal surgery
H Antineoplastic agents that have an antibiotic activity
H Immunocompromised state Nursing considerations
Incidence Key outcomes
H More common in people in nursing homes and day- The patient will:
care facilities H maintain stable vital signs
H One of the most common nosocomial infections H maintain normal electrolyte levels
(contracted by about 20% of hospitalized patients H maintain adequate fluid volume
taking antibiotics) H maintain skin integrity.

Common characteristics Nursing interventions

H Watery, foul-smelling diarrhea H Give prescribed drugs.
H Institute contact precautions for those with active
Complications diarrhea.
H Electrolyte abnormalities H Wash your hands with an antiseptic soap after direct
H Hypovolemic shock contact with the patient or his immediate environ-
H Toxic megacolon ment.
H Colonic perforation H Make sure reusable equipment is disinfected with a
H Peritonitis bleach-based solution before its used on another
H Sepsis patient.

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Monitoring
H Vital signs
H Intake and output
H Complications
H Serum electrolytes
H Adverse effects of medication
H Response to treatment
H Amount and characteristics of stools
H Skin integrity
H GI status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H proper hand-washing technique
H proper disinfection of contaminated clothing or
household items
H adequate fluid intake
H signs and symptoms of dehydration
H medications and possible adverse effects
H complications and when to notify the physician
H perirectal skin care.

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Clubfoot H Heredity
H Idiopathic
H Suspected muscle abnormalities, leading to varia-
tions in length and tendon insertions
Overview
Incidence
Description H 1 per 1,000 live births
H Foot deformity caused by a deformed talus and short- H Usually occurs bilaterally
ened Achilles tendon, giving the foot a characteristic H Twice as common in boys as in girls
clublike appearance H May be linked to other birth defects, such as
H In talipes equinovarus: foot points downward (equi- myelomeningocele, spina bifida, and arthrogryposis
nus) and turns inward (varus), and front of foot
curls toward the heel (forefoot adduction) Common characteristics
H Also known as talipes: most common congenital dis- H Inward deformity of the foot (see Recognizing club-
order of lower extremities foot)
Pathophysiology Complications
H Unknown, but contributing factors may include: H Abnormal gait
defective cartilage with ligamentous laxity H Stress changes on lateral side of the foot
muscle imbalance H Residual deformity
abnormal intrauterine position
central nervous system anomaly
persistence of a normal fetal relationship. Assessment
Causes History
H Combination of genetic and environmental factors in H Family history
utero H Muscular atrophy or dystrophy

Recognizing clubfoot
Clubfoot (talipes) may have TALIPES EQUINUS TALIPES CALCANEUS TALIPES CAVUS
various names, depending
on the orientation of the de-
formity, as shown in the il-
lustrations at right.

TALIPES VARUS TALIPES EQUINOVARUS TALIPES CALCANEOVARUS

TALIPES VALGUS TALIPES CALCANEOVALGUS TALIPES EQUINOVALGUS

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Physical findings H Proper foot alignment

H Deformed talus with a shortened Achilles tendon, the H Pain control
calcaneus somewhat shortened and flattened
H Shortened, underdeveloped calf muscles, with soft
tissue contractures at the site of the deformity Patient teaching
H Foot tight in its deformed position and resistant of
manual efforts to push it back into normal position Be sure to cover:
H the need for prompt treatment
Test results H signs of circulatory impairment
Imaging H proper skin care
H X-rays show superimposition of the talus and the H use of exercise, night splints, and orthopedic shoes
calcaneus and a ladderlike appearance of the to maintain alignment.
metatarsals.
Discharge planning
H Refer the patient to rehabilitation resources, as
Treatment needed.
General
H Correction of the deformity
H Activity according to ability
H Maintaining the correction until the foot regains nor-
mal muscle balance
H Close observation to prevent the deformity from re-
curring
Sequential correction
H For forefoot adduction: uncurling the front of the
foot away from the heel (forefoot abduction)
H For varus deformity: turning the foot so the sole faces
outward (eversion)
H For equinus: casting the foot with the toes pointing
up (dorsiflexion)
Medications
H Analgesics

Surgery
H Subcutaneous tenotomy of the Achilles tendon and
posterior capsulotomy of the ankle joint (may need
to be done with the equinus stage of correction)
H In severe cases, bone surgery, such as wedge resec-
tions, osteotomy, or astragalectomy possibly appro-
priate (After surgery, a cast is applied to preserve
the correction.)

Nursing considerations
Key outcomes
The patient will:
H maintain joint mobility and range of motion
H maintain muscle strength
H show no evidence of complications.

Nursing interventions
H After casting, elevate the childs feet with pillows.
H Perform proper skin and cast care.

Monitoring
H Neurovascular status of affected extremity after cast-
ing or surgery

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Coarctation of the aorta H Wide pulse pressure

H Signs and symptoms of heart failure

Complications
Overview H Heart failure
H Severe hypertension
Description H Cerebral aneurysms and hemorrhage
H A narrowing of the aorta, usually just below the left H Rupture of the aorta
subclavian artery, near the site where the ligamentum H Aortic aneurysm
arteriosum (the remnant of the ductus arteriosus, a H Infective endocarditis
fetal blood vessel) joins the pulmonary artery to the H Hypoperfusion of lower extremities
aorta
H May occur with aortic valve stenosis (usually of a bi-
cuspid aortic valve) and with severe cases of hypo- Assessment
plasia of the aortic arch, patent ductus arteriosus
(PDA), and ventricular septal defect History
H Ineffective pumping of the heart and increased risk H Tachypnea
due to heart failure caused by the obstruction of H Dyspnea
blood flow H Failure to thrive
H Headache
Pathophysiology H Vertigo
H Coarctation of the aorta may develop as a result of H Epistaxis
spasm and constriction of the smooth muscle in the H Claudication
ductus arteriosus as it closes.
H This contractile tissue extends into the aortic wall, Physical findings
causing narrowing. H Pallor
H The obstructive process causes hypertension in the H Hypertension
aortic branches above the constriction (arteries that H Crackles
supply the arms, neck, and head) and diminished H Edema
pressure in the vessel below the constriction. H Tachycardia
H Restricted blood flow through the narrowed aorta in- H Cardiomegaly
creases the pressure load on the left ventricle and H Hepatomegaly
causes dilation of the proximal aorta and ventricular H Hypertension
hypertrophy. H Pink upper arms and cyanotic legs
H As oxygenated blood leaves the left ventricle, a por- H Absent or diminished femoral pulses
tion travels through the arteries that branch off the H Arm blood pressure greater than leg blood pressure
aorta proximal to the coarctation. H Chest and arms more developed than legs
H If PDA is present, the rest of the blood travels
through the coarctation, mixes with deoxygenated Test results
blood from the PDA, and travels to the legs. Imaging
H If PDA is closed, the legs and lower portion of the H Chest X-rays may show left ventricular hypertrophy,
body must rely solely on the blood that gets through heart failure, a wide ascending and descending aorta,
the coarctation. and notching of the ribs undersurfaces due to ero-
sion by collateral circulation. (See Recognizing
Causes coarctation of the aorta.)
H Unknown H Echocardiography may show increased left ventricu-
H Turners syndrome lar muscle thickness, coexisting aortic valve abnor-
malities, and the coarctation site.
Incidence Diagnostic procedures
H Accounts for about 7% of all congenital heart defects H Electrocardiography may reveal left ventricular hy-
in children pertrophy.
H Twice as common in males as in females H Cardiac catheterization evaluates collateral circula-
H In females, commonly linked to Turners syndrome, a tion and measures pressure in the right and left ven-
chromosomal disorder that causes ovarian dysgene- tricles and in the ascending and descending aortas
sis (on both sides of the obstruction).
H Aortography locates the site and extent of coarcta-
Common characteristics tion.
H Resting systolic hypertension in the upper body
H Absent or diminished femoral pulses

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Recognizing coarctation of the aorta

Treatment
Collateral circulation develops to bypass the occluded aor-
General tic lumen, and can be seen on X-ray as notching of the
ribs. By adolescence, palpable, visible pulsations may be
H Low-sodium diet evident.
H Fluid restrictions
H Limited activity
Coarctation
Medications
H Cardiac glycoside such as digoxin
H Diuretic such as furosemide
H Oxygen
H Sedative such as chloral hydrate
H Prostaglandin infusion to keep the ductus open
H Antibiotic prophylaxis such as amoxicillin
H Antihypertensive such as enalaprilat

Surgery
H A flap of the left subclavian artery may be used to
reconstruct the aorta.
H Balloon angioplasty or resection with end-to-end
anastomosis or use of a tubular graft may also be
performed.

Nursing considerations
Key outcomes
The patient will:
H carry out activities of daily living without weakness or
fatigue
H maintain hemodynamic stability
H remain free from signs and symptoms of infection.

Nursing interventions
H Offer emotional support.
H Regulate environmental temperature.
H Give prescribed drugs.

Monitoring
H Hemodynamics
H Vital signs
H Intake and output
H Respiratory status
H Blood glucose levels
H Postoperative pain
H Signs of infection
H Cardiovascular status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H exercise restrictions
H endocarditis prophylaxis.

Discharge planning
H Stress the need for follow-up care, as ordered.

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Coccidioidomycosis Assessment
History
Overview H Living or traveling to an endemic area
H Fever
Description H Dry cough
H Fungal infection occurring primarily as a respiratory H Pleuritic chest pain
tract infection, although generalized dissemination H Sore throat
may occur H Chills
H Also known as valley fever or San Joaquin Valley H Malaise
fever H Headache
H Joint pain
Pathophysiology
H After spores are inhaled, cell activation and cytokine Physical findings
formation stimulate inflammatory cells and facilitate H Fever
killing of the organism. H Itchy macular rash
H Immunosuppression may delay resolution of the in- H Hemoptysis
fection. H Local swelling and redness in involved sites (with
musculoskeletal involvement)
Causes H Bronchial breath sounds
H Inhaled spores of Coccidioides immitis found in
the soil or dust from dressings or plaster casts of in- Test results
fected persons Laboratory
H Serum precipitins (immunoglobulins) are positive.
Risk factors H C. immitis spores is detected through immunodiffu-
H Occupational exposure to dust, such as with farmers sion testing of sputum, pus from lesions, and tissue
and construction workers biopsy.
H Impaired immune system H Antibodies are present in pleural and joint fluid and
a rising serum or body fluid antibody titer indicates
Incidence dissemination.
H Disseminated illness more common in dark-skinned H White blood cell count is increased.
males, pregnant females, and patients taking an im- H Eosinophil count is increased.
munosuppressant H Erythrocyte sedimentation rate is increased.
H Endemic to the southwestern United States, especially Imaging
between the San Joaquin Valley in California and H Chest X-ray shows bilateral diffuse infiltrates.
southwestern Texas; also found in Mexico, Guate- Other
mala, Honduras, Venezuela, Colombia, Argentina, H Coccidioidin skin test result is abnormal.
and Paraguay
H Generally affects Filipino Americans, Mexican Ameri-
cans, Native Americans, and Blacks because of popu- Treatment
lation distribution and an occupational link (com-
mon in migrant farm laborers) General
H Bed rest
Common characteristics H Symptomatic measures
Primary coccidioidomycosis
H Acute or subacute respiratory signs and symptoms Medications
H Fever that persists for weeks H I.V. fluids
Disseminated coccidioidomycosis H Antifungal such as amphotericin B
H Fever H Analgesics, such as acetaminophen and morphine
H Abscesses throughout the body, especially in skeletal, H Oxygen
central nervous system, splenic, hepatic, renal, and
subcutaneous tissues Surgery
H Excision or drainage of lesions
Complications H Lobectomy for severe pulmonary lesions
H Meningitis
H Bronchiectasis
H Osteomyelitis
H Hepatosplenomegaly
H Liver failure

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Nursing considerations
Key outcomes
The patient will:
H be free from pain
H maintain a patent airway
H cough effectively.

Nursing interventions
H Administer prescribed medications.
H Administer oxygen as prescribed.
H Encourage coughing, deep breathing, and incentive
spirometer use.
H Maintain a patent airway.
H Encourage bed rest, with head of the bed elevated
30 degrees.
H Encourage adequate fluid intake.
H Provide measures to relieve pain and increase
comfort.
Monitoring
H Pain control
H Intake and output
H Vital signs
H Sputum color, consistency, and amount
H Respiratory status
H Cardiovascular status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H proper hand-washing technique
H wound care.

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Colorectal cancer Assessment

Overview
Description
H Malignant tumors of colon or rectum almost always
adenocarcinomas (about one-half are sessile lesions
of rectosigmoid area; all others, polypoid lesions)
H Slow progression
H Five-year survival rate 50%; potentially curable in
75% of patients if early diagnosis allows resection
before nodal involvement
H Second most common visceral neoplasm in United
States and Europe
Pathophysiology
H Most lesions of the large bowel are moderately differ-
entiated adenocarcinomas.
H Tumors tend to grow slowly and produce no symp-
toms for long periods.
H Tumors in the sigmoid and descending colon under-
go circumferential growth and constrict the intestinal
lumen.
H Tumors in the ascending colon are usually large at
diagnosis and are palpable on physical examination.
Causes
H Unknown
History
H Right colon tumors: no signs and symptoms in early
stages because stool is liquid in that part of colon
H Transverse colon tumors: may cause cramps, gas,
partial or complete obstruction
H Descending colon tumors and rectal tumors: may
cause pencil-shaped stools if the tumor partially
obstructs the intestine
H Black, tarry stools
H Abdominal aching, pressure, or dull cramps
H Weakness
H Diarrhea, anorexia, obstipation, weight loss, and
vomiting
H Rectal bleeding
H Intermittent abdominal fullness
H Rectal pressure
H Urgent need to defecate on arising
Physical findings
H Abdominal distention or visible masses
H Enlarged abdominal veins
H Enlarged inguinal and supraclavicular nodes
H Abnormal bowel sounds
H Abdominal masses (right-side tumors that usually
feel bulky; tumors of transverse portion more easily
detected)
H Generalized abdominal tenderness

Risk factors Test results

H Excessive intake of saturated animal fat
H Digestive tract diseases
H Older than age 40
H History of ulcerative colitis
H Familial polyposis
H Family history of colon cancer
H High-protein, low-fiber diet
Incidence
H Equally distributed among males and females
H Greater in areas of higher economic development
Common characteristics
H Changes in bowel habits
H Symptoms of direct extension to bladder, prostate,
ureters, vagina, or sacrum
H Symptoms of local obstruction
Complications
H Abdominal distention and intestinal obstruction as
tumor growth encroaches on abdominal organs
H Anemia
Laboratory
H Fecal occult blood test may show blood in stools, a
warning sign of rectal cancer.
H Carcinoembryonic antigen allows patient monitoring
before and after treatment to detect metastasis or
recurrence.
Imaging
H Excretory urography verifies bilateral renal function
and allows inspection for displacement of the kid-
neys, ureters, or bladder by a tumor pressing against
these structures.
H Barium enema studies use a dual contrast of barium
and air and reveal the location of lesions that arent
detectable manually or visually. Barium examination
shouldnt precede colonoscopy or excretory urogra-
phy because barium sulfate interferes with these
tests.
H Computed tomography scan allows better visualiza-
tion if a barium enema yields inconclusive results or
if metastasis to the pelvic lymph nodes is suspected.
Diagnostic procedures
H Proctoscopy or sigmoidoscopy permits visualization
of the lower GI tract. It can detect up to 66% of co-
lorectal cancers.
H Colonoscopy permits visual inspection and photogra-
phy of the colon up to the ileocecal valve and pro-
vides access for polypectomies and biopsies of sus-
pected lesions.

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Other Monitoring
H Digital rectal examination can be used to detect al- H Stools
most 15% of colorectal cancers; specifically, it can H Diet
be used to detect suspicious rectal and perianal le- Postoperative
sions. H Vital signs
H Intake and output
H Hydration and nutritional status
Treatment H Electrolyte levels
H Wound and stoma site
General H Postoperative complications
H Radiation preoperatively and postoperatively to H GI status
induce tumor regression H Pain control
H High-fiber diet H Psychological status
H After surgery, avoidance of heavy lifting and contact H Respiratory status
sports H Cardiovascular status

Medications
H Antibiotics such as metronidazole postoperatively Patient teaching
H Chemotherapy, such as bevacizumab, capecitabine,
cetuximab, fluorouracil, irinotecan, oxaliplatin, and Be sure to cover:
panitumunab H the disease process, treatment, and postoperative
H Analgesic such as morphine course
H stoma care
Surgery H avoidance of heavy lifting
H Resection or right hemicolectomy for advanced dis- H the need for keeping follow-up appointments
ease; may include resection of the terminal segment H risk factors and signs of recurrence.
of the ileum, cecum, ascending colon, and right half
of the transverse colon with corresponding mesen- Discharge planning
tery for tumor of cecum and ascending colon H Refer the patient to resource and support services.
H Right colectomy that includes the transverse colon
and mesentery corresponding to midcolic vessels, or
segmental resection of the transverse colon and asso-
ciated midcolic vessels for proximal and middle
transverse colon tumor
H Resection usually limited to the sigmoid colon and
mesentery for sigmoid tumor
H Anterior or low anterior resection for upper rectal
tumor
H Abdominoperineal resection and permanent sigmoid
colostomy required for lower rectal tumor

Nursing considerations
Key outcomes
The patient will:
H maintain normal fluid volume
H maintain intact mucous membranes
H report feeling less pain
H express increased sense of well-being
H use support systems and employ coping strategies.

Nursing interventions
H Encourage early ambulation postoperatively.
H Encourage coughing, deep breathing, and incentive
spirometer use.
H Keep the head of the bed elevated at least 30 degrees
to prevent pneumonia.
H Provide support and encourage verbalization.
H Give prescribed drugs.
H Provide stoma care.

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Complications
Common cold H Secondary bacterial infection causing sinusitis, otitis
media, pharyngitis, or lower respiratory tract infec-
tion
Overview
Description Assessment
H Acute, usually afebrile viral infection that causes in-
flammation of the upper respiratory tract History
H Transmission through airborne respiratory droplets H Exposure to persons with the common cold
or through contact with contaminated objects, in- H Sore throat
cluding hands H Fatigue
H Accounts for 30% to 50% of time lost from work by H Malaise
adults and 60% to 80% of time lost from school by H Myalgia
children, more than any other illness H Fever
H Communicable for 2 to 3 days after onset of symp-
toms Physical findings
H Usually benign and self-limiting H Copious nasal discharge that commonly irritates the
nose
Pathophysiology H Increased erythema of nasal and pharyngeal mucous
H Rhinoviruses may infect cells by attaching to specific membranes
receptors. H Nasal quality to voice
H Infiltration with neutrophils, lymphocytes, plasma H Excoriated skin around nose
cells, and eosinophils occurs.
H Mucus-secreting glands become hyperactive and Test results
nasal turbinates become engorged. (See What hap- H There isnt an explicit diagnostic test.
pens in the common cold.) Laboratory
H White blood cell count and differential are within
Causes normal limits.
H Viral infection of the upper respiratory tract passages
and consequent mucous membrane inflammation re-
sponsible for 90% of cases Treatment
H More than 200 viruses, including rhinoviruses, coro-
naviruses, myxoviruses, adenoviruses, coxsackie- General
viruses, and echoviruses H Use of humidified inspired air
H Mycoplasma H Prevention of chilling
H Increased fluid intake
Risk factors H Rest periods, as needed
H Exposure to an infected person or contact with con-
taminated objects Medications
H Compromised immune system H Antipyretic such as acetaminophen
H Throat lozenges
Incidence H Antitussive such as dextromethorphan
H Most common infectious disease H In infants, saline nose drops and mucus aspiration
H More prevalent in children, adolescent boys, and with a bulb syringe
adult females
H In temperate climates, occurring more commonly in
the colder months Nursing considerations
H In the tropics, occurring more commonly during the
rainy season Key outcomes
The patient will:
Common characteristics H express feeling of increased comfort
H Initial complaints of nasal congestion, headache, and H cope effectively with illness
burning, watery eyes, chills, myalgia, arthralgia, H reestablish normal temperature
malaise, lethargy, sore throat, and a hacking, non- H have respiratory secretions that remain clear and
productive or nocturnal cough odorless
H Most patients afebrile, although fever possibly occur- H maintain adequate air exchange.
ring, especially in children

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What happens in the common cold

Virus-infected droplets enter the body and
attack the cells lining the throat and nose.
The virus particles then multiply rapidly.
Body cell
The immune system responds by send-
ing lymphocytes to the infected mucosa,
causing blood vessels in the nasal
mucosa to swell. This swelling causes
secretion of excess fluid the classic
cold symptom of a runny nose.

Infected
nasal lining

Virus
particles
Blood vessel

Lymphocyte

Phagocytes engulf and destroy dead virus

particles and damaged cells. Soon the cold
symptoms disappear.
Antibodies Some lymphocytes
immobilize the virus
Phagocyte particles with virus-
specific proteins
(antibodies); others
kill infected cells with
a chemical substance.

Chemicals

Damaged Lymphocyte
virus particles

Nursing interventions Patient teaching

H Give prescribed drugs.
H Provide a lubricant for nostrils to decrease irritation. Be sure to cover:
H Relieve throat irritation with sugarless hard candy or H advice against overuse of nose drops or sprays
cough drops. H how to avoid spreading colds
H A warm bath or heating pad can reduce aches and H proper hand-washing technique.
pains.
H Suggest a hot or cold steam vaporizer to relieve nasal Discharge planning
congestion. H Refer the patient for medical care if a high fever per-
sists, level of consciousness changes, or significant
Monitoring respiratory symptoms develop.
H Body temperature
H Respiratory status
H Response to treatment
H Adverse effects of medication
H Complications

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Complex regional pain H Muscle wasting (see Stages of complex regional

pain syndrome)
syndrome Test results
Imaging
H Bone X-rays rule out other conditions.
Overview
Description Treatment
H A chronic pain disorder resulting from abnormal
healing after minor or major injury to a bone, General
muscle, or nerve H Physical therapy
H Also known as reflex sympathetic dystrophy H Activity, as tolerated
(RSD/CRPS1) or causalgia (CRPS2)
Medications
Pathophysiology H Anti-inflammatory such as ibuprofen
H Abnormal functioning of the sympathetic nervous sys- H Antidepressant such as venlafaxine
tem causes development of symptoms commonly dis- H Analgesics, such as diclofenac and oxycodone
proportionate to the injurys severity.
H Interference with normal signals for sensations, tem- Surgery
perature, and blood flow may be caused by impaired H Nerve or regional blocks
communication between the damaged nerves of the
sympathetic nervous system and the brain.
Nursing considerations
Causes
H Exact cause unknown Key outcomes
Precipitating factors The patient will:
H Trauma H express increased comfort
H Neurologic disorder H use support systems and develop coping techniques
H Herpes zoster infection H demonstrate effective relaxation techniques.
H Myocardial infarction
H Musculoskeletal disorder (shoulder rotator cuff Nursing interventions
injury) H Offer emotional support.
H Malignancy H Apply antiembolism stockings.
H Apply heat or cold therapy.
Incidence
H Can occur at any age but is less common in children Monitoring
H Reported more commonly in women H Pain control
H Effects of medications
Common characteristics H Blood glucose level
H Severe, constant pain

Complications Patient teaching

H Impaired mobility
H Depression Be sure to cover:
H the disease and treatment
H relaxation techniques
Assessment H medication administration, dosage, and possible
adverse effects.
History
H Injury Discharge planning
H Severe pain that worsens after activity H Refer the patient for home therapy.
H Refer the patient to a pain care specialist.
Physical findings H Refer the patient for psychological counseling and
H Altered blood flow, feeling either warm or cool to the support groups, as indicated.
touch, with discoloration, sweating, or swelling to the
affected extremity
H Skin, hair, and nail changes
H Impaired mobility and weakness

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Stages of complex regional pain syndrome

Complex regional pain syndrome is divided into three stages. The stages arent always distinct and not all of the signs may
be present.

Stage Duration Pain, swelling, Skin Hair and Osteoporosis

and immobility nails
I (Acute)
Symptoms Gradual or abrupt Warm, red, Accelerated Early
begin within onset of severe dry skin at hair and nail osteoporosis
hours, days, aching, throbbing, onset; growth symptoms
or weeks of and burning pain at changes to
the injury; this site of injury bluish and
stage lasts Pain may be accom- becomes cold
several weeks panied by sensitivity and sweaty
to touch, swelling,
muscle spasm, stiff-
ness, and limited
mobility

II (Subacute or dystrophic)
Lasts 3 to Continuous burning, Cool, pale, Altered hair More apparent
6 months aching, or throbbing bluish, growth; osteoporosis
pain thats more se- sweaty cracked,
vere than stage I grooved, or
Swelling spreads ridged nails
and changes from
soft to brawny and
firm
Loss of range of
motion, muscle
wasting

III (Chronic or atrophic)

Lasts more Pain spreads proxi- Thin, shiny Increasingly Marked diffuse
than 6 months mally and may be in- brittle and osteoporosis
tractable, but some- ridged nails
times lessens and
stabilizes
More distinct dys-
trophic changes and
irreversible tissue
damage
Muscle atrophy and
contractures

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Concussion Assessment
History
Overview H Trauma to head
H Short-term loss of consciousness
Description H Vomiting
H Blow to the head forceful enough to jostle the brain H Antegrade and retrograde amnesia
and make it strike the skull H Change in level of consciousness (LOC)
H Acceleration-deceleration injury H Dizziness
H Causes temporary (less than 48 hours) neural dys- H Nausea
function H Severe headache

Pathophysiology Physical findings

H Concussion causes diffuse soft tissue damage. H Tenderness or hematomas on skull palpation
H Inflammation occurs.
H Structural damage is usually minimal. Test results
Imaging
Causes H Computed tomography scan and magnetic resonance
H Trauma to the head imaging help rule out fractures and more serious
injuries.
Incidence
H More than 2 million instances of concussion per year
in the United States Treatment
H May occur in up to 20% of football players
H More common in males than in females General
H Most commonly affects those ages 15 to 24 H Observation for changes in mental status
H Clear liquids if vomiting occurs
Common characteristics H Bed rest initially with head of the bed elevated at
H Short-term loss of consciousness least 30 degrees
H Nausea and vomiting H Avoidance of contact sports until fully recovered
H Dizziness
H Retrograde amnesia Medications
H Erratic behavior H Nonopioid analgesic such as acetaminophen
H Headache
H Blurred vision
Nursing considerations
Complications
H Seizures Key outcomes
H Persistent vomiting The patient will:
H Intracranial hemorrhage (rare) H state appropriate interactions for pain relief
H maintain stable vital signs
H identify factors that increase the potential for injury
What to look for after a concussion H recover or be rehabilitated from physical injuries to
Before the patients discharge, follow these teaching the extent possible.
guidelines: Instruct the caregiver to awaken the patient
every 2 hours through the night and to ask his name and
Nursing interventions
whether he can identify the caregiver. H Give prescribed drugs, and avoid opioids that may
Advise the caregiver to return the patient to the facility decrease LOC.
immediately if he is difficult to arouse, is disoriented, H Reorient the patient to time and place, if necessary.
has seizures, or experiences a persistent or worsening
headache, forceful or constant vomiting, blurred vision, Monitoring
changes in personality, abnormal eye movements, a stag- H Vital signs
gering gait, or twitching. If the patient is a child, explain to
H Neurologic status
the parents that some children have no apparent ill effects
H Pain control
immediately after a concussion but may grow lethargic or
somnolent a few hours later. Teach the patient the signs of
postconcussion syndrome headache, vertigo, anxiety,
personality changes, memory loss, and fatigue. Explain
that these signs may persist for several weeks.

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Patient teaching
Be sure to cover:
H the injury, diagnosis, and treatment
H nonopioid analgesics for a headache and avoidance
of products containing aspirin
H change in LOC or projectile vomiting, which requires
a return to the hospital
H signs and symptoms of increased intracranial pres-
sure.
Discharge planning
H Arrange for continued observation at home. (See
What to look for after a concussion.)

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Conjunctivitis H Transmission by contaminated towels, washcloths, or

ones own hand
H Systemic diseases, such as erythema multiforme and
thyroid disease
Overview H Candidal infection

Description Incidence
H Inflammation of palpebral or bulbar conjunctiva H Most common eye disorder in the Western hemi-
H Characterized by hyperemia of the conjunctiva sphere
H Usually spreads rapidly from one eye to the other H Responsible for about 30% of all eye complaints
H Usually benign and self-limiting
H Seldom affects vision Common characteristics
H If chronic, may signal degenerative changes or dam- H Reddened conjunctiva
age from repeated acute attacks H Edema of eyelid
H Acute bacterial conjunctivitis (pink eye) usually last- H Pain in the eye
ing about 2 weeks H Increased lacrimation
H Other viral conjunctival infections lasting 2 to H Burning in eyes
3 weeks; chronic and may produce severe disability
Complications
Pathophysiology H Tic
H Conjunctivitis is an inflammatory response of the H Corneal infiltrates
conjunctiva that usually begins in one eye and may H Corneal ulcers
rapidly spread to the other eye. H Eye loss
H Vernal conjunctivitis is linked to a severe form of im-
munoglobulin E-mediated mast cell hypersensitivity
reaction. Assessment
Causes History
H Allergens H Eye pain
H Bacteria H Photophobia
H Viruses H Burning, itching, and sensation of a foreign body in
H Chemical irritations the eye
H Sore throat and fever, in children

Recognizing conjunctival papillae
If you see papillae in the conjunctiva of the upper eyelid,
your patient may have vernal (allergic) conjunctivitis.
These cobblestone bumps are the telltale sign. They result
from swollen lymph tissue within the conjunctival mem-
brane.
Physical findings
H Conjunctival hyperemia
H Discharge
H Tearing
H Crust of sticky, mucopurulent discharge (in bacterial
conjunctivitis)
H Profuse, purulent discharge (in gonococcal conjunc-
tivitis)
H Copious tearing and minimal discharge (in viral con-
junctivitis)
H Conjunctival papillae (in vernal conjunctivitis) (see
Recognizing conjunctival papillae)
H Ipsilateral preauricular lymph node enlargement (in
viral conjunctivitis)
Test results
Laboratory
H Culture and sensitivity tests may identify the bacterial
pathogen.
H Stained smears of conjunctival scrapings may show
mostly monocytes with viral conjunctivitis; polymor-
phonuclear cells (neutrophils) are predominate with
bacterial conjunctivitis; and eosinophils are predom-
inate with allergic conjunctivitis.

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Treatment
General
H Warm compresses
H Depends on cause

Medications
H Antibiotics, such a ciprofloxacin, erythromycin, and
mixofloxacin
H Antiviral such as acyclovir
H Corticosteroid such as dexamethasone
H Histamine-1 receptor antagonist such as azelastine
H Oral antihistamine such as loratidine

Nursing considerations
Key outcomes
The patient will:
H maintain current health status
H sustain no harm or injury
H exhibit no signs of infection
H regain visual function.

Nursing interventions
H Apply warm compresses.
H Apply therapeutic ointment or eyedrops, as ordered.
H Avoid irrigating the eye to prevent the spread of in-
fection.
H Notify public health officials if culture results identify
Neisseria gonorrhoeae.
H Obtain culture specimens before antibiotic therapy.

Monitoring
H Response to treatment
H Signs and symptoms of complications
H Adverse reactions
H Visual acuity

Patient teaching
Be sure to cover:
H proper hand-washing technique
H instillation of eyedrops and ointments
H completing the prescribed antibiotics
H methods for preventing disease transmission
H importance of avoiding chemical irritants
H avoiding eye makeup and contact lens use until the
infection has cleared.

ALERT
Caution the patient to avoid rubbing the infected
eye so that he can prevent the spread of infection
to the other eye or to other people.

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Test results
Corneal abrasion Diagnostic procedures
H Fluorescein staining of the injured area of the cornea
appears green when illuminated.
Overview H Slit-lamp examination discloses the depth of the
abrasion.
Description
H Scratch on the epithelial surface of the cornea
H Prognosis usually good with appropriate treatment Treatment
Pathophysiology General
H Epithelial layers of cornea are lost due to trauma. H Eye irrigation (see Performing eye irrigation)
H Superficial abrasions dont involve Bowmans mem- H Removal of foreign body
brane. H Warm compresses
H Deep abrasions penetrate Bowmans membrane. H Eye patch for 24 hours
H Eye protection with potentially dangerous activities
Causes
H Eye trauma Medications
H Foreign bodies embedded under eyelid H Antibiotic eyedrops or ointment, such as ciproflox-
H Contact lenses acin, erythromycin, gentamicin, and tobramycin
H Chemicals H Corticosteroid such as dexamethasone
H Fingernails
H Hair brushes Surgery
H Tree branches H Surgical repair of corneal lacerations by an ophthal-
H Dust mologist
Incidence
H Affects males and females equally Nursing considerations
Common characteristics Key outcomes
H Difficulty opening the eye The patient will:
H Eye pain H regain visual function
H Erythema H sustain no harm or injury
H Feeling of foreign body in eye H express feelings of increased comfort
H Increased lacrimation H verbalize feelings and concerns.

Complications Nursing interventions

H Corneal erosion H Use a flashlight to inspect the cornea.
H Corneal ulceration H Check visual acuity before treatment begins.
H Permanent vision loss H If a foreign body is present, irrigate the eye with
H Secondary infection normal saline solution.
H Give prescribed antibiotics and cycloplegics.
H Instill prescribed topical anesthetics.
Assessment
History ALERT
H Eye trauma Never give the patient topical anesthetic drops for
H Prolonged contact lens wear self-administration. Abuse of this medication can
H Sensation of foreign body in eye delay healing, especially if the patient rubs the
H Sensitivity to light numb eye and further injures it.
H Decreased visual acuity
H Eye pain
Monitoring
Physical findings H Visual acuity
H Redness in eye H Response to treatment
H Increased tearing
H Possibly a foreign object embedded under the eyelid,
uncovered by eyelid eversion
H Disruption of corneal surface

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Performing eye irrigation

SQUEEZE BOTTLE I.V. TUBE MORGAN LENS

For moderate-volume irrigation to
remove eye secretions, for example
apply sterile ophthalmic irrigant to the
eye directly from the squeeze bottle
container. Direct the stream at the in-
ner canthus and position the patient so
that the stream washes across the
cornea and exits at the outer canthus.
For copious irrigation to treat chem-
ical burns, for example set up an
I.V. bag and tubing without a needle.
Use the procedure described for mod-
erate irrigation to flush the eye for at
least 15 minutes. Alkali burns may re-
quire irrigation for several hours.
Connected to irrigation tubing, a Mor-
gan lens permits continuous lavage
and delivers medication to the eye.
Use an adapter to connect the lens to
the I.V. tubing and the solution con-
tainer. Begin the irrigation at the pre-
scribed flow rate. To insert the device,
ask the patient to look down as you in-
sert the lens under the upper eyelid.
Then have her look up as you retract
and release the lower eyelid over the
lens.

ALERT
Pulse oximeter probes should be applied to the
middle, ring, or preferably little finger, but never
the index finger, in order to minimize the likeli-
hood of corneal abrasion, especially as patients
emerge from anesthesia.

Patient teaching
Be sure to cover:
H healing process
H proper instillation of antibiotic eyedrops or ointment
H effects of untreated corneal infection
H need to wear safety glasses in the workplace, if
appropriate
H contact lens care and instructions for wear.

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Coronary artery disease H Males eight times more susceptible than premeno-
pausal females
H Risk increased by positive family history
H White males more susceptible than nonwhite males;
Overview nonwhite females more susceptible than white fe-
males
Description H Occurs in about 11 million Americans
H Heart disease that results from narrowing of coro-
nary arteries over time due to atherosclerosis Common characteristics
H Primary effect: loss of oxygen and nutrients to myo- H Angina
cardial tissue because of diminished coronary blood
flow Complications
H Arrhythmias
Pathophysiology H Myocardial infarction (MI)
H Increased blood levels of low-density lipoprotein H Heart failure
(LDL) irritate or damage the inner layer of coronary
vessels.
H LDL enters the vessel after damaging the protective Assessment
barrier, accumulates, and forms a fatty streak.
H Smooth muscle cells move to the inner layer to en- History
gulf the fatty substance, produce fibrous tissue, and H Angina that may radiate to the left arm, neck, jaw, or
stimulate calcium deposition. shoulder blade
H Cycle continues, resulting in transformation of the H Commonly occurring after physical exertion but pos-
fatty streak into fibrous plaque and, eventually, a sibly following emotional excitement, exposure to
coronary artery disease (CAD) lesion evolves. cold, or ingestion of a large meal
H Oxygen deprivation forces the myocardium to shift H May develop during sleep; symptoms wake the
from aerobic to anaerobic metabolism, leading to patient
accumulation of lactic acid and reduction of cellu- H Nausea
lar pH. H Vomiting
H The combination of hypoxia, reduced energy avail- H Fainting
ability, and acidosis rapidly impairs left ventricular H Sweating
function. H Stable angina (predictable and relieved by rest or ni-
H The strength of contractions in the affected myocar- trates)
dial region is reduced as the fibers shorten inade- H Unstable angina (increases in frequency and dura-
quately, resulting in less force and velocity. tion and is more easily induced and generally indi-
H Wall motion is abnormal in the ischemic area, result- cates extensive or worsening disease and, untreated,
ing in less blood being ejected from the heart with may progress to MI)
each contraction. H Crescendo angina (an effort-induced pain occurring
with increasing frequency and decreasing provoca-
Causes tion)
H Atherosclerosis H Prinzmetals or variant angina pectoris (severe non-
H Dissecting aneurysm effort-produced pain occurs at rest without provoca-
H Infectious vasculitis tion due to spasm)
H Syphilis
H Congenital defects Physical findings
H Coronary artery spasm H Cool extremities
H Xanthoma
Risk factors H Arteriovenous nicking of the eye
H Family history H Obesity
H High cholesterol level H Hypertension
H Smoking H Positive Levines sign (holding fist to chest)
H Diabetes H Decreased or absent peripheral pulses
H Hormonal contraceptives
H Obesity Test results
H Sedentary lifestyle Imaging
H Stress H Myocardial perfusion imaging with radionucleotide
H Increased homocystine levels during treadmill exercise shows ischemic areas of
the myocardium, visualized as cold spots.
Incidence H Pharmacologic myocardial perfusion imaging in ar-
H Occurs after age 40 teries with stenosis shows decrease in blood flow
proportional to the percentage of occlusion.

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H Coronary angiography reveals the location and de-
gree of coronary artery stenosis or obstruction, col-
lateral circulation, and the condition of the artery
beyond the narrowing.
H Stress echocardiography may show abnormal wall
motion.
H Multiple-gated acquisition scanning demonstrates
cardiac wall motion and reflects injury to cardiac
tissue.
Diagnostic procedures
H Electrocardiography may be normal between anginal
episodes. During angina, it may show ischemic
changes.
H Exercise stress testing may be performed to detect
ST-segment changes during exercise, indicating
ischemia, and to determine a safe exercise prescrip-
tion.
Treatment
General
H Stress reduction techniques essential, especially if
known stressors precipitate pain
H Lifestyle modifications, such as smoking cessation
and maintaining ideal body weight (see Preventing
coronary artery disease)
H Low-fat, low-sodium diet
H Activity restrictions possible
H Regular exercise
Medications
H Antianginals, such as ranolazine and nitroglycerin
H Beta-adrenergic blocker such as metoprolol
H Calcium channel blocker such as diltiazem
H Antiplatelets, such as ticlopidine and aspirin
H Antilipemic such as simvastatin
H Antihypertensive such as lisinopril
Surgery
H Coronary artery bypass graft
H Keyhole or minimally invasive surgery
H Angioplasty
H Endovascular stent placement
H Laser angioplasty
H Atherectomy
Nursing considerations
Key outcomes
The patient will:
H maintain hemodynamic stability
H plan menus appropriate to prescribed diet
H demonstrate understanding of the disease process
H express concern about self-concept, self-esteem, and
body image
H express feelings of increased comfort and decreased
pain.
Preventing coronary artery disease
Because coronary artery disease is so widespread, pre-
vention is important. Dietary restrictions aimed at reduc-
ing the intake of calories (in obesity) and of salt, fats, and
cholesterol minimize the risk, especially when supple-
mented with regular exercise. Abstention from smoking
and reduction of stress are also essential.
Other preventive actions include control of hypertension
(with diuretics or sympathetic beta-adrenergic blockers),
control of elevated serum cholesterol or triglyceride levels
(with antilipemics such as HMG-CoA reductase inhibitors,
including atorvastatin, pravastatin, or simvastatin), and
measures to minimize platelet aggregation and the danger
of blood clots (with aspirin, for example).
Nursing interventions
H Ask the patient to grade the severity of his pain on a
scale of 0 to 10.
H Keep nitroglycerin available for immediate use. In-
struct the patient to call immediately whenever he
feels pain and before taking nitroglycerin.
H Observe for signs and symptoms that may signify
worsening of condition.
H Maintain bed rest immediately postoperatively with
the head of the bed elevated at least 30 degrees.
H Encourage coughing, deep breathing, and incentive
spirometer use postoperatively.
H Encourage early ambulation after surgery.
Monitoring
H Vital signs
H Hemodynamic status
H Intake and output
H Effectiveness of pain medication during anginal
episodes
H Abnormal bleeding and distal pulses following inter-
vention procedures
H Respiratory status
H Chest tube drainage, after surgery
H Cardiac rate and rhythm
H Cardiovascular status
Patient teaching
Be sure to cover:
H risk factors for CAD
H avoidance of activities that precipitate pain
H effective coping mechanisms to deal with stress
H the need to follow the prescribed drug regimen
H low-sodium and low-calorie diet
H the importance of regular, moderate exercise.
Discharge planning
H Refer the patient to a weight-loss program, if needed.
H Refer the patient to a smoking-cessation program, if
needed.
H Refer the patient to a cardiac rehabilitation program,
if indicated.
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Cor pulmonale H In response to hypoxia, the bone marrow produces

more red blood cells, causing polycythemia.
H The bloods viscosity increases, further aggravating
pulmonary hypertension. This increases the right
Overview ventricles workload, causing heart failure. (See Cor
pulmonale: An overview.)
Description
H Hypertrophy and dilation of the right ventricle sec- Causes
ondary to disease affecting the structure or function H Disorders affecting the pulmonary parenchyma
of the lungs or their vasculature H Chronic obstructive pulmonary disease
H Can occur at the end stage of various chronic disor- H Bronchial asthma
ders of the lungs, pulmonary vessels, chest wall, or H Primary pulmonary hypertension
respiratory control center H Vasculitis
H Also called right-sided heart failure H Pulmonary emboli
H External vascular obstruction resulting from a tumor
Pathophysiology or aneurysm
H An occluded vessel impairs the hearts ability to gen- H Kyphoscoliosis
erate enough pressure. H Pectus excavatum (funnel chest)
H Increased blood flow creates pulmonary hyperten- H Muscular dystrophy
sion. H Poliomyelitis
H Pulmonary hypertension increases the hearts work- H Obesity
load. H High altitude
H To compensate, the right ventricle hypertrophies to
force blood through the lungs. Incidence
H Accounts for 6% to 7% of all types of adult heart
disease in the United States
Cor pulmonale: An overview H Affects males and females equally

Although pulmonary restrictive disorders (such as fibrosis Common characteristics

or obesity), obstructive disorders (such as bronchitis), or H Dyspnea
primary vascular disorders (such as recurrent pulmonary H Tachypnea
emboli) may cause cor pulmonale, these disorders share H Signs of heart failure
this common pathway.
Complications
H Right- and left-sided heart failure
Pulmonary disorder
H Hepatomegaly
H Edema
H Ascites
H Pleural effusions
Anatomic alterations in the pulmonary blood vessels and H Thromboembolism due to polycythemia
functional alterations in the lung

Assessment
Increased pulmonary vascular resistance History
H Dyspnea
H Chronic productive cough
H Fatigue
H Weakness
Pulmonary hypertension
Physical findings
H Wheezing respirations
H Tachypnea
Right ventricular hypertrophy (cor pulmonale) H Dependent edema
H Enlarged, tender liver
H Hepatojugular reflux
H Jugular vein distention
H Tachycardia
HEART FAILURE H Pansystolic murmur at the lower left sternal border

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Test results Monitoring

Laboratory H Vital signs
H Arterial blood gas analysis detects decreased H Oxygenation
partial pressure of arterial oxygen (usually less H Intake and output
than 70 mm Hg and rarely more than 90 mm Hg). H Laboratory values
H Hematocrit is typically over 50%. H Respiratory status
H Serum hepatic tests may show an elevated level of H Cardiovascular status
aspartate aminotransferase levels.
Imaging
H Echocardiography demonstrates right ventricular Patient teaching
enlargement.
H Angiography shows right ventricular enlargement. Be sure to cover:
H Chest X-rays reveal large central pulmonary arteries H the disorder, diagnosis, and treatment
and right ventricular enlargement. H dietary restrictions
H Magnetic resonance imaging measures the right ven- H medication administration and possible adverse ef-
tricular mass, wall thickness, and ejection fraction. fects.
H Cardiac catheterization measures pulmonary vascular
pressures. Discharge planning
Diagnostic procedures H Refer the patient for home services, as indicated.
H Electrocardiography shows arrhythmias, such as pre-
mature atrial and ventricular contractions and atrial
fibrillation during severe hypoxia, and also right
bundle-branch block, right axis deviation, prominent
P waves, and an inverted T wave in right precordial
leads.
H Pulmonary function studies reflect underlying pulmo-
nary disease.
Other
H Pulmonary artery catheterization shows increased
right ventricular and pulmonary artery pressures.

Treatment
General
H Low-sodium diet
H Fluid restrictions
H Limited activity or bed rest
H Phlebotomy, if necessary

Medications
H Cardiac glycoside such as digoxin
H Antibiotics, such as amoxicillin and ampicillin
H Vasodilator such as isosorbide
H Oxygen

Nursing considerations
Key outcomes
The patient will:
H maintain adequate cardiac output
H maintain adequate ventilation
H use support services and develop coping mecha-
nisms.
Nursing interventions
H Reposition the patient often.
H Give prescribed drugs.
H Administer oxygen as prescribed.

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H Sporadic form of unknown etiology

Life-threatening disorder H Iatrogenic or acquired form due to inadvertent expo-
sure to CJD-contaminated equipment or material as
Creutzfeldt-Jakob a result of brain surgery, corneal grafts, or use of hu-
man pituitary-derived growth hormones or gonado-
disease tropin
Incidence
H About one case in 1 million people worldwide
Overview annually
H Most cases sporadic, accounting for about 85% of all
Description cases
H Rapidly progressive infectious disease attacking the H About 5% to 15% of cases familial, with an autoso-
central nervous system (CNS) mal dominant pattern of inheritance
H Manifested by progressive dementia, tremors, and H Usually patients older than age 55; median age of
muscle wasting death in the United States: 68
H Always fatal H Affects males and females of diverse ethnic back-
H Not transmitted by normal casual contact (although grounds
iatrogenic transmission can occur) H Most cases in Libya, North Africa, and Slovakia
H Has a 15- to 20-month incubation period
H Typical duration: 6 months Common characteristics
H New variant of Creutzfeldt-Jakob disease emerged in H Rapidly progressive dementia
Europe in 1996 (see Understanding new-variant H Prominent myoclonus
Creutzfeldt-Jakob disease)
H No cure and cant slow progression Complications
H Also known as CJD H Severe, progressive dementia
H CNS abnormalities
Pathophysiology H Death
H CJD is caused by the abnormal accumulation or me-
tabolism of prion proteins.
H These modified proteins are resistant to proteolytic Assessment
digestion and aggregate in the brain to produce rod-
like particles. History
H The accumulation of these modified cellular proteins H Mood changes
results in neuronal degeneration and spongiform H Emotional lability
changes in brain tissue. H Poor concentration
H Lethargy
Causes H Impaired judgment
H Familial or genetically inherited form H Memory loss
H Involuntary muscle movements
H Vision disturbances or other types of hallucinations
H Gait disturbances
Understanding new-variant
Creutzfeldt-Jakob disease Physical findings
Like conventional Creutzfeldt-Jakob disease (CJD), variant H Dementia
CJD (vCJD) is a rare, fatal neurodegenerative disease. H Myoclonus
Most cases have been reported in the United Kingdom, H Spasticity
and its most likely caused by exposure to bovine spongi- H Agitation
form encephalopathy (BSE), a fatal brain disease in cattle H Tremor
also known as mad cow disease. Ingestion of beef prod- H Clumsiness
ucts from cattle with BSE is the most probable route of
H Ataxia
exposure.
H Hypokinesis and rigidity
vCJD affects patients at a much younger age than CJD,
and the duration of the illness is much longer (14 months H Hyperreflexia
versus 6 months).
Regulations have been established in Europe to control
Test results
outbreaks of BSE in cattle and to prevent contaminated Laboratory
meat from entering the food supply. vCJD and its relation- H Cerebral spinal fluid (CSF) immunoassay may show
ship with BSE are still being explored by the Centers for abnormal protein species.
Disease Control and Prevention and the World Health Or- H CSF analysis may show mildly elevated protein level.
ganization.

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Imaging
H Computed tomography scan and magnetic resonance Patient teaching
imaging of the brain may show evidence of general-
ized cortical atrophy. Be sure to cover:
Diagnostic procedures H the disorder, diagnosis, and supportive treatment
H EEG may show burst suppression changes in brain- H prevention of disease transmission
wave activity. H effective coping strategies
H Brain biopsy may show spongiform changes. H safety precautions.
Other
H Autopsy of brain tissue allows definitive diagnosis. Discharge planning
H Refer the patient and his family to CJD support
groups.
Treatment H Refer the patient for hospice care, as appropriate.

General
H Palliative care to make the patient comfortable and to
ease symptoms
H Well-balanced diet
H Adequate fluid intake
H Activity, as tolerated

Medications
H Antiparkinsonian such as amantadine

Surgery
H Possible brain biopsy for diagnosis

Nursing considerations
Key outcomes
The patient will:
H verbalize feelings of anxiety and fear
H demonstrate effective coping techniques
H remain free from injury
H maintain social interaction to the extent possible
H utilize support systems.

Nursing interventions
H Assist the patient and his family through the grieving
process.
H Follow standard precautions.
H Encourage verbalization of concerns and fears.
H Encourage involvement of the patient and his family
in care decisions.
Monitoring
H Vital signs
H Intake and output
H Neurologic status

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Crohns disease H Perforation

H Nutritional deficiencies caused by malabsorption and
maldigestion
Overview
Assessment
Description
H Inflammatory bowel disease possibly affecting any History
part of the GI tract but commonly involving the termi- H Gradual onset of signs and symptoms, marked by pe-
nal ileum riods of remission and exacerbation
H Fifty percent of cases involving colon and small bow- H Fatigue and weakness
el; 33% involving terminal ileum; 10% to 20% involv- H Fever, flatulence, nausea
ing only colon H Steady, colicky, or cramping abdominal pain usually
H Extends through all layers of the intestinal wall; pos- occurring in the right lower quadrant
sibly involving regional lymph nodes and mesentery H Diarrhea possibly worsening after emotional upset
or ingestion of poorly tolerated foods, such as milk,
Pathophysiology fatty foods, and spices
H Crohns disease involves slow, progressive inflamma- H Weight loss
tion of the bowel.
H Lymphatic obstruction is caused by enlarged lymph Physical findings
nodes. H Possible soft or semiliquid stool, usually without
H Edema, mucosal ulceration, fissures, and abscesses gross blood
occur. H Right lower quadrant tenderness or distention
H Elevated patches of closely packed lymph follicles H Possible abdominal mass, indicating adherent loops
(Peyers patches) develop in the small intestinal lin- of bowel
ing. H Hyperactive bowel sounds
H Fibrosis occurs, thickening the bowel wall and caus- H Bloody diarrhea
ing stenosis. H Perianal and rectal abscesses
H Inflamed bowel loops adhere to other diseased or
normal loops. Test results
H The diseased bowel becomes thicker, shorter, and Laboratory
narrower. H Occult blood is seen in stools.
H Hemoglobin level and hematocrit are decreased.
Causes H White blood cell count and erythrocyte sedimentation
H Exact cause unknown rate are increased.
H Lymphatic obstruction and infection among con- H Serum potassium, calcium, and magnesium levels
tributing factors are decreased.
H Hypoproteinemia is present due to intestinal protein
Risk factors loss.
H History of allergies H Vitamin B12 and folate levels are decreased.
H Immune disorders Imaging
H Genetic predisposition 10% to 20% of patients H Small-bowel X-rays may show irregular mucosa, ul-
with the disease have one or more affected relatives; ceration, and stiffening.
sometimes occurs in monozygotic twins H Barium enema reveals the string sign (segments of
stricture separated by normal bowel) and may also
Incidence show fissures and narrowing of the lumen.
H Occurs equally in males and females Diagnostic procedures
H More common in Jewish people H Sigmoidoscopy and colonoscopy show patchy areas
H Onset usually before age 30 of inflammation and may also reveal the characteris-
tic coarse irregularity (cobblestone appearance) of
Common characteristics the mucosal surface.
H Diarrhea H Biopsy reveals granulomas in up to half of all speci-
H Abdominal pain mens.
H Weight loss

Complications Treatment
H Anal fistula
H Perineal abscess General
H Fistulas of the bladder or vagina or to the skin in an H Stress reduction
old scar area H Avoidance of foods that worsen diarrhea
H Intestinal obstruction H Adequate caloric, protein, and vitamin intake

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H Parenteral nutrition, if necessary

H Reduced physical activity Patient teaching
Medications Be sure to cover:
H Corticosteroid such as budesonide H information about the disease, symptoms, and com-
H Immunosuppressants, such as adalimumab and plications
infliximab H ordered diagnostic tests and pretest guidelines
H Sulfonamide such as sulfasalazine H the importance of adequate rest
H Antibacterials and antiprotozoals, such as metronida- H how the patient can identify and reduce sources of
zole and nitazoxanide stress
H Antidiarrheal such as octreotide H prescribed dietary changes
H Opioid such as morphine H prescribed medications, administration, and possible
H Vitamin supplements, such as vitamin B12 and folate adverse effects.
H Antispasmodic such as alosetron
H Iron supplement such as ferrous sulfate Discharge planning
H Refer the patient to a smoking-cessation program, if
Surgery appropriate.
H Indicated for acute intestinal obstruction H Refer the patient to enterostomal therapist, if indi-
H Colectomy with ileostomy cated.

Nursing considerations
Key outcomes
The patient will:
H maintain adequate caloric intake
H maintain normal fluid volume
H regain normal bowel movements
H verbalize understanding of the disease process and
treatment regimen
H exhibit adequate coping mechanisms and seek
appropriate sources of support.
Nursing interventions
H Provide emotional support to the patient and his
family.
H Provide meticulous skin care after each bowel
movement.
H Schedule patient care to include rest periods
throughout the day.
H Assist with dietary modification.
H Give prescribed iron supplements and blood
transfusions.
H Give prescribed analgesics.

Monitoring
H GI status
H Vital signs
H Intake and output, including amount of stool
H Daily weight
H Serum electrolyte, glucose, and Hb levels and stools
for occult blood
H Signs of infection or obstruction
H Bleeding, especially with steroid use
H Pain control
H Skin integrity

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Croup H Dehydration
H Ear infection
H Pneumonia
H Hypoxia
Overview H Hypercapnia

Description
H Viral infection causing severe inflammation and ob- Assessment
struction of the upper airway
H Childhood disease manifested by acute laryngotra- History
cheobronchitis (most commonly), laryngitis, acute H Recent upper respiratory infection
spasmodic laryngitis, and febrile rhinitis Laryngotracheobronchitis
H Incubation period about 3 to 6 days; contagious H Fever and breathing problems usually occurring at
while febrile night
H Recovery usually complete H Difficulty exhaling
Laryngitis in children
Pathophysiology H Mild sore throat
H Viral invasion of the laryngeal mucosa leads to in- H Cough
flammation, hyperemia, edema, epithelial necrosis, H Marked hoarseness (rare)
and shedding. H No respiratory distress
H This leads to irritation and cough, reactive paralysis Laryngitis in infants
and continuous stridor, or collapsible supraglottic or H Respiratory distress
inspiratory stridor and respiratory distress. Acute spasmodic laryngitis
H A thin, fibrinous membrane covers the mucosa of the H Mild to moderate hoarseness
epiglottis, larynx, and trachea. (See How croup af- H Nasal discharge
fects the upper airways.) H Characteristic cough and noisy inspiration
H Anxiety
Causes H Increased dyspnea
H Parainfluenza viruses H Transient cyanosis
H Adenoviruses
H Respiratory syncytial virus Physical findings
H Influenza viruses H Rhinorrhea
H Measles viruses H Use of accessory muscles
H Bacteria (pertussis and diphtheria) H Nasal flaring
H Barklike cough
Incidence H Hoarse, muffled vocal sounds
H Inspiratory stridor
Special populations H Diminished breath sounds
Laryngotracheobronchitis
Occurs mainly in children ages 3 months to 5 H Edema of bronchi and bronchioles
years. H Decreased breath sounds
H Expiratory rhonchi
H Affects boys more commonly than girls H Scattered crackles
H Usually occurs in late autumn and early winter Laryngitis
H Suprasternal and intercostal retractions
H Inspiratory stridor
Special populations
H Dyspnea, tachypnea
Acute spasmodic laryngitis affects children H Diminished breath sounds
between ages 1 and 3, particularly those with H Severe dyspnea and exhaustion in later stages
allergies. Acute spasmodic laryngitis
H Labored breathing with retractions
H Clammy skin
Common characteristics H Rapid pulse rate
H Sharp, barklike, or brassy cough progressing to
stridor Test results
H Hoarse or muffled vocal sounds Laboratory
H Throat cultures show bacteria and sensitivity to
Complications antibiotics.
H Airway obstruction
H Respiratory failure

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Imaging How croup affects the upper airways

H Neck X-ray may show upper airway narrowing and
edema in subglottic folds; helps to differentiate croup
from bacterial epiglotidititis.
H Computed tomography scan helps differentiate be-
tween croup, epiglotidititis, and noninfection.
Diagnostic procedures
H Laryngoscopy may reveal inflammation and obstruc-
tion in epiglottal and laryngeal areas.
In croup, inflammatory swelling and spasms constrict the
larynx, thereby reducing airflow. This cross-sectional
drawing (from chin to chest) shows the upper airway
changes caused by croup. Inflammatory changes almost
completely obstruct the larynx (which includes the epiglot-
tis) and significantly narrow the trachea.

Treatment
General Inflamed
H Home or hospitalized care laryngeal area
H Humidification during sleep
H Intubation if other means of preventing respiratory Inflamed
failure unsuccessful subglottic tissue
H Diet, as tolerated
H Parenteral fluids, if required
H Rest periods

Medications Narrowed
H Oxygen therapy, as needed trachea
H Antipyretic such as acetaminophen
H Antibiotics, such as cefuroxime and cefprozil, if
cause is bacterial
H Adrenergic, aerosolized racemic epinephrine for
moderately severe croup
H Corticosteroids for acute laryngotracheobronchitis
H Use sponge baths and hypothermia blanket, as or-
Surgery dered, for temperatures above 102 F (38.9 C).
H Tracheostomy (rare)
Monitoring
H Vital signs
Nursing considerations H Intake and output
H Respiratory status
Key outcomes H Signs and symptoms of dehydration
The patient will:
H maintain adequate ventilation
H maintain normal temperature Patient teaching
H maintain a patent airway
H use effective coping strategies Be sure to cover:
H verbalize understanding of the disorder. H the disorder, diagnosis, and treatment
H medications and possible adverse reactions
Nursing interventions H when to notify the physician
H Maintain a patent airway. H humidification
H Adminster oxygen, as prescribed. H hydration
H Administer I.V. fluids, as prescribed. H signs and symptoms of ear infection
H Give prescribed drugs. H signs and symptoms of pneumonia.
H Provide quiet diversional activities.
H Engage parents in the care of the infant or child.
H Position an infant in an infant seat or prop him up
with a pillow.
H Position an older child in Fowlers position.
H Provide humidification.
H Avoid milk-based fluids if the patient has thick mucus
or swallowing difficulties.
H Provide frequent mouth care.
H Isolate patients for respiratory syncytial virus and
parainfluenza infections.

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Physical findings
Cryptococcosis H Progressively severe frontal and temporal headache
H Diplopia, blurred vision, and papilledema
H Tinnitus, dizziness, ataxia, and aphasia
Overview H Vomiting
H Memory changes, inappropriate behavior, irritability,
Description and psychosis
H Fungal infection that usually begins as asymptomatic H Facial weakness
pulmonary infection in patient who presents with H Hyperactive reflexes and seizures in the late stage
meningoencephalitis H Pain in the long bones, skull, spine, and joints
H Also known as torulosis and European blastomyco- H Red facial papules and other skin abscesses, with or
sis without ulceration
H Rarely, pleural friction rub or crackles
Pathophysiology H Photophobia
H Small granulomas and cysts in the cerebral cortex
and, later, in deep cerebral tissues produce a mini- Test results
mal inflammatory response. Imaging
H In chronic cases, dense basilar arachnoiditis occurs. H Chest X-ray or computed tomography scan of the
H Lung lesions with intense granulomatous inflamma- chest reveals lesions in pulmonary cryptococcosis.
tion occur. Laboratory
H Analysis or cultures of the sputum, urine, prostatic
Causes secretions, or bone marrow aspirate show C. neo-
H Airborne fungus Cryptococcus neoformans found in formans.
dust particles contaminated by pigeon stool H Tissue or neural biopsy shows myriad cryptococci.
H Transmission by inhalation of cryptococci H India ink preparation of cerebrospinal fluid (CSF)
diagnosing CNS infection when C. neoformans is
Incidence detected.
H Prevalent in immunocompromised patients and those H Blood cultures are positive only in severe infection.
taking immunosuppressant drugs H Antigen titer in serum and CSF is elevated in dissemi-
H Increasing, especially in patients with acquired im- nated infection.
munodeficiency syndrome H Protein levels and white blood cell count are elevated
in CNS infection.
Common characteristics H CSF glucose levels are moderately decreased in about
H Disseminates to extrapulmonary sites, including the 50% of patients.
central nervous system (CNS), skin, bones, prostate Other
gland, liver, and kidneys H Lumbar puncture shows increased CSF pressure.
H Without treatment, leads to CNS infection and death
H Mortality dramatically reduced with treatment; neu-
rologic deficits, such as paralysis and hydrocephalus, Treatment
not necessarily reduced with treatment
General
Complications H Early treatment for cryptococcal disease
H Optic atrophy
H Ataxia Medications
H Hydrocephalus H Combination of antifungal antibiotics amphotericin B
H Deafness and flucytosine, or amphotericin B alone
H Paralysis
H Organic mental syndrome
H Personality changes Nursing considerations
H Coma
H Death Key outcomes
The patient will:
H be free from pain
Assessment H be free from injury
H maintain patent airway
History H increase activity, as tolerated.
H Human immunodeficiency virus infection or another
immunosuppressive disorder Nursing interventions
H Usually asymptomatic but patient may complain of H Maintain a patent airway.
dull chest pain and cough producing slight amount H Keep the head of the bed elevated at least 30 degrees.
of white, blood-streaked sputum H Give prescribed drugs.

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H Before therapy, obtain electrolyte and creatinine

levels.
H Observe for adverse effects such as diarrhea.
H Evaluate the need for long-term venous access for
administering amphotericin B.
H Provide psychological support to help the patient
cope with long-term treatment.
H If vision loss occurs, provide a safe environment.
H Encourage verbalization and provide support.

Monitoring
H Vital signs
H Neurologic checks
H Respiratory status
H Headache, vomiting, and nuchal rigidity
H Intake and output
H Blood urea nitrogen, creatinine levels, and complete
blood count results
H Urinalysis results
H Magnesium and potassium levels and liver function
test results
H Blood levels of flucytosine

Patient teaching
Be sure to cover:
H the disorder and treatment
H medication therapy, including dosage, desired drug
actions, adverse effects, and need for long-term treat-
ment.
Discharge planning
H Urge the patient to return for follow-up care and
evaluation every few months for 1 year.
H Refer the patient for resource and support services,
as needed.

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Cryptorchidism H True undescended testes remain along the path of

normal descent, while ectopic testes deviate from
that path.
Overview Causes
H Hormonal factors
Description H Testosterone deficiency
H Congenital disorder in which one or both testes fail H Structural factors
to descend into the scrotum, remaining in the ab- H Genetic predisposition
domen or inguinal canal or at the external ring
H May be bilateral, but more commonly affects the Incidence
right testis (see Varieties of cryptorchidism) H Occurs in 30% of premature male neonates, but in
only 3% of those born at term
Pathophysiology H In about 80% of affected infants: testes descend
H In the male fetus, testosterone normally stimulates spontaneously during first year; in the rest: testes
the formation of the gubernaculum. A fibromuscular may descend later
band connects the testes to the scrotal floor.
H This band probably helps pull the testes into the Common characteristics
scrotum by shortening as the fetus grows. H Testis on the affected side not palpable in the scro-
H Thus, cryptorchidism may result from inadequate tum; underdeveloped scrotum (unilateral cryp-
testosterone levels or a defect in the testes or the gu- torchidism)
bernaculum. H Scrotum enlarged on the unaffected side
H Because the testis is maintained at a higher tempera- H Infertility
ture, spermatogenesis is impaired, leading to re-
duced fertility.

Varieties of cryptorchidism

Descent interrupted beyond Partially descended Testis retained in

external inguinal ring abdomen

Descended but not to Normal

bottom of scrotum

218 Cryptorchidism
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Complications
H Sterility
H Increased risk for testicular cancer
H Increased vulnerability of the testes to trauma

Assessment
Physical findings
H Nonpalpable testes
H Underdeveloped scrotum

Test results
Laboratory
H Buccal smear (cells from oral mucosa) determines
genetic sex (a male sex chromatin pattern).
H Serum gonadotropin confirms the presence of testes
by showing presence of circulating hormone.

Treatment
Medications
H Human chorionic gonadotropin

Surgery
H Orchiopexy

Nursing considerations
Key outcomes
The patient will:
H express or demonstrate feelings of increased comfort
H be free from complications.

Nursing interventions
H Encourage the parents of the child with undescended
testes to express their concern about his condition.
H Tell the parents that a rubber band may be taped to
the patients thigh for about 1 week after surgery to
keep the testis in place. Explain that his scrotum may
swell but shouldnt be painful.
Monitoring
After surgery
H Vital signs
H Intake and output
H Operative site
H Pain control

Patient teaching
Be sure to cover:
H the disorder, treatment, and effect on reproduction
H surgery or medications prescribed.

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Cushings syndrome H Menstrual disturbances

H Sexual dysfunction
H Psychiatric problems, ranging from mood swings to
frank psychosis
Overview
Description Assessment
H Clinical manifestations of glucocorticoid excess, par-
ticularly cortisol History
H May also reflect excess secretion of mineralocorti- H Use of synthetic steroids
coids and androgens H Fatigue
H Classified as primary, secondary, or iatrogenic, de- H Muscle weakness
pending on etiology H Sleep disturbances
H Prognosis dependent on early diagnosis, identifica- H Polyuria
tion of underlying cause, and effective treatment H Thirst
H Frequent infections
Pathophysiology H Water retention
H A loss of normal feedback inhibition by cortisol H Amenorrhea
occurs. H Decreased libido
H Elevated levels of cortisol dont suppress hypothala- H Irritability; emotional instability
mic and anterior pituitary secretion of corticotropin- H Symptoms resembling those of hyperglycemia
releasing hormone and adrenocorticotropic hor- H Impotence
mone (ACTH). H Headache
H The result is excessive levels of circulating cortisol.
Physical findings
Causes H Thin hair
H Pituitary microadenoma H Moon-shaped face
H Excess production of corticotropin H Hirsutism
H Corticotropin-producing tumor in another organ H A buffalo-humplike back
H Chronic use of synthetic glucocorticoids or corti- H Thin extremities
cotropin H Muscle wasting and weakness
H Cortisol-secreting adrenal tumor H Petechiae, ecchymoses, and purplish striae
H Delayed wound healing
H Swollen ankles
Special populations
H Hypertension
In neonates, the usual cause of Cushings syndrome H Central obesity
is adrenal carcinoma. H Acne

Test results
Incidence Laboratory
H More common in females than in males H Salivary free cortisol level is elevated.
H Can affect a person at any age H ACTH is decreased in adrenal disease and excess
pituitary or ectopic secretion of ACTH is increased.
Common characteristics H Blood chemistry may show hypernatremia, hypo-
H Adiposity of the face, neck, and trunk kalemia, hypocalcemia, and elevated blood glucose
H Purple striae on the skin level.
H Truncal weight gain H Urinary free cortisol level is elevated.
H Glucose intolerance H Serum cortisol level is elevated in the morning.
H Glycosuria occurs.
Complications Imaging
H Osteoporosis and pathologic fractures H Ultrasonography, computed tomography scan, and
H Peptic ulcer magnetic resonance imaging may show the location
H Dyslipidemia of a pituitary or adrenal tumor.
H Impaired glucose tolerance Diagnostic procedures
H Diabetes mellitus H A low-dose dexamethasone suppression test shows
H Frequent infections failure of plasma cortisol levels to be suppressed.
H Slow wound healing
H Suppressed inflammatory response
H Hypertension
H Ischemic heart disease; heart failure

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With transsphenoidal approach to

Treatment hypophysectomy
H Keep the head of the bed elevated at least 30 degrees.
General H Maintain nasal packing.
H Management to restore hormone balance and re- H Provide frequent mouth care.
verse Cushings syndrome, including radiation, drug H Avoid activities that increase intracranial pressure
therapy, or surgery (ICP).
H High-protein, high-potassium, low-calorie, low-
sodium diet Monitoring
H Activity, as tolerated H Vital signs
H Intake and output
Medications H Daily weights
H Antihypertensive such as atenolol H Serum electrolyte results
H Diuretic such as furosemide After bilateral adrenalectomy and
H Glucocorticoid such as dexamethasone hypophysectomy
H Potassium supplements H Neurologic status
H Antihormone agents, such as ketoconazole, amino- H Severe nausea, vomiting, and diarrhea
glutethimide, and mitotane H GI status
H Pituitary hormone such as pitressin H Adrenal hypofunction
H Increased ICP
H Hypopituitarism
ALERT
H Transient diabetes insipidus
Glucocorticoid administration on the morning of H Hemorrhage and shock
surgery can help prevent acute adrenal insufficien- After transsphenoidal approach to
cy during surgery. Cortisol therapy is essential dur- hypophysectomy
ing and after surgery to help the patient tolerate H Cerebrospinal fluid leak
the physiologic stress caused by removal of the
pituitary or adrenal glands.
Patient teaching
Surgery Be sure to cover:
H Possible hypophysectomy or pituitary irradiation H the disorder, diagnosis, and treatment
H Bilateral adrenalectomy H medications and possible adverse effects
H Excision of nonendocrine, corticotropin-producing H when to notify the physician
tumor, followed by drug therapy H lifelong steroid replacement
H signs and symptoms of adrenal crisis
H medical identification bracelet
Nursing considerations H prevention of infection
H stress reduction strategies.
Key outcomes
The patient will: Discharge planning
H maintain skin integrity H Refer the patient to a mental health professional for
H remain free from infection additional counseling, if necessary.
H perform activities of daily living as tolerated within
the confines of the disorder
H express positive feelings about self
H express understanding of disorder.

Nursing interventions
H Give prescribed drugs.
H Consult a dietitian.
H Use protective measures to reduce the risk of
infection.
H Use meticulous hand-washing technique.
H Schedule adequate rest periods.
H Institute safety precautions.
H Provide meticulous skin care.
H Encourage verbalization of feelings.
H Offer emotional support.
H Help to develop effective coping strategies.

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Cystic fibrosis H Dyspnea

H Poor weight gain

Complications
Overview H Bronchiectasis
H Pneumonia
Description H Atelectasis
H Chronic, progressive, inherited, incurable disease af- H Dehydration
fecting exocrine (mucus-secreting) glands H Distal intestinal obstructive syndrome
H Transmitted as an autosomal recessive trait H Malnutrition
H Genetic mutation that involves chloride transport H Gastroesophageal reflux
across epithelial membranes (more than 100 specif- H Cor pulmonale
ic mutations of the gene identified) H Hepatic disease
H Characterized by major aberrations in sweat gland, H Diabetes
respiratory, and GI functions H Arthritis
H Accounts for almost all cases of pancreatic enzyme H Biliary disease
deficiency in children H Clotting problems
H Signs and symptoms apparent soon after birth or not H Retarded bone growth
for several years H Delayed sexual development
H Death typically from pneumonia, emphysema, or H Azoospermia in males
atelectasis H Secondary amenorrhea in females
H Electrolyte imbalances
Pathophysiology H Cardiac arrhythmias
H The viscosity of bronchial, pancreatic, and other mu- H Potentially fatal shock
cous gland secretions increases, obstructing glandu- H Death
lar ducts.
H The accumulation of thick, tenacious secretions in
the bronchioles and alveoli causes respiratory Assessment
changes, eventually leading to severe atelectasis and
emphysema. History
H The disease also causes characteristic GI effects in H Recurring bronchitis and pneumonia
the intestines, pancreas, and liver. H Nasal polyps and sinusitis
H Obstruction of the pancreatic ducts results in a defi- H Wheezing
ciency of trypsin, amylase, and lipase. This prevents H Dry, nonproductive cough
the conversion and absorption of fat and protein in H Shortness of breath
the intestinal tract and interferes with the digestion of H Abdominal distention, vomiting, constipation
food and absorption of fat-soluble vitamins. H Frequent, bulky, foul-smelling, and pale stool with a
H In the pancreas, fibrotic tissue, multiple cysts, thick high fat content
mucus, and fat replace the acini, producing signs of H Poor weight gain
pancreatic insufficiency. H Poor growth
H Ravenous appetite
Causes H Hematemesis
H Autosomal recessive mutation of gene on chromo-
some 7 Special populations
H Causes of symptoms: increased viscosity of bronchial,
pancreatic, and other mucous gland secretions and Neonates may exhibit meconium ileus and develop
consequent destruction of glandular ducts symptoms of intestinal obstruction, such as ab-
dominal distention, vomiting, constipation, dehy-
Incidence dration, and electrolyte imbalance.
H Most common fatal genetic disease of white children
H Twenty-five percent chance of transmission with each
pregnancy: both parents carriers of the recessive Physical findings
gene H Wheezy respirations
H Highest in people of northern European ancestry H Dry, nonproductive, paroxysmal cough
H Less common in Blacks, Native Americans, and peo- H Dyspnea
ple of Asian ancestry H Tachypnea
H Equally common in both sexes H Bibasilar crackles and hyperresonance
H Barrel chest
Common characteristics H Cyanosis, and clubbing of the fingers and toes
H Wheezy respirations H Distended abdomen
H Dry, nonproductive, paroxysmal cough H Thin extremities

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H Sallow skin with poor turgor

H Delayed sexual development
H Neonatal jaundice
H Hepatomegaly
H Rectal prolapse
H Failure to thrive
Test results
Laboratory
H Sweat test reveals sodium and chloride values.
H Stool specimen analysis shows absence of trypsin.
H Deoxyribonucleic acid testing shows presence of the
delta F 508 deletion.
H Liver enzyme tests may show hepatic insufficiency.
H Sputum culture may show such organisms as
Pseudomonas and Staphylococcus.
H Serum albumin level is decreased.
H Serum electrolytes may show hypochloremia and
hyponatremia.
H Arterial blood gas shows hypoxemia.
Imaging
H Chest X-rays may show early signs of lung obstruc-
tion.
H High-resolution chest computed tomography scan
shows bronchial wall thickening, cystic lesions, and
bronchiectasis.
Diagnostic procedures
H Pulmonary function tests show decreased vital capac-
ity, elevated residual volume, and decreased forced
expiratory volume in 1 second.
Nursing considerations
Key outcomes
The patient will:
H maintain a patent airway and adequate ventilation
H consume adequate calories daily
H use a support system to assist with coping
H express an understanding of the illness.
Nursing interventions
H Give prescribed drugs.
H Administer pancreatic enzymes with meals and
snacks.
H Perform chest physiotherapy and postural drainage.
H Administer oxygen therapy, as needed.
H Provide a well-balanced, high-calorie, high-protein
diet; include adequate fats.
H Provide vitamin A, D, E, and K supplements, if indi-
cated.
H Ensure adequate oral fluid intake.
H Provide exercise and activity periods.
H Encourage breathing exercises.
H Provide the young child with play periods.
H Enlist the help of the physical therapy department
and play therapists, if available.
H Provide emotional support.
H Include family members in all phases of the childs
care.
H Keep the head of the bed elevated at least 30 degrees.

Monitoring
Treatment H Vital signs
H Intake and output
General H Daily weight
H Based on organ systems involved H Hydration and nutrition
H Chest physiotherapy, nebulization, and breathing ex- H Pulse oximetry
ercises several times per day H Respiratory status
H Postural drainage H GI status
H Gene therapy (experimental)
H Salt supplements
H High-fat, high-protein, high-calorie diet Patient teaching
H Activity, as tolerated, encouraged
Be sure to cover:
Medications H the disorder, diagnosis, and treatment
H Pulmonary enzyme, such as dornase alfa, given by H medications and possible adverse effects
aerosol nebulizer H when to notify the physician
H Antibiotic, as appropriate H aerosol therapy
H Oxygen therapy, as needed H chest physiotherapy
H Oral pancreatic enzymes such as pancreatin H signs and symptoms of infection
H Bronchodilator such as albuterol H complications.
H Corticosteroid such as prednisone
H Vitamin A, D, E, and K supplements Discharge planning
H Annual influenza vaccination H Refer family members for genetic counseling, as
appropriate.
Surgery H Refer the patient and his family to a local support
H Heart-lung transplantation group such as the Cystic Fibrosis Foundation.
H Feeding tube placement for nutritional support

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Cytomegalovirus Neonatal complications

H Stillbirth

infection H Neonatal retinitis

H Microcephaly
H Mental retardation
H Seizures
Overview H Hearing loss
H Thrombocytopenia
Description H Hemolytic anemia
H Infection with a member of the herpesvirus group
H Also called generalized salivary gland disease and
cytomegalic inclusion disease Assessment
Pathophysiology History
H Cytomegalovirus (CMV) is found in the saliva, urine, H Immunosuppressive condition
semen, breast milk, feces, blood, and vaginal and
cervical secretions of infected people. It can be de- Physical findings
tected in body fluids for weeks or months after infec- H Fever common
tion. H Lethargy
H CMV usually remains latent, but reactivation occurs H In immunocompetent patient with CMV mononucleo-
when T-lymphocyte-mediated immunity is compro- sis, 3 or more weeks of irregular high fever may be
mised, as in organ transplantation, lymphoid neo- only finding
plasms, and certain acquired immunodeficiencies. H Tachypnea
H CMV spreads through the body in lymphocytes or H Dyspnea
mononuclear cells to the lungs, liver, GI tract, eyes, H Cyanosis
and central nervous system (CNS), typically produc- H Cough
ing inflammatory reactions. H Jaundice
H Spider angiomas
Causes H Hepatomegaly
H Results from a deoxyribonucleic acid virus belonging H Splenomegaly
to the herpes family H In infants, CNS damage (mental retardation, hearing
H Transmitted by human contact; once infected, CMV loss, seizures), jaundice, petechial rash, respiratory
carried for life distress
H Transmission through direct contact with secretions
and excretions, through blood transfusions, transpla- Test results
centally, and through transplanted organs Laboratory
H Isolating the virus or demonstrating increasing sero-
Risk factors logic titers by complement fixation studies, hemag-
H Poor hygiene glutination inhibition antibody tests and, in congeni-
H Immunosuppression tal infections, indirect immunofluorescent tests for
H Child care workers CMV immunoglobulin M antibody allows diagnosis.
Imaging
Incidence H Chest X-ray reveals bilateral, diffuse, white infiltrates.
H Occurs worldwide H Computed tomography scan or magnetic resonance
H Occurs in approximately 30% to 50% of acquired imaging shows CNS involvement.
immunodeficiency syndrome patients Diagnostic procedures
H One of the most opportunistic pathogens in patients H Endoscopy shows GI involvement.
infected with human immunodeficiency virus H Fundoscopy may show retinitis.

Common characteristics
H Mild fatigue, myalgia, and headache or no clinical Treatment
symptoms
General
Complications H Rest, as needed
H Pneumonia
H Hepatitis Medications
H Ulceration of the GI tract and esophagus H Antivirals, such as cidofovir and ganciclovir
H Retinitis H Immune serum such as cytomegalovirus immune
H Encephalopathy globulin

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Nursing considerations
Key outcomes
The patient will:
H maintain normal temperature
H maintain adequate caloric intake
H demonstrate skill in conserving energy while carrying
out daily activities to tolerance level
H verbally report having an increased energy level
H articulate factors that intensify pain and modify be-
havior accordingly
H maintain respiratory rate within 5 breaths of baseline
H express feeling of comfort while maintaining air
exchange.
Nursing interventions
H Institute standard precautions.
H Give prescribed drugs.
H If vision impairment occurs, provide a safe environ-
ment and encourage optimal independence.
Monitoring
H Intake and output
H Ventilation and oxygenation if the respiratory system
involved
H Vital signs

Patient teaching
Be sure to cover:
H proper hand-washing technique
H need for parents to wear gloves when in contact with
secretions or changing diapers and to dispose of dia-
pers or soiled articles properly and wash hands thor-
oughly
H need for female health care workers trying to get
pregnant to have CMV titers drawn to identify their
risk of contracting the infection
H need for an immunosuppressed or pregnant patient
to avoid contact with any person who has confirmed
or suspected CMV infection
H need for an immunosuppressed patient whos CMV-
seronegative to carry this information with him so he
wont be given CMV-positive blood.
Discharge planning
H Provide emotional support and counseling to the
parents of a child with severe CMV infection. Help
them find support systems, and coordinate referrals
to other health care professionals.
H For information and support, refer the patient and
his family to a local chapter of the National Center for
Infectious Diseases.

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DDacryocystitis
Overview
Description
H Infection of the lacrimal sac resulting from obstruc-
tion of the nasolacrimal duct
H Acute, chronic, or congenital

Pathophysiology
H The lacrimal excretory system is a mucous mem-
brane-lined tract thats contiguous with conjuctival
and nasal mucosa.
Risk factors
H Congenital blockage of nasolacrimal duct

Incidence
H More common in adults older than age 40
H More common on the left side than the right side
H Rare in blacks
H Affects females more commonly than males

Common characteristics
Acute form
H Sudden onset of pain
H Redness in the medial canthal region
Chronic form
H Incidious onset of watery eyes
H Conjuctival and nasal mucosa are normally colonized
with bacteria. Complications
H Inability to drain tears due to a blocked lacrimal H Hemorrhage
drainage system results in infection. (See A close H Infection
look at tears.) H Cerebrospinal fluid leakage

Causes
Acute form Assessment
H Staphylococcus aureus
H Beta-hemolytic streptococci History
Chronic form H Eye pain
H Streptococcus pneumonia H Fever
H Fungus, such as Actinomyces or Candida albicans
H Chronic mucosal degeneration
H Secondary tumors from sinuses, nose, and eye orbits

A close look at tears

Tears begin in the lacrimal gland and drain through the nasolacrimal duct into the nose.

Lacrimal gland

Punctum
Iris

Lacrimal canals
Pupil

Lacrimal sac
Sclera

Nasolacrimal duct

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Physical findings
H Severe erythematous swelling around nasal aspect of Patient teaching
lower eyelid
H Tenderness of eyelid Be sure to cover:
H Tearing H the disorder, diagnosis, and treatment
H Conjunctival injection H applying warm compresses and eyedrops
H Palpable mass inferior to the medial canthal tendon H reporting signs of worsening infection.
H Decreased visual acuity
H Orbital cellulitis

Test results
Laboratory
H Culture of discharge shows causative organism.
H Complete blood count shows elevated white blood
cell count.
Imaging
H X-ray after injection of radiopaque medium locates
atresia.
H Dacryocystography and dacryoscintigraphy identify
anatomical abnormalities of the nasolacrimal
drainage system.

Treatment
General
H Warm compresses
H Activity, as tolerated

Medications
H Antibiotic eyedrops such as polymyxin/trimethoprim
H Antibiotics, such as gentamicin, amoxicillin, and
clavulanate potassium
Surgery
H Incision and drainage
H Dacryocystorhinostomy (chronic cases)

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort
H remain free from signs of infection.

Nursing interventions
H Administer prescribed antibiotics.
H Apply compresses.

Monitoring
H Temperature
H Pain
H Visual acuity

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Dermatitis H Exposure to an allergen or irritant

H Intense itching

Physical findings
Overview H Depend on type of dermatitis
H Erythematous patches in excessively dry areas
Description
H Skin condition characterized by inflammation Special populations
H Can be acute or chronic
H Occurs in several forms, including contact, seborrhe- In children, look for lesions on the forehead,
ic, nummular, exfoliative, and stasis dermatitis (see cheeks, and extensor surfaces of the arms and legs.
Types of dermatitis, pages 230 and 231)
H Typically associated with other atopic diseases H Lesions usually at flexion points in adults
H During a flare-up: edema, scaling, and vesiculation;
Pathophysiology pus-filled vesicles
H The allergic mechanism of hypersensitivity results in H In chronic disease: multiple areas of dry, scaly skin,
a release of inflammatory mediators through sensi- with white dermatographism, blanching, and licheni-
tized antibodies of immunoglobulin (Ig) E. fication
H Histamine and other cytokines induce an inflamma-
tory response resulting in edema, skin breakdown, Test results
and pruritus. H Results depend on type of dermatitis.
Laboratory
Causes H Serum analysis shows elevated IgE levels.
H Exact cause unknown H Tissue cultures may rule out bacterial, viral, or fun-
H Possible underlying metabolic or biochemical causes gal superinfections.
H Possible genetic link to elevated serum IgE levels H Allergy testing may disclose allergic rhinitis or
H Possible defective T-cell function asthma.
H Precipitating factors: Diagnostic procedures
Infections H Patch testing and distribution of lesions are used to
Allergens pinpoint the provoking allergen.
Temperature extremes Other
Humidity H Firm stroking of the patients skin with a blunt instru-
Sweating ment causes a white not reddened hive to ap-
Stress pear on the skin of 70% of patients with atopic der-
matitis.
Incidence H Food elimination diet may help to identify at least one
H Common in infants and toddlers between ages 6 allergen.
months and 2 years
H Common in those with strong family histories of
atopic disease Treatment
Common characteristics General
H Pruritus H Dependent on type of dermatitis
H Skin lesions H Elimination of allergens
H Avoidance of precipitating factors
Complications H Ultraviolet B light therapy to increase the thickness of
H Permanent skin damage the stratum corneum
H Lichenification H Avoidance of food allergens
H Altered pigmentation H Avoidance of overheating
H Scarring
H Bacterial, fungal, and viral infections Medications
H Kaposis varicelliform eruption H Antihistamines, such as diphenhydramine
H Corticosteroids, such as betamethasone and hydro-
cortisone
Assessment H Antibiotics such as gentamicin
H Antifungals such as ketoconazole
History H Antivirals such as acyclovir
H Depends on type of dermatitis H Antipruritics such as hydroxyzine hydrochloride
H Family history of atopic dermatitis

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Surgery
H Vein stripping, sclerotherapy, or skin grafts in stasis
dermatitis

Nursing considerations
Key outcomes
The patient will:
H exhibit improved or healed lesions or wounds
H avoid complications
H demonstrate understanding of skin care regimen
H verbalize feelings about altered body image.

Nursing interventions
Nursing interventions are guided by the type of dermati-
tis.
H Assist with daily skin care, and avoid using perfumed
soaps.
H Apply intermittent occlusive dressings to lichenified
skin.
H Apply cool, moist compresses.
H Encourage verbalization of feelings.
H Offer emotional support and reassurance.
H Administer medications as prescribed.
H Prevent rubbing and scratching of the affected area.

Monitoring
H Adverse reactions
H Response to treatment
H Complications

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H skin care
H prescribed medications and possible adverse effects
H signs and symptoms of corticosteroid overdose and
notifying the practitioner immediately if they occur
H control of pruritus
H meticulous hand washing and good personal hygiene
H use of plain, tepid water (96 F [35.6 C]) and non-
perfumed soaps
H application of occlusive dressings when skin is
lichenified
H application of wet-to-dry dressings
H identification and avoidance of aggravating factors
H avoidance of temperature extremes.

Discharge planning
H Refer the patient to the American Academy of Derma-
tology.

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Types of dermatitis

Type Causes Assessment Diagnosis Treatment

findings and intervention
CHRONIC DERMATITIS

Characterized by Usually un- Thick, lichenified, sin- No characteris- Elimination of known aller-
inflammatory known but may gle or multiple lesions tic pattern or gens and decreased exposure
eruptions of the result from pro- on any part of the course; diag- to irritants, wearing protective
hands and feet gressive contact body (commonly on nosis based on clothing such as gloves, and
dermatitis the hands) detailed history washing immediately after
Secondary fac- Inflammation and and physical contact with irritants or aller-
tors: trauma, scaling findings gens
infections, re- Recurrence after long Antibiotics for secondary in-
distribution of remissions fection
normal flora, Avoidance of excessive wash-
photosensitivity, ing and drying of hands and
and food sensi- of accumulation of soaps and
tivity, which detergents under rings
may perpetuate Use of emollients with topical
this condition steroids

CONTACT DERMATITIS

Commonly, Mild irritants: Mild irritants and al- Patient history Same as for chronic dermati-
sharply demarcat- chronic expo- lergens: erythema and Patch testing tis
ed skin inflamma- sure to deter- small vesicles that to identify al- Topical anti-inflammatories
tion and irritation gents or sol- ooze, scale, and itch lergens (such as steroids), systemic
due to contact vents Strong irritants: blis- Shape and dis- steroids for edema and bullae,
with concentrated Strong irritants: ters and ulcerations tribution of le- antihistamines, and local ap-
substances to damage on con- Classic allergic re- sions plications of Burows solution
which the skin is tact with acids sponse: clearly de- (for blisters)
sensitive, such as or alkalis fined lesions, with Other nursing interventions
perfumes or Allergens: sen- straight lines follow- similar to those for atopic der-
chemicals sitization after ing points of contact matitis
repeated expo- Severe allergic reac-
sure tion: marked edema
of affected areas

EXFOLIATIVE DERMATITIS

Severe, chronic Progression of Generalized dermati- Identification Hospitalization, with protec-

skin inflammation preexisting skin tis, with acute loss of of the underly- tive isolation and hygienic
characterized by lesions to exfo- stratum corneum, and ing cause measures to prevent sec-
redness and wide- liative stage, as erythema and scaling ondary bacterial infection
spread erythema in contact der- Sensation of tight skin Open wet dressings, with col-
and scaling matitis, drug re- Hair loss loidal baths
action, lym- Possibly fever, sensi- Bland lotions over topical
phoma, or tivity to cold, shiver- steroids
leukemia ing, gynecomastia, Maintenance of constant envi-
and lymphadenopathy ronmental temperature to pre-
vent chilling or overheating
Careful monitoring of renal
and cardiac status
Systemic antibiotics and
steroids
Other nursing interventions
similar to those for atopic der-
matitis

LOCALIZED NEURODERMATITIS (LICHEN SIMPLEX CHRONICUS, ESSENTIAL PRURITUS)

Superficial skin Chronic Intense, sometimes Physical find- Scratching must stop; then
inflammation scratching or continual scratching ings erosions will disappear in
characterized by rubbing of a Thick, possibly dry, 2 weeks
itching and papu- primary lesion scaly lesions, with Fixed dressing or Unnas boot
lar eruptions that or insect bite, sharp borders and to cover affected area
appear on thick- or other skin raised papules Topical steroids (occlusive
ened, hyperpig- irritation Usually affects easily dressings or intralesional in-
mented skin reached areas, such jections)
as ankles, lower legs, Antihistamines and open wet
anogenital area, back dressings
of neck, and ears Emollients

230 Dermatitis
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Types of dermatitis (continued)

Type Causes Assessment Diagnosis Treatment

findings and intervention
NUMMULAR DERMATITIS

Chronic form of Possibly precip- Round, nummular Physical find- Elimination of known irritants
dermatitis charac- itated by stress; (coin-shaped) lesions, ings and pa- Measures to relieve dry skin:
terized by coin- or dryness, irri- usually on arms and tient history; increased humidification, lim-
shaped, vesicular, tants, or legs, with distinct bor- history of ited frequency of baths and
crusted scales scratching ders of crusts and atopic dermati- use of bland soap and bath
and, possibly, pru- scales tis in middle- oils, and application of emol-
ritic lesions Possibly oozing and aged or older lients
severe itching patient Wet dressings in acute phase
Summertime remis- Exclusion of Topical steroids (occlusive
sions common, with fungal infec- dressings or intralesional in-
wintertime recurrence tions, atopic or jections) for persistent lesions
contact der- Tar preparations and antihis-
matitis, and tamines for itching and anti-
psoriasis biotics for infection
Other interventions similar to
those for atopic dermatitis

SEBORRHEIC DERMATITIS

An acute or sub- Unknown; Eruptions in areas Patient history Removal of scales by frequent
acute disease that stress and neu- with many sebaceous and physical washing and shampooing
affects the scalp, rologic condi- glands (usually scalp, findings, espe- with selenium sulfide suspen-
face and, occa- tions may be face, and trunk) and cially distribu- sion, zinc pyrithione, tar and
sionally, other ar- predisposing in skin folds tion of lesions salicylic acid shampoo or ke-
eas and is charac- factors Itching, redness, and in sebaceous toconazole shampoo
terized by lesions inflammation of af- gland areas Application of topical steroids
covered with yel- fected areas; lesions Exclusion of and antifungal agents to non-
low or brownish that may appear psoriasis hairy areas
gray scales greasy; possibly For infants, baby shampoo
fissures
Indistinct, occasion-
ally yellowish scaly
patches from excess
stratum corneum
(dandruff may be mild
seborrheic dermatitis)

STASIS DERMATITIS

Condition usually Secondary to Varicosities and Positive his-
caused by im- peripheral vas- edema common, but
paired circulation cular diseases obvious vascular in-
and characterized affecting legs, sufficiency not always
by eczema of the such as recur- present
legs with edema, rent thrombo- Usually affects the
hyperpigmenta- phlebitis and re- lower leg, just above
tion, and persis- sultant chronic internal malleolus, or
tent inflammation venous insuffi- sites of trauma or irri-
ciency tation
Early signs: dusky red
deposits of hemo-
siderin in skin, with
itching and dimpling
of subcutaneous tis-
sue; later signs:
edema, redness, and
scaling of large area
of legs
Possibly fissures,
crusts, and ulcers
Measures to prevent venous
tory of venous stasis: avoidance of prolonged
insufficiency sitting or standing, use of
and physical support stockings, and weight
findings such reduction for obese patients
as varicosities Corrective surgery for under-
lying cause
After ulcer develops, rest peri-
ods with legs elevated; open
wet dressings; Unnas boot
(provides continuous pres-
sure to areas); and antibiotics
for secondary infection after
wound culture

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Developmental H Can be unilateral or bilateral

H Occurs in three forms of varying severity (see De-

dysplasia of the hip grees of hip dysplasia)

Pathophysiology
H Excessive or abnormal movement of the joint during
Overview a traumatic birth may cause dislocation.
H Displacement of bones within the joint may damage
Description joint structures, including articulating surfaces,
H An abnormality of the hip joint present at birth blood vessels, tendons, ligaments, and nerves.
H Most common disorder affecting the hip joints in H Disruption of blood flow to the joint may lead to is-
children younger than age 3 chemic necrosis.
Causes
Degrees of hip dysplasia H Unknown
Normally, the head of the femur fits snugly into the Risk factors
acetabulum, allowing the hip to move properly. In
developmental hip dysplasia, flattening of the acetabulum H Breech delivery
prevents the head of the femur from rotating adequately. H Elevated maternal relaxin (hormone secreted by the
The childs hip may be unstable, subluxated (partially corpus luteum during pregnancy that causes relax-
dislocated), or completely dislocated, with the femoral ation of pubic symphysis and cervical dilation)
head lying totally outside the acetabulum. The degree of H Large neonates and twins
dysplasia and the childs age are considered in
determining the treatment choice. Incidence
H About 85% of cases: female
NORMAL HIP
Common characteristics
H Level of knees uneven
H Limited abduction on the dislocated side
H Buttock fold on the affected side higher with the
child lying prone (see Ortolanis and Trendelen-
Acetabulum burgs signs)
Head of the femur
Complications
H Degenerative hip changes
H Abnormal acetabular development
H Lordosis (abnormally increased concave curvature of
the lumbar and cervical spine)
SUBLUXATED HIP H Joint malformation
H Sciatic nerve injury (paralysis)
H Avascular necrosis of femoral head
H Soft tissue damage
H Permanent disability

Assessment
History
H Traumatic birth
H Large birth size
DISLOCATED HIP H Twin

Physical findings
H Extra fold on the thigh of the affected side
H Limited abduction on the dislocated side
H Level of knees uneven
H Swaying from side to side (duck waddle) because
of uncorrected bilateral dysplasia
H Limp due to uncorrected unilateral dysplasia

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Test results Ortolanis and Trendelenburgs signs

Imaging
H X-rays show the location of the femur head and a
shallow acetabulum.
H Computed tomography scan shows the location and
extent of the deformity.
H Sonography and magnetic resonance imaging assess
reduction.
Other
H Physical examination helps to confirm the diagnosis.
Treatment
Treatment of developmental dysplasia of the hip varies
with the patients age.
Younger than age 3 months:
H Gentle manipulation to reduce the dislocation, fol-
lowed by splint-brace or Pavlik harness
H Splint-brace or Pavlik harness worn continuously for
2 to 3 months, then a night splint for another month
Older than age 3 months:
H Bilateral skin traction (in infants) or skeletal traction
(in children who have started walking)
H Bryants traction or divarication traction (both ex-
tremities placed in traction, even if only one is affect-
ed, to help maintain immobilization) for children
younger than 3 years and weighing less than 35 lb
(15.9 kg) for 2 to 3 weeks
H Immobilization in a spica cast for about 3 months for
children ages 6 to 12 months
Special populations
Treatment begun after age 5 rarely restores satis-
factory hip function.
A positive Ortolanis or Trendelenburgs sign confirms
developmental dysplasia of the hip.
Ortolanis sign
H Place the infant on his back, with hip flexed and in
abduction. Adduct the hip while pressing the femur
downward.
H Next, abduct the hip while moving the femur upward. A
click or a jerk (produced by the femoral head moving
over the acetabular rim) indicates subluxation in an
infant younger than 1 month. The sign indicates
subluxation or complete dislocation in an older infant.
Trendelenburgs sign
H When the child rests his weight on the side of the
dislocation and lifts his other knee, the pelvis drops on
the normal side because abductor muscles in the
affected hip are weak.
H However, when the child stands with his weight on the
normal side and lifts the other knee, the pelvis remains
horizontal.
H achieve the highest level of mobility possible within
the confines of the disease.
Nursing interventions
H Provide reassurance to the parents.
H Turn the child every 2 hours.
H Provide appropriate cast care.
Monitoring
H Parental care of cast or equipment
H Skin integrity
H Color, sensation, and motion of the infants legs and
feet
H Comfort

General Patient teaching

H Activity, as tolerated
H No dietary restrictions
Surgery
H Gentle closed reduction under general anesthesia to
further abduct the hips, followed by a spica cast for 3
months (if traction fails)
H In children older than age 18 months, open reduc-
tion and pelvic or femoral osteotomy to correct bony
deformity, followed by immobilization in a spica cast
for 6 to 8 weeks
H In children ages 2 to 5 years, skeletal traction and
subcutaneous adductor tenotomy (surgical cutting of
the tendon)
Be sure to cover:
H how to correctly splint or brace the hips, as ordered
H good hygiene
H signs and symptoms of cast compression (cyanosis,
cool extremities, or pain).
Discharge planning
H Stress the need for frequent checkups.
H Refer the child and parents to a child life specialist to
ensure continued developmental progress.

Nursing considerations
Key outcomes
The patient will:
H maintain joint mobility and range of motion
H maintain muscle strength

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Diabetes insipidus H Polydipsia

H Weight loss
H Fatigue

Overview Complications
H Hypovolemia
Description H Hyperosmolality
H Disorder in which secretion of antidiuretic hormone H Circulatory collapse
is inadequate, causing an inability to concentrate H Loss of consciousness
urine H CNS changes
H Two types: primary and secondary H Bladder distention
H May occur transiently during pregnancy, usually after H Hydroureter
the fifth or sixth month of gestation H Hydronephrosis
H Impaired or absent thirst mechanism increasing risk
of complications
H If uncomplicated, prognosis good Assessment
H If complicated by underlying disorder, such as can-
cer, prognosis variable History
H Also referred to as DI H Abrupt onset of extreme polyuria
H Extreme thirst
Pathophysiology H Extraordinarily large oral fluid intake
H Vasopressin (antidiuretic hormone) is synthesized in H Weight loss
the hypothalamus and stored by the posterior pitu- H Dizziness; weakness; fatigue
itary gland. H Constipation
H Once released into the general circulation, vaso- H Nocturia
pressin acts on the distal and collecting tubules of
the kidneys. Special populations
H Vasopressin increases the water permeability of the
tubules and causes water reabsorption. In children, reports of enuresis, sleep disturbances,
H The absence of vasopressin allows filtered water to irritability, anorexia, thirst, and decreased weight
be excreted in the urine instead of being reabsorbed. gain and linear growth are common.
Causes
H Failure of vasopressin secretion in response to nor- Physical findings
mal physiologic stimuli H Signs of dehydration
H Failure of the kidneys to respond to vasopressin, H Fever
called nephrogenic DI H Dyspnea
H Familial H Pale, voluminous urine
H Idiopathic H Poor skin turgor
H Congenital malformation of the central nervous sys- H Tachycardia
tem (CNS) H Decreased muscle strength
H Infection H Hypotension
H Trauma
H Tumors Test results
H Neurosurgery, skull fracture, or head trauma Laboratory
H Granulomatous disease H Urinalysis shows colorless urine with specific gravity
H Vascular lesions 1.005 or less and osmolality less than 200 mOsm/kg.
H Psychogenic H 24-hour urine sample shows decreased specific grav-
H Pregnancy (gestational DI) ity and increased volume.
H Damage to hypothalamus or pituitary gland H Serum chemistries show elevated sodium, blood urea
H Certain medications such as lithium nitrogen (BUN), and creatinine levels.
H Serum osmolality is increased.
Incidence H Serum vasopressin level is decreased.
H Affects males and females equally Diagnostic procedures
H Primary DI in 50% of patients H Dehydration test or water deprivation test shows an
increase in urine osmolality after vasopressin admin-
Common characteristics istration exceeding 9%.
H Polyuria with low specific gravity and osmolality H Magnetic resonance imaging may show a pituitary tu-
H Nocturia mor or brain tumor.
H Dehydration

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9400D.qxd 8/2/12 4:31 PM Page 235

H Computed tomography scan may reveal head trauma, H Signs and symptoms of hypovolemic shock
pituitary tumor, or brain tumor. H Changes in mental or neurologic status
H Cardiac rhythm

Treatment
Patient teaching
General
H Identification and treatment of underlying cause Be sure to cover:
H Control of fluid balance; administration of I.V. fluids H the disorder, diagnosis, and treatment
to match urine output H medications and possible adverse effects
H Dehydration prevention H when to notify the practitioner
H Free access to oral fluids H signs and symptoms of dehydration
H With nephrogenic DI, low-sodium diet H daily weight
H intake and output
Medications H use of a hydrometer to measure urine specific gravity
H Posterior pituitary hormones, such as vasopressin H need for medical identification jewelry
and desmopressin H need for ongoing medical care.
H Thiazide diuretics, such as hydrochlorothiazide, in
nephrogenic DI Discharge planning
H I.V. fluids: H Refer the patient to a mental health professional for
If serum sodium > 150 mEq/L: 5% dextrose in additional counseling, as indicated.
water
If serum sodium < 150 mEq/L: normal saline so-
lution
Surgery
H Not indicated, unless required to treat underlying
cause such as a tumor

Nursing considerations
Key outcomes
The patient will:
H demonstrate balanced fluid volume
H display adaptive coping behaviors
H avoid complications
H demonstrate normal laboratory values.

Nursing interventions
H Administer I.V. fluid to match urine output.
H Administer medications, as ordered.
H Provide meticulous skin and mouth care.

ALERT
Use caution when administering vasopressin to a
patient with coronary artery disease because it can
cause coronary artery constriction.

H Encourage verbalization of feelings.

H Offer encouragement while providing a realistic as-
sessment of the situation.
H Help the patient develop effective coping strategies.

Monitoring
H Intake and output
H Vital signs
H Daily weight
H Urine specific gravity
H Serum electrolytes and BUN

Diabetes insipidus 235

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Complications
Diabetes mellitus H Ketoacidosis
H Hyperosmolar hyperglycemic nonketotic syndrome
H Cardiovascular disease
Overview H Peripheral vascular disease
H Retinopathy, blindness
Description H Nephropathy
H Chronic disease of absolute or relative insulin defi- H Diabetic dermopathy
ciency or resistance H Impaired resistance to infection
H Characterized by disturbances in carbohydrate, pro- H Cognitive depression
tein, and fat metabolism H Hypoglycemia
H Two primary forms:
Type 1, characterized by absolute insufficiency Special populations
Type 2, characterized by insulin resistance with
varying degrees of insulin secretory defects Neonates of diabetic mothers have a two to three
times greater incidence of congenital malforma-
Pathophysiology tions and fetal distress, unless the mothers blood
H The effects of diabetes mellitus (DM) result from in- glucose levels are well-controlled before conception
sulin deficiency or resistance to endogenous insulin. and during pregnancy.
H Insulin allows glucose transport into the cells for use
as energy or storage as glycogen.
H Insulin also stimulates protein synthesis and free fatty Assessment
acid storage in the adipose tissues.
H Insulin deficiency compromises the body tissues ac- History
cess to essential nutrients for fuel and storage. H Polyuria, nocturia
H Dehydration
Causes H Polydipsia
H Genetic factors H Dry mucous membranes
H Autoimmune disease (type 1) H Poor skin turgor
H Weight loss and hunger
Risk factors H Weakness; fatigue
H Viral infections (type 1) H Vision changes
H Obesity (type 2) H Frequent skin and urinary tract infections
H Physiologic or emotional stress H Dry, itchy skin
H Sedentary lifestyle (type 2) H Sexual problems
H Pregnancy H Numbness or pain in the hands or feet
H Medication, such as thiazide diuretics, adrenal corti- H Postprandial feeling of nausea or fullness
costeroids, and hormonal contraceptives H Nocturnal diarrhea
Type 1
Incidence H Rapidly developing symptoms
H Type 1 usually occurs before age 30, although it Type 2
may occur at any age H Vague, long-standing symptoms that develop
H More common in males gradually
H Type 2 usually occurs in obese adults after age 30, H Family history of DM
although it may be seen in obese North American H Pregnancy
youths of African-American, Native American, or His- H Severe viral infection
panic descent H Other endocrine diseases
H Affects about 8% of the population of the United H Recent stress or trauma
States H Use of drugs that increase blood glucose levels
H About one-third of patients undiagnosed
H Increases with age (type 2) Physical findings
H Retinopathy or cataract formation
Common characteristics H Skin changes, especially on the legs and feet
H Polyuria H Muscle wasting and loss of subcutaneous fat (type 1)
H Polydipsia H Obesity, particularly in the abdominal area (type 2)
H Polyphagia H Poor skin turgor
H Weight loss H Dry mucous membranes
H Fatigue H Decreased peripheral pulses
H Cool skin temperature
H Diminished deep tendon reflexes

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H Orthostatic hypotension H Provide meticulous skin care, especially to the feet

H Characteristic fruity breath odor in ketoacidosis and legs.
H Possible hypovolemia and shock in ketoacidosis and H Treat all injuries, cuts, and blisters immediately.
hyperosmolar hyperglycemic state H Avoid constricting hose, slippers, or bed linens.
H Encourage adequate fluid intake.
Test results H Encourage verbalization of feelings.
Laboratory H Offer emotional support.
H Fasting plasma glucose level is greater than or equal H Help to develop effective coping strategies.
to 126 mg/dl on at least two occasions.
H Random blood glucose level is greater than or equal Monitoring
to 200 mg/dl. H Vital signs
H Two-hour postprandial blood glucose level is greater H Intake and output
than or equal to 200 mg/dl. H Daily weight
H Glycosylated hemoglobin (Hb A1C) level is increased. H Serum glucose
H Urinalysis may show acetone or glucose. H Urine acetone
Diagnostic procedures H Renal status
H Ophthalmologic examination may show diabetic H Cardiovascular status
retinopathy. H Signs and symptoms of:
Hypoglycemia
Hyperglycemia
Treatment Hyperosmolar coma
Urinary tract and vaginal infections
General Diabetic neuropathy
H Exercise and diet control
H Tight glycemic control for prevention of complica-
tions Patient teaching
H Modest caloric restriction for weight loss or mainte-
nance Be sure to cover:
H American Diabetes Association recommendations to H the disorder, diagnosis, and treatment
reach target glucose, Hb A1c lipid, and blood pres- H medications and possible adverse effects
sure levels H when to notify the practitioner
H Regular aerobic exercise H prescribed meal plan
H prescribed exercise program
Medications H signs and symptoms of:
H Exogenous insulin (type 1 or possibly type 2) urinary tract and vaginal infection
H Oral antidiabetics (type 2), such as arcabose, exe- hypoglycemia
natide, glimeperide, glipizide, glyburide, metformin, hyperglycemia
pioglitazone, and sitagliptin diabetic neuropathy
H self-monitoring of blood glucose
Surgery H complications of hyperglycemia
H Pancreas transplantation H foot care
H annual regular ophthalmologic examinations
H safety precautions
Nursing considerations H management of diabetes during illness.

Key outcomes Discharge planning

The patient will:
H maintain optimal body weight
H remain free from infection
H avoid complications
H verbalize understanding of the disorder and treat-
ment
H demonstrate adaptive coping behaviors.
Nursing interventions
H Administer prescribed drugs.
H Give rapidly absorbed carbohydrates for hypo-
glycemia or, if the patient is unconscious, glucagon
or I.V. dextrose, as ordered.
H Administer I.V. fluids and insulin replacement for hy-
perglycemic crisis, as ordered.
H Refer the patient to a dietitian.
H Refer the patient to a podiatrist, if indicated.
H Refer the patient to an ophthalmologist.
H Refer the adult patient who is planning a family for
preconception counseling.
H Refer the patient to the Juvenile Diabetes Research
Foundation, the American Association of Diabetes
Educators, and the American Diabetes Association to
obtain additional information.

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Diphtheria H In cutaneous diphtheria, yellow spots or skin lesions

(resembles impetigo)
Complications
Overview H Thrombocytopenia
H Myocarditis
Description H Neurologic involvement (primarily affecting motor
H Acute, highly contagious, toxin-mediated infection fibers but possibly also sensory neurons)
that usually infects the respiratory tract primarily H Renal involvement
the tonsils, nasopharynx, and larynx H Pulmonary involvement (bronchopneumonia)
H GI and urinary tracts, conjunctivae, and ears rarely
involved
Assessment
Pathophysiology
H The organism proliferates at the site of implantation. History
H Endotoxins are produced, absorbed by the blood, H Fever
and transported to the heart and central nervous sys- H Sore throat
tem. H Rasping cough
H Malaise
Causes H Vomiting
H Corynebacterium diphtheriae, a gram-positive rod H Dysphagia
H Transmission usually through intimate contact, air-
borne respiratory droplets, or a break in the skin Physical findings
H Hoarseness or stridor
Risk factors H Thick, patchy, grayish green membrane over the mu-
H Crowded living conditions cous membranes of the pharynx, larynx, tonsils, soft
H Poor hygiene palate, and nose
H Swelling of the palate
Incidence H Yellow spots or lesions (cutaneous)
H More prevalent during the colder months
H Rare in many parts of the world, including the United Test results
States Laboratory
H Cutaneous diphtheria on the increase since 1972, es- H Throat culture or culture of other suspect lesions
pecially in the Pacific Northwest and the Southwest grows C. diphtheriae.
H More prevalent in children younger than age 15 H Arterial blood gas results may reveal hypoxemia.

Common characteristics
H Thick, patchy, grayish green membrane over the mu- Treatment
cous membranes of the pharynx, larynx, tonsils, soft
palate, and nose General
H Symptoms similar to croup H Symptomatic
H Bleeding when membrane dislodged H Droplet precautions (see Droplet precautions)
H Activity, as tolerated
H Diet, as tolerated
H Endotracheal intubation and mechanical ventilation,
Droplet precautions as necessary

Droplet precautions prevent the spread of infectious dis- Medications

eases transmitted by contact with nasal or oral secretions H Diphtheria antitoxin
(droplets arising from coughing or sneezing) from the in- H Antibiotics, such as penicillin and erythromycin
fected patient with the mucous membranes of the suscep- H Oxygen therapy
tible host.
Effective droplet precautions require a single room Surgery
(not necessarily a negative-pressure room), and the door
H Tracheotomy (if airway obstruction occurs)
doesnt need to be closed. Persons having direct contact
with, or who will be within 3 feet of, the patient should
wear a surgical mask covering the nose and mouth.
When handling infants or young children who require
droplet precautions, you may also need to wear gloves
and a gown to prevent soiling of clothing with nasal and
oral secretions.

238 Diphtheria
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Nursing considerations
Key outcomes
The patient will:
H maintain patent airway
H have adequate ventilation
H remain free from signs and symptoms of infection.

Nursing interventions
H Enforce droplet precautions.
H Administer prescribed drugs.
H Obtain cultures, as ordered.
H Report all cases to local public health authorities.
H Keep the head of the bed elevated at least 30 degrees.
H Maintain a patent airway.

Monitoring
H Vital signs
H Pulse oximetry
H Respiratory status
H Signs of shock
H Cardiac rhythm and cardiovascular status
H Intake and output

Patient teaching
Be sure to cover:
H proper disposal of nasopharyngeal secretions
H maintaining isolation precautions until two consecu-
tive negative nasopharyngeal cultures at least 1
week after drug therapy stops.
Discharge planning
H Stress the need for childhood immunizations to all
parents.

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Dislocations and H Injuries may result in deposition of fracture frag-

ments between joint surfaces, damaging surrounding
subluxations structures.
H Joint function is impaired.

Causes
Overview H Congenital
H Trauma
Description H Pagets disease of surrounding joint tissues
H Dislocation displacement of joint bones so that ar-
ticulating surfaces totally lose contact (see Common Risk factors
dislocation) H Participation in contact sports
H Subluxation partial displacement of articulating
surfaces Incidence
H May accompany fractures of joints H Shoulder dislocations more than half of disloca-
tions seen in emergency departments
Pathophysiology H Hip dislocations from trauma, more common in
H Trauma causes displacement of the joint. those younger than age 35; from falls, more common
H Joint structures (blood vessels, ligaments, tendons, in those older than age 65
and nerves) are damaged.
Common characteristics
H Visible deformity of affected extremity
H Shortening of affected extremity
Common dislocation H Local pain
H Swelling
The elbow is a common site of dislocation.
H Limitation of function
H Numbness of affected extremity
NORMAL ELBOW JOINT
Complications
H Damage to surrounding muscle, ligaments, nerves,
and blood vessels
H Avascular necrosis
H Bone necrosis

Assessment
History
H Trauma or fall
H Extreme pain at injury site
H Participation in contact sports

Physical findings
ELBOW JOINT WITH
H Joint surface fractures
LATERAL DISLOCATION H Deformity around the joint
H Change in the length of the involved extremity
H Impaired joint mobility
H Point tenderness

Test results
Imaging
H X-rays confirm the diagnosis and reveal any associat-
ed fractures.

Treatment
General
H Ice application
H Immediate reduction and immobilization

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H Nothing by mouth if surgery scheduled H medication administration, dosage, and possible ad-
H Activity limitations based on injury verse effects.
H Active range-of-motion (ROM) exercises for adjacent
joints not immobilized Discharge planning
H Refer the patient to a rehabilitation program, if ap-
Medications propriate.
H Sedative, such as lorazepam H Refer the patient for home health care, if appropri-
H Analgesics, such as ibuprofen and oxycodone ate.
H Muscle relaxants, such as carisoprodol and cy-
clobenzaprine
Surgery
H Open reduction
H Skeletal traction
H Ligament repair

Nursing considerations
Key outcomes
The patient will:
H identify factors that intensify pain
H identify factors that increase the risk for injury
H maintain muscle strength and tone
H maintain joint ROM.

Nursing interventions
H Administer prescribed drugs.
H Provide proper positioning of the affected area.
H Apply ice, as ordered.
H Encourage ROM exercises, as ordered, for adjacent
nonmobilized joints.
H Provide meticulous skin care.

ALERT
Immediately report signs and symptoms of severe
vascular compromise, such as pallor, pain, loss of
pulse, paralysis, and paresthesia; the patient needs
an immediate orthopedic examination and emer-
gency reduction.

Monitoring
H Respiratory status when I.V. sedatives used
H Neurovascular status of involved extremity
H Integrity of skin

Patient teaching
Be sure to cover:
H the need to report numbness, pain, cyanosis, and
coldness of the extremity below the cast or splint
H how to evaluate skin integrity
H how to assess neurovascular status
H the use of assistive devices
H the importance of follow-up visits

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Common characteristics
Life-threatening disorder H Abnormal bleeding
H Hemorrhage

Disseminated Complications
intravascular H Cardiac tamponade
H Hemothorax

coagulation H Renal failure

Overview
Description
H Syndrome of activated coagulation characterized by
bleeding or thrombosis
H Complicates diseases and conditions that accelerate
clotting, causing occlusion of small blood vessels, or-
gan necrosis, depletion of circulating clotting factors
and platelets, and activation of the fibrinolytic system
H Also known as DIC, consumption coagulopathy,
and defibrination syndrome
Pathophysiology
H Typical accelerated clotting results in generalized ac-
tivation of prothrombin and a consequent excess of
thrombin.
H Excess thrombin converts fibrinogen to fibrin, pro-
ducing fibrin clots in the microcirculation.
H This process consumes exorbitant amounts of coagu-
lation factors (especially platelets, factor V, pro-
thrombin, fibrinogen, and factor VIII), causing
thrombocytopenia, deficiencies in factors V and VIII,
hypoprothrombinemia, and hypofibrinogenemia.
H Circulating thrombin activates the fibrinolytic system,
which lyses fibrin clots into fibrinogen degradation
products (FDPs).
H The hemorrhage that occurs may be due largely to
the anticoagulant activity of FDPs and depletion of
plasma coagulation factors.
Causes
H Infection, sepsis
H Obstetric complications
H Neoplastic disease
H Disorders that produce necrosis, such as extensive
burns and trauma
H Other disorders, such as heatstroke, shock, incom-
patible blood transfusion, drug reactions, cardiac ar-
rest, surgery necessitating cardiopulmonary bypass,
acute respiratory distress syndrome, diabetic ke-
toacidosis, pulmonary embolism, and sickle cell ane-
mia
H Snakebite
Incidence
H Dependent on the cause
H Hepatic damage
H Stroke
H Ischemic bowel
H Respiratory distress
H Death (mortality is greater than 50%)
H Intracerebral bleed
Assessment
History
H Abnormal bleeding without a history of a serious
hemorrhagic disorder; bleeding possibly occurring
at all bodily orifices
H Possible presence of one of the causes of DIC
H Possible signs of bleeding into the skin, such as
cutaneous oozing, petechiae, ecchymoses, and
hematomas
H Possible bleeding from surgical or invasive proce-
dure sites, such as incisions or venipuncture sites
H Possible nausea and vomiting; severe muscle, back,
and abdominal pain; chest pain; hemoptysis; epis-
taxis; seizures; and oliguria
H Possible GI bleeding, hematuria
Physical findings
H Petechiae
H Acrocyanosis
H Dyspnea, tachypnea
H Mental status changes, including confusion
Test results
Laboratory
H Serum platelet count is less than 150,000/mm3.
H Serum fibrinogen level is less than 170 mg/dl.
H Prothrombin time is more than 19 seconds.
H Partial thromboplastin time is more than 40 seconds.
H FDPs are increased (commonly greater than 45
mcg/ml, or positive at less than 1:100 dilution).
H Result of D-dimer test (specific fibrinogen test for
DIC) is positive at less than 1:8 dilution.
H Thrombin time is prolonged.
H Blood clotting factors V, VIII, X, XII, and protein C
are diminished.
H Complete blood count shows decreased hemoglobin
level (less than 10 g/dl).
H Blood urea nitrogen level is greater than 25 mg/dl,
and serum creatinine level is greater than 1.3 mg/dl.
H Antithrombin III level is decreased.

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H Limit venipunctures whenever possible.

Treatment H Watch for transfusion reactions and signs of fluid
overload.
General H Measure the amount of blood lost, weigh dressings
H Treatment of underlying condition and linen, and record drainage.
H Possibly supportive care alone if the patient not ac- H Weigh the patient daily, particularly in renal involve-
tively bleeding ment.
H Activity, as tolerated H Elevate the head of the bed at least 30 degrees.
H Fluid replacement H Provide nutritional support.
H Oxygen therapy H Maintain bed rest with range-of-motion exercises.
H Endotracheal intubation and mechanical ventilation,
as necessary Monitoring
H Vital signs
Medications H Results of serial blood studies
If the patient is actively bleeding H Signs of shock
H Administration of blood, fresh frozen plasma, H Intake and output, especially when administering
platelets, or packed red blood cells blood products
H Cryoprecipitate H Cardiovascular status
H Antithrombin III and gabexate H Respiratory status, including pulse oximetry
H Anticoagulant such as heparin
H Analgesics such as morphine
Patient teaching
Nursing considerations Be sure to cover (for the patient and his family):
H an explanation of the disorder
Key outcomes H the signs and symptoms of the problem, diagnostic
The patient will: procedures required, and treatment that the patient
H maintain balanced intake and output will receive.
H maintain adequate ventilation
H express feelings of increased comfort and decreased
pain
H have laboratory values return to normal
H use available support systems to assist in coping with
fears.
Nursing interventions

ALERT
Focus on early recognition of signs of abnormal
bleeding, prompt treatment of the underlying dis-
orders, and prevention of further bleeding.

H Provide emotional support.

H Provide adequate rest periods.
H Give prescribed analgesics as necessary.
H Reposition the patient every 2 hours, and provide
meticulous skin care.
H Give prescribed oxygen therapy.
H Maintain a patent airway.

ALERT
To prevent clots from dislodging and causing fresh
bleeding, dont vigorously rub the affected areas
when bathing.

H Protect the patient from injury.

H If bleeding occurs, use pressure and topical hemo-
static agents to control bleeding.

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Complications
Diverticular disease H Ruptured diverticula that cause abdominal abscesses
or peritonitis
H Intestinal obstruction
Overview H Rectal hemorrhage
H Portal pyemia
Description H Fistula
H Bulging pouches (diverticula) in GI wall pushing the H Sepsis
mucosal lining through surrounding muscle
H Sigmoid colon most common site, but possibly devel-
oping anywhere, from proximal end of the pharynx Assessment
to the anus
H Other typical sites: History
The duodenum, near the pancreatic border or the Diverticulosis
ampulla of Vater H May be symptom-free
The jejunum H Occasional intermittent pain in the left lower abdom-
H Diverticular disease of the ileum (Meckels diverticu- inal quadrant, which may be relieved by defecation
lum) most common congenital anomaly of the GI or the passage of flatus
tract H Alternating bouts of constipation and diarrhea
H Two clinical forms: Diverticulitis
Diverticulosis: diverticula present but dont cause H History of diverticulosis
symptoms H Low fiber consumption
Diverticulitis: diverticula inflamed and may cause H Recent consumption of foods containing seeds or
complications kernels or indigestible roughage, such as celery and
corn
Pathophysiology H Complaints of moderate dull or steady pain in the left
H Pressure in the intestinal lumen is exerted on weak lower abdominal quadrant, aggravated by straining,
areas, such as points where blood vessels enter the lifting, or coughing
intestine, causing a break in the muscular continuity H Mild nausea, gas, diarrhea, or intermittent bouts of
of the GI wall, creating a diverticulum. constipation, sometimes accompanied by rectal
H Diverticulitis occurs when retained undigested food bleeding
mixed with bacteria accumulates in the diverticulum,
forming a hard mass (fecalith). This substance cuts Physical findings
off the blood supply to the diverticulums thin walls, Diverticulitis
increasing its susceptibility to attack by colonic bac- H Distressed appearance
teria. H Left lower quadrant abdominal tenderness
H Inflammation follows bacterial infection, causing ab- H Low-grade fever
dominal pain. H Palpable mass
Acute diverticulitis
Causes H Muscle spasms
H Diminished colonic motility and increased intralumi- H Signs of peritoneal irritation
nal pressure H Guarding and rebound tenderness
H Defects in colon wall strength
Test results
Risk factors Laboratory
H Age H Complete blood count reveals leukocytosis.
H Low-fiber diet H Erythrocyte sedimentation rate is elevated (in diverti-
culitis).
Incidence H Stool test is positive for occult blood (in 25% of pa-
H Most common in adults ages 45 and older tients with diverticulitis).
H Affects 30% of adults older than age 60 Imaging
H Barium studies reveal barium-filled diverticula or
Common characteristics outlines, but barium doesnt fill diverticula blocked
H Left lower quadrant abdominal pain by impacted stools. This procedure isnt performed
H Generalized abdominal pain for acute diverticulitis due to potential rupture.
H Diarrhea or constipation H Radiography may reveal colonic spasm if irritable
H Palpable mass bowel syndrome accompanies diverticular disease.
H Nausea, vomiting H Abdominal X-rays rule out perforation.

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Diagnostic procedures
H Colonoscopy or flexible sigmoidoscopy shows diver-
ticula or inflamed mucosa. It isnt usually performed
in the acute phase.
H Biopsy results may rule out cancer.
H Computed tomography scan of the abdomen evalu-
ates the presence of abscess.
Treatment
General
H For asymptomatic diverticulosis, no treatment
H Bed rest
For symptomatic diverticulosis
H Liquid or low-residue diet (if experiencing pain)
H Increased water consumption, if appropriate
H High-residue diet
For severe diverticulitis
H Nothing by mouth
H Nasogastric (NG) decompression
Medications
For diverticulosis
H Stool softeners such as docusate sodium
H Bulk medication such as calcium polycarbophil
For diverticulitis
H Antibiotics, such as metronidazole and ceftazidime
H Analgesics such as morphine
H I.V. therapy for severe diverticulitis
Surgery
H Colon resection
H May require temporary colostomy to drain abscesses
or to rest the colon for 6 to 8 weeks
H Needed for rupture or to correct cases refractory to
medical treatment
Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort
H maintain normal fluid volume
H have bowel movements that return to normal
H verbalize understanding of the disease process and
treatment regimen.
Nursing interventions
ALERT
Remember that diverticulitis produces more seri-
ous signs and symptoms as well as complications,
and requires more interventions than diverticulo-
sis.
H If the patient is anxious, provide psychological sup-
port.
H Administer prescribed drugs.
H Maintain bed rest for acute diverticulitis.
H Maintain the prescribed diet.
H If surgery is scheduled, provide routine preoperative
care.
After colon resection
H Provide meticulous wound care.
H Encourage coughing and deep breathing and incen-
tive spirometer use to prevent atelectasis.
H Administer I.V. fluids and prescribed drugs.
H Provide colostomy care, if appropriate.
H Apply sequential compression device.
H Encourage early ambulation.
H Keep the head of the bed elevated at least 30 degrees.
Monitoring
H GI status
H Vital signs
H Pain control
H Stools for color, consistency, and frequency
H NG drainage, if appropriate
H Signs and symptoms of complications
After colon resection
H Signs of infection and postoperative bleeding
H Intake and output
Patient teaching
Be sure to cover:
H bowel and dietary habits (in uncomplicated divertic-
ulosis)
H the disorder, diagnosis, and treatment
H preoperative teaching (for a patient needing surgery)
H postoperative teaching (for a patient who must care
for his colostomy)
H the desired actions and possible adverse effects of
prescribed medications.
Discharge planning
H Refer the patient to an enterostomal therapist, if ap-
propriate.
H Refer the patient to a dietitian, if needed.
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Down syndrome H Brushfields spots on the iris

H Small skull
H Flat bridge across the nose
H Flattened face
Overview H Small external ears
H Short neck with excess skin
Description H Dry, sensitive skin with decreased elasticity
H A chromosomal aberration that results in mental and H Umbilical hernia
physical abnormalities H Short stature
H Average IQ between 30 and 50 (some higher) H Short extremities with broad, flat, and squarish
H Also known as mongolism and trisomy 21 syn- hands and feet
drome H Dysplastic middle phalanx of the fifth finger
H Wide space between the first and second toes
Pathophysiology H Abnormal fingerprints and footprints
H Down syndrome is an aberration in which chromo- H Impaired reflex development
some 21 has three copies instead of the normal two H Absent Moros reflex and hyperextensible joints
because of faulty meiosis (nondisjunction) of the H Impaired posture, coordination, and balance
ovum or, sometimes, the sperm. H Clubfoot
H Theres unbalanced translocation, in which the long H Imperforate anus
arm of chromosome 21 breaks and attaches to an- H Cleft lip and palate
other chromosome. H Pelvic bone abnormalities
H The result is a karyotype of 47 chromosomes instead
of the normal 46. Test results
Laboratory
Causes H Karyotype analysis or chromosome mapping shows
H Trisomy 21 the chromosomal abnormality and confirms the diag-
H Mosaicism and trisomy 21 nosis of Down syndrome.
H Robertsonian translation and partial trisomy 21 H Prenatal serum alpha-fetoprotein reveals reduced
levels of alpha-fetoprotein.
Risk factors Imaging
H Maternal age, especially older than age 35 H Prenatal ultrasonography can suggest Down syn-
drome if a duodenal obstruction or an atrioventricu-
Incidence lar canal defect is present.
H Occurs in 1 per 800 to 1,000 live births H Amniocentesis allows prenatal diagnosis.
H Increases with maternal age, especially after age 35 Other
H Developmental screening tests show severity and
Common characteristics progress of retardation.
H Mental retardation
H Abnormal facial features
H Heart defects Treatment
H Other congenital defects
General
Complications H Early intervention
H Death H Special education programs
H Congenital heart defects H Special athletic programs
H Premature senile dementia H Maximal environmental simulation for infants
H Leukemia H Safety precautions for children and adults in a con-
H Acute and chronic infections trolled environment
H Diabetes mellitus
H Thyroid disorders Medications
H Antibiotics, depending on the infective organism, for
recurrent infections
Assessment H Thyroid hormone replacement with levothyroxine for
hypothyroidism
History
H Neonate lethargic and a poor feeder Surgery
H Open-heart surgery to correct cardiac defects, such
Physical findings as ventricular or atrial septal defects
H Slanting, almond-shaped eyes H Plastic surgery to correct congenital abnormalities,
H Small, open mouth, protruding tongue such as protruding tongue, cleft lip, and cleft palate
H Single transverse palmar crease

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Nursing considerations
Key outcomes
The patient will:
H demonstrate age-appropriate skills and behaviors to
the extent possible
H perform health maintenance activities according to
level of ability
H participate in developmental stimulation programs to
increase skill levels.
Nursing interventions
H Establish a trusting relationship with the childs par-
ents.
H Encourage verbalization and provide support.
H Encourage the parents to hold and nurture their
child.
Monitoring
H Response to treatment
H Signs and symptoms of infection
H Complications
H Nutritional status
H Growth and development
H Thyroid function test results
H Cardiovascular status

Patient teaching
Be sure to cover:
H the need for adequate exercise and maximal environ-
mental stimulation
H realistic goals for the parents and child
H information about a balanced diet
H the importance of remembering the emotional needs
of other children in the family.
Discharge planning
H Refer the parents to infant stimulation classes.
H Refer the parents and older siblings for genetic and
psychological counseling, as appropriate.
H Refer the patient and his parents to support services.

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Dysmenorrhea H Obesity
H Smoking

Incidence
Overview H Affects more than 45% of females of reproductive age
H Usually peaks in the early 20s, then slowly decreases
Description
H Painful menstruation unassociated with pelvic dis- Common characteristics
ease H Sharp, intermittent, cramping, lower abdominal pain,
H Most common gynecologic complaint usually radiating to the back, thighs, groin, and vulva
H A primary disorder that begins 6 to 12 months after H Pain typically starting with or immediately before
the onset of ovulation menstrual flow and peaking within 24 hours
H A secondary disorder that typically begins between
ages 20 and 30, but possible any time after menarche Complications
H Dehydration
Pathophysiology
H Pain may result from increased prostaglandin secre-
tion in menstrual blood, which intensifies normal Assessment
uterine contractions.
H Prostaglandins intensify myometrial smooth muscle History
contraction and uterine blood vessel constriction, H Pelvic disease
thereby worsening the uterine hypoxia normally as- H Urinary frequency
sociated with menstruation. H Nausea
H Intense muscle contractions and hypoxia cause the H Vomiting
intense pain of dysmenorrhea. H Diarrhea
H Headache
Causes H Backache
Primary H Chills
H Increased prostaglandin secretion caused by slough- H Depression
ing endometrial cells H Irritability
Secondary
H Endometriosis Physical findings
H Cervical stenosis H Abdominal tenderness
H Uterine leiomyomas (benign fibroid tumors) H Painful breasts
H Pelvic inflammatory disease
H Pelvic tumors (see Causes of pelvic pain) Test results
Imaging
Risk factors H Laparoscopy, hysteroscopy, and pelvic ultrasound
Primary help diagnose underlying disorders (in secondary
H Early-onset menarche dysmenorrhea).
H Null parity Other
H Pelvic examination and a detailed patient history help
Causes of pelvic pain identify the cause.

The characteristic pelvic pain of dysmenorrhea must be

distinguished from the acute pain caused by many other
Treatment
disorders, such as:
H GI disorders: appendicitis, acute diverticulitis, acute or General
chronic cholecystitis, chronic cholelithiasis, acute pan- H Heat applied locally to the lower abdomen
creatitis, peptic ulcer perforation, intestinal obstruction H Increased fluid intake
H urinary tract disorders: cystitis, renal calculi H Activity, as tolerated
H reproductive disorders: acute salpingitis, chronic in-
flammation, degenerative fibroid, ovarian cyst torsion Medications
H pregnancy disorders: impending abortion (pain and
H Analgesics, such as acetaminophen, diclofenac, and
bleeding early in pregnancy), ectopic pregnancy, abrup-
tio placentae, uterine rupture, leiomyoma degeneration, ketoprofen
toxemia H Prostaglandin inhibitors, such as aspirin and ibupro-
H emotional conflicts: psychogenic (functional) pain. fen
Other conditions that may mimic dysmenorrhea include
ovulation and normal uterine contractions experienced in Surgery
pregnancy. H Surgical treatment of underlying disorders, such as
endometriosis or uterine leiomyomas (secondary)

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Nursing considerations
Key outcomes
The patient will:
H remain free from pain
H express understanding of disorder.

Nursing interventions
H Provide emotional support.
H Administer prescribed analgesics.

Monitoring
H Depression
H Hydration
H Pain control
H Menstrual cycle

Patient teaching
Be sure to cover:
H explanation of normal female anatomy and physiolo-
gy as well as the nature of dysmenorrhea
H information on pregnancy and contraception
H keeping a detailed record of her menstrual cycle and
symptoms
H seeking medical care if symptoms persist.

Discharge planning
H Refer the patient for psychological counseling, if
appropriate.

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E Life-threatening disorder

Ebola virus infection

Overview
Description
H An unclassified ribonucleic acid virus that results in
bleeding
H Four known strains: Ebola Zaire (EBO-Z), Ebola Su-
dan (EBO-S), Ebola Tai (EBO-C), and Ebola Reston
(affects only monkeys)
Risk factors
H Travel to endemic areas of Africa
H Exposure to animals, humans, or contaminated nee-
dles
Incidence
H Not endemic to the United States
H Affects males and females of all ages

Common characteristics
H Flulike symptoms
H Severe diarrhea
H Vomiting
H Internal and external hemorrhage
H Macular papular rash
H Poor prognosis
Complications
Pathophysiology H Liver and kidney dysfunction
H The virus is transmitted by direct contact with infect- H Dehydration
ed blood, body secretions, or infected tissues. H Hemorrhage
H It can be transmitted by nosocomial and community- H Abortion
acquired modes. H Myocarditis
H Viral replication causes focal tissue necrosis, most H Pulmonary edema
severely in the liver.
H Microvasculature damage causes increased vascular
permeability and bleeding. Assessment
H Ebola virus remains contagious even after the patient
has died. History
H Contact with an infected person
Causes H Headache
H EBO-Z, EBO-S, or EBO-C virus strains H Malaise
H Myalgia
H Fever
H Cough
Prevention H Sore throat
Preventing the spread of Ebola virus H Nausea
H Vomiting
The Centers for Disease Control and Prevention recom-
mends the following guidelines to help prevent the spread Physical findings
of this deadly disease:
H Keep the patient in isolation throughout the course of H Conjunctival injection
the disease. H Bruising
H If possible, place the patient in a negative-pressure H Maculopapular eruptions
room at the beginning of hospitalization to avoid the H Melena
need for transfer as the disease progresses. H Hematemesis
H Restrict nonessential staff members from entering the H Bleeding gums
patients room.
H Make sure that anyone who enters the patients room Test results
wears gloves and a gown to prevent contact with any
Laboratory
surface in the room that may have been soiled.
H Blood studies show specific antigens or antibodies
H Use barrier precautions to prevent skin and mucous
membrane exposure to blood or other body fluids, se-
and may show the isolated virus.
cretions, or excretions when caring for the patient. H Blood studies show neutrophil leukocytosis, hypo-
H If you must come within 3 (1 m) of the patient, also fibrinogenemia, thrombocytopenia, and microangio-
wear a face shield or a surgical mask and goggles or pathic hemolytic anemia.
eyeglasses with side shields. H Blood studies show elevated blood urea nitrogen and
H Dont reuse gloves or gowns unless they have been creatinine levels.
completely disinfected. H Blood studies show elevated aspartate aminotrans-
H Make sure any patient who dies of the disease is ferase and alanine aminotransferase levels.
promptly buried or cremated. Precautions to avoid
contact with the patients body fluids and secretions
should continue even after the patients death.

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Treatment
General
H Supportive care
H Strict isolation (see Preventing the spread of Ebola
virus)
H Diet as tolerated or total parental nutrition
H Bed rest or limited activity

Medications
H I.V. fluids
H Blood transfusions

Nursing considerations
Key outcomes
The patient will:
H maintain adequate fluid balance
H remain hemodynamically stable
H understand the implications of his illness.

Nursing interventions
H Enforce strict isolation.
H Provide emotional support.
H Administer prescribed I.V. solutions and blood prod-
ucts.
H Provide safety precautions.
H Provide nutritional support.

Monitoring
H Vital signs
H Signs of bleeding
H Intake and output
H Laboratory studies
H GI status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H signs of bleeding
H isolation precautions.

Discharge planning
H Refer the patient for home care, if appropriate.
H Stress to the patient the need for continued follow-up
care.

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Ectopic pregnancy H Previous surgery, such as tubal ligation or resection

H Transmigration of the ovum
H Congenital defects in reproductive tract
H Ectopic endometrial implants in the tubal mucosa
Overview H Sexually transmitted tubal infection
H Intrauterine device
Description H Smoking
H Implantation of a fertilized ovum outside the uterine H Hormonal contraceptives
cavity, most commonly in the fallopian tube (see Im-
plantation sites of ectopic pregnancy) Incidence
H Prognosis good with prompt diagnosis, appropriate H In whites, about 1 of 200 pregnancies
surgical intervention, and control of bleeding H In nonwhites, about 1 of 120 pregnancies
H Very few fetuses carried to term; rarely, with abdomi-
nal implantation, fetus survives to term Common characteristics
H About one in three chance of giving birth to live H Abdominal tenderness
neonate in subsequent pregnancy H Abdominal discomfort
H Minimal vaginal bleeding
Pathophysiology H Amenorrhea
H The transport of a blastocyst to the uterus is delayed.
H The blastocyst implants at another available vascular- Complications
ized site, usually the fallopian tube lining. H Rupture of fallopian tube
H Normal signs of pregnancy are initially present. H Hemorrhage
H Uterine enlargement occurs in about 25% of cases. H Shock
H Human chorionic gonadotropin (HCG) hormonal H Peritonitis
levels are lower than in uterine pregnancies. H Infertility
H If not interrupted, internal hemorrhage occurs with H Disseminated intravascular coagulation
rupture of the fallopian tube. H Death

Causes
H Abnormal reproductive organ anatomy Assessment
H Delay in reproductive events such as movement of
zygote to uterus History
H Unknown H Amenorrhea
H Abnormal menses (after fallopian tube implantation)
Risk factors H Slight vaginal bleeding
H Endosalpingitis H Unilateral pelvic pain over the mass
H Diverticula H If fallopian tube ruptures, sharp lower abdominal
H Tumors pressing against the tube pain, possibly radiating to the shoulders and neck

Implantation sites of ectopic pregnancy ALERT

In about 95% of patients with ectopic pregnancy, the
ovum implants in part of the fallopian tube: the fimbria,
ampulla, or isthmus. Other possible abnormal sites of im-
plantation include the interstitium, ovarian ligament,
ovary, abdominal viscera, and internal cervical os.
Ectopic pregnancy sometimes produces symptoms
of normal pregnancy or no symptoms other than
mild abdominal pain (especially in abdominal
pregnancy), making diagnosis difficult.

Ampulla
Physical findings
Fimbria H Possible extreme pain when cervix is moved and ad-
Isthmus
Interstitium
nexa palpated
H Boggy and tender uterus
H Adnexa possibly enlarged

Test results
Laboratory
Ovary H Serum HCG level is abnormally low; when repeated
in 48 hours, it remains lower than levels found in a
Ovarian ligament Internal cervical os normal intrauterine pregnancy.
Imaging
H Real-time ultrasonography shows intrauterine preg-
nancy or ovarian cyst.

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Diagnostic procedures H Signs of impending shock

H Laparoscopy may reveal pregnancy outside the H Cardiovascular status
uterus.
Patient teaching
Treatment
Be sure to cover:
General H the disorder, diagnosis, and treatment
H Initially, in the event of pelvic-organ rupture, man- H postoperative care
agement of shock H prevention of recurrent ectopic pregnancy
H Diet determined by clinical status H prompt treatment of pelvic infections
H Activity determined by clinical status H risk factors for ectopic pregnancy, including surgery
involving the fallopian tubes and pelvic inflammatory
Medications disease.
H Transfusion with packed red blood cells
H Broad-spectrum I.V. antibiotics, according to isolated Discharge planning
organism H Refer the patient to a mental health professional for
H Supplemental iron additional counseling, if necessary.
Surgery
H Laparotomy and salpingectomy; possibly after lap-
aroscopy to remove affected fallopian tube and con-
trol bleeding
H Microsurgical repair of the fallopian tube for patients
who wish to have children
H Oophorectomy for ovarian pregnancy
H Hysterectomy for interstitial pregnancy
H Laparotomy to remove the fetus for abdominal preg-
nancy

Nursing considerations
Key outcomes
The patient will:
H have stable vital signs
H express feelings about the current situation
H use available support systems to aid in coping.

Nursing interventions
H Prepare the patient with excessive blood loss for
emergency surgery.
H Administer prescribed blood transfusions.
H Provide emotional support.
H Give prescribed analgesics.
H Administer Rho(D) immune globulin (RhoGAM), as
ordered, if the patient is Rh-negative.
H Determine the date and description of her last men-
strual period.
H Provide a quiet, relaxing environment.
H Encourage the patient to express her feelings of fear,
loss, and grief.
H Help the patient to develop effective coping strate-
gies.
Monitoring
H Vital signs
H Vaginal bleeding
H Pain control
H Intake and output
H Signs of hypovolemia

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Life-threatening disorder Assessment

History
Electric shock H Exposure to electricity or lightning
H Loss of consciousness
H Muscle pain
Overview H Fatigue
H Headache
Description H Nervous irritability
H Electric current passing through body
H Physical damage depending on intensity of current, Physical findings
resistance of the tissues it passes through, type of H Determined by voltage exposure
current, and frequency and duration of current flow H Burns
H Classified as lightning, low voltage (less than 600 V), H Local tissue coagulation
and high voltage (greater than 600 V) H Entrance and exit injuries
H Burns the most common injury H Cyanosis
H Apnea
Pathophysiology H Markedly decreased blood pressure
H Electrical energy results in altered cell membrane H Cold skin
resting potential, causing depolarization in muscles H Unconsciousness
and nerves. H Numbness or tingling or sensorimotor deficits
H Electric shock alters normal electrical activity of the
heart and brain. Test results
H Electric shock resulting from a high-frequency cur- Laboratory
rent generates more heat in tissues than a low- H Laboratory test results evaluate internal damage and
frequency current, resulting in burns and local tissue guide treatment:
coagulation and necrosis. Arterial blood gas analysis may show hypoxemia
H Muscle tetany is elicited. and acid-base imbalance.
H Tissue destruction and coagulative necrosis occur. Urine may test positive for myoglobin.
Blood urea nitrogen and creatinine levels may be
Causes elevated.
H Accidental contact with an exposed part of an electri- Imaging
cal appliance or wiring H If chest injury or shortness of breath occurred, chest
H Lightning X-rays evaluate internal damage and guide treatment.
H Flash of electric arcs from high-voltage power lines Diagnostic procedures
or machines H Electrocardiography evaluates internal damage and
guides treatment.
Incidence
H Causes more than 1,000 deaths annually
H More common in males ages 20 to 40 Treatment
Common characteristics General
H Cutaneous burn H Separation of victim from current source
H Variable deep tissue damage H Stabilization of cervical spine
H Emergency measures to maintain airway, breathing,
Complications and circulation
H Sepsis H Treatment of acid-base imbalance
H Neurologic dysfunction H Vigorous fluid replacement
H Cardiac dysfunction H No dietary restrictions if swallowing ability intact
H Psychiatric dysfunction H Activity based on outcome of interventions
H Renal failure
H Electrolyte abnormalities Medications
H Peripheral nerve injuries H Tetanus prophylaxis with tetanus toxoid
H Vascular disruption
H Thrombi
H Death

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Nursing considerations
Key outcomes
The patient will:
H maintain stable cardiac rhythm
H maintain cardiac output
H regain skin integrity
H have wounds and incisions that appear clean, pink,
and free from purulent drainage.
Nursing interventions
H Separate the victim from the current source.
H Provide emergency treatment to maintain airway,
breathing, and circulation.
H Give rapid I.V. fluid infusion.
H Obtain a 12-lead electrocardiogram.
H Administer prescribed drugs.
H Provide wound care.

Monitoring
H Vital signs
H Cardiac rhythm (continuously) and cardiovascular
status
H Intake and output (hourly)
H Neurologic status
H Sensorimotor deficits
H Peripheral neurovascular status
H Respiratory status

Patient teaching
Be sure to cover:
H information about the injury, diagnosis, and treat-
ment
H how to avoid electrical hazards at home and at work
H electrical safety regarding children.

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Physical findings
Emphysema H Barrel chest
H Pursed-lip breathing
H Use of accessory muscles
Overview H Cyanosis
H Clubbed fingers and toes
Description H Tachypnea
H Progressive, chronic lung disease characterized by H Decreased tactile fremitus
permanent enlargement of air spaces distal to the H Decreased chest expansion
terminal bronchioles and by exertional dyspnea H Hyperresonance
H One of several diseases usually labeled collectively as H Decreased breath sounds
chronic obstructive pulmonary disease or chronic H Crackles
obstructive lung disease H Inspiratory wheeze
H Prolonged expiratory phase with grunting respira-
Pathophysiology tions
H Recurrent inflammation associated with the release H Distant heart sounds
of proteolytic enzymes from lung cells causes abnor-
mal, irreversible enlargement of the air spaces distal Test results
to the terminal bronchioles. Laboratory
H This enlargement leads to the destruction of alveolar H Arterial blood gas analysis shows decreased partial
walls, which results in a breakdown of elasticity. (See pressure of oxygen; partial pressure of carbon diox-
What happens in emphysema.) ide remains normal until late in the disease.
H Red blood cell count shows an increased hemoglo-
Causes bin level late in the disease.
H Cigarette smoking Imaging
H Air pollutants H Chest X-ray may show:
a flattened diaphragm
Risk factors reduced vascular markings at the lung periphery
H Genetic deficiency of alpha1-antitrypsin overaeration of the lungs
a vertical heart
Incidence enlarged anteroposterior chest diameter
H Most common cause of death from respiratory dis- large retrosternal air space.
ease in the United States Diagnostic procedures
H More prevalent in males than in females H Pulmonary function tests typically show:
H About 2 million U.S. residents affected increased residual volume and total lung capacity
H Affects 1 in 3,000 neonates reduced diffusing capacity
increased inspiratory flow.
Common characteristics H Electrocardiography may show tall, symmetrical P
H Exertional dyspnea waves in leads II, III, and aVF; a vertical QRS axis;
H Chronic cough and signs of right ventricular hypertrophy late in the
H Shortness of breath disease.
H Anorexia and weight loss
H Malaise
Treatment
Complications
H Recurrent respiratory tract infections General
H Cor pulmonale H Chest physiotherapy
H Respiratory failure H Possible transtracheal catheterization and home oxy-
H Peptic ulcer disease gen therapy
H Spontaneous pneumothorax H Adequate hydration
H Pneumomediastinum H High-protein, high-calorie diet
H Activity, as tolerated

Assessment Medications
H Bronchodilators such as formoterol
History H Anticholinergics such as tiotropium
H Smoking H Mucolytics such as acetylcysteine
H Shortness of breath H Corticosteroids such as fluticasone
H Chronic cough H Antibiotics according to the isolated organism
H Anorexia and weight loss H Oxygen
H Malaise

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H Immunizations, such as influenza virus vaccine and What happens in emphysema

pneumococcal vaccine In normal, healthy breathing, air moves in and out of the
Surgery lungs to meet metabolic needs. A change in airway size
compromises the lungs ability to circulate sufficient air.
H Chest tube insertion for pneumothorax In a patient with emphysema, recurrent pulmonary in-
H Lung volume reduction surgery flammation damages and eventually destroys the alveolar
walls, creating large air spaces. This breakdown leaves the
alveoli unable to recoil normally after expanding and re-
Nursing considerations sults in bronchiolar collapse on expiration. This traps air
within the lungs.
Key outcomes Associated pulmonary capillary destruction usually al-
The patient will: lows a patient with severe emphysema to match ventila-
tion to perfusion and thus avoid cyanosis.
H maintain a patent airway and adequate ventilation
H demonstrate energy conservation techniques NORMAL ALVEOLI
H express understanding of the illness
H demonstrate effective coping strategies. Bronchiole

Nursing interventions
H Administer prescribed drugs.
H Provide supportive care.
H Help the patient adjust to lifestyle changes necessitat-
ed by a chronic illness.
H Encourage the patient to express his fears and con- Alveoli
cerns.
H Perform chest physiotherapy.
H Provide a high-calorie, protein-rich diet.
H Give small, frequent meals. ABNORMAL ALVEOLI
H Encourage daily activity and diversional activities.
H Provide frequent rest periods.
H Keep the head of the bed elevated at least 30 degrees.
H Encourage oral fluid intake.

Monitoring
H Vital signs
H Intake and output
H Daily weight
H Complications
H Respiratory status
H Activity tolerance
H Cardiovascular status
H Nutritional status
ALERT
Patient teaching Urge the patient to notify the practitioner if he ex-
periences a sudden onset of worsening dyspnea or
Be sure to cover: sharp pleuritic chest pain exacerbated by chest
H the disorder, diagnosis, and treatment movement, breathing, or coughing.
H medications and possible adverse effects
H when to notify the practitioner
H avoidance of smoking and areas where smoking is Discharge planning
permitted H Refer the patient to a smoking-cessation program, if
H avoidance of crowds and people with known infec- indicated.
tions H Refer the patient for influenza and pneumococcal
H home oxygen therapy, if indicated pneumonia immunizations, as needed.
H transtracheal catheter care, if needed H Refer the family of patients with familial emphysema
H coughing and deep-breathing exercises for alpha1-antitrypsin deficiency screening.
H the proper use of handheld inhalers
H high-calorie, protein-rich diet
H adequate oral fluid intake
H avoidance of respiratory irritants
H signs and symptoms of pneumothorax.

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Encephalitis H Sore throat and upper respiratory tract symptoms

H Sudden onset of altered level of consciousness
H Seizures

Overview Physical findings

H Confusion, disorientation, or hallucinations
Description H Tremors
H Severe inflammation of the brain H Cranial nerve palsies
H Exaggerated deep tendon reflexes and absent superfi-
Pathophysiology cial reflexes
H Intense lymphocytic infiltration of brain tissues and H Paresis or paralysis of the arms and legs
the leptomeninges results in: H Stiff neck when the head is bent forward
cerebral edema H Fever
degeneration of the brains ganglion cells H Nausea and vomiting
diffuse nerve cell destruction (gray matter more H Cerebral hemispheres
than white). H Aphasia
H Involuntary movements
Causes H Ataxia
H Mosquito- or tick-borne arboviruses specific to rural H Sensory defects
areas
H Enteroviruses in urban areas (coxsackievirus, po- Test results
liovirus, and echovirus) Laboratory
H Herpesvirus H Blood analysis identifies the virus.
H Mumps virus H Serologic studies in herpes encephalitis show rising
H Adenoviruses titers of complement-fixing antibodies.
H Demyelinating diseases after measles, varicella, Imaging
rubella, or vaccination H Magnetic resonance imaging locates the lesion.
H Human immunodeficiency virus H Computed tomography scan shows cerebral edema.
Diagnostic procedures
Incidence H Cerebrospinal fluid (CSF) analysis identifies the
H About 1,500 cases annually in the United States virus.
H More common in elderly people and infants H Lumbar puncture discloses CSF pressure.
H EEG shows slowing of waveforms.
Common characteristics
H Dysuria; pyuria
H Fever Treatment
H Nausea and vomiting
H Myalgia General
H Photophobia H Supportive measures
H Stiff neck; headache H Airway maintenance
H Localized seizures H Oxygen administration
H Acute confusion or amnesic state H Adequate fluid and electrolyte intake
H Diet as tolerated
Complications H Activity as tolerated
H Bronchial pneumonia
H Urinary retention and urinary tract infection Medications
H Pressure ulcers H Osmotic diuretics such as mannitol
H Coma H Corticosteroids such as dexamethasone
H Epilepsy H Anticonvulsants such as phenytoin
H Parkinsonism H Antipyretics such as acetaminophen
H Mental deterioration H Antibiotics according to isolated organism
H Antivirals such as vidarabine
H Oxygen
Assessment H Stool softeners such as docusate sodium

History
H Headache
H Muscle stiffness and malaise

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Nursing considerations
Key outcomes
The patient will:
H maintain adequate ventilation
H exhibit fluid balance within normal limits
H exhibit temperature within normal limits
H consume adequate calorie requirements daily
H verbalize feelings of increased comfort and relief
from pain.
Nursing interventions
H Ensure adequate fluid intake.
H Administer prescribed drugs.
H Position and turn the patient often.
H Assist with range-of-motion exercises.
H Maintain adequate nutrition.
H Administer laxatives or stool softeners.
H Administer mouth care.
H Maintain a quiet environment.
H Start seizure precautions, if necessary.
H Reorient the patient often, if necessary.
H Keep the head of the bed elevated, as ordered.

Monitoring
H Vital signs
H Neurologic status
H Intake and output
H Response to medications
H Intracranial pressure (severe cases)
H Respiratory status
H Cardiovascular status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H transient behavior changes
H the medication regimen
H adverse effects of medication
H follow-up care.

Discharge planning
H Refer the patient to an outpatient rehabilitation pro-
gram, as indicated.

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Common characteristics
Endocarditis H Heart murmur

Complications
Overview H Valve stenosis or regurgitation
H Myocardial erosion
Description H Embolic debris lodged in the small vasculature of the
H Inflammation or infection of the endocardium, heart visceral tissue causing multiple organ infarcts
valves, or cardiac prosthesis H Stroke
H Classified as infective (bacterial or fungal) or nonin- H Myocardial infarction
fective H Heart failure
H Acute renal failure
Pathophysiology
H Fibrin, neutrophils, lymphocytes, and platelets clus-
ter on valve tissue and engulf bacteria, fungi, or Assessment
necrotic tissue. (See Degenerative changes in endo-
carditis.) History
H This produces vegetation, which may cover the valve H Predisposing condition
surfaces, causing deformities and destruction of H Complaint of nonspecific symptoms, such as weak-
valvular tissue, and may extend to the chordae ness, fatigue, weight loss, anorexia, arthralgia, night
tendineae, causing them to rupture, leading to valvu- sweats, and intermittent fever, that may recur for
lar insufficiency. weeks
H Vegetative growth on the heart valves, endocardial
lining of a heart chamber, or the endothelium of a Physical findings
blood vessel may embolize to the spleen, kidneys, H Petechiae on the skin (especially common on the up-
central nervous system, and lungs. per anterior trunk) and on the buccal, pharyngeal,
or conjunctival mucosa
Causes H Splinter hemorrhages under the nails
H Bacterial or fungal infection H Clubbing of the fingers in long-standing disease
H Advanced stages of cancer H Heart murmur in all patients except those with early
H Immune system disorders acute endocarditis and I.V. drug users with tricuspid
valve infection
Risk factors H Murmur that changes suddenly or new murmur that
H Cardiac valvular disease develops with a fever (classic physical sign)
H I.V. drug use H Oslers nodes
H Rheumatic heart disease H Roths spots
H Prosthetic heart valves H Janeway lesions
H Congenital heart disease H Splenomegaly in long-standing disease
H Mitral valve prolapse H Dyspnea, tachycardia, and bibasilar crackles possible
H Degenerative heart disease with left-sided heart failure
H Calcific aortic stenosis (in elderly patients) H Splenic infarction causing pain in the upper left
H Asymmetrical septal hypertrophy quadrant, radiating to the left shoulder, and abdomi-
H Marfan syndrome nal rigidity
H Syphilitic aortic valve H Renal infarction causing hematuria, pyuria, flank
H Long-term hemodialysis pain, and decreased urine output
H Streptococcal infection H Cerebral infarction causing hemiparesis, aphasia,
H Systemic lupus erythematosus and other neurologic deficits
H Pulmonary infarction causing cough, pleuritic pain,
Incidence pleural friction rub, dyspnea, and hemoptysis
H No underlying heart disease in up to 40% of patients H Peripheral vascular occlusion causing numbness and
Native valve endocarditis tingling in arm, leg, finger, or toe or signs of impend-
H More common in males than in females ing peripheral gangrene
H Most patients older than age 50
H Uncommon in children Test results
H Rheumatic valvular disease in about 25% of cases Laboratory
H Mitral valve most commonly involved valve H Three or more blood cultures over 24 to 48 hours
H Drug abusers with endocarditis (frequently young identify the causative organism in up to 90% of pa-
males) tients.
H White blood cell count with differential are normal
or elevated.

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H Complete blood count shows normocytic, normo- Degenerative changes in endocarditis

chromic anemia in subacute infective endocarditis. This illustration shows typical vegetations on the endo-
H Erythrocyte sedimentation rate and serum creatinine
cardium produced by fibrin and platelet deposits on infec-
levels are elevated. tion sites.
H Serum rheumatoid factor is positive in about half of
patients after the disease is present for 6 weeks.
H Urinalysis shows proteinuria and microscopic hema-
turia.
Imaging
H Echocardiography may identify valvular damage in up
to 80% of patients with native valve disease.
Diagnostic procedures
H Electrocardiography may show atrial fibrillation and
other arrhythmias that accompany valvular disease.

Treatment
General
H Prompt therapy that continues for several weeks
H Selection of anti-infective drug based on type of in-
fecting organism and sensitivity studies
H If blood cultures negative (10% to 20% of subacute
cases), possible I.V. antibiotic therapy (usually for 4 Monitoring
to 6 weeks) against probable infecting organism H Vital signs
H Sufficient fluid intake H Cardiac rhythm and cardiovascular status
H Bed rest H Respiratory status, including pulse oximetry
H Neurologic status
Medications H Intake and output
H Antiplatelets or antipyretics such as aspirin H Renal status
H Antibiotics, according to isolated organism H Arterial blood gas analysis, as needed

Surgery
H With severe valvular damage, especially aortic insuffi-
ciency or infection of a cardiac prosthesis, possible
corrective surgery if refractory heart failure develops
or if an infected prosthetic valve must be replaced
ALERT
Watch for signs of embolization, a common occur-
rence during the first 3 months of treatment. Tell
the patient to watch for and report these signs.

Nursing considerations Patient teaching

Key outcomes Be sure to cover:
The patient will: H the disorder, diagnosis, and treatment
H carry out activities of daily living without weakness or H anti-infectives the patient needs to continue taking
fatigue H the need to watch closely for fever, anorexia, and
H maintain hemodynamic stability with adequate car- other signs of relapse about 2 weeks after treatment
diac output stops
H exhibit no arrhythmias H the need for prophylactic antibiotics before dental
H maintain adequate ventilation work and some surgical procedures
H express feelings about diminished capacity to per- H proper dental hygiene and avoiding flossing the teeth
form usual roles. H how to recognize symptoms of endocarditis and to
notify the practitioner immediately if such symptoms
Nursing interventions occur.
H Stress the importance of bed rest.
H Provide a bedside commode. Discharge planning
H Allow the patient to express his concerns. H Encourage follow-up care with a cardiologist.
H Obtain a history of allergies.
H Administer antibiotics, as prescribed.
H Administer oxygen.
H Elevate the head of the bed at least 30 degrees.

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Endometriosis Assessment
History
Overview H Cyclic pelvic pain that peaks 5 to 7 days before
menses and lasts 2 to 3 days
Description H Infertility
H Poorly understood gynecologic condition character- H Acquired dysmenorrhea
ized by pain that occurs with menstruation H Pain in lower abdomen, vagina, posterior pelvis and
H Endometrial tissue appears outside uterine cavity back; often radiates down legs
lining H Additional symptoms depending on site of involve-
H Ectopic tissue generally confined to the pelvic ment:
area, but can appear anywhere in the body Hypermenorrhea (oviducts and ovaries)
Deep-thrust dyspareunia (ovaries and cul-de-sac)
Pathophysiology Suprapubic pain, dysuria, and hematuria (blad-
H Endometrial cells respond to estrogen and proges- der)
terone with proliferation and secretion. Dyschezia, rectal bleeding with menses, and pain
H During menstruation, ectopic tissue bleeds and caus- in the coccyx or sacrum (rectovaginal septum and
es inflammation of the surrounding tissues. colon)
H Inflammation leads to fibrosis. Nausea and vomiting that worsen before menses
H Fibrosis leads to adhesions that produce pain and in- (small bowel and appendix)
fertility. Abdominal cramps (small bowel and appendix)
Causes Physical findings
H Direct cause unknown H Multiple tender nodules on uterosacral ligaments or
H Familial susceptibility rectovaginal septum
H Direct implantation H Enlarged nodules (tender during menses)
H Transportation (retrograde menstruation) H Ovarian enlargement with endometrial cysts on the
H Formation in situ ovaries
H Induction of labor H Thickened, nodular adnexa
H Immune system defects
H Lymphatic spread theory Test results
H Inflammatory influence Diagnostic procedures
H Environmental contaminants H A scoring and staging system created by the American
Fertility Society quantifies endometrial implants ac-
Incidence cording to size, character, and location:
H Usually occurs between ages 20 and 40; uncommon Stage I indicates minimal disease (1 to 5 points).
before age 20 Stage II indicates mild disease (6 to 15 points).
H More common in females who postpone childbear- Stage III indicates moderate disease (16 to 40
ing points).
H More common in white females Stage IV indicates severe disease (more than 40
points).
Common characteristics H Laparoscopy confirms the diagnosis and identifies
H Early menarche the disease stage.
H Menstrual flow lasting longer than 7 days H Ultrasonography helps confirm the diagnosis.
H Cycles lasting longer than 27 days
H Family history of endometriosis
H Multiparity Treatment
H Cyclic pelvic pain
H Severe dysmenorrhea General
H Determined by stage of disease, patients age, and de-
Complications sire to have children
H Infertility H Pregnancy, if possible (provides temporary relief)
H Spontaneous abortion H Activity, as tolerated
H Anemia secondary to excessive bleeding
H Emotional problems secondary to infertility Medications
H Pelvic adhesions H Progestins such as medroxyprogesterone
H Severe dysmenorrhea H Hormonal contraceptives such as norethindrone
H Ovarian cyst H Gonadotropin-releasing hormone, such as goserelin
H Ovarian cancer and leuprolide
H Analgesics such as ibuprofen

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Surgery
H Laparoscopy to lyse adhesions, remove small im-
plants, and cauterize implants; for laser vaporization
of implants; usually followed by hormonal therapy to
suppress return of endometrial implants
H Total abdominal hysterectomy with bilateral
salpingo-oophorectomy in stages III and IV

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort
H exhibit no signs of infection
H express understanding of the disorder and treatment
H develop adequate coping behaviors.

Nursing interventions
H Encourage the patient to express her feelings about
the disorder.
H Offer emotional support.
H Encourage using open communication before and
during intercourse.
H Help the patient develop effective coping strategies.

Monitoring
H Effect of treatment
H Complications
H Adverse drug reactions
H Coping ability
H Pain control

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H associated complications
H avoiding minor gynecologic procedures immediately
before and during menstruation
H not postponing childbearing due to potential for in-
fertility
H annual pelvic examination and Papanicolaou test.

Discharge planning
H Refer the patient and her partner to a mental health
professional for additional counseling, if necessary.
H Refer the patient to a support group such as the En-
dometriosis Association.

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Enterobacteriaceae
infections
Overview
Description
H Variety of infections caused by a family of mostly aer-
obic, gram-negative bacilli
H Cause local and systemic infections, including inva-
sive diarrhea resembling shigellosis and noninvasive,
toxin-mediated diarrhea resembling cholera
H Escherichia coli: the cause of most nosocomial in-
fections
Pathophysiology
H When infected, incubation takes 12 to 72 hours.
H Noninvasive diarrhea results from two toxins pro-
duced by enterotoxigenic or enteropathogenic strains
of E. coli.
H Toxins interact with intestinal juices and promote ex-
cessive loss of chloride and water.
H The invasive form directly attacks the intestinal mu-
cosa without producing enterotoxins, causing local
irritation, inflammation, and diarrhea. This form
produces sporadic and outbreak-associated bloody
diarrhea due to hemorrhagic colitis, which can be
life-threatening at age extremes.
Causes
H Some strains of E. coli that are part of normal GI flo-
ra but cause infection in immunocompromised pa-
tients
H Infection usually from nonindigenous strains
H Transmission directly from an infected person
H Ingestion of contaminated food or water or contact
with contaminated utensils
H Enterotoxigenic E. coli (major cause of diarrhea
among those who travel from industrialized to devel-
oping regions)
H Most common food source: ground beef
Incidence
H May be major cause of diarrheal illness in children
in United States
H Incidence highest among travelers returning from
abroad, especially Mexico (noninvasive form),
Southeast Asia (noninvasive form), and South Ameri-
ca (invasive form)
Common characteristics
H Diarrhea (cardinal symptom)
Complications
H Bacteremia
H Severe dehydration and life-threatening electrolyte
disturbances
H Acidosis
H Shock
264 Enterobacteriaceae infections
Assessment
History
H Recent travel to another country
H Ingestion of contaminated food or water
H Recent close contact with a person who has diarrhea
H Abrupt onset of watery diarrhea
Physical findings
H Cramping abdominal pain with hyperactive bowel
sounds
H Blood and pus in infected stools
H Vomiting and anorexia
H Low-grade fever
H Signs of dehydration, especially in children
H Signs and symptoms of hyponatremia, hypokalemia,
hypomagnesemia, and hypocalcemia from electrolyte
losses
H Orthostatic hypotension
H Rapid, thready pulse
H Initially in infants, loose, watery stools that change
from yellow to green and contain little mucus or
blood
H Listlessness and irritability in infants
Test results
Laboratory
H Cultures growth of E. coli in a normally sterile lo-
cation, including the bloodstream, cerebrospinal flu-
id, biliary tract, pleural fluid, or peritoneal cavity
suggest E. coli infection at that site.
Treatment
General
H Contact enteric precautions
H Correction of fluid and electrolyte imbalances
H Initially, nothing by mouth
H Increased fluid intake (if appropriate)
H Avoidance of foods that cause diarrhea
H Small frequent meals until bowel function returns to
normal
H Activity, as tolerated
Medications
H I.V. antibiotics such as cotrimoxazole
Nursing considerations
Key outcomes
The patient will:
H regain or maintain normal fluid and electrolyte bal-
ance
H have an elimination pattern that returns to normal
H show no further evidence of weight loss
H maintain normal cardiac output.
9400E.qxd 8/2/12 4:32 PM Page 265

Nursing interventions
H Institute contact enteric precautions and use proper
hand-washing technique.
H Replace fluids and electrolytes, as needed.
H Clean the perianal area after each episode of diar-
rhea and apply skin protectant, as needed.
H Administer prescribed antibiotics.
H During epidemics, screen all facility personnel and
visitors for diarrhea, and prevent people with the dis-
order from having direct patient contact.
Monitoring
H Intake and output
H Stool volume measurement and presence of blood
and pus
H Serum electrolyte results
H Signs and symptoms of gram-negative septic shock
H Signs and symptoms of dehydration
H Vital signs
H GI status
H Cardiovascular status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H proper hand-washing technique
H the need to avoid unbottled water, ice, unpeeled fruit,
and uncooked vegetables in other countries
H signs of dehydration and seeking prompt medical at-
tention if these occur (if the patient will be cared for
at home).

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Incidence
Epididymitis H Usually affects males ages 19 to 40 or older than 60
H Affects 1 in 1,000 males anually
H Rare before puberty
Overview
Common characteristics
Description H Dull, aching groin pain
H Infection of the epididymis (cordlike excretory duct H Fever
of the testis)
H One of most common infections of the male repro- Complications
ductive tract H Orchitis (see Understanding orchitis)
H Sterility
Pathophysiology H Abscess
H Organisms enter the epididymis by the vas deferens H Atrophy
or lymphatics. H Pyocele
H Inflammation occurs. H Infarction
H Other organs, such as the testes and prostate, may be H Sepsis
affected.
Causes Assessment
H Pyogenic organisms, such as staphylococci, Es-
cherichia coli, streptococci, chlamydia, Neisseria History
gonorrhoeae, and Treponema pallidum H Chills
H Tuberculosis H Fever
H Sarcoidosis H Unilateral, dull, aching pain
H Brucellosis H Pain radiating to spermatic cord, lower abdomen,
H Leprosy and flank
H Trauma H Scrotal pain
H Certain drugs such as amiodarone H Dysuria, frequency, urgency, and urine retention
H Obstruction H Mild scrotal cellulitis
H Scrotal edema
Risk factors
H Urinary tract infection Physical findings
H Unprotected sex H Erythema
H Prostatitis H High fever
H Trauma H Characteristic waddle (attempt to protect groin and
scrotum while walking)
H Urethral discharge
Understanding orchitis H Prehn sign: elevation of hemiscrotum relieves pain
H Scrotal abscess
Orchitis, an infection of the testes, is a serious complica-
tion of epididymitis. It may also result from mumps, Test results
which can lead to sterility or, less commonly, another sys-
temic infection. Laboratory
Signs and symptoms H Urinalysis shows an increased white blood cell
Typical effects of orchitis include unilateral or bilateral ten- (WBC) count, indicating infection.
derness and redness, sudden onset of pain, and swelling H Urine culture and sensitivity tests may show the
of the scrotum and testes. Nausea and vomiting also oc- causative organism.
cur. Sudden cessation of pain indicates testicular is- H Serum WBC count is greater than 10,000/l, indicat-
chemia, which can cause permanent damage to one or ing infection.
both testes. Hydrocele may also be present. Imaging
Treatment H Ultrasonography shows an enlarged epididymis
Appropriate treatment consists of immediate antibiotic (larger than 17 mm) and can rule out testicular tor-
therapy in bacterial infection or, in mumps orchitis, injec-
sion.
tion of 20 ml of lidocaine near the spermatic cord of the
affected testis, which may relieve swelling and pain. Se-
vere orchitis may require surgery to incise and drain the
hydrocele and to improve testicular circulation. Other
Treatment
treatments are similar to those for epididymitis.
To prevent mumps orchitis, suggest that prepubertal
General
males receive the mumps vaccine (or gamma globulin in- H Scrotal elevation
jection after contracting mumps). H Ice bag to groin

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H Increased oral fluids

H Bed rest until condition improves
H Use of an athletic supporter until recovered

Medications
H Broad-spectrum antibiotics such as cefazolin
H Analgesics such as ibuprofen
H Antipyretics such as acetaminophen

Surgery
H Scrotal exploration for complications of acute epi-
didymitis
H Epididymectomy under local anesthesia, if disease is
refractory to antibiotic therapy

Nursing considerations
Key outcomes
The patient will:
H avoid or have minimal complications
H express feelings of increased comfort
H express concern about self-concept and body image
H express feelings about potential or actual changes in
sexual activity.
Nursing interventions
H Administer prescribed drugs.
H Apply ice packs for comfort.

Monitoring
H Signs of abscess formation
H Vital signs
H Pain control
H Intake and output

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medication administration, dosage, and possible ad-
verse effects
H the use of a scrotal support while sitting, standing, or
walking
H safer sex practices.

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Life-threatening disorder Assessment

History
Epidural hematoma H Injury to head
H Headache
H Nausea, vomiting
Overview H Change in mental status

Description Physical findings

H Acceleration-deceleration or coup-contrecoup in- H Head wound
juries that disrupt normal nerve functions in bruised H Neurologic signs based on the extent of bleeding
area and cause intracranial bleeding dilated pupils, weakness, sensory deficits, alterations
in reflexes, alterations in bladder or anal sphincter
Pathophysiology tone
H Injury is directly beneath the site of impact when the H Bradycardia and hypertension (with increased ICP)
brain rebounds against the skull from the force of a
blow (a beating with a blunt instrument, for exam- Test results
ple), when the force of the blow drives the brain Laboratory
against the opposite side of the skull, or when the H Coagulation studies show clotting abnormalities (if
head is hurled forward and stopped abruptly (as in cause is anticoagulation).
an automobile accident when a drivers head strikes Imaging
the windshield). H Computed tomography scan or magnetic resonance
H Brain continues moving and slaps against the skull imaging identifies abnormal masses or structural
(acceleration), then rebounds (deceleration). Brain shifts within the cranium.
may strike bony prominences inside the skull (espe-
cially the sphenoidal ridges), causing intracranial
hemorrhage or hematoma that may result in tentorial Treatment
herniation.
General
Causes H Supportive: airway, breathing, circulation
H Trauma H Wound care
H Anticoagulation H Head of the bed elevated 30 degrees with intracere-
H Thrombolysis bral injury
H Lumbar puncture H Diet based on extent of injury
H Epidural anesthesia H Nothing by mouth if surgery is necessary
H Coagulopathy or bleeding diathesis H Bed rest initially, then activity, as tolerated
H Hepatic disease with portal hypertension
H Vascular malformation Medications
H Disk herniation H Vitamin K, fresh frozen plasma, platelets, or clotting
H Paget disease of bone products (if coagulation studies are abnormal)
H Valsalvas maneuver H Analgesics such as codeine
H Hypertension H Osmotic diuretics such as mannitol
H Intracerebral lesion H Anticonvulsants such as phenytoin
H Prophylactic antibiotics
Incidence H Corticosteroids such as dexamethasone
H Rare in people younger than age 2 and older than
age 60 Surgery
H Four times more common in males than in females H Placement of burr holes
H Evacuation of the hematoma
Common characteristics H Craniotomy
H Brief loss of consciousness
H Headache
H Deteriorating mental status Nursing considerations
Complications Key outcomes
H Increased intracranial pressure (ICP) The patient will:
H Seizures H be hemodynamically stable
H Respiratory depression and failure H recover or be rehabilitated from physical injuries to
the greatest extent possible

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H use support systems to assist with coping

H express a feeling of increased comfort and pain
relief.
Nursing interventions
H Provide appropriate wound care.
H Administer prescribed drugs.
H Provide emotional support.
H Institute seizure precautions.

Monitoring
H Vital signs
H Neurologic status
H Wound healing
H Seizure activity
H Respiratory status
H Cardiovascular status, including cardiac rhythm

Patient teaching
Be sure to cover:
H reporting changes in neurologic status
H avoiding aspirin as a pain treatment
H observing for cerebrospinal fluid drainage and signs
of infection.
Discharge planning
H Refer the patient to physical, occupational, and
speech therapy, as appropriate.
H Refer the patient to social service for extended ser-
vices, as appropriate.

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H Apprehension
Life-threatening disorder H Irritability

Complications
Epiglottiditis H Airway obstruction
H Death
H Sepsis
Overview H Vocal cord paralysis

Description
H Acute inflammation of the epiglottis and surrounding Assessment
area
H Life-threatening emergency that rapidly causes ede- History
ma and induration H Recent upper respiratory tract infection
H If untreated, results in complete airway obstruction H Sore throat
H Mortality 8% to 12%, typically in children H Dysphagia
H Sudden onset of high fever
Pathophysiology
H An infection of the epiglottis and surrounding area Physical findings
leads to intense inflammation of the supraglottic re- H Stridor
gion. H Red and inflamed throat
H Swelling of the epiglottis, aryepiglottic folds, ary- H Fever
tenoid cartilage, and ventricular bands leads to acute H Drooling
airway obstruction. H Pale or cyanotic skin
H Restlessness and irritability
Causes H Nasal flaring
H Viral infection, usually Haemophilus influenzae H Tendency to sit in tripod position with mouth open
type B and tongue protruding
H Pneumococci or group A streptococci H Thick and muffled voice sounds
H Subcostal, suprasternal, and intercostal retractions
Incidence
H Higher incidence in Blacks and Hispanics Test results
H Most common in children ages 2 to 6 years Laboratory
H Occurs in any season H Arterial blood gas (ABG) analysis may show hypoxia.
H More common in males than females H Blood studies reveal elevated white blood cell count.
Imaging
Common characteristics H Lateral neck X-rays show an enlarged epiglottis and
H Sore throat distended hypopharynx.
H Dysphagia Diagnostic procedures
H Direct laryngoscopy shows swollen, beefy-red
epiglottis.
Airway crisis Other
H Pulse oximetry may show decreased oxygen satura-
Epiglottiditis can progress to complete airway obstruction tion.
within minutes. To prepare for this medical emergency,
keep these tips in mind:
H Watch for the inability to speak; weak, ineffective Treatment
cough; high-pitched sounds or no sounds while inhal-
ing; increased difficulty breathing; and possible General
cyanosis. These are warning signs of total airway ob-
H Emergency hospitalization
struction and the need for an emergency tracheotomy.
H Keep the following equipment available at the patients H Humidification of airway
bedside in case of sudden, complete airway obstruc- H Parenteral fluids
tion: a tracheotomy tray, endotracheal tubes, a hand- H Activity, as tolerated
held resuscitation bag, oxygen equipment, and a laryn- H Endotracheal intubation and mechanical ventilation
goscope with blades of various sizes.
H Remember that using a tongue blade or throat culture Medications
swab can initiate sudden, complete airway obstruction. H Parenteral antibiotics according to infective organism
H Before examining the patients throat, request trained H Corticosteroids such as hydrocortisone
personnel, such as an anesthesiologist, to stand by if H Oxygen therapy
emergency airway insertion is needed.

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Surgery
H Possible tracheotomy

Nursing considerations
Key outcomes
The patient will:
H maintain adequate ventilation
H maintain adequate fluid volume
H maintain a patent airway (see Airway crisis)
H use alternate means of communication.

Nursing interventions
H Administer prescribed drugs.
H Place the patient in a sitting position.
H Place the patient in a cool-mist tent.
H Encourage the parents to remain with their child.
H Offer reassurance and support.
H Ensure adequate fluid intake.
H Minimize external stimuli.
H Maintain a patent airway.

Monitoring
H Swallowing
H Vital signs
H Intake and output
H Respiratory status
H ABG results
H Pulse oximetry
H Signs and symptoms of secondary infection
H Signs and symptoms of dehydration
H Cardiovascular status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H prescribed medications and possible adverse effects
H when to call the practitioner
H humidification
H signs and symptoms of respiratory distress
H signs and symptoms of dehydration.

Discharge planning
H Refer the patient for H. influenzae b conjugate vac-
cine, preferably at age 2 months, if indicated.

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Epilepsy H Headache
H Mood changes
H Lethargy
H Myoclonic jerking
Overview H Description of an aura
H Pungent smell
Description H GI distress
H Neurologic condition characterized by recurrent H Rising or sinking feeling in the stomach
seizures H Dreamy feeling
H Good seizure control in about 80% of patients with H Unusual taste in the mouth
strict adherence to prescribed treatment H Vision disturbance
H Also known as seizure disorder H Incontinence

Pathophysiology Physical findings

H Seizures are paroxysmal events involving abnormal H Findings possibly normal while patient isnt having a
electrical discharges of neurons in the brain and cell seizure and when the cause is idiopathic
membrane potential. H Findings related to underlying cause of the seizure
H On stimulation, the neuron fires, the discharge
spreads to surrounding cells, and stimulation contin- Test results
ues to one side or both sides of the brain, resulting Laboratory
in seizure activity. H Serum glucose and calcium study results rule out
other diagnoses.
Causes Imaging
H Idiopathic in half of cases H Computed tomography scan and magnetic resonance
Nonidiopathic epilepsy imaging may indicate abnormalities in internal struc-
H Birth trauma tures.
H Anoxia H Skull radiography may show certain neoplasms with-
H Perinatal infection in the brain substance or skull fractures.
H Genetic abnormalities (tuberous sclerosis and H Brain scan may show malignant lesions when X-ray
phenylketonuria) findings are normal or questionable.
H Perinatal injuries H Cerebral angiography may show cerebrovascular ab-
H Metabolic abnormalities (hypoglycemia, pyridoxine normalities, such as aneurysm or tumor.
deficiency, hypoparathyroidism) Other
H Brain tumors or other space-occupying lesions H EEG shows paroxysmal abnormalities. (A negative
H Meningitis, encephalitis, or brain abscess EEG doesnt rule out epilepsy because paroxysmal
H Traumatic injury abnormalities occur intermittently.)
H Ingestion of toxins, such as mercury, lead, or carbon
monoxide
H Stroke Treatment
H Apparent familial incidence in some seizure disor-
ders General
H Airway protection during seizure
Incidence H Vagus nerve stimulation by pacemaker (see Vagus
H Patients usually younger than age 20 nerve stimulation)
H Affects both sexes H A detailed presurgical evaluation to characterize
H First seizure usually during childhood or after age 50 seizure type, frequency, site of onset, psychological
functioning, and degree of disability to select candi-
Common characteristics dates for surgery in medically intractable patients
H Recurring seizures H No dietary restrictions
H Safety measures
Complications H Activity, as tolerated
H Anoxia
H Traumatic injury Medications
H Anticonvulsants such as phenytoin
H Benzodiazepines such as lorazepam
Assessment
Surgery
History H Removal of a demonstrated focal lesion
H Seizure occurrence unpredictable and unrelated to H Correction of the underlying problem
activities
H Precipitating factors or events possibly reported

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Vagus nerve stimulation Discharge planning

H Refer the patient to the Epilepsy Foundation of Amer-
The vagus nerve stimulator is a Food and Drug Adminis-
trationapproved method to treat medically refractory ica.
epilepsy. The stimulator device is about the size of a pace- H Refer the patient to his states motor vehicle depart-
maker and is surgically placed in a pocket under the skin ment for information about a drivers license.
in the upper chest. Leadwires from the stimulator are tun-
neled under the skin to a neck incision where the vagus
nerve has been exposed. The electrode coils are then
placed around the nerve. The treating practitioner has a
computer, which can be used to alter the stimulation
parameters, thereby optimizing the treatment of seizures.
The device stimulates the vagus nerve for 30 seconds
every 5 minutes to prevent seizure occurrence. A magnet
over the area can activate the device to give extra, on-
demand stimulation if the patient feels a seizure coming
on. Adverse effects are voice change, throat discomfort,
shortness of breath, and coughing and are usually experi-
enced only when the device is on.

Nursing considerations
Key outcomes
The patient will:
H remain free from injury
H communicate understanding of the condition and
treatment regimen
H use support systems and develop adequate coping
H maintain usual participation in social situations and
activities.
Nursing interventions
H Institute seizure precautions.
H Prepare the patient for surgery, if indicated.
H Administer prescribed anticonvulsants.

Monitoring
H Neurologic status
H Response to anticonvulsants
H Vital signs
H Seizure activity
H Respiratory status
H Adverse drug reactions
H Associated injuries

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H maintaining a normal lifestyle
H compliance with the prescribed drug schedule
H adverse drug effects
H care during a seizure
H the importance of regular meals and checking with
the practitioner before dieting
H the importance of carrying a medical identification
card or wearing medical identification jewelry.

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Erectile dysfunction Assessment

History
Overview H Long-standing inability to achieve erection
H Sudden loss of erectile function
Description H Gradual decline in sexual function
H Inability to attain or maintain penile erection long H Medical disorders, drug therapy, or psychological
enough to complete intercourse trauma
H Classified as primary or secondary: H Achievement of erection through masturbation but
Primary impotence: never achieving sufficient not with a partner
erection
Secondary impotence: patient has achieved erec- Physical findings
tion and completed intercourse in the past H Anxious appearance
H Also called impotence H Signs of depression

Pathophysiology DSM-IV-TR criteria

H A lack of autonomic signal or impairment of perfu- H Diagnosis confirmed when patient meets criteria:
sion may interfere with arteriolar dilation due to in- Persistent or recurrent partial or complete failure
appropriate adrenergic stimulation. to attain or maintain erection until completion of
H Premature collapse of the sacs of the corpus caver- sexual activity
nosum occurs. Marked distress or interpersonal difficulty as a re-
H Pelvic steal syndrome can cause loss of erection be- sult of erectile dysfunction
fore ejaculation due to increased blood flow to pelvic Erectile dysfunction not better accounted for by
muscles. another Axis I disorder and not caused by a drug
or medical condition
Causes
H 80% of cases believed to have an organic cause, such Test results
as vascular insufficiency and veno-occlusive dysfunc- Laboratory
tion H Hormone levels may be decreased.
H 20% of cases believed to be psychogenic in origin Imaging
H Ultrasonography evaluates vascular function.
Risk factors Diagnostic procedures
H Medication H Angiography evaluates vaso-occlusive disease.
H Pelvic injury or surgery Other
H Alcohol use H Direct injection of prostaglandin E1 (alprostadil)
H Increasing age into the corpora evaluates the quality of erection.
H Smoking H Nocturnal penile tumescence testing helps distin-
H Obesity guish psychogenic impotence from organic impo-
H Hypertension tence.
H Diabetes mellitus
H Scleroderma
H Renal failure Treatment
H Cancer treatment
H Stroke General
H Multiple sclerosis H Sex therapy for psychogenic impotence
H Alzheimers disease H Treatment of cause for organic impotence
H Depression H Psychological counseling
H Avoidance of alcohol
Incidence H External vacuum device
H Affects males of all age-groups, but incidence in-
creases with age Medications
H Intracavernosal injection therapy
Common characteristics H Medicated Urethral System for Erections
H Depression intraurethral suppository
H Inability to obtain or maintain an erection H Hormone replacement such as testosterone
H Phosphodiesterase type-5 inhibitors, such as silde-
Complications nafil and vardenafil
H Serious disruption of marital or other sexual rela-
tionships

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Surgery
H Surgically inserted inflatable or semirigid penile
prosthesis

Nursing considerations
Key outcomes
The patient will:
H acknowledge a problem in sexual function
H discuss feelings and perceptions about changes in
sexual performance
H develop and maintain a positive attitude toward sexu-
ality and sexual performance.
Nursing interventions
H Encourage verbalization and provide support.
H As needed, refer the patient to a physician, nurse,
psychologist, social worker, or counselor trained in
sex therapy.
After penile prosthesis surgery
H Apply ice packs to the penis for 24 hours.
H Empty the drainage device when its full.
H If the patient has an inflatable prosthesis, provide in-
structions for use.
Monitoring
H Response to treatment
H Adverse effects of medication
H Complications
H Postoperative bleeding
H Postoperative infection

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the anatomy and physiology of the reproductive sys-
tem and the human sexual response cycle
H the need to avoid intercourse until the incision heals,
usually 6 weeks after penile implant surgery
H signs of infection.

Discharge planning
H Refer the patient to support services.

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H This can cause hemolytic disease even if fetal ery-

Life-threatening disorder throcytes dont escape into the maternal circulation
during pregnancy.
Erythroblastosis fetalis Rh incompatibility
H During her first pregnancy, an Rh-negative female be-
comes sensitized (during delivery or abortion) by ex-
posure to Rh-positive fetal blood antigens inherited
Overview from the father.
H A female may also become sensitized from receiving
Description blood transfusions with alien Rh antigens; from inad-
H Hemolytic disease of the fetus and neonate equate doses of Rh0(D) (RhoGAM); or from failure
H Stems from an incompatibility of fetal and maternal to receive Rh0(D) after significant fetal-maternal
blood leakage during abruptio placentae (premature de-
H Also known as hemolytic disease of the newborn tachment of the placenta).
H A subsequent pregnancy with an Rh-positive fetus
Pathophysiology provokes maternal production of agglutinating anti-
ABO incompatibility bodies, which cross the placental barrier, attach to
H Each blood group has specific antigens on red blood Rh-positive cells in the fetus, and cause hemolysis
cells (RBCs) and specific antibodies in the serum. and anemia.
H The maternal immune system forms antibodies H To compensate, the fetal blood-forming organs step
against fetal cells when blood groups differ. up the production of RBCs, and erythroblasts (imma-
ture RBCs) appear in the fetal circulation.
H Extensive hemolysis releases more unconjugated
bilirubin than the liver can conjugate and excrete,
causing hyperbilirubinemia and hemolytic anemia.
What happens in Rh isoimmunization Causes
H ABO incompatibility
H Rh isoimmunization (see What happens in Rh
Rh-negative woman before pregnancy isoimmunization)
Incidence
H Rh negativity 15% of Whites, 5% to7% of Blacks,
Pregnancy with Rh-positive fetus rare in Asians
H About 4,000 cases per year
H ABO incompatibility frequently occurs during first
pregnancy; present in about 12% of pregnancies
Placental separation
Common characteristics
H Jaundice
H Anemia
H Hepatosplenomegaly
Maternal sensitization to Rh-positive blood
H Hydrops fetalis

Complications
H Fetal death in utero
Next pregnancy with Rh-positive fetus H Severe anemia
H Heart failure
H Kernicterus

Maternal anti-Rh antibodies enter fetal circulation

Assessment
History
Anti-Rh antibody to fetal Rh-positive red blood cells (RBCs) H Mother Rh-positive; father Rh-negative
H Antigen-antibody response developed during previ-
ous pregnancy
H Blood transfusion
Hemolysis of fetal RBCs H Maternal history (for erythroblastotic stillbirths,
abortions, previously affected children, previous anti-
Rh titers)

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Physical findings H maintain fluid balance within normal limits

H Pallor H maintain normal temperature.
H Edema
H Petechiae Nursing interventions
H Bile-stained umbilical cord H Encourage expression of fears by parents concerning
H Yellow- or meconium-stained amniotic fluid possible complications of treatment.
H Mild to moderate hepatosplenomegaly H Promote normal parental bonding.
H Pulmonary crackles H Administer Rho(D) I.M., as ordered.
H Heart murmur
H Jaundice Monitoring
H Vital signs
Test results H Cardiac rhythm and rate
Laboratory H Temperature
H Paternal blood is typed for ABO and Rh. H Respiratory status
H Amniotic fluid analysis shows increased bilirubin and H Transfusion complications
anti-Rh titers. H Intake and output
H Direct Coombs test of umbilical cord blood mea-
sures RBC (Rh-positive) antibodies in the neonate
(positive only when the mother is Rh negative and Patient teaching
the fetus is Rh positive).
H Cord hemoglobin level in neonate is less than 10 g, Be sure to cover:
indicating severe disease. H the disorder, diagnosis, and treatment
H Many nucleated peripheral RBCs are present. H medications, drug routes, and administration
Imaging H preventive measures for reoccurrence.
H Radiologic studies show edema and, in hydrops fetal-
is, the halo sign (edematous, elevated, subcutaneous Discharge planning
fat layers) and the Buddha position (fetuss legs are H Encourage follow-up appointments.
crossed).

Treatment
General
H Phototherapy (exposure to ultraviolet light to reduce
bilirubin levels)
H Intubation of neonate
H Removal of excess fluid
H Maintenance of body temperature

Medications
H Intrauterine-intraperitoneal transfusion (if amniotic
fluid analysis suggests the fetus is severely affected
and not mature enough to deliver)
H Exchange transfusion
H Albumin infusion
H Gamma globulin containing anti-Rh antibody
(Rho[D])
Surgery
H Planned delivery (usually 2 to 4 weeks before term
date, depending on maternal history, serologic test
results, and amniocentesis)

Nursing considerations
Key outcomes
The patient will:
H exhibit adequate ventilation
H remain hemodynamically stable

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Esophageal cancer
Overview
Description
H Esophageal tumors usually fungating and infiltrating
and nearly always fatal
H Common sites of metastasis are liver and lungs
H Includes two types of malignant tumors: squamous
cell carcinoma and adenocarcinoma
H Grim prognosis (5-year survival rates occur in less
than 5% of cases; most patients die within 6 months
of diagnosis)
Pathophysiology
H Most esophageal cancers are poorly differentiated
squamous cell carcinomas, with 50% occurring in
the lower portion of the esophagus, 40% in the mid-
dle portion, and 10% in the upper or cervical esoph-
agus.
H Adenocarcinomas occur less frequently and are con-
tained to the lower third of the esophagus.
H The tumor partially constricts the lumen of the
esophagus.
H Regional metastasis occurs early by way of submu-
cosal lymphatics, often fatally invading adjacent vital
intrathoracic organs. (If the patient survives primary
extension, the liver and lungs are the usual sites of
distant metastases; unusual metastasis sites include
the bone, kidneys, and adrenal glands.)
Causes
H Unknown
Risk factors
H Human papillomavirus
H Chronic irritation from heavy smoking
H Excessive use of alcohol
H Stasis-induced inflammation, as in achalasia or stric-
ture
H Previous head and neck tumors
H Nutritional deficiency, such as in untreated sprue and
Plummer-Vinson syndrome
H Exposure to nitrosamines
Incidence
H Most common in males older than age 60
H Occurs worldwide, but most common in Japan, Rus-
sia, China, the Middle East, and the Transkei region
of South Africa
Common characteristics
H Dysphagia
H Weight loss
H Esophageal obstruction
H Acute pain
H Hoarseness, coughing
H Cachexia
Complications
H Direct invasion of adjoining structures
H Inability to control secretions
H Obstruction of the esophagus
H Loss of lower esophageal sphincter control (may re-
sult in aspiration pneumonia)
Assessment
History
H Feeling of fullness, pressure, indigestion, or subster-
nal burning
H Dysphagia and weight loss; the degree of dysphagia
varies, depending on the extent of disease
H Hoarseness
H Pain on swallowing or pain that radiates to the back
H Anorexia, vomiting, and regurgitation of food
Physical findings
H Chronic cough (possibly from aspiration)
H Cachexia and dehydration
Test results
Laboratory
H Complete blood count reveals anemia.
H Bleeding time may be prolonged.
Imaging
H X-rays of the esophagus, with barium swallow and
motility studies, are used to delineate structural and
filling defects and reduced peristalsis.
H Computed tomography scan may help to diagnose
and monitor esophageal lesions.
H Esophagogastroduodenoscopy shows tumor and per-
mits biopsy.
Diagnostic procedures
H Esophagoscopy, punch and brush biopsies, and exfo-
liative cytologic tests confirm esophageal tumors.
H Bronchoscopy (usually performed after an esopha-
goscopy) may reveal tumor growth in the tracheo-
bronchial tree.
H Endoscopic ultrasonography of the esophagus com-
bines endoscopy and ultrasound technology to mea-
sure the depth of penetration of the tumor.
Treatment
General
H Surgery and other treatments to relieve disease ef-
fects
H Palliative therapy used to keep esophagus open:
Dilatation of the esophagus
Laser therapy
Radiation therapy
Installation of prosthetic tubes (such as Celestins
tube)
H Liquid to soft diet, as tolerated
H High-calorie supplements

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Medications
H Chemotherapy such as fluorouracil
H Analgesics such as morphine

Surgery
H Radical surgery to excise tumor and resect esopha-
gus or stomach and esophagus
H Gastrostomy or jejunostomy

Other
H Endoscopic laser treatment and bipolar electrocoag-
ulation

Nursing considerations
Key outcomes
The patient will:
H maintain weight
H maintain fluid volumes within the normal range
H not aspirate
H express feelings of increased comfort and decreased
pain.
Nursing interventions
H Provide support and encourage verbalization.
H Position the patient with the head of the bed elevated
at least 30 degrees to prevent aspiration.
H Provide tube feedings, as ordered.
H Administer prescribed drugs.
H Encourage incentive spirometer use.

Monitoring
H Vital signs
H Hydration and nutritional status
H Electrolyte levels
H Intake and output
H Postoperative complications
H Swallowing ability
H Pain control
H Respiratory status

Patient teaching
Be sure to cover:
H the disease process, treatment, and postoperative
course
H dietary needs
H the need for rest between activities.

Discharge planning
H Arrange for home care follow-up after discharge.
H Refer the patient to the American Cancer Society.

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Exophthalmos Assessment
History
Overview H Vision changes
H Eye trauma
Description
H Unilateral or bilateral bulging or protrusion of the Physical findings
eyeballs or their apparent forward displacement H Eye protrusion (see Detecting unilateral exophthal-
(with lid retraction) mos)
H Also called proptosis H Visible rim of the sclera
H Infrequent blinking
Pathophysiology H Limited ocular movement
H Increase in volume within the fixed bony orbital con- H Ocular tenderness
fines displaces the globular orbit anteriorly.
Test results
Causes Laboratory
H Ophthalmic Graves disease H Culture of discharge determines the infecting organ-
H Trauma ism.
H Hemorrhage H Sensitivity testing indicates appropriate antibiotic
H Varicosities therapy.
H Thrombosis Imaging
H Edema H Computed tomography scan detects swollen extraoc-
H Infection ular muscles or lesions within the orbit.
H Orbital cellulitis Diagnostic procedures
H Panophthalmitis H Exophthalmometer readings confirm diagnosis by
H Tumors and neoplastic diseases showing the degree of anterior projection and asym-
H Vasculitis metry between the eyes. (Normal bar readings range
from 12 to 20 mm.)
Incidence
H Occurs more often in females than in males
H Can occur at any age, but more common between Treatment
ages 30 and 50
General
Common characteristics H Cold and warm compresses (trauma)
H Bulging eyeball (see Recognizing exophthalmos) H Activity, as tolerated
H Diplopia
Medications
Complications H Antibiotics such as cefazolin to treat infection
H Vision changes H Antithyroid therapy such as propylthyrouracil for
Graves disease
H Corticosteroids such as dexamethasone to treat optic
neuropathy
H Eye lubricants

Recognizing exophthalmos
This photo shows the characteristic forward protrusion of
the eyes from the orbit associated with exophthalmos.
Surgery
H Orbital decompression (removal of the superior and
lateral orbital walls) if vision threatened, followed by
lid (blepharoplasty) and muscle surgery
H Surgical exploration of the orbit and excision of the
tumor

Nursing considerations
Key outcomes
The patient will:
H maintain functional eyesight
H understand cause and treatment of exopthalmus
H experience normal eye movement.

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Detecting unilateral exophthalmos

If one of the patients eyes seems more prominent than
the other, examine both eyes from above the patients
head. Look down across his face, gently draw his lids up,
and compare the relationship of the corneas to the lower
lids. Abnormal protrusion of one eye suggests unilateral
exophthalmos.
Dont perform this test if you suspect eye trauma.

Nursing interventions
H Administer prescribed drugs.
H Apply cold and warm compresses, as ordered, for
fracture or other trauma.
H Provide postoperative care.
H Provide emotional support.
H Protect the exposed cornea with lubricants to prevent
corneal drying.
Monitoring
H Response to therapy
H Visual acuity

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H eye care
H prescribed medications and possible adverse effects
H proper administration of eyedrops.

Discharge planning
H Encourage follow-up care.

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FFailure to thrive
Overview
Description
H Failure to maintain weight (and sometimes height)
above the fifth percentile
H Deviation from established growth curve
H Three types
Organic
Nonorganic
Mixed
H Occurs in infants, children, adolescents, and adults
H Young or single mother without social supports
H Parents who are overly focused on career
H Caregivers with inadequate adaptive and social skills
H Depression (in parent or in adult patient with failure
to thrive)
Incidence
H Exact figures unknown
H 1% to 5% of children younger than age 2 years who
are admitted to hospitals
H An estimated 10% of children in primary care set-
tings
H Higher in children from families with medical and
psychosocial problems, those of low socioeconomic
status, and undeveloped countries
H Nonorganic form slightly higher in females
Pathophysiology
H Organic Common characteristics
Calorie intake is less than required for nutritional H Absence of weight gain or weight loss
needs due to the presence of a physiologic disor- H Altered body posture
der. H Thin appearance
H Nonorganic H Muscle wasting
A complex dynamic exists between the caregiver
and the patient, including a decreased emotional Complications
attachment. H Disease susceptibility
Sufficient food is available, but the patient may be H Growth retardation
fed an unusual or overly restricted diet. H Developmental delays
H Mixed H Impaired bonding
This is a combination of organic and nonorganic H Altered family relationships
explanations.
Causes Assessment
H Organic
Acute or chronic illness History
Defects in major organ systems H Prenatal
Malabsorption syndrome Use of drugs, alcohol, cigarettes
Endocrine deficiencies Diseases
Congenital heart defects H Labor and delivery
Fetal alcohol syndrome H Family medical and social history, including genetic
Cystic fibrosis disorders
Feeding difficulties H Early neonatal
Long-term gastroenteritis Birth weight
Premature birth Initial weight loss
Dementia (in adults) Birth defects
H Nonorganic H Feeding
Psychological problem between patient and prima- Nursing patterns of breast-fed infant; frequency
ry caregiver and time spent nursing
Failure to bond Maternal diet
Dysfunctional parenting behaviors Formula; type, amount, and frequency
Economic problems Current eating patterns
Poor eating habits H Psychosocial family problems
Neglect or abuse H Age at which the problem was first observed
Parental ignorance about appropriate child care H Previous growth information
H Mixed H Medications
Combination of organic and nonorganic causes H Caregivers knowledge of appropriate care

Risk factors Physical findings

H Untreated medical conditions H Short stature
H Low-birth-weight or premature infant H Weight below fifth percentile
H Domestic violence H Small head circumference
H Poverty H Decreased skin-fold thickness

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H Delayed motor function Nursing interventions

H Developmental delays
H Neuromuscular weakness
H Gaze avoidance
H Minimal smiling
H Signs and symptoms of underlying disease
H Caregiver-patient interactions
Test results
Laboratory
H Complete blood count shows anemia.
H Stool analysis shows abnormal absorption or blood
indicating possible underlying disorder.
H Erythrocyte sedimentation rate is elevated, indicating
possible underlying disorder.
H Decreased electrolyte levels show poor nutritional in-
take.
H Blood lead level indicates lead poisoning.
H Thyroid test results indicate a hyperthyroid state.
H Elevated liver function study results point to an un-
derlying disorder.
H Sweat-chloride test is done to rule out cystic fibrosis.
H Elevated glucose or glycosylated hemoglobin level in-
dicates diabetes.
H Elevated blood urea nitrogen and creatinine levels in-
dicate a kidney disorder.
X-rays
H GI studies may detect an organic cause.
H Bone X-rays establish bone age.
Other
H Short-term hospitalization determines whether disor-
der is nonorganic (child will gain weight).
H Developmental testing shows delays.
H Plot the childs growth and weight, as ordered.
H Assess for signs and symptoms of organic disease.
H Provide supportive environment.
H Encourage positive parenting.
Monitoring
H Signs and symptoms of complications
H Nutritional status
H Caregiver compliance with patients nutritional needs
H Weight
Patient teaching
Be sure to cover:
H the disorder and its treatment
H importance of maintaining the feeding schedule
H normal growth and development
H where and how to obtain help during crisis situations
H the proper care of infants and children.
Discharge planning
H Refer the patient to social worker and nutrition spe-
cialist, as appropriate.
H Refer the patient to community agencies, education
programs, stress management training, and support
groups, as indicated.

Treatment
General
H Underlying medical condition
H Liquid nutritional supplements
H High-calorie balanced diet

Medications
H Vitamins

Nursing considerations
Key outcomes
The patient will:
H receive appropriate medical care
H display age-appropriate nutrient intake
H demonstrate normal growth and development.
The caregiver will:
H verbalize understanding of the need for adequate nu-
trition
H demonstrate appropriate feeding techniques
H participate in developing a plan to promote parenting
skills, as appropriate
H seek psychological care and social assistance, as
needed.

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Complications
Fibrocystic breast H Benign condition usually not leading to breast cancer

disease H Makes it more challenging to do breast self-examina-

Overview
Description
H Common, benign breast condition
H Changes in breast tissue related to hormonal cycles
H Typically resolves after menopause
Pathophysiology
H Hormonal variations during the menstrual cycle are
normal.
H Estrogen and progesterone cause breast tissue cells
to grow and multiply.
H Prolactin, growth factor, insulin, and thyroid hor-
mone also affect breast tissue.
H They stimulate growth of breast glandular tissue and
increase the activity of blood vessels, cell metabo-
lism, and supporting tissue.
H Secretions produced by glandular cells may not be
completely reabsorbed, causing fibrosis.
H Secretions become trapped in glandular cells, form-
ing cysts.
Causes
H Fluctuations in hormone levels during menstrual
cycle
H Changes typically right before menstruation
H Dietary factors, including consumption of caffeine,
excessive saturated fats, and salts
H Estradiol excess (can occur from taking oral contra-
ceptives or other synthetic forms of estrogen)
H Diabetes or thyroid dysfunction
Risk factors
H Hormone replacement therapy
H Nullipara
H Irregular menstrual cycles
H Family history of fibrocystic breast disease or breast
cancer
H Dietary factors
Incidence
H Present in about 30% of females in United States
H Most common between the ages of 30 and 50
H Estimated to affect over 60% of all females
H Rare in postmenopausal females
Common characteristics
H Tends to be symmetrical but can occur in only one
breast
H Lumps that move freely in the breast tissue and vary
in texture and size
H Breast tenderness and pain ranging from mild to se-
vere
tions
H May make mammography more difficult to interpret;
early cancerous lesions possibly being overlooked
Assessment
History
H Premenstrual breast tenderness and swelling that im-
proves after menstrual period
H Dull, heavy pain and tenderness
H Feeling of fullness in breasts
H Nipple sensation changes; possibly itching
Physical findings
H Dense, irregular, and bumpy cobblestone consis-
tency in breast tissue
H Usually found in outer upper quadrants and under-
side of the breast
H Can occur as an isolated lump, in clusters, or wide-
spread
H Free movement of lumps in breast tissue
H Lumps usually smooth, round, fluid-filled, and slight-
ly elastic; varying in texture and size
H Possibly severe breast tenderness and pain
H Non-bloody nipple discharge; varying from clear and
watery to sticky
Test results
Imaging
H Mammography, ultrasonography, or magnetic reso-
nance imaging rule out malignancy.
Diagnostic procedures
H Needle aspiration and biopsy confirm benign condi-
tion.
Treatment
General
H Dietary changes such as:
Reducing or eliminating caffeine consumption
(controversial); includes chocolate, sodas, coffee,
and tea
Reducing sugar and salt intake
Limiting consumption of saturated fats
Avoiding commercially raised meats containing
hormones
Eating a high-fiber diet, including many plant-
based foods, fruits and vegetables, beans and peas,
raw seeds and nuts, and whole grains
Increasing seafood consumption, such as salmon,
trout, and mackerel (high in omega-3 fatty acids
and iodine)
H Increased vitamin and mineral intake
Vitamin A to reduce the pain symptoms and the
size of the breast lesions

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Vitamin E to reduce pain and tenderness as well as

size of cysts
Magnesium supplement to help relieve cyclic
breast pain
Evening primrose oil, a source of the essential fat-
ty acid, linoleic acid, and its chemical derivative,
gamma linolenic acid, to relieve symptoms and
possibly aid in correction of hormonal irregulari-
ties
H Application of heat to relieve pain
H Use of bra with good support to restrict motion
H Avoidance of estrogen supplementation

Medications
H Diuretics, such as furosemide, hydrochlorothiazide,
and triamterene
H Drugs that alter hormone levels, such as bromocrip-
tine, tamoxifen, and danazol
H Acetaminophen or nonsteroidal anti-inflammatory
drugs, such as ibuprofen and naproxen
Surgery
H Removal of lumps in the most severe cases

Nursing considerations
Key outcomes
The patient will:
H express feelings of comfort and reduced pain
H verbalize understanding of the disease and its treat-
ment
H demonstrate correct procedure for performing
breast self-examination
H acknowledge need to contact practitioner if changes
occur in breasts.
Nursing interventions
H Provide pain medication, as ordered.
H Assist with breast examination.

Monitoring
H Pain signs and symptoms
H Changes in breast lumps

Patient teaching
Be sure to cover:
H the disease and its treatment
H the correct method of breast self-examination
H dietary modifications
H when to contact the practitioner.

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Fibromyalgia syndrome H Sleep disturbances with frequent arousal and frag-

mented sleep or frequent waking throughout night
(patient unaware of arousals)
H Possible report of irritable bowel syndrome, tension
Overview headaches, puffy hands, and paresthesia
Description Physical findings
H A diffuse chronic pain syndrome H Tender points are elicited by applying a moderate
H Referred to as FMS amount of pressure to a specific location. (See Ten-
H Previously called fibrositis der points of fibromyalgia.)
Pathophysiology Test results
H Several theories describe FMS: H Diagnostic testing in FMS not associated with an un-
Blood flow to the muscle is decreased (due to derlying disease is generally negative for significant
poor muscle aerobic conditioning, rather than abnormalities.
other physiologic abnormalities).
Blood flow in the thalamus and caudate nucleus is
decreased, leading to a lowered pain threshold. Treatment
Endocrine dysfunction such as abnormal
pituitary-adrenal axis responses or abnormal General
levels of the neurotransmitter serotonin in brain H Massage therapy
centers affects pain and sleep. H Ultrasound treatments
The functioning of other pain-processing pathways H Regular, low-impact aerobic exercise program such
is abnormal. as water aerobics
H Preexercise and postexercise stretching to minimize
Causes injury
H Unknown
H May be primary disorder or associated with underly- Medications
ing disease H Serotonin reuptake inhibitors such as paroxetine
H Possible association with infection H Tricyclic antidepressants, such as amitriptyline and
H May be multifactorial and influenced by stress, physi- nortriptyline
cal conditioning, abnormal-quality sleep, neuroen- H Nonsteroidal anti-inflammatory drugs such as
docrine factors, psychiatric factors and, possibly, ibuprofen
hormonal factors (due to predominance in females) H Magnesium supplements
H Lidocaine injections
Incidence
H Observed in up to 15% of patients seen in general
rheumatology practice and 5% of general medicine Nursing considerations
clinic patients
H More common in females than in males Key outcomes
H May occur at almost any age; peak incidence among The patient will:
those ages 20 to 60 H express feelings of increased comfort and decreased
pain
Common characteristics H attain the highest degree of mobility possible within
H Widespread pain and fatigue the confines of the disease
H express feelings about limitations
Complications H express an increased sense of well-being.
H Pain
H Depression Nursing interventions
H Sleep deprivation H Administer prescribed drugs.
H Provide emotional support.
H Encourage the patient to perform regular stretching
Assessment exercises safely and effectively.
H Provide reassurance that FMS can be treated.
History
H Diffuse, dull, aching pain across neck and shoulders Monitoring
and in lower back and proximal limbs H Sensory disturbances
H Pain typically worse in morning, sometimes with stiff- H Pain control
ness; can be exacerbated by stress, lack of sleep, H Response to treatment
weather changes, and inactivity H Fatigue
H Depression

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Tender points of fibromyalgia

The patient with fibromyalgia syndrome may complain of specific areas of tenderness, which are shown in the
illustrations below.

Occiput:
Suboccipital muscle
insertions

Trapezius:
Midpoint of the upper
border

Supraspinatus: Low cervical:

Above the scapular spine Anterior aspects of the inter-
near the medial border transverse spaces at C5 to C7

Gluteal: Second rib:

Upper outer quadrants Second costochondral
of buttocks junctions

Greater trochanter: Lateral epicondyle:

Posterior to the 2 cm distal to the
trochanteric prominence epicondyles

Knee:
Medial fat pad proximal
to the joint line

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the importance of exercise in maintaining muscle
conditioning, improving energy and, possibly, im-
proving sleep quality
H the importance of taking the tricyclic antidepressant
dose 1 to 2 hours before bedtime, which can im-
prove sleep benefits while reducing the morning-
after effect
H the avoidance of decongestants and caffeine before
bedtime
H the need for a low-fat diet, high in complex carbohy-
drates, to decrease symptoms.
Discharge planning
H Refer the patient to appropriate counseling, as
needed.

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Folliculitis, Carbunculosis
H Abscess of adjacent furuncles

furunculosis, and H Develops more slowly

Pathophysiology
carbunculosis H The infecting organism invades the hair follicle.
H An inflammatory reaction within the hair follicle re-
sults. (See Hair follicles and bacterial infection.)
Overview
Causes
Description H Bacterial infection, typically coagulase-positive
Folliculitis Staphylococcus aureus
H Superficial bacterial infection of hair follicles that H Contamination from an infected wound elsewhere on
usually heals without scarring the body
H Characterized by the formation of pustules
H Typically a localized eruption Risk factors
H Predilection for perifollicular (hairy) areas and flex- H Poor personal hygiene
ural surfaces H Debilitation
H May occur in the beard region (sycosis barbae) H Immunosuppression
H May occur in the scalp or on extremities (follicular H Diabetes mellitus
impetigo) H Occlusive agents or chemicals such as cosmetics
H May lead to the development of furuncles (furuncu- H Tight-fitting clothing
losis) or carbuncles H Improper shaving technique
H Prognosis depending on severity, patients physical H Occlusive therapy, using steroids
condition, and ability to resist infection H Obesity
Furunculosis H Chronic colonization of S. aureus in nares or per-
H Deeper infections characterized by deeper, more ten- ineum
der, and erythematous nodules or boils
H Worsened by irritation, friction, or perspiration Incidence
Folliculitis
H Common infection
H Affects all ages
Hair follicles and bacterial infection
H Affects males more commonly than females
The degree of hair follicle involvement in bacterial skin in- Furunculosis
fection ranges from superficial folliculitis (erythema and a H Uncommon in children unless immunocompromised
pustule in a single follicle) to deep folliculitis (extensive H Increased frequency after puberty
follicle involvement), to furunculosis (red, tender nodules H More common in adolescents and young adults
that surround follicles with a single draining point) and, fi- H Affects males and females equally
nally, to carbunculosis (deep abscesses that involve sever- Carbunculosis
al follicles with multiple draining points). H Not uncommon for several family members to be af-
fected at the same time
Superficial folliculitis H More common in patients with diabetes and in pa-
tients who are immunocompromised
Deep folliculitis H Affects males more commonly than females

Furunculosis Common characteristics

H Pustules
Carbunculosis H Pain
H Erythema

Complications
H Cellulitis
H Septicemia
H Hematogenous seeding to heart valves, joints, and
other organs
H Residual scarring

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H report feelings of increased comfort

Assessment H demonstrate understanding of proper skin care regi-
men.
History
H Presence of risk factors Nursing interventions
H Pain and erythema for several days or longer H Perform wound care.
H Malaise H Properly dispose of contaminated dressings.
H Follow standard precautions.
Physical findings H Apply warm, moist compresses.
Folliculitis H Assist with general hygiene and comfort measures, as
H Localized pustules, usually on the scalp or extremi- needed.
ties H Administer prescribed pain medications and antibi-
H Pustules possibly also in beard area or on eyelids otics.
(styes)
Furunculosis Monitoring
H Hard, painful, or fluctuant nodules usually on neck, H Adverse drug reactions
face, axillae, or buttocks H Response to treatment
H If nodules enlarge and rupture, pus and necrotic ma- H Level of comfort
terial on the skin surface H Complications
H Erythema that may persist for days or weeks after
nodule rupture
Carbunculosis Patient teaching
H Fever
H Extremely painful, deep abscesses Be sure to cover:
H Abscesses drain through multiple openings onto the H the disorder, diagnosis, and treatment
skin surface H meticulous hand-washing technique
H Pain, tenderness, and edema around pustule sites H good personal hygiene
H Hard or fluctuant nodules under skin surface H how to prevent the spread of the infection
H Localized lymphadenopathy H lesion care
H the prescribed medication and possible adverse ef-
Test results fects.
Laboratory
H Wound culture and sensitivity results show the infect- Discharge planning
ing organism. H Refer patients with recurrent furunculosis for a phys-
H Complete blood count may reveal leukocytosis. ical examination to assess for underlying diseases.

Treatment
General
H Thorough cleaning of infected area with soap and
water
H Avoidance of occlusive agents
H Application of warm, moist compresses

Medications
H Topical or systemic antibiotics, according to the iso-
lated organism
Surgery
H Possible incision and drainage in patients with furun-
culosis or carbunculosis

Nursing considerations
Key outcomes
The patient will:
H avoid or minimize complications
H exhibit improved or healed wounds or lesions

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Fragile X syndrome Assessment

Overview
Description
H Most common inherited cause of mental retardation;
average IQ about 30 to 70
H Signs and symptoms of the syndrome apparent in
about 85% of males and 50% of females who inherit
the fragile X mental retardation-1 (FMR1) gene
H Distinct physical features, behavioral difficulties, and
cognitive impairment often found in postpubescent
males with syndrome
H More subtle symptoms usually found in females with
syndrome
Pathophysiology
H This X-linked condition doesnt follow a simple
X-linked inheritance pattern.
H Full mutation typically causes abnormal methylation
(methyl groups attach to components of the gene) of
FMR1.
H Methylation inhibits gene transcription and, thus,
protein production.
H The reduced or absent protein production leads to
the clinical features of fragile X syndrome.
Causes
H Genetic defect of the X-chromosome
H Well-defined mutation at a specific location on the
FMR1 gene
History
H Hyperactivity, speech difficulties, language delay, and
autistic-like behaviors
H Excessive shyness or social anxiety
Physical findings
H A prominent jaw and forehead
H Head circumference exceeding the 90th percentile
H Long, narrow face with long or large ears that may be
posteriorly rotated
H Hyperextension of the fingers
H Severe pectus excavatum
H Unusually large testes after puberty
Test results
Laboratory
H Positive genetic test, preferably deoxyribonucleic
acid analysis of blood or buccal samples, detects the
size of the cytosine-guanine-guanine repeat and the
methylation status of FMR1.
Imaging
H Echocardiography reveals a floppy mitral valve.
Treatment
General
H Early intervention during preschool years
H Special education tailored to the childs needs
H Activity, as tolerated

Incidence Medications
H Estimated to occur in about 1 in 1,500 males and H Anticonvulsants such as phenytoin
1 in 2,500 females H Antidepressants such as clomipramine
H Occurs in almost all races and ethnic populations H Sedatives such as diazepam

Common characteristics Surgery

Males H Mitral valve repair
H Physical manifestations
H Hyperactivity, speech difficulties, language delay, and
autistic-like behaviors Nursing considerations
Females
H Some degree of cognitive impairment, most com- Key outcomes
monly learning disabilities (math difficulties, lan- The patient will:
guage deficits, and attentional problems) H function at the highest level possible
H Autistic-like features (rare) H be free from signs and symptoms of infection
H Excessive shyness or social anxiety H demonstrate effective learning related to potential.

Complications Nursing interventions

H Behavioral or learning difficulties
H Cognitive impairment
H Connective tissue abnormalities
H Administer prescribed drugs.
H Provide emotional support to the patient and his
family.
H Encourage appropriate activities for the patients
ability.
H Encourage the family to follow a routine schedule.

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Monitoring
H Language development
H Seizures
H Hyperactivity

Patient teaching
Be sure to cover:
H medication administration and possible adverse ef-
fects.
Discharge planning
H Refer the patient and family for genetic counseling.
H Refer the family to a support group.
H Advocate for special education services and individu-
alized speech, language, and occupational therapy
services during the patients schooling.

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Common characteristics
Frostbite H First-degree frostbite characterized by white or blue
skin, edema, waxy appearance, spongy texture of the
tissue, and sensory deficits
Overview H Second-degree frostbite characterized by white,
blotchy, or blue skin; edema; and formation of vesi-
Description cles filled with clear or milky fluid (form within 24
H Damage to skin and other tissues caused by freezing hours of injury)
H Caused by sustained exposure to cold temperatures H Third-degree frostbite characterized by presence of
or to certain chemicals without proper protection blood-filled vesicles, which progress to a black es-
H Signs or symptoms persisting longer than 30 minutes char
after start of rewarming H Fourth-degree frostbite characterized by full-
H Classified by degree of injury as first-, second-, thickness damage affecting muscles, tendons, and
third-, or fourth-degree bone, with resultant tissue loss
H Frost nip: less severe cold exposure with complete
resolution within 30 minutes of starting to rewarm Complications
H Wound-related sepsis
Pathophysiology H Gangrene
H Loss of body heat causes a fall in tissue temperature. H Compartment syndrome
H Tissue hypoxia and acidosis occurs as blood vessels H Loss of affected part; amputation
narrow in response to cold. H Increased sensitivity to cold
H Tissues begin to freeze; ice crystals form and force H Pain with use of the affected area
water out of cells, causing cell death. H Altered sensation in the affected area, possibly lasting
H Blood no longer flows through the capillaries, and throughout life
clots form in the arterioles and venules from in- H Tetanus
creased blood viscosity. H Osteoporosis
H Inflammatory mediators are released, causing further H Muscle atrophy
damage. H Phantom pain of amputated extremities
H Extent of permanent injury depends on duration of H Death, when associated with hypothermia or sepsis
frozen tissue.
Causes Assessment
H Exposure to cold temperatures, without proper pro-
tection History
H Time for this to occur affected by air temperature, H Prolonged exposure to cold or exposure without ad-
wind speed, and moisture (in the air as well as wet equate protection
clothing and skin) H Numbness in affected part
H Chemical exposure, such as to dry ice or highly com- H Feeling of clumsiness and confusion
pressed gases H Possible shivering
H Pain, burning, or throbbing on rewarming
Risk factors
H Outdoor winter activities Physical findings
H Workers in cold environments H Skin
H Homelessness Color: White, blotchy, or blue; purple in large af-
H Alcohol consumption and smoking fected area
H Fatigue Waxy appearance
H Inadequate, tight, or wet clothing Stiff to touch
H Previous cold injury H Spongy feeling to underlying tissue
H Young children and older adults H Edema
H Diseases, including diabetes, atherosclerosis, and H Vesicles filled with clear or milky fluid or blood
thyroid disease H Joint stiffness and pain
H Infections H Sweating
H Medications such as beta-adrenergic blockers
Test results
Incidence Laboratory
H Hands or feet affected in 90% of injuries H Complete blood count may show hemoconcentration.
H Ears, nose, chin, cheeks, or penis affected in remain- Imaging
ing 10% of injuries H X-rays determine bone involvement.
H Males affected more often than females H Angiography determines extent of blood vessel dam-
age.

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H Thermography measures blood flow. H Assist with rewarming and other treatments, as or-
H Technetium-99 pertechnetate scintigraphy deter- dered.
mines extent of deep-tissue injury and assesses the H Maintain aseptic technique when changing dressings.
response of damaged tissue to therapy. H Provide pain medication, as ordered.

Monitoring
Treatment H Wound condition
H Pain level
General H Capillary refill time
H Replacement of wet or tight clothing with dry, loose H Sensation
clothing H Peripheral pulses
H Protection of injured area H Hydration status
H Rewarming affected part for 20 to 40 minutes in wa-
ter at 100 to 108 F (37.8 to 42.2 C) to halt ice
crystal formation and dilate blood vessels Patient teaching
H Hydration with warm fluids
H High-protein, high-calorie diet Be sure to cover:
H Physical therapy H the disorder and its treatment
H Acupuncture and homeopathic and botanical thera- H possible long-term effects
pies H need for smoking or alcohol cessation, if indicated
H Hyperbaric therapy H increased susceptibility to cold
H how to prevent future cold injuries. (See Preventing
Medications frostbite.)
H Tetanus toxoid immunization and appropriate antibi-
otics, if needed, with open injuries Discharge planning
H Nonsteroidal anti-inflammatory drugs, such as H Refer the patient to a social service agency, if indi-
ibuprofen and naproxen, for inflammation and pain cated.
H Opioids, such as morphine, meperidine, and
propoxyphene, for severe pain
H Vasodilators, such as nifedipine, to increase perfu-
sion
H Aloe vera cream to debride blisters and prevent fur-
ther trauma
H Anticlotting agent, tissue plasminogen activator, to re-
duce the risk of amputation (experimental)
Surgery
H Debridement or fasciotomy, if indicated
H Amputation, as needed (necessity usually unknown
for at least 1 month)

Nursing considerations
Prevention
Key outcomes Preventing frostbite
The patient will: H Anticipate poor weather, and dress appropriately.
H express understanding of the injury and how to pre- H Be aware that wet and windy conditions worsen the
vent future occurrences chill factor and increase the risk of cold injury.
H experience no further injury from frostbite H Limit exposure time.
H remain free from infection H Wear layers of loose-fitting clothing. Mittens provide
H express feelings of increased comfort and reduced more warmth than gloves.
pain H Wear head, face, and ear coverings at all times.
H show progressive wound healing H Wear two pairs of socks. An outer layer of wool socks
H maintain optimal perfusion to affected areas worn over synthetic socks that wick moisture away
H demonstrate effective coping. from the skin provides the best insulation.
H Wear waterproof shoes or boots.
Nursing interventions H Avoid smoking cigarettes and drinking alcohol, which
impair circulation.
H Provide a bed cradle to keep covers off lower ex- H Remove metal jewelry, which conducts cold.
tremities, if indicated.

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G Gas gangrene
Overview
Description
H Rare condition caused by local infection with anaero-
bic, spore-forming, gram-positive, rod-shaped bacil-
lus Clostridium perfringens or another clostridial
species
H Occurs in devitalized tissues and results from com-
promised arterial circulation
Pathophysiology
H Incubation is 1 to 4 days but can vary from 3 hours
H Most common in extremities and abdominal wounds;
less common in uterus
Common characteristics
H Sudden, severe pain at wound site

Complications
H Renal failure
H Hypotension and shock
H Hemolytic anemia
H Tissue death requiring amputation of the affected
body part

Assessment
to 6 weeks or longer. History
H C. perfringens invades soft tissues, producing H Recent surgery (within 72 hours)
thrombosis of regional blood vessels, tissue necrosis, H Traumatic injury
and localized edema. (See Effects of Clostridium H Septic abortion
perfringens.) H Delivery
H Necrosis releases carbon dioxide and hydrogen sub-
cutaneously, producing interstitial gas bubbles. Physical findings
H Normothermia, followed by a moderate increase,
Causes usually not above 101 F (38.3 C)
H C. perfringens H Toxemia (hypotension, tachycardia, tachypnea)
H Transmission when the organism enters the body H Localized swelling and discoloration (often dusky
during trauma or surgery brown or reddish)
H Bullae and tissue necrosis
Risk factors H Dark red or black necrotic muscle
H Diabetes mellitus H Foul-smelling, watery, or frothy discharge
H Subcutaneous emphysema (hallmark of gas gan-
Incidence grene)
H Rare, although more than 30% of deep wounds in- H In later stages, altered level of consciousness that
fected with clostridia may deteriorate to delirium and coma
H Most common in deep wounds, especially when tis-
sue necrosis further reduces oxygen supply Test results
Laboratory
H Anaerobic cultures of wound drainage disclose
Effects of Clostridium perfringens C. perfringens.
H Gram stain of wound drainage shows large,
As C. perfringens grows in a closed wound, it destroys gram-positive, rod-shaped bacteria.
cell walls and causes hemolysis, local tissue death, and H Blood studies show leukocytosis and, later,
increasing edema. hemolysis.
Imaging
C. perfringens H X-rays reveal gas in tissues.
and necrotic
muscle in

Increased
closed wound
Treatment
edema
General
H Hyperbaric oxygen therapy
Destruction
of cell walls H Adequate hydration
Edema H Nothing by mouth if surgery is planned
H Bed rest until recovery begins

Medications
Local H I.V. antibiotics such as vancomycin
tissue H Analgesics such as morphine
death Hemolysis

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Surgery
H Immediate wide surgical excision of all affected tis-
sues and necrotic muscle in myositis
H Amputation of the affected part

Nursing considerations
Key outcomes
The patient will:
H maintain hemodynamic stability
H have skin that remains warm, dry, and intact
H maintain collateral circulation
H express feelings of increased comfort and relief from
pain.
Nursing interventions
H Administer prescribed analgesics.
H Prepare for surgery, if indicated.
H Provide adequate fluid replacement.
H Maintain the airway and ventilation.
H Provide appropriate skin care and meticulous wound
care; place the patient on an air mattress or an
air-fluidized bed.
H Encourage verbalization and provide support.

Monitoring
H Vital signs
H Intake and output
H Pulmonary and cardiac status
H Wound site
H Pain control

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the need to report severe pain at the wound site im-
mediately
H the need to report foul odor or drainage from the
wound site.
Discharge planning
H After recovery, refer the patient for physical rehabili-
tation, as necessary.
H After extensive surgery, such as amputation, refer the
patient for psychological support, as necessary.

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Gastric cancer H Vague feeling of fullness, heaviness, and moderate

abdominal distention after meals
H Weight loss, nausea, vomiting
H Weakness and fatigue
Overview H Dysphagia

Description Physical findings

H Cancer of the GI tract classified according to gross
appearance (polypoid, ulcerating, ulcerating and in-
filtrating, or diffuse)
H Prognosis depending on stage of disease at time of
diagnosis (5-year survival rate about 15%)
Pathophysiology
H The most commonly affected areas of the stomach
are the pylorus and antrum.
H The remaining areas affected in order of descending
frequency are the lesser curvature of the stomach,
the cardia, the body of the stomach, and the greater
curvature of the stomach.
H Rapid metastasis occurs to the regional lymph nodes,
omentum, liver, and lungs.
Causes
H Unknown
Risk factors
H Gastritis with gastric atrophy
H Type A blood (10% increased risk)
H Family history of gastric cancer
H Smoked foods, pickled vegetables, and salted fish
and meat
H High alcohol consumption
H Smoking
H Helicobacter pylori infection
Incidence
H Common worldwide in all races
H Incidence greater in males older than age 40
H Mortality high in Japan, Iceland, Chile, and Austria
H Incidence decreased 50% over the past 25 years;
death rate now one-third that of 30 years ago
Common characteristics
H Feeling of fullness
H Abdominal distention
H Back, epigastric, or retrosternal pain
Complications
H Malnutrition
H GI obstruction
H Iron deficiency anemia
H Metastasis
Assessment
History
H Back, epigastric, or retrosternal pain not relieved
with nonprescription medications
H Abdominal distention
H Palpable mass
H Palpable lymph nodes, especially the supraclavicular
and axillary nodes
H Other assessment findings that depend on extent of
disease and location of metastasis
Test results
Laboratory
H Complete blood count may show iron deficiency ane-
mia.
H Liver function studies may be elevated with metastatic
spread of tumor to liver.
H Carcinoembryonic antigen radioimmunoassay may
be elevated.
Imaging
H Barium X-rays of the GI tract with fluoroscopy show
changes that suggest gastric cancer, including a tu-
mor or filling defect in the outline of the stomach,
loss of flexibility and distensibility, and abnormal gas-
tric mucosa with or without ulceration.
Diagnostic procedures
H Gastroscopy with fiber-optic endoscope helps rule
out other diffuse gastric mucosal abnormalities by al-
lowing direct visualization.
H Gastroscopic biopsy permits evaluation of gastric
mucosal lesions.
Other
H Gastric acid stimulation test discloses whether the
stomach secretes acid properly.
Treatment
General
H Radiation therapy combined with chemotherapy (not
indicated preoperatively because it may damage vis-
cera and impede healing)
H Diet based on the extent of the disorder and clinical
condition
H Parenteral feeding with an inability to consume ade-
quate calories
Medications
H Chemotherapy, such as fluorouracil and doxorubicin
H Antiemetics, such as aprepitant and dolasetron
H Opioid analgesics such as morphine
H Antibiotics such as tetracycline
Surgery
H Excision of lesion with appropriate margins (in more
than one-third of patients)
H Gastroduodenostomy
H Gastrojejunostomy

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H Partial gastric resection

H Total gastrectomy (If metastasis has occurred, omen-
tum and spleen may have to be removed.)

Nursing considerations
Key outcomes
The patient will:
H maintain weight
H express feelings of increased energy
H report feeling less tension and pain
H maintain skin integrity.

Nursing interventions
H Encourage coughing, deep breathing, and incentive
spirometer use.
H Provide a high-protein, high-calorie diet with dietary
supplements.
H Administer prescribed drugs.
H Provide parenteral nutrition, as appropriate.
H After surgery, provide supportive care.
H Elevate the head of the bed at least 30 degrees.

Monitoring
H Pain control
H Vital signs
H Nutritional status
H Nasogastric tube function and drainage
H Wound site
H Postoperative complications
H Effects of medication
H Intake and output
H Cardiovascular status
H Respiratory status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the dietary plan
H effective pulmonary toileting
H avoidance of crowds and people with known infec-
tion
H relaxation techniques
H medication administration, dosage, and possible ad-
verse effects.
Discharge planning
H Refer the patient and his family to support services.
H Refer the patient for home services, as necessary.
H Refer the patient for physical or occupational thera-
py, as necessary.

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Gastritis H Perforation
H Peritonitis
H Gastric cancer

Overview
Assessment
Description
H Inflammation of the gastric mucosa History
H May be acute or chronic H Exposure to one or more causative agents
H Most common stomach disorder (acute) H Rapid onset of symptoms (acute gastritis)
H Epigastric discomfort
Pathophysiology H Indigestion
Acute gastritis H Cramping
H The protective mucosal layer is altered. H Anorexia
H Acid secretion produces mucosal reddening, edema, H Nausea, hematemesis, and vomiting
and superficial surface erosion. H Coffee-ground emesis or melena (if GI bleeding is
Chronic gastritis present)
H Progressive thinning and degeneration of gastric mu-
cosa occur. Physical findings
H Possible normal appearance
Causes H Grimacing
Acute gastritis H Restlessness
H Chronic ingestion of irritating foods and alcohol H Pallor
H Drugs, such as aspirin and other nonsteroidal H Tachycardia
anti-inflammatory drugs (in large doses), cytotoxic H Hypotension
agents, caffeine, corticosteroids, antimetabolites, H Abdominal distention, tenderness, and guarding
phenylbutazone, and indomethacin H Normoactive to hyperactive bowel sounds
H Ingested poisons, especially dichloro-diphenyl-
trichloroethane (DDT), ammonia, mercury, carbon Test results
tetrachloride, or corrosive substances Laboratory
H Endotoxins released from infecting bacteria, such as H Occult blood is found in vomitus or stools (or both)
staphylococci, Escherichia coli, and salmonella if the patient has gastric bleeding.
H Complication of acute illness H Hemoglobin (Hb) level and hematocrit are de-
Chronic gastritis creased.
H Recurring exposure to irritating substances, such as H Urea breath test shows H. pylori.
drugs, alcohol, cigarette smoke, and environmental Diagnostic procedures
agents H Upper GI endoscopy reveals gastritis when its per-
H Pernicious anemia, renal disease, or diabetes melli- formed within 24 hours of bleeding.
tus H Biopsy reveals inflammatory process.
H Helicobacter pylori infection (common cause of
nonerosive gastritis)
Treatment
Risk factors
H Age older than 60 General
H Exposure to toxic substances H Elimination of cause
H Hemodynamic disorder H For massive bleeding:
Blood transfusion
Incidence Iced saline lavage
H May occur at any age; increased incidence of H. py- Angiography with vasopressin
lori in people older than age 60 H Nothing by mouth if bleeding occurs
H Occurs equally in both sexes H Elimination of irritating foods
H Acute gastritis in 8 of 1,000 people; chronic gastritis H Activity, as tolerated (encourage mobilization)
in 2 of 10,000 people
Medications
Common characteristics H Histamine antagonists, such as famotidine, ranitidine,
H Abdominal pain and cimetidine
H Indigestion H Proton pump inhibitors such as pantoprazole
H Prostaglandins such as misoprostol
Complications H Vitamin B12
H Hemorrhage H Antibiotic therapy, according to infective agent
H Obstruction

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Surgery
H When conservative treatment fails
H Vagotomy, pyloroplasty
H Partial or total gastrectomy (rarely)

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort
H maintain normal fluid volume
H maintain weight
H express concerns about current condition
H verbalize understanding of the disorder and treat-
ment regimen.
Nursing interventions
H Provide physical and emotional support.
H Administer prescribed drugs and I.V. fluids.
H Assist the patient with diet modification.
H If surgery is necessary, prepare the patient preopera-
tively and provide appropriate postoperative care.
H Consult a dietitian, as necessary.

Monitoring
H Vital signs
H Fluid intake and output
H Electrolyte and Hb levels
H Returning symptoms as food is reintroduced
H Response to medication
H Pain control
H GI status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H lifestyle and diet modifications
H preoperative teaching if surgery is necessary
H stress-reduction techniques
H medication administration and possible adverse ef-
fects.
Discharge planning
H Refer the patient to a smoking-cessation program, if
indicated.
H Refer the patient to an alcohol treatment program, if
indicated.

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Gastroenteritis H Viruses, such as adenoviruses, echoviruses, and cox-

sackieviruses
H Ingestion of toxins, such as poisonous plants and
toadstools
Overview H Drug reactions from antibiotics
H Food allergens
Description H Enzyme deficiencies
H Self-limiting inflammation of the stomach and small
intestine Risk factors
H Intestinal flu, travelers diarrhea, viral enteritis, and H Consumption of improperly prepared food or conta-
food poisoning minated water
H Travel or residence in areas of poor sanitation
Pathophysiology
H The bowel reacts to the various causes of gastroen- Incidence
teritis with increased luminal fluid that cant be ab- H Occurs at any age
sorbed. H Major cause of morbidity and mortality in underde-
H This results in abdominal pain, vomiting, severe diar- veloped nations
rhea (primarily), and secondary depletion of intra- H Ranks second to common cold as cause of lost work
cellular fluid. time in the United States
H Dehydration and electrolyte loss occur. H Fifth most common cause of death among young
children
Causes H Can be life-threatening in elderly and debilitated pa-
H Bacteria, such as Staphylococcus aureus, Salmonel- tients
la, Shigella, Clostridium botulinum, Clostridium
perfringens, and Escherichia coli Common characteristics
H Amoebas, especially Entamoeba histolytica H Diarrhea
H Parasites, such as Ascaris, Enterobius, and H Nausea and vomiting
Trichinella spiralis
Complications
Prevention H Severe dehydration
Preventing travelers diarrhea H Electrolyte imbalance

If the patient travels, especially to developing nations, dis-

cuss precautions that he can take to reduce his chances Assessment
of getting travelers diarrhea. Explain that travelers diar-
rhea is caused by inadequate sanitation and occurs after History
bacteria-contaminated food or water is ingested. These
organisms attach to the lining of the small intestine, H Acute onset of diarrhea
where they release a toxin that causes diarrhea and H Abdominal pain and discomfort
cramps. To minimize this risk, advise him to: H Nausea, vomiting
H Malaise and fatigue
H drink water (or brush his teeth with water) only if its
H Exposure to contaminated food
chlorinated or bottled (Chlorination protects the water
H Recent travel (see Preventing travelers diarrhea)
supply from bacterial contaminants such as Esche-
richia coli.) Physical findings
H avoid beverages in glasses that may have been washed
in contaminated water H Slight abdominal distention
H refuse ice cubes that may have been made from conta- H Poor skin turgor (with dehydration)
minated water H Hyperactive bowel sounds
H drink only beverages made with boiled water, such as H Decreased blood pressure
coffee and tea, or those in bottles or cans
H sanitize impure water by adding 2% tincture of iodine Test results
(5 drops/L of clear water, 10 drops/L of cloudy water) Laboratory
or by adding liquid laundry bleach (about 2 drops/L of H Gram stain, stool culture (by direct rectal swab), or
clear water; 4 drops/L of cloudy water)
H avoid uncooked vegetables, unpeeled fresh fruits, sal-
blood culture shows the causative bacteria.
ads, unpasteurized milk, and other dairy products
H beware of foods offered by street vendors.
Treatment
If travelers diarrhea occurs despite precautions, bis-
muth subsalicylate, diphenoxylate with atropine, or lo- General
peramide can be used to relieve symptoms. H Supportive treatment for nausea, vomiting, and diar-
rhea

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H Antidiarrheals generally not given; they can prolong

the infection
H Rehydration
H Initially, clear liquids as tolerated
H Electrolyte solutions
H Avoidance of milk products
H Activity, as tolerated (encourage mobilization)

Medications
H Antiemetics such as prochlorperazine
H Antibiotics, according to the infective organism
H I.V. fluids

Nursing considerations
Key outcomes
The patient will:
H maintain weight without further loss
H express feelings of increased comfort
H maintain adequate fluid volume
H maintain normal vital signs.

Nursing interventions
H Allow uninterrupted rest periods.
H Replace lost fluids and electrolytes through diet or
I.V. fluids.
H Administer prescribed drugs.

Monitoring
H Intake and output
H Vital signs
H Signs of dehydration
H Electrolytes
H GI status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H dietary modifications
H medication administration, dosage, and possible ad-
verse effects
H preventive measures
H how to perform warm sitz baths three times per day
to relieve anal irritation.

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Gastroesophageal reflux Assessment

disease History
H Minimal or no symptoms in one-third of patients
H Heartburn that typically occurs 112 to 2 hours after
Overview eating
H Heartburn that worsens with vigorous exercise,
Description bending, lying down, wearing tight clothing, cough-
H Backflow of gastric or duodenal contents, or both, ing, constipation, and obesity
into the esophagus and past the lower esophageal H Reported relief by using antacids or sitting upright
sphincter (LES), without associated belching or vom- H Regurgitation without associated nausea or belching
iting H Feeling of fluid accumulation in the throat with a
H Reflux of gastric acid, causing acute epigastric pain, sour or bitter taste
usually after a meal H Chronic pain radiating to the neck, jaws, and arms
H Popularly called heartburn that may mimic angina pectoris
H Also called GERD H Nocturnal hypersalivation and wheezing

Pathophysiology Physical findings

H Reflux occurs when LES pressure is deficient or pres-
sure in the stomach exceeds LES pressure. The LES
relaxes, and gastric contents regurgitate into the
esophagus.
H The degree of mucosal injury is based on the amount
and concentration of refluxed gastric acid, proteolyt-
ic enzymes, and bile acids.
Causes
H Pyloric surgery (alteration or removal of the py-
lorus), which allows reflux of bile or pancreatic juice
H Hiatal hernia with incompetent sphincter
H Condition or position that increases intra-abdominal
pressure
Risk factors
H Any agent that lowers LES pressure: acidic and fatty
food, alcohol, cigarettes, anticholinergics (atropine,
belladonna, propantheline) or other drugs (mor-
phine, diazepam, calcium channel blockers, meperi-
dine)
H Nasogastric (NG) intubation for longer than 4 days
Incidence
H Affects about 7 million U.S. residents
H Affects all ethnic groups and socioeconomic classes
H Most common in people ages 45 to 64
Common characteristics
H Epigastric pain, usually after a meal or when lying
down
Complications
H Reflux esophagitis
H Esophageal stricture
H Esophageal ulcer
H Barretts esophagus (metaplasia and possible in-
creased risk of neoplasm)
H Anemia from esophageal bleeding
H Reflux aspiration leading to chronic pulmonary dis-
ease
H Odynophagia (sharp substernal pain on swallowing),
possibly followed by a dull substernal ache
H Bright red or dark brown blood in vomitus
H Laryngitis and morning hoarseness
H Chronic cough
Test results
Imaging
H Barium swallow with fluoroscopy shows evidence of
recurrent reflux.
Diagnostic procedures
H Esophageal acidity test reveals degree of gastro-
esophageal reflux.
H Gastroesophageal scintillation testing shows reflux.
H Esophageal manometry reveals abnormal LES pres-
sure and sphincter incompetence.
H Acid perfusion (Bernstein) test confirms esophagitis.
H Esophagoscopy and biopsy confirm pathologic
changes in the mucosa.
Treatment
General
H Modification of lifestyle
H Positional therapy
H Removal of cause
H Weight reduction, if appropriate
H Avoidance of dietary causes
H Avoidance of eating 2 hours before sleep (see Fac-
tors affecting LES pressure)
H Parenteral nutrition or tube feedings
H No activity restrictions for medical treatment
H Lifting restrictions for surgical treatment
Medications
H Histamine-2 receptor antagonists, such as cimeta-
dine, ranitidine, and famotidine
H Proton pump inhibitors, such as esomeprazole, lan-
soprazole, pantoprazole, and rabeprazole

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Factors affecting LES pressure

Patient teaching
Various dietary and lifestyle elements can increase or de-
crease lower esophageal sphincter (LES) pressure. Take
these into account as you plan the patients treatment pro- Be sure to cover:
gram. H the disorder, diagnosis, and treatment
What increases LES pressure H causes of gastroesophageal reflux
H Protein H prescribed antireflux regimen of medication, diet,
H Carbohydrates and positional therapy
H Nonfat milk H developing a dietary plan
H Low-dose ethanol H the need to identify situations or activities that in-
What decreases LES pressure crease intra-abdominal pressure
H Fat
H the need to refrain from using substances that reduce
H Whole milk
H Orange juice
sphincter control
H signs and symptoms to watch for and report.
H Tomatoes
H Antiflatulent (simethicone)
H Chocolate
Discharge planning
H High-dose ethanol H Refer the patient to a dietitian, as appropriate.
H Cigarette smoking
H Lying on right or left side
H Sitting

Surgery
H Hiatal hernia repair
H Vagotomy or pyloroplasty
H Esophagectomy

Nursing considerations
Key outcomes
The patient will:
H state and demonstrate understanding of the disorder
and its treatment
H express feelings of increased comfort
H show no signs of aspiration
H have minimal or no complications.

Nursing interventions
H Administer prescribed drugs.
H Offer emotional and psychological support.
H Assist with diet modification.
H Perform chest physiotherapy.
H Use semi-Fowlers position for the patient with an NG
tube.
H Elevate the head of the bed at least 30 degrees.

Monitoring
H Response to therapy
H Adverse effects of medication
After surgery
H Respiratory status
H Pain control
H Intake and output
H Vital signs
H Chest tube drainage
H GI status

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Generalized anxiety H Anger

H Difficulty concentrating, eating, and sleeping

disorder Physical findings

H Trembling
H Shortness of breath
Overview H Tachycardia
H Sweating
Description
H Feeling of apprehension sometimes described as an DSM-IV-TR criteria
exaggerated feeling of impending doom, dread, or A diagnosis is confirmed when the patients symptoms
uneasiness match the following criteria:
H Reaction to an internal threat H Excessive anxiety and worry about a number of
H Uncontrollable, unreasonable worry that persists for events or activities occur more days than not for at
at least 6 months and narrows perceptions or inter- least 6 months.
feres with normal functioning H The person finds it difficult to control the worry.
H The anxiety and worry are associated with at least
Pathophysiology three of the following six symptoms:
H Aberration in benzodiazepine receptor regulation oc- restlessness or feeling keyed up or on edge
curs. being easily fatigued
difficulty concentrating or mind going blank
Causes irritability
H Unknown muscle tension
H Roles played by biologic and physiologic factors sleep disturbances (difficulty falling or staying
asleep, or restless, unsatisfying sleep).
Risk factors H The focus of the anxiety and worry isnt confined to
H Stressful life situations features of an axis disorder.
H Learned maladaptive behaviors H The anxiety, worry, or physical symptoms cause clini-
cally significant distress or impairment in social, oc-
Incidence cupational, or other important areas of functioning.
H Can begin at any age but typically begins between H The disturbance isnt due to the direct physiologic ef-
ages 20 and 40 fects of a substance or a general medical condition
H Twice as common in females as in males and doesnt occur exclusively during a mood disor-
der, a psychotic disorder, or a pervasive, develop-
Common characteristics mental disorder.
Mild anxiety
H Psychological symptoms Test results
H Unusually self-aware and alert to surroundings Laboratory
Moderate anxiety H Tests, such as cardiac enzymes, troponin level, and
H Selective inattention, but can concentrate on a single thyroid studies, rule out organic causes of symptoms.
task Diagnostic procedures
Severe anxiety H Electrocardiography excludes myocardial ischemia.
H Inability to concentrate on more than scattered de- Other
tails of a task H Psychiatric evaluation helps confirm the diagnosis.
H Panic state with acute anxiety causing complete loss
of concentration, typically with unintelligible speech
Treatment
Complications
H Impaired social or occupational functioning General
H Substance abuse H Psychotherapy
H Relaxation techniques

Assessment Medications
H Benzodiazepines, such as diazepam and lorazepam
History H Tricyclic antidepressants such as doxepin
H Muscle aches and spasms H Serotonin receptor reuptake inhibitors, such as ser-
H Headaches traline, paroxetine, and escitalopram
H Inability to relax
H Apprehension
H Fear

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Nursing considerations
Key outcomes
The patient will:
H develop effective coping strategies
H identify anxiety triggers
H experience reduced anxiety.

Nursing interventions
H Administer prescribed drugs.
H Reduce environmental stimuli.
H Help identify triggers to anxiety.
H Provide emotional support.

Monitoring
H Response to therapy

Patient teaching
Be sure to cover:
H prescribed drugs
H relaxation techniques
H effective coping strategies.

Discharge planning
H Refer the patient for psychological counseling.

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Common characteristics
Genital herpes H Fluid-filled vesicles that develop into shallow, painful
ulcers with yellow, oozing centers
H Fever
Overview H Malaise
H Dysuria
Description
H Acute inflammatory disease of the genitalia Complications
H Usually self-limiting but able to cause painful local or H Herpetic keratitis, which may lead to blindness
systemic disease (see Understanding the genital H Herpetic encephalitis
herpes cycle)
Pathophysiology Assessment
H Virus invades and replicates in neurons and epider-
mal and dermal cells. History
H Virions travel to sensory dorsal root ganglion. H Intimate contact with an infected person
H Replication in the sensory ganglia leads to recurrent H Fever
clinical outbreaks. H Malaise
H Dysuria
Causes H Leukorrhea (females)
H Herpes simplex virus (HSV), type 1 or type 2
H Typically transmitted through sexual intercourse, Physical findings
orogenital sexual activity, kissing, hand-to-body con- H Shallow, reddened, painful ulcers with yellow, oozing
tact, and vaginal delivery centers usually on the cervix (the primary infection
site) and possibly on the labia, perianal skin, vulva,
Risk factors or vagina and on the glans penis, foreskin, or penis
H Unprotected sexual activity H Extragenital lesions, possibly on the mouth or anus
H Marked edema
Incidence H Tender inguinal lymph nodes
H One in five adults in the United States serologically
HSV-positive Test results
Laboratory
H Vesicular fluid reveals HSV.
H Antigen testing identifies specific antigens.
Understanding the genital herpes cycle
After a patient is infected with genital herpes, a latency pe-
riod follows. The virus takes up permanent residence in
Treatment
the nerve cells surrounding the lesions, and intermittent
viral shedding may take place. General
Repeated outbreaks may develop at any time, again fol- H Adequate rest periods
lowed by a latent stage during which the lesions heal
completely. Outbreaks may recur as often as three to eight Medications
times yearly. H Antivirals, such as acyclovir, famciclovir, and valacy-
Although the cycle continues indefinitely, some people
remain symptom-free for years.
clovir

INITIAL INFECTION Nursing considerations

Highly infectious period marked by fever, aches, adenopathy, pain,
and ulcerated skin and mucous membranes
Key outcomes
The patient will:
H express an understanding of the disorder and its
LATENCY treatment
Intermittently infectious period marked by viral dormancy or viral H practice safe sex
shedding and no disease symptoms H report feelings of increased comfort
H demonstrate improved skin integrity.

Nursing interventions
RECURRENT INFECTION
Highly infectious period similar to initial infection with milder H Encourage expression of feelings and concerns.
symptoms that resolve faster H Keep lesions dry.

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Monitoring
H Response to treatment
H Skin integrity
H Wound healing

Patient teaching
Be sure to cover:
H avoiding sexual intercourse during the active stage of
this disease (while lesions are present)
H using condoms during all sexual encounters
H urging sexual partners to seek medical examination
H having a Papanicolaou test every 6 months (females).

Discharge planning
H Refer the patient to the Herpes Resource Center for
support.

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Genital warts H Genital tract dysplasia

Overview
Description
H Papillomas that consist of fibrous tissue overgrowth
from the dermis and thickened epithelial coverings
H Also known as venereal warts and condylomata
acuminata
Pathophysiology
H Infection is transmitted by sexual contact and incu-
bates for 1 to 6 months (2 months, average) before
warts erupt.
H Infection of the basal cells occurs, with proliferation
of all epidermal layers, producing acanthosis, para-
keratosis, and hyperkeratosis.
H Cervical and vulvar cancer in females, penile cancer
in males, and some rectal carcinomas in both sexes
Assessment
History
H Unprotected sexual contact with a partner with a
known infection, a new partner, or many partners
Physical findings
H Warts on moist genital surfaces (subpreputial sac,
urethral meatus, penile shaft, scrotum, vulva, vaginal
and cervical walls) and around the anus and inside
the rectum
H Tiny red or pink swellings that may grow as large as
10 cm and that may be pedunculated
H Infected lesions that become malodorous

Causes Test results

H Infection with one of more than 60 strains of human Laboratory
papillomavirus (HPV) H Dark-field microscopy of wart-cell scrapings shows
marked epidermal cell vascularization.
Risk factors H Application of 5% acetic acid (white vinegar) turns
H Unprotected sexual activity warts white if theyre papillomas.
Incidence
H One of the most common sexually transmitted dis- Treatment
eases (STDs) in the United States
General
Common characteristics H Good hygiene practices
H Appearance of small, pink to red, moist warts with ir- H Contact precautions
regular surfaces (see Recognizing genital warts)
H Usually located around the external genitalia and Medications
possibly inside the urethra or vagina or on the cervix H Topical interferon alfa 2-b
H No symptoms in most patients H Vaccine preparations such as HPV recombinant vac-
cine
Complications H Immune response modifier such as imiquimod
H During pregnancy, genital warts in the vaginal and
cervical walls that grow large enough to impede vagi- Surgery
nal delivery H Cryosurgery
H Electrodesiccation
Recognizing genital warts H Surgical excision
H Laser ablation
Genital warts are marked by clusters of flesh-colored pap-
H Circumcision to prevent recurrence
illary growths that may be barely visible or several inches
in diameter.
Nursing considerations
Key outcomes
The patient will:
H remain free from all signs and symptoms of infection
H exhibit improved or healed lesions or wounds
H acknowledge the change in body image
H voice feelings about potential or actual changes in
sexuality
H express feelings of increased comfort and decreased
pain.

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Nursing interventions
H Provide a nonthreatening, nonjudgmental atmos-
phere that encourages verbalization, and provide
support.
H Institute contact precautions to avoid transmission.

Monitoring
H Response to treatment
H Adverse effects of medication
H Signs and symptoms of infection (postoperative)
H Concomitant STDs or infections
H Papanicolaou (Pap) test results

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the need for sexual abstinence or condom use during
intercourse until healing is complete
H evaluation of the patients sexual partners
H the importance of testing for human immunodefi-
ciency virus infection and other STDs
H the emphasis that genital warts can recur and that the
virus can mutate, causing infection with warts of a
different strain
H recommendation that female patients have a Pap test
every 6 months.

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H Roughly 5% incidence of preeclampsia progressing

Life-threatening disorder to eclampsia
Common characteristics
Gestational H Hypertension

hypertension H Sudden weight gain

H Irritability
H Emotional tension

Overview Complications
H Abruptio placentae
Description H HELLP syndrome: hemolysis, elevated liver enzyme
H High blood pressure, most commonly occurring after levels, low platelet count
the 20th week of gestation in a nulliparous woman H Coagulopathy
H Carries a high risk for fetal mortality because of the H Stillbirth
increased incidence of premature delivery H Seizures
H Among the most common causes of maternal death H Coma
in developed countries (especially when complica- H Premature labor
tions occur) H Renal failure
H Nonconvulsive form (also called preeclampsia) oc- H Maternal hepatic damage
curring after the 20th week of gestation; may be mild
or severe
H Convulsive form (also called eclampsia) occurring Assessment
between the 24th week of gestation and the end of
the first postpartum week History
H Sudden weight gain
Pathophysiology H Irritability
H Generalized arteriolar vasoconstriction is thought to H Emotional tension
cause decreased blood flow through the placenta and H Severe frontal headache
maternal organs. H Blurred vision
H This leads to intrauterine growth retardation or re- H Epigastric pain or heartburn
striction, placental infarcts, and abruptio placentae.
Physical findings
Causes H Preeclampsia: blood pressure of 160/110 mm Hg or
H Unknown higher
H Contributing factors: H Eclampsia: systolic blood pressure of 180 or
Geographic, ethnic, racial, nutritional, immuno- 200 mm Hg or higher
logic, and familial factors H Generalized edema, especially of the face
Preexisting vascular disease H Pitting edema of the legs and feet
Maternal age H Hyperreflexia
Autolysis of placental infarcts H Oliguria
Autointoxication H Vascular spasm, papilledema, retinal edema or de-
Uremia tachment, and arteriovenous nicking or hemorrhage
Maternal sensitization to total proteins (seen on ophthalmoscopy)
Pyelonephritis H Seizures
Diabetes
Test results
Special populations Laboratory
H In preeclampsia: proteinuria is more than
Adolescents and primiparas older than age 35 are 300 mg/24 hours [1+].
at higher risk for preeclampsia. H In severe eclampsia: proteinuria is 5 g/24 hours
[5+] or more.
H In HELLP syndrome: hemolysis, elevated liver en-
Risk factors zymes and decreased platelet count are evident.
H First-time pregnancy Imaging
H Multiple fetuses H Ultrasonography aids evaluation of fetal well-being.
H History of vascular disease Diagnostic procedures
H Stress and nonstress tests and biophysical profiles
Incidence help evaluate fetal well-being.
H Occurs in about 7% of pregnancies; more common
in females from lower socioeconomic groups

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Emergency interventions for gestational

Treatment hypertension

General When caring for a patient with gestational hypertension,

be prepared to perform the following interventions:
H Measures to halt progression of the disorder and en- H Observe for signs of fetal distress by closely monitor-
sure fetal survival ing results of stress and nonstress tests.
H Prompt labor induction, especially if the patient is H Keep emergency resuscitative equipment and anticon-
near term (advocated by some clinicians) vulsants at hand in case of seizures and cardiac or res-
H Adequate nutrition piratory arrest.
H Low-sodium diet, if indicated H Carefully monitor magnesium sulfate administration.
H Limited caffeine Signs of drug toxicity include absence of patellar re-
H Complete bed rest flexes, flushing, muscle flaccidity, decreased urinary
output, significant blood pressure drop (> 15 mm Hg),
H Left lateral lying position
and a respiratory rate below 12 per minute. Keep cal-
Medications cium gluconate at the bedside to counteract the toxic
effects of magnesium sulfate.
H Antihypertensives H Prepare for emergency cesarean delivery, if indicated.
H Magnesium sulfate Alert the anesthesiologist and pediatrician.
H Oxytocin H To protect the patient from injury, maintain seizure pre-
H Oxygen cautions. Dont leave an unstable patient unattended.
Maintain a patent airway, and have supplemental oxy-
Surgery gen readily available.
H Possible cesarean delivery

Nursing considerations Patient teaching

Key outcomes Be sure to cover:
The patient will: H the disorder, diagnosis, and treatment
H maintain normal vital signs H signs and symptoms of preeclampsia and eclampsia
H maintain adequate fluid volume H importance of bed rest in the left lateral position, as
H avoid complications ordered
H remain oriented to the environment. H adequate nutrition and a low-sodium diet
H good prenatal care
Nursing interventions H control of preexisting hypertension
H Administer prescribed drugs. H early recognition and prompt treatment of
H Elevate edematous arms or legs. preeclampsia
H Eliminate constricting hose, slippers, and bed linens. H likelihood that the neonate will be small for gesta-
H Assist with or insert an indwelling urinary catheter, if tional age, with the probability that hell do better
necessary. than other premature neonates of the same weight.
H Provide a quiet, darkened room.
H Enforce absolute bed rest. Discharge planning
H Provide emotional support. H Refer the patient for professional counseling, as indi-
H Encourage the patient to express feelings. cated.
H Help the patient develop effective coping strategies.
(See Emergency interventions for gestational
hypertension.)
Monitoring
H Vital signs
H Fetal heart rate
H Vision
H Edema
H Daily weight
H Intake and output
H Level of consciousness
H Deep tendon reflexes
H Headache unrelieved by medication
H Complications

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Giardiasis H Drinking of suspect water

H Institutionalization

Overview
Description
H Infection of the small bowel by Giardia lamblia, a
symmetrical flagellate protozoan
H Reinfection possible because infection doesnt confer
immunity
H Also called G. enteritis and lambliasis
Pathophysiology
H Cysts enter the small bowel and release trophozoites,
which attach to the bowels epithelial surface.
H Attachment causes superficial mucosal invasion and
destruction, inflammation, and irritation.
H Trophozoites become encysted again, travel down the
colon, and are excreted. (Unformed stool may con-
tain trophozoites as well as cysts.)
Causes
H Ingestion of G. lamblia cysts in stool-contaminated
water
H Fecal-oral transfer of cysts from an infected person
Incidence
H Occurs worldwide but most common in developing
countries and other areas where sanitation and hy-
giene are poor (G. lamblia has been found in mu-
nicipal water sources, nursing homes, and day-care
centers.)
H Children generally more likely to develop giardiasis
than adults
H In the United States, most common in travelers re-
cently returned from endemic areas, campers who
drink water from contaminated streams, male homo-
sexuals, patients with congenital immunoglobulin A
deficiency, and children in day-care centers
Common characteristics
H Diarrhea
H Abdominal pain
H Bloating
H Belching
H Flatus
H Nausea and vomiting
Complications
H Malabsorption
H Dehydration
H Lactose intolerance
H Possible death, in hypogammaglobulinemia
Assessment
Physical findings
H Possibly, no intestinal symptoms in mild infection
H Abdominal cramps, bloating
H Belching, flatus
H Nausea, vomiting
H Explosive pale, loose, greasy, malodorous, frequent
stools (occurring 2 to 10 times daily)
H Fatigue, weight loss
H Hyperactive bowel sounds in the right upper and left
lower quadrants just before bowel movements
H General upper and right lower quadrant discomfort
and guarding
Test results
Laboratory
H Examination of a fresh stool specimen shows cysts or
examination of duodenal aspirate or biopsy shows
trophozoites.
Treatment
General
H Examination for possible testing and treatment for
people living with an infected person or those having
had sexual contact with an infected person
H Parenteral fluid replacement to prevent dehydration
Medications
H Antiprotozoals, such as nitazoxanide and tinidazole
Nursing considerations
Key outcomes
The patient will:
H avoid skin breakdown or infection
H maintain stable vital signs
H maintain normal electrolyte levels
H have an elimination pattern that returns to normal
H express feelings of increased comfort and relief from
pain.
Nursing interventions
H Institute enteric contact precautions, and quickly dis-
pose of all fecal material.
H Place a child or an incontinent adult in a private
room.
H Keep the perianal area clean, especially after each
bowel movement.
H Administer I.V. fluid therapy, as needed.
H Provide nutritionally adequate foods.
H Administer prescribed drugs.
H Report to public health authorities.

History Monitoring
H Recent travel to an area with poor sanitation H Frequency and characteristics of bowel movements
H Sexual practices that involve oral-anal contact H Nutritional intake (to prevent malnutrition)

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H Adverse drug effects

H Skin integrity
H Signs and symptoms of dehydration
H Intake and output

Patient teaching
Be sure to cover:
H prescribed medications, including precautions and
adverse effects
H need for the patient whos taking metronidazole or
furazolidone to avoid alcohol while taking the drug
and for 3 days after completing treatment
H need for the family and others in contact with the pa-
tient to have their stools tested for G. lamblia cysts
H need for good personal hygiene, especially proper
hand washing as well as correct handling of infec-
tious material by the patient and his family
H importance of safer sex practices
H need for campers to purify all stream and lake water
before drinking it
H need for travelers to endemic areas to avoid drinking
tap or suspect water and to avoid eating uncooked
and unpeeled fruits or vegetables.
Discharge planning
H Encourage the patient to return for follow-up ap-
pointments because relapses can occur.

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Risk factors
Glaucoma Open-angle glaucoma
H Family history
H Myopia
Overview H Ethnic origin
Angle-closure glaucoma
Description H Family history
H Eye disorder characterized by high intraocular pres- H Cataracts
sure (IOP) and optic nerve damage H Hyperopia
H Two forms:
Open-angle (also known as chronic, simple, or Incidence
wide-angle) glaucoma, which begins insidiously H A leading cause of blindness; accounts for about 12%
and progresses slowly of newly diagnosed blindness in the United States
Angle-closure (also known as acute or narrow- H Affects about 2% of Americans older than age 40
angle) glaucoma, which occurs suddenly and can H Highest incidence among males and Black and Asian
cause permanent vision loss in 48 to 72 hours populations
H Open-angle glaucoma commonly familial
Pathophysiology
Open-angle glaucoma Common characteristics
H Degenerative changes in the trabecular meshwork H Decreased visual acuity
block the flow of aqueous humor from the eye, in- H Nausea and vomiting (from increased IOP)
creasing IOP and resulting in optic nerve damage. H Eye pain
Angle-closure glaucoma
H Obstruction to the outflow of aqueous humor is Complications
caused by an anatomically narrow angle between the H Varying degrees of vision loss
iris and the cornea. H Total blindness
H IOP increases suddenly.

Causes Assessment
Open-angle glaucoma
H Degenerative changes History
Angle-closure glaucoma Open-angle glaucoma
H Anatomically narrow angle between the iris and the H Possibly no symptoms
cornea H Dull, morning headache
H Attacks triggered by trauma, pupillary dilation, stress, H Mild aching in the eyes
or ocular changes that push the iris forward H Loss of peripheral vision
H Halos around lights
H Reduced visual acuity (especially at night) not cor-
rected by glasses
Optic disk changes Angle-closure glaucoma
H Pain and pressure over the eye
Ophthalmoscopy and slit-lamp examination show cupping H Blurred vision
of the optic disk, which is characteristic of glaucoma. H Decreased visual acuity
H Halos around lights
H Nausea and vomiting

Physical findings
H Unilateral eye inflammation
H Cloudy cornea
H Moderately dilated pupil, nonreactive to light
H With gentle fingertip pressure to the closed eyelids,
one eye feels harder than the other (in angle-closure
glaucoma)
Test results
Diagnostic procedures
H Tonometry measurement shows increased IOP.
H Slit-lamp examination shows effects of glaucoma on
the anterior eye structures. (See Optic disk
changes.)

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H Gonioscopy shows angle of the eyes anterior cham- Monitoring

ber.
H Ophthalmoscopy aids visualization of the fundus.
H Perimetry or visual field tests show extent of periph-
eral vision loss.
H Fundus photography shows optic disk changes.
Treatment
ALERT
Angle-closure glaucoma typically has a rapid onset
and is an emergency.
General
H Reduction of IOP by decreasing aqueous humor pro-
duction with medications
H Bed rest (with acute angle-closure glaucoma)
Medications
H Beta-adrenergic blockers, such as levobunolol and
timolol
H Prostaglandin analogues such as bimatoprost
H Selective alpha2 agonists such as brimonidine
H Vital signs
H Response to treatment
H Visual acuity
Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H need for meticulous compliance with prescribed
drug therapy
H all procedures and treatments, especially surgery
H the fact that lost vision cant be restored but treat-
ment can usually prevent further loss
H modification of the patients environment for safety
H signs and symptoms that require immediate medical
attention, such as sudden vision change or eye pain
H the importance of glaucoma screening for early de-
tection and prevention.

ALERT
Occasionally, systemic absorption of a beta-
adrenergic blocker from eyedrops can be sufficient
to cause bradycardia, hypotension, heart block,
bronchospasm, impotence, or depression.

Surgery
H For patients unresponsive to drug therapy:
Argon laser trabeculoplasty
Trabeculectomy
Angle-closure glaucoma
H Laser iridectomy
H Surgical peripheral iridectomy
H In end-stage glaucoma, tube shunt or valve

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort
H express feelings and concerns
H sustain no harm or injury
H maintain present vision.

Nursing interventions
H Administer prescribed drugs.
H Prepare for surgery, if indicated.
H After surgery, protect the affected eye.
H Encourage ambulation immediately after surgery.
H Encourage the patient to express his concerns relat-
ed to the chronic condition.

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Glomerulonephritis Special populations

Goodpastures syndrome, a type of RPGN, is rare,
but occurs most commonly in males ages 20 to 30.
Overview
Description Common characteristics
H Bilateral inflammation of the glomeruli, typically fol- H Decreased urination or oliguria
lowing a streptococcal infection H Smoky or coffee-colored urine
H Also called poststreptococcal acute glomerulo- H Dyspnea and orthopnea
nephritis or PSAGN H Periorbital edema
H Mild to severe hypertension
Pathophysiology
H Epithelial or podocyte layer of the glomerular mem- ALERT
brane is disturbed, resulting in a loss of negative
charge. The presenting features of glomerulonephritis in
H Acute poststreptococcal glomerulonephritis results children may be encephalopathy with seizures and
from the entrapment and collection of antigen- local neurologic deficits. An elderly patient with
antibody complexes in the glomerular capillary glomerulonephritis may report vague, nonspecific
membranes, after infection with group A beta- symptoms, such as nausea, malaise, and arthral-
hemolytic streptococcus. gia.
H Antigens stimulate the formation of antibodies.
H Circulating antigen-antibody complexes become
lodged in the glomerular capillaries. Complications
H Complexes initiate complement activation and the re- H Pulmonary edema
lease of immunologic substances that lyse cells and H Heart failure
increase membrane permeability. H Sepsis
H Antibody damage to basement membranes causes H Renal failure
crescent formation. H Severe hypertension
H Antibody or antigen-antibody complexes in the H Cardiac hypertrophy
glomerular capillary wall activate biochemical medi-
ators of inflammation complement, leukocytes,
and fibrin. Assessment
H Activated complement attracts neutrophils and
monocytes, which release lysosomal enzymes that History
damage the glomerular cell walls and cause a prolif- H Decreased urination
eration of the extracellular matrix, affecting glomeru- H Recent streptococcal infection of the respiratory tract
lar blood flow. H Household member with PSAGN
H Membrane permeability increases and causes a loss H May be asymptomatic
of negative charge across the glomerular membrane
as well as enhanced protein filtration. Physical findings
H Membrane damage leads to platelet aggregation, and H Smoky or coffee-colored urine
platelet degranulation releases substances that in- H Dyspnea
crease glomerular permeability. H Periorbital edema
H Increased blood pressure
Causes H Pallor
H Streptococcal infection
H Impetigo Test results
H Immunoglobulin A nephropathy (Bergers disease) Laboratory
H Lipoid nephrosis H Throat culture shows group A beta-hemolytic strepto-
coccus.
Incidence H Electrolyte, blood urea nitrogen, and creatinine lev-
H Acute glomerulonephritis most common in boys ages els are elevated.
3 to 7 but can occur at any age H Serum protein level is decreased.
H Rapidly progressive glomerulonephritis (RPGN) most H Hemoglobin level is decreased in chronic glomeru-
common between ages 50 and 60 lonephritis.
H Antistreptolysin-O titers are elevated.
H Streptozyme and anti-DNase B levels are elevated.
H Serum complement levels are low.

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H Urinalysis shows red blood cells, white blood cells,

mixed cell casts, protein, fibrin-degradation prod- Patient teaching
ucts, and C3 protein.
Imaging Be sure to cover:
H Kidney-ureter-bladder X-ray shows bilateral kidney H taking prescribed drugs
enlargement (acute glomerulonephritis). H how to assess ankle edema
H Chest X-ray reveals congestion caused by fluid reten- H reporting signs of infection
tion. H recording daily weight
Diagnostic procedures H following a low-sodium diet.
H Renal biopsy confirms diagnosis.
Discharge planning
H Refer the patient to social services, as appropriate.
Treatment H Refer the patient to renal disease support group.

General
H Treatment of the primary disease
H Bed rest
H Fluid restriction
H Sodium-restricted diet
H Correction of electrolyte imbalance
H Dialysis
H Plasmapheresis

Medications
H Antibiotics, according to the infective agent
H Anticoagulants such as heparin
H Diuretics such as furosemide
H Vasodilators such as hydralazine
H Corticosteroids, such as methylprednisolone and
prednisone
Surgery
H Kidney transplantation

Nursing considerations
Key outcomes
The patient will:
H maintain adequate fluid balance
H identify risk factors that exacerbate the condition,
and modify lifestyle accordingly
H maintain hemodynamic stability
H have laboratory values return to normal.

Nursing interventions
H Provide appropriate skin care and oral hygiene.
H Encourage the patient to express his feelings about
the disorder.
H Administer prescribed drugs.
H Elevate the head of the bed at least 30 degrees.

Monitoring
H Vital signs
H Intake and output
H Daily weight
H Laboratory studies
H Respiratory status
H Renal function
H Cardiovascular status

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Goiter or the use of goitrogenic drugs (such as propyl-

thiouracil, methimazole, iodides, and lithium)
Incidence
Overview H Decreases with age
H More common in females than in males
Description
H Thyroid gland enlargement not caused by inflamma- Common characteristics
tion or a neoplasm H Mildly enlarged gland to a massive, multinodular
H Commonly classified as toxic (associated with hyper- goiter
thyroidism) or nontoxic (not associated with hyper-
thyroidism or hypothyroidism) Complications
H Tracheal compression
Pathophysiology H Hyperthyroidism
H Thyroid gland cant produce enough thyroid hor- H Lymphoma
mone to meet metabolic requirements. H Abscess
H Thyroid gland enlarges to compensate for inadequate
hormone synthesis.
Assessment
Causes
H Thyroid growth-stimulating immunoglobulins History
H Inherited defects H Respiratory distress
H Inadequate dietary intake of iodine H Dysphagia
H Ingestion of large amounts of goitrogenic foods
(such as rutabagas, cabbage, soybeans, peanuts, Physical findings
peaches, peas, strawberries, spinach, and radishes) H Swelling and distention of the neck, which may be
mildly to massively enlarged (see Understanding
simple goiter)
Test results
Understanding simple goiter
Laboratory
A simple (nontoxic) goiter is any enlargement of the thy- H Thyroid-stimulating hormone level is high or normal.
roid gland not caused by inflammation or neoplasm. The H Serum thyroxine concentrations are low-normal or
thyroid mass increases to compensate for inadequate hor- normal.
mone synthesis. Its most common in females, occurring H Iodine-131 uptake is normal or increased (50% of
when thyroid hormone secretion fails to meet metabolic the dose at 24 hours).
needs.
Other
Sporadic goiter follows ingestion of goitrogenic drugs
H Patient history and physical examination help to con-
(such as propylthiouracil) and iodides or foods (such as
rutabagas and cabbage). Endemic goiter results from firm the diagnosis.
geographically related nutritional factors such as iodine-
depleted soil. Inherited defects may contribute to either
type of goiter.
Treatment
The patient may report respiratory distress and dyspha-
gia from compression of the trachea and esophagus and General
dizziness or syncope when raising her arms over her H Avoidance of known goitrogenic drugs and foods
head. A firm, irregular enlargement and stridor caused by
tracheal compression may be found. Medications
Diagnostic tests reveal normal serum thyroid hormone H Thyroid hormone such as levothyroxine
levels; abnormalities rule out this diagnosis. Thyroid anti-
H Small doses of iodine
body titers are usually normal. Iodine 131 uptake is usu-
ally normal but may increase with iodine deficiency or a Surgery
biosynthetic defect. Urinalysis may show low urinary ex-
cretion of iodine. H Subtotal thyroidectomy
Treatment to reduce thyroid hyperplasia involves thyroid
hormone replacement. Iodide administration commonly
relieves goiters caused by iodine deficiency. Sporadic goi-
Nursing considerations
ter requires avoidance of goitrogenic drugs and food. Ra-
dioiodine ablation therapy aids some patients. Rarely, par- Key outcomes
tial thyroidectomy is needed to relieve pressure on the The patient will:
surrounding structures. H remain hemodynamically stable
H have a reduced goiter

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H express feelings of increased comfort

H not demonstrate respiratory or swallowing difficulty.

Nursing interventions
H Administer prescribed drugs.
H Encourage the patient to express feelings and con-
cerns.
Monitoring
H Vital signs
H Neck circumference
H Response to therapy
H Respiratory status

Patient teaching
Be sure to cover:
H medication administration, dosage, and possible ad-
verse effects
H symptoms of thyroid toxicosis
H use of iodized salt.

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Gonadotropin deficiency H Depending on age of onset: inadequate sexual differ-

entiation, microphallus and partial or complete lack
of testicular descent, poor secondary sex characteris-
tics and muscle development
Overview
Complications
Description H Infertility
H Lack of hormones (follicle-stimulating hormone H Sexual dysfunction
[FSH] and luteinizing hormone [LH]) that stimulate
the sex glands, primarily the testes and ovaries
H If chronic and untreated, can cause infertility and os- Assessment
teopenia
History
Pathophysiology H Illness that affects testes
H Gonadotropin-releasing hormone (Gn-RH) is secret- H Underdeveloped secondary sex characteristics
ed by the hypothalamus and causes the anterior pitu- H Mood and behavior changes
itary to secrete the gonadotropins testosterone, H Sexual dysfunction
estrogen, FSH, and LH. H Infertility
H Estrogen, progesterone, and testosterone, produced
by the gonads, function in a negative-feedback loop Physical findings
that regulates Gn-RH secretion. H Testicular atrophy
H Mechanisms that cause Gn-RH deficiency include: H Underdeveloped secondary characteristics
pituitary tumor producing another hormone that H Decreased body hair
impinges on the gonadotropin-producing cells and H Fine wrinkles around eyes and lips
physically impairs Gn-RH biosynthesis
medical treatments such as radiation (impairs Test results
Gn-RHproducing cells) Laboratory
oversecretion of estrogen, progesterone, or testos- H Testosterone level is low, and Gn-RH level is high in
terone by dysfunctional target glands, causing primary testicular failure.
Gn-RH inhibition through the negative-feedback H Estrogen level is low, and Gn-RH level is high in pri-
loop mary ovarian failure.
prolactin (inhibits pituitary secretion of Gn-RH; H Gn-RH and testosterone or estrogen levels are low in
prolactin-secreting tumors can cause Gn-RH defi- hypothalamic or pituitary dysfunction.
ciency) H Human chorionic gonadotropin stimulation test re-
reduced Gn-RH secretion due to response of hypo- sults are abnormal.
thalamus to physical stress, obesity, or starvation. H Gn-RH stimulation test reveals insufficient elevation
of LH or FSH levels.
Causes
H Pituitary tumor or hemorrhage
H Oversecretion of target gland hormone, such as es- Treatment
trogen, progesterone, or testosterone
H Prolactin-secreting tumor General
H Hypothalamic suppression of Gn-RH during periods H Stress reduction
of physical or emotional stress, obesity, and starva- H Weight gain or loss
tion
H Genetics Medications
H Gonadotropin, estrogen, or testosterone replacement
Incidence
H Can occur at any age Surgery
H Affects males more commonly than females H Removal of tumors

Common characteristics
H Decreased libido, strength, and body hair, and fine Nursing considerations
wrinkles around the eyes and lips (adults)
H Amenorrhea; vaginal, uterine, and breast atrophy; Key outcomes
clitoral enlargement; voice deepening; and beard The patient will:
growth (females) H relate an understanding of the disorder and its treat-
H Testicular atrophy, reduction in beard growth, and ment
erectile dysfunction (males) H express positive feelings regarding body image
H Mood and behavior changes H seek appropriate support measures.
H Anosmia

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Nursing interventions
H Administer prescribed drugs.
H Provide emotional support.

Monitoring
H Laboratory results

Patient teaching
Be sure to cover:
H the disorder and treatment
H taking prescribed drugs.

Discharge planning
H Stress to the patient the importance of obtaining on-
going follow-up care.

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Gonorrhea H Pneumonia
H Acute respiratory distress syndrome

Overview Assessment
Description History
H Common sexually transmitted disease (STD) that H Unprotected sexual contact (vaginal, oral, or anal)
usually starts as infection of the genitourinary tract; with an infected person, an unknown partner, or
can also begin in rectum, pharynx, or eyes multiple sex partners
H Left untreated, spreads through the blood to the H History of STD
joints, tendons, meninges, and endocardium
H In females, can lead to chronic pelvic inflammatory Physical findings
disease (PID) and sterility H Fever
H Purulent discharge from urethral meatus
Pathophysiology H Female urethral meatus possibly red and edematous
H Gonococci infect mucus-secreting epithelial surfaces H Friable cervix and a greenish yellow discharge
and penetrate through or between the cells to the H Engorged, red, swollen vagina with profuse purulent
connective tissue. discharge
H Inflammation and spread of the infection results. H Rectal infection
H Ocular infection
Causes H Pharyngeal infection
H Transmission of Neisseria gonorrhoea, the causative H Papillary skin lesions on hands and feet
organism, through sexual contact with an infected H PID
person H Perihepatitis
H For a child born to an infected mother, acquisition of H Pain and a cracking noise when moving an involved
gonococcal ophthalmia neonatorum during passage joint
through the birth canal
H Acquisition of gonococcal conjunctivitis by touching Test results
the eyes with a contaminated hand Laboratory
H Culture from the infection site of the urethra, cervix,
Risk factors rectum, or pharynx reveals N. gonorrhea.
H Unprotected sexual activity H Culture of conjunctival scrapings confirms gonococ-
cal conjunctivitis.
Incidence H In males, a Gram stain showing gram-negative diplo-
H Among sexually active individuals, incidence highest cocci may confirm gonorrhea.
in those with multiple partners, teenagers, non- H Identification of gram-negative diplococci on smear
whites, the poor, the poorly educated, city dwellers, from joint fluid and skin lesions indicates gonococ-
and unmarried people who live alone cal arthritis.
H Reinfection common H Complement fixation and immunofluorescent assays
of serum reveal antibody titers four times the normal
Common characteristics rate.
H Possible dysuria in males H Venereal Disease Research Laboratory test may be re-
H Possible absence of symptoms (in both sexes) or active.
symptoms related to the area infected H Rapid plasma reagin test may be reactive.
H Vagina most common site in female children older
than age 1
Treatment
Complications
H PID General
H Acute epididymitis H Follow-up cultures 4 to 7 days after treatment and
H Proctitis again in 6 months
H Salpingitis H For a pregnant patient, final follow-up before delivery
H Septic arthritis H Effective therapy (ends communicability within
H Dermatitis hours)
H Perihepatitis H Abstinence from sexual activity until infection is
H Corneal ulceration treated
H Blindness
H Meningitis Medications
H Osteomyelitis H Antibiotics, such as ceftriaxone, doxycycline, and
azithromycin

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Prevention Monitoring
Preventing gonorrhea H Response to treatment
H Adverse drug effects
To prevent gonorrhea, provide the following patient teach-
H Complications
ing:
H Follow-up culture results
H Tell the patient to avoid sexual contact until cultures
prove negative and infection is eradicated.
H Advise the patients partner to receive treatment even if Patient teaching
the partner doesnt have a positive culture. Recom-
mend that the partner avoid sexual contact with anyone
Be sure to cover:
until treatment is complete because reinfection is ex-
H the disorder, diagnosis, and treatment
tremely common.
H Counsel the patient and all sexual partners to be tested H informing all sexual partners of the infection so that
for the human immunodeficiency virus and hepatitis B they can seek treatment
infection. H avoiding sexual contact until cultures are negative
H Instruct the patient to be careful when coming into and infection is eradicated
contact with any bodily discharges to avoid contami- H being careful when coming into contact with any
nating the eyes. bodily discharges to avoid contaminating the eyes
H Tell the patient to take anti-infectives for the entire time H safer sex practices
prescribed. H taking anti-infectives for the time prescribed
H To prevent reinfection, tell the patient to avoid sexual H the importance of returning for follow-up testing
contact with anyone suspected of being infected, to
(see Preventing gonorrhea).
use condoms during intercourse, to wash genitalia
with soap and water before and after intercourse, and
to avoid sharing washcloths or douche equipment.
H Advise the patient to return for follow-up testing.

H 1% silver nitrate drops or erythromycin ointment in

neonates to prevent gonococcal ophthalmia neonato-
rum

Nursing considerations
Key outcomes
The patient will:
H express concern about self-concept, esteem, and
body image
H state infection risk factors
H identify signs and symptoms of infection
H remain free from signs and symptoms of infection
H practice safer sex.

Nursing interventions
H Isolate the patient if his eyes are infected.
H With gonococcal arthritis, apply moist heat to ease
pain in affected joints.
H Administer prescribed drugs.
H Report all cases of gonorrhea to the local public
health authorities as required.
H Report all cases of gonorrhea in children to child
abuse authorities.
H Routinely instill prophylactic drugs, according to fa-
cility protocol, in the eyes of all neonates on admis-
sion to the nursery.
H Check the neonate of an infected mother for signs of
infection, and obtain specimens for culture from the
neonates eyes, pharynx, and rectum.

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Goodpastures H Immunofluorescence of GBM shows linear deposi-

syndrome
Overview
Description
H Pulmonary renal syndrome characterized by hemop-
tysis and rapidly progressive glomerulonephritis
Pathophysiology
H Abnormal production and deposition of antibodies
against glomerular basement membrane (GBM) and
alveolar basement membrane activate the comple-
ment and inflammatory responses.
H This results in glomerular and alveolar tissue dam-
age.
Causes
H Unknown
H May be associated with exposure to hydrocarbons or
with type II hypersensitivity reaction
H Possible genetic predisposition
Incidence
H Occurs at any age; most commonly in males between
ages 20 and 30
tion of immunoglobulins.
H Serum anti-GBM antibody test reveals circulating
anti-GBM antibodies, which distinguish Goodpas-
tures syndrome from other pulmonary-renal syn-
dromes, such as Wegeners granulomatosis, poly-
arteritis, and systemic lupus erythematosus.
H Serum creatinine and blood urea nitrogen (BUN)
levels typically two to three times normal.
H Urinalysis may reveal red blood cells and cellular
casts, which typify glomerular inflammation; may
also show granular casts and proteinuria.
Imaging
H Chest X-rays reveal pulmonary infiltrates in a diffuse,
nodular pattern.
Diagnostic procedures
H Lung biopsy shows interstitial and intra-alveolar
hemorrhage with hemosiderin-laden macrophages.
H Renal biopsy usually shows focal necrotic lesions and
cellular crescents.
Treatment
General
H Plasmapheresis
H Dialysis
H Low-protein, low-sodium diet
H Activity, as tolerated

Common characteristics Medications

H Hemoptysis H High-dose I.V. corticosteroids such as methylpred-
H Rapidly progressive glomerulonephritis nisolone
Complications Surgery
H Renal failure H Kidney transplantation
H Pulmonary edema and hemorrhage

Nursing considerations
Assessment
Key outcomes
History The patient will:
H Possible complaint of malaise, fatigue, and pallor H maintain a patent airway and adequate ventilation
H Possible pulmonary bleeding for months or years be- H maintain adequate fluid balance
fore developing overt hemorrhage and signs of renal H express feelings of increased energy
disease H avoid complications.

Physical findings Nursing interventions

H Hematuria
H Decreased urine output
H Dyspnea, tachypnea, orthopnea
H Restlessness
H Hemoptysis, ranging from a cough with blood-tinged
sputum to frank pulmonary hemorrhage
H Pulmonary crackles and rhonchi
Test results
Laboratory
H Immunofluorescence of alveolar basement mem-
brane shows linear deposition of immunoglobulins
as well as C3 and fibrinogen.
H Elevate the head of the bed at least 30 degrees, and
administer humidified oxygen, as ordered.
H Encourage the patient to conserve his energy.
H Assist with range-of-motion exercises.
H Assist with activities of daily living, and provide fre-
quent rest periods.
H Transfuse blood and administer corticosteroids, as
ordered. Watch closely for signs and symptoms of
adverse reactions.
H Encourage coughing, deep breathing, and incentive
spirometer use.

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Monitoring
H Respiratory status
H Vital signs
H Arterial blood gas levels
H Cardiovascular status
H Intake and output
H Daily weight
H Creatinine clearance, BUN, and serum creatinine
levels
H Hematocrit and coagulation studies

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the importance of conserving energy
H an explanation that fluid intake may be restricted
H the name, dosage, purpose, and adverse effects of all
medications
H how to effectively deep-breathe and cough
H how to recognize the signs of respiratory or geni-
tourinary bleeding and the need to report such signs
to the practitioner at once.
Discharge planning
H If dialysis or kidney transplantation is required, refer
the patient to a renal support group.
H Encourage regular follow-up care.

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Gout H Coronary thrombosis

H Hypertension
H Infection when tophi rupture

Overview
Assessment
Description
H Inflammatory arthritis caused by uric acid and crystal History
deposits H Sedentary lifestyle
H Red, swollen, and acutely painful joints H Hypertension
H Mostly affects feet, great toe, ankle, and midfoot H Renal calculi
H Primary gout: patient symptom-free for years be- H Waking during the night with pain in great toe
tween attacks H Initial moderate pain that grows intense
H Sudden strike and quick peak in first acute attack H Chills; mild fever
H Delayed attacks associated with olecranon bursitis
H Chronic polyarticular gout the final, unremitting Physical findings
stage of the disease marked by persistent painful H Swollen, dusky red or purple joint
polyarthritis H Limited movement of joint
H Tophi, especially in the outer ears, hands, and feet
Pathophysiology (see Recognizing gouty tophi)
H Uric acid crystallizes in blood or body fluids, and the H Skin over tophi that may ulcerate and release chalky
precipitate accumulates in connective tissue (tophi). white exudate or pus
H Crystals trigger an immune response. H Secondary joint degeneration
H Neutrophils secrete lysosomes for phagocytosis. H Erosions, deformity, and disability
H Lysosomes damage tissue and exacerbate the im- H Warmth over joint
mune response. H Extreme tenderness
H Fever
Causes H Hypertension
H Exact cause unknown
H Decreased renal excretion of uric acid Test results
H Genetic defect in purine metabolism (hyper- Laboratory
uricemia) H Serum uric acid levels are elevated with a gout at-
H Secondary gout that develops with other diseases: tack.
Obesity H White blood cell count is elevated in an acute attack.
Diabetes mellitus H Urine uric acid level is elevated in 20% of patients.
Hypertension Imaging
Polycythemia H X-ray of the articular cartilage and subchondral bone
Leukemia shows evidence of chronic gout.
Myeloma Diagnostic procedures
Sickle cell anemia H Needle aspiration of synovial fluid shows needlelike
Renal disease intracellular crystals.
H Secondary gout that follows treatment with drugs
(hydrochlorothiazide or pyrazinamide)
Treatment
Incidence
H Primary gout typically in males older than age 30 and General
postmenopausal females taking diuretics H Termination of acute attack
H Protection of inflamed, painful joints
Common characteristics H Treatment for hyperuricemia
H Extreme pain in affected joints H Local application of cold
H Redness and swelling in joints H Prevention of recurrent gout
H Tophi in great toe, ankle, or pinna of ear H Prevention of renal calculi
H Elevated skin temperature H Weight loss program, if indicated
H Avoidance of alcohol
Complications H Sparing use of purine-rich foods (such as anchovies,
H Renal calculi liver, and sardines)
H Atherosclerotic disease H Bed rest (in acute attack)
H Cardiovascular lesions H Immobilization of joint
H Stroke

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Recognizing gouty tophi Monitoring

H Intake and output
In advanced gout, urate crystal deposits develop into
H Serum uric acid levels
hard, irregular, yellow-white nodules called tophi. These
bumps commonly protrude from the great toe and ear. H Acute gout attacks 24 to 96 hours after surgery
H Pain control

Patient teaching
Tophus Be sure to cover:
H the disorder, diagnosis, and treatment
H the need to drink plenty of fluids (up to 2 qt [2 L]
per day)
H relaxation techniques
H compliance with the prescribed medication regimen
H dietary adjustments
H the need to control hypertension.

Discharge planning
H Refer the patient to a weight-reduction program, if
appropriate.
Tophi

Medications
H Analgesics such as oxycodone
H Nonsteroidal anti-inflammatory drugs, such as sundi-
lac and naproxen
H Antigout drugs, such as allopurinol, colchicine,
probenecid, and sulfinpyrazone

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort and decreased
pain
H maintain joint mobility and range of motion
H perform activities of daily living within confines of
the disease
H demonstrate knowledge of the condition and treat-
ment regimen.
Nursing interventions
H Allow adequate time for self-care.
H Institute bed rest.
H Use a bed cradle, if appropriate.
H Give pain medication, as needed.
H Apply cold packs to affected areas.
H Identify techniques and activities that promote rest
and relaxation.
H Administer anti-inflammatories, as prescribed.
H Provide a purine-poor diet.

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Graft rejection Assessment

syndrome
Overview
Description
H Rejection of a donated organ occurring when the
hosts immune responses are directed against the
graft
H Three subtypes based on time of onset and mecha-
nisms involved:
Hyperacute rejection
Acute rejection
Chronic rejection
Pathophysiology
H Hyperacute rejection occurs within minutes to hours
after graft transplantation.
H Circulating host antibodies recognize and bind to
graft antigens.
H Binding of these antibodies leads to initiation of the
complement cascade, recruitment of neutrophils,
platelet activation, damage to graft endothelial cells,
and stimulation of coagulation reactions.
H Acute rejection may occur several hours to days
(even weeks) after transplantation.
H Alloantigen-reactive T cells from the host infiltrate
the graft and are activated by contact with foreign,
graft-related proteins that are presented to them by
antigen-presenting cells.
H These T cells may cause graft tissue damage.
H Chronic rejection is characterized by the develop-
ment of blood vessel luminal occlusion due to pro-
gressive thickening of the intimal layers of medium
and large arterial walls.
H Large amounts of intimal matrix are produced, lead-
ing to increasingly occlusive vessel wall thickening.
H A slowly progressing reduction in blood flow results
in regional tissue ischemia, cell death, and tissue fi-
brosis.
Causes
H Immune system response to a graft
Incidence
H Hyperacute rejection rare; affects less than 1% of
transplant recipients
H Acute rejection in 50% of transplant patients (only
10% progress to graft loss)
H Chronic rejection in 50% of transplant patients with-
in 10 years after transplantation
Common characteristics
H Rapid or gradual progression of organ dysfunction
History
H Signs and symptoms that vary markedly, depending
on type of rejection, underlying illnesses, and type of
organ transplanted
Physical findings
H Oliguria and increasing serum creatinine and blood
urea nitrogen levels with kidney transplant
H Elevated transaminase levels, decreased albumin lev-
els, and hypocoagulability with liver transplant
H Hypotension, heart failure, and edema with heart
transplant
Test results
Diagnostic procedures
H Biopsy of the transplanted tissue confirms rejection.
H Hyperacute rejection is characterized by large num-
bers of polymorphonuclear leukocytes in the graft
blood vessels, widespread microthrombi, platelet ac-
cumulation, and interstitial hemorrhage with little or
no interstitial inflammation.
Treatment
General
H Close monitoring of function of grafted organ
H Surveillance, with prophylactic measures against op-
portunistic infections
H Dietary restrictions based on organ system affected
H Activity, as tolerated
H Hemodialysis
H Mechanical ventilation
Medications
H Immunosuppressants, such as azathioprine and
basiliximab
H Antirejection therapies such as cyclosporine
H Antibiotics, according to infective organism
Nursing considerations
Key outcomes
The patient will:
H not experience fever, chills, and other signs and
symptoms of illness
H use support systems to assist with coping
H express his feelings about the condition
H comply with the treatment regimen.
Nursing interventions
H Administer prescribed medications.
H Provide emotional support.

Complications Monitoring
H Rapid thrombosis H Vital signs
H Loss of graft function H Function of the transplanted organ

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H Signs and symptoms of infection

H Signs and symptoms of rejection
H Respiratory status
H Intake and output
H Cardiovascular status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H how to recognize signs and symptoms of organ dys-
function
H the need to immediately report fever, chills, and oth-
er symptoms of infection
H the need for lifelong medication compliance.

Discharge planning
H Refer the patient and his family to social support, in-
cluding psychological support services, as indicated.

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H Aspiration
Life-threatening disorder H Respiratory tract infections
H Life-threatening respiratory and cardiac compromise

Guillain-Barr
Assessment
syndrome
History
H Minor febrile illness 1 to 4 weeks before current
Overview symptoms
H Tingling and numbness (paresthesia) in the legs
Description H Progression of symptoms to the arms, the trunk and,
H A form of polyneuritis finally, the face
H Acute, rapidly progressive, and potentially fatal H Stiffness and pain in the calves
H Three phases:
Acute: beginning from first symptom, ending in 1 Physical findings
to 3 weeks H Muscle weakness (the major neurologic sign)
Plateau: lasting several days to 2 weeks H Sensory loss, usually in the legs (spreads to arms)
Recovery: coincides with remyelination and axonal H Difficulty talking, chewing, and swallowing
process regrowth; extends over 4 to 6 months and H Paralysis of the ocular, facial, and oropharyngeal
may take up to 2 to 3 years; recovery possibly not muscles
complete H Loss of position sense
H Diminished or absent deep tendon reflexes
Pathophysiology
H Segmented demyelination of peripheral nerves oc- Test results
curs, preventing normal transmission of electrical Diagnostic procedures
impulses. H Cerebrospinal fluid (CSF) analysis may show a nor-
H Sensorimotor nerve roots are affected; autonomic mal white blood cell count, an elevated protein count
nerve transmission may also be affected. (See Under- and, in severe disease, increased CSF pressure.
standing sensorimotor nerve degeneration.) Other
H Electromyography may demonstrate repeated firing
Causes of the same motor unit instead of widespread sec-
H Unknown tional stimulation.
H Nerve conduction studies show marked slowing of
Risk factors nerve conduction velocities.
H Surgery
H Rabies or swine influenza vaccination
H Viral illness Treatment
H Hodgkins or some other malignant disease
H Lupus erythematosus General
H Supportive measures
Incidence H Possible endotracheal intubation or tracheotomy
H Occurs equally in both sexes with mechanical ventilation
H Occurs between ages 30 and 50 H Fluid volume replacement
H Plasmapheresis
Common characteristics H Possible tube feedings
H Symmetrical muscle weakness initially in lower ex- H Adequate caloric intake
tremities and progressing to upper extremities H Exercise program to prevent contractures
H Paresthesia H Emotional support
H Diplegia H Maintenance of skin integrity
H Dysphagia
H Hypotonia Medications
H Areflexia H Corticosteroids such as methylprednisolone
H I.V. immune globulin
Complications
H Thrombophlebitis Surgery
H Pressure ulcers H Possible tracheostomy
H Contractures H Possible gastrostomy or jejunotomy feeding tube in-
H Muscle wasting sertion

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Understanding sensorimotor nerve

degeneration
Guillain-Barr syndrome attacks the peripheral nerves so
that they cant transmit messages to the brain correctly.
Heres what goes wrong:
The myelin sheath degenerates for unknown reasons.
This sheath covers the nerve axons and conducts electri-
cal impulses along the nerve pathways. With degeneration
comes inflammation, swelling, and patchy demyelination.
As this disorder destroys myelin, the nodes of Ranvier (at
the junctures of the myelin sheaths) widen. This delays
and impairs impulse transmission along the dorsal and
ventral nerve roots.
Because the dorsal nerve roots handle sensory function,
the patient may experience sensations, such as tingling
and numbness, when the nerve root is impaired. Similarly,
because the ventral roots are responsible for motor func-
tion, impairment causes varying weakness, immobility,
and paralysis.
Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H effective means of communication
H the appropriate home care plan
H instructions about medications
H adverse medication reactions.
Discharge planning
H Refer the patient to physical rehabilitation sources,
as indicated.
H Refer the patient to occupational and speech rehabil-
itation resources, as indicated.
H Refer the patient to the Guillain-Barr Syndrome
Foundation.

Nursing considerations
Key outcomes
The patient will:
H maintain a patent airway and adequate ventilation
H develop an alternate means of communication
H maintain required caloric intake daily
H maintain joint mobility and range of motion (ROM).

Nursing interventions
H Establish a means of communication before intuba-
tion is required, if possible.
H Turn and reposition the patient.
H Encourage coughing, deep breathing, and incentive
spirometer use.
H Provide meticulous skin care.
H Provide passive ROM exercises.
H In case of facial paralysis, provide eye and mouth
care.
H Administer prescribed drugs.
H Provide emotional support.
H Elevate the head of the bed at least 30 degrees.

Monitoring
H Vital signs
H Respiratory status
H Arterial blood gas values
H Neurologic status
H Pulse oximetry
H Signs of thrombophlebitis
H Signs of urine retention
H Response to medications
H Skin integrity
H Cardiovascular status

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Gynecomastia Special populations

In neonates, gynecomastia may be associated with
galactorrhea (witchs milk). This sign usually
Overview disappears within a few weeks but may persist
until age 2.
Description
H Enlargement of breast tissue in males
H Usually bilateral, except in males older than age 50 Incidence
when its usually unilateral H Affects up to 65% of adolescent males
H Usually resolves spontaneously in 6 to 12 months H True gynecomastia: affects 1% of adult males
H Pseudogynecomastia: accumulation of fat deposits,
not breast tissue. Special populations
Pathophysiology Most males have physicologic gynecomastia at
H Disturbance in the normal ratio of active androgen to some time during adolescence, usually around age
estrogen results in proliferation of the fibroblastic 14. This gynecomastia is usually asymmetrical and
stroma and the duct system of the breast. tender; it commonly resolves within 2 years and
rarely persists beyond age 20.
Causes
H Testicular tumors
H Obesity Common characteristics
H Pituitary tumors H Enlarged breast tissue (at least 2 cm in diameter),
H Some hypogonadism syndromes either unilateral or bilateral, beneath the areola
H Liver disease causing inability to break down normal
male estrogen secretions Complications
H Chronic renal failure H Malignancy
H Chronic obstructive lung disease H Complications of surgery:
H Other causes (see Drugs and treatments causing Infection
gynecomastia) Scarring
Sensory change
Hematoma
Breast asymmetry

Drugs and treatments causing

Assessment
gynecomastia
History
In addition to the common causes of gynecomastia, vari- H Causative tumor
ous drugs and treatments may also cause this disorder. H Change in size of breast tissue
Drugs H History of causative factors
When gynecomastia is an effect of drugs, its typically H Breast pain
painful and unilateral. Estrogens used to treat prostate
cancer, including diethylstilbestrol (DES), estramustine, Physical findings
and chlorotrianisene, directly affect the estrogen-
androgen ratio. Drugs that have an estrogen-like effect, H Enlarged breast tissue beneath the areola
such as cardiac glycosides and human chorionic go- H Further physical findings depending on cause
nadotropin, may do the same.
Regular use of alcohol, marijuana, or heroin reduces
Test results
plasma testosterone levels, causing gynecomastia. Other Laboratory
drugs such as flutamide, cyproterone, spironolactone, H Estrogen levels are excessively high and testosterone
cimetidine, and ketoconazole produce this sign by levels are normal in drug- and tumor-induced hyper-
interfering with androgen production or action. Some estrogenism.
common drugs, including phenothiazines, tricyclic antide- H Testosterone levels are very low and estrogen levels
pressants, and antihypertensives, produce gynecomastia,
are normal in hypergonadism.
but it isnt known how.
Treatments Diagnostic procedures
H Biopsy rules out malignancy.
Gynecomastia may develop within weeks of starting
hemodialysis for chronic renal failure. It may also follow
major surgery or testicular irradiation.

332 Gynecomastia
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Treatment
General
H Treatment of cause

Medications
H Androgens, such as testosterone and methyltestos-
terone
Surgery
H Resection of extra breast tissue for cosmetic reasons
H Liposuction-assisted mastectomy

Nursing considerations
Key outcomes
The patient will:
H express understanding of the condition and its cause
H express positive feelings concerning body image.

Nursing interventions
H Apply cold compresses.
H Encourage verbalization of feelings and concerns.
H Provide emotional support.

Monitoring
H Vital signs
H Breast size
After surgery
H Pain control
H Wound site

Patient teaching
Be sure to cover:
H cause of condition and related treatment
H medication administration, dosage, and possible ad-
verse effects
H preoperative teaching, if appropriate.

Gynecomastia 333
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HHaemophilus
influenzae infection
Overview
Description
H Infection that most commonly attacks respiratory sys-
tem
H Common cause of epiglottiditis, laryngotracheobron-
chitis, pneumonia, bronchiolitis, otitis media, and
meningitis
H Infrequent cause of bacterial endocarditis, conjunc-
H Pericarditis, pleural effusion
H Respiratory failure due to pneumonia

Assessment
History
H Possible report of recent viral infection
H Malaise
H Fatigue
H Fever

Physical findings
Epiglottiditis
H Restlessness and irritability
tivitis, facial cellulitis, septic arthritis, and osteo- H Use of accessory muscles, inspiratory retractions,
myelitis stridor
H Sitting up, leaning forward with mouth open, tongue
Pathophysiology protruding, and nostrils flaring
H Antigenic response occurs with invasion of bacteria. H Expiratory rhonchi; diminishing breath sounds as the
H Systemic disease results from invasion and condition worsens
hematogenous spread to distant sites (meninges, H Pharyngeal mucosa that may look reddened (rarely,
bones, and joints). with soft yellow exudate)
H Local invasion occurs on the mucosal surfaces. H Epiglottis that appears cherry red with considerable
H Otitis media occurs when bacteria reach the middle edema
ear through the eustachian tube. H Severe pain that makes swallowing difficult or impos-
sible
Causes Pneumonia
H H. influenzae, a gram-negative, pleomorphic aero- H Shaking chills
bic bacillus H Tachypnea
H Transmission by direct contact with secretions or air- H Productive cough
borne droplets H Impaired or asymmetrical chest movement caused by
pleuritic pain
Incidence H Dullness over areas of lung consolidation
H H. influenzae type B (Hib) infection incidence lower Meningitis
when vaccine is administered at ages 2, 4, 6, and 15 H Altered level of consciousness
months H Seizures and coma as disease progresses
H Occurs in fewer than 2 in 100,000 children in the H Positive Brudzinskis and Kernigs signs
United States H Exaggerated and symmetrical deep tendon reflexes
H H. influenza epiglottiditis most common in children H Nuchal rigidity
between ages 3 and 7 but can occur at any age H Opisthotonos
H Higher incidence of meningitis due to Hib in black
children Test results
H Ten times higher incidence in Native Americans, pos- Laboratory
sibly due to exposure, socioeconomic conditions, H Isolation of the organism in blood culture confirms
and genetic differences in immune response infection.
H Cause of 5% to 10% of bacterial meningitis cases in H Hib meningitis is detected in cerebrospinal fluid
adults cultures.
H 3% to 5% mortality rate

Common characteristics Treatment

H Generalized malaise
H High fever General
H Airway maintenance (critical in epiglottiditis)
Complications H Diet based on respiratory status (possible need for
H Permanent neurologic sequelae from meningitis, small, frequent meals)
including hearing loss H Nothing by mouth with inability to swallow ade-
H Complete upper airway obstruction from epiglotti- quately
ditis H Activity, as tolerated
H Cellulitis

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Medications
H Cephalosporin
H Chloramphenicol and ampicillin (alternate regimen)
H Glucocorticoids, such as dexamethasone, betametha-
sone, and methylprednisone

Nursing considerations
Key outcomes
The patient will:
H have no adventitious breath sounds
H maintain adequate gas exchange
H have arterial blood gas (ABG) levels that return to
normal
H have no pathogens appear in cultures
H remain free from signs and symptoms of infection.

Nursing interventions
H Maintain respiratory isolation.
H Maintain adequate respiratory function through cool
humidification, oxygen, as needed, and croup or face
tents.
H Keep emergency resuscitation equipment readily
available.
H Suction, as needed.
H Administer prescribed drugs.
H Maintain adequate nutrition and elimination.

Monitoring
H Pulse oximetry
H ABG results
H Complete blood count for signs of bone marrow de-
pression when therapy includes ampicillin or chlor-
amphenicol
H Intake and output
H Respiratory status
H Neurologic status
H Vital signs

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the importance of continuing the prescribed antibiot-
ic until the entire prescription is finished
H using a room humidifier or breathing moist air from
a shower or bath, as necessary, for home treatment
of a respiratory infection
H coughing and deep-breathing exercises to clear
secretions
H the safe disposal of secretions and use of proper
hand-washing technique.
Discharge planning
H Refer the patient to an infectious disease specialist, if
necessary.
H Encourage the patient to receive vaccinations to pre-
vent future infections.

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Hantavirus pulmonary H Fever

H Headache

syndrome H Nausea
H Vomiting
H Cough

Overview Complications
H Respiratory failure
Description H Death (in 80% of cases)
H Viral disease that causes flulike symptoms
H Rapidly progresses to respiratory failure
Assessment
Pathophysiology
H Rodents shed virus in stool, urine, and saliva. History
H Human infection occurs from inhalation, ingestion H Rodent exposure (2 weeks before symptoms)
(of contaminated food or water, for example), con- H Fever
tact with rodent excrement, or rodent bites. (See Sin H Myalgia
Nombre virus.) H Abdominal discomfort
H Dizziness
Causes
H Hantaviruses Physical findings
H Transmission with exposure to infected rodents H Cough
(deer mice, pinion mice, brush mice, and western H Hypotension
chipmunks) H Tachycardia
H Farming, hiking, or camping in rodent-infested areas H Tachypnea
and occupying rodent-infested dwellings H Severe hypoxemia and respiratory failure

Incidence Test results

H Occurs mainly in southwestern United States
H More commonly affects whites
H Affects males more than females
Common characteristics
H Noncardiogenic pulmonary edema
H Myalgia
Sin Nombre virus
This illustration shows the Sin Nombre virus, the most
common cause of Hantavirus pulmonary syndrome in the
United States and Canada. It exists primarily in western
states and provinces.
H The Centers for Disease Control and Prevention and
state health departments can perform definitive test-
ing for hantavirus exposure and antibody formation.
Laboratory
H White blood cell count is elevated with a predomi-
nance of neutrophils, myeloid precursors, and atypi-
cal lymphocytes.
H Hematocrit is elevated.
H Platelet count is decreased.
H Partial thromboplastin time is prolonged.
H Fibrinogen level is normal.
H Serum creatinine levels are no greater than
2.5 mg/dl.
Imaging
H Chest X-rays eventually show bilateral diffuse infil-
trates in almost all patients (findings consistent with
acute respiratory distress syndrome).

Treatment
General
H Intubation and aggressive respiratory management
H Adequate oxygenation
H Stabilization of heart rate and blood pressure
H Cautious fluid volume replacement
H Nothing by mouth until recovery begins
H Activity, as tolerated, with frequent rest periods

Medications
H Vasopressors, such as dopamine, dobutamine, and
norepinephrine
H Ribavirin

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Nursing considerations
Key outcomes
The patient will:
H maintain a respiratory rate within 5 breaths/minute
of baseline
H maintain adequate gas exchange
H cough effectively
H expectorate mucus.

Nursing interventions
H Maintain a patent airway by suctioning, if necessary.
H Ensure adequate humidification, and check mechani-
cal ventilator settings frequently.
H Administer prescribed drugs.
H Provide I.V. fluid therapy based on results of hemody-
namic monitoring.
H Provide emotional support.
H Report cases of Hantavirus pulmonary syndrome to
your state health department.
Monitoring
H Serum electrolyte levels
H Respiratory status
H Neurologic status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the need to immediately report signs or symptoms of
respiratory distress
H prevention guidelines, with a focus on rodent con-
trol.
Discharge planning
H Refer the patient for follow-up with a pulmonologist,
if indicated.

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Headache Tourettes syndrome

Ischemic stroke
Depression
Overview Incidence
Headache
Description H Affects 60% to 80% of people in the United States at
H Head pain that may be a symptom of an underlying any point in time
disorder Migraine
H Classified as primary (headaches having no organic H Appears in childhood or adolescence
or structural cause) or secondary (indicative of an H Recurs throughout adulthood
underlying structural or organic disease) H Affects 17% of females and 6% of males in the United
States
Pathophysiology H Strong familial incidence
Headache
H Sustained muscle contractions directly deform pain Common characteristics
receptors. H Pain thats aching or tight
H Inflammation or direct pressure affects the cranial H Hatbandlike pattern around head
nerves. H Nausea
H Pain-sensitive structures respond, including the skin, H Photophobia
scalp, muscles, arteries, and veins; cranial nerves V, H Phonophobia
VII, IX, and X; and cervical nerves 1, 2, and 3. H Blurred vision
Migraine
H Biochemical abnormalities occur, including local Complications
leakage of a vasodilator polypeptide through the di- H Worsening of existing hypertension
lated arteries and a decreased plasma level of sero- H Photophobia
tonin. H Emotional lability
H Motor weakness
Causes H Loss of work
Headache
H Underlying intracranial disorder
H Systemic disorder Assessment
H Psychological disorders
H Allergy History
H Tension (muscle contraction) Headache
H Emotional stress H Location (frontal, temporal, or cervical), character-
H Fatigue istics (frequency and intensity), onset and duration
H Menstruation (continuous or intermittent)
H Environmental stimuli H Precipitating factors: tension, menstruation, loud
H Glaucoma noises, menopause, alcohol consumption, stress,
H Hormone replacement therapy and food allergies
H Inflammation of the eyes or mucosa of the nasal or H Aggravating factors: coughing, sneezing, and sunlight
paranasal sinuses H Associated symptoms: nausea or vomiting, weakness,
H Disorder of the scalp, teeth, extracranial arteries, or facial pain, and scotomas
external or middle ear H Use of headache-inducing medications
H Muscle spasms of the face, neck, or shoulders H Familial history of headaches
H Vasodilators Migraine
H Hypoxia H Unilateral, pulsating pain gradually becoming more
H Hypertension generalized
H Head trauma and tumors H May be preceded by scintillating scotoma, hemianop-
H Intracranial bleeding, abscess, or aneurysm sia, unilateral paresthesia, or speech disorders
H Caffeine withdrawal H May be accompanied by irritability, anorexia, nausea
H Overuse of over-the-counter headache medications or vomiting, and photophobia
(rebound headache)
Migraine Physical findings
H Constriction and dilation of intracranial and ex- Headache
tracranial arteries H Findings based on cause
H Associated with: H If no underlying problem, normal physical findings
Epilepsy H Possible crepitus or tender spots of the head and
Hereditary hemorrhagic telangiectasia neck

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Migraine H express an increased sense of well-being

H Pallor
H Possible extraocular muscle palsies
H Possible ptosis
H Possible neurologic deficits
Test results
Imaging
H Skull X-rays may show skull fracture (with trauma).
H Sinus X-rays may show sinusitis.
H Computed tomography scan may show tumor or sub-
arachnoid hemorrhage or other intracranial patholo-
gy; may show pathology of sinuses.
H Magnetic resonance imaging may also show tumor.
Diagnostic procedures
H Lumbar puncture may show increased intracranial
pressure, suggesting tumor, edema, or hemorrhage.
H EEG may show alterations in the brains electrical
activity, suggesting intracranial lesion, head injury,
meningitis, or encephalitis.
Other
H Patient questionnaire tool evaluates functional status
and quality of life.
Treatment
General
H Yoga, meditation, or other relaxation therapy
H Identification and elimination of causative factors
(including environmental)
H Psychotherapy, if emotional stress involved
H For migraine patient, adequate oral fluid intake and
avoidance of dietary triggers
H For migraine patient, bed rest in dark, quiet room
H use support systems to assist with coping
H understand causative factors or triggers.
Nursing interventions
H Encourage the use of relaxation techniques.
H Keep the patients room dark and quiet.
H Place ice packs on the patients forehead or a cold
cloth over his eyes.
H Administer prescribed drugs for pain.
Monitoring
H Pain control
H Response to alternative treatment
H Vital signs, especially blood pressure
H Neurologic status
Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H avoidance of migraine triggers
H lifestyle changes
H nonpharmacologic strategies
H monitoring of headaches with headache diary
H appropriate use of preventive medications
H possible adverse reactions to prescribed drugs.
Discharge planning
H Refer the patient to the National Headache Founda-
tion.

Medications
Headache
H Analgesics, such as acetaminophen, aspirin, and
ibuprofen
H Tranquilizers, such as alprazolam, diazepam, and
lorazepam
H Muscle relaxants, such as carisopradol and tizani-
dine
Migraine
H Ergotamine preparations
H Preventive drugs, such as clonidine, propranolol,
topiramate, and valproate
H Triptan agents, such as electriptan, sumatriptan, and
naratriptan

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort and decreased
pain
H demonstrate methods of promoting relaxation and
inner well-being

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Hearing loss H May be transmitted as a dominant, autosomal domi-

nant, autosomal recessive, or sex-linked recessive
trait
Hearing loss in neonates
Overview H Trauma during delivery
H Toxicity
Description H Infection during pregnancy or delivery
H Mechanical or nervous impediment to the transmis- H Hereditary disorders
sion of sound waves to the brain H Maternal exposure to rubella or syphilis during preg-
H Classified as sensorineural, conductive, or mixed nancy
H Presbycusis (age related): most common type of H Use of ototoxic drugs during pregnancy
sensorineural hearing loss H Prolonged fetal anoxia during delivery
H Congenital hearing loss: may be conductive or sen- H Congenital abnormalities of the ears, nose, or throat
sorineural Sudden hearing loss
H Sudden hearing loss: may be conductive, senso- H Occlusion of internal auditory artery by spasm or
rineural, or mixed; usually affects only one ear thrombosis
H Depending on the cause, with prompt treatment H Subclinical mumps
(within 48 hours), hearing possibly restored H Bacterial and viral infections
H Noise-induced hearing loss possibly transient or H Acoustic neuroma
permanent H Mnires disease
H Metabolic, vascular, or neurologic disorders
Pathophysiology H Blood dyscrasias
H In conductive hearing loss, sound wave transmission H Ototoxic drugs
is interrupted between the external canal and inner
ear (junction of the stapes and oval window). Risk factors
H In sensorineural hearing loss, sound wave transmis-
sion is interrupted between the inner ear and brain, Special populations
and theres cochlea or acoustic nerve dysfunction.
H In mixed hearing loss, a combination of dysfunction Premature or low-birth-weight neonates with
of conduction and sensorineural transmission is in- congenital hearing loss are most likely to have
volved. structural or functional hearing impairments.
Causes H Neonates with serum bilirubin levels greater than
Conductive hearing loss 20 mg/dl (toxic effects on the brain)
H Cerumen impaction H Erythroblastosis fetalis
H Blockage of the external ear H Maternal infection or drug abuse
H Tympanic membrane thickening, retraction, scarring, H Frequent ear infections
or perforation H Repeated exposure to very loud noise
H Otitis media, otitis externa
H Otosclerosis Incidence
H Serous otitis H Most common disability in the United States
Sensorineural hearing loss H Third most prevalent disorder in adults older than
H Impairment of the cochlea, eighth cranial or acoustic age 65
nerve H Presbycusis prevalent in adults older than age 50
H Loss of hair cells and nerve fibers in the cochlea
H Drug toxicity Common characteristics
H Vascular occlusion of the anterior cerebellar artery H Hearing loss
H Infectious diseases H Tinnitus
H Arteriosclerosis
H Otospongiosis Complications
H Head or ear trauma H Tympanic membrane perforation
H Organ of Corti degeneration H Cholesteatoma
H Prolonged exposure to loud noise (85 to 90 dB) H Permanent hearing loss
H Perilymphatic fistula H Speech and language delay in children
H Brief exposure to extremely loud noise (greater than
90 dB)
H Acoustic neuroma
Congenital hearing loss
H Sensorineural or conductive

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Assessment Nursing considerations

History Key outcomes
H Deficient response to auditory stimuli within 2 to 3 The patient will:
days after birth H express understanding of the condition and treat-
H Older child with hearing loss that impairs speech de- ment
velopment H exhibit adequate coping mechanisms
H Recent upper respiratory tract infection H regain hearing or develop alternate means of com-
H Use of ototoxic substances munication.
Sudden deafness
H Recent exposure to loud noise Nursing interventions
H Brief exposure to extremely loud noise H Face the patient when speaking and enunciate words
H Persistent tinnitus clearly, slowly, and in a normal tone.
H Transient vertigo H Provide an alternative method of communication.

Physical findings Monitoring

H Obvious hearing difficulty H Response to medications
H Progression of hearing loss
Test results H Adaptation to hearing aid
Imaging
H Computed tomography scan shows vestibular and au-
ditory pathways. Patient teaching
H Magnetic resonance imaging shows acoustic tumors
and brain lesions. Be sure to cover:
Diagnostic procedures H hearing loss, its causes, and treatments
H Auditory brain response shows activity in auditory H tests and procedures
nerve and brain stem. H preoperative and postoperative instructions
H Pure tone audiometry shows presence and degree of H operation and maintenance of a hearing aid
hearing loss. H lip-reading lessons, which may increase the effective-
H Electronystagmography shows vestibular function. ness
H Otoscopic or microscopic examination shows middle H the danger of excessive noise exposure
ear disorders; removes debris. H the use of protective devices in a noisy environment
H Rinne and Webers tests show whether hearing loss is H the danger of exposure to drugs, chemicals, and in-
conductive or sensorineural. fection (with pregnancy)
H the proper technique for ear cleaning or irrigation
H how to instill otic medications
Treatment H medication use and possible adverse effects.

General Discharge planning

H Varies with the type and cause of impairment
H Hearing aids or other effective means of aiding com-
munication
H Avoidance of activities that allow water to enter ear, if
eardrum perforated
H If hearing deteriorates, refer the patient for speech
and hearing rehabilitation.
H Refer a child to an audiologist or otolaryngologist for
further evaluation, as indicated.
H Refer to community resources, as appropriate.

Medications
H Antibiotics as appropriate for infecting organism
H Agents to dissolve cerumen such as triethanolamine
polypeptide oleate-condensate
Surgery
H Correction of tympanic membrane perforation
H Cochlear implants

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Complications
Life-threatening disorder H Pulmonary edema
H Organ failure, especially the brain and kidneys
H MI
Heart failure
Assessment
Overview History
H A disorder or condition that can precipitate heart
Description failure
H Fluid buildup in the heart from myocardium that H Dyspnea or paroxysmal nocturnal dyspnea
cant provide sufficient cardiac output H Peripheral edema
H Usually occurs in a damaged left ventricle but may H Fatigue
occur in right ventricle either primarily or secondary H Weakness
to left-sided heart failure H Insomnia
H Anorexia
Pathophysiology H Nausea
Left-sided heart failure H Sense of abdominal fullness (particularly in right-
H Pumping ability of the left ventricle fails and cardiac sided heart failure)
output falls. H Substance abuse (alcohol, drugs, tobacco)
H Blood backs up into the left atrium and lungs, caus-
ing pulmonary congestion. Physical findings
Right-sided heart failure H Cough that produces pink, frothy sputum
H Ineffective contractile function of the right ventricle H Cyanosis of the lips and nail beds
leads to blood backing up into the right atrium and H Pale, cool, clammy skin
the peripheral circulation, which results in peripher- H Diaphoresis
al edema and engorgement of the kidneys and other H Jugular vein distention
organs. H Ascites
H Tachycardia
Causes H Pulsus alternans
H Mitral stenosis secondary to rheumatic heart disease, H Hepatomegaly and, possibly, splenomegaly
constrictive pericarditis, or atrial fibrillation H Decreased pulse pressure
H Mitral or aortic insufficiency H S3 and S4 heart sounds
H Arrhythmias H Moist, bibasilar crackles, rhonchi, and expiratory
H Hypertension wheezing
H Atherosclerosis with myocardial infarction (MI) H Decreased pulse oximetry
H Myocarditis H Peripheral edema
H Ventricular and atrial septal defects H Decreased urinary output
H Constrictive pericarditis
H Pregnancy Test results
H Thyrotoxicosis Laboratory
H Pulmonary embolism H B-type natriuretic peptide immunoassay is elevated.
H Infections Imaging
H Anemia H Chest X-rays show increased pulmonary vascular
H Emotional stress markings, interstitial edema, or pleural effusion and
H Increased sodium or water intake cardiomegaly.
Diagnostic procedures
Incidence H Electrocardiography reflects heart strain or enlarge-
H Affects 1% of people older than age 50 ment or ischemia. It may also reveal atrial enlarge-
H Affects 10% of people older than age 80 ment, tachycardia, extrasystole, or atrial fibrillation.
H Pulmonary artery pressure monitoring typically
Common characteristics shows elevated pulmonary artery and pulmonary
H Reduced cardiac output artery wedge pressures, left ventricular end-diastolic
H Shortness of breath pressure in left-sided heart failure, and elevated right
H Peripheral edema atrial or central venous pressure in right-sided heart
H Dyspnea on exertion failure.

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Monitoring
Treatment H Daily weight for peripheral edema and other signs
and symptoms of fluid overload
General H Cardiac rhythm
H Antiembolism stockings H Intake and output
H Elevation of lower extremities H Response to treatment
H Sodium-restricted diet H Vital signs
H Fluid restriction H Mental status
H Calorie restriction, if indicated H Peripheral edema
H Low-fat diet, if indicated
H Walking program ALERT
H Activity, as tolerated
Auscultate for abnormal heart and breath sounds,
Medications and report changes immediately.
H Oxygen
H Diuretics, such as furosemide, bumetanide, torse- H Blood urea nitrogen and serum creatinine, potassi-
mide, and metolazone um, sodium, chloride, and magnesium levels
H Inotropic drugs, such as digoxin, dobutamine, and H Prothrombin time and INR
dopamine
H Vasodilators, such as nitrates, isosorbide, and nesiri-
tide Patient teaching
H Angiotensin converting enzyme inhibitors, such as
captopril, enalapril, and lisinopril Be sure to cover:
H Angiotensin receptor blockers, such as losartan, val- H the disorder, diagnosis, and treatment
sartan, and irbesartan H signs and symptoms of worsening heart failure
H Calcium channel blockers such as amiodipine H when to notify the physician
H Potassium supplements H the importance of follow-up care
H Beta-adrenergic blockers, such as atenolol, metopro- H the need to avoid high-sodium foods
lol, and carvedilol H the need to avoid fatigue
H Anticoagulants such as warfarin H instructions about fluid restrictions
H the need to weigh himself every morning, at the same
Surgery time, before eating, and after urinating; keeping a
H For valvular dysfunction with recurrent acute heart record of his weight, and reporting a weight gain of
failure, surgical replacement 3 to 5 lb (1.5 to 2.5 kg) in 1 week
H Heart transplantation H the importance of smoking cessation, if appropriate
H Ventricular assist device H weight reduction, as needed
H Stent placement H medication administration, dosage, possible adverse
effects, and monitoring needs.
Nursing considerations Discharge planning
H Encourage follow-up care.
Key outcomes H Refer the patient to a smoking-cessation program,
The patient will: if appropriate.
H maintain hemodynamic stability
H maintain adequate cardiac output
H carry out activities of daily living without excess
fatigue or decreased energy
H maintain adequate ventilation
H maintain adequate fluid balance.

Nursing interventions
H Place the patient in Fowlers position, and give sup-
plemental oxygen.
H Provide continuous cardiac monitoring during acute
and advanced stages.
H Assist the patient with range-of-motion exercises.
H Apply antiembolism stockings. Check for calf pain
and tenderness.
H Administer prescribed drugs.
H Provide emotional support.

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Common characteristics
Life-threatening disorder H Temperature in excess of 105.8 F (41 C)
H Tachycardia (greater than 130 beats/minute)

Heat syndrome H Widened pulse pressure

H Changes in level of consciousness (LOC)
H Tonic-dystonic contractions of the muscles
H Coma
Overview H Tachypnea
H Hypoxia
Description
H Heat exhaustion: acute heat injury with hyperthermia Complications
caused by dehydration H Hypovolemic shock
H Heat stroke: extreme hyperthermia with thermo- H Cardiogenic shock
regulatory failure H Cardiac arrhythmias
H Renal failure
Pathophysiology H Disseminated intravascular coagulation
H Normal regulation of temperature is by evaporation H Hepatic failure
(30% of bodys heat loss) or vasodilation. When heat
is generated or gained by the body faster than it can
dissipate, the thermoregulatory mechanism is Assessment
stressed and eventually fails.
H Hyperthermia accelerates. History
H Cerebral edema and cerebrovascular congestion oc- Heat exhaustion
cur. H Prolonged activity in a very warm or hot environment
H Cerebral perfusion pressure increases and cerebral H Muscle cramps
perfusion decreases. H Nausea and vomiting
H Tissue damage occurs when temperature exceeds H Thirst
107.6 F (42 C), resulting in tissue necrosis, organ H Weakness
dysfunction, and failure. H Headache
H Fatigue
Causes Heat stroke
H Illness H Exposure to high temperature and humidity without
H Heart disease air circulation
H Endocrine disorders H Same signs as heat exhaustion
H Neurologic disorder H Blurred vision
H Infection (fever) H Confusion
H Dehydration H Hallucinations
H Behavior H Decreased muscle coordination
H Excessive physical activity H Syncope
H Excessive clothing
H Lack of acclimatization Physical findings
H Hot environment without ventilation Heat exhaustion
H Inadequate fluid intake H Rectal temperature greater than 100 F (37.8 C)
H Drugs, such as phenothiazines, anticholinergics, and H Pale skin
amphetamines H Thready, rapid pulse
H Sudden discontinuation of Parkinsons disease med- H Cool, moist skin
ications H Decreased blood pressure
H Irritability
Risk factors H Syncope
H Obesity H Impaired judgment
H Sodium and water depletion H Hyperventilation
H Alcohol use Heat stroke
H Poor physical condition H Rectal temperature of at least 104 F (40 C)
H Age H Red, diaphoretic, hot skin in early stages
H Socioeconomic status H Gray, dry, hot skin in later stages
H Tachycardia
Incidence H Slightly elevated blood pressure in early stages
H Affects males and females equally H Decreased blood pressure in later stages
H Increased incidence among elderly patients and H Signs of central nervous system dysfunction
neonates during excessively hot summer days H Altered mental status
H Hyperpnea

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H Cheyne-Stokes respirations
H Anhydrosis (late sign) Patient teaching
Test results Be sure to cover:
Laboratory H the disorder, diagnosis, and treatment
H Abnormal serum electrolytes may show hyponatrem- H how to avoid reexposure to high temperatures
ia and hypokalemia. H the need to maintain adequate fluid intake
H Arterial blood gas levels may show respiratory alka- H limiting activity in hot weather
losis. H steps to prevent recurrence. (See Preventing heat
H Complete blood count may show leukocytosis and illness.)
thrombocytopenia.
H Coagulation studies may show increased bleeding Discharge planning
and clotting times. H Refer the patient to social services, if appropriate.
H Urinalysis may show concentrated urine and protein-
uria with tubular casts and myoglobinuria.
H Blood urea nitrogen level may be elevated.
H Serum calcium level may be decreased.
H Serum phosphorus level may be decreased.

Treatment
General
Heat exhaustion
H Cool environment
H Oral or I.V. fluid administration
Heat stroke
H Lowering the body temperature as rapidly as possible
H Evaporation, hypothermia blankets, and ice packs to
the groin, axillae, and neck
H Supportive respiratory and cardiovascular measures
H Increased hydration; cool liquids only
H Avoidance of caffeine and alcohol
H Rest periods, as needed

Nursing considerations Prevention

Preventing heat illness
Key outcomes
Heat illness can occur insidiously if precautions arent
The patient will:
taken. The patient should follow these guidelines:
H maintain adequate ventilation
H Drink plenty of fluids during outdoor activities, espe-
H maintain a normal body temperature cially on hot days. (Water and sports drinks are the
H prevent recurrent episodes of hyperthermia drinks of choice; avoid tea, coffee, soda, and alcohol
H express understanding of the need to maintain ade- because these can lead to dehydration. He should at-
quate fluid intake. tempt to take in more than hes losing.)
H Take frequent breaks for drinks and to mist himself
Nursing interventions with a spray bottle of water to help with cooling.
H Perform rapid cooling procedures. H Wear lightweight, tightly woven, loose-fitting clothing
H Provide supportive measures. in light colors.
H Provide adequate fluid intake. H Schedule vigorous activity and sports for cooler times
H Administer prescribed drugs. of the day.
H Protect himself from direct sun exposure by wearing a
Monitoring hat, sunglasses, and using an umbrella.
H Gradually increase time spent outdoors to get his body
H Vital signs acclimated to the heat.
H Pulse oximetry readings H Try to spend as much time as possible in a cooled or
H Complications air conditioned environment on very hot and humid
H LOC days.
H Cardiac rhythm H Discuss chronic conditions with his practitioner for
H Intake and output disease specific precautions.
H Myoglobin test results

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Hemophilia H Pain and swelling in a weight-bearing joint, such as

the hip, knee, or ankle
H With mild hemophilia or after minor trauma, lack of
spontaneous bleeding, but prolonged bleeding with
Overview major trauma or surgery
H Moderate hemophilia producing only occasional
Description spontaneous bleeding episodes
H Hereditary bleeding disorder H Severe hemophilia causing spontaneous bleeding
H Characterized by greatly prolonged coagulation time H Prolonged bleeding after surgery or trauma or joint
H Results from deficiency of specific clotting factors pain in spontaneous bleeding into muscles or joints
H Hemophilia A (classic hemophilia): affects more H Signs of internal bleeding, such as abdominal, chest,
than 80% of hemophiliacs; results from factor VIII or flank pain; episodes of hematuria or hematemesis;
deficiency and tarry stools
H Hemophilia B (Christmas disease): affects 15% of H Activity or movement limitations and need for assis-
hemophiliacs; results from factor IX deficiency tive devices, such as splints, canes, or crutches
H Incurable
Physical findings
Pathophysiology H Hematomas on extremities, torso, or both
H Low level or absence of the blood protein necessary H Joint swelling in episodes of bleeding into joints
for clotting causes disruption of normal intrinsic co- H Limited and painful joint range of motion in episodes
agulation cascade. of bleeding into joints
H Abnormal bleeding, which may be mild, moderate,
or severe, depending on the degree of protein factor Test results
deficiency, occurs. Laboratory
H A platelet plug forms at the bleeding site, but the lack HEMOPHILIA A
of clotting factors impairs formation of a stable fibrin H Factor VIII assay is 0% to 25% of normal.
clot. H Partial thromboplastin time (PTT) is prolonged.
H Immediate hemorrhage isnt prevalent; delayed H Platelet count and function, bleeding time, and pro-
bleeding is common. thrombin time are normal.
HEMOPHILIA B
Causes H Factor IX assay is deficient.
H Hemophilia A and B usually inherited as X-linked H Baseline coagulation results are similar to those of
recessive traits hemophilia A, with normal factor VIII.
H Spontaneous mutation HEMOPHILIA A OR B
H Acquired immunologic process H Degree of factor deficiency defines severity:
Mild hemophilia factor levels are 5% to 25% of
Incidence normal.
H Most common X-linked genetic disease Moderate hemophilia factor levels are 1% to
H Occurs in about 400 live male births in the United 5% of normal.
States each year; rare in females Severe hemophilia factor levels are less than
1% of normal.
Common characteristics
H Abnormal tendency to bleed
H Painful and swollen joints Treatment
Complications General
H Pain, swelling, extreme tenderness, and permanent H Correct treatment to quickly stop bleeding by in-
joint and muscle deformity creasing plasma levels of deficient clotting factors
H Peripheral neuropathies, pain, paresthesia, and mus- H Diet consisting of foods high in vitamin K
cle atrophy H Activity guided by degree of factor deficiency
H Ischemia and gangrene
H Shock and death Medications
H Aminocaproic acid
Hemophilia A
Assessment H Cryoprecipitated antihemophilic factor (AHF),
lyophilized AHF, or both
History H Desmopressin
H Familial history of bleeding disorders Hemophilia B
H Prolonged bleeding with circumcision H Factor IX concentrate
H Concomitant illness

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H the need to notify the physician immediately after

Nursing considerations
Key outcomes
The patient will:
H maintain hemodynamic stability
H have peripheral pulses that remain palpable and
strong
H express feelings of increased comfort and decreased
pain
H maintain range of motion (ROM) and joint mobility
H demonstrate adequate coping skills
H verbalize understanding of disease process and treat-
ment regimen.
Nursing interventions
H Follow standard precautions.
H Provide emotional support and reassurance when in-
dicated.
During bleeding episodes
H Apply pressure to bleeding sites.
H Administer the deficient clotting factor or plasma, as
ordered, until bleeding stops.
H Apply cold compresses or ice bags, and elevate the
injured part.
H To prevent recurrence of bleeding, restrict activity for
48 hours after bleeding is under control.
H Control pain with prescribed analgesics.
H Avoid I.M. injections.
H Avoid aspirin and aspirin-containing drugs.
During bleeding into a joint
H Immediately elevate the joint.
H To restore joint mobility, begin ROM exercises at
least 48 hours after the bleeding is controlled.
H Restrict weight bearing until bleeding stops and
swelling subsides.
H Administer prescribed analgesics.
H Apply ice packs and elastic bandages to alleviate
pain.
Monitoring
H PTT
H Adverse reactions to blood products
H Signs and symptoms of decreased tissue perfusion
H Vital signs
H Bleeding from the skin, mucous membranes, and
wounds
even a minor injury
H the need for parents to watch for signs of internal
bleeding
H the importance of avoiding aspirin, combination
medications that contain aspirin, and over-the-
counter anti-inflammatory agents (use acetamino-
phen instead)
H the importance of good dental care and the need to
check with the physician before dental extractions or
surgery
H the need to wear medical identification jewelry at all
times
H how to administer blood factor components at home,
if appropriate
H the need to keep blood factor concentrate and infu-
sion equipment available at all times
H adverse reactions that can result from replacement
factor procedures
H signs, symptoms, and treatment of anaphylaxis
H the need for the patient or parents to watch for early
signs of hepatitis
H the need to follow standard precautions.
Discharge planning
H Refer new patients to a hemophilia treatment center
for evaluation.
H For more information, refer the patients family to the
National Hemophilia Foundation.

Patient teaching
Be sure to cover:
H the benefits of regular isometric exercises
H how parents can protect their child from injury while
avoiding unnecessary restrictions that impair normal
development
H the need to avoid contact sports
H if an injury occurs, directions for parents to apply
cold compresses or ice bags and to elevate the in-
jured part or apply light pressure to bleeding

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Hemorrhoids H Pregnancy
H Obesity

Incidence
Overview H Occur in both sexes
H Most cases occurring in people ages 20 to 50
Description
H Varicosities found in the superior or inferior hemor- Common characteristics
rhoidal venous plexus H Painless, intermittent bleeding during defecation
H Classified as first, second, third, or fourth degree,
depending on their severity Complications
H First-degree hemorrhoids: confined to the anal canal H Constipation
H Second-degree hemorrhoids: prolapse during strain- H Local infection
ing but reduce spontaneously H Thrombosis of hemorrhoids
H Third-degree hemorrhoids: prolapsed hemorrhoids H Secondary anemia from severe or recurrent bleeding
requiring manual reduction after each bowel move-
ment
H Fourth-degree hemorrhoids: irreducible Assessment
Pathophysiology History
H Dilation and enlargement of the superior plexus of H Bright red blood on stool or toilet tissue
the superior hemorrhoidal veins above the dentate H Anal itching
line cause internal hemorrhoids. H Vague feeling of anal discomfort
H Enlargement of the plexus of the inferior hemor- H Pain
rhoidal veins below the dentate line causes external
hemorrhoids, which may protrude from the rectum. Physical findings
(See Comparing types of hemorrhoids.) H Prolapse of rectal mucosa
H Anal tenderness on palpation
Causes H Internal hemorrhoids (with digital examination)
H Prolonged sitting
H Straining at defecation
H Constipation, low-fiber diet

Comparing types of hemorrhoids

Covered by mucosa, internal hemorrhoids bulge into the rectal lumen and may prolapse during defecation. Covered by skin,
external hemorrhoids protrude from the rectum and are more likely to thrombose than internal hemorrhoids. The illustra-
tions below show both frontal and cross-sectional views.
INTERNAL HEMORRHOIDS EXTERNAL HEMORRHOIDS

348 Hemorrhoids
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Test results
Diagnostic procedures
H Anoscopy and flexible sigmoidoscopy visualize inter-
nal hemorrhoids.

Treatment
General
H High-fiber diet, increased fluid intake
H Avoidance of prolonged sitting
H Warm sitz baths to relieve pain

Medications
H Local anesthetic agents
H Hydrocortisone cream and suppositories

Surgery
H Injection sclerotherapy or rubber band ligation
H Hemorrhoidectomy by cauterization or excision

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort
H have reduced occurrence of hemorrhoids
H express understanding of the disorder and treatment
regimen.
Nursing interventions
H Administer enemas preoperatively.
H Administer prescribed drugs.
H Keep the wound site clean.
H Provide sitz baths.

Monitoring
H Bleeding
H Pain

Patient teaching
Be sure to cover:
H avoiding stool softeners after surgery
H the importance of regular bowel habits and good
anal hygiene
H avoiding too-vigorous wiping with washcloths and
use of harsh soaps
H the use of medicated astringent pads and white, un-
scented toilet paper.

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Hemothorax H Anxiety
H Cyanosis
H Stupor
H Affected side may expand and stiffen
Overview H Unaffected side may rise with gasping respirations
H Dullness over affected side
Description H Decreased or absent breath sounds over affected side
H Blood in the pleural cavity H Symptoms associated with blunt trauma
H May result in lung collapse H Tachycardia
H Hypotension
Pathophysiology
H Damaged intercostal, pleural, mediastinal, and some- Test results
times lung parenchymal vessels cause blood to enter Laboratory
the pleural cavity. H Pleural fluid analysis shows hematocrit greater than
H The amount of bleeding and the cause is associated 50% of serum hematocrit.
with varying degrees of lung collapse and mediastinal H Arterial blood gas (ABG) analysis may show in-
shift. creased partial pressure of carbon dioxide and
decreased partial pressure of oxygen.
Causes H Serum hemoglobin level may be decreased, depend-
H Blunt or penetrating chest trauma ing on blood loss.
H Pulmonary infarction Imaging
H Necrotizing infections H Chest X-rays and computed tomography scan of the
H Pulmonary arteriovenous fistulas thorax show the presence and extent of hemothorax
H Hereditary hemorrhagic telangiectasis and help to evaluate treatment.
H Heart or thorax surgery Diagnostic procedures
H Neoplasm H Thoracentesis may yield blood or serosanguineous
H Dissecting thoracic aneurysm fluid.
H Anticoagulant therapy
H Thoracic endometriosis
H Central venous catheter insertion Treatment
H Tuberculosis
General
Incidence H Stabilization of the patients clinical condition
H Occurs in about 30% of patients with chest trauma H Stoppage of bleeding
H Thoracentesis
Common characteristics H Insertion of chest tube
H Chest pain H Blood transfusion, or autotransfusion if blood loss
H Sudden shortness of breath approaches or exceeds 1 L (see Using autotransfu-
sion for chest wounds)
Complications H Diet, as tolerated
H Mediastinal shift H I.V. therapy
H Ventilatory compromise H Activity, as tolerated
H Lung collapse
H Cardiopulmonary arrest Medications
H Pneumothorax H Oxygen
H Empyema H Analgesics

Surgery
Assessment H Thoracotomy if chest tube doesnt improve condition

History
H Recent trauma Nursing considerations
H Recent thoracic surgery
H Metastatic disease Key outcomes
The patient will:
Physical findings H maintain adequate ventilation
H Tachypnea H maintain fluid volume balance
H Dusky skin color H express feelings of increased comfort and decreased
H Diaphoresis pain
H Hemoptysis H verbalize understanding of the illness.
H Restlessness

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Using autotransfusion for chest wounds

Autotransfusion is used most commonly in patients with
chest wounds, especially those that involve hemothorax.
Through autotransfusion, a patients own blood is collected,
filtered, and reinfused. The procedure may also be used
when two or three units of pooled blood can be recovered,
such as in cardiac or orthopedic surgery.
Autotransfusion eliminates the patients risk of transfusion
reaction or blood-borne disease, such as cytomegalovirus,
hepatitis, and human immunodeficiency virus. Its contra-
indicated in patients with sepsis or cancer.
How autotransfusion works
A large-bore chest tube connected to a closed drainage sys-
tem is used to collect the patients blood from a wound or
chest cavity. This blood passes through a filter, which
catches most potential thrombi, including clumps of fibrin
and damaged red blood cells (RBCs). The filtered blood
passes into a collection bag. From the bag, the blood is rein-
fused immediately, or it may be processed in a commercial
cell washer that reduces anticoagulated whole blood to
washed RBCs for later infusion.
Assisting with autotransfusion
Set up the blood collection system as you would any closed
chest drainage system. Attach the collection bag according
to the manufacturers instructions.
If ordered, inject an anticoagulant, such as heparin or
acid-citrate-dextrose solution, into the self-sealing port on
the connector of the patients drainage tubing.
During reinfusion, monitor the patient for complications,
such as blood clotting, hemolysis, coagulopathies, thrombo-
cytopenia, particulate and air emboli, sepsis, and citrate toxi-
city (from the acid-citrate-dextrose solution).

Drainage tube From patient

To suction

Locking connectors to
collection bag

Self-sealing
ports

Microfilter

Water-seal chamber

Autotransfusion
collection bag

Nursing interventions Patient teaching

H Administer prescribed drugs.
H Promote comfort and relaxation. Be sure to cover:
H Administer prescribed oxygen. H the disorder, diagnosis, and treatment
H Administer prescribed I.V. fluids and blood transfu- H prescribed drugs and possible adverse effects
sions. H when to notify the physician
H Assist with thoracentesis. H preoperative and postoperative care, if needed
H Prepare the patient for surgery, if needed. H mechanical ventilation, if needed
H Change the chest tube dressing, and provide chest H deep-breathing exercises
tube care, as needed. H smoking cessation, if appropriate.

Monitoring
H Vital signs
H Intake and output
H Chest tube drainage
H Central venous pressure
H ABG results
H Chest X-ray results
H Complete blood count results
H Respiratory status
H Complications
H Signs and symptoms of infection

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Common characteristics
Life-threatening disorder H Changes in mental status and personality
H Jaundice

Hepatic encephalopathy H Muscle tremors

H Fruity breath odor

Complications
Overview H Irreversible coma
H Death
Description
H A neurologic syndrome that develops as a complica-
tion of aggressive fulminant hepatitis or chronic he- Assessment
patic disease
H Most common in patients with cirrhosis History
H In advanced stages, prognosis extremely poor despite Prodromal stage
vigorous treatment H Slight personality changes, such as agitation, belliger-
H Acute form occurring with acute fulminant hepatic ence, disorientation, and forgetfulness
failure; possibly fatal H Difficulty concentrating or thinking clearly
H Chronic form occurring with chronic liver disease; H Fatigue
usually reversible H Mental changes, such as confusion and disorienta-
H Also called hepatic coma tion
H Sleep-wake reversal
Pathophysiology Impending stage
H Normally, the ammonia produced by protein break- H Mental changes, such as confusion and disorienta-
down in the bowel is metabolized to urea in the liver. tion
When portal blood shunts past the liver, ammonia di- Stuporous stage
rectly enters the systemic circulation and is carried H Marked mental confusion
to the brain. Comatose stage
H Such shunting may result from the collateral venous H Unable to arouse
circulation that develops in portal hypertension or
from surgically created portal-systemic shunts. Physical findings
H Cirrhosis further compounds this problem because Prodromal stage
impaired hepatocellular function prevents conver- H Slurred or slowed speech
sion of ammonia that reaches the liver. H Slight tremor
Impending stage
Causes H Tremors that have progressed to asterixis
H Ammonia intoxication of the brain H Lethargy
H Exact cause unknown H Aberrant behavior
H Apraxia
Risk factors H Possible incontinence
H Excessive protein intake Stuporous stage
H Sepsis H Drowsy and stuporous
H Excessive accumulation of nitrogenous body wastes H Noisy and abusive when aroused
(from constipation or GI hemorrhage) H Hyperventilation
H Bacterial action on protein and urea to form ammo- H Muscle twitching
nia H Asterixis
H Hepatitis Comatose stage
H Diuretic therapy H Obtunded
H Alcoholism H Seizures
H Fluid and electrolyte imbalance (especially metabolic H Hyperactive reflexes
alkalosis) H Positive Babinskis sign
H Hypoxia H Fetor hepaticus (musty, sweet breath odor)
H Azotemia
H Impaired glucose metabolism Test results
H Infection Laboratory
H Use of sedatives, opioids, and general anesthetics H Serum ammonia levels are elevated and, together
with characteristic clinical features, strongly suggest
Incidence hepatic encephalopathy.
H Occurs in about 4 of 100,000 people H Serum bilirubin level is elevated and prothrombin
H Observed in 70% of patients with cirrhosis time is prolonged.

352 Hepatic encephalopathy

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Diagnostic procedures
H EEG shows slowing waves as the disease progresses. Patient teaching
Be sure to cover:
Treatment H the disorder, diagnosis, and treatment
H signs of complications or worsening symptoms
General H dietary modifications
H Elimination of underlying cause H medication administration, dosage, and possible ad-
H I.V. fluid administration verse effects.
H Control of GI bleeding
H Life-support measures, if appropriate Discharge planning
H Bowel cleansing H Refer the patient to social services, as indicated.
H Limited protein intake
H Nothing by mouth with decreased responsiveness
H Parenteral or enteric feedings, if appropriate
H Bed rest until condition improves
H No alcohol use

Medications
H Lactulose
H Neomycin
H Potassium supplements
H Salt-poor albumin
H Sorbitol-induced catharsis

Surgery
H Possible liver transplant

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort
H maintain orientation to environment
H maintain stable vital signs
H maintain normal fluid volume
H maintain skin integrity.

Nursing interventions
H Promote rest, comfort, and a quiet atmosphere.
H Administer prescribed drugs.
H Use appropriate safety measures to protect the pa-
tient from injury.
H Maintain skin integrity.
H Perform passive range-of-motion exercises.
H Provide emotional support.

Monitoring
H Level of consciousness and neurologic status
H Intake and output
H Fluid and electrolyte balance
H Weight and abdominal girth
H Signs of anemia, alkalosis, GI bleeding, and infection
H Serum ammonia level

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Hepatitis, nonviral arthralgias, lymphadenopathy, and epigastric or

right upper quadrant pain.

Overview Complications
H Fulminant hepatic failure
Description H Renal failure
H Inflammation of the liver H Liver fibrosis
H Classified as toxic or drug-induced (idiosyncratic) H Cirrhosis

Pathophysiology
H Hepatocellular damage and necrosis are usually Assessment
caused by toxins and is dose-dependent.
H Nonvrial hepatitis occurs primarily in connection History
with acetaminophen overdose. H Exposure to causative agent
H Anorexia
Causes H Nausea
H Acetaminophen overdose H Vomiting
H Alcohol overuse H Possibly abdominal pain
H Aspirin and nonsteroidal anti-inflammatory drugs H Pruritus
H Direct hepatotoxicity
H Lack of bile excretion Physical findings
H Possibly direct hepatotoxicity from hormonal contra- H Jaundice
ceptives or anabolic steroids H Dark-colored urine
H Hypersensitivity to phenothiazine derivatives such as H Hepatomegaly
chlorpromazine H Clay-colored stools
H Statin drugs
H Inhaled anesthetics such as halothane Test results
H Antifungal medications, such as ketoconazole and Laboratory
amphotericin B H Serum aspartate aminotransferase and alanine
H Herbal supplements, such as cascava, kava, and aminotransferase levels are elevated.
ma-huang H Total and direct bilirubin (with cholestasis) levels
H Industrial chemicals such as for cleaning use or are elevated.
herbicidals H Alkaline phosphatase level is elevated.
H Antibiotics H White blood cell count is elevated.
H Thyroid medications H Eosinophil count is elevated (possible in the drug-
H Antidiabetic drugs induced type).
H Cytotoxic drugs Diagnostic procedures
H Cholestatic reactions H Liver biopsy may help identify the underlying path-
H Metabolic and autoimmune disorders ology.
H Infectious agents

Incidence Treatment
H Can affect males and females (autoimmune affects
females more commonly) General
H Can occur at any age H Removal of causative agent by lavage, catharsis, or
hyperventilation, depending on the route of exposure
Common characteristics H Nutritious diet and adequate fluid intake
H Clinical features of toxic and drug-induced hepatitis H Activity, as tolerated
vary with the severity of liver damage and the causa-
tive agent Medications
H Symptoms resemble those of viral hepatitis H Acetylcysteine (acetaminophen poisoning)
H Corticosteroids (drug-induced hepatitis)
ALERT
Carbon tetrachloride poisoning also produces Nursing considerations
headache, dizziness, drowsiness, and vasomotor
collapse; halothane-related hepatitis produces Key outcomes
fever, moderate leukocytosis, and eosinophilia; The patient will:
chlorpromazine produces a rash, abrupt fever, H demonstrate an understanding of the disorder and
treatment regimen

354 Hepatitis, nonviral

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H remain free from complications

H express feelings of increased comfort.

Nursing interventions
H Administer prescribed drugs.
H Provide emotional support.

Monitoring
H Response to treatment
H Laboratory values
H Vital signs
H Complications

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medication administration, dosage, and possible ad-
verse effects
H proper handling of cleaning agents and solvents.

Discharge planning
H Encourage follow-up care.

Hepatitis, nonviral 355

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Common characteristics
Hepatitis, viral H Malaise, fatigue
H Dark-colored urine, clay-colored stools
H Abdominal tenderness
Overview H Fever
H Jaundice
Description H Nausea; loss of appetite
H Infection and inflammation of the liver caused by a
virus Complications
H Six types recognized (A, B, C, D, E, and G), and a H Life-threatening fulminant hepatitis
seventh suspected H Chronic active hepatitis (in hepatitis B)
H Marked by hepatic cell destruction, necrosis, and au- H Syndrome resembling serum sickness, characterized
tolysis, leading to anorexia, jaundice, and hepato- by arthralgia or arthritis, rash, and angioedema; can
megaly lead to misdiagnosis of hepatitis B as rheumatoid
H In most patients, hepatic cells eventually regenerate arthritis or lupus erythematosus
with little or no residual damage, allowing recovery H Primary liver cancer (in hepatitis B or C)
H Complications more likely with old age and serious H In hepatitis D, mild or asymptomatic form of hepati-
underlying disorders tis B that flares into severe, progressive chronic ac-
H Prognosis poor if edema and hepatic encephalopathy tive hepatitis and cirrhosis
develop
Pathophysiology Assessment
H Hepatic inflammation caused by virus leads to diffuse
injury and necrosis of hepatocytes. History
H Hypertrophy and hyperplasia of Kupffer cells and H 50% to 60% of people with hepatitis B have no signs
sinusoidal lining cells occurs. or symptoms
H Bile obstruction may occur. H 80% of people with hepatitis C have no signs or
symptoms
Causes H Revelation of a source of transmission
H Infection with the causative viruses for each of six Prodromal stage
major forms of viral hepatitis H Patient easily fatigued, with generalized malaise
Type A H Anorexia, mild weight loss
H Transmittal by the fecal-oral or parenteral route H Depression
H Ingestion of contaminated food, milk, or water H Headache, photophobia
Type B H Weakness
H Transmittal by contact with contaminated human H Arthralgia, myalgia (hepatitis B)
blood, secretions, and stool H Nausea or vomiting
Type C H Changes in the senses of taste and smell
H Transmittal primarily by sharing of needles by I.V. Clinical jaundice stage
drug users, through blood transfusions, or tattoo H Pruritus
needles H Abdominal pain or tenderness
Type D H Indigestion
H Found only in patients with an acute or a chronic H Anorexia
episode of hepatitis B H Possible jaundice of sclerae, mucous membranes,
Type E and skin
H Transmittal by parenteral route and commonly water- Posticteric stage
borne H Most symptoms decreasing or subsided
Type G
H Thought to be blood-borne, with transmission simi- Physical findings
lar to that of hepatitis B and C Prodromal stage
H Fever (100 to 102 F [37.8 to 38.9 C])
Incidence H Dark-colored urine
Hepatitis A H Clay-colored stools
H Approximately 4 new cases per 100,000 annually Clinical jaundice stage
H May occur as an epidemic outbreak H Rashes, erythematous patches, or hives
Hepatitis B H Abdominal tenderness in the right upper quadrant
H Estimated 1.25 million chronically infected Americans H Enlarged and tender liver
H Highest rate of disease occurs in people ages 20 H Splenomegaly
to 49 H Cervical adenopathy
Hepatitis C Posticteric stage
H Estimated 3.9 million chronically infected Americans H Decrease in liver enlargement

356 Hepatitis, viral

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Test results Medications

Laboratory
H In suspected viral hepatitis, hepatitis profile routinely
performed; results identify antibodies specific to the
causative virus and establishing the type of hepatitis:
Type A detection of an antibody to hepatitis A
confirms the diagnosis.
Type B presence of hepatitis B surface antigens
and hepatitis B antibodies confirm the diagnosis.
Type C diagnosis depends on serologic testing
for the specific antibody 1 or more months after
the onset of acute illness; until then, diagnosis is
principally established by obtaining negative test
results for hepatitis A, B, and D.
Type D detection of intrahepatic delta antigens
or immunoglobulin (Ig) M antidelta antigens in
acute disease (or IgM and IgG in chronic disease)
establishes the diagnosis.
Type E detection of hepatitis E antigens sup-
ports the diagnosis; however, diagnosis may also
rule out hepatitis C.
Type G detection of hepatitis G ribonucleic acid
supports the diagnosis.
H Additional findings from liver function studies sup-
port the diagnosis:
Serum aspartate aminotransferase and serum ala-
nine aminotransferase levels are increased in the
prodromal stage of acute viral hepatitis.
Serum alkaline phosphatase levels are slightly in-
creased.
Serum bilirubin levels are elevated; levels may re-
main elevated late in the disease, especially with
severe disease.
Prothrombin time (PT) is prolonged. (PT more
than 3 seconds longer than normal, indicates
severe liver damage.)
White blood cell counts commonly reveal transient
neutropenia and lymphopenia followed by lymph-
ocytosis.
Diagnostic procedures
H Liver biopsy shows chronic hepatitis.
Treatment
General
For hepatitis A
H Supportive care
For hepatitis B
H Supportive care
For hepatitis C
H Aimed at clearing hepatitis C from the body, stopping
or slowing of hepatic damage, and symptom relief
H Symptomatic
H Small, high-calorie, high-protein meals (reduced
protein intake if signs of precoma lethargy, confu-
sion, mental changes develop)
H Parenteral feeding, if appropriate
H Alcohol cessation
H Frequent rest periods, as needed
H Avoidance of contact sports and strenuous activity
H Standard immunoglobulin
H Vaccine (hepatitis A and B)
H Alfa-2b interferon (hepatitis B, C, and D)
H Antiemetics such as prochlorperazine
H Cholestyramine
H Lamivudine (hepatitis B)
H Ribavirin (hepatitis C)
Surgery
H Possible liver transplant (hepatitis C)
Nursing considerations
Key outcomes
The patient will:
H develop no complications
H maintain stable vital signs
H perform activities of daily living within the confines
of the disease process
H express understanding of the disorder and treatment
regimen.
Nursing interventions
H Observe standard precautions to prevent transmis-
sion of the disease.
H Provide rest periods throughout the day.
H Administer prescribed drugs.
H Encourage oral fluid intake.
Monitoring
H Hydration and nutritional status
H Daily weight
H Intake and output
H Stool for color, consistency, amount, and frequency
H Signs of complications
Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H measures to prevent the spread of disease
H the importance of rest and a proper diet
H the need to abstain from alcohol
H medication administration, dosage, and possible ad-
verse effects
H the need to avoid over-the-counter medications un-
less approved by the physician
H the need for follow-up care.
Discharge planning
H Refer the patient to Alcoholics Anonymous, if indi-
cated.
H Refer the patient to social services as needed.

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ecchymoses, and spider hemangiomas of varying size

Life-threatening disorder (see Typical lesions of hereditary hemorrhagic
telangiectasia)
Hereditary hemorrhagic H Clubbing of the digits

telangiectasia
Overview
Description
H Inherited vascular disorder of the blood vessels that
can cause excessive bleeding
H Also called Osler-Weber-Rendu disease
Pathophysiology
H Venules and capillaries dilate to form fragile masses
of thin convoluted vessels (telangiectases), resulting
in an abnormal tendency to hemorrhage.
Causes
H Transmitted by autosomal dominant inheritance
Incidence
H Affects both sexes but may cause less severe bleeding
in females
H Occurs in 5,000 to 10,000 people
Test results
Laboratory
H Platelet count may be abnormal.
H Complete blood count and anemia panel may show
hypochromic, microcytic anemia
H Arterial blood gas analysis shows hypoxia.
Imaging
H Chest X-rays may show lesions in the lungs.
H Echocardiography may show high-output cardiac
failure.
Typical lesions of hereditary
hemorrhagic telangiectasia
The illustrations below show the commonly encountered
lesions of hereditary hemorrhagic telangiectasia.
Dilated capillaries, either flat or raised, appear in local-
ized aggregations, as on the fingers.

Common characteristics
H Recurrent epistaxis
H Telangiectases

Complications
H Secondary iron deficiency anemia
H Vascular malformation causing pulmonary arteriove-
nous (AV) fistulas (rare)
H Recurring cerebral embolism and brain abscess
H Hemorrhagic shock
H Intracranial hemorrhage

On the face, spider hemangiomas reflect capillary

Assessment fragility.

History
H Established familial pattern of bleeding disorders
H Epistaxis, hemoptysis, or tarry stools
H Appearance of telangiectasia during late childhood
or adolescence
Physical findings
H Localized aggregations of dilated capillaries on the
skin of the face, ears, tongue, lips, conjunctivae,
scalp, hands, arms, and feet and under the nails
H Characteristic telangiectases: violet, bleed sponta-
neously, flat or raised, blanch on pressure, and non-
pulsatile
H Signs of capillary fragility (may exist without overt
telangiectasia): spontaneous bleeding, petechiae,

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H Endoscopy may show bleeding tendency and may

rule out other disorders.
Diagnostic procedures
H Bone marrow aspiration shows depleted iron stores
and confirms secondary iron deficiency anemia.
H Genetic testing confirms the disorder in most cases.
Treatment
General
H Supportive therapy, including blood transfusions and
supplemental iron administration
H Ancillary treatment consisting of applying pressure
and topical hemostatic agents to bleeding sites, cau-
terizing bleeding sites not readily accessible, and
protecting the patient from trauma and unnecessary
bleeding
H Avoidance of activities with the potential for trauma
H Air humidification to keep mucuous membranes
moist
Medications
H Parenteral iron
H Antipyretics or antihistamines
H Laser treatment to destroy vessel
Patient teaching
Be sure to cover:
H the disorder, signs and symptoms, and treatment
H iron supplements, including the importance of fol-
lowing dosage instructions and of taking oral iron
with meals to minimize GI irritation
H a warning that iron turns stools dark green or black
and may cause constipation
H the management of constipation
H the management of minor bleeding episodes, espe-
cially recurrent epistaxis
H how to recognize major bleeding episodes that re-
quire emergency intervention.
Discharge planning
H Refer the patient for genetic counseling, as appro-
priate.

Other
H Embolization
H Endoscopic procedures to address GI bleeding

Nursing considerations
Key outcomes
The patient will:
H maintain hemodynamic stability
H have laboratory values that return to normal
H demonstrate positive signs of coping
H exhibit no signs or symptoms of infection.

Nursing interventions
H Provide emotional and psychological support.
H Administer prescribed blood transfusions.
H Encourage fluid intake if the patient is bleeding or
hypovolemic.
H Provide meticulous skin care and hygiene.
H Use aseptic technique when caring for the patient.

Monitoring
H Vital signs
H Intake and output
H Signs of febrile or allergic transfusion reaction
H Indications of GI bleeding
H Laboratory values to detect possible renal, hepatic,
or respiratory failure

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Hernia, hiatal

Esophageal ulceration and perforation
Hemorrhage
Peritonitis
Mediastinitis
Overview Aspiration
Strangulation and gangrene of herniated portion of
Description stomach
H Defect in the diaphragm that permits a portion of the H Iron deficiency anemia
stomach to pass through the diaphragmatic opening H Chronic cough
into the chest H Dysphagia
H Three types: sliding hernia, paraesophageal (rolling)
hernia, and mixed hernia (sliding and rolling her-
nia) Assessment
Pathophysiology History
Sliding hernia H Heartburn 1 to 4 hours after eating; aggravated by re-
H The muscular collar around the esophageal and di- clining, belching, or conditions that increase intra-
aphragmatic junction loosens. abdominal pressure
H Increased intra-abdominal pressure causes the lower H Regurgitation or vomiting
portion of the esophagus and the upper portion of H Retrosternal or substernal chest pain (typically after
the stomach to rise into the chest. meals or at bedtime)
Paraesophageal hernia H Feeling of fullness after eating
H The stomach isnt properly anchored below the di- H Feeling of breathlessness or suffocation
aphragm. H Chest pain resembling angina pectoris
H Increased intra-abdominal pressure causes the up- H Reflux
per portion of the stomach to slide through the H Chronic cough
esophageal hiatus. H Belching

Causes Physical findings

Sliding hernia H Possibly none
H Normal aging H Dysphagia
H Secondary to esophageal carcinoma, kyphoscoliosis,
trauma, or surgery Test results
H Diaphragmatic malformations that can cause congen- Laboratory
ital weakness H Serum hemoglobin level and hematocrit are de-
H Chronic esophagitis creased in patients with paraesophageal hernia, if
Paraesophageal hernia bleeding from esophageal ulceration is present.
H Not fully understood H Fecal occult blood test may be positive.
H Analysis of gastric contents may reveal blood.
Risk factors Imaging
H Obesity H Chest X-rays reveal an air shadow behind the heart in
H Smoking a large hernia; lower lobe infiltrates with aspiration.
H Pregnancy H Barium swallow with fluoroscopy detects a hiatal
H Presence of ascites hernia and diaphragmatic abnormalities.
Diagnostic procedures
Incidence H Endoscopy and biopsy results identify the mucosal
H Sliding hernia 3 to 10 times more common than junction and the edge of the diaphragm indenting the
paraesophageal and mixed hernias combined esophagus; differentiate hiatal hernia, varices, ero-
H Increases with age sions, ulcers, Barretts esophagus, and other small
H 60% of people have hiatal hernias by age 60 gastroesophageal lesions; and rule out malignant tu-
H Higher prevalence in females than in males mors.
H Esophageal motility studies reveal esophageal motor
Common characteristics or lower esophageal pressure abnormalities before
H May produce no symptoms surgical repair of the hernia.
H Heartburn H pH studies identify reflux of gastric contents.
H Acid perfusion (Bernstein) test identifies esophageal
Complications reflux.
H Esophageal stricture
H Incarceration (with paraesophageal hernia)
H In association with gastroesophageal reflux disease:
Esophagitis

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Treatment Patient teaching

General Be sure to cover:
H Smoking cessation (smoking stimulates gastric acid H the disorder, diagnosis, and treatment
production) H the development of a dietary plan
H Six small meals per day H the need to sit upright after meals and snacks
H No fluids or food 1 to 2 hours before bedtime H situations or activities that increase intra-abdominal
H Elimination of spicy or irritating foods, alcohol, and pressure
coffee H desired drug actions and potential adverse effects
H Weight reduction, as appropriate H the need to sleep with the head of the bed elevated
H Upright posture for 2 to 3 hours after eating about 6 (15 cm).
H Restriction of activities that increase intra-abdominal
pressure Discharge planning
H Refer the patient to a smoking-cessation program, if
Medications appropriate.
H Antacids, such as aluminum hydroxide and calcium H Refer the patient to a weight-reduction program, if
carbonate appropriate.
H Histamine-2 receptor antagonists, such as cimeti-
dine, famotidine, and ranitidine
H Anticholinergic agents, such as glycopyrrolate and
hyoscyamine
H Motility agent, such as metoclopramide and
urecholine
H Antiemetics such as prochlorperazine
H Cough suppressants, such as benzonatate and dex-
tromethorphan
H Proton pump inhibitors, such as omeprazole, lanso-
prazole, and rabeprazole
Surgery
H Hernia repair (rare)

Nursing considerations
Key outcomes
The patient will:
H avoid or have minimal complications
H show no evidence of aspiration
H maintain a patent airway
H express feelings of increased comfort
H express understanding of the disorder and treatment
regimen.
Nursing interventions
H Prepare the patient for diagnostic tests.
H Teach positional therapy.
H If surgery is necessary, provide appropriate preoper-
ative and postoperative care.
Monitoring
ALERT
After endoscopy, watch for signs of perforation, in-
cluding decreasing blood pressure, rapid pulse,
shock, and sudden pain.

H Patient response to prescribed antacids and other

drugs

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Herniated H Paresthesia
H Motor weakness

intervertebral disk H Peripheral neuropathy

Overview
Description
H Rupture of fibrocartilaginous material that surrounds
the intervertebral disk, allowing protrusion of the nu-
cleus pulposus
H Results in pressure on spinal nerve roots or spinal
cord that causes back pain and other symptoms of
nerve root irritation
H Most common site for herniation is L4-L5 disk space;
other sites include L5-S1, L2-L3, L3-L4, C6-C7, and
C5-C6
H Clinical manifestations determined by:
Location and size of the herniation into the spinal
canal
Amount of space that exists inside the spinal canal
H Also known as herniated nucleus pulposus, slipped
disk, or ruptured disk
Pathophysiology
H The ligament and posterior capsule of the disk are
usually torn, allowing the nucleus pulposus to ex-
trude, compressing the nerve root.
H Occasionally, the injury tears the entire disk loose,
causing protrusion onto the nerve root or compres-
sion of the spinal cord.
H Large amounts of extruded nucleus pulposus or
complete disk herniation of the capsule and nucleus
pulposus may compress the spinal cord.
Causes
H Improper lifting or twisting
H Direct injury
H Degenerative disk disease
Risk factors
H Advanced age
H Congenitally small lumbar spinal canal
H Osteophytes along the vertebrae
H Work environment
Incidence
H About 90% affect lumbar (L) and lumbosacral spine;
8% in cervical (C) spine; 1% to 2% in thoracic (T)
spine
H Lumbar herniation more common in people ages
20 to 45
H Cervical herniation more common in people ages
45 and older
H Herniated disks more common in males than in
females
Common characteristics
H Pain
H Limited range of motion (ROM)
Complications
H Neurologic deficits
H Bowel and bladder dysfunction
H Sexual dysfunction
Assessment
History
H Previous traumatic injury or back strain
H Unilateral, lower back pain
H Pain possibly radiating to the buttocks, legs, and feet
H Pain possibly beginning suddenly, subsiding in a few
days, and then recurring at shorter intervals with
progressive intensity
H Sciatic pain beginning as a dull ache in the buttocks,
worsening with Valsalvas maneuver, coughing, sneez-
ing, or bending
H Pain possibly subsiding with rest
H Muscle spasms
H Chronic repetitive injury
Physical findings
H Limited ability to bend forward
H Posture favoring the affected side
H Muscle atrophy, in later stages
H Tenderness over the affected region
H Radicular pain with straight-leg raising in lumbar
herniation
H Increased pain with neck movement in cervical her-
niation
H Referred upper trunk pain with cervical neck com-
pression
Test results
Imaging
H X-rays of the spine show degenerative changes.
H Myelography shows the level of the herniation.
H Computed tomography scan shows bone and soft-
tissue abnormalities; can also show spinal canal
compression.
H Magnetic resonance imaging shows soft-tissue abnor-
malities.
Other
H Electromyography measures muscle response to
nerve stimulation.
H Nerve conduction studies show sensory and motor
loss.
Treatment
General
H Initial treatment conservative and symptomatic, un-
less neurologic impairment progresses rapidly
H Possible traction
H Supportive devices such as a brace

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H Heat or ice applications ALERT

H Transcutaneous electrical nerve stimulation
H Chemonucleolysis During conservative treatment, watch for a deteri-
H Avoidance of repetitive activity oration in neurologic status, especially during the
H Diet, as tolerated first 24 hours after admission, which may indicate
H Bed rest, initially an urgent need for surgery.
H Prescribed exercise program
H Physical therapy After surgery
H Enforce bed rest, as ordered.
Medications H Use the logrolling technique to turn the patient.
H Nonsteroidal anti-inflammatory drugs, such as H Assist the patient during his first attempt to walk.
ibuprofen, ketorolac, and naproxen H Provide a straight-backed chair for the patient to sit
H Corticosteroids in, as allowed.
H Muscle relaxants, such as methocarbamol, cariso-
prodol, and cyclobenzaprine Monitoring
H Analgesics, such as codeine, hydromorphone, oxy- H Vital signs
codone, and acetaminophen H Intake and output
H Pain control
Surgery H Mobility
H Laminectomy H Motor strength
H Spinal fusion H Deep vein thrombosis
H Microdiskectomy H Bowel and bladder function
After surgery
H Blood drainage system
Nursing considerations H Drainage
H Incisions
Key outcomes H Dressings
The patient will: H Neurovascular status
H express feelings of increased comfort H Bowel sounds and abdominal distention
H demonstrate adequate joint mobility and ROM
H perform activities of daily living within the confines
of the disorder Patient teaching
H achieve the highest level of mobility possible
H demonstrate strategies to prevent self-injury. Be sure to cover:
H the disorder, diagnosis, and treatment
Nursing interventions H prescribed drugs and possible adverse effects
H Administer prescribed drugs. H when to notify the physician
H Plan a pain-control regimen. H bed rest
H Offer supportive care. H traction
H Provide encouragement. H heat application
H Help the patient cope with chronic pain and im- H the exercise program
paired mobility. H myelography, if indicated
H Include the patient and his family in all phases of his H preoperative and postoperative care, if indicated
care. H relaxation techniques
H Encourage the patient to express his concerns. H proper body mechanics
H Encourage performance of self-care. H skin care.
H Help the patient identify activities that promote rest
and relaxation. Discharge planning
H Prepare the patient for myelography, if indicated. H Refer the patient to physical therapy, if indicated.
H Periodically remove traction to inspect the skin. H Refer the patient to occupational therapy, if indi-
H Prevent deep vein thrombosis. cated.
H Prevent footdrop. H Refer the patient to a weight-reduction program, if
H Ensure a consistent regimen of leg- and back- appropriate.
strengthening exercises.
H Encourage adequate oral fluid intake.
H Encourage coughing and deep-breathing exercises.
H Provide meticulous skin care.
H Provide a fracture bedpan for the patient on com-
plete bed rest.

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Herpes simplex
Overview
Description
H Common viral infection that may be latent for years
H After initial herpes simplex virus (HSV) infection, pa-
tient becomes carrier susceptible to recurrent at-
tacks
H Recurrent infections may be provoked by fever,
menses, stress, heat, cold, lack of sleep, sun expo-
sure, and contact with reactivated disease (kissing,
sharing cosmetics, sexual intercourse)
Pathophysiology
H Virus enters mucosal surfaces or abraded skin sites
and initiates replication in cells of the epidermis and
dermis.
H Replication continues to permit infection of sensory
or autonomic nerve endings.
H Virus enters the neuronal cell and is transported
intra-axonally to nerve cell bodies in ganglia (where
the virus establishes latency) and spreads by the pe-
ripheral sensory nerves. (See Understanding the
genital herpes cycle.)
Causes
H Type 1 (HSV-1) Herpesvirus hominis transmitted
primarily by contact with oral secretions; mainly af-
fects oral, labial, ocular, or skin tissues
H Type 2 (HSV-2) Herpesvirus hominis transmitted
primarily by contact with genital secretions; mainly
affects genital structures
Incidence
H Occurs worldwide and equally in males and females
H Lower socioeconomic groups infected more com-
monly, probably due to crowded living conditions
H Infection with HSV-1 more common, occurring earli-
er in life than infection with HSV-2
Common characteristics
H Fever, malaise, and headache
H Tender inguinal adenopathy
H Typical primary lesions erupting after prodromal tin-
gling and itching
H Ruptured vesicles producing painful ulcers followed
by yellow crusting
Complications
H Primary (or initial) HSV infection during pregnancy
leading to spontaneous abortion, premature labor,
microcephaly, and intra-uterine growth retardation
H Congenital herpes transmitted during vaginal birth,
producing a subclinical neonatal infection or severe
infection with seizures, chorioretinitis, skin vesicles,
and hepatosplenomegaly
H HSV-1 causing life-threatening nonepidemic en-
cephalitis in infants
364 Herpes simplex
H Gingivostomatitis in children ages 1 to 3
H Blindness from ocular infection
H Increased risk for cervical cancer
H Urethral stricture from recurrent genital herpes
H Perianal ulcers
H Colitis
H Esophagitis (more frequent in the impaired host)
H Pneumonitis
H Neurologic disorders
H Uremia with multiple organ involvement
Assessment
History
H Oral, vaginal, or anal sexual contact with an infected
person or other direct contact with lesions
H With recurrent infection, various precipitating factors
identified
Physical findings
Primary perioral HSV
H Sore throat, fever, anorexia, adenopathy
H Increased salivation
H Severe mouth pain, halitosis
H Small vesicles on an erythematous base possibly pre-
sent on pharyngeal and oral mucosa
Primary genital HSV
H Malaise
H Tender inguinal adenopathy
H Dysuria, leukorrhea
H Dyspareunia
H Fluid-filled vesicles on the cervix, labia, perianal
skin, vulva, and vagina; glans penis, foreskin, and
penile shaft
H Extragenital lesions possibly seen on the mouth or
anus
Primary ocular infection
H Photophobia, excessive tearing
H Follicular conjunctivitis, chemosis
H Blepharitis, vesicles on eyelids
H Lethargy and fever
H Regional adenopathy
Test results
Laboratory
H Tissue culture shows isolation of virus (gold stan-
dard).
H Staining of scrapings from the base of the lesion
demonstrate characteristic giant cells or intranuclear
inclusions of herpes virus infection.
H Tissue analysis shows HSV antigens or deoxyribonu-
cleic acid in scrapings from lesions.
Treatment
General
H Symptomatic and supportive therapy
H Ophthalmologist treatment for eye infections
H Avoidance of acidic foods (with stomatitis)
9400H.qxd 8/2/12 4:35 PM Page 365

H Abstinence from sexual activity during active phase Understanding the genital herpes cycle
(with genital lesions)
After a patient is infected with genital herpes, a latency pe-
Medications riod follows. The virus takes up permanent residence in
the nerve cells surrounding the lesions, and intermittent
H Antipyretics and analgesics such as acetominophen viral shedding may take place.
H Anesthetic mouthwashes Repeated outbreaks may develop at any time, again fol-
H Bicarbonate-based mouth rinse lowed by a latent stage during which the lesions heal
H Drying agents such as astringents completely. Outbreaks may recur as often as three to eight
H Ophthalmic drugs times yearly.
H Antivirals, such as acyclovir, valacyclovir, and famci- Although the cycle continues indefinitely, some people
clovir remain symptom-free for years.
H Docosanol
INITIAL INFECTION
Highly infectious period marked by fever, aches,
Nursing considerations adenopathy, pain, and ulcerated skin
and mucous membranes
Key outcomes
The patient will:
H exhibit improved or healed lesions or wounds LATENCY
H express feelings of increased comfort and decreased Intermittently infectious period marked by viral domancy
pain or viral shedding and no disease symptoms
H exhibit no complications related to trauma to oral
mucous membranes
H voice feelings about potential or actual changes in
RECURRENT INFECTION
sexuality.
Highly infectious period similar to initial infection with
Nursing interventions milder symptoms that resolve faster

H Observe standard precautions.

H Administer prescribed drugs.
H Encourage the patient to express his feelings, and
provide support. Discharge planning
H Refer the patient with an eye infection to an ophthal-
Monitoring mologist.
H Response to treatment H Refer the patient to a support group such as the Her-
H Adverse reactions to medications pes Resource Center, as appropriate.
H Complications H If child abuse is suspected, make a report to local
H Lesions authorities and social services.
H Fluid and electrolyte balance

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H proper hand-washing technique
H the recommended use of lip balm with sunscreen
(with oral lesions)
H instructions to keep lesions dry, except for applying
prescribed topical drugs
H medication administration, dosage, and possible ad-
verse effects
H the use of sunscreen to prevent skin-induced recur-
rences
H the recommendation that sexual partners be
screened for sexually transmitted diseases (with gen-
ital herpes)
H for a patient with genital herpes, the recommenda-
tion to use warm compresses or take sitz baths sever-
al times per day and avoid all sexual contact during
outbreaks of active infection.

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Herpes zoster H Possibly more prevalent in people who had chicken-

pox at a young age
Common characteristics
Overview H Localized vesicular skin lesions, confined to a der-
matome; thoracic, cervical and ophthalmic der-
Description matomes most commonly involved
H Acute unilateral and segmental inflammation of dor- H Severe neuralgic pain in peripheral areas innervated
sal root ganglia that remains in people who have had by the nerves arising in the inflamed root ganglia
chickenpox H Pain generally precedes rash by 2 to 3 days
H Also called shingles H Lesions pustulate, crust, and heal in 3 to 4 weeks

Pathophysiology Complications
H Herpes zoster erupts when the virus reactivates after H Deafness
dormancy in the cerebral ganglia (extramedullary H Bells palsy
ganglia of the cranial nerves) or the ganglia of poste- H Secondary skin infection
rior nerve roots. H Postherpetic neuralgia
H The virus may multiply as it reactivates, and antibod- H Meningoencephalitis
ies remaining from the initial infection may neutral- H Cutaneous dissemination
ize it. H Ocular involvement with facial zoster
H Without opposition from effective antibodies, the H Hepatitis
virus continues to multiply in the ganglia, destroys H Pneumonitis
neurons, and spreads down the sensory nerves to the H Peripheral motor weakness
skin, causing localized vascular eruptions. H Guillain-Barr syndrome
H Cranial nerve syndrome
Causes
H Dormant varicella-zoster virus (herpesvirus that also
causes chickenpox) that reactivates Assessment
Incidence History
H Most common in adults ages 50 and older H Typically no history of exposure to others with the
H Bone marrow transplant patients especially at risk varicella-zoster virus
H Fever
H Malaise
H Pain that mimics appendicitis
H Pleurisy
A look at herpes zoster
H Musculoskeletal pain
These characteristic herpes zoster lesions are fluid-filled H Severe, deep pain
vesicles that dry and form scabs after about 10 days. Uni- H Pruritus
lateral vesicular lesions in a dermatomal pattern should H Paresthesia or hyperesthesia (usually affecting the
rapidly lead to a diagnosis of herpes zoster. trunk and occasionally the arms and legs)
Physical findings
H Small, red, vesicular skin lesions spread unilaterally
around the thorax or vertically over the arms or legs
H May see vesicles filled with clear fluid or pus
H Vesicles drying, forming scabs or even becoming
gangrenous (see A look at herpes zoster)
H Enlarged regional lymph nodes
Geniculate involvement
H Vesicle formation in the external auditory canal and
ipsilateral facial palsy
H Hearing loss, dizziness, and loss of taste
Trigeminal involvement
H Eye pain
H Corneal and scleral damage and impaired vision
H Conjunctivitis, extraocular weakness, ptosis, and par-
alytic mydriasis
H Secondary glaucoma

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Test results H Lesions

Laboratory H Signs and symptoms of infection
H Vesicular fluid and infected tissue analyses show
eosinophilic intranuclear inclusions and varicella
virus. Patient teaching
H Staining antibodies from vesicular fluid and identifi-
cation under fluorescent light aid differentiation of Be sure to cover:
herpes zoster from herpes simplex virus. H the disorder, diagnosis, and treatment
H Specific antibody immune globulin measurement of H prescribed drugs and possible adverse effects
varicella antibodies is elevated. H the use of a soft toothbrush, eating soft foods, and
H Cerebrospinal fluid analysis demonstrates increased using a saline- or bicarbonate-based mouthwash and
protein levels and, possibly, pleocytosis. oral anesthetics to decrease discomfort from oral le-
Diagnostic procedures sions
H Lumbar puncture indicates increased pressure. H the need for meticulous hygiene to prevent spreading
infection to other body parts
H that the virus can be transmitted if the blisters break
Treatment H the need to avoid scratching lesions
H advice to apply a cold compress if vesicles rupture
General H local treatment of vesicles.
H Transcutaneous peripheral nerve stimulation for
postherpetic neuralgia Discharge planning
H Soothing baths H Refer the patient to an ophthalmologist for ocular in-
H Cold compresses volvement.
H Refer the patient to a pain management specialist for
Medications postherpetic neuralgia.
H Antivirals, such as acyclovir, valacyclovir, and fami-
clovir
H Antipruritics, such as hydroxyzine and diphenhy-
dramine
H Analgesics, such as acetominophen and ibuprofen
H Tricyclic antidepressants, such as amitriptyline and
imipramine
H Systemic antibiotic as appropriate for infecting
organisms
H Corticosteroids, topical and oral, such as betametha-
sone, dexamethasone, and hydrocortisone
H Tranquilizers and sedatives, such as diazepam and
lorazepam
H Patient-controlled analgesia
H Vaccine for at-risk people age 60 or older

Nursing considerations
Key outcomes
The patient will:
H exhibit improved or healed lesions or wounds
H express feelings of increased comfort and decreased
pain
H remain free from complications.

Nursing interventions
H Administer prescribed drugs.
H Maintain meticulous hygiene to prevent spreading the
infection to other parts of the patients body.
H With open lesions, follow contact isolation precau-
tions to prevent the spread of infection.
Monitoring
H Response to treatment
H Adverse reaction to medications

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Common characteristics
Life-threatening disorder H Impaired function
H Deformity

Hip fracture H Edema

H Muscle spasm
H Pain and tenderness
H Impaired sensation
Overview
Complications
Description H Pneumonia
H Break in the head or neck of the femur (usually the H Venous thrombosis
head) H Pressure ulcers
H Most common fall-related injury resulting in hospi- H Social isolation
talization H Depression
H Leading cause of disability among older adults H Bladder dysfunction
H May permanently change level of functioning and H Deep vein thrombosis
independence H Pulmonary embolus
H Almost 25% of patients die within 1 year after hip H Hip dislocation
fracture H Death

Pathophysiology
H With bone fracture, the periosteum and blood vessels Assessment
in the marrow, cortex, and surrounding soft tissues
are disrupted. History
H This results in bleeding from the damaged ends of H Falls or trauma to the bones
the bone and from the neighboring soft tissue. H Pain in the affected hip and leg
H Clot formation occurs within the medullary canal, be- H Pain exacerbated by movement
tween the fractured bone ends, and beneath the pe-
riosteum. Physical findings
H Bone tissue immediately adjacent to the fracture dies, H Outward rotation of affected extremity
and the necrotic tissue causes an intense inflammato- H Affected extremity possibly appearing shorter
ry response. H Limited or abnormal range of motion (ROM)
H Vascular tissue invades the fracture area from sur- H Edema and discoloration of the surrounding tissue
rounding soft tissue and marrow cavity within 48 H In an open fracture, bone protruding through the
hours, increasing blood flow to the entire bone. skin
H Bone-forming cells in the periosteum, endosteum,
and marrow are activated to produce subperiosteal Test results
procallus along the outer surface of the shaft and Imaging
over the broken ends of the bone. H X-rays show the location of the fracture.
H Collagen and matrix, which become mineralized to H Computed tomography scan shows abnormalities in
form callus, are synthesized by osteoblasts within the complicated fractures.
procallus.
H During the repair process, remodeling occurs; un-
necessary callus is resorbed, and trabeculae are Treatment
formed along stress lines.
H New bone, not scar tissue, is formed over the healed General
fracture. H Depends on age, comorbidities, cognitive function-
ing, support systems, and functional ability
Causes H Possible skin traction
H Falls H Physical therapy
H Trauma H Nonweight-bearing transfers
H Cancer metastasis H Well-balanced diet
H Osteoporosis H Foods rich in vitamin A and C, calcium, and protein
H Skeletal disease H Adequate vitamin D
H Bed rest, initially
Incidence H Ambulation as soon as possible after surgery
H Affects more than 300,000 people each year
H Occurs in one of five females by age 80 Medications
H More common in females than in males H Analgesics, such as butorphanol, meperidine, and
H More common in white females ketorolac initially, then acetaminophen and ibupro-
fen

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H Anticoagulants, such as warfarin, for deep vein ALERT

thrombosis prophylaxis
After surgery, assess the patient for complications,
Surgery such as deep vein thrombosis, pulmonary embolus,
H Total hip arthroplasty and hip dislocation.
H Hemiarthroplasty
H Percutaneous pinning
H Internal fixation using a compression screw and Patient teaching
plate
Be sure to cover:
H the disorder, diagnosis, and treatment
Nursing considerations H prescribed drugs and possible adverse effects
H ROM exercises
Key outcomes H meticulous skin care
The patient will: H proper body alignment
H identify factors that increase the potential for injury H wound care
H maintain muscle strength and tone and joint ROM H signs of infection
H verbalize feelings of increased comfort H coughing and deep-breathing exercises and incentive
H attain the highest degree of mobility possible within spirometry
the confines of the injury H assistive devices
H maintain skin integrity. H activity restrictions and lifestyle changes
H safe ambulation practices
Nursing interventions H nutritious diet and adequate fluid intake
H Administer prescribed drugs. H decreasing risk for additional injury. (See Prevent-
H Administer prescribed prophylactic anticoagulation ing hip fracture.)
after surgery.
H Maintain traction. Discharge planning
H Maintain proper body alignment. H Refer the patient to physical and occupational thera-
H Use logrolling techniques to turn the patient in bed. py programs, as indicated.
H Maintain nonweight-bearing status. H Refer the patient to home health or intermediate
H Increase the patients activity level, as prescribed. care.
H Consult physical therapy as early as possible.
H Assist with active ROM exercises to unaffected limbs. Prevention
H Encourage coughing and deep-breathing exercises. Preventing hip fracture
H Keep the patients skin clean and dry.
H Prevent skin breakdown. Hip fractures are debilitating, with only 25% of those
H Encourage good nutrition; offer high-protein, high- treated making a complete recovery. Its important to dis-
calorie snacks. cuss prevention, especially with aging patients. Steps that
H Perform daily wound care. can be taken to minimize the risk of hip fracture include
H Provide antiembolism stockings. the following:
H Obtain a baseline bone density test at menopause to
assess bone status.
ALERT H Ensure proper dietary calcium and vitamin D intake and
take supplements as appropriate.
Dont massage the patients legs and feet to pro- H Perform weight-bearing exercises, such as walking, to
mote circulation because this could increase the encourage increased bone density, strength, and bal-
risk of thromboembolism. ance.
H Avoid smoking and excessive alcohol intake which
decrease bone density.
Monitoring H Take prescribed medication for osteoporosis, such as
H Vital signs alendronate, risedronate, raloxifene, or calcitonin.
H Intake and output H Assess the home environment for fall risks, such as
H Pain electrical cords, throw rugs, and unlighted stairs.
H Install grab bars in the bathroom and non-slip mats in
H Mobility and ROM
the tub or shower.
H Incision and dressings
H Wear flat, slip-resistant shoes.
H Complications H Avoid heavy lifting and climbing on step ladders or
H Coagulation study results chairs.
H Signs of bleeding H Wear glasses as prescribed and follow-up with routine
H Neurovascular status vision screenings.
H Skin integrity H Be aware of adverse effects of medications that might
H Signs and symptoms of infection cause dizziness or weakness.

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Hirschsprungs disease H Overflow diarrhea caused by increased water secre-

tion into bowel with bowel obstruction
In children
H Intractable constipation caused by decreased GI
Overview motility
H Abdominal distention caused by retention of stool
Description H Easily palpated fecal masses caused by retention of
H Congenital disorder of the large intestine character- stool
ized by the absence or marked reduction of parasym- H Wasted extremities (in severe cases) caused by im-
pathetic ganglion cells in the colorectal wall paired intestinal motility and its effects on nutrition
H Usually coexists with other congenital anomalies, and intake
particularly trisomy 21 and anomalies of the urinary H Loss of subcutaneous tissue (in severe cases) caused
tract such as megaloureter by malnutrition
H Also called congenital megacolon and congenital H Large protuberant abdomen caused by retention of
aganglionic megacolon stool and consequent changes in fluid and electrolyte
homeostasis
Pathophysiology In adults
H Parasympathetic ganglion cells in the colorectal wall H Abdominal distention from decreased bowel motility
are absent or markedly reduced in number. and constipation
H The aganglionic bowel segment contracts without the H Chronic intermittent constipation caused by impaired
reciprocal relaxation needed to propel feces for- intestinal motility
ward.
H Impaired intestinal motility causes severe, intractable Complications
constipation. H Bowel perforation
H Colonic obstruction can ensue, causing bowel dila- H Electrolyte imbalances
tion and subsequent occlusion of surrounding blood H Nutritional deficiencies
and lymphatic vessels. H Enterocolitis
H Ensuing mucosal edema, ischemia, and infarction H Hypovolemic shock
draw large amounts of fluid into the bowel, causing H Sepsis
copious amounts of liquid stool.
H Continued infarction and destruction of the mucosa
can lead to infection and sepsis. Assessment
Causes History
H Familial congenital defect H Familial history of difficult stool passage
H Failure to pass meconium within the first 24 to 48
Incidence hours after birth
H Occurs in 1 in 2,000 to 1 in 5,000 live births H Vomiting of bile-stained or fecal contents
H Up to seven times more common in males than in fe- H Anorexia
males (although the aganglionic segment is usually H Nausea
shorter in males) H Lethargy
H Most prevalent in whites H Constipation
H Both sexes equally affected by total aganglionosis
H Females with Hirschsprungs disease at higher risk Physical findings
for having affected children H Distended abdomen
H Tachypnea
Common characteristics H Rectum without stools
In neonates
H Failure to pass meconium within 24 to 48 hours be- Test results
cause of inability to propel intestinal contents for- Imaging
ward H Barium enema reveals a narrowed segment of distal
H Bile-stained or fecal vomiting as a result of bowel ob- colon with a saw-toothed appearance and a funnel-
struction shaped segment above it.
H Abdominal distention caused by to retention of in- H Upright plain abdominal X-rays show marked colonic
testinal contents and bowel obstruction distention.
H Irritability caused by resultant abdominal distention Diagnostic procedures
H Feeding difficulties and failure to thrive caused by H Rectal biopsy confirms diagnosis by showing the ab-
retention of intestinal contents and abdominal dis- sence of ganglion cells.
tention H Rectal manometry detects failure of the internal anal
H Dehydration caused by subsequent feeding difficul- sphincter to relax and contract.
ties and inability to ingest adequate fluids

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H that complete continence may take several years to

Treatment develop and that constipation may recur at times
H with parents, participation in the childs care as
General much as possible, if appropriate.
H Daily colonic lavage (to empty the infants bowel until
the time of surgery) Discharge planning
H Oral feeding with breast milk or predigested formula H Refer the parents to an enterostomal therapist for
when bowel sounds return (infants) information on ostomy care.

ALERT
Without prompt treatment, an infant with colonic
obstruction may die within 24 hours from entero-
colitis that leads to severe diarrhea and hypo-
volemic shock.

Surgery
H Corrective surgery to pull the normal ganglionic seg-
ment through to the anus (usually delayed until the
infant is at least age 10 months)
H Temporary colostomy or ileostomy to compress the
colon in instances of total bowel obstruction

Nursing considerations
Key outcomes
The patient will:
H maintain adequate caloric intake
H avoid complications
H have bowel function return to normal patterns
H maintain fluid balance.

Nursing interventions
H Maintain fluid and electrolyte balance and prevent
shock.
H Provide adequate nutrition and hydrate with I.V. flu-
ids, as needed.
H Relieve respiratory distress by keeping the patient in
an upright position.
After colostomy or ileostomy
H Place the infant in a heated incubator, with the tem-
perature set at 98 to 99 F (36.7 to 37.2 C), or in
a radiant warmer.
Monitoring
H Vital signs
H Signs of sepsis and enterocolitis
H Intake and output
H Laboratory values

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H recognizing the signs of fluid loss, dehydration, and
enterocolitis
H withholding foods that have increased the number of
stools previously

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Histoplasmosis
Overview
Description
H Fungal infection
H Three forms in the United States
Primary acute histoplasmosis
Progressive disseminated histoplasmosis (acute
disseminated or chronic disseminated disease)
Chronic pulmonary (cavitary) histoplasmosis
H Also known as Ohio Valley disease, Central Missis-
sippi Valley disease, Appalachian Mountain dis-
ease, and Darlings disease
Pathophysiology
H Spores reach alveoli and are transformed into bud-
ding forms, carried to regional lymphatics, and then
disseminated throughout the body.
H Intense granulomatous reaction occurs and case-
ation necrosis or calcification (resembling tubercu-
losis) occurs.
H Transient dissemination can leave granulomas in the
spleen.
Causes
H Caused by Histoplasma capsulatum, which is found
in the stool of birds and bats and in soil contaminat-
ed by their stool (near roosts, chicken coops, barns,
caves, and underneath bridges)
H Transmitted to humans by inhalation of H. capsula-
tum or H. capsulatum var. duboisii spores or inva-
sion of spores after minor skin trauma
Incidence
H Occurs worldwide, but especially in temperate areas
of Asia, Africa, Europe, and North and South America
H In the United States, most prevalent in southeastern,
mid-Atlantic, and central states
H Primary acute histoplasmosis most common in in-
fants, young children, and immunocompromised
patients
Common characteristics
H Incubation period ranges from 3 to 17 days, al-
though chronic pulmonary histoplasmosis may
progress slowly for many years
H Chronic pulmonary infections occur more commonly
in males older than age 40, particularly with a history
of cigarette smoking or chronic lung disease
Complications
H Vascular or bronchial obstruction
H Acute pericarditis
H Pleural effusion
H Mediastinal fibrosis or granuloma
H Intestinal ulceration
372 Histoplasmosis
H Addisons disease
H Endocarditis
H Meningitis
Assessment
History
H Possible history of an immunocompromised condi-
tion
H Exposure to contaminated soil in an endemic area
Physical findings
H Fever, which may rise as high as 105 F (40.6 C)
Primary acute histoplasmosis
H Usually no characteristic signs
H Mild respiratory illness, cough
H Malaise, headache, myalgia, anorexia
H Chest pain
Progressive disseminated histoplasmosis
H Anorexia and weight loss
H Pain
H Hoarseness, tachypnea in later stages
H Ulceration of the oropharynx, dysphagia
H Pallor from anemia
H Jaundice and ascites
H Hepatosplenomegaly
H Lymphadenopathy
Chronic pulmonary histoplasmosis
H Productive cough, dyspnea, hemoptysis
H Shortness of breath, cyanosis
H Extreme weakness, weight loss
H Upper lobe fibrocavitary pneumonia
Test results
Laboratory
H Blood cultures done by lysis-centrifugation technique
reveal organism causing the infection.
H In disseminated forms, culture of bone marrow, mu-
cosal lesions, liver, and bronchoalveolar lavage help
show organisms in disseminated histoplasmosis.
H Sputum cultures are preferred in chronic pulmonary
histoplasmosis, may take 2 to 4 weeks to culture, and
show growth of the organism.
H Radioactive assay for histoplasma antigen in blood or
urine shows presence of histoplasma antigen.
Imaging
H Chest X-rays show lung damage.
Treatment
General
H Oxygen for respiratory distress
H Parenteral fluids for dysphagia caused by oral or la-
ryngeal ulcerations
H Smoking cessation
H Cool mist humidifier
H Soft, bland foods (with oropharyngeal ulceration)
9400H.qxd 8/2/12 4:35 PM Page 373

H Small, frequent meals H Refer the patient with chronic pulmonary or dissemi-
H Frequent rest periods nated histoplasmosis for psychological support to
cope with long-term treatment, if needed.
Medications H Refer the patient to a social worker or an occupa-
H Antifungal therapy, such as amphotericin B and tional therapist, as needed.
itraconazole H Help the parents of a child with this disease arrange
H Glucocorticoids for a visiting teacher.
Surgery
H Lung resection to remove pulmonary nodules
H Shunt for increased intracranial pressure
H Cardiac repair for constrictive pericarditis
H Laser surgery (photo coagulation) for ocular
histoplasmosis syndrome

Nursing considerations
Key outcomes
The patient will:
H be free from pain
H maintain adequate ventilation
H express feelings of increased comfort in maintaining
air exchange
H experience no further weight loss
H maintain hemodynamic stability.

Nursing interventions
H Administer prescribed drugs.
H Provide oxygen therapy, if needed.
H Plan rest periods.
H Consult with a dietitian and the patient concerning
food preferences.
Monitoring
H Hypoglycemia and hyperglycemia, which indicate
adrenal dysfunction
H Respiratory status
H Neurologic status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medication administration, dosage, and possible
adverse effects
H cardiac and pulmonary signs that could indicate
effusions
H the need to watch for early signs of this infection and
to seek treatment promptly to help prevent histoplas-
mosis for people in endemic areas
H the need for patients who risk occupational exposure
to contaminated soil to wear face masks.
Discharge planning
H Stress the need for follow-up care on a regular basis
for at least 1 year.

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H Enlarged, rubbery lymph nodes in the neck (which

Life-threatening disorder enlarge during periods of fever and then revert to
normal size)
Hodgkins disease Test results
Laboratory
H Hematologic tests show mild to severe normocytic
Overview anemia, normochromic anemia in 50% of patients,
and elevated, normal, or reduced white blood cell
Description count and differential show any combination of
H Neoplastic disorder characterized by painless, pro- neutrophilia, lymphocytopenia, monocytosis, and
gressive enlargement of lymph nodes, spleen, and eosinophilia.
other lymphoid tissue H Serum alkaline phosphatase levels are elevated, indi-
H With appropriate treatment, 5-year survival rate cating liver or bone involvement.
about 90% Diagnostic procedures
H Tests must first rule out other disorders that enlarge
Pathophysiology the lymph nodes.
H Enlarged lymphoid tissue results from proliferation H Lymph node biopsy confirms the presence of Reed-
of lymphocytes, histiocytes, eosinophils, and Sternberg cells, abnormal histiocyte proliferation,
Reed-Sternberg cells. and nodular fibrosis and necrosis. Lymph node biop-
H Untreated Hodgkins disease follows a variable but sy is also used to determine lymph node and organ
relentlessly progressive and ultimately fatal course. involvement.
H A staging laparotomy is necessary for patients
Causes younger than age 55 and for those without obvious
H Exact cause unknown stage III or IV disease, lymphocyte predominance
subtype histology, or medical contraindications.
Risk factors
H Genetic factors
H Viral factors Treatment
H Environmental factors
General
Common characteristics H For patient with stage I or IIA disease, radiation ther-
H Painless swelling of lymph nodes apy alone
H Fever, night sweats H For patient with stage IIB or III disease, radiation
therapy and chemotherapy
Incidence H For patient with stage IV disease, chemotherapy
H Occurs in all races; slightly more common in whites alone (or chemotherapy and radiation therapy to in-
H Peaks in two age-groups: ages 15 to 38 and people volved sites), sometimes inducing complete remis-
older than age 50 sion
H Most common in young adults, except in Japan (ex- H Autologous bone marrow transplantation or autolo-
clusively in people older than age 50) gous peripheral blood sternal transfusions and im-
H Greater incidence in males than in females munotherapy
H Well-balanced diet
Complications H Frequent rest periods
H Multiple organ failure
Medications
H Chemotherapy
Assessment H Antiemetics, such as prochlorperazine and metoclo-
pramide
History H Sedatives, such as alprazolam and lorazepam
H Painless swelling of one of the cervical, axillary, or H Antidiarrheals, such as loperamide/simethicone and
inguinal lymph nodes diphenoxylate/atropine
H Persistent fever and night sweats
H Weight loss despite an adequate diet, with resulting
fatigue and malaise Nursing considerations
H Increasing susceptibility to infection
Key outcomes
Physical findings The patient will:
H Edema of the face and neck and jaundice H have no further weight loss

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H express feelings of increased energy

H demonstrate adequate skin integrity
H demonstrate effective coping mechanisms
H express feelings of increased comfort and decreased
pain.
Nursing interventions
H Provide a well-balanced, high-calorie, high-protein
diet.
H Provide for periods of rest.
H Administer prescribed drugs.
H Provide emotional support.

Monitoring
H Complications of treatment
H Pain control
H Lymph node enlargement
H Body temperature
H Fatigue
H Daily weight
H Signs and symptoms of infection
H Response to treatment
H Signs and symptoms of dehydration

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H signs and symptoms of infection
H the importance of maintaining good nutrition
H the pacing of activities to counteract therapy-induced
fatigue
H the importance of good oral hygiene
H the avoidance of crowds and people with known
infection
H the importance of checking the lymph nodes
H medication administration, dosage, and possible ad-
verse effects.
Discharge planning
H Refer the patient to resource and support services.

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Hookworm disease Assessment

History
Overview H Recent walking (barefoot) in an area with contami-
nated soil
Description H Irritation and pruritus at entry site
H Infection of the upper intestine caused by Ancy- H Fatigue
lostoma duodenale (found in the Eastern Hemi- H Cough, hoarseness
sphere) or Necator americanus (in the Western H Abdominal pain
Hemisphere) H Fever
H Occurs mostly in tropical and subtropical climates H Nausea
H Also called uncinariasis or ground itch H Weight loss
H Dizziness
Pathophysiology H Diarrhea
H Disease is transmitted to humans through direct skin
penetration (usually in the foot) by hookworm larvae Physical findings
in soil contaminated with feces containing hook- H Papulovasicular rash
worm ova. H Crackles (with lung involvement)
H These ova develop into infectious larvae in 1 to 3 H Irregular respirations
days. H Bloody sputum
H The larvae travel through the lymphatics to the pul- H Black, tarry stools
monary capillaries, where they penetrate alveoli and H Edema
move up the bronchial tree to the trachea and
epiglottis. There they are swallowed and enter the GI Test results
tract. Laboratory
H When they reach the small intestine, they mature, at- H Stool specimen reveals larvae.
tach to the jejunal mucosa, and suck blood, oxygen, H Hemoglobin level is decreased to as low as 5 to
and glucose from the intestinal wall. 9 g/dl (in severe case).
H These mature worms then deposit ova, which are ex- H Leukocyte count is increased to as high as 47,000/l.
creted in the stool, starting the cycle anew. Hook- H Eosinophil count is increased to as high as 500 to
worm larvae mature in about 5 to 6 weeks. 700/l.
Causes
H Transmission of A. duodenale (found in the Eastern Treatment
Hemisphere) or N. americanus (in the Western
Hemisphere) General
H Blood transfusions (if anemia severe)
Incidence H Nutritious high-protein, high-iron diet
H May produce no symptoms H Activity, as tolerated, with frequent rest periods
H Affects one billion people worldwide
H More common in whites Medications
H Children more at risk because of playing or walking H Mebendazole
barefoot in contaminated soil H Pyrantel pamoate
H Albendazole
Common characteristics H Iron supplements
H Irritation, pruritus, and edema at the site of entry H Topical thiabendazole (cutaneous larva migrans)
H Secondary bacterial infection with pustule formation
H Pneumonitis and hemorrhage with fever, sore throat,
crackles, and cough (larvae in lungs) Nursing considerations
H Fatigue, nausea, weight loss, dizziness, melena, and
uncontrolled diarrhea (larvae in intestines) Key outcomes
The patient will:
Complications H experience no further weight loss
H Anemia H report having increased energy levels
H Cardiomegaly H have decreased episodes of diarrhea
H Heart failure H maintain a normal respiratory rate.
H Generalized massive edema

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Nursing interventions
H Follow standard precautions.
H Isolate the incontinent patient.
H Teach proper hand-washing technique.
H For severe anemia, administer oxygen, as ordered.
H Encourage coughing and deep breathing.
H Allow frequent rest periods.
H Reposition frequently.
H Assess family members for symptoms.

Monitoring
H Intake and output
H Nutritional status
H Quantity and frequency of stools
H Daily weight
H Skin integrity

Patient teaching
Be sure to cover:
H proper hand-washing technique
H the need to wear shoes when outdoors
H nutritious diet
H proper hygiene after toileting
H use of prescribed iron supplements and how this
treatment affects stools
H the need to start another course of treatment if stool
examination remains positive for larvae
H medication administration, dosage, and possible
adverse effects.

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Human papillomavirus H More than 50% of sexually active people becoming

infected during their lifetimes
H About 80% of females infected by age 50

Overview Common characteristics

Description
H Sexually transmitted disease (STD)
H Group of viruses with more than 100 different strains
H About 30 types spread through sexual contact
H Low-risk and high-risk types
H Primarily infects genital area; mouth and throat pos-
sible but rare
H Causes benign papillomas (warts)
H Affects both sexes
Pathophysiology
H Human papillomavirus is very contagious.
H It may produce proteins that interfere with cell func-
tions that normally prevent excessive cell growth.
H Its contracted during oral, vaginal, or anal sex with
an infected person.
H About two-thirds of those who have sexual contact
with an infected person develop papillomas, usually
within 3 months of contact.
Papillomas can be single or multiple cauliflower-
like growths or may be flat and white or barely vis-
ible areas commonly producing no symptoms.
These growths affect the penis, scrotum, vulva,
anus, and the linings of the vagina, cervix, or rec-
tum.
H Initial growths may spread to other areas of the geni-
tals or to the anal area.
H Most infected individuals having no symptoms and
clearing the infection on their own
H Symptoms (if they develop) that occur 2 to 3 months
after infection; possibly developing as early as 3
weeks and as late as many years after infection
H For 90% of females, cervical HPV infection becoming
undetectable within 2 years
Complications
H High-risk HPV possibly leading to cancer of the
mouth, cervix, vulva, vagina, anus, or penis
H Pregnant females passing HPV to neonate during
vaginal delivery (rare)
H Large vaginal papillomas that cause excessive bleed-
ing with vaginal birth
H Associated with an increased risk of anal cancer in
males receiving anal sex
Assessment
History
H Sexual partner with HPV or genital warts
H Multiple sex partners
H May exhibit no signs or symptoms
H Possible discharge from the vagina or penis
H Previous STD
H Abnormal Papanicolaou (Pap) test

Causes Physical findings

H Human papillomavirus (HPV)
H HPV 6 and HPV 11
Low-risk viruses
Most commonly associated with genital warts
Cause most visible genital warts
H HPV 16 and HPV 18
Most common high-risk viruses
Growths usually flat and nearly invisible
Majority resolving on their own
H Genital warts
Soft, moist, pink, or flesh-colored swellings
Raised or flat; possibly cauliflower-shaped
Individual or grouped
Small or large
Location: groin, thigh, vulva, vagina, anus, urethra,
cervix, penis, or scrotum
H HPV 16 and HPV 18: no visible genital warts
H Patient possibly unaware of warts

Risk factors Test results

H Impaired immune system Genital warts are typically diagnosed by visual inspec-
H Multiple sex partners tion.
H Partner with multiple sex partners or HPV-infected Laboratory
sex partners H Pap tests (most common means of diagnosis for fe-
H Possibly, uncircumcised males males) are abnormal.
H Sexual activity before age 18 H Confirmatory follow-up test for HPV deoxyribonucle-
H Unprotected sexual contact ic acid can identify 13 of the high-risk types of HPV
associated with the development of cervical cancer.
Incidence H No testing is available for males.
H About 20 million people currently infected
H About 6.2 million new infections in United States
each year

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Treatment Patient teaching

General
H No cure for HPV infection; wart removal doesnt
eliminate infection or communicability
H Geared toward warts and precancerous cervical
changes
H Genital warts possibly disappearing without treatment
H 20% to 50% of people experiencing recurrence of
warts
H Treatment varying based on size and location of
warts; can be painful and may cause scarring
Medications
H Topical, applied by physician, such as podophyllin
resin, trichloroacetic acid, and fluorouracil cream
H Interferon injection into wart
H Topical, prescriptions applied at home, such as im-
iquimod cream and podofilox lotion or gel
Surgery
H Cryosurgery
H Electrocautery
H Laser treatment
H Surgical excision
H Loop electrosurgical excision procedure
Be sure to cover:
H need to inform sexual partners about the risk of
genital warts
H need for regular Pap testing and careful medical
follow-up
H reasons for not using nonprescription wart removal
products
H use of female condoms
H limitations of male and female condoms
H that podophyllin and fluorouracil cream cant be
used during pregnancy
H availability of HPV vaccine, Gardasil, which blocks
HPV 6, 11, 16, and 18, recommended for females
ages 9 to 26 before first sexual contact.

Nursing considerations
Key outcomes
The patient will:
H verbalize an understanding of the disease
H state infection risk factors
H remain free from complications
H express feelings of comfort after treatment
H communicate feelings about changes in body image
H voice feelings about the need for changes in sexual
activity.
Nursing interventions
H Use standard precautions when theres a risk of con-
tact with genital secretions.
H Administer pain medication as ordered.
H Provide a nonthreatening, nonjudgmental atmo-
sphere that encourages the patient to verbalize feel-
ings about perceived changes in sexual identity and
behavior.
Monitoring
H Sites treated with topical medication
H Surgical sites
H Pap test results
H Psychological status

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Huntingtons disease Assessment

History
Overview Findings vary depending on disease progression.
H Familial history
Description H Emotional and mental changes
H Degenerative disease of the brain causing dementia H Insidious onset
H Death usually 10 to 15 years after onset H Total dependency through:
H Also called Huntingtons chorea, hereditary chorea, Intellectual decline
chronic progressive chorea, and adult chorea Emotional disturbances
Loss of musculoskeletal control
Pathophysiology H Described as clumsy, irritable, or impatient
H Degeneration in the cerebral cortex and basal gan- H Subject to fits of anger
glia leads to chronic progressive chorea (dancelike H Periods of suicidal depression, apathy, or elation
movements). H Ravenous appetite, especially for sweets
H The final stage is mental deterioration, which ends in H Loss of bladder and bowel control in later stages
dementia.
Physical findings
Causes H Choreic movements
H Genetic link H Rapid, usually violent, and purposeless movements
H Transmitted as autosomal dominant trait (either sex H Cognitive decline
can transmit and inherit it) Early stages
H Mild fidgeting
Incidence H Grimacing, tongue smacking
H Most common between ages 30 and 45 H Dysarthria
H 2% of cases in children H Athetoid movements related to emotional state
H 5% of cases as late as age 60 H Torticollis
H Each child of a parent with this disease: 50% chance H Deficits in short-term memory
of inheritance Later stages
H Cant be passed on by child who doesnt inherit it H Constant writhing and twitching
H Affects males and females equally H Unintelligible speech
H Difficulty chewing and swallowing
Common characteristics H Ambulation impossible
H Chorea H Appears emaciated and exhausted
H Emotional changes, irritability
H Clumsiness, bradykinesia Test results
H Incontinence Laboratory
H Increased appetite H Deoxyribonucleic acid analysis may show disease.
H Bouts of anger Imaging
H Purposeless movements H Positron-emission tomography may show disease.
H Grimacing H Magnetic resonance imaging shows characteristic
H Dysarthria butterfly dilation of the brains lateral ventricles.
H Writhing and twitching H Computed tomography scan shows brain atrophy.
H Loss of motor control; rigidity
H Dysphagia
H Oral apraxia, aprosody Treatment
Complications General
H Choking and aspiration H No known cure
H Pneumonia H Supportive and symptomatic treatment
H Heart failure H Psychotherapy
H Infections H Possibly soft diet
H Suicide H Safety measures
H Electroconvulsive therapy

Medications
H Tranquilizers such as clonazepam
H Dopamine agonists such as haloperidol

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H Neuroleptics, such as chlorpromazine and tetra-

benazine
H Selective serotonin reuptake inhibitors, such as flu-
oxetine and sertraline
H Tricyclic antidepressants, such as nortriptyline and
imipramine

Nursing considerations
Key outcomes
The patient will:
H maintain a patent airway without evidence of aspira-
tion
H maintain joint mobility and range of motion
H remain free from infection
H express positive feelings about self
H perform activities of daily living
H develop alternative means of communication to
express self.
Nursing interventions
H Provide psychological support.
H Identify self-care deficits.
H Encourage the patient to be independent.
H Provide communication aids.
H Help the patient with difficulty walking.
H Maintain a turning schedule.
H Elevate the head of the bed during eating.
H Administer prescribed drugs.
H Protect the patient from infections.

Monitoring
H Response to prescribed drugs
H Possible suicide ideation
H Temperature
H White blood cell count

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H prescribed medications and possible adverse effects
H aspiration precautions
H signs and symptoms of infection
H communication strategies.

Discharge planning
H Refer the patient to the Huntingtons Disease Society
of America.
H Refer the patient to appropriate community organiza-
tions.
H Refer the family for genetic counseling.
H Refer the patient for psychotherapy, as appropriate.

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Physical findings
Hydrocele H Soft, nontender fullness within the hemiscrotum
H Transillumination of the scrotum revealing a ho-
mogenous glow without internal shadows
Overview
Test results
Description Imaging
H A collection of fluid between the visceral and parietal H Abdominal X-rays distinguish acute hydrocele from
layers of the testicles tunica vaginalis or along the an incarcerated hernia.
spermatic cord H Ultrasound distinguishes spermatoceles from hydro-
H The most common cause of scrotal swelling celes and identifies torsion or tumor.
H Described as communicating or noncommunicating Other
H Transillumination to distinguish fluid-filled from sol-
Pathophysiology id mass (a tumor doesnt transilluminate).
Communicating
H A patency between the scrotal sac and the peritoneal
cavity allows peritoneal fluids to collect in the scro- Treatment
tum.
Noncommunicating General
H Fluid accumulation may be caused by infection, trau- H Frequently resolves spontaneously
ma, tumor, an imbalance between the secreting and H Scrotal elevation
absorptive capacities of scrotal tissue, or an obstruc- H No dietary restrictions
tion of lymphatic or venous drainage in the spermatic H Activity, as tolerated
cord. H Postoperatively avoidance of vigorous activity for
H This leads to a displacement of fluid in the scrotum, short time
outside the testes.
H Subsequent swelling results, leading to reduced Medications
blood flow to the testes. H Nonsteroidal anti-inflammatory drugs, such as
ibuprofen and naproxen
Causes H Nonopioid analgesics, such as acetaminophen, as-
H Congenital malformation (infants) pirin, and diflunisal
H Trauma to the testes or epididymis
H Infection of the testes or epididymis Surgery
H Testicular tumor H Operative exploration if underlying pathology sus-
pected
Incidence H Surgical repair to avoid strangulation of the bowel
H Apparent in 6% of full-term male neonates (inguinal hernia with bowel present in the sac)
H Incidence in adult males unknown H Aspiration of fluid and injection of sclerosing drug
into the scrotal sac for a tense hydrocele impeding
Common characteristics blood circulation or causes pain
H Scrotal swelling and feeling of heaviness H Excision of tunica vaginalis for recurrent hydroceles
H Inguinal hernia (commonly present in congenital H Suprainguinal excision for testicular tumor detected
hydrocele) by ultrasound
H Size varying from slightly larger than the testes to the
size of a grapefruit or larger
H Fluid collection with either flaccid or tense mass Nursing considerations
H Pain with acute epididymal infection or testicular
torsion Key outcomes
H Scrotal tenderness due to severe swelling The patient (or his parents) will:
H express feeling or demonstrate behavior of comfort
Complications and relief from pain
H Epididymitis H express understanding of disorder, diagnosis, and
H Testicular atrophy treatment.
Nursing interventions
Assessment H Place a rolled towel between the patients legs and el-
evate the scrotum to help reduce severe swelling.
History H Apply heat or ice packs to the scrotum.
H Scrotal tenderness H Provide preoperative teaching.
H Inguinal hernia H Provide postoperative wound care, if appropriate.

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Monitoring
H Swelling
H Worsening of condition

Patient teaching
Be sure to cover:
H the need to wear a loose-fitting athletic supporter
lined with soft cotton dressings
H how to take a sitz bath
H the need to avoid tub baths postoperaively for 5 to
7 days
H the possibility that the hydrocele may reaccumulate
for 1 month postoperatively because of edema.
Discharge planning
H Follow-up visits may be required biweekly, monthly,
or every 2 to 3 months, depending on recovery rate.

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Common characteristics
Life-threatening disorder H Enlargement of head clearly disproportionate to
growth
Hydrocephalus H Distended scalp veins
H Thin, shiny, fragile-looking scalp skin
H Underdeveloped neck muscles
H Depressed orbital roof
Overview H Downward displacement of eyes
H High-pitched, shrill cry; irritability
Description H Projectile vomiting
H A variety of conditions characterized by an excess of H Skull widening
fluid within the cranial vault, subarachnoid space, or
both Complications
H Occurs because of interference with cerebrospinal H Mental retardation
fluid (CSF) flow caused by increased fluid produc- H Impaired motor function
tion, obstruction within the ventricular system, or de- H Vision loss
fective reabsorption of CSF H Death (increased intracranial pressure [ICP])
H Types include: H Infection and malnutrition (more common in
Noncommunicating hydrocephalus: obstruction infants)
within the ventricular system
Communicating hydrocephalus: impaired absorp-
tion of CSF Assessment
Pathophysiology History
H The obstruction of CSF flow associated with hydro- Infants
cephalus produces dilation of the ventricles proximal H History that may disclose cause
to the obstruction. H High-pitched, shrill cry; irritability
H The obstructed CSF is under pressure, causing atro- H Anorexia
phy of the cerebral cortex and degeneration of the H Episodes of projectile vomiting
white matter tracts, with selective preservation of Adults and older children
gray matter. H Frontal headaches
H When excess CSF fills a defect caused by atrophy, a H Nausea and vomiting (may be projectile)
degenerative disorder, or a surgical excision, the flu- H Symptoms causing wakening or occurring on awak-
id isnt under pressure, and atrophy and degenera- ening
tive changes arent induced. H Diplopia
H Restlessness
Causes
Noncommunicating hydrocephalus Physical findings
H Congenital abnormalities in the ventricular system Infants
H Mass lesions such as a tumor that compresses one of H Enlarged head clearly disproportionate to the infants
the structures of the ventricular system growth
H Aqueduct stenosis H Head possibly appearing normal in size with bulging
H Arnold-Chiari malformation fontanels
Communicating hydrocephalus H Distended scalp veins
H Adhesions from inflammation, such as with meningi- H Thin, fragile, and shiny scalp skin
tis or subarachnoid hemorrhage H Underdeveloped neck muscles
H Compression of the subarachnoid space by a mass H Depression of the roof of the eye orbit
such as a tumor H Displacement of the eyes downward
H Congenital abnormalities of the subarachnoid space H Prominent sclera (sunset sign)
H High venous pressure within the sagittal sinus H Abnormal leg muscle tone
H Head injury Adults and older children
H Cerebral atrophy H Decreased level of consciousness (LOC)
H Ataxia
Incidence H Impaired intellect
H Rare cases of congenital hydrocephalus H Incontinence
H Noncommunicating hydrocephalus more common in H Signs of increased ICP
children
H Communicating hydrocephalus more common in
adults

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Test results Monitoring

Imaging H Fontanels for tension or fullness
H Skull X-rays show thinning of the skull with separa- H Head circumference
tion of sutures and widening of the fontanels in in- H Signs and symptoms of increased ICP
fants. H Complications
H Angiography, computed tomography scan, and mag- H Growth and development
netic resonance imaging show differentiation be- H Neurologic status
tween hydrocephalus and intracranial lesions and H Intake and output
Arnold-Chiari deformity. After surgery
H Signs and symptoms of meningitis
H Redness, swelling, and other signs and symptoms of
Treatment local infection
H Dressing for drainage
General H Response to analgesics
H Shunting of CSF directly from the ventricular system
to some point beyond the obstruction ALERT
H Small, frequent feedings
H Slow feeding of infant Monitor the patient for vomiting, which may be an
H Decreased movement during and immediately after early sign of shunt malfunction.
meals
Medications Patient teaching
H Possible preoperative and postoperative antibiotics
Be sure to cover:
Surgery H the disorder, diagnosis, and treatment
H Surgical correction (the only treatment for hydro- H shunt surgery: hair loss and the visibility of a me-
cephalus): chanical device
Removal of obstruction to CSF flow H postoperative shunt care
Implantation of a ventriculoperitoneal shunt to di- H signs and symptoms of increased ICP or shunt mal-
vert CSF flow from the brains lateral ventricle into function
the peritoneal cavity H signs and symptoms of infection
With concurrent abdominal problem, ventriculo- H signs and symptoms of paralytic ileus
atrial shunt to divert CSF flow from the brains lat- H the need for periodic shunt surgery to lengthen the
eral ventricle into the right atrium of the heart shunt as the child grows older.
Discharge planning
Nursing considerations H Refer the patient to special education programs, as
appropriate.
Key outcomes
The patient will:
H maintain adequate ventilation
H develop no signs and symptoms of infection
H maintain and improve current LOC
H develop no signs and symptoms of increased ICP.

Nursing interventions
H Elevate the head of the bed to 30 degrees or put an
infant in an infant seat.
H Administer prescribed oxygen, as needed.
H Provide small, frequent feedings.
H Decrease the patients movement during and immedi-
ately after meals.
H Provide skin care.
After shunt surgery
H Place the patient on the side opposite the operative
site.
H Administer prescribed I.V. fluids.
H Administer prescribed analgesics.

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Hydronephrosis Assessment
History
Overview H Possibly no initial symptoms, but increasing pressure
behind the obstruction eventually resulting in renal
Description dysfunction
H Abnormal dilation of the renal pelvis and calyces of H Varies depending on cause of obstruction
one or both kidneys H No symptoms or complaint of only mild pain and
H Caused by obstruction of urine flow in the genitouri- slightly decreased urine flow
nary tract H Severe, colicky renal pain or dull flank pain that ra-
H May be acute or chronic diates to the groin
H Hematuria
Pathophysiology H Pyuria
H With obstruction in the urethra or bladder, hydro- H Dysuria
nephrosis is usually bilateral. H Alternating oliguria and polyuria, anuria
H With obstruction in a ureter, hydronephrosis is usu- H Nausea
ally unilateral. H Vomiting
H Obstructions distal to the bladder cause the bladder H Abdominal fullness
to dilate, acting as a buffer zone, delaying hydro- H Pain on urination
nephrosis. H Dribbling
H Total obstruction of urine flow with dilation of the H Urinary hesitancy
collecting system ultimately causes complete cortical H Change in voiding pattern
atrophy and glomerular filtration ceases.
Physical findings
Causes H Hematuria
H Benign prostatic hyperplasia (BPH) H Pyuria
H Urethral strictures H Urinary tract infection
H Renal calculi H Palpable kidney
H Strictures or stenosis of the ureter or bladder outlet H Lower extremity edema
H Congenital abnormalities H Distended bladder
H Bladder, ureteral, or pelvic tumors H Costovertebral angle tenderness
H Blood clots
H Neurogenic bladder Test results
H Ureterocele Laboratory
H Tuberculosis H Renal function study results are abnormal.
H Gram-negative infection H Urine studies confirm inability to concentrate urine,
glomerular filtration rate is decreased, and pyuria
Incidence occurs if infection is present.
H About 1 in 100 people affected by unilateral hydro- H Leukocytosis indicates infection.
nephrosis Imaging
H About 1 in 200 people affected by bilateral hydro- H Excretory urography, retrograde pyelography, and re-
nephrosis nal ultrasonography confirm diagnosis.
H I.V. urogram may show site of obstruction.
Common characteristics H Nephrogram may show delayed appearance time.
H Decreased urine output H Radionuclide scan may show site of obstruction.
H Flank pain H Computed tomography scan may indicate cause.

Complications
H Renal calculi Treatment
H Sepsis
H Renovascular hypertension General
H Obstructive nephropathy H For inoperable obstructions, decompression and
H Infection drainage of the kidney, using a nephrostomy tube
H Pyelonephritis placed temporarily or permanently in the renal pelvis
H Paralytic ileus H If renal function affected, low-protein, low-sodium,
H Renal failure and low-potassium diet
H Urinary catheterization

386 Hydronephrosis
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Medications
H Antibiotic therapy as appropriate for infecting
organism
H Analgesics
H Oral alkalinization therapy (for uric acid calculi)
such as allopurinol
H Steroid therapy (for retroperitoneal fibrosis)

Surgery
H Dilatation for urethral stricture
H Prostatectomy for BPH
H Placement of percutaneous nephrostomy tube

Nursing considerations
Key outcomes
The patient will:
H avoid or have minimized complications
H maintain fluid balance
H report increased comfort
H maintain hemodynamic stability
H demonstrate skill in managing urinary elimination.

Nursing interventions
H Administer prescribed drugs.
H Administer prescribed I.V. fluids.
H Allow the patient to express his fears and anxieties.

Monitoring
H Renal function studies
H Intake and output
H Vital signs
H Fluid and electrolyte status
H Nephrostomy tube function and drainage, if appro-
priate
H Wound site (postoperatively)

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the procedure and postoperative care, if surgery is
scheduled
H nephrostomy tube care, if appropriate
H medication administration, dosage, and possible ad-
verse effects
H dietary changes
H hydronephrosis symptom recognition and reporting.

Discharge planning
H Follow-up imaging studies may be required to evalu-
ate recovery.
H Follow-up laboratory studies may be needed to as-
sess renal function.

Hydronephrosis 387
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Hyperaldosteronism H Fatigue
H Headache
H Paresthesia
H Possibly tetany (resulting from metabolic alkalosis)
Overview
Complications
Description H Neuromuscular irritability, tetany, paresthesia
H Hypersecretion of the mineralocorticoid aldosterone H Seizures
by the adrenal cortex H Left ventricular hypertrophy, heart failure, death
H Causes excessive reabsorption of sodium and water H Metabolic alkalosis, nephropathy, azotemia
and excessive renal excretion of potassium
H May be primary (uncommon) or secondary
Assessment
Pathophysiology
In primary hyperaldosteronism History
(Conns syndrome) H Vision disturbances
H Chronic excessive secretion of aldosterone is inde- H Nocturnal polyuria
pendent of the renin-angiotensin system and sup- H Polydipsia
presses plasma renin activity. H Fatigue
H This aldosterone excess enhances sodium and water H Headaches
reabsorption and potassium loss by the kidneys,
which leads to mild hypernatremia and, simultane- Physical findings
ously, hypokalemia and increased extracellular fluid H Muscle weakness
volume. H Intermittent, flaccid paralysis
H Expansion of intravascular fluid volume also occurs H Paresthesia
and results in volume-dependent hypertension and H High blood pressure
increased cardiac output.
Test results
ALERT Laboratory
H Serum potassium levels are persistently low.
Excessive ingestion of English black licorice or H Plasma renin level is low and fails to increase appro-
licorice-like substances can produce a syndrome priately during volume depletion (upright posture,
similar to primary hyperaldosteronism because of sodium depletion) and plasma aldosterone level is
the mineralocorticoid action of glycyrrhizic acid. high during volume expansion by salt loading (con-
firm primary hyperaldosteronism in a hypertensive
In secondary hyperaldosteronism patient without edema).
H Secondary hyperaldosteronism results from an extra- H Serum bicarbonate level is elevated.
adrenal abnormality that stimulates the adrenal gland H Urine aldosterone levels are markedly increased.
to increase aldosterone production. H Plasma aldosterone levels are increased.
H Plasma renin levels are increased (secondary).
Causes H Suppression test differentiates between primary and
H Benign aldosterone-producing adrenal adenoma (in secondary hyperaldosteronism.
70% of patients) Imaging
H Bilateral adrenocortical hyperplasia (in children) or H Chest X-rays show left ventricular hypertrophy caused
carcinoma (rarely) by chronic hypertension.
H Conditions that reduce renal blood flow and extracel- H Adrenal angiography or computed tomography scan
lular fluid volume (renal artery stenosis) localizes tumor.
H Conditions that produce a sodium deficit (Wilms Diagnostic procedures
tumor) H Electrocardiography shows signs of hypokalemia
H Nephrotic syndrome (ST-segment depression and U waves).
H Bartters syndrome
H Hepatic cirrhosis with ascites
H Heart failure Treatment
Incidence General
H Three times more common in females than in males H Treatment of underlying cause (secondary)
H Most common between ages 30 and 50 H Low-sodium, high-potassium diet

Common characteristics
H Muscle weakness
H Intermittent, flaccid paralysis

388 Hyperaldosteronism
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Medications
H Potassium-sparing diuretics (primary) such as
spironolactone
Surgery
H Unilateral adrenalectomy (primary)

Nursing considerations
Key outcomes
The patient will:
H maintain hemodynamic stability
H express feelings of increased comfort
H maintain adequate fluid balance
H express understanding of the condition and treat-
ment modalities.
Nursing interventions
H Watch for signs of tetany (muscle twitching,
Chvosteks sign, Trousseaus sign).
H Administer potassium replacement, and keep I.V. cal-
cium gluconate available.
H After adrenalectomy, watch for weakness, hypona-
tremia, rising serum potassium levels, and signs of
adrenal hypofunction, especially hypotension.
Monitoring
H Intake and output
H Vital signs
H Weight
H Serum electrolyte levels
H Cardiac arrhythmias

Patient teaching
Be sure to cover:
H adverse effects of spironolactone, including hyper-
kalemia, impotence, and gynecomastia, if appropri-
ate
H the importance of wearing medical identification
jewelry while taking steroid hormone replacement
therapy.

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Hyperbilirubinemia, H Heme fragments form unconjugated (indirect)

unconjugated
Overview
Description
H Excessive serum bilirubin levels and mild jaundice
H The result of hemolytic processes in the neonate
H Can be physiologic (with jaundice the only symptom)
or pathologic (resulting from an underlying disease)
H Also called neonatal jaundice
Pathophysiology
H As erythrocytes break down at the end of their neo-
natal life cycle, hemoglobin separates into globin
(protein) and heme (iron) fragments.
Causes of hyperbilirubinemia
The infants age at onset of hyperbilirubinemia may pro-
vide clues as to the sources of this jaundice-causing dis-
order.
Day 1
H Blood type incompatibility (Rh, ABO, other minor blood
groups)
H Intrauterine infection (rubella, cytomegalic inclusion
body disease, toxoplasmosis, syphilis and, occasion-
ally, bacteria such as Escherichia coli, Staphylococcus,
Pseudomonas, Klebsiella, Proteus, and Streptococcus)
Day 2 or 3
H Infection (usually from gram-negative bacteria)
H Polycythemia
H Enclosed hemorrhage (skin bruises, subdural
hematoma)
H Respiratory distress syndrome (hyaline membrane dis-
ease)
H Heinz body anemia from drugs and toxins (vitamin K3,
sodium nitrate)
H Transient neonatal hyperbilirubinemia
H Abnormal red blood cell morphology
H Red cell enzyme deficiencies (glucose-6-phosphate
dehydrogenase, hexokinase)
H Physiologic jaundice
H Blood group incompatibilities
Days 4 and 5
H Breast-feeding, respiratory distress syndrome, mater-
nal diabetes
H Crigler-Najjar syndrome (congenital nonhemolytic
icterus)
H Gilbert syndrome
Day 7 and later
H Herpes simplex
H Pyloric stenosis
H Hypothyroidism
H Neonatal giant cell hepatitis
H Infection (usually acquired in neonatal period)
H Bile duct atresia
H Galactosemia
H Choledochal cysts.
bilirubin, which binds with albumin for transport to
liver cells to conjugate with glucuronide, forming di-
rect bilirubin.
H Because unconjugated bilirubin is fat-soluble and
cant be excreted in the urine or bile, it may escape
to extravascular tissue, especially fatty tissue and the
brain, resulting in hyperbilirubinemia.
H Hyperbilirubinemia may develop when:
certain factors disrupt conjugation and usurp
albumin-binding sites, including drugs (such as
aspirin, tranquilizers, and sulfonamides) and
conditions (such as hypothermia, anoxia, hypo-
glycemia, and hypoalbuminemia)
decreased hepatic function results in reduced
bilirubin conjugation
increased erythrocyte production or breakdown
results from hemolytic disorders or Rh or ABO in-
compatibility
biliary obstruction or hepatitis results in blockage
of normal bile flow
maternal enzymes present in breast milk inhibit
the infants glucuronyl-transferase conjugating
activity.
Causes
See Causes of hyperbilirubinemia.
Incidence
H Common in neonates
H More common in males than females
H Less common in Black infants than in White infants
Common characteristics
H Jaundice
Complications
H Kernicterus
H Cerebral palsy
H Epilepsy
H Mental retardation
Assessment
History
H Previous sibling with neonatal jaundice
H Familial history of anemia, bile stones, splenectomy,
liver disease
H Maternal illness suggestive of viral or other infection
H Maternal drug intake
H Delayed cord clamping
H Birth trauma with bruising
Physical findings
H Yellowish skin, particularly in the sclerae
Test results
Laboratory
H Serum bilirubin levels are elevated.

390 Hyperbilirubinemia, unconjugated

9400H.qxd 8/2/12 4:35 PM Page 391

Treatment
General
H Phototherapy
H Exchange transfusions

Medications
H Albumin
H Phenobarbital (rarely used)
H Rh (D) immune globulin (human) (to Rh-negative
o
mother)

Nursing considerations
Key outcomes
The patient will:
H exhibit normal body temperature
H maintain normal fluid balance
H maintain skin integrity
H have a reduced bilirubin level.

Nursing interventions
H Reassure parents that most infants experience some
degree of jaundice.
H Keep emergency equipment available when transfus-
ing blood.
H Administer Rh
o(D) immune globulin (human), to an
Rh-negative mother after amniocentesis, or to
prevent hemolytic disease in subsequent infants to
an Rh-negative mother during the third trimester, af-
ter the birth of an Rh-positive infant, or after sponta-
neous or elective abortion.
Monitoring
H Jaundice
H Bilirubin levels
H Body temperature
H Intake and output
H Bleeding and complications

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H that the infants stool contains some bile and may be
greenish.

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Hypercalcemia H Anorexia
H Constipation
H Nausea, vomiting
H Polyuria
Overview
Physical findings
Description H Confusion
H Excessive levels of serum calcium H Muscle weakness
H Hyporeflexia
Pathophysiology H Decreased muscle tone
H Together with phosphorus, calcium is responsible for
the formation and structure of bones and teeth. Test results
H Calcium helps to maintain cell structure and func- Laboratory
tion. H Serum calcium levels are greater than 10.5 mg/dl.
H It plays a role in cell membrane permeability and im- H Ionized calcium levels are greater than 5.8 mg/dl.
pulse transmission. H Albumin level is elevated.
H It affects the contraction of cardiac muscle, smooth Diagnostic procedures
muscle, and skeletal muscle. H Electrocardiography shows shortened QT interval
H It participates in the blood-clotting process. and ventricular arrhythmias.
H Hypercalcemia leads to multiple-organ system dys-
function.
Treatment
Causes
H Hyperparathyroidism General
H Hypervitaminosis D H Treatment of the underlying cause
H Certain cancers H Activity, as tolerated
H Multiple fractures and prolonged immobilization H Hemodialysis with kidney failure
H Certain drugs (see Drugs causing hypercalcemia)
Medications
Incidence H Normal saline solution
H Considerably higher in females than in males H Loop diuretics, such as furosemide, bumetamide,
H No gender predominance in elevated calcium levels and torsemide
related to cancer H Corticosteroids to counter effects of excess vitamin D
H Increases with age

Common characteristics Nursing considerations

See Clinical effects of hypercalcemia.
Key outcomes
Complications The patient will:
H Renal calculi H maintain stable vital signs
H Coma H maintain adequate cardiac output
H Cardiac arrest H express an understanding of the disorder and treat-
ment regimen.
Assessment
Clinical effects of hypercalcemia
History
Dysfunction Effects
H Underlying cause
H Lethargy Cardiovascular Signs of heart block, cardiac ar-
rest, hypertension
H Weakness
Gastrointestinal Anorexia, nausea, vomiting, con-
stipation, dehydration, polydipsia
Drugs causing hypercalcemia
Musculoskeletal Weakness, muscle flaccidity, bone
These drugs can cause or contribute to hypercalcemia: pain, pathologic fractures
H antacids that contain calcium
H calcium preparations (oral or I.V.) Neurologic Drowsiness, lethargy, headaches,
H lithium depression or apathy, irritability,
confusion
H thiazide diuretics
H vitamin A Other Renal polyuria, flank pain and,
H vitamin D. eventually, azotemia

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Nursing interventions
H Provide safety measures and institute seizure precau-
tions, if appropriate.
H Administer prescribed I.V. fluids.
H Watch for signs of heart failure.

Monitoring
H Cardiac rhythm
H Seizures
H Calcium levels

Patient teaching
Be sure to cover:
H avoiding nonprescription drugs high in calcium
H increasing fluid intake
H following a low-calcium diet.

Discharge planning
H Refer the patient to a dietitian and social services, if
indicated.

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Complications
Hyperchloremia H Metabolic acidosis
H Hypervolemia
H Coma
Overview
Description Assessment
H Excessive serum levels of the chloride anion
H Usually accompanied by sodium and water retention History
H Risk factors for high chloride level
Pathophysiology H Altered level of consciousness
H Chloride accounts for two-thirds of all serum anions.
H Chloride is secreted by stomach mucosa as hydro- Physical findings
chloric acid; it provides an acid medium that aids di- H Agitation
gestion and activation of enzymes. H Pitting edema
H Chloride helps maintain acid-base and body water H Dyspnea
balances, influences the osmolality or tonicity of ex- H Rapid deep breathng (Kussmauls respirations)
tracellular fluid, plays a role in the exchange of oxy- H Weakness
gen and carbon dioxide in red blood cells, and helps H Tachypnea
activate salivary amylase (which, in turn, activates the H Hypertension
digestive process).
H An inverse relationship exists between chloride and Test results
bicarbonate. When the level of one goes up, the level H Serum chloride level is greater than 108 mEq/L.
of the other goes down. (See Anion gap and meta- H With metabolic acidosis, serum pH is less than
bolic acidosis.) 7.35 and serum carbon dioxide level is less than
H Chloride imbalanace can lead to metabolic acidosis 22 mEq/L and anion gap is normal.
and altered fluid balance if left untreated. H Serum sodium level is greater than 145 mEq/L.

Causes
H Hyperparathyroidism Treatment
H Renal tubular acidosis
H Metabolic acidosis General
H Hypernatremia H Treatment of underlying cause
H Prolonged diarrhea H Activity, as tolerated
H Loss of pancreatic secretion H Restoring fluid, electrolyte, and acid base balance
H Certain drugs (see Drugs causing hyperchloremia) H Restricted sodium and chloride intake

Incidence Medications
H Associated with other acid-base disorders and rarely H Sodium bicarbonate I.V.
occurs alone. H Lactated Ringers solution
H Diuretics, such as furosemide, bumetanide, and
Common characteristics hydrochlorothiazide
H Agitation, tachycardia, hypertension, pitting edema,
dyspnea
H Deep, rapid breathing; weakness; diminished cogni- Nursing considerations
tive ability; and, ultimately, coma (if in metabolic aci-
dosis) Key outcomes
The patient will:
H maintain adequate cardiac output
Anion gap and metabolic acidosis H maintain stable vital signs

Hyperchloremia increases the likelihood that a patient will

develop hyperchloremic metabolic acidosis. Drugs causing hyperchloremia
How it happens
If a patient with metabolic acidosis has a normal anion These drugs can cause or contribute to hyperchloremia:
gap, the acidosis is probably caused by a loss of bicar- H acetazolamide
bonate ions by the kidneys or the GI tract. In such cases, H ammonium chloride
a corresponding increase in chloride ions also occurs. H phenylbutazone
Acidosis can also result from an accumulation of chlo- H sodium polystyrene sulfonate (Kayexalate)
ride ions in the form of acidifying salts. A corresponding H salicylates (overdose)
decrease in bicarbonate ions occurs at the same time. H triamterene.

394 Hyperchloremia
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H maintain adequate fluid volume

H avoid complications.

Nursing interventions
H Provide a safe environment.
H Administer prescribed I.V. fluids.
H Evaluate muscle strength and adjust activity level.
H Reorient the confused patient when necessary.

Monitoring
H Serum electrolyte levels
H Respiratory status
H Signs of metabolic alkalosis
H Intake and output
H Neurologic status
H Cardiac rhythm
H Arterial blood gas values

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H dietary or fluid restrictions, as indicated
H medication administration, dosage, and possible ad-
verse effects.

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Complications
Life-threatening disorder H Cardiac arrhythmia
H Metabolic acidosis

Hyperkalemia H Cardiac arrest

Assessment
Overview
History
Description H Irritability
H Excessive serum levels of the potassium anion H Paresthesia
H Commonly induced by other treatments H Muscle weakness
H Nausea
Pathophysiology H Abdominal cramps
H Potassium facilitates contraction of both skeletal and H Diarrhea
smooth muscles, including myocardial contraction.
H Potassium figures prominently in nerve impulse con- Physical findings
duction, acid-base balance, enzyme action, and cell H Hypotension
membrane function. H Irregular heart rate
H Slight deviation in serum levels can produce pro- H Cardiac arrhythmia (possible)
found clinical consequences.
H Potassium imbalance can lead to muscle weakness Test results
and flaccid paralysis due to an ionic imbalance in Laboratory
neuromuscular tissue excitability. H Serum potassium levels are greater than 5 mEq/L.
H Arterial pH is decreased.
Causes Diagnostic procedures
H Renal dysfunction or failure H Electrocardiography shows a tall, tented T wave.
H Use of potassium-sparing diuretics such as triam-
terene by patients with renal disease
H Burns Treatment
H Crushing injuries
H Adrenal gland insufficiency General
H Dehydration H Treatment of the underlying cause
H Diabetic acidosis H Hemodialysis or peritoneal dialysis
H Increased intake of potassium H Activity, as tolerated
H Decreased urinary excretion of potassium
H Severe infection
H Large quantities of blood transfusions
H Certain drugs (see Drugs causing hyperkalemia)

Incidence Clinical effects of hyperkalemia

H Affects males and females equally
H Diagnosed in up to 8% of hospitalized patients in the Dysfunction Effects
United States Acid-base Metabolic acidosis
balance
Common characteristics
See Clinical effects of hyperkalemia. Cardiovascular Tachycardia and later bradycardia,
electrocardiogram changes (tented
and elevated T waves, widened
QRS complex, prolonged PR inter-
val, flattened or absent P waves,
depressed ST segment), cardiac
Drugs causing hyperkalemia arrest (with levels > 7 mEq/L)

These drugs may increase potassium levels:

Gastrointestinal Nausea, diarrhea, abdominal
cramps
H angiotensin-converting enzyme inhibitors
H antibiotics Genitourinary Oliguria, anuria
H beta-adrenergic blockers
H chemotherapeutic drugs Musculoskeletal Muscle weakness, flaccid paralysis
H nonsteroidal anti-inflammatory drugs
H potassium (in excessive amounts) Neurologic Hyperreflexia progressing to weak-
ness, numbness, tingling, flaccid
H spironolactone. paralysis

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Avoiding false results

When a patient receives a laboratory test result indicating
a high potassium level, and the result doesnt make sense,
make sure its a true result. If the sample was drawn using
poor technique, the results may be falsely high. These are
some of the causes of falsely high potassium levels:
H drawing the sample above an I.V. infusion containing
potassium
H using a recently exercised arm or leg for the venipunc-
ture site
H causing hemolysis (cell damage) as the sample is
obtained.

Medications
H Rapid infusion of 10% calcium gluconate (decreases
myocardial irritability)
H Insulin and 10% to 50% glucose I.V.
H Sodium polystyrene sulfonate with 70% sorbitol

Nursing considerations
Key outcomes
The patient will:
H maintain hemodynamic stability
H maintain a normal potassium level
H understand potential adverse effects of prescribed
drugs.
Nursing interventions
H Check the serum sample. (See Avoiding false
results.)
H Administer prescribed drugs.
H Insert an indwelling urinary catheter.
H Implement safety measures.
H Be alert for signs of hypokalemia after treatment.

Monitoring
H Serum potassium levels
H Cardiac rhythm
H Intake and output

Patient teaching
Be sure to cover:
H prescribed medications and possible adverse effects
H monitoring intake and output
H preventing future episodes of hyperkalemia
H need for potassium-restricted diet.

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Hyperlipoproteinemia Assessment
History
Overview Type I
H Recurrent attacks of severe abdominal pain
Description H Abdominal pain usually preceded by fat intake
H Increased plasma concentrations of one or more H Malaise and anorexia
lipoproteins Type II
H Primary form: at least five distinct and inherited H History of premature and accelerated coronary
metabolic disorders atherosclerosis
H May occur secondary to other conditions such as di- H Symptoms that typically develop in 20s or 30s
abetes mellitus Type III
H Clinical changes ranging from relatively mild symp- H No clinical symptoms until after age 20
toms, managed by diet, to potentially fatal pancre- H Aggravating factors, such as obesity, hypothyroidism,
atitis and diabetes mellitus
Type IV
Pathophysiology H Atherosclerosis
H Low-density lipoprotein (LDL) level is increased and H Early CAD
high-density lipoprotein (HDL) level is decreased. H Excessive alcohol consumption
H Development of atherosclerosis is accelerated. H Poorly controlled diabetes mellitus
H Birth control pills containing estrogen (can precipi-
Causes tate severe hypertriglyceridemia)
H Primary hyperlipoproteinemia H Hypertension
Types I and III transmitted as autosomal recessive H Hyperuricemia
traits Type V
Types II, IV, and V transmitted as autosomal domi- H Abdominal pain associated with pancreatitis
nant traits H Complaints related to peripheral neuropathy
H Secondary hyperlipoproteinemia
Diabetes mellitus Physical findings
Pancreatitis Type I
Hypothyroidism H Papular or eruptive xanthomas over pressure points
Renal disease and extensor surfaces
H Ophthalmoscopic examination: lipemia retinalis
Incidence (reddish white retinal vessels)
Type I H Abdominal spasm, rigidity, or rebound tenderness
H Relatively rare; present at birth H Hepatosplenomegaly, with liver or spleen tenderness
Type II H Fever possibly present
H Onset between ages 10 and 30 Type II
Type III H Tendinous xanthomas on the Achilles tendons and
H Uncommon; usually occurring after age 20 tendons of the hands and feet
Type IV H Tuberous xanthomas, xanthelasma
H Relatively common, especially in middle-aged males H Juvenile corneal arcus
Type V Type III
H Uncommon; usually occurring in late adolescence or H Tuberoeruptive xanthomas over elbows and knees
early adulthood H Palmar xanthomas on the hands, particularly the fin-
gertips
Common characteristics Type IV
H Increased plasma concentrations of one or more H Obesity
lipoproteins H Xanthomas possibly noted during exacerbations
Type V
Complications H Eruptive xanthomas on extensor surface of arms and
H Coronary artery disease (CAD) legs
H Pancreatitis H Ophthalmoscopic examination: lipemia retinalis
H Hepatosplenomegaly

Test results
Laboratory
H Serum lipid profiles show elevated levels of total cho-
lesterol, triglycerides, very low-density lipoproteins,
LDLs, or HDLs.

398 Hyperlipoproteinemia
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Treatment Nursing considerations

General
H Weight reduction
H Elimination or treatment of aggravating factors, such
as diabetes mellitus, alcoholism, and hypothyroidism
H Reduction of risk factors for atherosclerosis
H Smoking cessation
H Treatment of hypertension
H Avoidance of hormonal and estrogen-containing
contraceptive drugs
H Restriction of cholesterol and saturated animal fat
intake
H Avoidance of alcoholic beverages to decrease plasma
triglyceride levels
H Inclusion of polyunsaturated vegetable oils (reduces
plasma LDLs)
H Maintenance of exercise and physical fitness pro-
gram
Type I
H Restricted fat intake (less than 20 g/day); 20- to
40-g/day, medium-chain triglyceride diet to supple-
ment calorie intake
Type II
H Restriction of cholesterol intake to less than 300 mg/
day for adults and less than 150 mg/day for children;
restricted triglyceride intake (to less than 100 mg/
day for children and adults); and diet high in polyun-
saturated fats
Type III
H Restricted cholesterol intake (to less than 300 mg/
day) and carbohydrates; increased polyunsaturated
fats
Type IV
H Restricted cholesterol intake; increased polyunsatu-
rated fats
Type V
H Long-term maintenance of a low-fat diet; 20- to 40-g/
day medium-chain triglyceride diet
Medications
H Statins, such as rosuvastatin, atorvastatin, and sim-
vastatin
H Nicotinic acid (niacin)
H Bile acid resins, such as cholestyramine-sucrose and
colestipol
H Fibrates, such as gemfibrozil and fenofibrate
Surgery
H If unable to tolerate drug therapy, surgical creation
of an ileal bypass
H For severely affected homozygote children, portacav-
al shunt as a last resort to reduce plasma cholesterol
levels
Key outcomes
The patient will:
H develop no complications
H maintain stable vital signs
H verbalize understanding of the disorder and treat-
ment regimen.
Nursing interventions
H Administer prescribed antilipemics.
H Prevent or minimize adverse reactions.
H Urge the patient to adhere to the prescribed diet.
H Assist the patient with additional lifestyle changes.
H Encourage verbalization of fears related to premature
CAD.
Monitoring
H Vital signs
H Adverse reactions
H Serum lipoproteins
H Response to treatment
H Signs and symptoms related to CAD or its sequelae
Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the need to maintain a steady weight and strictly ad-
here to the prescribed diet (for the 2 weeks preced-
ing serum cholesterol and serum triglyceride tests),
and to fast for 12 hours before the test
H the need to avoid excessive sugar intake and alco-
holic beverages
H minimized intake of saturated fats (higher in meats
and coconut oil)
H increased intake of polyunsaturated fats (vegetable
oils)
H avoidance of hormonal contraceptives or drugs that
contain estrogen
H foods high in cholesterol and saturated fats
H the prescribed medication regimen and possible
adverse effects
H signs and symptoms requiring medical evaluation.
Discharge planning
H Refer the patient for a medically supervised exercise
program.
H Refer the patient to a smoking-cessation program, if
indicated.
H Refer the patient to a dietitian, if necessary.

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Incidence
Hypermagnesemia H Rarely occurs in the United States

Common characteristics
Overview See Clinical effects of hypermagnesemia.
Description Complications
H Excessive serum levels of the magnesium cation H Respiratory depression
H Cardiac arrhythmia
Pathophysiology H Cardiac arrest
H Magnesium enhances neuromuscular integration and
stimulates parathyroid hormone secretion, thus regu-
lating intracellular fluid calcium levels. Assessment
H Magnesium may also regulate skeletal muscles
through its influence on calcium utilization by de- History
pressing acetylcholine release at synaptic junctions. H Nausea
H Magnesium activates many enzymes for proper car- H Vomiting
bohydrate and protein metabolism, aids in cell me- H Drowsiness
tabolism and the transport of sodium and potassium H Confusion
across cell membranes, and influences sodium,
potassium, calcium, and protein levels. Physical findings
H About one-third of magnesium taken into the body is H Flushed appearance
absorbed through the small intestine and is eventual- H Hypotension
ly excreted in the urine; remaining unabsorbed mag- H Weak pulse
nesium is excreted in the stool. H Muscle weakness
H Hyporeflexia (see Testing the patellar reflex)
Causes
H Chronic renal insufficiency Test results
H Use of magnesium-containing laxatives, especially Laboratory
with renal insufficiency (see Drugs and supplements H Serum magnesium levels are greater than 2.5 mEq/L.
causing hypermagnesemia) Diagnostic procedures
H Overuse of magnesium-containing antacids H Electrocardiography shows prolonged PR interval,
H Severe dehydration (resulting oliguria can cause widened QRS complex, and tall T waves.
magnesium retention)
H Overcorrection of hypomagnesemia
H Addisons disease Treatment
H Adrenocortical insufficiency
H Untreated diabetic ketoacidosis General
H Identification and correction of the underlying cause
Risk factors H Increased fluid intake
H Advanced age H Peritoneal dialysis or hemodialysis
H Pregnancy
H Neonates whose mothers received magnesium sulfate Medications
during labor H Loop diuretics, such as furosemide, with impaired
H Patients receiving magnesium sulfate to control renal function
seizures H Calcium gluconate (10%)

Clinical effects of hypermagnesemia

Drugs and supplements causing
hypermagnesemia
Monitor your patients magnesium level closely if hes
receiving:
H an antacid (Di-Gel, Gaviscon, Maalox)
H a laxative (milk of magnesia, Haleys M-O, magnesium
citrate)
H a magnesium supplement (magnesium oxide, magne-
sium sulfate).
Dysfunction Effects
Cardiovascular Bradycardia, weak pulse, hypoten-
sion, heart block, cardiac arrest
Neurologic Drowsiness, flushing, lethargy,
confusion, diminished sensorium
Neuromuscular Diminished reflexes, muscle weak-
ness, flaccid paralysis, respiratory
muscle paralysis that may cause
respiratory embarrassment

400 Hypermagnesemia
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Testing the patellar reflex

One way to gauge your pa- Sitting Supine position
tients magnesium status is to Have the patient sit on the side of the Flex the patients knee at a 45-degree angle, and
test his patellar reflex, one of bed with his legs dangling freely, as place your nondominant hand behind it for support
the deep tendon reflexes that shown below. Then test the reflex. (as shown below). Then test the reflex.
the magnesium level affects.
To test the reflex, strike the
patellar tendon just below
the patella with the patient
sitting or lying in a supine
position, as shown. Look for
leg extension or contraction
of the quadriceps muscle in
the front of the thigh.
If the patellar reflex is ab-
sent, notify the physician
immediately. This finding
may mean the patients mag-
nesium level is 7 mEq/L or
higher.

Nursing considerations Patient teaching

Key outcomes Be sure to cover:
The patient will: H avoidance of abusing laxatives and antacids contain-
H maintain hemodynamic stability ing magnesium, particularly in elderly patients or
H attain and maintain a normal magnesium level those patients with compromised renal function
H understand the causes of high magnesium levels H hydration requirements
H have a normal electrocardiogram. H medication administration, dosage, and possible ad-
verse effects.
Nursing interventions
H Provide sufficient fluids for adequate hydration and
maintenance of renal function.
H Administer prescribed drugs.
H Report abnormal serum electrolyte levels imme-
diately.
H Watch patients receiving a cardiac glycoside and
calcium gluconate simultaneously because calcium
excess enhances the cardiac glycoside.
Monitoring
H Vital signs
H Magnesium levels
H Electrolyte levels
H Intake and output
H Cardiac rhythm
H Neuromuscular system
H Level of consciousness
H Respiratory status

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Incidence
Hypernatremia H Occurs in about 1% of hospitalized patients (usually
elderly patients)
H Affects males and females equally
Overview
Common characteristics
Description H Pulmonary edema
H Excessive serum levels of the sodium cation relative H Circulatory disorders
to body water H Decreased level of consciousness (see Clinical
effects of hypernatremia)
Pathophysiology
H Sodium is the major cation (90%) in extracellular Complications
fluid; potassium, the major cation in intracellular H Seizures
fluid. H Coma
H During repolarization, the sodium-potassium pump H Permanent neurologic damage
continually shifts sodium into the cells and potassium
out of the cells; during depolarization, it does the re-
verse. Assessment
H Sodium cation functions include maintaining tonicity
and concentration of extracellular fluid, acid-base History
balance (reabsorption of sodium ion and excretion H Fatigue
of hydrogen ion), nerve conduction and neuromus- H Restlessness, agitation
cular function, glandular secretion, and water bal- H Weakness
ance. H Disorientation
H Increased sodium causes high serum osmolality (in- H Lethargy
creased solute concentrations in the body), which
stimulates the hypothalmus and intiates the sensation Physical findings
of thirst. H Flushed skin
H Dry, swollen tongue
Causes H Sticky mucous membranes
H Decreased water intake H Low-grade fever
H Excess adrenocortical hormones, as in Cushings syn- H Twitching
drome H Hypertension, dyspnea (with hypervolemia)
H Antidiuretic hormone deficiency (diabetes insipidus) H Orthostatic hypotension and oliguria (with hypo-
H Salt intoxication (less common), which may be pro- volemia)
duced by excessive table salt ingestion
H Excessive I.V. administration of sodium solutions Test results
H Certain drugs (see Drugs causing hypernatremia) Laboratory
H Serum sodium level is greater than 145 mEq/L.
Risk factors H Urine sodium level is less than 40 mEq/24 hours,
H People unable to drink voluntarily with high serum osmolality.

Clinical effects of hypernatremia

Dysfunction Effects
Cardiovascular Hypertension, tachycardia, pitting
edema, excessive weight gain
Drugs causing hypernatremia Cutaneous Flushed skin; dry, sticky mem-
branes
Ask the patient if hes taking any of these drugs that can
elevate his sodium level: Gastrointestinal Rough, dry tongue; intense thirst
H antacids with sodium bicarbonate
H antibiotics such as ticarcillin disodium-clavulanate Genitourinary Oliguria
potassium (Timentin) Neurologic Fever, agitation, restlessness,
H salt tablets seizures
H sodium bicarbonate injections (such as those given
during cardiac arrest) Respiratory Dyspnea, respiratory arrest, death
H I.V. sodium chloride preparations (from dramatic rise in osmotic
H sodium polystyrene sulfonate (Kayexalate). pressure)

402 Hypernatremia
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Treatment
General
H Treatment of underlying cause
H Administration of sodium-free solutions (such as
dextrose in water) followed by infusion of half-
normal saline solution to prevent hyponatremia
H Discontinuation of drugs that promote sodium
retention
H Sodium-restricted diet
H Activity, as tolerated

Nursing considerations
Key outcomes
The patient will:
H maintain adequate fluid volume
H maintain a normal sodium level
H maintain stable vital signs
H remain alert and oriented to his environment.

Nursing interventions
H Obtain a drug history to check for drugs that pro-
mote sodium retention.
H Assist with oral hygiene.
H Observe for signs of cerebral edema during fluid
replacement therapy.
Monitoring
H Serum sodium levels
H Intake and output
H Neurologic status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the importance of sodium restriction
H low-sodium diet
H prescribed drugs
H signs and symptoms of hypernatremia
H avoiding over-the-counter medications that contain
sodium.

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Hyperparathyroidism H Vascular damage

H Heart failure
H Muscle atrophy
H Depression
Overview
Description Assessment
H Characterized by a greater than normal secretion of
parathyroid hormone (PTH) History
H Classified as either primary or secondary H Recurring nephrolithiasis
H Polyuria
Pathophysiology H Hematuria
H In primary hyperparathyroidism, one or more of the H Chronic lower back pain
parathyroid glands enlarges, increasing PTH secre- H Easy fracturing
tion and elevating serum calcium levels or an adeno- H Osteoporosis
ma secretes PTH, unresponsive to negative feedback H Constant, severe epigastric pain that radiates to the
of serum calcium. back
H In secondary hyperparathyroidism, excessive com- H Abdominal pain
pensatory production of PTH stems from a hypocal- H Anorexia, nausea, and vomiting
cemia-producing abnormality outside the parathy- H Constipation
roid gland, which isnt responsive to PTH such as H Polydipsia
decreased intestinal absorption of calcium or vita- H Muscle weakness, particularly in the legs
min D. H Lethargy
H Increased PTH levels act directly on the bone and the H Personality disturbances
kidney tubules, resulting in an increase in extracellu- H Depression
lar calcium. H Overt psychosis
H Renal excretion and uptake into the soft tissues or H Cataracts
skeleton cant compensate for increased calcium. H Anemia
Causes
H Adenoma Physical findings
H Genetic disorders H Muscle weakness and atrophy
H Multiple endocrine neoplasia H Psychomotor disturbances
H Dietary vitamin D or calcium deficiency H Stupor and, possibly, coma
H Decreased intestinal absorption of vitamin D or H Skin necrosis
calcium H Subcutaneous calcification
H Chronic renal failure
H Osteomalacia Test results
H Ingestion of drugs such as phenytoin Laboratory
H Laxative ingestion IN PRIMARY DISEASE
H Idiopathic H Alkaline phosphatase level is increased.
H Osteocalcin level is increased.
Incidence H Tartrate-resistant acid phosphatase level is increased.
H More common in females than in males H Serum PTH level is increased.
H Increased incidence in postmenopausal females H Serum phosphorus level is decreased.
H Onset usually between ages 35 and 65 H Urine and serum calcium and serum chloride levels
are increased.
Common characteristics H Creatinine levels may be increased.
H Bone pain and tenderness H Basal acid secretion may be increased.
H Renal calculi H Serum amylase may be increased.
H Abdominal distress IN SECONDARY DISEASE
H Anxiety and depression H Serum calcium level is normal or slightly decreased.
H Serum phosphorus level is variable.
Complications H Serum PTH level is increased.
H Osteoporosis Imaging
H Subchondral fractures H X-rays show diffuse bone demineralization, bone
H Traumatic synovitis cysts, outer cortical bone absorption, and subperi-
H Renal calculi and colic osteal erosion of the phalanges and distal clavicles in
H Renal insufficiency and failure primary disease.
H Peptic ulcers H X-ray spectrophotometry shows increased bone
H Cholelithiasis turnover in primary disease.
H Cardiac arrhythmias

404 Hyperparathyroidism
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H Esophagography, thyroid scan, parathyroid thermog- H Help the patient develop effective coping strategies.
raphy, ultrasonography, thyroid angiography, com- After parathyroidectomy
puted tomography scan, and magnetic resonance H Keep a tracheotomy tray and endotracheal tube setup
imaging may show location of parathyroid lesions. at the bedside.
H Maintain seizure precautions.
H Place the patient in semi-Fowlers position.
Treatment H Support the patients head and neck with sandbags.
H Have the patient ambulate as soon as possible.
General
H In primary disease, treatment to decrease calcium ALERT
levels
H In renal failure, dialysis Watch for complaints of tingling in the hands and
H In secondary disease, treatment to correct underlying around the mouth. If these symptoms dont subside
cause of parathyroid hypertrophy quickly, they may be prodromal signs of tetany, so
H Increased oral fluid intake keep I.V. calcium gluconate or calcium chloride
H Activity, as tolerated available for emergency administration.
Medications
Primary disease Monitoring
H Bisphosphonates H Vital signs
H Oral sodium or potassium phosphate H Intake and output
H Calcitonin H Serum calcium levels
H Plicamycin, if primary disease is metastatic H Respiratory status
Secondary disease H Cardiovascular status
H Vitamin D therapy After parathyroidectomy
H Aluminum hydroxide H Increased neuromuscular irritability
H Glucocorticoids H Complications
Postoperatively H Neck edema
H I.V. magnesium and phosphate H Chvosteks sign
H Sodium phosphate H Trousseaus sign
H Supplemental calcium
H Vitamin D or calcitriol
Patient teaching
Surgery
H With primary hyperparathyroidism, removal of ade- Be sure to cover:
noma or all but one-half of one gland H the disorder, diagnosis, and treatment
H prescribed medications and possible adverse effects
H when to notify the physician
Nursing considerations H the signs and symptoms of tetany, respiratory dis-
tress, and renal dysfunction
Key outcomes H the need for periodic blood tests
The patient will: H avoidance of calcium-containing antacids and thi-
H maintain current weight azide diuretics
H express feelings of increased comfort H the need to wear medical identification jewelry.
H maintain adequate cardiac output
H maintain balanced fluid volume status
H perform activities of daily living without excessive
fatigue
H express positive feelings about self.

Nursing interventions
H Obtain baseline serum potassium, calcium, phos-
phate, and magnesium levels before treatment.
H Provide at least 3 qt (3 L) of fluid per day.
H Institute safety precautions.
H Schedule frequent rest periods.
H Provide comfort measures.
H Administer prescribed drugs.
H Help the patient turn and reposition every 2 hours.
H Support affected extremities with pillows.
H Offer emotional support.

Hyperparathyroidism 405
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Common characteristics
Hyperphosphatemia H Usually remains asymptomatic
H May result in hypocalcemia with tetany and seizures

Overview Complications
H Soft tissue calcifications
Description H Hypocalcemia
H Excessive serum levels of phosphate H Bone fractures
H Reflects the kidneys inability to excrete excess phos-
phorus
Assessment
Pathophysiology
H Phosphorus exists primarily in inorganic combina- History
tion with calcium in teeth and bones. H Anorexia
H In extracellular fluid, the phosphate ion supports H Decreased mental status
several metabolic functions: utilization of B vitamins, H Nausea and vomiting
acid-base homeostasis, bone formation, nerve and
muscle activity, cell division, transmission of heredi- Physical findings
tary traits, and metabolism of carbohydrates, pro- H Hyperreflexia
teins, and fats. H Hypocalcemic electrocardiogram changes
H Renal tubular reabsorption of phosphate is inversely H Muscle weakness and cramps
regulated by calcium levels an increase in phos- H Papular eruptions
phorus causes a decrease in calcium. An imbalance H Paresthesia
causes hypophosphatemia or hyperphosphatemia. H Presence of Chvosteks or Trousseaus sign
H Abdominal spasm
Causes H Tetany
H Hypocalcemia H Visual impairment
H Hypervitaminosis D H Conjunctivitis
H Hypoparathyroidism
H Renal failure Test results
H Overuse of laxatives with phosphates or phosphate Laboratory
enemas H Serum phosphorus level is greater than 4.5 mg/dl.
H Certain drugs (see Drugs and supplements causing H Serum calcium level is less than 8.9 mg/dl.
hyperphosphatemia) H Blood urea nitrogen and creatinine levels are in-
H Acid-base imbalance creased.
Imaging
Risk factors H X-ray studies may reveal skeletal changes caused by
H Muscle necrosis osteodystrophy in chronic hyperphosphatemia.
H Infection Diagnostic procedures
H Heat stroke H Electrocardiography may show changes characteris-
H Trauma tic of hypercalcemia.
H Chemotherapy

Incidence Treatment
H Occurs most commonly in children, who tend to
consume more phosphorus-rich foods and beverages General
than adults H Treatment of the underlying cause
H Greater incidence in children and adults with renal H Peritoneal dialysis or hemodialysis (if severe)
insufficiency H Discontinuation of drugs associated with hyperphos-
phatemia
H Low-phosphorus diet
Drugs and supplements causing H Activity, as tolerated
hyperphosphatemia H I.V. saline solution

These drugs may cause hyperphosphatemia: Medications

H enemas such as Fleet enemas H Aluminum
H laxatives containing phosphorus or phosphate
H Magnesium
H oral phosphorus supplements
H Calcium gel
H parenteral phosphorus supplements (sodium phos-
H Phosphate-binding antacids
phate, potassium phosphate)
H vitamin D supplements.

406 Hyperphosphatemia
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Foods high in phosphorus

These foods have a high phosphorus content:
H beans H lentils
H bran H milk
H cheese H nuts
H chocolate H peanut butter
H dark-colored sodas H seeds
H ice cream H yogurt.

Nursing considerations
Key outcomes
The patient will:
H maintain a patent airway
H maintain adequate vital signs
H have a normal phosphorus level
H express understanding of condition and treatment
H maintain a low-phosphorus diet.

Nursing interventions
H Provide safety measures.
H Be alert for signs of hypocalcemia.
H Administer prescribed drugs.
H Give phosphate-binding antacids with meals to in-
crease their effectiveness.
H Prepare the patient for dialysis, if appropriate.
H Assist with selecting a low-phosphorus diet.

Monitoring
H Vital signs
H Phosphorus and calcium levels
H Intake and output
H Renal studies

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H prescribed medications
H avoidance of preparations that contain phosphorus
H avoidance of high-phosphorus foods. (See Foods
high in phosphorus.)
Discharge planning
H Refer the patient to a dietitian and social services, if
indicated.

Hyperphosphatemia 407
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Hyperpituitarism H Glucose intolerance

H Diabetes mellitus
H Severe psychological stress

Overview
Assessment
Description
H Chronic, progressive disease marked by hormonal History
dysfunction and startling skeletal overgrowth H Gradual onset of acromegaly
H Prognosis dependent on cause H Relatively abrupt onset of gigantism
H Life expectancy usually reduced H Soft-tissue swelling
H Appears in two forms: acromegaly and gigantism H Hypertrophy of the face and extremities
H Also referred to as growth hormone (GH) excess H Diaphoresis, oily skin
H Fatigue, sleep disturbances
Pathophysiology H Weight gain
H Progressive excessive secretion of pituitary GH H Headaches, decreased vision
occurs. H Decreased libido, impotence
H Acromegaly occurs after epiphyseal closure, causing H Oligomenorrhea, infertility
bone thickening and transverse growth and viscero- H Joint pain
megaly. H Hypertrichosis
H Gigantism occurs before epiphyseal closure with ex- H Irritability, hostility, and other psychological distur-
cess GH, causing proportional overgrowth of all body bances
tissues.
H A large tumor may cause loss of other trophic hor- Physical findings
mones, such as thyroid-stimulating hormone, H Enlarged jaw, thickened tongue
luteinizing hormone, follicle-stimulating hormone, H Enlarged and weakened hands
and corticotropin, which may cause dysfunction of H Coarsened facial features
target organs. H Oily or leathery skin
H Prominent supraorbital ridge
Causes H Deep, hollow-sounding voice
H GH-producing adenoma of the anterior pituitary H Cartilaginous and connective tissue overgrowth
gland H Skeletal abnormalities
H Excessive GH secretion
H Excessive GH-releasing hormone Special populations
H Possible genetic cause
In infants, inspection reveals a highly arched
Incidence palate, muscular hypotonia, slanting eyes, and
Acromegaly exophthalmos.
H Occurs equally in males and females
H Usually occurs between ages 30 and 50
Gigantism Test results
H Affects infants and children Laboratory
H GH radioimmunoassay shows increased plasma GH
Common characteristics levels and levels of insulin-like growth factor I.
H Progressive enlargement of the face, hands and feet, H Glucose suppression test fails to suppress the hor-
thorax, and soft tissue mone level to below the accepted norm of 2 ng/ml.
H Coarsening of features Imaging
H Headache H Skull X-rays, computed tomography scan, or magnet-
H Menstrual disturbances ic resonance imaging shows location of pituitary tu-
mor.
Complications H Bone X-rays show a thickening of the cranium and
H Arthritis long bones and osteoarthritis in the spine.
H Carpal tunnel syndrome
H Osteoporosis
H Kyphosis Treatment
H Hypertension
H Arteriosclerosis General
H Cardiomegaly and heart failure H Treatment to curb overproduction of GH
H Blindness H Pituitary radiation therapy
H Severe neurologic disturbances

408 Hyperpituitarism
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Medications H avoidance of activities that increase ICP

H Replacement of thyroid, cortisone, and gonadal hor- H deep breathing through the mouth if nasal packing is
mones postoperatively if entire pituitary removed in place postoperatively
H GH synthesis inhibitor H hormone replacement therapy, if ordered
H Long-acting analogue of somatostatin H the need to wear a medical identification bracelet
H follow-up examinations
Surgery H possible tumor recurrence.
H Transsphenoidal hypophysectomy
Discharge planning
H Refer the patient for psychological counseling to help
Nursing considerations deal with body image changes and sexual dysfunc-
tion, as needed.
Key outcomes
The patient will:
H demonstrate age-appropriate skills and behaviors to
the extent possible
H express feelings of increased comfort
H express positive feelings about self
H maintain joint mobility and range of motion (ROM).

Nursing interventions
H Provide emotional support.
H Provide reassurance that mood changes result from
hormonal imbalances and can be reduced with treat-
ment.
H Administer prescribed drugs.
H Provide comfort measures.
H Perform or assist with ROM exercises.
H Evaluate muscle weakness.
H Institute safety precautions.
H Provide meticulous skin care.
H Assist with early postoperative ambulation.

ALERT
Report large increases in urine output after
surgery, which may indicate diabetes insipidus.

Monitoring
H Vital signs
H Intake and output
H Serum glucose levels
H Signs and symptoms of hyperglycemia
After surgery
H Signs and symptoms of increased intracranial pres-
sure (ICP) and intracranial bleeding
H Respiratory status
H Surgical incisions and dressings
H Complications
H Signs and symptoms of infection
H Signs and symptoms of hormonal deficiency

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H prescribed medications and possible adverse effects
H when to notify the physician

Hyperpituitarism 409
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Hypersplenism Assessment
History
Overview H Frequent bacterial infection
H Frequent bruising
Description H Spontaneous hemorrhaging from the mucous mem-
H Exaggerated splenic activity and, possibly, spleno- branes and GI or genitourinary tract
megaly H Fever
H Results in peripheral blood cell deficiency as the H Weakness
spleen traps and destroys peripheral blood cells H Palpitations
H May be primary or secondary H Weight loss

Pathophysiology Physical findings

H The spleens normal filtering and phagocytic func- H Ulcerations of the mouth, legs, and feet
tions accelerate indiscriminately, automatically re- H Bruising
moving antibody-coated, aging, and abnormal cells, H Splenomegaly
even though some cells may be functionally normal. H Jaundice
H The spleen may also temporarily sequester normal H Pallor
platelets and red blood cells (RBCs), withholding
them from circulation. In this manner, the enlarged Test results
spleen may trap as many as 90% of the bodys Laboratory
platelets and up to 45% of its RBC mass. H Hemoglobin level is decreased (as low as 4 g/dl).
H White blood cell count is decreased (less than
Causes 4,000/l).
H Idiopathic (see Causes of splenomegaly) H Platelet count is decreased (less than 125,000/l).
H An extrasplenic disorder, such as chronic malaria, H Reticulocyte count is elevated (more than
polycythemia vera, or rheumatoid arthritis 75,000/l).
Imaging
Incidence H Ultrasound or splenic scan shows enlarged spleen or
H Affects all ages possible underlying cause such as a tumor.
H Affects males and females equally H A high spleen-liver ratio of radioactivity indicates
splenic destruction or sequestration.
Common characteristics
H Anemia
H Leukopenia Treatment
H Thrombocytopenia
H Splenomegaly General
H Easy bruising H Treatment of underlying disease (secondary)
H Limited activity
Complications H Nothing by mouth if surgery indicated
H Bleeding
H Postsplenectomy infection and thromboembolic Medications
disease H Antibiotics if infection present
H Pneumococcal vaccine (after splenectomy)

Surgery
H Splenectomy only in transfusion-dependent patients
Causes of splenomegaly refractory to medical therapy
Congestive
H Cirrhosis, thrombosis
Cystic or neoplastic
Nursing considerations
H Cysts, leukemia, lymphoma, myelofibrosis
Hyperplastic
Key outcomes
H Hemolytic anemia, polycythemia The patient will:
Infectious H express understanding of the disorder and treatment
H Acute (abscesses, subacute infective endocarditis), H maintain stable vital signs
chronic (tuberculosis, malaria, Feltys syndrome) H understand restrictions imposed by illness
Infiltrative H not show signs of bleeding.
H Gauchers disease, Niemann-Pick disease

410 Hypersplenism
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Nursing interventions
H If splenectomy is scheduled, administer preoperative
transfusions of blood or blood products (fresh
frozen plasma and platelets) to replace deficient
blood elements, as ordered.
H Treat symptoms or complications of any underlying
disorder.
H Provide emotional support.

Monitoring
H Vital signs
H Signs of bleeding
H Complete blood cell count
H Signs of infection
After surgery
H Pain control
H Wound site

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H signs and symptoms of infection
H activity restrictions.

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Common characteristics
Hypertension H Serial blood pressure measurements:
prehypertension: systolic blood pressure (SBP)
120 to 139 mm Hg or diastolic blood pressure
Overview (DBP) 80 to 89 mm Hg
stage 1: SBP 140 to 159 mm Hg or DBP 90 to
Description 99 mm Hg
H Intermittent or sustained elevation of diastolic or sys- stage 2: SBP 160 mm Hg or DBP 100 mm Hg
tolic blood pressure
H Usually begins as benign disease, slowly progressing Complications
to accelerated or malignant state H Cardiac disease
H Two major types: essential (also called primary or H Renal failure
idiopathic) hypertension and secondary hyperten- H Blindness
sion, which results from renal disease or another H Stroke
identifiable cause
H Malignant hypertension, a medical emergency: a se-
vere, fulminant form commonly arising from both Assessment
types
History
Pathophysiology H In many cases, no symptoms, and disorder revealed
Several theories incidentally during evaluation for another disorder
H Changes in arteriolar bed cause increased peripheral or during a routine blood pressure screening pro-
vascular resistance. gram
H Abnormally increased tone in the sympathetic ner- H Symptoms that reflect the effect of hypertension on
vous system originating in the vasomotor system cen- the organ systems
ters causes increased peripheral vascular resistance. H Awakening with a headache in the occipital region,
H Increased blood volume results from renal or hor- which subsides spontaneously after a few hours
monal dysfunction. H Dizziness, fatigue, confusion
H Increase in arteriolar thickening caused by genetic H Palpitations, chest pain, dyspnea
factors leads to increased peripheral vascular resis- H Epistaxis
tance. H Hematuria
H Abnormal renin release results in the formation of H Blurred vision
angiotensin II, which constricts the arterioles and
increases blood volume. Physical findings
H Bounding pulse
Causes H S4
H Unknown, in most cases H Peripheral edema in late stages
H 5% to 10% due to underlying condition, certain H Hemorrhages, exudates, and papilledema of the eye
medications, or illicit drugs in late stages if hypertensive retinopathy present
H Pulsating abdominal mass, suggesting an abdominal
Risk factors aneurysm
H Family history H Elevated blood pressure on at least two consecutive
H Blacks in the United States occasions after initial screenings
H Stress H Bruits over the abdominal aorta and femoral arteries
H Obesity or the carotids
H High-sodium, high-saturated fat diet
H Use of tobacco Test results
H Use of hormonal contraceptives Laboratory
H Excess alcohol intake H Urinalysis may show protein, red blood cells, or
H Sedentary lifestyle white blood cells, suggesting renal disease, or glu-
H Aging cose, suggesting diabetes mellitus.
H Serum potassium levels less than 3.5 mEq/L may in-
Incidence dicate adrenal dysfunction (primary hyperaldostero-
H Affects about 33% of adults in the United States nism).
H Essential hypertension: 90% to 95% of cases H Blood urea nitrogen levels normal or elevated to
more than 20 mg/dl and serum creatinine levels nor-
mal or elevated to more than 1.5 mg/dl suggest renal
disease.

412 Hypertension
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Imaging
H Excretory urography may reveal renal atrophy, indi-
cating chronic renal disease; one kidney more than
5
8(1.6 cm) shorter than the other suggests unilater-
al renal disease.
H Chest X-rays may demonstrate cardiomegaly.
H Renal arteriography may show renal artery stenosis.
Diagnostic procedures
H Electrocardiography may show left ventricular hyper-
trophy or ischemia.
H An oral captopril challenge may be done to test for
renovascular hypertension.
H Ophthalmoscopy reveals arteriovenous nicking and,
in hypertensive encephalopathy, edema.
Treatment
General
H Lifestyle modification, such as weight control, limit-
ing alcohol, regular exercise, and smoking cessation
H For a patient with secondary hypertension, correc-
tion of the underlying cause and control of hyperten-
sive effects
H Low-saturated fat and low-sodium diet
H Adequate calcium, magnesium, and potassium in diet
Medications
H Diuretics, such as furosemide, hydrochlorothiazide,
and indapamide
H Beta-adrenergic blockers, such as atenolol and
metoprolol
H Calcium channel blockers, such as felodipine and
nisoldipine
H Angiotensin-converting enzyme inhibitors, such as
benazepril, captopril, and enalapril
H Alpha-blockers, such as doxazosine and prazosin
H Vasodilators, such as hydralazine and minoxidil
H Angiotensin-receptor blockers, such as olmesartan,
candesartan, and irbesartan
H Aldosterone antagonists, such as eplerenone and
spironolactone
H Combination alpha- and beta-blockers, such as
carvedilol and labetalol
H Alpha-receptor antagonist such as clonidine
H Help the patient identify risk factors and modify his
lifestyle, as appropriate.
Monitoring
H Vital signs, especially blood pressure
H Signs and symptoms of target end-organ damage
H Complications
H Response to treatment
H Risk factor modification
H Adverse effects of antihypertensive agents
Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H how to use a self-monitoring blood pressure cuff and
to record the reading in a journal for review by the
physician
H the importance of compliance with antihypertensive
therapy and establishing a daily routine for taking
prescribed drugs
H the need to report adverse effects of drugs
H the need to avoid high-sodium antacids and over-
the-counter cold and sinus medications containing
harmful vasoconstrictors
H examining and modifying lifestyle, including diet
H the need for a routine exercise program, particularly
aerobic walking
H dietary restrictions
H the importance of follow-up care.
Discharge planning
H Refer the patient to stress-reduction therapies or
support groups, as needed.

Nursing considerations
Key outcomes
The patient will:
H maintain adequate cardiac output
H maintain hemodynamic stability
H develop no arrhythmias
H express feelings of increased energy
H comply with the therapy regimen.

Nursing interventions
H Administer prescribed drugs.
H Encourage dietary changes, as appropriate.

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Complications
Hyperthyroidism H Arrhythmias
H Left ventricular hypertrophy
H Heart failure
Overview H Muscle weakness and atrophy
H Paralysis
Description H Osteoporosis
H An alteration in thyroid function in which thyroid H Vitiligo
hormones (TH) exert greater than normal responses H Skin hyperpigmentation
H Management determined by cause H Corneal ulcers
H Hyperthyroidism: a form of thyrotoxicosis in which H Myasthenia gravis
excess thyroid hormones are secreted by the thyroid H Impaired fertility
gland H Decreased libido
H Thyrotoxicoses not associated with hyperthyroidism: H Gynecomastia
subacute thyroiditis, ectopic thyroid tissue, and in- H Thyrotoxic crisis or thyroid storm
gestion of excessive TH H Hepatic or renal failure
H Graves disease: also known as toxic diffuse goiter;
an autoimmune disease, the most common form of
hyperthyroidism Assessment
H Also known as thyrotoxicosis
History
Pathophysiology Graves disease
H In Graves disease, thyroid-stimulating antibodies H Nervousness, tremor
bind to and stimulate the thyroid-stimulating hor- H Heat intolerance
mone (TSH) receptors of the thyroid gland. H Weight loss despite increased appetite
H The trigger for this autoimmune disease is unclear. H Sweating
H Its associated with the production of autoantibodies H Frequent bowel movements
possibly caused by a defect in suppressor-T-lympho- H Palpitations
cyte function that allows the formation of these au- H Poor concentration
toantibodies. H Shaky handwriting
H Clumsiness
Causes H Emotional instability and mood swings
H Diseases that can cause hyperthyroidism: H Thin, brittle nails
Graves disease H Hair loss
Toxic multinodular goiter H Nausea and vomiting
Thyroid cancer H Weakness and fatigue
Increased TSH secretion H Oligomenorrhea or amenorrhea
Genetic and immunologic factors H Fertility problems
H Precipitating factors: H Diminished libido
Excessive iodine intake H Diplopia
Stress
Surgery Physical findings
Infection Graves disease
Toxemia of pregnancy H Enlarged thyroid (goiter)
Diabetic ketoacidosis H Exophthalmos
H Tremor
Incidence H Smooth, warm, flushed skin
H Graves disease: most common between ages 30 and H Fine, soft hair
60; more common in females than in males H Premature graying and increased hair loss
H Increased among monozygotic twins H Friable nails and onycholysis
H More common with family history of thyroid abnor- H Pretibial myxedema
malities H Thickened skin
H Only 5% of hyperthyroid patients younger than age 15 H Accentuated hair follicles
H Tachycardia at rest
Common characteristics H Full, bounding pulses
H Increased metabolic rate H Arrhythmias, especially atrial fibrillation
H Heat intolerance H Wide pulse pressure
H Increased tissue sensitivity to sympathetic nervous H Possible systolic murmur
system stimulation H Dyspnea
H Goiter (almost always present) H Hepatomegaly
H Exophthalmos H Hyperactive bowel sounds

414 Hyperthyroidism
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H Weakness, especially in proximal muscles, and H Offer small, frequent meals.

atrophy H Provide meticulous skin care.
H Possible generalized or localized paralysis H Reassure the patient and his family that mood swings
H Gynecomastia and nervousness usually subside with treatment.
H Increased tearing H Encourage verbalization of feelings.
H Help the patient identify and develop coping strate-
Test results gies.
Laboratory H Offer emotional support.
H Radioimmunoassay shows increased serum tri- H Administer prescribed drugs.
iodothyronine and thyroxine concentrations. H Avoid excessive palpation of the thyroid.
H Serum protein-bound iodine is increased. After thyroidectomy
H Serum cholesterol and total lipid levels are H Change dressings and perform wound care, as or-
decreased. dered.
H TSH level is decreased. H Keep the patient in semi-Fowlers position.
Imaging H Support the patients head and neck with sandbags.
H Thyroid scan shows increased uptake of radioactive
iodine (131I). Monitoring
H Ultrasonography shows subclinical ophthalmopathy. H Vital signs
H Daily weight
H Intake and output
Treatment H Daily neck circumference
H Serum electrolyte results
General H Hyperglycemia and glycosuria
H Adequate caloric intake H Electrocardiogram for arrhythmias and ST-segment
H Activity, as tolerated changes
H Complete blood count results
Medications H Signs and symptoms of heart failure
H Treatment with 131I: a single oral dose; treatment of H Frequency and characteristics of stools
choice for females past reproductive age or males After thyroidectomy
and females not planning to have children H Dressings
H Thyroid hormone antagonists, such as methimazole H Signs and symptoms of hemorrhage into the neck
and propylthiouracil (PTU) H Surgical incision
H Beta-adrenergic blockers, such as atenolol and H Dysphagia or hoarseness
metoprolol H Signs and symptoms of hypocalcemia
H Corticosteroids
H Sedatives, such as diazepam and lorazepam
Patient teaching
Surgery
H Subtotal (partial) thyroidectomy Be sure to cover:
H Surgical decompression H the disorder, diagnosis, and treatment
H prescribed drugs and possible adverse effects
H when to notify the physician
Nursing considerations H the need for regular medical follow-up visits
H the need for lifelong thyroid hormone replacement
Key outcomes H the importance of wearing medical identification
The patient will: jewelry
H maintain stable vital signs H precautions with 131I therapy
H maintain normal cardiac output H signs and symptoms of hypothyroidism and hyperthy-
H maintain balanced fluid status roidism
H have normal bowel movements H eye care for ophthalmopathy.
H remain normothermic.

Nursing interventions
H Minimize physical and emotional stress.
H Balance rest and activity periods.
H Keep the patients room cool and quiet and the
lights dim.
H Encourage the patient to dress in loose-fitting, cotton
clothing.
H Consult a dietitian to ensure a nutritious diet with ad-
equate calories and fluids.

Hyperthyroidism 415
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Hypocalcemia H Cardiac arrhythmia

H Respiratory arrest

Overview Assessment
Description History
H Deficient serum levels of calcium H Underlying cause
H Anxiety
Pathophysiology H Irritability
H Together with phosphorous, calcium is responsible H Seizures
for the formation and structure of bones and teeth. H Muscle cramps
H Calcium helps maintain cell structure and function. H Diarrhea
H It plays a role in cell membrane permeability and im-
pulse transmission. Physical findings
H It affects the contraction of cardiac muscle, smooth H Twitching
muscle, and skeletal muscle. H Carpopedal spasm
H It also participates in the blood-clotting process. H Tetany
H Decreased calcium levels can result in multi-system H Hypotension
dysfunction. H Confusion
H Positive Chvosteks and Trousseaus sign (see Elicit-
Causes ing signs of hypocalcemia)
H Inadequate dietary intake of calcium and vitamin D
H Hypoparathyroidism Test results
H Malabsorption or loss of calcium from the GI tract Laboratory
H Severe infections or burns H Serum calcium levels are less than 8.5 mg/dl.
H Overcorrection of acidosis H Ionized calcium levels are less than 4.5 mg/dl.
H Pancreatic insufficiency Diagnostic procedures
H Renal failure H Electrocardiography shows lengthened QT interval,
H Hypomagnesemia prolonged ST segment, and arrhythmias.
Incidence
H Occurs equally in males and females Treatment
H Affects persons of all ages
General
Common characteristics H Treatment of the underlying cause
See Clinical effects of hypocalcemia. H Diet high in calcium and vitamin D
H Activity, as tolerated
Complications
H Laryngeal spasm Medications
H Seizures H Oral calcium and vitamin D supplements
H Calcium gluconate I.V.

Clinical effects of hypocalcemia Nursing considerations

Dysfunction Effects
Cardiovascular Arrhythmias, hypotension
Gastrointestinal Increased GI motility, diarrhea
Musculoskeletal Paresthesia, tetany or painful tonic
muscle spasms, facial spasms, ab-
dominal cramps, muscle cramps,
spasmodic contractions
Neurologic Anxiety, irritability, twitching around
mouth, laryngospasm, seizures,
Chvosteks sign, Trousseaus sign
Other Blood-clotting abnormalities
Key outcomes
The patient will:
H maintain stable vital signs
H maintain adequate cardiac output
H express an understanding of the disorder and treat-
ment.
Nursing interventions
H Provide safety measures; institute seizure precau-
tions, if appropriate.
H Administer prescribed calcium replacement.

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9400H.qxd 8/2/12 4:35 PM Page 417

Eliciting signs of hypocalcemia H Assess I.V. sites if administering calcium I.V. (infiltra-

When the patient complains of muscle spasms and pares-

tion causes sloughing).
thesia in his limbs, try eliciting Chvosteks and Trous- Monitoring
seaus signs indications of tetany associated with cal-
cium deficiency. H Cardiac rhythm
Follow the procedures described here, keeping in mind H Seizures
the discomfort they typically cause. If you detect these H Calcium levels
signs, notify the physician immediately. During these
tests, watch the patient for laryngospasm, monitor his
cardiac status, and have resuscitation equipment nearby. Patient teaching
Chvosteks sign
To elicit this sign, tap the patients facial nerve just in front Be sure to cover:
of the earlobe and below the zygomatic arch or between H proper administration of calcium supplements
the zygomatic arch and the corner of the mouth, as shown H the need to follow a high-calcium diet.
below.
Discharge planning
H Refer the patient to a dietitian and social services, if
indicated.

A positive response (indicating latent tetany) ranges

from simple mouth-corner twitching to twitching of all fa-
cial muscles on the side tested. Simple twitching may be
normal in some patients. However, a more pronounced re-
sponse usually confirms Chvosteks sign.

Trousseaus sign
In this test, occlude the brachial artery by inflating a blood
pressure cuff on the patients upper arm to a level between
diastolic and systolic blood pressure. Maintain this infla-
tion for 3 minutes while observing the patient for carpal
spasm (shown below), which is Trousseaus sign.

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Complications
Hypochloremia H Respiratory arrest
H Seizures
H Coma
Overview
Description Assessment
H Deficient serum levels of the chloride anion
History
Pathophysiology H Risk factors for low chloride levels
H Chloride accounts for two-thirds of all serum anions. H Agitation
H Chloride is secreted by the stomachs mucosa as hy- H Irritability
drochloric acid; it provides an acid medium that aids
digestion and activation of enzymes. Physical findings
H It participates in maintaining acid-base and body wa- H Muscle weakness
ter balances, influences the osmolality or tonicity of H Twitching
extracellular fluid, plays a role in the exchange of H Tetany
oxygen and carbon dioxide in red blood cells, and H Shallow, depressed breathing
helps activate salivary amylase (which, in turn, acti- H Hyperactive deep tendon reflexes
vates the digestive process). H Muscle cramps
H When serum chloride levels drop, levels of sodium, H Cardiac arrhythmias
potassium, calcium, and other electrolytes may be af-
fected. Test results
H When chloride levels decrease, bicarbonate levels Laboratory
rise to compensate. H Serum chloride level is less than 98 mEq/L.
H Serum sodium level is less than 135 mEq/L.
Causes H Supportive values in metabolic alkalosis, include:
H Untreated diabetic ketoacidosis serum pH greater than 7.45
H Addisons disease serum carbon dioxide level greater than
H Chloride-deficient formula (for infants) 32 mEq/L.
H Sodium-restricted diets
H Prolonged use of mercurial diuretics
H Administration of dextrose I.V. without electrolytes Treatment
H Prolonged diarrhea or diaphoresis
H Loss of hydrochloric acid in gastric secretions due to General
vomiting, gastric suctioning, or gastric surgery H Treatment of underlying condition
H Certain drugs (see Drugs causing hypochloremia) H High-sodium diet
H Activity, as tolerated
Risk factors H Treatment of associated metabolic acidosis or elec-
H Cystic fibrosis trolyte imbalances
H Pyloric obstruction
H Draining fistula Medications
H Ileostomy H Normal saline I.V. solution
H Heart failure H Ammonium chloride
H Potassium chloride (for metabolic acidosis)
Common characteristics
H Muscle weakness and twitching
H Muscle hypertonicity
H Tetany
H Shallow, depressed breathing (if metabolic alkalosis
occurs) Dietary sources of chloride
These foods provide chloride:
Drugs causing hypochloremia H fruits
H vegetables
These kinds of diuretics may cause hypochloremia: H table salt
H loop (such as furosemide) H salty foods
H osmotic (such as mannitol) H processed meats
H thiazide (such as hydrochlorothiazide). H canned vegetables.

418 Hypochloremia
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Nursing considerations
Key outcomes
The patient will:
H maintain adequate cardiac output
H maintain stable vital signs
H maintain adequate fluid volume
H avoid complications.

Nursing interventions
H Offer foods high in chloride. (See Dietary sources of
chloride.)
H Provide environmental safety.
H Administer prescribed I.V. fluids and drugs.

Monitoring
H Level of consciousness
H Muscle strength and movement
H Cardiac rhythm
H Arterial blood gas levels
H Serum electrolyte levels
H Respiratory status
H Signs of metabolic alkalosis

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H signs and symptoms of electrolyte imbalance
H dietary supplements
H medication administration, dosage, and possible ad-
verse effects.

Hypochloremia 419
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Incidence
Life-threatening disorder H Affects up to 20% of hospitalized patients (significant
in only about 4% to 5% of these patients)
Hypokalemia H Affects up to 14% of outpatients mildly
H Approximately 80% of patients who receive diuretics
become hypokalemic
H Males and females affected equally
Overview
Common characteristics
Description See Clinical effects of hypokalemia.
H Deficient serum levels of the potassium anion
H Normal range for a serum potassium level narrow Complications
(3.5 to 5 mEq/L); a slight decrease can have a pro- H Cardiac arrhythmia
found consequence H Cardiac arrest
H Rhabdomyolysis
Pathophysiology
H Potassium facilitates contraction of both skeletal and
smooth muscles, including myocardial contraction. Assessment
H Potassium figures prominently in nerve impulse con-
duction, acid-base balance, enzyme action, and cell History
membrane function. H Muscle weakness
H A slight deviation in serum levels can produce pro- H Paresthesia
found clinical consequences. H Abdominal cramps
H Potassium imbalance can lead to muscle weakness H Anorexia
and flaccid paralysis due to an ionic imbalance in H Nausea, vomiting
neuromuscular tissue excitability. H Constipation
H Polyuria
Causes
H Excessive GI or urinary losses, such as vomiting, Physical findings
gastric suction, diarrhea, dehydration, anorexia, H Hyporeflexia
or chronic laxative abuse H Weak, irregular pulse
H Trauma (injury, burns, or surgery) H Orthostatic hypotension
H Chronic renal disease, with tubular potassium H Decreased bowel sounds
wasting
H Certain drugs, especially potassium-wasting diuretics,
steroids, and certain sodium-containing antibiotics
(carbenicillin) (see Drugs causing hypokalemia)
H Acid-base imbalances
H Prolonged potassium-free I.V. therapy
H Hyperglycemia
Clinical effects of hypokalemia
H Cushings syndrome
Dysfunction Effects
H Primary hyperaldosteronism
H Excessive ingestion of licorice Acid-base balance Metabolic alkalosis
H Severe serum magnesium deficiency Cardiovascular Dizziness, hypotension, arrhythmias,
H Low-potassium diet electrocardiogram changes (flat-
tened T waves, elevated U waves,
decreased ST segments), cardiac
arrest (with levels < 2.5 mEq/L)
Drugs causing hypokalemia
Gastrointestinal Nausea, vomiting, anorexia, diarrhea,
These drugs can deplete potassium and cause hypoka- abdominal distention, paralytic ileus
lemia: or decreased peristalsis
H adrenergics, such as albuterol and epinephrine
H antibiotics, such as amphotericin B, carbenicillin, and Genitourinary Polyuria
gentamicin Musculoskeletal Muscle weakness and fatigue, leg
H cisplatin cramps
H corticosteroids
H diuretics, such as furosemide and thiazide Neurologic Malaise, irritability, confusion, men-
H insulin tal depression, speech changes, de-
H laxatives (when used excessively). creased reflexes, respiratory paraly-
sis

420 Hypokalemia
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Test results
Laboratory Patient teaching
H Serum potassium levels are less than 3.5 mEq/L.
H pH and bicarbonate levels are elevated. Be sure to cover:
H Serum glucose level is slightly elevated. H the disorder, diagnosis, and treatment
Diagnostic procedures H prescribed medications and possible adverse effects
H Characteristic electrocardiography changes, such as H monitoring intake and output
flattened T wave, depressed ST segment and U wave, H preventing future episodes of hypokalemia
are present. H need for a high-potassium diet (see Dietary sources
of potassium)
H warning signs and symptoms to report to the physi-
Treatment cian.
General
H Treatment of the underlying cause
H High-potassium diet
H Activity, as tolerated

Medications
H Potassium chloride (I.V. or orally)

ALERT
A patient taking a diuretic may be switched to a
potassium-sparing diuretic to prevent excessive
urinary loss of potassium.

Nursing considerations
Key outcomes
The patient will:
H maintain hemodynamic stability
H maintain a normal potassium level
H understand potential adverse effects of medications
H express an understanding of high-potassium foods.

Nursing interventions
H Administer prescribed drugs.
H Insert an indwelling urinary catheter.
H Implement safety measures.
H Be alert for signs of hyperkalemia after treatment.
H Administer I.V. fluids.

Monitoring
H Serum potassium levels
H Cardiac rhythm
H Intake and output
H Vital signs Dietary sources of potassium
H Respiratory status
These foods provide potassium:
H avocados H molasses
ALERT H bananas H oranges
H cantaloupe H peaches
A patient taking a cardiac glycoside, especially if H citrus juices H potatoes
hes also taking a diuretic, should be monitored H dried apricots H prunes
closely for hypokalemia, which can potentiate the H fresh fish and meat H tomato or prune juice
action of the cardiac glycoside and cause toxicity. H grapefruit H tomatoes
H honeydew melons H whole grains.

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H Hypoparathyroidism
Life-threatening disorder H Hypercalcemia
H Excessive release of adrenocortical hormones

Hypomagnesemia H Certain drugs (see Drugs causing hypomagne-

semia)
Risk factors
Overview H Sepsis
H Serious burns
Description H Wounds requiring debridement
H Deficient serum levels of the magnesium cation
H Relatively common imbalance Incidence
H Occurs in 10% to 20% of hospitalized patients (50%
Pathophysiology to 60% of patients in the intensive care unit)
H Magnesium enhances neuromuscular integration and H Occurs in 25% of outpatients with diabetes
stimulates parathyroid hormone secretion, thus regu- H Occurs in 30% to 80% of alcoholics
lating intracellular fluid calcium levels. H Affects males and females equally
H Magnesium may also regulate skeletal muscles.
H It activates many enzymes for proper carbohydrate Common characteristics
and protein metabolism, aids in cell metabolism and See Clinical effects of hypomagnesemia.
the transport of sodium and potassium across cell
membranes, and influences sodium, potassium, cal- Complications
cium, and protein levels. H Laryngeal stridor
H About one-third of magnesium taken into the body is H Seizures
absorbed through the small intestine and is eventual- H Respiratory depression
ly excreted in the urine; the remaining unabsorbed H Cardiac arrhythmia
magnesium is excreted in the stool. H Cardiac arrest
H Decreased serum levels of magnesium, primarily
lead to dysfunction of the central nervous system and
neuromuscular, GI, and cardiac systems. Assessment
Causes History
H Malabsorption syndrome H Dysphagia
H Chronic diarrhea H Nausea
H Postoperative complications after bowel resection H Vomiting
H Chronic alcoholism H Drowsiness
H Prolonged diuretic therapy H Confusion
H Nasogastric suctioning H Leg and foot cramps
H Administration of parenteral fluids without magne-
sium salts Physical findings
H Starvation or malnutrition H Tachycardia
H Severe dehydration H Hypertension
H Diabetic acidosis H Muscle weakness, tremors, twitching
H Hyperaldosteronism H Hyperactive deep tendon reflexes

Drugs causing hypomagnesemia

Monitor the patients magnesium level if hes taking any of Clinical effects of hypomagnesemia
these drugs that can cause or contribute to hypomagne-
semia: Dysfunction Effects
H aminoglycoside antibiotic, such as amikacin, genta-
Cardiovascular Arrhythmias, vasomotor changes
micin, streptomycin, or tobramycin (vasodilation and hypotension) and,
H amphotericin B occasionally, hypertension
H cisplatin
H cyclosporine Neurologic Confusion, delusions, hallucinations,
H insulin seizures
H laxative
Neuromuscular Hyperirritability, tetany, leg and foot
H loop or thiazide diuretic, such as bumetanide,
cramps, Chvosteks sign (facial mus-
furosemide, and torsemide cle spasms induced by tapping the
H pentamidine isethionate. branches of the facial nerve)

422 Hypomagnesemia
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H Chvosteks and Trousseaus signs Patient teaching

H Cardiac arrhythmia
Be sure to cover:
Test results H the disorder, diagnosis, and treatment
Laboratory H prescribed drugs
H Serum magnesium levels are less than 1.5 mEq/L. H avoidance of drugs that deplete magnesium, such as
H Other electrolyte abnormalities, such as below-nor- diuretics and laxatives
mal serum potassium or calcium level, are present. H the need to adhere to a high-magnesium diet
Diagnostic procedures H danger signs and when to report them.
H Electrocardiography shows abnormalities, such as
prolonged QT interval and atrioventricular block. Discharge planning
H Refer the patient to Alcoholics Anonymous if appro-
priate.
Treatment
General
H Treatment of the underlying cause
H Dietary replacement of magnesium
H Activity, as tolerated

Medications
H Magnesium oxide
H Magnesium sulfate (I.M. or I.V.)

Nursing considerations
Key outcomes
The patient will:
H maintain hemodynamic stability
H maintain a normal magnesium level
H understand the causes of high magnesium levels.

Nursing interventions
H Institute seizure precautions.
H Administer prescribed drugs.
H Report abnormal serum electrolyte levels
immediately.

ALERT
A low magnesium level may increase the bodys re-
tention of a cardiac glycoside. Be alert for signs of
digoxin toxicity if your patient is taking digoxin.

H Ensure patient safety.

H Reorient the patient as needed.

Monitoring
H Vital signs
H Magnesium levels
H Electrolyte levels
H Intake and output
H Cardiac rhythm
H Level of consciousness
H Respiratory status

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Hyponatremia H Trauma, surgery (wound drainage), or burns

H Adrenal gland insufficiency (Addisons disease) or
hypoaldosteronism
H Cirrhosis of the liver with ascites
Overview H Syndrome of inappropriate antidiuretic hormone
(SIADH), resulting from brain tumor, stroke, pul-
Description monary disease, or neoplasm with ectopic antidiuret-
H Deficient serum levels of the sodium cation in rela- ic hormone production
tion to body water H Certain drugs, such as chlorpropamide and clofi-
brate (see Drugs causing hyponatremia)
Pathophysiology
H Sodium is the major cation (90%) in extracellular Incidence
fluid; potassium, the major cation in intracellular H Occurs in about 1% of hospitalized patients (30% of
fluid. patients in intensive care unit)
H During repolarization, the sodium-potassium pump H More common in the very young and very old
continually shifts sodium into the cells and potassium H Affects males and females equally
out of the cells; during depolarization, it does the re-
verse. Common characteristics
H Sodium cation functions include maintaining tonicity H Pulmonary edema
and concentration of extracellular fluid, acid-base H Circulatory disorders
balance (reabsorption of sodium ion and excretion H Decreased level of consciousness (LOC) (see Clini-
of hydrogen ion), nerve conduction and neuromus- cal effects of hyponatremia)
cular function, glandular secretion, and water bal-
ance. Complications
H Sodium depletion causes dysfunction of multiple H Seizures
organ systems. H Coma
H Permanent neurologic damage
Causes
H Vomiting
H Suctioning Assessment
H Diarrhea
H Excessive perspiration or fever History
H Use of potent diuretics H Altered LOC
H Tap water enemas H Nausea
H Excessive water intake H Headache
H Infusion of I.V. dextrose in water without other H Muscle weakness
solutes H Abdominal cramps
H Malnutrition or starvation
H Low-sodium diet, usually in combination with one of Physical findings
the other causes H Orthostatic hypotension
H Dry mucous membranes
H Poor skin turgor
Drugs causing hyponatremia
Drugs can contribute to the development of hyponatremia Clinical effects of hyponatremia
by potentiating the action of antidiuretic hormone, by
causing syndrome of inappropriate antidiuretic hormone, Dysfunction Effects
or by inhibiting sodium reabsorption in the kidney (diuret-
ics). Cardiovascular Hypotension; tachycardia; with
severe deficit, vasomotor collapse,
Anticonvulsants Diuretics thready pulse
H carbamazepine H bumetanide
Antidiabetics H ethacrynic acid Gastrointestinal Nausea, vomiting, abdominal
H chlorpropamide H furosemide cramps
H tolbutamide (rarely) H thiazides
Genitourinary Oliguria or anuria
Antineoplastics Sedatives
H cyclophosphamide H barbiturates Integumentary Cold, clammy skin; decreasing skin
H vincristine H morphine turgor
Antipsychotics
H fluphenazine Neurologic Anxiety, headaches, muscle twitch-
H thioridazine ing and weakness, seizures
H thiothixene
Respiratory Cyanosis with severe deficiency

424 Hyponatremia
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H Rapid, bounding pulse

H Muscle twitching

Test results
Laboratory
H Serum sodium level is less than than 135 mEq/L.
H Urine specific gravity is less than 1.010.
H Serum osmolality is less than 280 mOsm/kg (dilute
blood).
H Urine specific gravity is increased and urine sodium
level is elevated (0.20 mEq/L) in patients with
SIADH.

Treatment
General
H Treatment of the underlying cause
H Restricted fluid intake
H High-sodium diet
H Activity, as tolerated

Medications
H Oral sodium supplements
H Demeclocycline or lithium
H Administration of normal saline solution
H Hypertonic (3% or 5%) saline solutions (with serum
sodium levels less than 110 mEq/L)

Nursing considerations
Key outcomes
The patient will:
H maintain adequate fluid volume
H maintain a normal sodium level
H maintain stable vital signs
H remain alert and oriented to his environment.

Nursing interventions
H Restrict fluid intake.
H Administer prescribed I.V. fluids.
H Provide a safe environment.

Monitoring
H Vital signs
H Serum sodium levels
H Urine specific gravity
H Intake and output
H Neurologic status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H drug therapy and possible adverse effects
H dietary changes and fluid restrictions
H monitoring daily weight
H signs and symptoms to report to the physician.

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Common characteristics
Hypoparathyroidism H Muscle spasms
H Hyperreflexia
H Neuromuscular excitability
Overview
Complications
Description H Heart failure
H Deficiency in parathyroid hormone (PTH) secretion H Cataracts
by the parathyroid glands or the decreased action of H Tetany
PTH in the periphery H Increased intracranial pressure
H Because parathyroid glands primarily regulate calci- H Irreversible calcification of basal ganglia
um balance, neuromuscular symptoms range from H Bone deformities
paresthesia to tetany H Laryngospasm, respiratory stridor, anoxia
H May be acute or chronic H Vocal cord paralysis
H Classified as idiopathic, acquired, or reversible H Seizures
H Death
Pathophysiology
H PTH normally maintains serum calcium levels by in- Special populations
creasing bone resorption and by stimulating renal
conversion of vitamin D to its active form, which en- Hypoparathyroidism that develops during child-
hances GI absorption of calcium and bone resorp- hood results in malformed teeth.
tion.
H PTH also maintains the inverse relationship between
serum calcium and phosphate levels by inhibiting Assessment
phosphate reabsorption in the renal tubules and en-
hancing calcium reabsorption. History
H Abnormal PTH production in hypoparathyroidism H Neck surgery or irradiation
disrupts this delicate balance. H Malabsorption disorders
H Alcoholism
Causes H Tingling in the fingertips, around the mouth and,
H Autoimmune genetic disorder occasionally, in the feet
H Congenital absence or malformation of the parathy- H Muscle tension and spasms
roid glands H Feeling like throat is constricted
H Accidental removal of or injury to one or more H Dysphagia
parathyroid glands during surgery H Difficulty walking and a tendency to fall
H Ischemia or infarction of the parathyroid glands dur- H Nausea, vomiting, abdominal pain
ing surgery H Constipation or diarrhea
H Hemochromatosis H Personality changes
H Sarcoidosis H Fatigue
H Amyloidosis
H Tuberculosis Physical findings
H Neoplasms H Brittle nails
H Trauma H Dry skin
H Massive thyroid irradiation H Coarse hair, alopecia
H Hypomagnesemia-induced impairment of hormone H Transverse and longitudinal ridges in the fingernails
secretion H Loss of eyelashes and fingernails
H Suppression of normal gland function due to hyper- H Stained, cracked, and decayed teeth
calcemia H Tetany
H Delayed maturation of parathyroid function H Positive Chvosteks and Trousseaus signs
H Abnormalities of the calcium-sensor receptor H Increased deep tendon reflexes
H Irregular, slow or rapid pulse
Incidence
H Idiopathic and reversible forms most common in Test results
children Laboratory
H Acquired form most common in older patients who H Radioimmunoassay for PTH is decreased.
have undergone thyroid gland surgery H Serum and urine calcium levels are decreased.
H Serum phosphate levels are increased.
H Urine creatinine levels are decreased.

426 Hypoparathyroidism
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Imaging H Electrocardiogram for QT interval changes and

H Computed tomography scan may show frontal lobe arrhythmias
and basal ganglia calcifications. H Signs and symptoms of decreased cardiac output
H X-rays may show increased bone density and bone H Chvosteks sign
malformation. H Trousseaus sign
Diagnostic procedures
H Electrocardiography shows a prolonged QT interval. ALERT
Closely monitor the patient receiving digoxin and
Treatment calcium because calcium potentiates the effect of
digoxin. Stay alert for signs of digoxin toxicity.
General
H To restore the calcium and associated mineral bal-
ance within the body Patient teaching
H Supportive care necessary for an acute, life-
threatening attack or hypoparathyroid tetany Be sure to cover:
H High-calcium, low-phosphorus diet H the disorder, diagnosis, and treatment
H Activity, as tolerated H prescribed medications and possible adverse effects
H when to notify the physician
Medications H follow-up care
H Vitamin D H complications
H Supplemental calcium H periodic checks of serum calcium levels.
H Calcitriol
Acute, life-threatening tetany Discharge planning
H I.V. administration of 10% calcium gluconate, 10% H Refer the patient to an alcoholism treatment program
calcium glucepate, or 10% calcium chloride for additional counseling, if necessary.
H Sedatives
H Anticonvulsants

Surgery
H To treat underlying cause such as tumor

Nursing considerations
Key outcomes
The patient will:
H maintain normal cardiac output
H maintain stable vital signs
H maintain adequate ventilation
H maintain intact skin integrity
H verbalize an understanding of the disorder and treat-
ment regimen.
Nursing interventions
H Administer prescribed drugs.
H Maintain a patent I.V. line.
H Keep emergency equipment readily available.
H Maintain seizure precautions.
H Provide meticulous skin care.
H Institute safety precautions.
H Encourage the patient to express his feelings.
H Offer emotional support.
H Help the patient develop effective coping strategies.

Monitoring
H Vital signs
H Intake and output
H Serum calcium and phosphorus levels

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Hypophosphatemia H Arrhythmias
H Rhabdomyolysis
H Seizures
H Coma
Overview
Description Assessment
H Deficient serum phosphate levels
History
Pathophysiology H Anorexia
H Phosphorus exists primarily in inorganic combina- H Memory loss
tion with calcium in teeth and bones. H Muscle and bone pain
H In extracellular fluid, the phosphate ion supports H Fractures
several metabolic functions: utilization of B vitamins, H Chest pain
acid-base homeostasis, bone formation, nerve and
muscle activity, cell division, transmission of heredi- Physical findings
tary traits, and metabolism of carbohydrates, pro- H Tremor and weakness in speaking voice
teins, and fats. H Confusion
H Renal tubular reabsorption of phosphate is inversely H Bruising and bleeding
regulated by calcium levels an increase in phos-
phorus causes a decrease in calcium. An imbalance Test results
causes hypophosphatemia or hyperphosphatemia. H Serum phosphorus levels are less than 2.5 mg/dl.

Causes
H Inadequate dietary intake Treatment
H Commonly related to malnutrition resulting from a
prolonged catabolic state or chronic alcoholism General
H Intestinal malabsorption H Treatment of the underlying cause
H Chronic diarrhea H Discontinuation of drugs that may cause hypophos-
H Hyperparathyroidism with resultant hypercalcemia phatemia (see Drugs that may cause hypophos-
H Hypomagnesemia phatemia)
H Vitamin D deficiency H High-phosphorus diet
H Chronic use of antacids containing aluminum hy- H Activity, as tolerated
droxide
H Use of parenteral nutrition solution with inadequate Medications
phosphate content H Phosphate salt tablets or capsules
H Renal tubular defects H Potassium phosphate I.V.
H Tissue damage in which phosphorus is released by
injured cells
H Diabetic acidosis Nursing considerations
Incidence Key outcomes
H Varies according to the underlying cause The patient will:
H Occurs in about 1% to 5% of hospitalized patients H maintain a patent airway
H Patients with alcoholism, diabetic ketoacidosis, or H maintain adequate vital signs
sepsis: 40% to 80% incidence H maintain a normal phosphorus level.
H More than 50% of renal transplant patients experi-
encing low phosphate levels; many chronically
Common characteristics
H Anorexia
H Muscle weakness Drugs that may cause hypophosphatemia
H Tremor
H Paresthesia The following drugs may cause hypophosphatemia:
H acetazolamide, thiazide diuretics (chlorothiazide and
H Osteomalacia (when persistent)
hydrochlorothiazide), loop diuretics (bumetanide and
H Peripheral hypoxia
furosemide), and other diuretics
H antacids, such as aluminum carbonate, aluminum hy-
Complications droxide, calcium carbonate, and magnesium oxide
H Heart failure H insulin
H Shock H laxatives.

428 Hypophosphatemia
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Nursing interventions
H Provide safety measures.
H Administer prescribed phosphorus replacement.
H Assist with ambulation and activities of daily living.

Monitoring
H Respiratory status
H Neurologic status
H Phosphorus and calcium levels
H Intake and output

Patient teaching
Be sure to cover:
H proper administration of phosphorus supplements
H the need to adhere to a high-phosphorus diet. (See
Foods high in phosphorus, page 407.)
Discharge planning
H Refer the patient to a dietitian and social services, if
indicated.

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Hypopituitarism H Corticotropin deficiency

H Gonadotropin and prolactin deficiency
H Pituitary apoplexy (a medical emergency)
H High fever, shock, coma, and death
Overview H Diabetes insipidus

Description
Special populations
H Partial or complete failure of the anterior pituitary
gland to produce its vital hormones: corticotropin, In children, hypopituitarism can cause dwarfism
thyroid-stimulating hormone (TSH), luteinizing hor- and pubertal delay.
mone (LH), follicle-stimulating hormone (FSH),
growth hormone (GH), and prolactin
H May be primary or secondary, resulting from dys- Assessment
function of the hypothalamus
H Development of clinical features typically slow and History
not apparent until 75% of the pituitary gland is de- H Signs and symptoms dependent on which pituitary
stroyed hormones are deficient, patients age, and severity of
H Total loss of all hormones fatal without treatment disorder
H Prognosis good with adequate replacement therapy Gonadotropin (FSH and LH) deficiency
and correction of the underlying causes in females
H Panhypopituitarism: absence of all hormones H Amenorrhea
H Dyspareunia
Pathophysiology H Infertility
H The pituitary gland is extremely vulnerable to is- H Reduced libido
chemia and infarction because its highly vascular. Gonadotropin (FSH and LH) deficiency in
H Any event that leads to circulatory collapse and com- males
pensatory vasospasm may result in gland ischemia, H Impotence
tissue necrosis, or edema. H Reduced libido
H Expansion of the pituitary within the fixed compart- TSH deficiency
ment of the sella turcica further impedes blood sup- H Cold intolerance
ply to the pituitary. H Constipation
H Menstrual irregularity
Causes H Lethargy
H Tumor H Severe growth retardation in children despite treat-
H Congenital defects ment
H Pituitary gland hypoplasia or aplasia Corticotropin deficiency
H Pituitary infarction H Fatigue
H Partial or total hypophysectomy by surgery, irradia- H Nausea, vomiting, anorexia
tion, or chemical agents H Weight loss
H Granulomatous disease Prolactin deficiency
H Deficiency of hypothalamus releasing hormones H Absent postpartum lactation
H Idiopathic H Amenorrhea
H Infection
H Trauma Physical findings
GH deficiency
Incidence H Physical signs possibly not apparent in neonate
H Relatively rare H Growth retardation usually apparent at age 6 months
H Occurs in adults and children In children:
H Affects males and females equally H Chubbiness from fat deposits in the lower trunk
H Short stature
Common characteristics H Delayed secondary tooth eruption
H Metabolic dysfunction H Delayed puberty
H Sexual immaturity H Average height of 4 (1.2 m), with normal propor-
H Growth retardation tions
H Fatigue H More subtle signs in adults (fine wrinkles near the
mouth and eyes)
Complications Gonadotropin (FSH and LH) deficiency
H Any combination of deficits in the production of the in women
six major hormones H Breast atrophy
H GH deficiency H Sparse or absent axillary and pubic hair
H TSH deficiency H Dry skin

430 Hypopituitarism
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Gonadotropin (FSH and LH) deficiency in men Special populations

H Decreased muscle strength
H Testicular softening and shrinkage Children with hypopituitarism may also need
H Retarded secondary sexual hair growth adrenal and thyroid hormone replacement and, as
TSH deficiency they approach puberty, sex hormones.
H Dry, pale, puffy skin
H Slow thought processes
H Bradycardia Surgery
Corticotropin deficiency H For pituitary tumor
H Depigmentation of skin and nipples
H Hypothermia and hypotension during periods of
stress Nursing considerations
Prolactin deficiency
H Sparse or absent growth of pubic and axillary hair Key outcomes
Panhypopituitarism The patient will:
H Mental abnormalities, including lethargy and psy- H maintain body weight
chosis H maintain normal body temperature
H Physical abnormalities, including orthostatic hypo- H demonstrate age-appropriate skills and behavior to
tension and bradycardia the extent possible
H verbalize feelings of positive self-esteem.
Test results
Laboratory Nursing interventions
H Serum thyroxin levels are decreased in diminished H Administer prescribed drugs.
thyroid gland function due to lack of TSH. H Encourage maintenance of adequate calorie intake.
H Radioimmunoassay shows decreased plasma levels of H Offer small, frequent meals.
some or all of the pituitary hormones. H Keep the patient warm.
H Increased prolactin levels may indicate a lesion in H Institute safety precautions.
the hypothalamus or pituitary stalk. H Provide emotional support.
H Oral administration of metyrapone may show the H Encourage the patient to express his feelings.
source of low hydroxycorticosteroid levels in serum
or urine. Monitoring
H Insulin administration shows low levels of cortico- H Laboratory tests for hormonal deficiencies
tropin, indicating pituitary or hypothalamic failure. H Calorie intake
H Dopamine antagonist administration evaluates pro- H Daily weight
lactin secretory reserve. H Vital signs
H I.V. administration of gonadotropin-releasing hor- H Neurologic status
mone may distinguish pituitary and hypothalamic H Signs and symptoms of pituitary apoplexy, a medical
causes of gonadotropin deficiency. emergency
H Provocative testing shows persistently low GH and H Signs and symptoms of hypoglycemia
insulin-like growth factor-1 levels, confirming GH
deficiency.
Imaging Patient teaching
H Computed tomography scans, magnetic resonance
imaging, or cerebral angiography may show the pres- Be sure to cover:
ence of intrasellar or extrasellar tumors. H the disorder, diagnosis, and treatment
H long-term hormonal replacement therapy and ad-
verse reactions
Treatment H when to notify the physician
H regular follow-up appointments
General H energy-conservation techniques
H If caused by a lesion or tumor, removal, radiation, or H the need for adequate rest
both, followed by possible lifelong hormone replace- H the need for a balanced diet.
ment therapy
H Endocrine substitution therapy for affected organs Discharge planning
H High-calorie, high-protein diet H Refer the parents for psychological counseling or to
H Regular exercise program community resources.
H Rest periods for fatigue

Medications
H Hormone replacement, appropriate to deficiency

Hypopituitarism 431
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Hypothermia H Low core body temperature

H Rigid muscles
H Irregular heart and respiratory rates
H Unconsciousness
Overview
Complications
Description H Fatal coagulation disorders
H Lowering of the core body temperature to below H Renal failure
95 F (35 C) H Cardiac arrhythmias
H Systemic reaction, rather than localized H Cardiorespiratory arrest
H Produces chemical changes in body
H Can be fatal
Assessment
Pathophysiology
H Exposure to cold temperatures slows the actions of History
enzymes throughout body. H One or more risk factors
H The body attempts to generate heat by inducing shiv- H Exposure to cold temperatures
ering (involuntary contraction and expansion of
muscle tissue). Physical findings
H Muscle action creates heat through friction. H Mild core body temperature between 90 and
H Body is unable to generate sufficient heat. 95 F (32.2 and 35 C)
H Metabolic changes slow the functions of most major Cool skin
organ systems, including decreased renal flow and Fatigue
glomerular filtration. Slow gait
Apathy
Causes Slurred speech
H Interference with the bodys temperature regulation Confusion
by alterations in heat production, conduction, con- Shivering
vection, radiation, evaporation, or respiration Muscle weakness
H Examples: H Moderate core body temperature between 82
Cold-water near drowning and 86 F (27.8 and 30 C)
Prolonged exposure to cold temperatures Cold skin
Administration of blood products Cyanosis
Disease processes Bradycardia
Atrial and ventricular arrhythmias
Risk factors Hypotension
H Youth Stupor or coma
H Increased age Muscular rigidity
H Lack of insulating subcutaneous body fat Generalized edema
H Wet or inadequate clothing Slowed reflexes
H Drug abuse Poorly reactive pupils
H Cardiac disease Oliguria
H Hypothyroidism H Severe core body temperature below 82 F
H Fatigue (27.8 C)
H Malnutrition Very cold skin
H Excessive alcohol intake Muscle rigidity
H Smoking Apnea
H Certain medications Ventricular fibrillation
Unresponsiveness
Incidence Fixed pupils
H About 600 elderly people in the United States dying
each year from hypothermia Test results
H One study shows about 12,000 people dying during Laboratory
one 15-year period; about 50% of these deaths were H Complete blood count may indicate hemoconcentra-
in people older than age 65; males were affected tion or anemia from blood loss or cell damage.
more than females; and whites were affected less fre- H Liver enzyme studies may be increased due to organ
quently than people of other races damage.
Common characteristics
H Change in mental status
H Uncontrollable shivering

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Treatment Patient teaching

General Be sure to cover:
H Protecting the patient from further heat loss H the disorder, diagnosis, and treatment
H Insulation to conserve body heat H ways to prevent recurrence
H Dry clothing if necessary H effects of alcohol, smoking, and drugs that increase
H Passive rewarming risks
No external methods used H diseases that may predispose patient to recurrence.
Body regains heat slowly
H Active rewarming
Heating blankets and other objects
Warm-water immersion
Radiant heat
H Active core rewarming
Heated I.V. fluids
Genitourinary tract irrigation
Peritoneal, gastric, and mediastinal lavage
Hemodialysis
H Cardiopulmonary resuscitation (CPR) and defibrilla-
tion, if necessary
H Oxygen and controlled ventilation

Medications
H Antiarrhythmic agents such as lidocaine, if indicated

Nursing considerations
Key outcomes
The patient will:
H show signs of adequate cardiac output
H express feelings of comfort and warmth
H verbalize an understanding of the condition and how
to prevent recurrence
H attain and maintain normal body temperature
H maintain adequate ventilation.

Nursing interventions
H Administer CPR if necessary.
H Assist with rewarming procedures, as ordered.
H Administer medications, as ordered.
H Provide supportive environment for anxious patient
and family.
Monitoring
H Vital signs
H Temperature
H Cardiac and ventilatory status
H Neurologic status
H Intake and output
H Skin integrity during rewarming due to possible
burns
H Complete blood count
H Coagulation and liver enzyme study results
H Urinalysis test results
H Serum amylase, glucose, electrolyte, and blood urea
nitrogen levels
H Arterial blood gas levels

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Hypothyroidism H Cardiomegaly
H Heart failure
H Pleural and pericardial effusion
GI complications
Overview H Achlorhydria
H Anemia
Description H Dynamic colon
H Clinical condition characterized by either decreased H Megacolon
circulating levels of or resistance to free thyroid hor- H Intestinal obstruction
mone (TH) H Bleeding tendencies
H Classified as primary or secondary Other complications
H Severe hypothyroidism known as myxedema H Conductive or sensorineural deafness
H Psychiatric disturbances
Pathophysiology H Carpal tunnel syndrome
H In primary hypothyroidism, a decrease in TH pro- H Benign intracranial hypertension
duction is a result of the loss of thyroid tissue. H Impaired fertility
H This results in an increased secretion of thyroid- H Myxedema coma
stimulating hormone (TSH) that leads to a goiter.
H In secondary hypothyroidism, the pituitary typically
fails to synthesize or secrete adequate amounts of Assessment
TSH, or target tissues fail to respond to normal blood
levels of TH. History
H Either type may progress to myxedema, which is clin- H Vague and varied symptoms that developed slowly
ically more severe and considered a medical emer- over time
gency. H Energy loss, fatigue
H Forgetfulness
Causes H Sensitivity to cold
H Autoimmune thyroiditis (Hashimotos) (most com- H Unexplained weight gain
mon cause) H Constipation
H Thyroid gland surgery H Anorexia
H Radioactive iodine therapy H Decreased libido
H Inflammatory conditions H Menorrhagia
H Endemic iodine deficiency H Paresthesia
H Antithyroid drugs H Joint stiffness
H Congenital defects H Muscle cramping
H Amyloidosis
H Sarcoidosis Physical findings
H External radiation to the neck H Slight mental slowing to severe obtundation
H Drugs, such as iodides and lithium H Thick, dry tongue
H Pituitary failure to produce TSH H Hoarseness; slow, slurred speech
H Hypothalamic failure to produce thyrotropin- H Dry, flaky, inelastic skin
releasing hormone H Puffy face, hands, and feet
H Postpartum pituitary necrosis H Periorbital edema; drooping upper eyelids
H Pituitary tumor H Dry, sparse hair with patchy hair loss
H Idiopathic H Loss of outer third of eyebrow
H Thick, brittle nails with transverse and longitudinal
Incidence grooves
H Most prevalent in females H Ataxia, intention tremor; nystagmus
H In the United States, increased incidence in people H Doughy skin that feels cool
older than age 40 H Weak pulse and bradycardia
H Muscle weakness
Common characteristics H Sacral or peripheral edema
H Decreased energy metabolism H Delayed reflex relaxation time
H Decreased heat production H Possible goiter
H Absent or decreased bowel sounds
Complications H Hypotension
Cardiovascular complications H A gallop or distant heart sounds
H Hypercholesterolemia H Adventitious breath sounds
H Arteriosclerosis H Abdominal distention or ascites
H Ischemic heart disease
H Peripheral vascular disease

434 Hypothyroidism
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Test results H Encourage the patient to express his feelings.

Laboratory H Help the patient develop effective coping strategies.
H Radioimmunoassay shows decreased serum levels of
T3 and T4. Monitoring
H Serum TSH level is increased with thyroid insufficien- H Vital signs
cy and decreased with hypothalamic or pituitary H Intake and output
insufficiency. H Daily weight
H Serum cholesterol, alkaline phosphatase, and triglyc- H Cardiovascular status
erides levels are elevated. H Pulmonary status
H Serum electrolytes show low serum sodium levels in H Edema
myxedema coma. H Bowel sounds, abdominal distention, frequency of
H Arterial blood gas analysis shows decreased pH and bowel movements
increased partial pressure of carbon dioxide in H Mental and neurologic status
myxedema coma. H Signs and symptoms of hyperthyroidism
Imaging
H Skull X-rays, computed tomography scan, and mag-
netic resonance imaging may show pituitary or hypo- Patient teaching
thalamic lesions.
H Thyroid scan and uptake evaluates structure and Be sure to cover:
function. H the disorder, diagnosis, and treatment
H prescribed medications and possible adverse effects
H when to notify the physician
Treatment H physical and mental changes
H signs and symptoms of myxedema
General H the need for lifelong hormone replacement therapy
H To restore and maintain a normal thyroid state H the need to wear a medical identification bracelet
H Need for long-term thyroid replacement H the importance of keeping accurate records of daily
H Low-fat, low-cholesterol, high-fiber, low-sodium diet weight
H Possibly fluid restriction H the need to adhere to a well-balanced, high-fiber,
H Activity, as tolerated low-sodium diet
H energy-conservation techniques.
Medications
H Synthetic hormone levothyroxine Discharge planning
H Synthetic liothyronine H Refer the patient and family members to a mental
health professional for additional counseling, if
Surgery needed.
H For underlying cause such as pituitary tumor

Nursing considerations
Key outcomes
The patient will:
H maintain adequate cardiac output
H maintain stable vital signs
H demonstrate normal laboratory values
H maintain balanced fluid volume status
H consume adequate daily calorie requirements
H express positive feelings about self.

Nursing interventions
H Administer prescribed drugs.
H Provide adequate rest periods.
H Apply antiembolism stockings.
H Encourage coughing and deep-breathing exercises.
H Maintain fluid restrictions and a low-sodium diet.
H Provide a high-bulk, low-calorie diet.
H Reorient the patient, as needed.
H Offer support and encouragement.
H Provide meticulous skin care.
H Keep the patient warm, as needed.

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I Idiopathic
thrombocytopenic
purpura
Overview
Description
H A deficiency of platelets occurring when the immune
system destroys the bodys own platelets
H May be acute, as in postviral thrombocytopenia, or
chronic, as in essential thrombocytopenia or autoim-
Assessment
History
H Epistaxis
H Bleeding gums
H Menorrhagia
H Recent viral illness

Physical findings
H Petechiae or ecchymosis
H Bleeding into mucous membranes
H Splenomegaly

Test results
mune thrombocytopenia Laboratory
H Excellent prognosis for acute form; recovery in near- H Platelet count is less than 20,000/l.
ly four of five patients without treatment H Bleeding time is prolonged.
H Good prognosis for chronic form; remissions com- H Platelets are of abnormal size and appearance.
monly lasting weeks or years, especially among fe- H Hemoglobin level is decreased (if bleeding oc-
males curred).
H Bone marrow studies show abundant megakaryo-
Pathophysiology cytes (platelet precursor cells) and a circulating
H Circulating immunoglobulin (Ig) G molecules react platelet survival time of only several hours to a few
with host platelets, which are then destroyed in the days.
spleen and, to a lesser degree, in the liver. H Humoral tests measure platelet-associated IgG (one-
H Normally, the life span of platelets in circulation is 7 half of all patients with ITP display elevated IgG
to 10 days. In idiopathic thrombocytopenic purpura levels).
(ITP), platelets survive 1 to 3 days or less.
Causes Treatment
H Viral infection
H Immunization with a live virus vaccine General
H Immunologic disorders H Rest periods between activities
H Drug reactions H Complete bed rest during active bleeding
H Well-balanced diet
Incidence
Medications
Special populations Acute
H Glucocorticoids to prevent further platelet destruc-
Acute ITP usually affects children between ages 2 tion by immunosuppression
and 6; chronic ITP mainly affects adults younger H IgG or Rho immunoglobulin
than age 50, especially women between ages 20 H Rituximab
and 40. H Chemotherapy
Chronic
H Vitamin K
Common characteristics H Corticosteroids such as prednisone
H Epistaxis
H Bleeding gums Surgery
H Hemorrhages into the skin, mucous membranes, and H Splenectomy (when splenomegaly accompanies the
other tissues causing red discoloration of skin (pur- initial thrombocytopenia)
pura)
H Small, purplish hemorrhagic spots on skin (pete- Other
chiae) H Platelet transfusion with profuse bleeding
H Excessive menstrual bleeding

Complications
H Hemorrhage
H Cerebral hemorrhage
H Purpuric lesions of vital organs (such as the brain
and kidney)

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Nursing considerations
Key outcomes
The patient will:
H demonstrate the use of protective measures, includ-
ing conserving energy, maintaining a balanced diet,
and getting plenty of rest
H demonstrate effective coping mechanisms
H express positive feelings about self.

Nursing interventions
H Administer prescribed platelets.
H Provide emotional support.
H Protect all areas of petechia and ecchymoses from
further injury.
Monitoring
H Signs of bleeding
H Platelet count
H Intake and output
H Vital signs
When receiving immunosuppressants
H Bone marrow depression
H Infection
H Mucositis
H GI ulcers
H Severe diarrhea or vomiting

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H how to observe for petechiae, ecchymoses, and other
signs of recurrence
H avoiding aspirin and ibuprofen
H avoiding straining during defecation and coughing
H bleeding precautions.

Discharge planning
H Advise the patient to carry medical identification to
alert others about the condition.

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Risk factors
Impetigo H Poor hygiene
H Untreated minor trauma
H Overcrowded living conditions
Overview H Lesions of preexisting eczema, chickenpox, scabies
H Other skin rashes
Description H Anemia
H Contagious, superficial bacterial skin infection H Malnutrition
H Nonbullous and bullous forms
H May complicate chickenpox, eczema, and other skin Incidence
disorders marked by open lesions H Most common among infants, children, and young
H Most commonly appears on face, arms, and legs adults
H More common in warm ambient temperatures
Pathophysiology H Predominant during late summer and early fall
Nonbullous impetigo
H Eruption occurs when bacteria inoculate traumatized Common characteristics
skin cells. H Painlessness
H Lesions begin as small vesicles, which rapidly erode. H Tender, red macule or papule
H Honey-colored crusts surrounded by erythema are H Pustules
formed.
Bullous impetigo Complications
H Eruption occurs in nontraumatized skin via bacterial H Acute glomerulonephritis
toxin or exotoxin. H Ecthyma (see Comparing ecthyma and impetigo)
H Lesions begin as thin-walled bullae and vesicles. H Exfoliative eruption (staphylococcal scalded-skin
H Lesions contain clear to turbid yellow fluid; some syndrome)
crusting exists. (See Recognizing impetigo.)
Causes Assessment
H Bacterial infection
H Spread by autoinoculation through scratching History
H Presence of risk factors
H Absence of pain
Recognizing impetigo H Possible pruritus

In impetigo, when the vesicles break, crust forms from the Physical findings
exudate. This infection is especially contagious among Nonbullous impetigo
young children. H Small, red macule or vesicle becoming pustular with-
in a few hours
H Characteristic thick, honey-colored crust forming
from the exudate
H Satellite lesions due to autoinoculation
Bullous impetigo
H Thin-walled vesicle
H Thin, clear crust forming from exudate
H Lesion appearing as a central clearing circumscribed
by an outer rim
Test results
Laboratory
H Gram stain of vesicular fluid shows infecting
organism.
H Culture and sensitivity testing of exudate or denuded
crust shows infecting organism.
H White blood cell count is elevated.

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Comparing ecthyma and impetigo

Treatment
Ecthyma is a superficial skin infection that usually causes
General scarring. It generally results from infection by group A
beta-hemolytic streptococci.
H Removal of exudate by washing lesions two to three Ecthyma differs from impetigo in that its characteristic
times per day with soap and water ulcer results from deeper penetration of the skin by the in-
H Warm soaks or compresses of normal saline solution fecting organism (involving the lower epidermis and der-
or a diluted soap solution for stubborn crusts mis), and the overlying crust tends to be raised (38 to
H Prevention with use of benzoyl peroxide soap 114) [1 to 3 cm]).
These lesions are usually found on the legs after a
Medications scratch or an insect bite. Autoinoculation can transmit ec-
H Antibiotics as appropriate thyma to other parts of the body, especially to sites that
have been scratched open.
H Antihistamines
Therapy for ecthyma is basically the same as for im-
petigo, beginning with removal of the crust, but the pa-
Nursing considerations tients response may be slower. Parenteral antibiotics are
also used.
Key outcomes
The patient will:
H exhibit improved or healed wounds or lesions
H report feelings of increased comfort
Discharge planning
H demonstrate proper skin care regimen H Encourage the patient to schedule follow-up appoint-
H verbalize feelings about changed body image. ments as recommended by his physician.
Nursing interventions
H Use meticulous hand-washing technique.
H Follow standard precautions.
H Remove crusts by gently washing with bactericidal
soap and water.
H Soften stubborn crusts with cool compresses.
H Administer prescribed drugs.
H Encourage verbalization of feelings about body
image.
H Comply with local public health standards and
guidelines.
Monitoring
H Response to treatment
H Adverse drug reactions
H Complications

Patient teaching Prevention

Be sure to cover:
H the disorder, diagnosis, and treatment
H prevention techniques (see Preventing the spread of
impetigo)
H trimming fingernails short
H regular bathing with bactericidal soap
H identification of characteristic lesions
H completion of prescribed medications
H possible adverse reactions
H lesion care.
Preventing the spread of impetigo
The spread of impetigo can be prevented by following
these guidelines:
H Practice meticulous hand-washing techniques after
touching linens.
H Use a clean towel and washcloth with each bath if
impetigo is present.
H Avoid sharing clothes and linens.
H Avoid sharing razors, towels, and washcloths.
H Clean all minor cuts and scrapes with soap and water.

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Infectious Assessment
mononucleosis History
H Contact with a person having infectious mononu-
cleosis
Overview H Headache
H Malaise
Description H Fatigue
H An acute infectious disease that causes fever, sore H Sore throat
throat, and cervical lymphadenopathy H Fever
H Loss of appetite
Pathophysiology H Muscle aches or stiffness
H Virus enters and replicates in epithelial cells of the
oropharynx and B cells of tonsillar tissue, causing al- Physical findings
teration of shape and function of the infected cells. H Exudative tonsillitis, pharyngitis
H Infected B cells activate cell-mediated immunity with H Palatal petechiae
proliferation of abnormal cytotoxic T cells in lym- H Periorbital edema
phoid tissues. H Maculopapular rash that resembles rubella
H Lymphoproliferation stops when cytotoxic T cells are H Cervical adenopathy; possible inguinal and axillary
able to destroy infected B cells. adenopathy
H Splenomegaly, hepatomegaly, jaundice
Causes
H Epstein-Barr virus (EBV), a member of the herpes Test results
group Laboratory
H Spread by contact with oral secretions (kissing) H White blood cell (WBC) count is increased 10,000 to
H Also transmitted during bone marrow transplantation 20,000/l during the second and third weeks of ill-
and blood transfusion ness; lymphocytes and monocytes account for 50% to
70% of the total WBC count; 10% of the lymphocytes
Incidence are atypical.
H Primarily affects young adults and children H Fourfold increase in heterophil antibodies (agglu-
H Common and widespread in early childhood in de- tinins for sheep red blood cells) during the acute
veloping countries and socioeconomically depressed phase and at 3- to 4-week intervals.
populations H Antibodies to EBV and cellular antigens are shown by
indirect immunofluorescence.
Common characteristics H Liver function studies are abnormal.
H Incubation period of about 4 to 6 weeks in young
adults
H Prodromal symptoms include headache, malaise, Treatment
and profound fatigue
H After 3 to 5 days, triad of symptoms, including sore General
throat, cervical lymphadenopathy, and temperature H Essentially supportive
fluctuations, with an evening peak of 101 to 102 F H Nutritious diet
(38.3 to 38.9 C) H Soft food (with throat soreness)
H Frequent rest periods
Complications H Avoidance of strenuous activity or contact sports until
H Splenic enlargement or rupture fully recovered
H Aseptic meningitis
H Encephalitis Medications
H Hemolytic anemia H Acetaminophen or ibuprofen
H Pericarditis H Steroids such as prednisone
H Guillain-Barr syndrome
H Secondary bacterial throat infection Surgery
H Hepatitis H Splenectomy for splenic rupture

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Prevention
Nursing considerations Preventing the spread of infectious
mononucleosis
Key outcomes
The spread of infectious mononucleosis can be limited by
The patient will: teaching the patient to follow these guidelines:
H maintain temperature within normal limits H Avoid sharing food, dishes, glasses, and utensils.
H conserve energy while performing daily activities to H Avoid kissing for several days after fever has subsided.
tolerance level H Use good hand-washing techniques.
H identify factors that intensify pain and change behav- H Dont donate blood for at least 6 months from onset of
ior accordingly illness.
H express needs and communicate whether needs are
met.
Nursing interventions
H Administer prescribed drugs.
H Provide warm saline gargles for symptomatic relief of
sore throat.
H Provide adequate fluids and nutrition.
H Plan care to provide frequent rest periods.

Monitoring
H Response to treatment
H Fatigue
H Nutritional status
H Liver function tests
H Complications

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H expectation that convalescence may take several
weeks
H need for bed rest during the acute illness
H explanation that theres a period of prolonged com-
municability
H prevention techniques (see Preventing the spread of
infectious mononucleosis)
H benefits of bland foods, milk shakes, fruit juices, and
broths to minimize throat discomfort.
Discharge planning
H Refer the patient to an otolaryngologist for marked
tonsillar swelling or a neurologist for a central ner-
vous system complication.

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Complications
Influenza H Pneumonia
H Myositis
H Exacerbation of chronic obstructive pulmonary
Overview disease
H Reyes syndrome
Description H Myocarditis
H An acute, highly contagious infection of the respirato- H Pericarditis
ry tract H Transverse myelitis
H Has capacity for antigenic variation (ability to mutate H Encephalitis
into different strains so that no immunologic resis-
tance is present in those at risk)
H Antigenic variation characterized as antigenic drift Assessment
(minor changes occurring yearly or every few years)
and antigenic shift (major changes that lead to pan- History
demics) H Usually, recent exposure (typically within 48 hours)
H Also called the grippe or the flu to a person with influenza
H Patient not receiving influenza vaccine during the
Pathophysiology past season
H The virus invades the epithelium of the respiratory H Headache
tract, causing inflammation and desquamation. H Malaise
H After attaching to the host cell, viral ribonucleic acid H Myalgia
enters the cell and uses host components to replicate H Fatigue, listlessness, weakness
its genetic material and protein, which are then as-
sembled into new virus particles. Physical findings
H Newly produced viruses burst forth to invade other H Fever (usually higher in children)
healthy cells. H Signs of croup, dry cough
H Viral invasion destroys host cells, impairing respira- H Red, watery eyes; clear nasal discharge
tory defenses (especially mucociliary transport sys- H Erythema of the nose and throat without exudate
tem) and predisposing the patient to secondary bac- H Tachypnea, shortness of breath, cyanosis
terial infection. H With bacterial pneumonia, purulent or bloody
sputum
Causes H Cervical adenopathy and tenderness
H Type A, most prevalent; strikes annually with new H Breath sounds may be diminished in areas of con-
serotypes causing epidemics every 3 years solidation
H Type B also annual; causes epidemics only every 4 H Nausea, vomiting, and diarrhea possibly occurring,
to 6 years but more common in children than adults
H Type C endemic; causes only sporadic cases
H Infection transmitted by inhaling a respiratory Test results
droplet from an infected person or by indirect con- H After an epidemic is confirmed, diagnosis requires
tact (drinking from a contaminated glass) only observation of clinical signs and symptoms.
Laboratory
Incidence H Inoculation of chicken embryos with nasal secretions
H Affects all age-groups; highest incidence among from infected patients shows influenza virus.
school-age children H Throat swabs, nasopharyngeal washes, or sputum
H Greatest severity (may lead to death) in young chil- culture shows isolation of the influenza virus.
dren, elderly people, and those with chronic diseases H Immunodiagnostic techniques show viral antigens in
H Occurs sporadically or in epidemics (usually during tissue culture or in exfoliated nasopharyngeal cells
colder months) with peak within 2 to 3 weeks after obtained by washings.
initial cases and lasting 2 to 3 months H Leukocyte counts are elevated in secondary bacterial
infection.
Common characteristics H Leukocyte counts are decreased in overwhelming
H Flu symptoms after incubation period of 24 to viral or bacterial infection.
48 hours
H Sudden onset of chills, fever (101 to 104 F [38.3
to 40 C]), headache, malaise, myalgia (particularly Treatment
in the back and limbs), photophobia, a nonproduc-
tive cough and, occasionally, laryngitis, hoarseness, General
rhinitis, and rhinorrhea H Fluid and electrolyte replacements
H Oxygen and assisted ventilation, if indicated

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H Increased fluid intake Prevention

H Rest periods, as needed Preventing the spread of influenza
Medications The spread of influenza can be limited by teaching the pa-
tient to follow these guidelines:
H Acetaminophen H Wash hands frequently and use good hand-washing
H Guaifenesin or expectorant techniques.
H Amantadine for influenza A H Cover mouth and nose when coughing or sneezing.
H Dispose of tissues properly.
H Avoid touching eyes, nose, and mouth.
Nursing considerations H Avoid close contact with others.
H Stay home and rest when sick.
Key outcomes H Get plenty of sleep, fluids, and nutritious foods.
The patient will: H High-risk patients should take antiviral drugs as
H report increased energy level prescribed.
H Get the influenza vaccine yearly.
H maintain a normal temperature
H express feelings of increased comfort and relief from
pain
H maintain adequate fluid volume
H maintain respiratory rate within 5 breaths/minute of
baseline.
Nursing interventions
H Administer prescribed drugs.
H Follow standard precautions.
H Administer oxygen therapy, if warranted.

Monitoring
H Temperature
H Signs and symptoms of dehydration
H Respiratory status
H Response to treatment
H Complications

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H mouthwash or warm saline gargles to ease sore
throat
H importance of increased fluids to prevent dehydra-
tion
H warm bath or a heating pad to relieve myalgia
H prevention techniques. (See Preventing the spread
of influenza.)

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Inguinal hernia H Direct hernias: more common in middle-aged and

elderly people
Common characteristics
Overview H A lump that appears over the herniated area when
the patient stands or strains and that disappears
Description when the patient is in a supine position
H Protrusion of part of an internal organ through an H Tension on the herniated contents possibly causing a
abnormal opening in the wall of the cavity that sur- sharp, steady pain in the groin that fades when the
rounds it hernia is reduced
H The most common type of hernia (see Common H Strangulation that produces severe pain possibly
sites of hernia) leading to partial or complete bowel obstruction and
H May be direct or indirect intestinal necrosis
H Also called rupture
Complications
Pathophysiology H Strangulation
H In an inguinal hernia, the large or small intestine, H Intestinal obstruction
omentum, or bladder protrudes into the inguinal H Infection (after surgery)
canal.
H In an indirect hernia, abdominal viscera leave the
abdomen through the inguinal ring and follow the Assessment
spermatic cord (in males) or round ligament (in fe-
males); they emerge at the external ring and extend History
down into the inguinal canal, typically into the scro- H Sharp or catching pain when lifting or straining
tum or labia.
H In a direct inguinal hernia, instead of entering the Physical findings
canal through the internal ring, the hernia passes H Obvious swelling or lump in the inguinal area (large
through the posterior inguinal wall, protrudes direct- hernia) (see Identifying a hernia)
ly through the transverse fascia of the canal (in an
area known as Hesselbachs triangle), and comes Test results
out at the external ring. Laboratory
H White blood cell count is elevated (with intestinal
Causes obstruction).
H Indirect weakness in fascial margin of internal
inguinal ring
H Direct weakness in fascial floor of inguinal canal Treatment
H Either weak abdominal muscles (caused by con-
genital malformation, trauma, or aging) or increased General
intra-abdominal pressure (caused by heavy lifting, H Manual reduction
pregnancy, obesity, or straining) H Truss
H Activity, as tolerated
Incidence H Nothing by mouth if surgery necessary
H Indirect hernias: more common; may develop at any
age; three times more common in males; especially Medications
prevalent in infants H Analgesics
H Antibiotics as appropriate
H Electrolyte replacement
Identifying a hernia
Surgery
Palpation of the inguinal area while the patient is perform-
H Herniorrhaphy
ing Valsalvas maneuver confirms the diagnosis of ingui-
H Hernioplasty
nal hernia. To detect a hernia in a male patient, ask the pa-
H Bowel resection (with strangulation or necrosis)
tient to stand with his ipsilateral leg slightly flexed and his
weight resting on the other leg. Insert an index finger into
the lower part of the scrotum and invaginate the scrotal
skin so the finger advances through the external inguinal
Nursing considerations
ring to the internal ring (about 12 to 2 [1 to 5 cm]
through the inguinal canal). Tell the patient to cough. If Key outcomes
pressure is felt against the fingertip, an indirect hernia ex- The patient will:
ists; if pressure is felt against the side of the finger, a di- H express feelings of increased comfort
rect hernia exists. H have normal bowel function
H avoid complications.

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Common sites of hernia
There are four common sites of hernia: umbilical, incisional,
inguinal, and femoral. Here are descriptions of each type
with an illustration demonstrating where each type is lo-
cated.
Umbilical
Umbilical hernia results from abnormal muscular structures
around the umbilical cord. This hernia is quite common in
neonates but also occurs in females who are obese or who
have had several pregnancies. Because most umbilical her-
nias in infants close spontaneously, surgery is warranted
only if the hernia persists for more than 4 to 5 years. Taping
or binding the affected area or supporting it with a truss may
relieve symptoms until the hernia closes. A severe congeni-
tal umbilical hernia, which allows the abdominal viscera to
protrude outside the body, must be repaired immediately.
Incisional
Incisional (ventral) hernia develops at the site of previous
surgery, usually along vertical incisions. This hernia may re-
sult from a weakness in the abdominal wall, caused by an
infection, impaired wound healing, inadequate nutrition, ex-
treme abdominal distention, or obesity. Palpation of an inci-
Umbilical
Incisional
Inguinal
Femoral
Nursing interventions
H Apply a truss after a hernia has been reduced.
H Administer prescribed drugs for pain.
H Encourage coughing and deep breathing.
Monitoring
H Vital signs
H Pain control
H Signs of strangulation or incarceration
sional hernia may reveal several defects in the surgical scar.
Effective repair requires pulling the layers of the abdominal
wall together without creating tension or, if this isnt possi-
ble, the use of Teflon, Marlex mesh, or tantalum mesh to
close the opening.
Inguinal
Inguinal hernia can be direct or indirect. An indirect inguinal
hernia causes the abdominal viscera to protrude through the
inguinal ring and follow the spermatic cord (in males) or
round ligament (in females). A direct inguinal hernia results
from a weakness in the fascial floor of the inguinal canal.
Femoral
Femoral hernia occurs where the femoral artery passes into
the femoral canal. Typically, a fatty deposit within the femo-
ral canal enlarges and eventually creates a hole big enough
to accommodate part of the peritoneum and bladder. A fem-
oral hernia appears as a swelling or bulge at the pulse point
of the large femoral artery. Its usually a soft, pliable, re-
ducible, nontender mass but commonly becomes incarcer-
ated or strangulated.
Patient teaching
Be sure to cover:
H avoidance of lifting heavy objects or straining during
bowel movements
H signs and symptoms of infection (oozing, tenderness,
warmth, and redness) at the incision site
H wound care
H after surgery, not resuming normal activity or return-
ing to work without the surgeons permission.
Discharge planning
H Encourage the patient to schedule follow-up appoint-
ments as recommended by the surgeon.
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Insect bites and stings Assessment

History
Overview Tick bite
H Itching at the affected site
Description H Tick observed at lesion
H Bite or sting from an insect or other arthropod, such Brown recluse spider bite
as a tick, brown recluse spider, black widow spider, H Minimal initial pain that increases over time
scorpion, bee, wasp, yellow jacket, or fire ant, that H Fever, chills, malaise, weakness
causes pain or a local systemic reaction H Nausea, vomiting
H Joint pain
Pathophysiology Black widow spider bite
H A bite or sting can injure the skin, and secretions re- H Pinprick sensation, followed by dull, numbing pain
leased from a bite or sting can cause a physiologic H Leg bite: severe pain and large-muscle cramping
response specific to the insect or arthropod. H Vertigo
H Reactions to secretion exposure range from barely H Chills and sweats
noticeable to life-threatening. Bee, wasp, or yellow jacket sting
H Transmission of disease may result from a bite or H Pain and pruritus
sting. H Generalized weakness
H Mouth parts of an insect or arthropod are classified H Chest tightness
as piercing-sucking, sponging, or biting-chewing. H Dizziness
H Nausea and vomiting
Causes H Abdominal cramps
H Toxic effects of venom H Throat constriction
H Hypersensitivity response Fire ant sting
H Immediate pain, itching, and burning
Incidence
H Unknown Physical findings
Tick bite
Common characteristics H Tick paralysis
Local reaction H Expanding skin lesion, erythema migrans
H Mild discomfort to moderate or severe pain Brown recluse spider bite
H Erythema and warmth H Bleb (blister)
H Tenderness H Bluish ring around bite
H Edema of surrounding tissues H Joint pain
H Severe local reaction H Seizures
H Generalized erythema H Petechiae
H Urticaria Black widow spider bite
H Pruritic edema H Rigid, painful abdomen
Systemic response H Rigidity and pain in the chest, shoulders, and back
H All of the above symptoms (if arm bite)
H Anxiety, disorientation H Extreme restlessness (systemic)
H Weakness H Pallor
H GI disturbances H Seizures, especially in children
H Dizziness H Hyperactive reflexes
H Hypotension H Hypertension
H Stridor H Tachycardia with thready pulse
H Dyspnea and cough H Circulatory collapse
H Cardiovascular collapse Bee, wasp, or yellow jacket sting
H Raised, reddened wheal, possibly with a protruding
Complications stinger from the bee, wasp, or yellow jacket
H Anaphylaxis H Wheezing
H Hemolytic anemia H Hypotension
H Rarely, thrombocytopenia (brown recluse spider Fire ant sting
only) H Clear vesicles with surrounding erythema
H Pustule

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Test results Surgery

Laboratory H Lesion excision for brown recluse spider bite
H Urinalysis shows hematuria (black widow spider
bite).
H White blood cell count is increased (black widow Nursing considerations
spider bite).
H Anemia panel shows hemolytic anemia (brown Key outcomes
recluse spider bite). The patient will:
H Platelet count shows thrombocytopenia (brown H maintain adequate ventilation and a patent airway
recluse spider bite). H express feelings of increased comfort
Other H regain skin integrity
H Identification of the insect is difficult unless stung by H maintain normal fluid volume.
a honeybee or bumblebee, which typically leaves a
stinger with a venom sac in the lesion. Nursing interventions
H Keep the affected part immobile.
Treatment H Clean the bite or sting site with antiseptic.
H Apply ice.
General H Administer prescribed drugs.
H Provide emergency resuscitation.
Tick bite Tick bite
H Tick removal H Remove the tick promptly and carefully.
H Symptomatic therapy for severe symptoms H Use tweezers to grasp the tick near its head or
Brown recluse spider bite mouth, and gently pull to remove the whole tick with-
H Cool compresses and elevation of extremity out crushing it.
H I.V. fluids H If possible, seal the tick in a plastic bag and keep it
Black widow spider bite in case the patient needs to see a physician. Other-
H Ice packs wise, flush the tick down the toilet or burn it.
Bee, wasp, yellow jacket, or fire ant sting Brown recluse spider bite
H Ice application H Clean the lesion with a 1:20 Burows aluminum
H Elevation of affected extremity acetate solution.
H Supportive treatment H Apply antibiotic ointment, as ordered.
H No dietary restrictions Black widow spider bite
H Nothing by mouth if severe, systemic reaction H Remove all jewelry.
H Rest to limit toxic effects of venom H Apply cool compresses.
H Avoid cutting into the wound or applying suction.
Medications Bee, wasp, or yellow jacket sting
Tick bite H Scrape stinger off; dont pull or squeeze it, which
H Antipruritics releases more toxin.
H Antibiotics Fire ant sting
Doxycycline, amoxicillin, or cefuroxime axetil for H Apply cool compresses.
Lyme disease H Gently wash the bite area, leaving the blister intact.
Doxycycline for Rocky Mountain spotted fever H Be prepared to intervene for an acute severe allergic
Brown recluse spider bite reaction (rare).
H Corticosteroids
H Antibiotic ointment Monitoring
H Antihistamines H Vital signs
H Tranquilizers H Respiratory status
H Tetanus prophylaxis H General appearance
Black widow spider bite H Changes at the bite or sting site
H Antivenin I.V.
H Calcium gluconate I.V. Patient teaching
H Muscle relaxants
H Adrenaline or antihistamines Be sure to cover:
H Tetanus immunization H avoidance of insect bites and stings
H Oxygen for respiratory difficulty H examination of the body for ticks after being outdoors
Bee, wasp, yellow jacket, or fire ant sting H removal of ticks
H Antihistamines such as diphenhydramine H medical identification jewelry or card
H Steroids for severe reactions H anaphylaxis kit use
H Bronchodilator such as epinephrine H insect repellent use.

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Common characteristics
Life-threatening disorder H Abdominal pain
H Change in bowel habits

Intestinal obstruction Complications

H Perforation
H Peritonitis
Overview H Septicemia
H Secondary infection
Description H Metabolic alkalosis or acidosis
H Partial or complete blockage of the lumen of the H Death
small or large bowel
H Usually a medical emergency
H Most likely after abdominal surgery or with congeni- Assessment
tal bowel deformities
H Without treatment, complete obstruction in any part History
of bowel causing death within hours from shock and H Recent change in bowel habits
vascular collapse H Hiccups
Mechanical obstruction
Pathophysiology H Colicky pain
H Mechanical or nonmechanical (neurogenic) block- H Nausea, vomiting
age of the lumen occurs. H Constipation
H Fluid, air, or gas collects near the site. Nonmechanical obstruction
H Peristalsis increases temporarily in an attempt to H Diffuse abdominal discomfort
break through the blockage. H Frequent vomiting
H Intestinal mucosa is injured, and distention at and H Severe abdominal pain (if obstruction results from
above the site of obstruction occurs. vascular insufficiency or infarction)
H Venous blood flow is impaired, and normal absorp-
tive processes cease. Physical findings
H Water, sodium, and potassium are secreted by the Mechanical obstruction
bowel into the fluid pooled in the lumen. H Distended abdomen
H Borborygmi and rushes (occasionally loud enough to
Causes be heard without a stethoscope)
Mechanical obstruction H Abdominal tenderness
H Adhesions H Rebound tenderness
H Strangulated hernias Nonmechanical obstruction
H Carcinomas H Abdominal distention
H Foreign bodies H Decreased bowel sounds (early), then absent bowel
H Compression of the bowel wall from stenosis, sounds
intussusception, volvulus of the sigmoid or cecum,
tumors, and atresia Test results
Nonmechanical obstruction Laboratory
H Paralytic ileus H Serum sodium, chloride, and potassium levels are
H Electrolyte imbalances decreased.
H Toxicity, such as that associated with uremia or H White blood cell counts are elevated.
generalized infection H Serum amylase level is elevated if pancreas is irritat-
H Neurogenic abnormalities ed by a bowel loop.
H Thrombosis or embolism of mesenteric vessels H Blood urea nitrogen level is increased (with dehydra-
tion).
Risk factors Imaging
H Abdominal surgery H Abdominal X-rays reveal the presence and location of
H Radiation therapy intestinal gas or fluid. In small-bowel obstruction, a
H Gallstones typical stepladder pattern emerges, with alternating
H Inflammatory bowel disease fluid and gas levels apparent in 3 to 4 hours.
H Barium enema reveals a distended, air-filled colon or
Incidence a closed loop of sigmoid with extreme distention (in
H Diagnosed in about 20% of hospital admissions for sigmoid volvulus).
abdominal illness
H Occurs equally in males and females

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Treatment Patient teaching

General
H Correction of fluid and electrolyte imbalances
H Decompression of the bowel to relieve vomiting and
distention
H Treatment of shock and peritonitis
H Nothing by mouth if surgery planned
H Parenteral nutrition until bowel is functioning
H High-fiber diet when obstruction relieved
H Bed rest during acute phase
H Postoperatively, avoidance of lifting and contact
sports
Medications
H Broad-spectrum antibiotics
H Analgesics
H Blood replacement
Surgery
H Usually the treatment of choice (exception is paralyt-
ic ileus in which nonoperative therapy is usually at-
tempted first)
H Type of surgery depends on cause of blockage
Be sure to cover:
H the disorder (focusing on the patients type of intesti-
nal obstruction), diagnosis, and treatment
H techniques for coughing and deep breathing, and use
of an incentive spirometer
H colostomy or ileostomy care, if appropriate
H incision care
H postoperative activity limitations and why these re-
strictions are necessary
H medication administration, dosage, and possible ad-
verse effects
H importance of following a structured bowel regimen,
particularly if the patient had a mechanical obstruc-
tion due to fecal impaction.
Discharge planning
H Refer the patient to an enterostomal therapist, if
indicated.

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort
H maintain normal fluid volume
H return to normal bowel function
H maintain caloric requirement
H maintain stable vital signs.

Nursing interventions
H Insert a nasogastric (NG) tube and attach to
low-pressure, intermittent suction.
H Maintain the patient in semi-Fowlers position.
H Provide mouth and nose care.
H Begin and maintain I.V. therapy, as ordered.
H Administer prescribed drugs.

Monitoring
H Vital signs
H Signs and symptoms of shock
H Bowel sounds and signs of returning peristalsis
H NG tube function and drainage
H Pain control
H Abdominal girth measurement to detect progressive
distention
H Hydration and nutritional status
H Electrolytes and signs and symptoms of metabolic de-
rangements
H Wound site (postoperatively)

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H Lymphoid hyperplasia
Life-threatening disorder H Meckels diverticulum
H Alterations in intestinal motility

Intussusception In adults
H Benign or malignant tumors (65% of patients)
H Polyps
H Meckels diverticulum
Overview H Gastroenterostomy with herniation
H Appendiceal stump
Description
H Condition in which a portion of the bowel telescopes Incidence
or invaginates into an adjacent bowel portion (see H Most common in infants
Understanding intussusception) H Three times more common in males than in females
H Can be fatal if treatment delayed more than 24 hours H About 87% of children with intussusception younger
H Pediatric emergency than age 2; about 70% of these children between
ages 4 and 11 months
Pathophysiology H Seasonal peaks in late spring and early summer
H A bowel section invaginates and is propelled by peri-
stalsis. Common characteristics
H More bowel is pulled in, causing edema, obstruction, H Intermittent attacks of colicky pain
and pain. H Vomiting
H Abdominal guarding
Causes
H Intussusception may be linked to viral infections due Complications
to seasonal peaks. H Strangulation of the intestine
In infants H Gangrene of the bowel
H Unknown H Shock
In older children H Bowel perforation
H Polyps H Peritonitis
H Hemangioma H Death
H Lymphosarcoma

Understanding intussusception
In intussusception, a bowel section invaginates and is pro-
pelled along by peristalsis, pulling in more bowel. This il-
lustration shows intussusception of a portion of the trans-
verse colon. Intussusception typically produces edema,
hemorrhage from venous engorgement, incarceration, and
obstruction.
Invaginated bowel
Cecum
Assessment
History
H Intermittent attacks of colicky pain
H Pain that causes the child to scream, draw his legs up
to his abdomen, turn pale and diaphoretic and, pos-
sibly, grunt
H Vomiting, initially stomach contents; later,
bile-stained or fecal material
H Currant jelly stools, which contain mixture of
blood and mucus
Physical findings
H Distended, tender abdomen
H Guarding over the intussusception site
H Palpable sausage-shaped abdominal mass in the right
upper quadrant or in the midepigastric area if trans-
verse colon involved
H Bloody mucus on rectal examination
H In adults, abdominal pain localized in right lower
quadrant, radiating to the back, and increasing with
eating
Test results
Laboratory
H White blood cell count up to 15,000/l indicates
obstruction; more than 15,000/l, strangulation;
and more than 20,000/l, bowel infarction.

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Imaging
H Barium enema confirms colonic intussusception
when it shows the characteristic coiled-spring sign;
it also delineates the extent of intussusception.
H Upright abdominal X-rays may show a soft-tissue
mass and signs of complete or partial obstruction,
with dilated loops of bowel.
Treatment
General
H Hydrostatic reduction
H Bowel decompression
H Nothing by mouth until bowel functions properly
H Bed rest until condition is resolved
Medications
H Analgesics
H Antibiotics if infection occurs
Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medication administration, dosage, and possible ad-
verse effects
H wound care
H signs and symptoms of infection
H parental participation in their childs care to mini-
mize the stress of hospitalization (visiting hours
should be flexible).
Discharge planning
H Encourage the patients family to make follow-up ap-
pointments as recommended by his physician.

Surgery
H Indicated for children with recurrent intussuscep-
tion, those who show signs of shock or peritonitis,
and those in whom symptoms present longer than
24 hours
H In adults, always the treatment of choice

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort
H avoid complications
H maintain normal fluid volume
H have family members who understand the disorder
and treatment regimen.
Nursing interventions
H Offer reassurance and emotional support to the pa-
tient and, if the patient is a child, to his parents.
H Administer prescribed I.V. fluids.
H Encourage coughing and deep breathing.
H Administer prescribed antibiotics.

Monitoring
H Vital signs
H Intake and output
H Hydration status
H Nasogastric tube function and drainage
H Bowel sounds, stools, abdominal distention
H Wound site (after surgery)
H For recurrence in the first 36 to 48 hours after
reduction

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Irritable bowel H Contributing psychological factors, such as a recent

stressful life change, that may have triggered or ag-
syndrome gravated symptoms
H Anxiety and fatigue

Physical findings
Overview H Normal bowel sounds
H Tympany over a gas-filled bowel
Description
H Common condition marked by chronic or periodic Test results
diarrhea alternating with constipation H Assessment involves studies to rule out other, more
H Accompanied by straining and abdominal cramps serious disorders.
H Initial episodes early in life and late teens to twenties Laboratory
H Prognosis good H Stool examination is negative for occult blood, para-
H Also known as spastic colon, spastic colitis, mu- sites, and pathogenic bacteria.
cous colitis H Complete blood count, serologic tests, serum albu-
min, and erythrocyte sedimentation rate are normal.
Pathophysiology Imaging
H Precise etiology unclear H Barium enema may reveal colonic spasm and a tubu-
H Involves a change in bowel motility, reflecting an ab- lar appearance of the descending colon. Its also
normality in the neuromuscular control of intestinal used to rule out certain other disorders, such as di-
smooth muscle verticula, tumors, and polyps.
Diagnostic procedures
Causes H Sigmoidoscopy may disclose spastic contractions.
H Anxiety and stress
H Dietary factors, such as fiber, raw fruits, coffee, alco-
hol, and foods that are cold, highly seasoned, or lax- Treatment
ative in nature
Other possible triggers General
H Hormones H Stress management
H Laxative abuse H Lifestyle modifications
H Allergy to certain foods or drugs H Diet based on the patients symptoms
H Lactose intolerance H Initially, an elimination diet
H Avoidance of sorbitol, nonabsorbable carbohydrates,
Incidence and lactose-containing foods
H Occurs mostly in females, with symptoms first emerg- H Increased dietary bulk
ing before age 40 H Increased fluid intake
H Regular exercise
Common characteristics
H Chronic constipation or diarrhea Medications
H Lower abdominal pain H Bulk-forming laxatives/fiber supplements, such as
psyllium and methylcellulose
Complications H Anticholinergics and antispasmodics
H Diverticulitis and colon cancer H Antidiarrheals such as loperamide
H Chronic inflammatory bowel disease H Antiemetics
H Simethicone
H Mild tranquilizers
Assessment H Tricyclic antidepressants, such as impiramine and
amitriptyline
History H 5HT3-receptor antagonist such as alosetron
H Chronic constipation, diarrhea, or both
H Lower abdominal pain (typically in the left lower
quadrant) usually relieved by defecation or passage Nursing considerations
of gas
H Small stools with visible mucus or pasty, pencil-like Key outcomes
stools instead of diarrhea The patient will:
H Dyspepsia H express feelings of increased comfort
H Abdominal bloating H maintain adequate caloric intake
H Heartburn H have normal bowel function
H Faintness and weakness H express positive feelings about self

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H maintain normal laboratory values

H understand the disease process and treatment
regimen.
Nursing interventions
H Because the patient generally isnt hospitalized for ir-
ritable bowel syndrome, nursing interventions almost
always focus on patient teaching.
Monitoring
H Weight
H Diet
H Bowel movements

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H dietary plans and implementation
H need to drink 8 to 10 glasses of water or other com-
patible fluids daily
H proper use of prescribed medication, reviewing de-
sired effects and possible adverse reactions
H need to implement lifestyle changes that reduce
stress
H smoking cessation
H need for regular physical examinations. (For patients
older than age 40, emphasize the need for colorectal
cancer screening, including annual proctosigmoid-
oscopy and rectal examinations.)

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J
Juvenile rheumatoid
arthritis
Overview
Description
H Several inflammatory conditions characterized by
chronic synovitis and joint swelling, pain, and ten-
derness
H Major types systemic (Stills disease or acute
febrile type), polyarticular, and pauciarticular
Pathophysiology
H If juvenile rheumatoid arthritis (JRA) isnt arrested,
the inflammatory process in the joints occurs in four
stages:
Synovitis develops from congestion and edema of
the synovial membrane and joint capsule.
Pannus covers and invades cartilage and eventually
destroys the joint capsule and bone.
Fibrous tissue and ankylosis occludes the joint
space.
Fibrous tissue calcifies, resulting in bony ankylosis
and total immobility.
Physical findings
Systemic JRA
H Mild, transient arthritis or frank polyarthritis with
fever and rash
H Behavior may clearly suggest joint pain and fatigue
H Painful breathing and nonspecific abdominal pain
H Fatigue, shortness of breath, palpitations, and fever
H Resting or exertional tachycardia; arrhythmias; jugu-
lar vein distention; heart murmurs
H Hepatic, splenic, and lymph node enlargement
H Friction rub associated with pericarditis
Polyarticular JRA
H Pain in the wrists, elbows, knees, ankles, and small
joints of the hands and feet
H Pain in larger joints, including the temporomandibu-
lar, cervical spine, hips, and shoulders
H Tenderness, stiffness, and swelling of joints
H Possible low-grade fever with daily peaks
H Weight loss
H Noticeable developmental retardation
H Hepatic, splenic, and lymph node enlargement
H Subcutaneous nodules on the elbows or heels
Pauciarticular JRA
H Pain in the hips, knees, heels, feet, ankles, and el-
bows
H Eye redness, blurred vision, and photophobia
H Lower back pain

Causes Test results

H Unknown Laboratory
H Suggested link to genetic factors or an abnormal im- H Serum hemoglobin levels are decreased, and neu-
mune response trophil (neutrophilia) and platelet (thrombocytosis)
H Viral or bacterial (streptococcal) infection, trauma, levels are increased; other findings include elevated
and emotional stress erythrocyte sedimentation rate and elevated C-reac-
tive protein, serum haptoglobin, immunoglobulin,
Incidence and C3 complement levels.
H May occur as early as age 6 weeks but seldom before H Antinuclear antibody test is positive in patients with
age 6 months; peak onset between ages 1 and 3 and polyarticular JRA and in those with pauciarticular
8 and 12 JRA with chronic iridocyclitis.
H Occurs in an estimated 150,000 to 250,000 children H Rheumatoid factor (RF) appears in about 15% of pa-
in United States; affects twice as many girls as boys tients with JRA. (In contrast, about 85% of patients
with rheumatoid arthritis test positive for RF; patients
Common characteristics with polyarticular JRA may test positive for RF.)
H Joint stiffness in the morning H Human leukocyte antigen-B27 forecasts later devel-
opment of ankylosing spondylitis.
Complications Imaging
H Flexion contractures H X-ray studies demonstrate early structural changes
H Ocular damage and loss of vision associated with JRA. These include soft-tissue
H Retarded growth and development swelling, effusion, and periostitis in affected joints.
Later evidence includes osteoporosis and accelerated
bone growth followed by subchondral erosions,
Assessment joint-space narrowing, bone destruction, and fusion.
History
H Common complaint of joint stiffness in morning or Treatment
after periods of inactivity
H In young children, typically irritability and listless- General
ness H Physical therapy
H Splints
H Heat application during passive exercises

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H Adequate iron, protein, calcium, and caloric intake
H Activity, as tolerated
Medications
H Analgesic such as acetaminophen
H Nonsteroidal anti-inflammatory drugs (NSAIDs)
H Disease-modifying antirheumatic drugs, such as
methotrexate, penicillamine, gold salts, and the anti-
malarial drug hydroxychloroquine.
Surgery
H Soft-tissue releases to improve mobility
H Joint replacement (delayed until child matures physi-
cally and can tolerate vigorous rehabilitation)
H signs and symptoms of exacerbation, and the need to
notify the pediatrician about these symptoms
H need for proper nutrition and caloric consumption
H childs special needs (telling teachers and the school
principal).
Discharge planning
H Consult an occupational therapist to assess the pa-
tients home care needs.

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort and decreased
pain
H recognize and express feelings about limitations due
to illness
H identify factors that increase risk for injury
H maintain optimum mobility.

Nursing interventions
H Focus nursing care on reducing pain and promoting
mobility.
H During inflammatory exacerbations, administer
NSAIDs or prescribed medication on a regular
schedule.
H Allow the patient to rest frequently throughout the
day to conserve energy for times when she must be
mobile.
H Arrange the patients environment for participation in
activities of daily living so that she feels capable of
accomplishing tasks.
Monitoring
H Pain level
H Response to treatment
H Signs and symptoms of bleeding
H Nutritional status
H Joint mobility
H Adverse drug effects

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H need to encourage the child to be as independent as
possible
H need for regular slit-lamp examinations to enable
early diagnosis and treatment of iridocyclitis
H signs and symptoms of bleeding caused by NSAID
therapy (instructing the patient to take these medica-
tions with meals or milk to reduce adverse GI reac-
tions)

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KKaposis sarcoma
Overview
Description
H Most common acquired immunodeficiency syndrome
(AIDS)related cancer
H Characterized by obvious, colorful lesions
H Most common internal sites: lungs and GI tract
(esophagus, oropharynx, and epiglottis)
Pathophysiology
H Kaposis sarcoma causes structural and functional
H Untreated lesions that may appear as large, ulcerative
masses
H Dyspnea
H Edema from lymphatic obstruction
H Wheezing and hypoventilation

Test results
Diagnostic procedures
H Tissue biopsy shows the type and stage of the lesion.
(See Laubensteins stages in Kaposis sarcoma.)

Treatment
General
damage. H Radiation therapy for palliation of symptoms (pain
H When associated with AIDS, it progresses aggressive- from obstructing lesions in the oral cavity or extremi-
ly, involving the lymph nodes, the viscera and, possi- ties and edema caused by lymphatic blockage); also
bly, GI structures. for cosmetic improvement
H High-calorie, high-protein diet
Causes H Small meals
H Exact cause unknown H Limited activity
H Frequent rest periods
Risk factors
H Males, especially white Medications
H Immunosuppression and immune deficiency H Chemotherapy
H People of Mediterranean or Middle Eastern descent H Biological response modifier
H Africans
Surgery
Incidence H Removal of lesion from skin (especially if lesion is
H Originally affected 35% of AIDS patients; now declin- small), using local excision, electrodesiccation and
ing with earlier detection of AIDS curettage, or cryotherapy
H 1 in 200 transplant patients in the United States

Common characteristics
H History of AIDS
H Lesions of various shapes, sizes, and colors

Complications
H Severe pulmonary involvement, resulting in respira- Laubensteins stages in Kaposis
tory distress sarcoma
H GI involvement, leading to digestive problems
L.J. Laubenstein proposed this staging system to evaluate
and treat patients with acquired immunodeficiency syn-
Assessment drome and Kaposis sarcoma:
H Stage I locally indolent cutaneous lesions
History H Stage II locally aggressive cutaneous lesions
H Stage III mucocutaneous and lymph node
H Possible history of AIDS
involvement
H Pain (in advanced cases) H Stage IV visceral involvement.
Within each stage, a patient may have different symp-
Physical findings toms further classified as stage subtype A or B, which are:
H Several lesions of various shapes, sizes, and colors H Subtype A no systemic signs or symptoms
(ranging from red-brown to dark purple) on the H Subtype B one or more systemic signs and
skin, buccal mucosa, hard and soft palates, lips, symptoms, including 10% weight loss, fever of
gums, tongue, tonsils, conjunctiva, and sclera (the unknown origin that exceeds 100 F (37.8 C) for
most common sites) longer than 2 weeks, chills, lethargy, night sweats,
H In advanced disease, lesions that may merge, becom- anorexia, and diarrhea.
ing one large plaque

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Nursing considerations
Key outcomes
The patient will:
H have no further weight loss
H express positive feelings about self
H maintain adequate ventilation
H maintain a patent airway
H exhibit no signs and symptoms of infection.

Nursing interventions
H Encourage verbalization and offer support.
H Inspect the skin for new lesions and skin breakdown.
H Administer prescribed drugs.
H Provide rest periods.

Monitoring
H Adverse effects of treatment
H Vital signs
H Pain control
H Nutritional status
H Respiratory status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medication administration, dosage, and possible ad-
verse effects
H infection prevention techniques and, if necessary, ba-
sic hygiene measures to prevent infection (especially
if the patient also has AIDS)
H the need for ongoing treatment and care.

Discharge planning
H Refer the patient to available resources and support
services.

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Kawasaki syndrome H Skin desquamation, especially in the groin, on the

palms, and soles
H Possible aneurysms leading to sudden death
Convalescent phase
Overview H Occurs between the 25th and 40th days
H May continue beyond 40 days without distinguishing
Description features
H A noncontagious, febrile, self-limited disorder of un-
known origin Complications
H Affects the mucus membranes, lymph nodes, blood H Vasculitis leading to aneurysm and myocardial infarc-
vessels, and heart tion
H Occurs in stages: acute, subacute, and convalescent H Death (2% of patients with Kawasaki syndrome dying
H Cardiac complications most serious sequelae from coronary vasculitis)
H Full recovery expected H Future coronary bypass surgery if coronary artery
H Also known as mucocutaneous lymph node syn- disease develops
drome and infantile polyarteritis H Myocarditis
H Pericarditis
Pathophysiology H Cardiac arrhythmias
H An infection results in altered immune function. H Abnormal valve functioning
H Antibodies increase as a result of the infection and
cause inflammation of blood vessels.
H Blood vessel inflammation increases platelet accu- Assessment
mulation and results in thrombi.
H Thrombi result in obstruction of heart and systemic History
blood vessels. H Fever of 5 days or more, unresponsive to antipyretics
H Occurrence of characteristic symptoms
Causes
H Possible genetic role after exposure to an unknown Physical findings
virus, bacteria, or other pathogen H Reddened, swollen hands and feet
H Inflamed mucous membrane of eyes
Risk factors H Strawberry tongue with red, cracked lips
H None known H Rash in trunk area
H No known preventive measures H Enlarged cervical lymph nodes
H Reddened, swollen joints
Incidence H Possible enlarged gallbladder
H Peak incidence in boys younger than age 4, but can
occur up to puberty Test results
H Affects boys 112 times more commonly than girls Laboratory
H Occurs more commonly in late winter and spring H White blood cell count and erythrocyte sedimentation
H Most common in Japan or in Japanese or Korean rate are elevated in acute phase.
children living elsewhere H Platelet count is elevated in the subacute phase.
H Commonly occurs in clusters within a geographic H Culture results are all negative.
location H Liver function test results are elevated.
H Rarely occurs twice in the same household H Complete blood count shows anemia.
H Urinalysis may show pyuria or proteinuria.
Common characteristics Imaging
Acute phase H Sequential echocardiograms detect artery disease.
H High fever for 5 days or more (up to 106.5 F H Chest X-ray rules out cardiomegaly or subclinical
[41.4 C]) unresponsive to antipyretics pneumonitis.
H Lethargy and irritability
H Reddened, swollen hands and feet
H Inflamed mucous membrane of eyes Treatment
H Strawberry tongue with red, cracked lips
H Rash in trunk area General
H Enlarged cervical lymph nodes H Hospitalization
H Abdominal pain, anorexia, and diarrhea resulting H Symptomatic
from internal lymph node swelling H Prevention of complications
H Reddened, swollen joints H Soft, nonirritating foods
Subacute phase H Avoidance of citrus (mouth sores)
H Begins about 10 days after the onset of symptoms H Activity, as tolerated

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Medications
H I.V. gamma globulin
H Aspirin

Nursing considerations
Key outcomes
The patient will:
H maintain adequate tissue perfusion
H have normal vital signs
H have a capillary refill time of less than 5 seconds
H experience a tolerable pain level
H experience increased comfort
H maintain adequate nutrition.

Nursing interventions
H Observe for signs of heart failure, such as tachycar-
dia, dyspnea, crackles, and edema.
H Inspect the extremities for color, temperature, and
capillary refill.
H Observe and report joint swelling and redness.
H Observe and report nature of rash.
H Keep clothing from constricting or irritating rash.
H Moisten lips with lip balm to prevent cracking.
H Offer frequent fluids.
H Observe for signs of GI upset, such as nausea and
vomiting.
H Avoid pressure on the extremities with edema.
H Administer prescribed drugs.

Monitoring
H Complications such as chest pain, arrhythmias, and
electrocardiogram changes
H Edema changes
H Intake and output
H Nutritional status
H Response to treatment
H Adverse effects of I.V. immunoglobulin: allergic reac-
tions, fever, chills, headache, transfusion reactions,
and pulmonary edema

Patient teaching
Be sure to cover:
H the disorder, diagnosis and treatment
H aspirin therapy during and after hospitalization
H reporting exposure to viral illnesses, such as influen-
za or chickenpox, while taking aspirin, in order to
prevent Reyes syndrome
H possibility of long-term management if cardiac com-
plications exist
H need to delay immunizations (especially the measles-
mumps-rubella and chickenpox vaccines) when im-
munoglobulin is given.
Discharge planning
H Encourage the patient to schedule a follow-up exami-
nation in 2 to 3 weeks.

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Common characteristics
Keratitis H Photophobia
H Pain
H Lacrimation
Overview
Complications
Description H Blindness
H Infection of the cornea H Corneal scarring or perforation
H Usually affects only one eye
H May be acute or chronic
Assessment
Pathophysiology
H Inflammation of the cornea results from corneal History
infection. H Recent upper respiratory tract infection, accompa-
H Inflammation may be deep or superficial. nied by cold sores
H Eye pain
Causes H Central vision loss
H Viral, bacterial, or fungal infection H Sensitivity to light
H Congenital syphilis H Sensation of a foreign body in eye
H Blurred vision
Risk factors
H Tear deficiency Physical findings
H Denervation H Cornea lacks normal luster
H Immune reactions H Characteristic branched lesion of the cornea with
H Ischemia herpes simplex virus type 1
H Trauma
H Contact lenses Test results
Diagnostic procedures
Incidence H Slit-lamp examination with sodium fluorescein stain-
H Fairly common ing may show corneal inflammation or abrasion;
H May develop at any age small branchlike (dendritic) lesions indicate possi-
ble herpes simplex virus infection. (See Examining
the eye with a slit lamp.)

Treatment
Examining the eye with a slit lamp
General
An ophthalmologist uses the slit lamp, an instrument
H Eye shield or patch
equipped with a special lighting system and a binocular
microscope, to view the eyelids, eyelashes, conjunctiva, Medications
sclera, cornea, tear film, anterior chamber, iris, crystalline
lens, and vitreous face. The examiner may adjust the size, Acute dendritic keratitis
shape, intensity, and depth of the light source as well as H Trifluridine eyedrops
the magnification of the microscope, to evaluate normally H Vidarabine ophthalmic ointment
transparent or near-transparent ocular fluids and tissues. H Broad-spectrum antibiotic
If he notes abnormalities, he can attach special devices to Chronic dendritic keratitis
the slit lamp to allow more detailed investigation. H Vidarabine therapy
Preparing the patient H Long-term topical therapy may be necessary
H Tell the patient that the slit-lamp examination evaluates H Antiviral such as acyclovir
the front portion of the eyes and that it requires that he
Fungal keratitis
remain still. Reassure him that the examination is
H Natamycin
painless.
H If the patient wears contact lenses, tell him to remove Surgery
them for the test, unless the test is being performed to
evaluate the fit of the lens. H Corneal transplantation for severe ulcerations with
H If the test calls for dilating eyedrops, check the residual scarring
patients history for adverse reactions to mydriatics
and for the presence of angle-closure glaucoma before
giving the drops. Dilating eyedrops arent used in
routine eye examinations, but some diseases require
pupillary dilation before slit-lamp examination.

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Prevention
Nursing considerations Preventing the spread of keratitis
Key outcomes The spread of keratitis can be prevented by following
these guidelines:
The patient will: H Use meticulous hand-washing techniques.
H sustain no harm or injury H Avoid touching the eyes after touching the mouth,
H express feelings of increased comfort especially in patients with cold sores.
H regain visual function. H Dont share eyedrops or ointment.
H Dont touch the eyedropper or ointment tip to the eye.
Nursing interventions H Wash hands before and after administering eyedrops.
H Follow the providers directions and complete antibiotic
or antifungal treatment course as prescribed.
ALERT H Take antiviral as prescribed.
H Keep follow-up appointments.
Watch for keratitis in patients predisposed to cold
H Use artificial tears as directed.
sores. Corneal infection is commonly caused by a H Wear protective eye wear to prevent further injury.
virus, such as adenovirus or herpes simplex, the
same viruses that cause cold sores. Be sure to tell
patients never to touch their eyes after touching
their mouths.

H Wear gloves when in contact with eyes or ocular

drainage with herpes simplex virus.
H Apply warm compresses.
H Dim the lights in case of photophobia.
H Administer prescribed drugs.

Monitoring
H Response to treatment
H Visual acuity

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medication administration, dosage, and possible ad-
verse effects
H how stress, traumatic injury, fever, colds, and sun
overexposure can trigger flare-up
H wearing sunglasses for photophobia
H preventing spread of infection. (See Preventing the
spread of keratitis.)

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Causes
Kidney cancer H Unknown

Risk factors
Overview H Heavy cigarette smoking
H Regular hemodialysis treatments
Description
H Proliferation of cancer cells in the kidney Incidence
H 85%: originate in kidneys; 15%: metastasize from H Twice as common in males as in females
various primary-site carcinomas H More common after age 40
H Also called nephrocarcinoma, renal carcinoma, H Renal pelvic tumors and Wilms tumor most common
hypernephroma, and Grawitzs tumor in children
Pathophysiology Common characteristics
H Most kidney tumors are large, firm, nodular, encap- H Hematuria
sulated, unilateral, and solitary. H Flank pain
H Kidney cancer may affect either kidney; occasionally
tumors are bilateral or multifocal. (See Unilateral Complications
kidney tumor.) H Hemorrhage
H Renal cancers arise from the tubular epithelium. H Metastasis
H Tumor margins are usually clearly defined.
H Tumors can include areas of ischemia, necrosis, and
focal hemorrhage. Assessment
H Tumor cells may be well differentiated to anaplastic.
H Kidney cancer can be separated histologically into History
clear cell, granular cell, and spindle cell types. H Hematuria
H The prognosis is better for patients with the clear cell H Dull, aching flank pain
type than for the other types; in general, however, the H Weight loss (rare)
prognosis depends more on the cancers stage than H Fatigue
on its type. The overall prognosis has improved con- H Intermittent fever
siderably, with a 5-year survival rate of about 50%.
Physical findings
H Palpable smooth, firm, nontender abdominal mass
Unilateral kidney tumor
Test results
In kidney cancer, tumors such as this one in the upper Laboratory
kidney pole usually occur unilaterally. H Alkaline phosphatase, bilirubin, and transaminase
levels are increased.
H Prothrombin time is prolonged.
Imaging
H Renal ultrasonography and computed tomography
scan can be used to verify renal cancer.
H Excretory urography, nephrotomography, and
kidney-ureter-bladder radiography are used to aid
diagnosis and help in staging.

Treatment
General
H Because of radiation resistance, radiation used only
when cancer has spread into perinephric region or
lymph nodes or when primary tumor or metastatic
sites cant be completely excised
H Low-protein diet
H Postoperatively, no heavy lifting or contact sports for
6 to 8 weeks
Medications
H Chemotherapy

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H Biotherapy with lymphokine-activated killer cells

plus recombinant interleukin-2
H Interferon

Surgery
H Radical nephrectomy, with or without regional lymph
node dissection

Nursing considerations
Key outcomes
The patient will:
H maintain fluid balance
H report increased comfort
H communicate understanding of medical regimen,
medications, diet, and activity restrictions
H maintain ventilation
H utilize support services.

Nursing interventions
H Administer prescribed drugs.
H Encourage verbalization and provide support.

Monitoring
H Wound site
H Intake and output
H Complete blood count; serum chemistry results
H Pain control

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medication administration, dosage, and possible ad-
verse effects
H need for a healthy, well-balanced diet and regular ex-
ercise
H importance of checking with the physician before
taking vitamins or other dietary supplements
H importance of follow-up care.

Discharge planning
H Refer the patient to support services.
H Refer the patient to a smoking-cessation program, if
indicated.

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Klinefelter syndrome
Overview
Description
H Relatively common genetic abnormality that results
from an extra X chromosome, creating an XXY sex
chromosome constitution
H Affects only males and usually becomes apparent at
puberty, when secondary sex characteristics develop
H Failure of the testicles to mature and degenerative
testicular changes that eventually result in irre-
versible infertility
Pathophysiology
H The extra chromosome responsible for Klinefelter
syndrome probably results from either meiotic
nondisjunction during parental gametogenesis or
from mitotic nondisjunction in the zygote.
Turners syndrome
In Turners syndrome, one of the X chromosomes (or part
of the second X chromosome) may be lost from either the
ovum or sperm through nondisjunction or chromosome
lag. Mixed aneuploidy may result from mitotic nondisjunc-
tion.
This disorder occurs in 1 in 2,500 to 7,000 births; up to
95% of affected fetuses are spontaneously aborted.
Signs and symptoms
In utero, the fetus may have a cystic hygroma, seen on ul-
trasound; however, these may also be seen in fetuses that
dont have Turners syndrome. The mother may have ele-
vated or low levels of serum alpha-fetoprotein.
At birth, 50% of infants with this syndrome measure
below the third percentile in length. Many have swollen
hands and feet, a wide chest with laterally displaced nip-
ples, and a low hairline that becomes more obvious as
they grow. They may have webbing of the neck and
coarse, enlarged, prominent ears. Gonadal dysgenesis is
seen at birth and typically causes sterility in adult females
(unless they have the mosaic form).
Cardiovascular defects, such as a bicuspid aortic valve
and coarctation of the aorta, occur in 10% to 40% of pa-
tients. Short stature (usually under 59 [150 cm]) is the
most common adult sign.
Most patients have average or slightly below-average
intelligence; they commonly exhibit spatial defects,
rightleft disorientation for extrapersonal space, and de-
fective figure drawing.
Diagnosis and treatment
Turners syndrome can be diagnosed by chromosome
analysis. Differential diagnosis should rule out mixed go-
nadal dysgenesis, Noonans syndrome, and other similar
disorders.
Treatment should begin in early childhood and may in-
clude hormonal therapy (androgens, human growth hor-
mone and, possibly, small doses of estrogen). Later, prog-
esterone and estrogen can induce sexual maturation, but
most patients remain sterile.
464 Klinefelter syndrome
H The incidence of meiotic nondisjunction increases
with maternal age.
Causes
H One extra X chromosome creating 47,XXY comple-
ment instead of the normal 46,XY
H In the rare mosaic form, some cells containing extra
X chromosomes; others containing normal XY com-
plement
H Turners syndrome, the lack of one X chromosome
(45,X), possibly being a cause (see Turners syn-
drome)
Incidence
H In the United States, approximately 1 in 500 to 1,000
males born with an extra sex chromosome; over
3,000 affected males born yearly
H Prevalence: 5 to 20 times higher in neonates with
mental retardation
Common characteristics
H May not be apparent until puberty (or later in mild
cases)
H Behavioral problems in adolescence
H Infertility
Complications
H Aspermatogenesis and infertility
H Learning disabilities and behavioral problems
H Osteoporosis
H Breast cancer due to the extra X chromosome
Assessment
History
H Sexual dysfunction (impotence, lack of libido)
H In some individuals, behavioral problems beginning
in adolescence
H Increased incidence of pulmonary disease and vari-
cose veins
Physical findings
H Small penis and prostate gland
H Small testicles
H Sparse facial and abdominal hair
H Feminine distribution of pubic hair (triangular
shape)
H In fewer than 50% of patients, gynecomastia
H In the mosaic form, delay of pathologic changes and
resulting infertility
H Abnormal body build (long legs with short, obese
trunk)
H Tall stature
Test results
Laboratory
H A karyotype (chromosome analysis) is determined by
culturing lymphocytes from the patients peripheral
blood.
H Urinary 17-ketosteroid levels are decreased.
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H Follicle-stimulating hormone excretion is increased.

H Plasma testosterone levels are decreased after
puberty.

Treatment
General
H Activity, as tolerated
H Diet, as tolerated
H Psychological counseling

Medications
H Supplemental testosterone

Surgery
H Mastectomy in patients with persistent gynecomastia.

Nursing considerations
Key outcomes
The patient will:
H express feelings about the disorder
H demonstrate effective coping mechanisms
H comply with prescribed treatment.

Nursing interventions
H Encourage the patient to discuss his feelings of con-
fusion and rejection that may arise, and try to rein-
force his male identity.
H Administer prescribed drugs.

Monitoring
H Response to treatment

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the potential benefits and adverse effects of testos-
terone administration.
Discharge planning
H Send the fertile patient with the mosaic form of the
syndrome for genetic counseling.

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LLabyrinthitis
Overview
Description
H Inflammation of the labyrinth of the inner ear
H Typically produces severe vertigo with head move-
ment and sensorineural hearing loss
H Viral labyrinthitis most prevalent form

Pathophysiology
H Lesion within vestibular pathways (inner ear to cere-
bral cortex) results in an imbalance in the vestibular
Complications
H Meningitis
H Permanent balance disability
H Permanent hearing loss

Assessment
History
H Severe vertigo from any movement of the head
H Nausea and vomiting
H Unilateral or bilateral hearing loss
H Recent upper respiratory tract infection
H Loss of balance and falling in the direction of the af-
fected ear
system.
Physical findings
Causes H Spontaneous nystagmus
H Viral or bacterial infections H Jerking movements of eyes toward unaffected ear
H Cholesteatoma H Purulent drainage
H Drug toxicity
H Head injury Test results
H Tumor Laboratory
H Vasculitis H Culture and sensitivity tests show the infecting
H Allergies organism.
Imaging
Risk factors H Computed tomography scanning results rule out
H Current or recent viral infection, especially brain lesion.
respiratory Diagnostic procedures
H Allergies H Audiometric testing reveals sensorineural hearing
H Smoking loss.
H Excess alcohol intake H A flat tympanogram may suggest fluid in the middle
H Stress ear, a perforated tympanic membrane, or impacted
cerumen. Fluctuations on the tympanogram, syn-
Incidence chronous with the patients pulse, suggest a gloman-
H Affects all ages beyond infancy gioma in the middle ear.
H Affects males and females equally H Electronystagmography may show decreased velocity
from one side that indicates hypofunction or canal
Common characteristics paresis. An inability to induce nystagmus with ice
H Severe vertigo with head movement water denotes a dead labyrinth.
H Nausea and vomiting
H Sensorineural hearing loss
H Tinnitus Treatment
General
H Based on relieving symptoms
H Increased oral fluids
H During acute attacks, bed rest in darkened room
Managing labyrinthitis with head immobilized between pillows
H Tell the patient to avoid sudden position changes. Medications
H Help the patient assess how much this disability will af-
H Meclizine to relieve vertigo
fect his daily life.
H Work with the patient to identify hazards in the home, H Antiemetics such as prochlorperazine
such as throw rugs and dark stairways. H Benzodiazepines such as valium
H Discuss the patients anxieties and concerns about ver- H I.V. fluids for severe dehydration
tigo attacks and decreased hearing. H Antibiotics as appropriate
H Stress the importance of maintaining and resuming
normal diversions or social activities when balance dis-
turbance is absent.

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Surgery
H Surgical excision of cholesteatoma
H Drainage of middle and inner ear infected areas
H Labyrinthectomy

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort
H maintain normal fluid volumes
H be free from injury
H verbalize understanding of the condition and treat-
ment.
Nursing interventions
H Offer the patient reassurance when appropriate.
H Maintain bed rest in a darkened room with his head
immobilized during acute attacks.
H Administer prescribed drugs.
H Encourage oral fluid intake.
For the patient with hearing loss
H Encourage expression of concerns about hearing
loss.
H Give clear, concise explanations.
H Face him when speaking.
H Enunciate words clearly, slowly, and in a normal
tone.
H Provide a pencil and paper to aid communication.
H Alert staff to communication needs.

Monitoring
H Response to medication
H Vital signs
H Signs of dehydration
H Intake and output
H Auditory acuity
H Complications

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H limitation of activities to avoid danger from vertigo
H recovery time (up to 6 weeks)
H prompt treatment of upper respiratory tract and sys-
temic infections
H controlling use of salicylates and other potentially
toxic substances
H completion of the prescribed medication regimen
H medication administration, dosage, and possible ad-
verse effects
H preoperative and postoperative instructions, as indi-
cated
H management of labyrinthitis (see Managing
labyrinthitis).

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Incidence
Lactose intolerance H High incidence among certain ethnic groups, includ-
ing Blacks, Asians, Native Americans, Greek Cypriots,
and some Ashkenazic Jews
Overview
Common characteristics
Description H Abdominal pain and distention after ingesting dairy
H Inability to digest and absorb lactose, the main car- products
bohydrate in milk
H Stems from an insufficiency of the enzyme lactase Complications
H May be congenital (rare) or acquired H Dehydration
H Deficiency continues for life

Pathophysiology
See Understanding lactase insufficiency.
Causes
H Genetic basis
H Medical conditions that disrupt the intestinal mucosa
(secondary)
H Medications that cause GI disturbances
H Ionizing radiation to the abdomen and abdominal
surgery
Understanding lactase insufficiency
Normally, the enzyme lactase hydrolyzes dietary lactose in
the jejunum and proximal ileus. The hydrolysis splits lac-
tose into glucose and galactose, which bind to glucose
carriers and eventually pass into the portal vein. If lactase
levels are insufficient to split the lactose, a chain of effects
is triggered.
Available lactase is insufficient to
hydrolyze dietary lactose.
Unsplit lactose remains as unabsorbed glucose
in the small intestine.
Unabsorbed glucose acts osmotically
to draw in and retain intraluminal fluid,
leading to diarrhea.
Intestinal bacteria ferment the lactose,
breaking it down into hydrogen, carbon dioxide,
water, and organic acids.
Accumulation of gases causes discomfort,
flatulence, and distention.
Assessment
History
H GI signs and symptoms, such as diarrhea, abdominal
cramping, discomfort, distention, flatulence, and
borborygmus (intestinal rumbling), following inges-
tion of milk products
H History of a medical disorder or treatment that dis-
rupts the GI mucosa
Physical findings
H Abdominal distention
H Nonverbal signs of patient distress, such as doubling
over or holding the abdomen
H Rectal tissue irritation and excoriation related to di-
arrhea
H Hyperactive bowel sounds
Test results
Laboratory
H Lactose tolerance testing: A blood sample is taken af-
ter the patient has fasted overnight. Then the patient
ingests a specified oral lactose load. Serum glucose
levels are taken on blood samples drawn at specified
intervals following lactose ingestion and on the fast-
ing blood sample. A minimal increase (less than
20 mg/dl) in the serum glucose level and GI symp-
toms (cramping, flatulence and, perhaps, diarrhea)
confirm lactase deficiency.
H Breath hydrogen analysis measures excess hydrogen
exhalation resulting from bacterial fermentation of
lactose in the colon. (Hydrogen from the colon pass-
es to the blood and then to the lungs.) Increased hy-
drogen content of expired air confirms lactose intol-
erance.
Other
H Lactose challenge test produces diarrhea and bloat-
ing within minutes to hours.
H Lactose-free diet testing eliminates lactose from the
patients diet for a period of time such as 5 days. If
he becomes asymptomatic, the diagnosis is upheld.
H Small-bowel biopsy (rarely used) determines
whether lactose intolerance is primary or secondary.
Only the secondary form shows abnormal epithe-
lium.

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H checking product labels carefully for lactose content

Treatment and avoiding products that list milk solids, milk sug-
ars, whey, or casein
General H the need to eliminate all sources of lactose from his
H Lactose-free diet diet until he is symptom free
H how to use lactase enzyme products
Medications H avoiding vitamin D and calcium deficiencies.
H Lactase enzyme products available as chewable
tablets, tablets, and capsules
H Antidiarrheal agents, such as loperamide and bis-
muth subsalicylate
H Calcium supplement

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort
H have normal bowel function
H have fluid volume within normal parameters
H maintain adequate caloric intake.

Nursing interventions
H Administer prescribed antidiarrheal agents.
H Administer prescribed lactase enzyme products.
H Assess the patient for abdominal discomfort.
H Encourage relaxation and diversion techniques to
relieve discomfort.
H Initiate patient care measures to protect the rectal
skin and mucous membranes.
H Assess the patient for signs of dehydration.
H Offer emotional support.
H Provide patient privacy.

Monitoring
H Elimination pattern
H Diet
H Skin integrity

Patient teaching
Be sure to cover:
H lactose intolerance and its associated signs and
symptoms, risks, and treatment, especially dietary
management
H avoiding foods that contain lactose, such as milk
(whole, low-fat, skim, evaporated, condensed, but-
termilk, cream), ice cream, cheese, sour cream, cus-
tards, milk-based puddings, butter, drinks prepared
with chocolate or malted milk powder, cream sauces
and gravies, cream-based soups, chocolate candy, in-
stant potatoes, baked products made with milk, and
frozen or canned fruits and vegetables containing
lactose

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Laryngeal cancer Assessment

History
Overview Stage I
H Complaints of local throat irritation
Description H 2-week history of hoarseness
H Malignant cells in the tissues of the larynx or voice Stages II and III
box H Hoarseness
H Squamous cell carcinoma: most common form (95% H Sore throat
of cases) H Voice volume reduced to whisper
H Adenocarcinoma and sarcoma: rare (5% of cases) Stage IV
H Tumor intrinsic (located on the true vocal cords; H Pain radiating to ears
tends not to spread because underlying connective H Dysphagia
tissues lack lymph nodes), or extrinsic (located on H Dyspnea
another part of the larynx; tends to spread easily)
Physical findings
Pathophysiology Stage I
H Laryngeal cancer is classified by its location: H None
supraglottic (on the false vocal cords) Stage II
glottic (on the true vocal cords) H Possible abnormal movement of vocal cords
subglottic (rare downward extension from the Stage III
vocal cords). H Abnormal movement of vocal cords; possible lym-
H Malignant cells that proliferate can cause swallowing phadenopathy
and breathing impairment. Stage IV
H A tumor can decrease mobility of the vocal cords. H Neck mass or enlarged cervical nodes

Causes Test results

H Unknown Imaging
H Xeroradiography, laryngeal tomography, computed
Risk factors tomography scan, and laryngography confirm the
H Smoking presence of a mass.
H Alcoholism H Chest X-ray rules out metastasis.
H Chronic inhalation of noxious fumes Diagnostic procedures
H Familial disposition H Laryngoscopy allows definitive staging by obtaining
H History of gastroesophageal reflux disease multiple biopsy specimens to establish a primary di-
agnosis, to determine the extent of the disease, and
Incidence to identify additional premalignant lesions or second
H About nine times more common in males than primaries.
females Other
H Most victims between ages 50 and 65 H Biopsy identifies cancer cells.

Common characteristics
Intrinsic laryngeal cancer Treatment
H Hoarseness lasting longer than 3 weeks
Extrinsic laryngeal cancer General
H Lump in the throat H Precancerous lesions laser surgery
H Pain or burning of the throat when drinking hot liq- H Early lesions laser surgery or radiation therapy
uid or citrus drinks H Advanced lesions radiation therapy and
With metastasis chemotherapy
H Dysphagia H Speech preservation
H Dyspnea H Speech rehabilitation (when speech preservation im-
H Cough possible) esophageal speech, prosthetic devices,
H Pain, most commonly radiating to the ear or experimental surgical reconstruction of the voice
H Enlarged cervical lymph nodes box
H Diet based on treatment options
Complications H May require enteral feeding
H Increased swallowing difficulty and pain H Frequent rest periods
H Metastasis

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Medications Discharge planning

H Chemotherapeutic agents H Arrange for rehabilitation measures (including laryn-
H Analgesics geal speech, esophageal speech, an artificial larynx,
and various mechanical devices).
Surgery H Refer the patient to local resources and support ser-
H Cordectomy vices.
H Partial or total laryngectomy
H Supraglottic laryngectomy or total laryngectomy with
laryngoplasty

Nursing considerations
Key outcomes
The patient will:
H express feelings regarding illness
H express feelings of increased comfort
H maintain a patent airway
H utilize available support systems.

Nursing interventions
H Provide supportive psychological, preoperative, and
postoperative care.
H Encourage verbalization and provide support.
H Assist with establishing a method of communication.
H Prepare the patient for functional losses (inability to
smell, blow his nose, whistle, gargle, sip, or suck on
a straw).
H Provide frequent mouth care.
H Suction when needed.
H After total laryngectomy, elevate the head of the bed
30 to 45 degrees and support the back of the neck to
prevent tension on sutures and, possibly, wound de-
hiscence.
Monitoring
After partial laryngectomy
H Hydration and nutritional status
H Tracheostomy tube care
H Use of voice
After total laryngectomy
H Laryngectomy tube care
H Vital signs
H Postoperative complications
H Pain control
H Nasogastric (NG) tube placement and function

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H appropriate oral hygiene practices (before partial or
total laryngectomy)
H postoperative procedures, such as suctioning, NG
tube feeding, and laryngectomy tube care
H preparation for any functional losses.

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Laryngitis Assessment
History
Overview H Hoarseness ranging from mild to complete loss of
voice
Description H Feeling of throat rawness
H Acute or chronic inflammation of vocal cords H Throat pain
H Isolated infection or part of a generalized bacterial H Dry cough
or viral upper respiratory tract infection H Malaise
H Typical viral infection mild, with limited duration H Difficulty swallowing
H Inflammatory changes caused by repeated attacks
(associated with chronic laryngitis) Physical findings
H Cough
Pathophysiology H Fever
H Inflammatory response to cell damage by viruses re- H Regional lymphadenopathy
sults in hyperemia and fluid exudation. H Stridor (in children)
H Irritant receptors are triggered.
H Kinins and other inflammatory mediators may induce Test results
spasm of upper airway smooth muscle. Laboratory
H White blood cell count is elevated in bacterial
Special populations infection.
Diagnostic procedures
Developmental differences in the upper airway H Indirect laryngoscopy reveals red, inflamed and,
structures of young children may result in severe occasionally, hemorrhagic vocal cords exudate.
narrowing of the upper airways with inflamma-
tion, to the degree that respiratory failure may re-
sult from hypoventilation. Treatment
Causes General
H Infection H Symptom-based
H Overuse of the voice H Elimination of underlying cause
H Inhalation of smoke or fumes H Resting the voice (primary treatment)
H Aspiration of caustic chemicals H Humidification
H Chronic laryngitis H Avoidance of smoking
H Chronic upper respiratory tract disorders H Avoidance of whispering
H Mouth breathing H Cold fluids
H Smoking H Rest during febrile period, with head of bed elevated
H Constant exposure to dust or other irritants
H Alcohol abuse Medications
H Gastroesophageal reflux H Analgesics
H Reflux esophagitis H Throat lozenges
H Antibiotics as appropriate (bacterial infection)
Incidence
H Common disorder Surgery
H Affects all ages H Tracheotomy in chronic laryngitis
H Affects males and females equally

Common characteristics Nursing considerations

H Hoarseness
H Dry cough Key outcomes
The patient will:
Complications H express feelings of increased comfort
H Chronic hoarseness H exhibit an adequate breathing pattern
H Permanent laryngeal tissue changes H show no signs of infection
H Airway obstruction H express understanding of the condition and treat-
ment.

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Nursing interventions
H Encourage discussion of concerns.
H Keep tracheotomy tray at bedside.
H Encourage modification of predisposing factors.
H Restrict verbal communication.
H Provide alternative communication means.
H Anticipate needs.
H Administer prescribed drugs.

Monitoring
H Response to treatment
H Respiratory status

ALERT
In severe, acute laryngitis, monitor the patient for
signs and symptoms of airway obstruction.

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H why the patient shouldnt talk
H alternate methods of communication
H speaking softly rather than whispering
H maintenance of adequate humidification
H smoking cessation
H medication and possible adverse reactions
H importance of completing prescribed antibiotics
H avoidance of occupational hazards.

Discharge planning
H Refer the patient to a smoking-cessation program, if
indicated.

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Complications
Life-threatening disorder H Respiratory obstruction
H Systemic vascular collapse

Latex allergy H Death

Assessment
Overview
History
Description H Exposure to latex
H An immunoglobulin (Ig) Emediated immediate hy-
persensitivity reaction to products that contain natur- Physical findings
al latex H Signs of anaphylaxis
H Can range from local dermatitis to life-threatening H Rash
anaphylactic reaction H Angioedema
H Conjunctivitis
Pathophysiology H Wheezing, stridor
H Mast cells release histamine and other secretory
products. Test results
H Vascular permeability increases and vasodilation and Diagnosis of latex allergy is based mainly on history and
bronchoconstriction occur. physical assessment.
H Chemical sensitivity dermatitis is a type IV delayed hy- Laboratory
persensitivity reaction to the chemicals used in pro- H Radioallergosorbent test shows specific IgE antibod-
cessing rather than the latex itself. ies to latex (safest for use in patients with history of
H In a cell-mediated allergic reaction, sensitized T lym- type I hypersensitivity).
phocytes are triggered, stimulating the proliferation
of other lymphocytes and mononuclear cells, result-
ing in tissue inflammation and contact dermatitis. Products that contain latex
Causes Medical products
H Frequent contact with latex-containing products (see H Adhesive bandages
Products that contain latex) H Airways, Levin tube
H Blood pressure cuff, tubing, and bladder
Risk factors H Catheter leg straps
H Medical and dental professionals H Catheters
H Workers in latex companies H Dental dams
H Patients with spina bifida or other conditions that re- H Elastic bandages
H Electrode pads
quire multiple surgeries involving latex material H Fluid-circulating hypothermia blankets
H History of:
H Handheld resuscitation bags
Asthma or other allergies, especially to bananas, H Hemodialysis equipment
avocados, tropical fruits, or chestnuts H I.V. catheters
Multiple intra-abdominal or genitourinary surg- H Latex or rubber gloves
eries H Medication vials
Frequent intermittent urinary catheterization H Pads for crutches
H Protective sheets
Incidence H Reservoir breathing bags
H Present in 1% to 5% of population of the United H Rubber airways and endotracheal tubes
States H Tape
H Tourniquets
H Affects 10% to 30% of health care workers
H Most prevalent (20% to 68%) in patients with spina
Nonmedical products
H Adhesive tape
bifida and urogenital abnormalities H Balloons (excluding Mylar)
H Affects males and females equally H Cervical diaphragms
H Condoms
Common characteristics H Disposable diapers
H Hypotension H Elastic stockings
H Tachycardia H Glue
H Urticaria and pruritus H Latex paint
H Difficulty breathing, bronchospasm, wheezing, and H Nipples and pacifiers
stridor H Rubber bands
H Angioedema H Tires

474 Latex allergy

9400L.qxd 8/2/12 4:37 PM Page 475

Other
H Patch test results in hives with itching or redness as a
positive response.

Treatment
General
H Prevention of exposure, including use of latex-free
products to decrease possible exacerbation of hyper-
sensitivity
H Maintenance of patent airway

Medications
H Use before and after possible exposure to latex
H Corticosteroids
H Antihistamines
H Histamine-2 receptor blockers

Acute treatment
H Epinephrine 1:1,000
H Oxygen therapy
H Volume expanders
H I.V. vasopressors
H Aminophylline and albuterol

Nursing considerations
Key outcomes
The patient will:
H maintain a patent airway
H remain hemodynamically stable
H identify latex products in order to avoid exposure.

Nursing interventions
H Maintain airway, breathing, and circulation.
H Administer prescribed drugs.

ALERT
When adding medication to an I.V. bag, inject the
drug through the spike port, not the rubber latex
port.

H Keep the patients environment latex free.

Monitoring
H Vital signs
H Respiratory status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H potential for life-threatening reaction
H wearing medical identification jewelry that identifies
allergy
H how to use an epinephrine autoinjector.

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Incidence
Lead poisoning H Sharp decline for the past 30 years due to education
and regulations
H About 4.4% of children in the United States having an
Overview elevated lead level
H Black, non-Hispanic children at greatest risk
Description H Highest between ages 1 and 5 and adult workers
H Toxicity from repeated or excessive exposure to lead
which occurs naturally in the environment Common characteristics
H Present in: H Anemia
Lead-based paint H Anorexia
Soil and dust H Constipation
Drinking water
Air Complications
Food H Renal failure
H Major worldwide health hazard H Mental retardation
H Encephalopathy
Pathophysiology H Exposure during pregnancy associated with low birth
H Lead replaces calcium in the bones, affecting rapidly weight and premature birth
growing bones; it appears as lines on X-rays.
H Substances, such as sodium citrate, ascorbate, amino
acids, vitamin D, protein and fat, and lactose, bind to Assessment
lead and enhance its absorption.
H Lead is metabolized in blood, skeleton, soft tissues, History
and bile, and other body fluids. H Commonly produces no symptoms until severe
H It affects every body system but primarily red blood H Possible myalgia or paresthesia
cell chemistry, the kidneys, and the nervous system. H Fatigue or lethargy
H Brain damage occurs at low lead levels and isnt re- H Irritability
versible. H Abdominal discomfort
H Difficulty concentrating
Causes H Headache
H Inhalation of lead dust or fumes H Tremors
H Ingestion of lead H Vomiting
H Weight loss
Risk factors H Seizures
H Children with pica or iron deficiency anemia H Delayed developmental milestones
H Living where more than 27% of the housing was built
before 1950 Physical findings
H Exposure to leaded-paint surfaces H Typically normal
H Dust from clothing of lead worker H Abdominal tenderness, possibly severe
H Water from lead or lead-soldered plumbing H Possible symptoms of neuropathy or encephalopathy
H Lead-glazed ceramics
H Soil and dust near lead industries and roads Test results
H Hobbies Laboratory
Glazed pottery making H Serum lead levels are elevated.
Target shooting at firing ranges H Complete blood count may show microcytic anemia.
Painting H Free erythrocyte protoporphyrin level is elevated.
Stained glass making H Zinc protoporphyrin level is elevated.
H Home remodeling H Provocative chelation test estimates the total body
H Occupational exposuremore than 900 occupa- burden of lead and the efficacy of treatment.
tions, including: Imaging
Plumbers H Abdominal X-rays
Auto mechanics H Long-bone X-rays may show growth retardation.
Glass manufacturers
Printers
Construction workers
H Herbal folk remedies

476 Lead poisoning

9400L.qxd 8/2/12 4:37 PM Page 477

Treatment
General
H Based on blood lead level
H Separate individual from source of exposure
H Possibly intestinal irrigation
H Chelation therapy to promote lead excretion
Medications
H Calcium disodium edetate, usually I.V. but may be
given I.M.
H Dimercaprol given I.M.
H Oral agents
D-penicillamine (used for about 30 years but still
not FDA approved for chelation therapy)
Succimer (DMSA)
H Diazepam for initial seizure control, if indicated
Nursing considerations
Key outcomes
The patient (or parent) will:
H verbalize understanding of the disease and its treat-
ment
H express understanding of preventive measures
H eliminate sources of lead from the home.
The patient will:
H verbalize reduced or absent pain
H show age-appropriate skills and activities
H show developmental progress
H demonstrate increased energy.
Nursing interventions
H Administer prescribed drugs.
H Provide the prescribed diet, and encourage dietary
changes.
H Encourage activities that can be completed in short
periods.
H Help the patient (or parent) identify risk factors and
modify lifestyle, as appropriate.
H Facilitate screening of all family members.
Prevention
Preventing lead poisoning
Lead poisoning can be prevented by following these
guidelines:
H Discuss screening family members for lead with health
care provider.
H Identify sources of lead in the home, such as in tap
water, handmade pots or pottery, imported cans of
food, and lead paint.
H Keep children away from lead paint and other sources
of lead in the home.
H Eat foods high in iron, calcium, and vitamin C, which
limit lead absorption.
H Wash hands after playing or working outside, before
eating, and before bed.
H Have the home inspected before doing major
remodeling and repairs, and reside elsewhere while the
lead source is being removed.
H If family members work with lead, they should change
their clothes before coming home from work, take off
shoes before entering the home, and shower before
playing with children.
H Discard toys that may contain lead paint.
H Dont let children play near major roadways or bridges.
H Run cold water for at least 1 minute before using.
H Dont use hot water for drinking, mixing formula, or
cooking.
Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H importance of follow-up care and monitoring lead
levels
H lead poisoning prevention. (See Preventing lead
poisoning.)

Monitoring
H Response to treatment
H Adverse reactions to prescribed drugs
H Level of pain
H Growth and development
H Laboratory values
H Urine output
H Complications
H Risk factor and lifestyle modifications

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Legg-Calv-Perthes
disease
Overview
Description
H Ischemic necrosis leading to eventual flattening of
the head of the femur due to vascular interruption
H Typically unilateral, occurs bilaterally in 20% of pa-
tients
H Also called coxa plana
H Usually runs its course in 3 to 4 years
H May lead to premature osteoarthritis later in life from
misalignment of the acetabulum and flattening of the
femoral head
Pathophysiology
H The first stage, synovitis, is characterized by synovial
inflammation and increased joint fluid, and typically
lasts 1 to 3 weeks.
H In the second (avascular) stage, vascular interrup-
tion causes necrosis of the ossification center of the
femoral head (usually in several months to 1 year).
H In the third stage, revascularization, a new blood
supply causes bone resorption and deposition of im-
mature bone cells. New bone replaces necrotic bone
and the femoral head gradually reforms.
H The final, or residual stage, involves healing and
regeneration. Immature bone cells are replaced by
normal bone cells, thereby fixing the joints shape.
There may be residual deformity, based on the
degree of necrosis that occurred in stage two.
Causes
H Exact vascular obstructive changes that initiate dis-
ease unknown
H Current etiologic theories:
Venous obstruction with secondary intraepiphyseal
thrombosis
Trauma to retinacular vessels
Vascular irregularities (congenital or developmen-
tal)
Vascular occlusion secondary to increased intra-
capsular pressure from acute transient synovitis
Increased blood viscosity resulting in stasis and
decreased blood flow
Incidence
H Occurs most frequently in boys ages 4 to 10
H Tends to occur in families
Common characteristics
H Persistent thigh pain or limp that becomes progres-
sively more severe
H Mild pain in the hip, thigh, or knee aggravated by
activity and relieved by rest
H Muscle spasm
H Atrophy of muscles in the upper thigh
478 Legg-Calv-Perthes disease
H Slight shortening of the leg
H Severely restricted abduction and internal rotation of
the hip
Complications
H Permanent disability
H Premature osteoarthritis
Assessment
History
H Family history
H Limp that becomes progressively worse
H Persistent pain in the groin, anterior thigh, or knee
aggravated by activity and relieved by rest
Physical findings
H Muscle atrophy
H Slight shortening of the affected leg
H Restricted hip abduction and internal rotation
H Adductor muscle spasm in the affected hip
Test results
Imaging
H Hip X-rays taken every 3 to 4 months confirm the di-
agnosis, with findings that vary according to the stage
of the disease.
H Anterior-posterior X-rays and magnetic resonance
imaging enhance early diagnosis of necrosis and
visualization of articular surface.
Treatment
General
H Protection of the femoral head from further stress
and damage by containing it within the acetabulum
H Reduced weight bearing by means of bed rest in bilat-
eral split counterpoised traction, then application of
hip abduction splint or cast, or weight bearing while
a splint, cast, or brace holds the leg in abduction
(braces remaining in place for 6 to 18 months)
H Physical therapy with passive and active range-of-
motion (ROM) exercises after cast removal
H Well-balanced diet
Medications
H Analgesics
Surgery
H For a young child in the early stages of the disease,
osteotomy and subtrochanteric derotation providing
maximum confinement of the epiphysis within the
acetabulum allowing return of the femoral head to
normal shape and full ROM; proper placement of
the epiphysis thus allowing remolding with ambula-
tion; postoperatively, requiring a hip-spica cast for
about 2 months
9400L.qxd 8/2/12 4:37 PM Page 479

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort and decreased
pain
H perform activities of daily living within the confines
of the disease
H express understanding of the disorder and treatment
regimen.
Nursing interventions
H Provide cast care.
H Administer prescribed analgesics.
H Provide emotional support.

Monitoring
H Intake and output
H Neurovascular status of affected extremity
H Skin integrity

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H proper cast care and monitoring of skin integrity.

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Legionnaires disease H Hypotension

H Delirium
H Seizures
H Heart failure
Overview H Arrhythmias
H Renal failure
Description H Shock
H An acute bronchopneumonia produced by a gram-
negative bacillus
H Illness ranging from mild (with or without pneu- Assessment
monitis) to serious multilobed pneumonia with mor-
tality as high as 15% History
H Outbreaks (usually in late summer and early fall) H Presence at a suspected source of infection
epidemic or confined to a few cases H Prodromal symptoms, including anorexia, malaise,
myalgia, and headache
Pathophysiology
H The legionella enter the lungs after aspiration or in- Physical findings
halation. H Rapidly rising fever with chills
H Although alveolar macrophages phagocytize the le- H Grayish or rust-colored, nonpurulent, occasionally
gionella, the organisms arent killed and proliferate blood-streaked sputum
intracellularly. H Tachypnea
H The cells rupture, releasing the legionella, and the H Bradycardia (in about 50% of patients)
cycle starts again. H Neurologic signs (altered level of consciousness
H Lesions develop a nodular appearance, and alveoli [LOC])
become filled with fibrin, neutrophils, and alveolar H Dullness over areas of secretions and consolidation
macrophages. or pleural effusions
H Fine crackles that develop into coarse crackles as the
Causes disease progresses
H Legionella pneumophila, an aerobic, gram-negative
bacillus most likely transmitted by air Test results
H Water distribution systems (such as whirlpool spas Laboratory
and decorative fountains): a primary reservoir for H Gram staining reveals numerous neutrophils but no
the organism organism.
H Definitive method of diagnosis involves isolation of
Risk factors the organisms from respiratory secretions or bron-
H Smoking chial washings or through thoracentesis.
H Diabetes H Definitive tests include direct immunofluorescence of
H Cancer, especially hematologic or pulmonary L. pneumophila and indirect fluorescent serum anti-
H Acquired immunodeficiency syndrome body testing.
H End-stage renal disease H Leukocytosis and increased erythrocyte sedimenta-
H Chronic cardiopulmonary disease tion rate are present.
H Advanced age H Partial pressure of arterial oxygen is decreased, and
H Alcohol abuse partial pressure of arterial carbon dioxide is initially
H Recent surgery decreased.
H Serum sodium level less than 131 mg/L indicates
Incidence hyponatremia.
H Most likely to affect males more than females Imaging
H Others at increased risk: H Chest X-ray typically shows patchy, localized infiltra-
Elderly patients tion, which progresses to multilobed consolidation
Immunocompromised patients (usually involving the lower lobes) and pleural effu-
Patients with chronic underlying disease such as sion.
diabetes H In fulminant disease, chest X-ray reveals opacifica-
Alcoholics tion of the entire lung.
Cigarette smokers
Common characteristics Treatment
H Nonspecific prodromal symptoms
H Initial nonproductive cough that becomes productive General
H Fluid replacement
Complications H Oxygen administration
H Hypoxia and acute respiratory failure

480 Legionnaires disease

9400L.qxd 8/2/12 4:37 PM Page 481

Medications
H Antibiotics, such as levofloxacin and azithromycin
H Antipyretics such as acetominophen

Nursing considerations
Key outcomes
The patient will:
H cough effectively
H expectorate sputum effectively
H express feelings of increased comfort in maintaining
air exchange
H regain and maintain normal fluid and electrolyte bal-
ance
H have normal breath sounds.

Nursing interventions
H Give tepid sponge baths or use hypothermia blankets
to lower fever.
H Provide frequent mouth care. If necessary, apply
soothing cream to irritated nostrils.
H Replace fluids and electrolytes, as needed.
H Institute seizure precautions.
H Administer prescribed drugs.

Monitoring
H Vital signs
H Respiratory status and arterial blood gas values
H LOC

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H prevention of infection
H importance of disinfection of water supply
H purpose of postural drainage, and how to perform
coughing and deep-breathing exercises
H proper hand washing and disposal of soiled tissues
to prevent disease transmission.
Discharge planning
H Refer the patient to a pulmonologist, if necessary.

Legionnaires disease 481

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Life-threatening disorder
Leukemia, acute
Overview
Description
H Malignant proliferation of white blood cell (WBC)
precursors, or blasts, in bone marrow or lymph tis-
sue; blasts accumulate in peripheral blood, bone
marrow, and body tissues
H Most common form of cancer among children
H Common forms:
Acute lymphoblastic (lymphocytic) leukemia
(ALL), characterized by abnormal growth of lym-
phocyte precursors (lymphoblasts)
Acute myeloblastic (myelogenous) leukemia
(AML); causes rapid accumulation of myeloid pre-
cursors (myeloblasts)
Acute monoblastic (monocytic) leukemia, or
Schillings type; results in marked increase in
monocyte precursors (monoblasts)
H ALL: treatment induces remissions in 90% of chil-
dren (average survival time: 5 years) and 65% of
adults (average survival time: 1 to 2 years); children
ages 2 to 8 have best survival rate about 50%
with intensive therapy
H AML: average survival time is only 1 year after diag-
nosis, even with aggressive treatment (remissions
lasting 2 to 10 months in 50% of children; adult sur-
vival, only about 1 year after diagnosis, even with
treatment)
H Without treatment, invariably fatal
Pathophysiology
H Immature, nonfunctioning WBCs appear to accumu-
late first in the tissue where they originate, such as
lymphocytes in lymph tissue and granulocytes in
bone marrow.
H The immature, nonfunctioning WBCs spill into the
bloodstream and overwhelm red blood cells (RBCs)
and platelets; from there, they infiltrate other tissues.
Causes
H Unknown
Risk factors
H Radiation (especially prolonged exposure)
H Certain chemicals and drugs
H Viruses
H Genetic abnormalities
H Chronic exposure to benzene
In children
H Down syndrome
H Ataxia
H Telangiectasia
482 Leukemia, acute
H Congenital disorders, such as albinism and congeni-
tal immunodeficiency syndrome
Incidence
H More common in males than females
H More common in whites (especially of Jewish ances-
try)
H More common in children between ages 2 and 5
(80% in this age-groupALL), and those who live in
urban and industrialized areas
Common characteristics
H Sudden onset of high fevers
H Night sweats
H Malaise
H Bone and joint pain
H Shortness of breath during physical activity
H Excessive bleeding or bruises
Complications
H Infection
H Organ malfunction through encroachment or hemor-
rhage
Assessment
History
H Sudden onset of high fever
H Abnormal bleeding
H Fatigue and night sweats
H Weakness, lassitude, recurrent infections, and chills
H Abdominal or bone pain in patients with ALL, AML,
or acute monoblastic leukemia
Physical findings
H Tachycardia, palpitations, and a systolic ejection
murmur
H Decreased ventilation
H Pallor
H Lymph node enlargement
H Liver or spleen enlargement
Test results
Laboratory
H Blood counts show thrombocytopenia and neutro-
penia, and a WBC differential shows the cell type.
Imaging
H Computed tomography scan shows the affected or-
gans, and cerebrospinal fluid analysis shows abnor-
mal WBC invasion of the central nervous system.
Diagnostic procedures
H Bone marrow aspiration that shows a proliferation of
immature WBCs confirms acute leukemia; if the aspi-
rate is dry or free from leukemic cells but the patient
has other typical signs of leukemia, a bone marrow
biopsy, usually of the posterior superior iliac spine,
must be performed.
H Lumbar puncture is used to detect meningeal in-
volvement.
9400L.qxd 8/2/12 4:37 PM Page 483

Monitoring
Treatment H Complications from treatment
H Hydration and nutritional status
General H Urine pH (should be above 7.5)
H Transfusions of platelets to prevent bleeding H Vital signs
H Transfusions of RBCs to treat anemia H Signs and symptoms of bleeding
H Bone marrow transplantation in some patients
H Radiation therapy in case of brain or testicular infil-
tration Patient teaching
H Chemotherapeutic and radiation treatment, depend-
ing on diagnosis Be sure to cover:
H Well-balanced diet H the disorder, diagnosis, and treatment
H Frequent rest periods H medication administration, dosage, and possible ad-
verse effects
Medications H use of a soft toothbrush and avoidance of hot, spicy
For meningeal infiltration foods and commercial mouthwashes
H Intrathecal instillation of methotrexate or cytarabine H signs and symptoms of infection
with cranial radiation H signs and symptoms of abnormal bleeding
For ALL H planned rest periods during the day.
H Vincristine, prednisone, high-dose cytarabine, and
daunorubicin Discharge planning
H Intrathecal methotrexate or cytarabine because ALL H Refer the patient to available resources and support
carries 40% risk of meningeal infiltration services.
For AML
H Combination of I.V. daunorubicin and cytarabine (if
these fail to induce remission, treatment with some
or all of the following drugs: a combination of cyclo-
phosphamide, vincristine, prednisone, or methotrex-
ate; high-dose cytarabine alone or with other drugs;
amsacrine; etoposide; and 5-azacytidine and mitox-
antrone)
For acute monoblastic leukemia
H Cytarabine and thioguanine with daunorubicin or
doxorubicin
H Anti-infectives, such as antibiotics, antifungals, antivi-
rals and granulocyte injections

Nursing considerations
Key outcomes
The patient will:
H have no further weight loss
H exhibit intact mucous membranes
H experience no chills, fever, or other signs and symp-
toms of illness
H express feelings of increased comfort
H utilize available support systems.

Nursing interventions
H Encourage verbalization and provide comfort.
H Provide adequate hydration.
H After bone marrow transplantation, keep the patient
in a sterile room, administer antibiotics, and trans-
fuse packed RBCs as necessary.
H Administer prescribed drugs.
H Control mouth ulceration by checking often for obvi-
ous ulcers and gum swelling and by providing fre-
quent mouth care and saline rinses.

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Leukemia, chronic H Hemorrhage

H Pain

granulocytic
Overview
Description
H Type of leukemia characterized by abnormal over-
growth of granulocytic precursors (myeloblasts,
promyelocytes, metamyelocytes, and myelocytes) in
bone marrow, peripheral blood, and body tissues
H Always fatal (average survival time 3 to 4 years after
onset of chronic phase and 3 to 6 months after onset
of acute phase)
H Clinical course in two distinct phases:
insidious chronic phase (characterized by anemia
and bleeding abnormalities)
acute phase (blast crisis, or myeloblasts, the most
primitive granulocytic precursors, proliferating
rapidly)
H During acute phase, may develop either lymphoblas-
tic or myeloblastic disease (despite vigorous treat-
ment, chronic granulocytic leukemia rapidly advanc-
ing after onset of acute phase)
H Also called chronic myelogenous (or myelocytic)
leukemia (CML)
Pathophysiology
H CML is a myeloproliferative disorder, originating in a
progenitor stem cell.
H Malignant transformation is identified in erythroid,
megakaryocytic, and macrophage cell lines.
H Malignant transformation arises from pluripotential
stem cells or lymphoid stem cells.
Causes
H Exact cause unknown
Risk factors
H Presence of the Philadelphia chromosome (found in
almost 90% of patients)
H Myeloproliferative diseases
Incidence
H Most common in young and middle-aged adults
H Slightly more common in males than in females, and
rare in children
H In United States, 3,000 to 4,000 cases annually
(about 20% of all leukemias)
Common characteristics
H Fatigue
H Weakness
H Weight loss
H History of gouty arthritis or renal calculi
Complications
H Infection
Assessment
History
H Renal calculi or gouty arthritis
H Fatigue, weakness, dyspnea, decreased exercise tol-
erance, and headache
H Recent weight loss and anorexia
Physical findings
H Evidence of bleeding and clotting disorders
H Low-grade fever and tachycardia
H Pallor
H Difficulty breathing
H Retinal hemorrhage
H Hepatosplenomegaly with abdominal discomfort and
pain
H Sternal and rib tenderness
Test results
Laboratory
H Chromosomal studies of peripheral blood or bone
marrow show the Philadelphia chromosome.
H Low leukocyte alkaline phosphatase levels confirm
chronic granulocytic leukemia.
H Complete blood count reveals:
white blood cell (WBC) abnormalities, including
leukocytosis (WBC count over 50,000/l, rising
as high as 250,000/l), occasionally leukopenia
(WBC count under 5,000/l), and neutropenia
(neutrophil count under 1,500/l) despite high
WBC count
increased circulating myeloblasts
decreased hemoglobin level (below 10 g/dl), and
low hematocrit (less than 30%)
thrombocytosis (more than 1 million thrombo-
cytes/l).
H Serum uric acid level may exceed 8 mg/dl.
Imaging
H Computed tomography scan may show the affected
organs.
Diagnostic procedures
H Bone marrow aspirate or biopsy (performed only if
the aspirate is dry) may be hypercellular, character-
istically showing bone marrow infiltration by a signif-
icantly increased number of myeloid elements; in the
acute phase, myeloblasts predominate.
Treatment
General
H Bone marrow transplantation (chronic phase, more
than 60% of patients who receive transplant achiev-
ing remission)
H Local splenic radiation

484 Leukemia, chronic granulocytic

9400L.qxd 8/2/12 4:37 PM Page 485

H Leukapheresis (selective leukocyte removal) to re- Discharge planning

duce WBC count H Refer the patient to available resources and support
H Well-balanced diet services.
H Frequent rest periods

Medications
H Antineoplastics, such as hydroxyurea or imatinib

Surgery
H Splenectomy

Nursing considerations
Key outcomes
The patient will:
H have no further weight loss
H have intact mucous membranes
H experience no chills, fever, or other signs and symp-
toms of illness
H express feelings of increased comfort and energy
H utilize available support systems.

Nursing interventions
H Plan care to minimize fatigue.
H Regularly check skin and mucous membranes for
pallor, petechiae, and bruising.
H Encourage deep-breathing and coughing exercises.
H Encourage verbalization and provide comfort.
H Administer prescribed drugs.
H After bone marrow transplantation, keep the patient
in a sterile room and give prescribed antibiotics and
packed red blood cells.
Monitoring
H Adverse effects of treatment
H Signs and symptoms of bleeding
H Signs and symptoms of infection
H Complete blood count
H Vital signs
H Hydration and nutritional status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H how to minimize bleeding and infection risks (such
as by using a soft-bristled toothbrush, an electric ra-
zor, and other safety devices)
H high-calorie, high-protein diet
H reinforcement of the physicians explanation of the
procedure, possible outcome, and potential adverse
effects (if the patient will undergo bone marrow
transplantation)
H medication administration, dosage, and possible
adverse effects
H signs and symptoms of infection and thrombocyto-
penia.

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Physical findings
Leukemia, chronic H Macular or nodular eruptions and evidence of skin

lymphocytic infiltration
H Enlarged lymph nodes, liver, and spleen
H Bone tenderness and edema from lymph node ob-
struction
Overview H Pallor, dyspnea, tachycardia, bleeding, and infection
from bone marrow involvement
Description H Signs of opportunistic fungal, viral, or bacterial in-
H The most benign and the most slowly progressive fections
form of leukemia
H Prognosis poor if anemia, thrombocytopenia, neu- Test results
tropenia, bulky lymphadenopathy, and severe lym- Laboratory
phocytosis develop H Miscellaneous blood tests reveal the disease. (Typi-
cally, chronic lymphocytic leukemia is an incidental
Pathophysiology finding during a routine complete blood count that
H Chronic lymphocytic leukemia is a generalized, pro- reveals numerous abnormal lymphocytes.)
gressive disease marked by an uncontrollable spread In the early stages, white blood cell (WBC) count
of abnormal, small lymphocytes in lymphoid tissue, is mildly but persistently elevated; granulocytope-
blood, and bone marrow. nia is the rule, although WBC count climbs as dis-
H Once these cells infiltrate bone marrow, lymphoid ease progresses.
tissue, and organ systems, clinical signs begin to Hemoglobin level is less than 11 g/dl.
appear. WBC differential shows neutropenia (less than
H Gross bone marrow replacement by abnormal lym- 1,500/l) and lymphocytosis (more than
phocytes is the most common cause of death, usually 10,000/l).
within 4 to 5 years of diagnosis. Platelet count shows thrombocytopenia (less than
150,000/l).
Causes Serum protein electrophoresis shows hypogamma-
H Exact cause unknown globulinemia.
Imaging
Risk factors H Computed tomography scan shows affected organs.
H Hereditary factors Diagnostic procedures
H Undefined chromosomal abnormalities H Bone marrow aspiration and biopsy show lympho-
H Certain immunologic defects, such as acquired cytic invasion.
agammaglobulinemia or ataxia-telangiectasia
Incidence Treatment
H Most common in elderly people; nearly all afflicted
are males older than age 50 General
H Chronic lymphocytic leukemia almost one-third of H Radiation therapy to relieve symptoms (generally for
new leukemia cases annually patient with enlarged lymph nodes, painful bony le-
H Higher incidence recorded within families sions, or massive splenomegaly)
H High-calorie, high-protein diet
Common characteristics H Avoidance of hot and spicy foods for patient with
H Fever, malaise, weakness impaired oral membranes
H Enlarged lymph nodes H Frequent rest periods

Complications Medications
H Infection H Systemic chemotherapy, such as fludarabine, chlo-
H In end-stage disease: anemia, progressive spleno- rambucil, and cyclophosphamide
megaly, leukemic cell replacement of the bone mar- H Other antineoplastics, such as rituximab and alem-
row, and profound hypogammaglobulinemia, which tuzumab
usually terminates with fatal septicemia
Nursing considerations
Assessment
Key outcomes
History The patient will:
H Fatigue, malaise, fever, weight loss, and frequent in- H have no further weight loss
fections H have intact mucous membranes
H Weakness, palpitations

486 Leukemia, chronic lymphocytic

9400L.qxd 8/2/12 4:37 PM Page 487

H experience no chills, fever, or other signs and symp-

toms of illness
H express feelings of increased comfort and energy
H utilize available support systems.

Nursing interventions
H Help establish an appropriate rehabilitation program
during remission.
H Place in reverse isolation, if necessary.
H Administer prescribed drugs.
H Encourage verbalization and provide support.
H Administer blood component therapy, as necessary.

Monitoring
H Signs and symptoms of bleeding and thrombo-
cytopenia
H Adverse effects of treatment
H Nutritional status
H Pain control
H Vital signs
H Signs and symptoms of infection

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H use of a soft toothbrush and avoidance of commer-
cial mouthwashes to prevent irritating the mouth
ulcers that result from chemotherapy
H medication administration, dosage, and possible
adverse effects
H signs and symptoms of infection, bleeding, and
recurrence
H staying away from anyone with an infection
H importance of follow-up care
H signs and symptoms of recurrence.

Discharge planning
H Refer the patient to available resources and support
services.

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Listeriosis
Overview
Description
H An infection caused by the weakly hemolytic, gram-
positive bacillus Listeria monocytogenes
H Occurs most commonly in fetuses, in neonates (dur-
ing the first 3 weeks of life), and in older or im-
munosuppressed adults; infected fetus usually still-
born or born prematurely
H Infection producing milder illness in pregnant fe-
males and varying degrees of illness in older and im-
munosuppressed patients; prognoses dependent on
severity of underlying illness
Pathophysiology
H L. monocytogenes is a nonspore producing, motile
gram-positive bacillus with aerobic and anaerobic
characteristics.
H It grows best at neutral to slightly alkaline pH.
H Transmission occurs:
in utero (through the placenta) or during passage
through an infected birth canal
by inhaling contaminated dust
by drinking contaminated, unpasteurized milk
Preventing listeriosis
Follow these general guidelines to prevent listeriosis:
H Thoroughly cook raw food from animal sources, such
as beef, pork, or poultry.
H Wash raw vegetables thoroughly before eating.
H Keep uncooked meats separate from vegetables and
from cooked foods and ready-to-eat foods.
H Avoid unpasteurized (raw) milk or foods made from
unpasteurized milk.
H Wash hands, knives, and cutting boards after handling
uncooked foods.
Patients at high risk, such as those with weakened im-
mune systems and pregnant women, should follow the
general guidelines, plus:
H Avoid hot dogs, luncheon meats, and deli meats, un-
less they are reheated until steaming hot.
H Avoid cross-contaminating other foods, utensils, and
food preparation surfaces with fluid from hot dog pack-
ages, and wash hands after handling hot dogs, lun-
cheon meats, and deli meats.
H Dont eat soft cheeses, such as feta, Brie, Camembert,
blue-veined cheeses, and Mexican-style cheeses such
as queso blanco fresco.
H Dont eat refrigerated pts or meat spreads. Canned or
shelf-stable pts and meat spreads may be eaten.
H Dont eat refrigerated smoked seafood, such as
salmon, trout, whitefish, cod, tuna, or mackerel, unless
its in a cooked dish such as a casserole.
488 Listeriosis
by coming in contact with infected animals, conta-
minated sewage or mud, or soil contaminated with
feces organism. (See Preventing listeriosis.)
Causes
H Contamination with L. monocytogenes
Risk factors
H Age extremes
H Pregnancy
H Weakened immune system
H Handling or eating uncooked or undercooked meat,
soft cheese, and unpasturized milk
H Occupations involving contact with animals, such as
butchers, veterinarians, and farmers
Incidence
H 7.4 cases per million population
H Affects females of childbearing age
Common characteristics
H Transient asymptomatic carrier state
H Bacteremia and a febrile, generalized illness
H In a pregnant female, especially during the third
trimester: a mild illness with malaise, chills, fever,
and back pain (possibly also severe uterine infection,
abortion, premature delivery, or stillbirth)
H Transplacental infection possibly causing early
neonatal death or granulomatosis infantiseptica,
which produces organ abscesses in infants
Complications
H Stillbirth
H Meningitis
H Septic arthritis
H Endocarditis
Assessment
History
H Ingestion of infected food
H Eye or skin exposure to laboratory animals or ani-
mals seen in veterinary practice
Physical findings
H Back pain and malaise
H Fever
H Nausea and diarrhea
H Headache, stiff neck
H Confusion, loss of balance, seizures
H Skin lesions on trunk and extremities
H Signs of sepsis
Test results
Laboratory
H L. monocytogenes is identified by its diagnostic tum-
bling motility on a wet mount of the culture.
H Positive culture of blood, spinal fluid, drainage from
cervical or vaginal lesions, or lochia from a mother
9400L.qxd 8/2/12 4:37 PM Page 489

with an infected neonate is present; isolation of the

organism from these specimens is generally difficult.

Treatment
General
H Symptomatic
H Activity, as tolerated
H Diet, as tolerated

Medications
H Antibiotics, such as penicillin G and ampicillin

Nursing considerations
Key outcomes
The patient will:
H maintain fluid balance
H maintain stable vital signs
H show improvement in signs and symptoms.

Nursing interventions
H Follow standard precautions.
H Provide adequate nutrition by total parenteral nutri-
tion, nasogastric tube feedings, or a soft diet, as
ordered.
Monitoring
H Neurologic status
H Fontanels (in neonates)
H Vital signs
H Intake and output

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H how to avoid infective materials on farms where
listeriosis is endemic among livestock.

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Liver cancer H Nausea and vomiting

H Initially, dull aching abdominal pain
H Severe pain in the epigastrium or right upper
quadrant
Overview
Physical findings
Description H Jaundice
H Malignant cells growing in the tissues of the liver H Dependent edema
H Rapidly fatal, usually within 6 months H Abdominal bruit, hum, or rubbing sound
H After cirrhosis, the leading cause of fatal hepatic dis- H Tender, nodular, enlarged liver
ease H Ascites
H Liver metastasis occurring as solitary lesion (the first H Palpable mass in the right upper quadrant
sign of recurrence after a remission)
Test results
Pathophysiology Laboratory
H Most (90%) primary liver tumors originate in the H Liver function studies are abnormal.
parenchymal cells and are hepatomas. Others origi- H Alpha-fetoprotein levels are greater than
nate in the intrahepatic bile ducts (cholangiomas). 500 mcg/ml.
H Approximately 30% to 70% of patients with hepato- H Electrolyte study results are abnormal.
mas also have cirrhosis. Imaging
H Rare tumors include a mixed-cell type, Kupffer cell H Liver scan may show filling defects and lesions in
sarcoma, and hepatoblastoma. the liver.
H The liver is one of the most common sites of metasta- H Arteriography may define large tumors.
sis from other primary cancers. Cells metastasize to H Ultrasound and computed tomography scans may
gallbladder, mesentery, peritoneum, and diaphragm reveal lesions in the liver.
by direct extension. Diagnostic procedures
H Liver biopsy by needle or open biopsy reveals can-
Causes cerous cells.
H Immediate cause unknown
H Environmental exposure to carcinogens
H Possibly androgens and oral estrogens Treatment
H Hepatitis B virus
H Hepatitis C virus General
H Hepatitis D virus H Radiation therapy (alone or with chemotherapy)
H High-calorie, low-protein diet
Risk factors H Frequent rest periods
H Cirrhosis H Postoperative avoidance of heavy lifting and contact
H Excessive alcohol intake sports
H Malnutrition
Medications
Incidence H Chemotherapeutics, such as doxorubicin, 5-fluo-
H Most prevalent in males older than age 60 rouracil, and cisplatin
H Primary liver cancer roughly 2% of all cancers in
North America and 10% to 50% of cancers in Africa Surgery
and parts of Asia H Resection (lobectomy or partial hepatectomy)
H Liver transplantation
Common characteristics
H Right upper quadrant pain
H Fatigue Nursing considerations
Complications Key outcomes
H GI hemorrhage The patient will:
H Progressive cachexia H maintain stable hemodynamic status
H Liver failure H maintain adequate cardiac output
H exhibit adequate coping behaviors
H maintain normal fluid volume
Assessment H express feelings of increased comfort.

History Nursing interventions

H Weight loss H Administer prescribed drugs.
H Weakness, fatigue, and fever H Provide meticulous skin care.

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H Encourage verbalization and provide support.

Monitoring
H Vital signs
H Hydration and nutritional status
H Weight
H Pain control
H Neurologic status
H Complete blood count; liver function tests
H Postoperative complications
H Wound site

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H dietary restrictions
H relaxation techniques
H medication administration, dosage, and possible
adverse effects.
Discharge planning
H Refer the patient and family to support services.

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Liver failure H The cause may be the accumulation of vasoactive

substances that cause inappropriate constriction of
renal arterioles, leading to decreased glomerular fil-
tration and oliguria.
Overview H The vasoconstriction may also be a compensatory re-
sponse to portal hypertension and the pooling of
Description blood in the splenic circulation.
H Inability of the liver to function properly, usually as
the end result of any liver disease Causes
H Causes a complex syndrome involving the impair- H Viral hepatitis
ment of many different organs and body functions H Nonviral hepatitis
(see Understanding liver functions) H Cirrhosis
H Two conditions occurring in liver failure hepatic H Liver cancer
encephalopathy and hepatorenal syndrome H Acetaminophen toxicity
H Liver transplantation only cure H Malnutrition
H Long-term alcohol abuse
Pathophysiology H Hemochromatosis
H Manifestations of liver failure include hepatic en- H Ingestion of wild, poisonous mushrooms
cephalopathy and hepatorenal syndrome.
Hepatic encephalopathy Risk factors
H The liver cant detoxify the blood. H Obesity
H Liver dysfunction and collateral vessels that shunt H Diabetes
blood around the liver to the systemic circulation H Hyperlipidemia
permit toxins absorbed from the GI tract to circulate H Abdominal surgery removing large sections of the
freely to the brain. small intestines
H The normal liver transforms ammonia (a by-product H Certain medications
of protein metabolism) to urea, which the kidneys
excrete. Incidence
H When the liver cant transform ammonia to urea, am- H Patients younger than age 10 and older than age 40
monia blood levels rise, and the ammonia is deliv- faring poorly
ered to the brain.
H Short-chain fatty acids, serotonin, tryptophan, and Common characteristics
false neurotransmitters may also accumulate in the H Jaundice
blood. H Abdominal pain or tenderness
Hepatorenal syndrome H Nausea and anorexia
H Renal failure is concurrent with liver disease; the H Fatigue
kidneys appear to be normal but abruptly cease func- H Weight loss
tioning. H Pruritus
H Blood volume expands, hydrogen ions accumulate, H Oliguria
and electrolyte disturbances occur. H Splenomegaly
H Ascites
H Peripheral edema
H Varices of the esophagus, rectum, and abdominal
wall
Understanding liver functions H Bleeding tendencies
To understand how liver disease affects the body, you H Petechia
need to understand its main functions. The liver: H Amenorrhea
H detoxifies poisonous chemicals, including alcohol, and H Gynecomastia (in males)
drugs (prescribed and over-the-counter as well as ille-
gal substances) Complications
H makes bile to help digest food H Variceal bleeding
H stores energy by stockpiling sugar (carbohydrates, glu- H GI hemorrhage
cose, and fat) until needed H Coma
H stores iron reserves as well as vitamins and minerals
H Death
H manufactures new proteins
H produces important plasma proteins necessary for
blood coagulation, including prothrombin and fibrino-
gen
Assessment
H serves as a site for hematopoiesis during fetal develop-
ment.
History
H Liver disorder

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H Fatigue Monitoring
H Weight loss H Level of consciousness
H Nausea H Vital signs
H Anorexia H Laboratory values
H Pruritus H Intake and output
H Weight and abdominal girth
Physical findings
H Jaundice
H Abdominal tenderness Patient teaching
H Splenomegaly
H Ascites Be sure to cover:
H Peripheral edema H the disorder, diagnosis, and treatment
H signs of complications and when to notify the
Test results physician
Laboratory H importance of following a low-protein diet
H Liver function tests reveal elevated levels of aspartate H importance of avoiding alcohol.
aminotransferase, alanine aminotransferase, alkaline
phosphatase, and bilirubin. Discharge planning
H Blood studies reveal anemia, impaired red blood cell H Refer the patient to available support services, as
production, elevated bleeding and clotting times, low appropriate.
blood glucose levels, and increased serum ammonia
levels.
H Urine osmolarity is increased.

Treatment
General
H Paracentesis to remove ascitic fluid
H Balloon tamponade to control bleeding varices
H Low-protein, high-carbohydrate diet
H Activity, as tolerated

Medications
H Lactulose
H Potassium-sparing diuretics (for ascites)
H Potassium supplements
H Vasoconstrictors (for variceal bleeding)
H Vitamin K

Surgery
H Sclerosis to stop bleeding varices
H Shunt placement
H Liver transplantation

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort
H maintain stable vital signs
H stabilize fluid status
H remain oriented to his surroundings.

Nursing interventions
H Reorient patient, as needed.
H Provide a safe environment.
H Provide emotional support.

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Lung cancer H Dyspnea

H Hemoptysis
H Chest pain
H Cushings and carcinoid syndromes
Overview H Hypercalcemia
Adenocarcinoma and large-cell
Description H Fever
H Malignant tumors arising from the respiratory epithe- H Weakness
lium H Weight loss
H Most common types are epidermoid (squamous H Anorexia
cell), adenocarcinoma, small-cell (oat cell), and H Shoulder pain
large-cell (anaplastic) H Gynecomastia
H Most common site is wall or epithelium of bronchial H Hypertrophic pulmonary osteoarthropathy
tree
H For most patients, poor prognosis, depending on ex- Complications
tent of cancer when diagnosed and cells growth rate H Spread of primary tumor to intrathoracic structures
(only about 13% of patients with lung cancer surviv- H Tracheal obstruction
ing 5 years after being diagnosed) H Esophageal compression with dysphagia
H Phrenic nerve paralysis with hemidiaphragm eleva-
Pathophysiology tion and dyspnea
H Individuals with lung cancer demonstrate bronchial H Sympathetic nerve paralysis with Horners syndrome
epithelial changes progressing from squamous cell H Spinal cord compression
alteration or metaplasia to carcinoma in situ. H Lymphatic obstruction with pleural effusion
H Tumors originating in the bronchi are thought to be H Hypoxemia
more mucus producing. H Anorexia and weight loss, sometimes leading to
H Partial or complete obstruction of the airway occurs cachexia, digital clubbing, and hypertrophic os-
with tumor growth, resulting in lobar collapse distal teoarthropathy
to the tumor. H Neoplastic and paraneoplastic syndromes, including
H Early metastasis occurs to other thoracic structures, Pancoasts syndrome and syndrome of inappropriate
such as hilar lymph nodes or the mediastinum. antidiuretic hormone
H Distant metastasis occurs to the brain, liver, bone,
and adrenal glands.
Assessment
Causes
H Exact cause unknown History
H Possibly no symptoms
Risk factors H Exposure to carcinogens
H Smoking H Coughing
H Exposure to carcinogenic and industrial air pollu- H Hemoptysis
tants (asbestos, arsenic, chromium, coal dust, iron H Shortness of breath
oxides, nickel, radioactive dust, and uranium) H Hoarseness
H Radon exposure H Fatigue
H Genetic predisposition
Physical findings
Incidence H Dyspnea on exertion
H Family susceptibility H Finger clubbing
H Edema of the face, neck, and upper torso
H Dilated chest and abdominal veins (superior vena
Special populations
cava syndrome)
Lung cancer is the most common cause of death H Weight loss
from cancer for men and women ages 50 to 75. H Enlarged lymph nodes
H Enlarged liver
H 15% of new cancer cases H Decreased breath sounds
H 29% of all cancer deaths H Wheezing
H Pleural friction rub
Common characteristics
Epidermoid and small-cell Test results
H Smokers cough Laboratory
H Hoarseness H Cytologic sputum analysis shows diagnostic evidence
H Wheezing of pulmonary malignancy.

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H Liver function studies are abnormal especially with

metastasis. Nursing considerations
Imaging
H Chest X-rays show advanced lesions and can show a Key outcomes
lesion up to 2 years before signs and symptoms ap- The patient will:
pear; findings may indicate tumor size and location. H maintain normal fluid volume
H Contrast studies of the bronchial tree (chest tomog- H maintain adequate ventilation
raphy, bronchography) demonstrate size and loca- H maintain a patent airway
tion as well as spread of lesion. H express feelings of increased comfort and decreased
H Bone scan is used to detect metastasis. pain.
H Computed tomography (CT) scan of the chest is used
to detect malignant pleural effusion. Nursing interventions
H CT scan of the brain is used to detect metastasis. H Provide supportive care.
H Positron-emission tomography aids in the diagnosis H Encourage verbalization.
of primary and metastatic sites. H Give prescribed drugs.
Diagnostic procedures
H Bronchoscopy can be used to identify the tumor site. Monitoring
Bronchoscopic washings provide material for cyto- H Chest tube function and drainage
logic and histologic study. H Postoperative complications
H Needle biopsy of the lungs (relies on biplanar fluoro- H Wound site
scopic visual control to locate peripheral tumors be- H Vital signs
fore withdrawing a tissue specimen for analysis) al- H Sputum production
lows firm diagnosis in 80% of patients. H Hydration and nutrition
H Tissue biopsy of metastatic sites (including supra- H Oxygenation
clavicular and mediastinal nodes and pleura) is used H Pain control
to assess disease extent. Based on histologic findings,
staging describes the diseases extent and prognosis
and is used to direct treatment. Patient teaching
H Thoracentesis allows chemical and cytologic exami-
nation of pleural fluid. Be sure to cover:
H Gallium scans of the liver and spleen help detect H the disorder, diagnosis, and treatment
metastasis. H postoperative procedures and equipment
H Exploratory thoracotomy is performed to obtain H chest physiotherapy
biopsy. H exercises to prevent shoulder stiffness
H medication administration, dosage, and possible
adverse effects
Treatment H risk factors for recurrent cancer.

General Discharge planning

H Various combinations of surgery, radiation therapy,
and chemotherapy to improve prognosis
H Palliative (most treatments)
H Preoperative and postoperative radiation therapy
H Laser therapy
H Well-balanced diet
H Activity, as tolerated per breathing capacity
H Refer smokers to local branches of the American
Cancer Society or Smokenders.
H Provide information about group therapy, individual
counseling, and hypnosis.
H Refer the patient to available resources and support
services.

Medications
H Chemotherapy combinations
H Erletin
H Biologicals such as bevacizumab

Surgery
H Partial removal of lung (wedge resection, segmental
resection, lobectomy, radical lobectomy)
H Total removal of lung (pneumonectomy, radical
pneumonectomy)

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Lupus erythematosus
Overview
Description
H Chronic inflammatory disorder of the connective tis-
sues appearing in two forms: discoid lupus erythe-
matosus, which affects only the skin, and systemic
lupus erythematosus (SLE), which affects multiple
organ systems as well as the skin and possibly fatal
H Characterized by recurring remissions and exacerba-
tions, especially common during the spring and sum-
mer
H Prognosis improving with early detection and treat-
ment but remaining poor for patients who develop
cardiovascular, renal, or neurologic complications,
or severe bacterial infections
Pathophysiology
H Autoimmunity is believed to be the prime mechanism
involved with SLE.
H The body produces antibodies against components of
its own cells such as the antinuclear antibody (ANA),
and immune complex disease follows.
H Patients with SLE may produce antibodies against
many different tissue components, such as red blood
cells (RBCs), neutrophils, platelets, lymphocytes, or
almost any organ or tissue in the body.
Causes
H Exact cause unknown
Risk factors
H Physical or mental stress
H Streptococcal or viral infections
H Exposure to sunlight or ultraviolet light
H Immunization
H Pregnancy
H Abnormal estrogen metabolism
H Treatment with certain drugs, such as procainamide
(Pronestyl), hydralazine (Apresoline), and anticon-
vulsants
Incidence
H Affects 14 to 50 people per 100,000 in the United
States
H Affects females more than males
H Affects all ages, but peak incidence is young adult-
hood
Common characteristics
See Signs of systemic lupus erythematosus.
Complications
H Concomitant infections
H Urinary tract infections
H Renal failure
H Osteonecrosis of hip from long-term steroid use
496 Lupus erythematosus
Assessment
History
H History of contributing factor
H Fever
H Weight loss
H Malaise
H Fatigue
H Polyarthralgia
H Abdominal pain
H Headaches, irritability, and depression (common)
H Nausea, vomiting, diarrhea, constipation
H Irregular menstrual periods or amenorrhea during
the active phase of SLE
Physical findings
H Rashes
H Joint involvement, similar to rheumatoid arthritis (al-
though the arthritis of lupus usually nonerosive)
H Skin lesions, most commonly an erythematous rash
in areas exposed to light (classic butterfly rash over
the nose and cheeks in less than 50% of patients) or
a scaly, papular rash (mimics psoriasis), especially
in sun-exposed areas
H Vasculitis (especially in the digits), possibly leading
to infarctive lesions, necrotic leg ulcers, or digital
gangrene
H Patchy alopecia and painless ulcers of the mucous
membranes
H Lymph node enlargement (diffuse or local, and non-
tender)
Test results
Laboratory
H Antidouble-stranded deoxyribonucleic acid anti-
body, the most specific test for SLE, correlates with
disease activity, especially renal involvement, and
helps monitor response to therapy; it may be low or
absent in remission.
H Complete blood count with differential may show
anemia and a decreased white blood cell (WBC)
count.
H Platelet count is decreased.
H Erythrocyte sedimentation rate is elevated.
H Serum hypergammaglobulin is elevated.
H ANA and lupus erythematosus cell tests show positive
results in active SLE.
H Urine studies may show RBCs and WBCs, urine casts
and sediment, and significant protein loss (more
than 0.5 g/24 hours).
H Serum complement blood studies show decreased
serum complement (C3 and C4) levels indicating
active disease.
H Lupus anticoagulant and anticardiolipin tests may be
positive in some patients (usually in patients prone to
antiphospholipid syndrome of thrombosis, abortion,
and thrombocytopenia).
Imaging
H Chest X-ray may show pleurisy or lupus pneumonitis.
9400L.qxd 8/2/12 4:37 PM Page 497

Diagnostic procedures Signs of systemic lupus erythematosus

H Electrocardiography may show a conduction defect
Systemic lupus erythematosus (SLE) often mimics other
with cardiac involvement or pericarditis. diseases, making it difficult to diagnose. Symptoms may
H Kidney biopsy determines disease stage and extent of be vague and vary greatly among patients.
renal involvement. For these reasons, the American Rheumatism Associa-
tion issued a list of criteria for classifying SLE to be used
primarily for consistency in epidemiologic surveys. Usu-
Treatment ally, four or more of these signs are present at some time
during the course of the disease:
General H malar or discoid rash
H Symptomatic H photosensitivity
H oral or nasopharyngeal ulcerations
H Dialysis or kidney transplant for renal failure
H nonerosive arthritis (of two or more peripheral joints)
H Diet restrictions based on extent of disorder
H pleuritis or pericarditis
H Activity, as tolerated
H profuse proteinuria (more than 0.5 g/day) or excessive
H Frequent rest periods cellular casts in the urine
H seizures or psychoses
Medications H hemolytic anemia, leukopenia, lymphopenia, or throm-
H Nonsteroidal anti-inflammatory drugs, including bocytopenia
aspirin H antidouble-stranded deoxyribonucleic acid or positive
H Topical corticosteroid creams, such as hydrocorti- findings of antiphospholipid antibodies (elevated im-
sone buteprate and triamcinolone munoglobulin [Ig] G or IgM anticardiolipin antibodies,
H Intralesional corticosteroids or antimalarials such as positive test result for lupus anticoagulant, or false-
hydroxychloroquine sulfate positive serologic test results for syphilis)
H abnormal antinuclear antibody titer.
H Systemic corticosteroids

Nursing considerations
Discharge planning
Key outcomes H Arrange for physical therapy and occupational coun-
The patient will: seling, as appropriate.
H remain free from infection H Refer the patient to the Lupus Foundation of America
H remain hemodynamically stable and the Arthritis Foundation, as necessary.
H express understanding of disease and treatment.

Nursing interventions
H Provide a balanced diet. Renal involvement may man-
date a low-sodium, low-protein diet.
H Urge the patient to get plenty of rest. Schedule diag-
nostic tests and procedures to allow adequate rest.
H Explain all tests and procedures.
H Apply heat packs to relieve joint pain and stiffness.
H Encourage regular exercise to maintain full range of
motion (ROM) and prevent contractures.
Monitoring
H Signs and symptoms
H Vital signs
H Intake and output
H Laboratory reports

Patient teaching
Be sure to cover:
H ROM exercises as well as body alignment and postur-
al techniques
H expected benefit of prescribed medications as well as
adverse effects
H cosmetic tips, such as suggesting the use of hypoal-
lergenic makeup and referral to a hairdresser who
specializes in scalp disorders.

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Lyme disease If untreated in acute phase

Overview
Description
H A multisystem disorder caused by a spirochete
Pathophysiology
H A tick injects spirochete-laden saliva into the blood-
stream or deposits fecal matter on the skin.
H After incubating for 3 to 32 days, the spirochetes mi-
grate outward on the skin, causing a rash, and dis-
seminate to other skin sites or organs through the
bloodstream or lymph system.
H Spirochetes may survive for years in the joints or die
after triggering an inflammatory response in the host.
Causes
H The spirochete Borrelia burgdorferi, carried by the
minute tick Ixodes dammini (also called I. scapu-
laris) or another tick in the Ixodidae family
Risk factors
H Outdoor occupations
H Outdoor activities, such as camping and hunting
H Geographic location with tick infestation
Incidence
H Affects all ages and both sexes
H Onset during the summer months
H Occurs in geographic ranges of ixodid ticks
Common characteristics
H Typically begins with classic skin lesion, erythema
migrans (EM)
H Skin lesions with bright red outer rims and white
centers appearing on axilla, thigh, and groin
H Initial reported symptoms, such as fatigue, malaise,
migratory myalgia, and arthralgia
H Cardiac, neurologic, or joint abnormalities possibly
developing weeks or months later
Complications
H Myocarditis
H Pericarditis
H Arrhythmias
H Meningitis
Differentiating Lyme disease
Lyme disease, or chronic neuroborreliosis, needs to be
differentiated from chronic fatigue syndrome or fibromyal-
gia, which is difficult late in the disease because of
chronic pain and fatigue. The other diseases produce
more generalized and disabling symptoms; also, patients
lack evidence of joint inflammation, have normal neuro-
logic tests, and have a greater degree of anxiety and de-
pression than patients with Lyme disease.
H Encephalitis
H Cranial or peripheral neuropathies
H Arthritis
Assessment
History
H Recent exposure to ticks
H Onset of symptoms in warmer months
H Severe headache and stiff neck with rash eruption
H Fever (up to 104 F [40 C]) and chills
Physical findings
H Regional lymphadenopathy
H Tenderness in the skin lesion site or the posterior
cervical area
Early stage
H Tachycardia or irregular heartbeat
H Mild dyspnea
H EM
H Headache
H Myalgia
H Arthralgia
Later stage
H Neurologic signs such as memory impairment
H Bells palsy
H Intermittent arthritis (see Differentiating Lyme dis-
ease)
H Cardiac symptoms, such as heart failure, pericarditis,
and dyspnea
H Neurologic symptoms, such as memory impairment
and myelitis
H Fibromyalgia
H Ocular signs such as conjunctivitis
Test results
Laboratory
H Assays for anti-B. burgdorferi show evidence of pre-
vious or current infection.
H Enzyme-linked immunosorbent assay or indirect im-
munofluorescence microscopy shows immunoglobu-
lin (Ig) M levels peak 3 to 6 weeks after infection,
IgG antibodies are detected several weeks after infec-
tion and may continue to develop for several months
and generally persist for years.
H Positive Western blot assay shows serologic evidence.
of past or current infection with B. burgdorferi
H Polymerase chain reaction is used when joint and
cerebrospinal fluid involvement are present.
ALERT
Serologic testing isnt useful early in the course of
Lyme disease because of its low sensitivity. Howev-
er, it may be more useful in later disease stages,
when sensitivity and specificity of the test are im-
proved.

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Diagnostic procedures Prevention

H Lumbar puncture with analysis of cerebrospinal fluid
may show antibodies to B. burgdorferi.
H Skin biopsy may be used to detect B. burgdorferi.
Treatment
General
H Prompt tick removal using proper technique
H Rest periods when needed
Medications
H I.V. or oral antibiotics (initiated as soon as possible
after infection), such as doxycycline, amoxicillin,
ceftriaxone, and cefuroxime axetil
Preventing lyme disease
Lyme disease can be prevented by following these guide-
lines:
H Avoid tick-infested areas.
H Cover the skin with light-colored clothing to make ticks
more visible.
H Wear long sleeves and pants and tuck pant legs into
socks.
H Use insect repellants, such as DEET or permethricin
(on clothing only).
H Inspect the body and scalp for attached ticks at least
every 4 hours and remove. Lyme disease is less likely
if the tick is removed in less than 48 hours.
H Check pets for ticks.

Nursing considerations
Key outcomes
The patient will:
H maintain hemodynamic stability
H maintain adequate cardiac output
H express relief from pain
H attain the highest degree of mobility possible.

Nursing interventions
H Plan care to provide adequate rest.
H Administer prescribed drugs.
H Assist with range-of-motion and strengthening exer-
cises (with arthritis).
H Encourage verbalization and provide support.

Monitoring
H Skin lesions
H Response to treatment
H Adverse drug reactions
H Complications

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medication administration, dosage, and possible ad-
verse effects
H importance of follow-up care and reporting recur-
rent or new symptoms to the physician
H prevention of Lyme disease (see Preventing Lyme
disease)
H information about the vaccine for persons at risk for
contracting Lyme disease.
Discharge planning
H If the patient is in the late stages of the disease, refer
him to a dermatologist, neurologist, cardiologist, or
infectious disease specialist, as indicated.

Lyme disease 499

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Lymphocytic
choriomeningitis
Overview
Description
H A mild, biphasic, febrile illness lasting about 2 weeks
H Asymptomatic in one-third of individuals and re-
solves without serious sequelae in most cases
H Rarely fatal (less than 1% mortality rate)
H Also known as LCM or lymphocytic meningitis
Pathophysiology
H Infected mice or other hosts excrete lymphocytic
choriomeningitis virus (LCMV) in saliva, urine, and
feces.
H Human infection is through inhalation of infectious
aerosolized particles of host urine, feces, or saliva;
food contaminated with virus; or contamination of
mucous membranes, skin lesions, or cuts with infect-
ed body fluids.
H The incubation period is 8 to13 days and is followed
by a biphasic, febrile illness.
H The initial viremia extensively seeds extra-central
nervous system tissue and sometimes cortical tissue.
H The leptomeninges are infiltrated mainly by lympho-
cytes and histiocytes, with few neutrophils.
H The hosts immune response to the infected cells
produces various symptoms.
H Natural killer cells are first to respond, then cytotox-
ic T cells respond with interferon.
H Meningeal symptoms appear in 15 to 21 days.
Causes
H LCMV
H Arenavirus
Risk factors
H Handling infected animals or their excreta
Incidence
H Prevalence of LCM in humans: 2% to 10%, but im-
portant to note that LCM historically underreported
H Individuals of all ages susceptible, but more common
in young adults
H Cases reported in Europe, North America, South
America, Australia, and Japan, but most cases occur-
ring in the northeast and eastern seaboard areas of
the United States
H More common during fall and winter
H Infection occurring equally in males and females
Common characteristics
H Early: fever, malaise, anorexia, weakness, muscle
aches, retro-orbital headache, nausea, and vomiting
(other symptoms appearing less commonly include
500 Lymphocytic choriomeningitis
sore throat, nonproductive cough, joint pain, chest
pain, testicular pain, and parotid [salivary gland]
pain)
H Late: include alopecia and signs and symptoms of
meningitis (fever, increased headache, and stiff
neck) or encephalitis (drowsiness, confusion, senso-
ry disturbances, and motor abnormalities such as
paralysis)
Complications
H Temporary or permanent neurologic damage possi-
ble (meningitis, paralysis, coma)
H Possible maternal transmission (Pregnancy-related
infection associated with abortion, congenital hydro-
cephalus, chorioretinitis, and mental retardation)
H Myelitis presenting with muscle weakness, paralysis,
or changes in body sensation
H Guillain-Barrtype syndrome
H Orchitis (usually unilateral) or parotitis
H Cardiac involvement such as myocarditis
H Psychosis
H Joint pain and arthritis during convalescence, espe-
cially in the metacarpophalangeal and proximal in-
terphalangeal joints
H Prolonged convalescence, with continuing dizziness,
somnolence, and fatigue
Assessment
History
H Exposure to rodents, hamsters, or their excreta 1 to
3 weeks before symptom onset
Physical findings
H Lymphadenopathy
H Maculopapular rash
H Fever
H Cough
H Possible bradycardia
Test results
Laboratory
PHASE I
H White blood cell (WBC) count is decreased (leuko-
penia).
H Platelet count is decreased (thrombocytopenia).
H Liver enzymes are mildly elevated.
PHASE II
H Protein levels are increased.
H WBC count is increased.
H Glucose levels in cerebrospinal fluid (CSF) are
decreased.
Diagnostic procedures
H Enzyme-linked immunosorbent assay detects immu-
noglobulin M antibodies from serum or CSF (the
preferred diagnostic test).
H Lumbar puncture: In patients with meningeal signs,
CSF is typically abnormal, consisting of an increased
9400L.qxd 8/2/12 4:37 PM Page 501

opening pressure, increased protein levels, and a Prevention

lymphocytic pleocytosis, usually in the range of Preventing lymphocytic
several hundred WBCs. choriomeningitis
Lymphocytic choriomeningitis can be prevented by fol-
Treatment lowing these guidelines:
H Use meticulous hand-washing techniques using soap
and water after handling pet rodents.
General H Clean cages in a well-ventilated area.
H Hospitalization and supportive treatment based on H Use a liquid disinfectant, such as diluted household
severity bleach, to clean up rodent droppings.
H Activity, as tolerated H Avoid putting rodents near your face.
H Closely supervise children and make sure they follow
Medications good hand-washing practices after touching rodents.
H No specific treatment
H Anti-inflammatory drugs possibly useful
H Ribavirin (effective against LCMV in vitro)
H Analgesics (for symptom relief)

Surgery H Refer paralyzed or comatose patients to physical

H Acute hydrocephalus possibly requiring surgical therapy or occupational therapy, as needed.
shunting to relieve increased intracranial pressure H Refer psychotic patients for follow-up with a psychia-
trist.
Nursing considerations
Key outcomes
The patient will:
H report acute symptom relief
H use precautions in handling rodents in the future
H have a plan to manage potential complications dur-
ing convalescence
H understand the importance of follow-up appoint-
ments.
Nursing interventions
H Encourage rest and fluids after lumbar puncture.
H Administer prescribed drugs.
H Administer total care if the patient is paralyzed or in
a coma.
H Encourage diet and activity, as tolerated.

Monitoring
H Vital signs
H Acute hydrocephalus
H Cardiac signs and symptoms
H Skin integrity
H If lumbar puncture, complications

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H prevention techniques (see Preventing lymphocytic
choriomeningitis)
H use of a personal respirator.

Discharge planning
H Refer pregnant patients to an obstetrician for moni-
toring.

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Lymphoma, H Meningitis
H Anemia

non-Hodgkins H Liver, kidney, and lung problems (with tumor

Overview
Description
H Heterogeneous group of malignant diseases that orig-
inate in lymph glands and other lymphoid tissue
H Usually classified according to histologic, anatomic,
and immunomorphic characteristics developed by
the National Cancer Institute (Rappaport histologic
and Lukes and Collins classifications also used in
some facilities)
H New categories of non-Hodgkins lymphoma, called
mantle zone lymphoma and marginal zone lym-
phoma
H Also called malignant lymphoma and lymphosarco-
ma
Pathophysiology
H Non-Hodgkins lymphoma seems to be similar to
Hodgkins disease, but Reed-Sternberg cells arent
present, and the lymph node destruction is different.
H Lymphoid tissue is defined by the pattern of infiltra-
tion as diffuse or nodular. Nodular lymphomas yield
a better prognosis than the diffuse form, but in both
the prognosis is less hopeful than in Hodgkins dis-
ease.
Causes
H Exact cause unknown
Risk factors
H History of autoimmune disease
Incidence
H Three times more common than Hodgkins disease
H Incidence increasing, especially in patients with au-
toimmune disorders and those receiving immuno-
suppressant treatment or those with acquired im-
munodeficiency syndrome
Special populations
Males older than age 60 have the highest incidence
of non-Hodgkins lymphoma.
Common characteristics
H Enlarged, painless lymph nodes
H Fever, malaise
H Weight loss
growth)
H Central nervous system involvement possibly leading
to increased intracranial pressure
Assessment
History
H Symptoms mimicking those of Hodgkins disease
H Painless, swollen lymph glands (swelling that may
have appeared and disappeared over several
months)
H Complaints of fatigue, malaise, weight loss, fever, and
night sweats
H Trouble breathing, cough (usually children)
Physical findings
H Enlarged tonsils and adenoids
H Rubbery nodes in the cervical and supraclavicular
areas
Test results
Laboratory
H Complete blood count shows anemia.
H Uric acid levels are normal or elevated.
H Calcium level is elevated due to bone lesions.
Imaging
H Miscellaneous scans (chest X-rays; lymphangiogra-
phy; liver, bone, and spleen scans; a computed to-
mography scan of the abdomen; and excretory urog-
raphy) show disease progression.
Diagnostic procedures
H Biopsies of lymph nodes; of tonsils, bone marrow,
liver, bowel, or skin; or, as needed, of tissue removed
during exploratory laparotomy help to differentiate
non-Hodgkins lymphoma from Hodgkins disease.
H The same staging system used for Hodgkins disease
is used for non-Hodgkins lymphomas.
Treatment
General
H Radiation therapy mainly during the localized stage
of the disease
H Total nodal irradiation usually effective in nodular
and diffuse lymphomas
H Well-balanced, high-calorie, high-protein diet
H Increased fluid intake
H Small, frequent meals
H Limited activity
H Frequent rest periods

Complications Medications
H Hypercalcemia H Chemotherapy in combinations
H Hyperuricemia
H Lymphomatosis

502 Lymphoma, non-Hodgkins

9400L.qxd 8/2/12 4:37 PM Page 503

Surgery
H Total or subtotal gastrectomy to treat perforation
(common in patients with gastric lymphomas) before
chemotherapy

Nursing considerations
Key outcomes
The patient will:
H have no further weight loss
H demonstrate effective coping mechanisms
H express feelings of increased comfort and decreased
pain.
Nursing interventions
H Administer prescribed drugs.
H Provide time for rest periods.
H Encourage verbalization and provide support.

Monitoring
H Adverse effects of treatment
H Vital signs
H Pain control
H Hydration and nutritional status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H preoperative and postoperative procedures
H dietary plan
H mouth care using a soft-bristled toothbrush and
avoidance of commercial mouthwashes
H relaxation and comfort measures
H medication administration, dosage, and possible
adverse effects
H symptoms that require immediate attention.

Discharge planning
H Refer the patient to available resources and support
services.

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MOverview
Description
Life-threatening disorder

Major depression

H Persistent sad, dysphoric mood; may be life-

threatening
H Unipolar depressive disorder with onset in early
adulthood and recurrences throughout life (at least
two more episodes in 50% to 60% of patients)
H Patient appearing unhappy and apathetic

Complications
H Profound alteration of social, family, and occupation-
al functioning
H Suicide

H Recurrences possible after protracted symptom-free
period or occurring sporadically, increasing in fre-
quency, or occurring in clusters
Pathophysiology
H Changes occur in the receptor-neurotransmitter rela-
tionships in the limbic system.
H Changes in the hypothalamic-pituitary-adrenal regu-
lation system may be an adaptive deregulation of the
stress response.
H Theres a possible defect on chromosome II or X.
Causes
H Psychological stress
H Genetic, familial, biochemical, physical, psychologi-
cal, and social causes
H Many physical causes result in secondary depression
H Seasonal depression
Risk factors
H Female sex
H Family history of major depression or bipolar disor-
der
H Chronic illness
H Chronic pain
H Substance abuse
H Adverse reaction to medication such as beta-
adrenergic blockers
Incidence
H Affects about 17.6 million Americans each year
H Affects 5% to 20% of general population at some
time in their lives
H 6% to 8% of patients in care settings meet diagnostic
criteria
H Incidence increases with age
H Twice as common in females as in males, regardless
of age
Common characteristics
H Depressed mood daily for 2 weeks or longer
H History of personal loss or severe stress
H Patient expressing doubts about self-worth or ability
to cope
Assessment
History
H Profound loss of pleasure in all enjoyable activities
for a full month to 1 or more years
H Life problems or losses
H Physical disorder
H Use of prescription, nonprescription, or illicit drugs
H Change in eating and sleeping patterns
H Lack of interest in sex
H Constipation or diarrhea
Physical findings
H Difficulty concentrating or thinking clearly
H Easily distracted
H Indecisiveness
H Delusions of persecution or guilt
H Agitation
H Psychomotor retardation
DSM-IV-TR criteria
A diagnosis is confirmed when five or more of the fol-
lowing symptoms present during the same 2-week peri-
od and represent a change from previous functioning:
H Depressed mood (irritable mood in children and
adolescents) most of the day, nearly every day, as in-
dicated by either subjective account or observation
by others
H Markedly diminished interest or pleasure in all, or
almost all, activities most of the day, nearly every day
H Significant weight loss or weight gain (greater than
5% of the patients body weight in a month) when not
dieting, or a change in appetite nearly every day
H Insomnia or hypersomnia nearly every day
H Psychomotor agitation or retardation nearly every
day
H Fatigue or loss of energy nearly every day
H Feelings of worthlessness and excessive or inappro-
priate guilt nearly every day
H Diminished ability to think or concentrate, or indeci-
siveness, nearly every day
H Recurrent thoughts of death, recurrent suicidal
ideation without a specific plan, or suicide attempt or
a specific plan for committing suicide (see Suicide
prevention guidelines)
H Symptoms not due to a mixed episode, a medical
condition, the effects of a medication or other sub-
stance, or bereavement

504 Major depression

9400M.qxd 8/2/12 4:39 PM Page 505

Test results Suicide prevention guidelines

Laboratory
H Toxicology screening suggests a drug-induced
depression.
H Dexamethasone suppression test may show a failure
to suppress cortisol secretion.
Other
H Beck Depression Inventory shows the onset, severity,
duration, and progression of depressive symptoms.
Treatment
General
H Electroconvulsive therapy
H Short-term psychotherapy (a combination of individ-
ual, family, or group psychotherapy)
H Well-balanced diet
H Scheduled activities of daily living
Medications
H Selective serotonin-reuptake inhibitors, such as flu-
oxetine, paroxetine, and sertraline
H Maprotiline
H Tricyclic antidepressants, such as amitriptyline and
desipramine
H Monoamine oxidase inhibitors such as phenelzine
Nursing considerations
Key outcomes
The patient will:
H voice feelings related to self-esteem
H make a verbal contract not to harm self
H engage in social interactions with others
H verbally and behaviorally demonstrate a positive self-
evaluation.
Nursing interventions
H Encourage participation in individual and group
therapy.
H Encourage verbalization and expression of feelings.
H Listen attentively and respectfully.
H Provide a structured routine.
H Encourage interaction with others.
H Document observations and significant conversa-
tions.
H Assume an active role in initiating communication.
H Plan activities for when the patients energy levels are
highest.
H Provide distraction from self-absorption.
To help deter potential suicide in the patient with major
depression, keep in mind these guidelines.
Assess for clues to suicide
Watch for such clues as communicating suicidal
thoughts, threats, and messages; hoarding medication;
talking about death and feelings of futility; giving away
prized possessions; describing a suicide plan; and chang-
ing behavior, especially as depression begins to lift.
Provide a safe environment
Check patient areas and correct dangerous conditions,
such as exposed pipes, windows without safety glass, and
access to the roof or open balconies.
Remove dangerous objects
Remove such objects as belts, razors, suspenders, light
cords, glass, knives, nail files, and clippers from the pa-
tients environment.
Consult with staff
Recognize and document verbal and nonverbal suicidal
behaviors, keep the physician informed, share data with
all staff, clarify the patients specific restrictions, assess
risk and plan for observation, and clarify day and night
staff responsibilities and frequency of consultation.
Observe the suicidal patient
Be alert when the patient is using a sharp object (shav-
ing), taking medication, or using the bathroom (to prevent
hanging or other injury). Assign the patient to a room near
the nurses station and with another patient. Continuously
observe the acutely suicidal patient.
Maintain personal contact
Help the suicidal patient feel that he isnt alone or without
resources or hope. Encourage continuity of care and con-
sistency of primary nurses. Building emotional ties to oth-
ers is the ultimate technique for preventing suicide.
Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H depression and its effects on daily living
H need for adherence to medication regimen
H medication administration, dosage, and possible ad-
verse effects and interactions with other substances.
Discharge planning
H Refer the patient to available support services and
community assistance.

Monitoring
H Adverse effects of medication
H Suicidal ideations
H Self-care
H Social interaction
H Functioning level
H Response to treatment

Major depression 505

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Malabsorption flat and has lost absorptive surface. Symptoms gener-

ally disappear when gluten is removed from the diet.
H Lactase deficiency is a disaccharide deficiency syn-
drome. Lactase is an intestinal enzyme that splits
Overview nonabsorbable lactose (a disaccharide) into the ab-
sorbable monosaccharides glucose and galactose.
Description Production may be deficient, or another intestinal
H Defect in the GI tract in which the intestinal mucosa disease may inhibit the enzyme.
fails to absorb single or multiple nutrients efficiently H After gastrectomy, poor mixing of chyme with gastric
H Absorption of amino acids, fat, sugar, or vitamins secretions is the cause of postsurgical malabsorp-
possibly impaired tion.
H Resulting inadequate movement of nutrients from the H In Zollinger-Ellison syndrome, increased acidity in
small intestine to the bloodstream or lymphatic sys- the duodenum inhibits release of cholecystokinin,
tem which stimulates pancreatic enzyme secretion. Pan-
H Manifestations primarily dependent on what isnt creatic enzyme deficiency leads to decreased break-
being absorbed down of nutrients and malabsorption.
H Bacterial overgrowth in the duodenal stump (loop
Pathophysiology created in the Billroth II procedure) causes malab-
H The mechanism of malabsorption depends on the sorption of vitamin B12.
cause.
H In celiac sprue, dietary gluten a product of wheat, Causes
barley, rye, and oats is toxic to the patient, caus- H Prior gastric surgery
ing injury to the mucosal villi. The mucosa appears H Pancreatic disorders
H Hepatobiliary disease
H Disease of the small intestine
Causes of malabsorption H Hereditary disorders
H Drug toxicity (see Causes of malabsorption)
Many disorders from systemic to organ-specific dis-
eases may lead to malabsorption.
Diseases of the small intestine
Incidence
Primary small-bowel disease H Depends on cause of malabsorption
H Bacterial overgrowth from stasis in afferent loop after
Billroth II gastrectomy Common characteristics
H Massive bowel resection H Weight loss and generalized malnutrition
H Nontropical sprue (celiac disease) H Diarrhea
H Regional enteritis H Steatorrhea
H Tropical sprue
H Flatulence and abdominal distention
Ischemic small-bowel disease
H Nocturia
H Chronic heart failure
H Weakness and fatigue
H Mesenteric atherosclerosis
Systemic disease involving small bowel H Edema
H Acute enteritis H Amenorrhea
H Giardiasis H Anemia
Drug-induced malabsorption H Glossitis, cheilosis
H Calcium carbonate H Peripheral neuropathy
H Neomycin H Bruising, bleeding tendency
Hepatobiliary disease H Bone pain, skeletal deformities, fractures
H Biliary fistula H Tetany, paresthesia
H Biliary tract obstruction
H Cirrhosis and hepatitis Complications
Hereditary disorder H Fractures
H Primary lactase deficiency
H Anemias
Pancreatic disorders
H Chronic pancreatitis H Bleeding disorders
H Cystic fibrosis H Tetany
H Pancreatic cancer H Malnutrition
H Pancreatic resection
H Zollinger-Ellison syndrome
Previous gastric surgery Assessment
H Billroth II gastrectomy
H Pyloroplasty History
H Total gastrectomy H Fatigue
H Vagotomy
H Diarrhea
H Steatorrhea

506 Malabsorption
9400M.qxd 8/2/12 4:39 PM Page 507

Physical findings H Intake and output

H Orthostatic hypotension H Laboratory values
H Signs of weight loss or muscle wasting
H Abdominal distention
H Hyperactive bowel sounds Patient teaching
H Pallor
H Ecchymosis Be sure to cover:
H Peripheral edema H the disorder, diagnosis, and treatment
H following a gluten-free diet.
Test results
Laboratory Discharge planning
H Stool specimen for fat reveals excretion of greater H Encourage follow-up visits, as ordered.
than 6 g of fat per day.
H D-xylose absorption test shows less than 20% of 25 g
of D-xylose in the urine after 5 hours (reflects disor-
ders of proximal bowel).
H Schilling test reveals deficiency of vitamin B12 ab-
sorption.
H Culture of duodenal and jejunal contents confirms
bacterial overgrowth in the proximal bowel.
Imaging
H GI barium studies show characteristic features of the
small intestine.
Diagnostic procedures
H Small intestine biopsy reveals the atrophy of mucosal
villi.

Treatment
General
H Identification of cause and appropriate correction
H Gluten-free diet to stop progression of celiac disease
and malabsorption
H Lactose-free diet to treat lactase deficiency

Medications
H Dietary supplementation
H Vitamin B12 injections

Nursing considerations
Key outcomes
The patient will:
H have improved absorption of nutrients
H maintain or improve weight
H express understanding of cause of disorder.

Nursing interventions
H Watch for signs of dehydration, such as dry skin and
mucous membranes and poor skin turgor.
H Protect patients with osteomalacia from injury by
keeping the side rails up and assisting with ambula-
tion, as necessary.
Monitoring
H Nutritional status
H Calorie intake
H Weight

Malabsorption 507
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Malaria cystlike structures containing thousands of mero-

zoites.
H Upon release, each merozoite invades an erythrocyte
and feeds on hemoglobin.
Overview H Eventually, the erythrocyte ruptures, releasing heme
(malaria pigment), cell debris, and more mero-
Description zoites, which, unless destroyed by phagocytes, enter
H An acute infectious disease: caused by protozoa of other erythrocytes.
the genus Plasmodium: P. falciparum, P. vivax, P.
malariae, and P. ovale Causes
H Mosquito vectors transmitting the disease to humans H Bite of female Anopheles mosquitoes
H Falciparum malaria: the most severe form of the dis-
ease Risk factors
H Untreated primary attacks: last from 1 week to 1 H Resident of, or travel to, an endemic area
month or longer H Pregnancy
H Relapses common and possibly recurring sporadical- H Lack of immunity
ly for several years H Poverty
H Hepatic parasites (P. vivax, P. ovale, and P. malari- H Lack of access to health care
ae) possibly persisting for years in the liver; respon-
sible for the chronic carrier state Incidence
H 300 to 500 million cases annually (internationally)
Pathophysiology H Since 1940, few cases of malaria contracted in the
H Plasmodium sporozoites are injected by the bite of a United States; most of these transmitted by blood
mosquito vector. transfusions or the use of contaminated needles by
H The infective sporozoites migrate by blood circula- drug addicts
tion to parenchymal cells of the liver; there they form
Common characteristics
H Chills
H Fever
Special considerations for H Headache
antimalarial drugs H Myalgia
H Interspersed periods of well-being (the hallmark of
Chloroquine the benign form of malaria)
H Perform baseline and periodic ophthalmologic exami- Acute attack
nations, and report blurred vision, increased sensitivity H Occurs when erythrocytes rupture
to light, and muscle weakness to the physician.
H Three stages:
H Consult with the physician about altering therapy if
muscle weakness appears in a patient on long-term
cold stage, lasting 1 to 2 hours, ranging from
therapy. chills to extreme shaking
H Monitor the patient for tinnitus and other signs of oto- hot stage, lasting 3 to 4 hours, characterized by
toxicity, such as nerve deafness and vertigo. high fever up to 107 F (41.7 C)
H Caution the patient to avoid excessive exposure to the wet stage, lasting 2 to 4 hours, characterized by
sun to prevent exacerbating drug-induced dermatoses. profuse sweating
Primaquine Falciparum malaria
H Give with meals or antacids. H Persistent high fever
H Discontinue administration if you observe a sudden fall H Orthostatic hypotension
in hemoglobin concentration or in erythrocyte or leuko- H Red blood cell (RBC) sludging that leads to capillary
cyte count or marked darkening of the urine, suggest-
obstruction at various sites
ing impending hemolytic reaction.
Pyrimethamine Complications
H Give with meals to minimize GI distress.
H Check blood counts (including platelets) twice a week. H Renal failure
If signs of folic or folinic acid deficiency develop, re- H Liver failure
duce or discontinue dosage while patient receives par- H Heart failure
enteral folinic acid until blood counts become normal. H Pulmonary edema
Quinine H Disseminated intravascular coagulation
H Use with caution in patients with cardiovascular condi- H Circulatory collapse
tions, asthma, hemolytic anemia, and granulocytosis, H Severe normocytic anemia
in a severe reaction. H Seizures
H Monitor blood pressure frequently while administering H Hypoglycemia
quinine I.V. infusion. Rapid administration causes
H Splenic rupture
marked hypotension.
H Cerebral dysfunction
H Death

508 Malaria
9400M.qxd 8/2/12 4:39 PM Page 509

Assessment Nursing considerations

History Key outcomes
H Travel to endemic area The patient will:
H Recent blood transfusion H have stable vital signs
H I.V. drug abuse H have adequate fluid volume
H Chills, fever H express feelings and fears about current situation.
H Headache, backache
Nursing interventions
Physical findings H Obtain a detailed patient history.
H Pale skin H Follow proper hand-washing and aseptic techniques.
H Urticaria H Follow standard precautions.
H Jaundice H Record symptom pattern, fever, type of malaria, and
H Petechial rash systemic signs.
H Hepatosplenomegaly (P. vivax and P. ovale) H Report all cases of malaria to local public health
authorities.
Test results
Laboratory Monitoring
H Peripheral blood smears identify parasites in RBCs. H Vital signs
H Hemoglobin levels are decreased. H Response to treatment
H Leukocyte count may be decreased (as low as H Intake and output
3,000/l).
H Protein and leukocytes are present in urine sedi-
ment. Patient teaching
FALCIPARUM MALARIA
H Platelet numbers are reduced (20,000 to 50,000/l). Be sure to cover:
H Prothrombin time is prolonged (18 to 20 seconds). H the disorder, diagnosis, and potential for relapse
H Partial thromboplastin time is prolonged (60 to H medication administration, dosage, and possible ad-
100 seconds). verse effects.
H Plasma fibrinogen is decreased.

Treatment
General
H Symptomatic
H Activity, as tolerated (bed rest during acute phase)
H Increased fluid intake

Medications
H Oral chloroquine (for all forms except chloroquine-
resistant P. falciparum)
H Oral quinine (for malaria caused by P. falciparum)
given concurrently with pyrimethamine and a sulfon-
amide, such as sulfadiazine
H Primaquine phosphate (for hepatic phase) (see
Special considerations for antimalarial drugs)
H Other antimalarials, such as doxycycline and
hydroxycholorquine sulfate
H Antipyretics

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Mastitis H Occurs occasionally in nonlactating females

H Rare in males

Common characteristics
Overview H Red, swollen, warm, and tender breasts
H Nipple cracks or fissures
Description H Enlarged axillary lymph nodes
H Inflammation of the breast tissue
H Lactating breast infection Complications
H Good prognosis H Abscess

Pathophysiology
H A pathogen (typically originating in nursing infants Assessment
nose or pharynx) invades the breast tissue, entering
through a fissured or abraded nipple. History
H The result is parenchymatous inflammation of the H Fever
mammary glands, which disrupts normal lactation. H Malaise
H Systemic manifestations of inflammation may result. H Flulike symptoms
H Tenderness
Causes
H Most common pathogen Staphylococcus aureus; Physical findings
less frequently, S. epidermidis or beta-hemolytic H Nipple abrasion or fissure
streptococci H Enlarged axillary lymph nodes
H Disseminated tuberculosis (rare) H Involved breast red, edematous, warm, and hard
H Mumps virus (rare)
Test results
Risk factors Laboratory
H Fissure or abrasion of the nipple H Cultures of expressed milk confirm generalized
H Blocked milk ducts mastitis.
H Incomplete letdown reflex H Cultures of breast skin confirm localized mastitis.
H Tight bra
H Prolonged intervals between breast-feedings
Treatment
Incidence
H Usually occurring in first 3 months postbirth but General
possibly occurring at any time during breast-feeding H Warm soaks
H More common in breast-feeding primiparas H Avoidance of tight bras and clothing
H Continuation of breast-feeding in both breasts to pre-
vent engorgement, with proper infant sucking and
changing of feeding positions to drain the milk
Preventing mastitis Medications
To help your patient prevent mastitis from recurring, fol- H Antibiotics according to infecting organism
low these guidelines: H Analgesics
H Stress to the patient the importance of emptying the
breasts completely because milk stasis can cause in- Surgery
fection and mastitis. H Breast abscess incision and drainage
H Teach the patient to alternate feeding positions and to
rotate pressure areas on the nipples.
H Remind the patient to position the infant properly on
the breast with the entire areola in his mouth.
Nursing considerations
H Advise the patient to expose sore nipples to the air as
often as possible.
Key outcomes
H Teach the patient proper hand-washing technique and The patient will:
personal hygiene. H express feelings of increased comfort
H Instruct the patient to get plenty of rest and consume H exhibit no signs or symptoms of infection
sufficient fluids and a balanced diet to enhance H resume breast-feeding without further complications
breast-feeding. H maintain skin integrity.
H Suggest that the patient apply a warm, wet towel to the
affected breast or take a warm shower to relax and im- Nursing interventions
prove breast-feeding.
H Administer prescribed drugs.
H Provide warm soaks.

510 Mastitis
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H Use meticulous hand-washing technique.

H Provide meticulous skin care.

Monitoring
H Signs and symptoms of infection
H Abscess development
H Breast engorgement
H Skin integrity
H Breast-feeding

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medication administration, dosage, and possible ad-
verse effects
H reassurance that breast-feeding wont harm the infant
because hes the source of the infection
H offering the infant the unaffected breast first to pro-
mote complete emptying and prevent clogged ducts
H need to stop breast-feeding with abscessed breast
H use of a breast pump until abscess heals
H continuation of breast-feeding on the unaffected side
H prevention of mastitis. (See Preventing mastitis.)

Discharge planning
H Refer the patient to a lactation specialist, if indicated.

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Melanoma, malignant
Overview
Description
H Neoplasm that arises from melanocytes
H Potentially the most lethal of the skin cancers
H Common sites: head and neck in males, legs and
chest in females, and backs of people exposed to
excessive sunlight
H Four types:
Superficial spreading melanoma most common
type; usually develops between ages 40 and 50
Nodular melanoma grows vertically, invades the
dermis, and metastasizes early; usually develops
between ages 40 and 50
Acral-lentiginous melanoma occurs on the
palms and soles and under the tongue; most com-
mon among Hispanics, Asians, and Blacks
Lentigo maligna melanoma relatively rare; most
benign, slowest growing, and least aggressive of
the four types; most commonly occurs in areas
heavily exposed to the sun; arises from a lentigo
maligna on an exposed skin surface; usually oc-
curs between ages 60 and 70
Pathophysiology
H Melanomas arise as a result of malignant degenera-
tion of melanocytes located either along the basal
layer of the epidermis or in a benign melanocytic
nevus.
H Up to 70% of malignant melanomas arise from a pre-
existing nevus.
H Malignant melanoma spreads through the lymphatic
and vascular systems and metastasizes to the regional
lymph nodes, skin, liver, lungs, and central nervous
system.
H Malignant melanoma follows an unpredictable
course; recurrence and metastasis may not appear
for more than 5 years after resection of the primary
lesion.
Causes
H Ultraviolet rays from the sun that damage the skin
Risk factors
H Excessive exposure to sunlight
H Skin type (blond or red hair, fair skin, and blue
eyes; prone to sunburn; and Celtic or Scandinavian
ancestry)
H Hormonal factors (pregnancy)
H Family history
H Past history of melanoma
H Preexisting pigmented mole or nevus
Incidence
H Lifetime U.S. incidence: 1 in 60 people
H Most common cancer in females ages 25 to 29
H Unusual in children
512 Melanoma, malignant
H Peak incidence between ages 50 and 70, but inci-
dence in younger age-groups increasing
Common characteristics
H Nonhealing sore
H Preexisting lesion or nevus that enlarges
H Signs of melanoma:
Asymmetrical lesion
Border irregularity
Color varied
Diameter larger than 6 mm
Complications
H Metastasis to the lungs, liver, or brain
Assessment
History
H A sore that doesnt heal, a persistent lump or
swelling, and changes in preexisting skin markings,
such as moles, birthmarks, scars, freckles, or warts
H Preexisting skin lesion or nevus that enlarges,
changes color, becomes inflamed or sore, itches, ul-
cerates, bleeds, changes texture, or shows signs of
surrounding pigment regression
Physical findings
H Lesions on the ankles or the inside surfaces of the
knees
H Uniformly discolored nodule on knee or ankle
H Small, elevated tumor nodules that may ulcerate and
bleed
H Palpable polypoid nodules that resemble the surface
of a blackberry
H Pigmented lesions on the palms and soles or under
the nails
H Long-standing lesion that has ulcerated
H Flat nodule with smaller nodules scattered over the
surface
Test results
Laboratory
H Complete blood count with differential shows
anemia.
H Erythrocyte sedimentation rate is elevated.
H Platelet count is abnormal if metastasis has occurred.
H Liver function studies are abnormal if metastasis has
occurred.
Imaging
H Chest X-rays and computed tomography scan help in
staging.
Diagnostic procedures
H Excisional biopsy and full-depth punch biopsy with
histologic examination can show tumor thickness
and disease stage.
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Prevention
Treatment Preventing malignant melanoma

General Malignant melanoma can be prevented by following these

guidelines:
H Close long-term follow-up care to detect metastasis H Apply sunscreen and protective lip balm every day at
and recurrences least 30 minutes before going outside, even on cloudy
H Radiation therapy (usually for metastatic disease) days.
H Well-balanced diet H Use sun protective factor (SPF) of 15 or greater.
H Avoidance of sun exposure H Reapply sunscreen every 2 to 3 hours and after
sweating or swimming.
Medications H Wear protective clothing, such as long-sleeved shirts,
H Chemotherapy hats, and sunglasses with UV protection.
H Avoid lying in the sun.
H Biotherapy
H Avoid sun exposure between the hours of 10 a.m. and
H Immunotherapy such as interferon
4 p.m.
H Avoid sunbeds and tanning salons.
Surgery H Have health care provider check suspicious spots or
H Surgical resection to remove tumor and 3- to 5-cm moles and have them removed if needed.
margin H Perform monthly self skin examinationespecially if
H Regional lymphadenectomy theres a family history of skin cancer.

Nursing considerations
Discharge planning
Key outcomes H Refer the patient to available resources and support
The patient will: services.
H maintain weight
H express positive feelings about self
H demonstrate effective coping mechanisms
H experience healing of wound without signs of
infection
H express feelings of increased comfort.

Nursing interventions
H Encourage verbalization and provide support.
H Provide appropriate wound care.
H Administer prescribed drugs.
H Provide a high-protein, high-calorie diet.

Monitoring
H Complications of treatment
H Pain control
H Wound site
H Postoperative complications

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H preoperative and postoperative care
H need for close follow-up care to detect recurrences
early
H signs and symptoms of recurrence
H detrimental effects of overexposure to solar radiation
and benefits of regular use of a sunblock or a sun-
screen and protective clothing. (See Preventing ma-
lignant melanoma.)

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Mnires disease H History of smoking

H Alcohol use

Overview ALERT
In some females, premenstrual edema may precipi-
Description tate outbreaks of Mnires disease.
H Inner ear disease that results from a labyrinthine
dysfunction
H Causes severe vertigo, sensorineural hearing loss, Incidence
and tinnitus H Usually affects adults between ages 30 and 60; rare in
H Usually, only one ear involved children
H After multiple attacks over several years, possibly H Slightly more common in males than in females
incapacitating residual tinnitus and hearing loss
H Also known as endolymphatic hydrops Common characteristics
H Sudden severe spinning, whirling vertigo, lasting
Pathophysiology from 10 minutes to several hours
H Mnires disease may result from overproduction or H Tinnitus
decreased absorption of endolymphthe fluid con- H Hearing impairment
tained in the labyrinth of the ear. H Feeling of fullness or blockage in the affected ear
H Accumulated endolymph dilates the semicircular preceding an attack
canals, utricle, and saccule and causes degeneration H Severe nausea, vomiting, sweating, and pallor during
of the vestibular and cochlear hair cells. an acute attack
H Overstimulation of the vestibular branch of cranial H Nystagmus
nerve VIII impairs postural reflexes and stimulates H Loss of balance and falling to the affected side
the vomiting reflex. (See Normal vestibular func-
tion.) Complications
H Perception of sound is impaired as a result of this ex- H Continued tinnitus
cessive cranial nerve stimulation, and injury to sen- H Hearing loss
sory receptors for hearing may affect auditory acuity. H Injury

Causes
H Unknown, but possibly associated with: Assessment
Family history
Immune disorder History
Migraine headaches H Vertigo
Middle ear infection H Nausea
Head trauma H Tinnitus
Autonomic nervous system dysfunction H Falls
Premenstrual edema
Physical findings
Risk factors H Inability to maintain upright posture
H Recent viral infection H Unsteady gait
H Stress H Diplopia
H Fatigue H Hypotension
H Allergies
Test results
Imaging
Normal vestibular function H Computed tomography scan and magnetic resonance
imaging rule out acoustic neuroma as a cause of
The three semicircular canals and the vestibule of the inner
symptoms.
ear are responsible for equilibrium and balance. Each of
the semicircular canals lies at a 90-degree angle to the oth-
Diagnostic procedures
H Audiometric testing shows a sensorineural hearing
ers. Head movement in one direction causes the endo-
lymph inside each semicircular canal to move in the oppo- loss and loss of discrimination and recruitment.
site direction and causes vestibular otoliths (crystals of H Electronystagmography shows normal or reduced
calcium salts) to shift in their gel medium. This movement vestibular response on the affected side.
stimulates hair cells, sending electrical impulses to the H Cold caloric testing shows impairment of oculo-
brain through the vestibular portion of cranial nerve VIII. vestibular reflex.
Together, these organs help detect the bodys present posi- H Electrocochleography shows increased ratio of sum-
tion as well as any change in its direction or motion. mating potential to action potential.

514 Mnires disease

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H Brain stem evoked response audiometry test rules H avoidance of sudden position changes and any tasks
out acoustic neuroma, brain tumor, and vascular that vertigo makes hazardous
lesions in the brain stem. H restriction of caffeine, nicotine, and alcohol.

Treatment
General
H Lying down to minimize head movement, and avoid-
ing sudden movements and glaring lights to reduce
dizziness (during an attack)
H Sodium restriction

Medications
H Promethazine or prochlorperazine
H Atropine
H Dimenhydrinate
H Central nervous system depressants, such as lo-
razepam and diazepam during an acute attack
H Antihistamines, such as meclizine and diphenhy-
dramine
For long-term management
H Diuretics
H Betahistine dihydrochloride
H Vasodilators
H Antihistamines or mild sedatives
H Systemic streptomycin (chemical ablation)

Surgery
H Endolymphatic drainage and shunt procedures
H Vestibular nerve resection
H Labyrinthectomy
H Cochlear implantation

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort
H remain safe from injury
H maintain adequate fluid balance
H seek appropriate support to assist with coping.

Nursing interventions
H Maintain a safe environment; provide assistance
when necessary.
H Administer prescribed drugs.

Monitoring
H Intake and output
H Frequency of attacks
H Response to treatment

Patient teaching
Be sure to cover:
H avoidance of reading and exposure to glaring lights
to reduce dizziness

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Incidence
Life-threatening disorder H Infants, children, and elderly people at highest risk

Common characteristics
Meningitis H Nuchal rigidity
H Headache
H Fever
Overview H Meningismus, typically with signs of cerebral
dysfunction
Description H Seizures
H Inflammation of brain and spinal cord meninges
H May affect all three meningeal membranes (dura Complications
mater, arachnoid membrane, and pia mater) H Visual impairment; optic neuritis
H Usually follows onset of respiratory symptoms H Cranial nerve palsies; deafness
H Sudden onset, causing serious illness within 24 H Paresis or paralysis
hours H Endocarditis
H Prognosis usually good; complications rare H Coma
H Bacterial meningitis: acute infection in the subarach- H Vasculitis
noid space H Cerebral infarction
H Seizures
Special populations
Prognosis is poor for infants and elderly people. Assessment
History
Pathophysiology H Headache
H Inflammation of pia-arachnoid and subarachnoid H Fever
space progresses to congestion of adjacent tissues. H Nausea, vomiting
H Nerve cells are destroyed. H Weakness
H Intracranial pressure (ICP) increases due to exu- H Myalgia
dates. H Photophobia
H Results can include: H Confusion, delirium
engorged blood vessels H Seizures
disrupted blood supply
edema of the brain tissue Physical findings
thrombosis H Meningismus
rupture H Rigors
acute hydrocephalus. H Profuse sweating
H Kernigs and Brudzinskis signs (elicited in only 50%
Causes of adults)
H Bacterial infection, usually from Neisseria meningi- H Declining level of consciousness (LOC)
tidis and Streptococcus pneumoniae (Before the H Cranial nerve palsies
1990s, Haemophilus influenzae type b [Hib] was H Rash (with meningococcemia)
the leading cause of bacterial meningitis. However, H Focal neurologic deficits such as visual field defects
new vaccines have reduced its occurrence in chil- H Signs of increased ICP (in later stages)
dren.)
H Viruses Special populations
H Protozoa
H Fungi Meningismus and fever are commonly absent in
H Secondary to another bacterial infection such as neonates and the only clinical clues may be non-
pneumonia specific, such as refusal to feed, high-pitched cry,
H May follow skull fracture, penetrating head wound, and irritability.
lumbar puncture, or ventricular shunting procedures
Risk factors Special populations
H I.V. drug abuse
H Crowded living conditions Elderly patients may experience an insidious onset,
H Age older than 60 or younger than 5 exhibiting lethargy and variable signs of meningis-
H Diabetes mus and no fever.
H Alcoholism or cirrhosis

516 Meningitis
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Test results Monitoring

Laboratory H Neurologic status
H White blood cell count shows leukocytosis. H Vital signs
H Blood cultures are positive in bacterial meningitis, H Signs and symptoms of cranial nerve involvement
depending on the pathogen. H Signs and symptoms of increased ICP
Imaging H LOC
H Chest X-rays may reveal a coexisting pneumonia. H Seizures
H Neuroimaging techniques, such as computed tomog- H Respiratory status
raphy scanning and magnetic resonance imaging, H Arterial blood gas results
may detect complications and a parameningeal H Fluid balance
source of infection. H Response to medications
Diagnostic procedures H Complications
H Lumbar puncture and cerebrospinal fluid analysis
shows:
increased opening pressure Patient teaching
neutrophilic pleocytosis
elevated protein Be sure to cover:
hypoglycorrhachia H the disorder, diagnosis, and treatment
positive Gram stain H contagion risks for close contacts
positive culture. H medication administration, dosage, and possible ad-
verse effects
H signs and symptoms of meningitis
Treatment H polysaccharide meningococcal vaccine, pneumococ-
cal vaccine, and Hib vaccine.
General
H Hypothermia
H Fluid therapy
H Pain control
H Bed rest (in acute phase)

Medications
H Antibiotics, such as vancomycin and meropenem
H Antiarrhythmics
H Osmotic diuretics
H Anticonvulsants
H Aspirin or acetaminophen

Nursing considerations
Key outcomes
The patient will:
H maintain adequate ventilation
H have normal temperature
H express feelings of increased comfort and pain relief
H maintain normal fluid volume
H have intact skin.

Nursing interventions
H Follow standard precautions.
H Maintain respiratory isolation for first 24 hours (with
meningococcal meningitis).
H Administer prescribed oxygen.
H Position the patient in proper body alignment.
H Encourage active range-of-motion (ROM) exercises
when appropriate.
H Provide passive ROM exercises when appropriate.
H Maintain adequate nutrition.
H Administer prescribed laxatives or stool softeners.
H Provide meticulous skin and mouth care.
H Administer prescribed drugs.

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Complications
Metabolic syndrome H Coronary artery disease
H Diabetes
H Hyperlipidemia
Overview H Premature death

Description
H A cluster of symptoms triggered by insulin resistance: Assessment
abdominal fat; obesity; high blood pressure; and high
levels of blood glucose, triglycerides, and cholesterol History
H Increased risk of diabetes, heart disease, and stroke H Familial history
H Commonly unrecognized H Hypertension
H Also known as syndrome X, insulin resistance syn- H High low-density lipoproteins (LDL) and triglyceride
drome, dysmetabolic syndrome, and multiple levels
metabolic syndrome H Low high-density lipoproteins (HDL) levels
H Abdominal obesity
Pathophysiology H Sedentary lifestyle
H The body breaks down food into basic components, H Poor diet
one of which is glucose.
H Glucose provides energy for cellular activity. Physical findings
H Excess glucose is stored in cells for future use. Its H Abdominal obesity
guided into storage cells by insulin, which is secreted
by the pancreas. Test results
H In those with metabolic syndrome, glucose doesnt Laboratory
respond to insulins attempt to guide it into storage H Blood glucose levels are high.
cells. This is called insulin resistance. H LDL and triglyceride levels are high.
H To overcome this resistance, the pancreas produces H HDL levels are low.
excess insulin, which causes damage to arterial H Hyperinsulinemia is present.
lining. H Serum uric acid level is elevated.
H Excessive insulin secretion also promotes fat storage Other
deposits and prevents fat breakdown. H Blood pressure is greater than 130/85 mm/Hg.
H This series of events can lead to diabetes, blood
clots, and coronary events.
Treatment
Causes
H Genetic predisposition General
H Acquired H Weight-reduction program
H Low alcohol intake
Risk factors H Low-cholesterol diet
H Obesity H Diet high in complex carbohydrates (grains, beans,
H Improper diet vegetables, fruit) and low in refined carbohydrates
H Insufficient physical activity (soda, table sugar, high fructose corn syrup)
H Aging H Daily physical activity of at least 20 minutes
H Hyperinsulinemia/impaired glucose tolerance
H Previous myocardial infarction Medications
H Oral antidiabetic agents
Incidence H Antihypertensives
H Affects an estimated 47 million Americans H Statins
H Most common in Mexican Americans (highest rate at
32%)
H In Black and Mexican American populations, females Nursing considerations
more susceptible than males; otherwise, males and
females equally affected Key outcomes
The patient will:
Common characteristics H maintain a healthy weight
H Waist size: more than 40 (101.6 cm) in men; more H increase his level of activity
than 35 (88.9 cm) in women (see Why abdominal H consume a proper diet.
obesity is dangerous)
H Lethargy, especially after eating

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Why abdominal obesity is dangerous

People with excess weight around the waist have a greater
risk of developing metabolic syndrome than people with
excess weight around the hips. Thats because intra-
abdominal fat tends to be more resistant to insulin than
fat in other areas of the body. Insulin resistance increases
the release of free fatty acid into the portal system, lead-
ing to increased apolipoprotein B, increased low-density
lipoprotein, decreased high-density lipoprotein, and in-
creased triglyceride levels. As a result, the risk of cardio-
vascular disease increases.

Nursing interventions
H Promote lifestyle changes and provide appropriate
support.
Monitoring
H Blood pressure
H Ordered laboratory tests

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H principles of healthy diet
H relationship of diet, inactivity, and obesity to metabol-
ic syndrome
H benefits of increased physical activity
H medication administration, dosage, and possible ad-
verse effects.
Discharge planning
H Refer the patient to a dietitian and an exercise
program, as appropriate.
H Stress the importance of follow-up.

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Methicillin-resistant Assessment
Staphylococcus aureus History
H Possible risk factors for MRSA
H Carrier patient typically asymptomatic
Overview
Physical findings
Description H In symptomatic patients, signs and symptoms related
H A mutation of a very common bacterium easily to the primary diagnosis (respiratory, cardiac, or
spread by direct person-to-person contact other major system symptoms)
H Also known as MRSA
Test results
Pathophysiology Laboratory
H 90% of Staphylococcus aureus isolates or strains H Cultures from suspicious wounds, skin, urine, or
are penicillin-resistant, and about 27% of all S. au- blood show MRSA.
reus isolates are resistant to methicillin, a penicillin
derivative. These strains may also resist cephalo-
sporins, aminoglycosides, erythromycin, tetracycline, Treatment
and clindamycin.
H When natural defense systems break down (after in- General
vasive procedures, trauma, or chemotherapy), the H Transmission precautions: contact isolation for
usually benign bacteria can invade tissue, proliferate, wound, skin, and urine infection; respiratory isola-
and cause infection. tion for sputum infection
H The most frequent colonization site is the anterior H No treatment needed for patient with colonization
nares (40% of adults and most children become only
transient nasal carriers). The groin, armpits, and in- H High-protein diet
testines are less common colonization sites. H Rest periods, as needed

Causes Medications
H MRSA that enters a health care facility through an in- H Vancomycin and imipenem
fected or colonized patient (symptom-free carrier of
the bacteria) or colonized health care worker
H Transmitted mainly by health care workers hands Nursing considerations
(MRSA possibly remaining viable for days on sur-
faces and clothing) Key outcomes
The patient will:
Risk factors H maintain collateral circulation
H Immunosuppression H attain hemodynamic stability
H Prolonged facility stays H maintain adequate cardiac output
H Extended therapy with multiple or broad-spectrum H remain afebrile
antibiotics H have an adequate fluid volume.
H Proximity to others colonized or infected with MRSA
H Invasive devices such as indwelling catheters Nursing interventions
H Provide emotional support to the patient and family.
Incidence H Consider grouping infected patients together and
H Endemic in nursing homes, long-term care facilities, having the same nursing staff care for them.
and community facilities H Use proper hand-washing technique.
H Use contact and standard precautions.
Common characteristics
H Dependent on body system affected Monitoring
H Vital signs
Complications H Culture results
H Sepsis H Response to treatment
H Death H Adverse drug reactions
H Complications

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Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H difference between MRSA and colonization
H prevention of MRSA spread
H proper hand-washing technique
H need for family and friends to wear protective garb
(and to dispose of it properly) when they visit the
patient
H medication administration, dosage, and possible
adverse effects
H need to take antibiotics for the full prescription peri-
od, even if the patient begins to feel better.
Discharge planning
H Refer the patient to an infectious disease specialist, if
indicated.

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Complications
Mitral stenosis H Cardiac arrhythmias, especially atrial fibrillation
H Thromboembolism

Overview
Assessment
Description
H Narrowing of the mitral valve orifice, which is nor- History
mally 3 to 6 cm Mild mitral stenosis
H Mild mitral stenosis: valve orifice of 2 cm H Asymptomatic
H Severe mitral stenosis: valve orifice of 1 cm Moderate to severe mitral stenosis
H Gradual decline in exercise tolerance
Pathophysiology H Dyspnea on exertion; shortness of breath
H Valve leaflets become diffusely thickened by fibrosis H Paroxysmal nocturnal dyspnea
and calcification. H Orthopnea
H The mitral commissures and the chordae tendinae H Weakness
fuse and shorten, the valvular cusps become rigid, H Fatigue
and the valves apex becomes narrowed. H Palpitations
H This obstructs blood flow from the left atrium to the H Cough
left ventricle, resulting in incomplete emptying.
H Left atrial volume and pressure increase, and the Physical findings
atrial chamber dilates. H Hemoptysis
H Increased resistance to blood flow causes pulmonary H Peripheral and facial cyanosis
hypertension, right ventricular hypertrophy and, H Malar rash
eventually, right-sided heart failure and reduced car- H Jugular vein distention
diac output. H Ascites
H Peripheral edema
Causes H Hepatomegaly
H Rheumatic fever H A loud S1 or opening snap
H Congenital anomalies H A diastolic murmur at the apex (see Identifying the
H Atrial myxoma murmur of mitral stenosis)
H Endocarditis H Crackles over lung fields
H Systemic lupus erythematosus H Right ventricular lift
H Rheumatoid arthritis H Resting tachycardia; irregularly irregular heart
rhythm
Incidence
H Two-thirds of all mitral stenosis patients female Test results
H Occurs in approximately 40% of patients with Imaging
rheumatic heart disease H Chest X-rays show left atrial and ventricular enlarge-
ment (in severe mitral stenosis), straightening of the
Common characteristics left border of the cardiac silhouette, enlarged pulmo-
H Gradual decline in exercise tolerance nary arteries, dilation of the upper lobe pulmonary
H Dyspnea on exertion veins, and mitral valve calcification.
H Shortness of breath H Echocardiography discloses thickened mitral valve
H Chest pain, palpitations leaflets and left atrial enlargement.
Diagnostic procedures
H Cardiac catheterization shows a diastolic pressure
gradient across the valve, elevated pulmonary artery
Identifying the murmur of mitral stenosis wedge pressure (greater than 15 mm Hg), and pul-
monary artery pressure in the left atrium with severe
A low, rumbling crescendo-decrescendo murmur in the
pulmonary hypertension.
mitral valve area characterizes mitral stenosis.
H Electrocardiography reveals left atrial enlargement,
right ventricular hypertrophy, right axis deviation,
SYSTOLE DIASTOLE SYSTOLE and (in 40% to 50% of cases) atrial fibrillation.
S1 S2 S1 S2

522 Mitral stenosis

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Treatment Patient teaching

General Be sure to cover:
H Synchronized electrical cardioversion to correct atri- H the disorder, diagnosis, and treatment
al fibrillation H need to plan for periodic rest in daily routine
H Sodium-restricted diet H how to take the pulse
H Activity, as tolerated H dietary restrictions
H medication administration, dosage, and possible ad-
Medications verse effects
H Digoxin H signs and symptoms to report
H Diuretics H importance of consistent follow-up care
H Oxygen H when to notify the physician
H Beta-adrenergic blockers such as metoprolol H use of prophylactic antibiotics for procedures.
H Calcium channel blockers such as diltiazem
H Anticoagulants such as warfarin
H Infective endocarditis antibiotic prophylaxis
H Nitrates

Surgery
H Commissurotomy or valve replacement
H Percutaneous balloon valvuloplasty

Nursing considerations
Key outcomes
The patient will:
H carry out activities of daily living without weakness or
fatigue
H maintain hemodynamic stability and adequate car-
diac output
H have no complications due to fluid excess
H exhibit adequate coping mechanisms.

Nursing interventions
H Check for hypersensitivity reaction to antibiotics.
H If the patient needs bed rest, stress its importance.
H Provide a bedside commode to encourage energy
conservation.
H Allow the patient to express concerns over her inabil-
ity to meet responsibilities due to activity restrictions.
H Place the patient in an upright position to relieve dys-
pnea, if needed.
H Provide a low-sodium diet.

Monitoring
H Vital signs and hemodynamics
H Intake and output
H Signs and symptoms of heart failure and pulmonary
edema
H Signs and symptoms of thromboembolism
H Adverse drug reactions
H Cardiac arrhythmias
H Postoperatively: hypotension, arrhythmias, and
thrombus formation

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Mitral valve H Papillary muscle disorders such as coronary artery

disease
insufficiency Incidence
H Can occur at any age
H Affects both sexes equally
Overview
Common characteristics
Description H Dyspnea
H Valvular disease of the mitral valve that allows the H Peripheral edema
backflow of blood from the left ventricle to the left H Tachycardia
atrium
H May be acute (sudden volume overload of the left Complications
ventricle), chronic compensated (left ventricle com- H Heart failure
pensates and left ventricular enlargement occurs), or H Pulmonary edema
chronic decompensated (left ventricle unable to sus- H Thromboembolism
tain forward cardiac output) H Endocarditis
H Also known as mitral regurgitation H Arrhythmias
H Shock
Pathophysiology
H Blood from the left ventricle flows back into the left
atrium during systole, causing the atrium to enlarge Assessment
to accommodate the backflow.
H As a result, the left ventricle dilates to accommodate History
the increased volume of blood from the atrium and H Causal occurrence
to compensate for diminishing cardiac output. H Orthopnea
H Ventricular hypertrophy and increased end-diastolic H Dyspnea
pressure result in increased pulmonary artery pres- H Fatigue
sure, eventually leading to left- and right-sided heart H Angina
failure. H Palpitations

Causes Physical findings

H Trauma H Tachycardia
H Rheumatic fever H Crackles in the lungs
H Systemic lupus erythematosus H Hepatomegaly (right-sided failure)
H Scleroderma H Holosystolic murmur at the apex (see Identifying
H Hypertrophic cardiomyopathy the murmur of mitral valve insufficiency)
H Infective endocarditis H Possible split S2
H Mitral valve prolapse H S3
H Myocardial infarction
H Severe left-sided heart failure Test results
H Ruptured chordae tendineae Imaging
H Associated with congenital anomalies such as trans- H Chest X-ray reveals left atrial and ventricular enlarge-
position of the great arteries ment and pulmonary congestion.
H Echocardiography shows abnormal valve leaflet mo-
tion and left atrial enlargement.
Identifying the murmur of mitral Diagnostic procedures
valve insufficiency H Cardiac catheterization reveals mitral insufficiency
A high-pitched, rumbling pansystolic murmur that radi- with increased left ventricular end-diastolic volume
ates from the mitral area to the left axillary line character- and pressure, increased atrial pressure and pulmo-
izes mitral valve insufficiency. nary artery wedge pressure, and decreased cardiac
output.
SYSTOLE DIASTOLE SYSTOLE H Electrocardiography may show left atrial and ventric-
S1 S2 S1 S2 ular hypertrophy, sinus tachycardia, or atrial fibrilla-
tion.

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Treatment
General
H Treat underlying cause appropriately
H Low-sodium diet
H Activity, as tolerated

Medications
H Diuretics, such as furosemide and spironolactone
H Inotropic agents, such as digoxin and milrinone
H Angiotensin-converting enzyme inhibitors
H Oxygen
H Anticoagulants such as warfarin
H Prophylactic antibiotics before and after surgery or
dental care to prevent endocarditis
H Antiarrhythmics, such as amiodarone and digoxin, to
treat atrial fibrillation or atrial flutter
H Vasodilators such as nitroprusside

Surgery
H Annuloplasty or valvuloplasty to reconstruct or repair
the valve
H Valve replacement with a prosthetic valve

Nursing considerations
Key outcomes
The patient will:
H carry out activities of daily living without weakness or
fatigue
H maintain hemodynamic stability
H maintain adequate ventilation.

Nursing interventions
H Administer prescribed oxygen.
H Watch for signs of heart failure or pulmonary edema.

Monitoring
H Vital signs and pulse oximetry
H Cardiac rhythm
H Pulmonary artery catheter readings
H Intake and output
H Adverse effects of drug therapy

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H dietary restrictions and medication
H medication administration, dosage, and possible ad-
verse effects.

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Test results
Mitral valve prolapse Imaging
H Echocardiography may reveal mitral valve prolapse
(MVP) with or without mitral insufficiency.
Overview Diagnostic procedures
H Electrocardiography is usually normal but may reveal
Description atrial or ventricular arrhythmia.
H Portion of the mitral valve (MV) prolapses into the H Signal-averaged electrocardiography may show ven-
left atrium during ventricular contraction (systole) tricular and supraventricular arrhythmias.
H Holter monitor worn for 24 hours may show an ar-
Pathophysiology rhythmia.
H Myxomatous degeneration of MV leaflets with redun-
dant tissue leads to prolapse of the MV into the left
atrium during systole. Treatment
H In some patients, this results in leakage of blood into
the left atrium from the left ventricle. General
H Usually requires no treatment; only regular monitor-
Causes ing
H Connective tissue disorders, such as systemic lupus H Decreased caffeine intake
erythematosus and Marfan syndrome H Fluid intake to maintain hydration
H Congenital heart disease
H Acquired heart disease, such as coronary artery dis- Medications
ease and rheumatic heart disease H Beta-adrenergic blockers, such as atenolol and
metoprolol
Incidence H Anticoagulants such as warfarin
H More prevalent in females than males H Antiarrhythmics as appropriate
H Usually detected in young adulthood
H Affects 2.5% to 5% of the general population
Nursing considerations
Special populations Key outcomes
Mitral valve prolapse is most common in females The patient will:
ages 20 to 40. H carry out activities of daily living without fatigue or
decreased energy
H maintain adequate cardiac output, without arrhyth-
Common characteristics mias
H Palpitations H exhibit adequate coping mechanisms.
H Atypical chest pain
H Dyspnea Nursing interventions
H Provide reassurance and comfort if the patient expe-
Complications riences anxiety.
H Arrhythmias H If fatigue is a concern, plan rest periods.
H Infective endocarditis H Discuss the patients drug therapy including dosage,
H Mitral insufficiency from chordal rupture adverse reactions, and when to notify the physician if
H Mitral regurgitation a problem arises.
H Discuss the importance of adequate hydration.

Assessment Monitoring
H Vital signs
History H Blood pressure while lying, sitting, and standing
H Usually asymptomatic H Heart sounds
H Possible fatigue, syncope, palpitations, chest pain, or H Signs and symptoms of mitral insufficiency
dyspnea on exertion H Serial echocardiograms
H Electrocardiograms for arrhythmias
Physical findings
H Orthostatic hypotension
H Mid-to-late systolic click and late systolic murmur

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Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H need to perform the most important activities of the
day when energy levels are highest
H need for antibiotic prophylaxis therapy before dental
or surgical procedures as indicated (not all patients
with MVP require antibiotic prophylaxis)
H avoidance of foods and beverages high in caffeine
H taking medications as prescribed
H using caution with over-the-counter medications that
contain stimulants.
Discharge planning
H If the patient is being discharged with a Holter moni-
tor, make sure she understands the importance of
documenting her activities throughout the monitor-
ing process.
H Refer the patient to an MVP support group.
H Refer the patient to a planned exercise program.

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Motion sickness Assessment

History
Overview H Recent travel
H Exposure to smoke, carbon monoxide, or fumes
Description H Recent illness, such as cold or ear infection
H Sensory conflict about body motion H Anxiety
H Involvement of: H Panic attack
Visual receptors H Malaise
Vestibular receptors H Fatigue
Body proprioceptors H Weakness
H Also induced when patterns of motion differ from H Confusion
those previously experienced H Vision disturbances
H Nervous system affected H Vertigo

Pathophysiology Physical findings

H Central cholinergic pathways, possibly in the vestibu- H Nausea
lar nuclei, may play a role in motion sickness. H Vomiting
H Motion sickness may be mediated by vasopressin re- H Diaphoresis
leased from the pituitary. H Pallor
H Associated with increases in blood levels of epineph- H Hypersalivation
rine and norepinephrine; levels are also increased in H Yawning
certain brain regions. H Hyperventilation

Causes Test results

H Body, inner ear, and the eyes sending conflicting sig- Laboratory
nals to the brain H Blood tests rule out other disorders.
H Anticipating movement possibly producing anxiety Imaging (with frequent episodes)
and symptoms H Computed tomography scan and magnetic resonance
imaging rule out other disorders.
Risk factors Diagnostic procedures
H Motion (automobile, plane, boat, amusement rides) H Possible EEG, if prolonged episode, rules out other
H Travel disorders.
H Visual stimuli (such as a moving horizon)
H Poor ventilation (fumes, smoke, carbon monoxide)
H Emotions (fear, anxiety) Treatment
H Illness or poor health
General
Incidence H Removing triggers
H Unknown H Minimizing exposure
H Children ages 2 to 12 affected more commonly than H Improving ventilation
adults H Acupressure on point 2 cm proximal from transverse
crease of palmar side of wrist, between tendons
Common characteristics (Pericardium 6 [P6])
H Occurs during or after motion or visual stimuli H Diet
H GI disturbances Decrease oral intake; frequent small meals
H Nervous system disturbances Avoidance of alcohol
H Semirecumbent seating
Complications H Fix vision at 45-degree angle above horizon
H Hypotension H Avoidance of fixation of vision on moving objects
H Dehydration such as waves
H Depression H Avoidance of reading while in moving automobile or
H Panic boat
H Syncope H Mind-body practices, such as cognitive-behavioral
therapy and biofeedback

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Medications Prevention
H Scopolamine Preventing motion sickness
H Promethazine
Motion sickness can be prevented by following these
H Cyclizine
guidelines:
H Dimenhydrinate H Avoid reading.
H Meclizine H Choose seating with good ventilation.
H Ginger H Sit in a semirecumbent position.
H Sit in a place with the least possible movement, such
as the middle of the plane or boat or in the front of the
Nursing considerations car.
H Fix vision at 45 degrees above the horizon on a
Key outcomes stationary object.
The patient will: H Avoid alcohol.
H Dont smoke.
H express reduced levels of anxiety
H Decrease dietary intake or eat small, frequent meals.
H verbalize understanding of the disorder and its treat-
H Premedicate with over-the-counter or prescription
ment drugs as advised.
H express improvement in symptoms H Engage in distracting mental activities.
H maintain adequate hydration.

Nursing interventions
H Administer prescribed drugs.
H Remove triggers or noxious stimuli.
H Help the patient identify risk factors and make modi-
fications to reduce symptoms, as appropriate.
H Provide reassurance and support.

Monitoring
H Response to treatment
H Adverse reactions to prescribed drugs
H Intake and output
H Risk-factor modification

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medication administration, dosage, and possible ad-
verse effects
H use of acupressure to reduce symptoms
H prevention techniques. (See Preventing motion
sickness.)

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Multiple myeloma H History of repeated pneumonia, bladder or kidney

infections, or sinusitis
H Pain on movement or weight bearing, especially in
the thoracic and lumbar vertebrae
Overview
Physical findings
Description H Noticeable thoracic deformities and reduction in
H Disseminated neoplasm of marrow plasma cells body height of 5 (12.7 cm)
H Prognosis usually poor because by diagnosis, the ver-
tebrae, pelvis, skull, ribs, clavicles, and sternum in- Test results
filtrated Laboratory
H With early diagnosis and treatment, life commonly H Complete blood count shows moderate or severe
prolonged by 3 to 5 years anemia; the differential may show 40% to 50% lym-
H Without treatment, fatal in 52% of patients within 3 phocytes but seldom more than 3% plasma cells;
months of diagnosis; in 90% within 2 years Rouleau formation, commonly the first clue, is seen
H Also called malignant plasmacytoma, plasma cell on differential smear and results from elevation of
myeloma, and myelomatosis the erythrocyte sedimentation rate.
H Urine studies may show protein urea, Bence Jones
Pathophysiology protein, and hypercalciuria; absence of Bence Jones
H Infiltration of the bone produces osteolytic lesions protein doesnt rule out multiple myeloma, but its
throughout the skeleton. presence almost invariably confirms the disease.
H In late stages, the malignant plasma cells infiltrate H Serum electrophoresis shows an elevated globulin
the lymph nodes, liver, spleen, and kidneys. spike thats electrophoretically and immunologically
H Infiltrates prevent normal function. abnormal.
H Serum calcium level is elevated.
Causes Imaging
H Exact cause unknown H X-rays during the early stages may reveal only diffuse
osteoporosis. Eventually, they show the characteristic
Risk factors lesions of multiple myeloma: multiple, sharply cir-
H Genetic factors cumscribed osteolytic, or punched out lesions, par-
H Occupational exposure to radiation ticularly on the skull, pelvis, and spine.
H Obesity Diagnostic procedures
H Bone marrow aspiration reveals myelomatous cells
Incidence and abnormal number of immature plasma cells
H Most common in males older than age 50 (10% to 95% instead of the normal 3% to 5%).
H More common in blacks

Common characteristics Treatment

H History of neoplastic fractures
H Joint and back pain General
H Adjuvant local radiation
Complications H Dialysis (if renal complications develop)
H Infections (such as pneumonia) H Plasmapheresis to remove the M protein from the
H Pyelonephritis, renal calculi, and renal failure blood and return the cells to the patient (temporary
H Hematologic imbalance effect)
H Fractures H Peripheral blood stem cell transplantation
H Hypercalcemia H Well-balanced diet
H Hyperuricemia H Activity, as tolerated
H Dehydration
Medications
H Bisphosphonates
Assessment H Analgesics
H Chemotherapeutics, such as melphalan, cyclophos-
History phamide, and vincristine
H History of neoplastic fractures H Thalidomide or lenalidomide
H Severe, constant back pain, which may increase with H Immunotherapy
exercise H Corticosteroids such as dexamethasone
H Arthritic symptoms H Proteasome inhibitor such as bortezomib
H Peripheral paresthesia
H Progressive weakness and fatigue

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Surgery
H Laminectomy if the patient develops vertebral com-
pression

Nursing considerations
Key outcomes
The patient will:
H express feelings regarding illness
H maintain adequate ventilation
H express feelings of increased comfort and decreased
pain
H demonstrate effective coping skills.

Nursing interventions
H Encourage fluid intake (3 to 4 qt [3 to 4 L] daily).
H Administer prescribed drugs.
After surgery
H Encourage mobilization.

Monitoring
H Complications of treatment
H Signs and symptoms of severe anemia and fractures
H Proper positioning (alignment)
H Pain control

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H importance of deep breathing and changing position
every 2 hours after surgery
H appropriate dress for weather conditions (because
the patient may be sensitive to cold)
H avoidance of crowds and people with infections
H medication administration, dosage, and possible
adverse effects
H safety precautions to prevent falls.

Discharge planning
H Refer the patient to available resources and support
services.

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Complications
Multiple sclerosis H Injuries from falls
H Urinary tract infections
H Constipation
Overview H Contractures
H Pressure ulcers
Description H Pneumonia
H Progressive demyelination of white matter of brain H Depression
and spinal cord
H Characterized by exacerbations and remissions
H May progress rapidly, causing death within months Assessment
H Prognosis varies (70% of patients with multiple scle-
rosis lead active lives with prolonged remissions) History
H Also known as MS H Symptoms related to extent and site of myelin de-
struction, extent of remyelination, and adequacy of
Pathophysiology subsequent restored synaptic transmission
H Sporadic patches of demyelination occur in the cen- H Symptoms possibly transient or last for hours or
tral nervous system, resulting in widespread and var- weeks
ied neurologic dysfunction. H Chronic, progressive loss or deterioration
H Symptoms unpredictable and difficult to describe
Causes H Visual problems and sensory impairment (the first
H Exact cause unknown signs)
H Slow-acting viral infection H Blurred vision or diplopia
H An autoimmune response of the nervous system H Urinary problems (such as urgency, frequency,
H Allergic response incontinence)
H Events that precede the onset: H Emotional lability
emotional stress H Dysphagia
overwork H Bowel disturbances (involuntary evacuation or
fatigue constipation)
pregnancy H Fatigue (typically the most disabling symptom)
acute respiratory tract infections
H Genetic factors possibly also involved Physical findings
H Poor articulation
Risk factors H Muscle weakness of the involved area
H Trauma H Spasticity; hyperreflexia
H Anoxia H Intention tremor
H Toxins H Gait ataxia
H Nutritional deficiencies H Paralysis, ranging from monoplegia to quadriplegia
H Vascular lesions H Nystagmus; scotoma
H Anorexia nervosa H Optic neuritis
H Ophthalmoplegia
Incidence
H Highest in females Test results
H Highest among people in northern urban areas H Years of testing and observation may be required for
H Highest in higher socioeconomic groups diagnosis.
H Low incidence in Japan Laboratory
H Family history increases incidence H Cerebrospinal fluid analysis shows mononuclear cell
H Increased incidence with living in a cold, damp cli- pleocytosis, an elevation in the level of total immu-
mate noglobulin (Ig) G, and presence of oligoclonal Ig.
H Major cause of chronic disability in young adults Imaging
ages 20 to 40 H Magnetic resonance imaging is the most sensitive
method of detecting multiple sclerosis focal lesions.
Common characteristics Other
H Dependent on the extent and site of myelin destruc- H EEG abnormalities occur in one-third of patients with
tion MS.
H Sensory impairment H Evoked potential studies show slowed conduction of
H Muscle dysfunction nerve impulses.
H Bladder and bowel disturbances
H Speech problems
H Fatigue

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Describing multiple sclerosis

Treatment
General
H Symptomatic treatment for acute exacerbations and
related signs and symptoms
H High fluid diet and fiber intake in case of constipa-
tion
H Frequent rest periods
Medications
H Antineoplastics such as mitoxantrone
H Muscle relaxants, such as baclofen and tizandine
H I.V. steroids followed by oral steroids
H Immunosuppressants
H Biological response modifiers, such as glatiramer,
interferon beta-1a, and interferon beta-1b
H Natalizumab (use restricted to special distribution
programs)
Various terms are used to decribe multiple sclerosis (MS).
H Elapsing-remitting: clear relapses (or acute attacks or
exacerbations) with full recovery and lasting disability.
Between attacks, the disease doesnt worsen.
H Primary progressive: steadily progressing or worsen-
ing with minor recovery or plateaus. This form is un-
common and may involve different brain and spinal
cord damage from other forms.
H Secondary progressive: beginning as a pattern of clear-
cut relapses and recovery but becoming steadily pro-
gressive and worsening between acute attacks.
H Progressive-relapsing: steadily progressing from the
onset but also has clear, acute attacks. This form is
rare. In addition, differential diagnosis must rule out
spinal cord compression, foramen magnum tumor
(which may mimic the exacerbations and remissions of
MS), multiple small strokes, syphilis or another infec-
tion, thyroid disease, and chronic fatigue syndrome.

Nursing considerations
Key outcomes
Patient teaching
The patient will: Be sure to cover:
H perform activities of daily living H disease process (see Describing multiple sclerosis)
H remain free from infection H medication administration, dosage, and possible ad-
H maintain joint mobility and range of motion verse effects
H express feelings of increased energy and decreased H avoidance of stress, infections, and fatigue
fatigue H maintaining independence
H develop regular bowel and bladder habits H avoiding exposure to bacterial and viral infections
H use available support systems and coping mecha- H nutritional management
nisms. H adequate fluid intake and regular urination.

Nursing interventions Discharge planning

H Provide emotional and psychological support.
H Assist with physical therapy program.
H Provide adequate rest periods.
H Promote emotional stability.
H Keep the bedpan or urinal readily available because
the need to void is immediate.
H Provide bowel and bladder training, if indicated.
H Administer prescribed drugs.
H Refer the patient to the National Multiple Sclerosis
Society.
H Refer the patient to physical and occupational reha-
bilitation programs, as indicated.
H Refer the patient for counseling.

Monitoring
H Response to medications
H Adverse drug reactions
H Sensory impairment
H Muscle dysfunction
H Energy level
H Signs and symptoms of infection
H Speech
H Elimination patterns
H Vision changes
H Laboratory results

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Mumps Assessment
History
Overview H Inadequate immunization and exposure to someone
with mumps within the preceding 2 to 3 weeks
Description H Myalgia, headache
H An acute inflammation of one or both parotid glands, H Malaise, fever
and sometimes the sublingual or submaxillary glands H Earache aggravated by chewing
H Also called infectious or epidemic parotitisan
Physical findings
Pathophysiology H Swelling and tenderness of the parotid glands
H Virus replication occurs in the epithelium of the up- H Simultaneous or subsequent swelling of one or more
per respiratory tract, leading to viremia. other salivary glands (see Parotid inflammation in
H Infection of the central nervous system (CNS) or mumps)
glandular tissues (or both) occurs, resulting in
perivascular and interstitial mononuclear cell infil- Test results
trates with edema. H Glandular swelling confirms the diagnosis.
H Necrosis of acinar and epithelial duct cells occurs in Laboratory
the salivary glands and germinal epithelium of the H Serologic testing shows mumps antibodies.
seminiferous tubules.
Causes Treatment
H A paramyxovirus found in the saliva of an infected
person General
H Transmitted by droplets or by direct contact with the H Rest
saliva of an infected person H Cold compresses for swollen glands
H Use of athletic supporter if testicles are tender
Risk factors H Liquid to mechanical soft diet until able to swallow
H Travel outside the United States H Increased fluid intake
H Unvaccinated status H Bed rest until fever resolves
H Rest periods when fatigued
Incidence
H Seldom occurring in infants younger than age 1 be- Medications
cause of passive immunity from maternal antibodies H Analgesics
H About 50% of cases in young adults; remainder in H Antipyretics
young children or immunocompromised adults
H Peak incidence during late winter and early spring
Nursing considerations
Common characteristics
H Usually begins with prodromal symptoms that last for Key outcomes
24 hours The patient will:
H Myalgia, anorexia, malaise, headache, an earache ag- H remain afebrile
gravated by chewing, and pain when drinking sour or H express feelings of increased comfort and decreased
acidic liquids; may have a fever of 101 to 104 F pain
(38.3 to 40 C) H maintain adequate fluid volume
H achieve adequate nutritional intake.
Complications
H Epididymoorchitis Nursing interventions
H Meningoencephalitis H Apply warm or cool compresses to the neck area to
H Sterility relieve pain.
H Pancreatitis H Administer prescribed drugs.
H Transient sensorineural hearing loss H Provide scrotal support, if needed.
H Arthritis H Report all cases of mumps to local public health au-
H Nephritis thorities.
H Spontaneous abortion (with contact during the first H Disinfect articles soiled with nose and throat secre-
trimester) tions.

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Parotid inflammation in mumps

The mumps virus (paramyxovirus) attacks the parotid glands the main salivary glands. Inflammation causes characteristic
swelling and discomfort with eating, drinking, swallowing, and talking.

Parotid gland

Monitoring
H Response to treatment
H Signs of CNS involvement
H Auditory acuity
H Complications

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H need to stay away from school or work from days 12
through 25 after exposure
H importance of having children immunized with live
attenuated mumps vaccine at age 15 months or
older, if applicable
H if epididymoorchitis occurs, reassurance that it wont
cause impotence and sterility (occurs only with bilat-
eral orchitis)
H need for bed rest during febrile period
H need to avoid spicy, irritating foods, and those that
require much chewing; advise a soft, bland diet
H need for family members to follow respiratory isola-
tion precautions until symptoms subside.
Discharge planning
H Refer the patient to a urologist for orchitis, if indi-
cated.

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Muscular dystrophy Duchennes

H Onset insidious
H Onset between ages 3 and 5
H Pelvic muscle weakness
Overview H Interferes with childs ability to run, climb, and walk
Beckers
Description H Onset after age 5
H Hereditary disorder characterized by progressive H Symptoms the same as Duchennes, but slower pro-
symmetrical wasting of skeletal muscles gression
H No neural or sensory defects Landouzy-Dejerine
H Four main types: Duchennes (pseudohypertrophic), H Onset before age 10
Beckers (benign pseudohypertrophic), Landouzy- H Weakness of eye, face, and shoulder muscles
Dejerine (facioscapulohumeral) dystrophy, and Erbs H Inability to raise arms over head
(limb-girdle) dystrophy H Inability to close eyes
H Duchennes beginning during early childhood, death H Inability to pucker lips or whistle
occurring within 10 to 15 years H Abnormal facial movements
H Absence of facial movements when laughing or cry-
Pathophysiology ing
H Muscle fibers necrotize and regenerate in various H Pelvic muscles weaken as disease progresses
states. Erbs
H Regeneration slows and degeneration dominates. H Symptoms the same as in Landouzy-Dejerine but
H Fat and connective tissue replace muscle fibers. slower progression
H Weakness results. H Less of a disability than in Landouzy-Dejerine
H Onset between ages 6 and 10
Causes H Muscle weakness of upper arm and pelvic muscles
H Various genetic mechanisms (band Xp 21)
H Duchennes and Beckers X-linked recessive Physical findings
H Landouzy-Dejerine autosomal dominant Duchennes and Beckers
H Erbs usually autosomal recessive H Wide stance and waddling gait
H Gowers sign when rising from a sitting or supine
Incidence position
H Duchennes and Beckers: affect males almost exclu- H Muscle hypertrophy and atrophy
sively H Calves enlarged due to fat infiltration into the muscle
H Landouzy-Dejerine and Erbs: affect both sexes about H Posture changes
equally H Lordosis and a protuberant abdomen
H Scapular winging or flaring when raising arms
Common characteristics H Contractures
H Waddling gait H Tachypnea and shortness of breath
H Toe walking Landouzy-Dejerine
H Lumbar lordosis H Pendulous lower lip
H Frequent falls H Possible disappearance of nasolabial fold
H Dyspnea H Diffuse facial flattening leading to a masklike expres-
H Dysphagia sion
H Inability to suckle (infants)
Complications H Scapulae with a winglike appearance; inability to
H Crippling disability raise arms above head
H Contractures Erbs
H Pneumonia H Apparent effects of muscle weakness
H Arrhythmias H Muscle wasting
H Cardiac hypertrophy H Winging of the scapulae
H Dysphagia H Lordosis with abdominal protrusion
H Waddling gait
H Poor balance
Assessment H Inability to raise the arms

History Test results

H Evidence of genetic transmission Laboratory
H Progressive muscle weakness H Urine creatinine, serum creatine kinase, lactate dehy-
drogenase, alanine aminotransferase, and aspartate
aminotransferase levels are elevated.

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Diagnostic procedures
H Muscle biopsy result confirms the diagnosis.
H Immunologic and biological results facilitate prenatal
and postnatal diagnosis.
H Electromyography shows abnormal muscle move-
ments.
H Amniocentesis detects sex of fetus for high-risk
family.
Other
H Genetic testing may be used to detect the gene defect
that leads to muscular dystrophy in some families.
Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H maintenance of peer relationships
H how to maintain mobility and independence
H possible complications and prevention
H signs and symptoms of respiratory tract infections
H need for a low-calorie, high-protein, high-fiber diet
H need to avoid long periods of bed rest and inactivity.

Discharge planning
Treatment H Refer the patient for sexual counseling, if indicated.
H Refer the patient for physical therapy, vocational re-
General habilitation, social services, and financial assistance.
H No known treatment to stop progression H Refer the patient to the Muscular Dystrophy Associa-
H Orthopedic appliances tion.
H Low-calorie, high-protein, high-fiber diet H Refer the patient for genetic counseling.
H Tube feedings, as needed
H Exercise, as tolerated
H Physical therapy

Medications
H Stool softeners
H Possible steroids

Surgery
H Surgery to correct contractures
H Spinal fusion

Nursing considerations
Key outcomes
The patient will:
H perform activities of daily living without muscle
fatigue or intolerance
H maintain muscle strength, joint mobility, and range of
motion
H show no evidence of complications
H maintain respiratory rate within 5 breaths/minute of
baseline.
Nursing interventions
H Encourage coughing and deep-breathing exercises.
H Take steps to prevent muscle atrophy.
H Use splints, braces, grab bars, and overhead slings.
H Use a footboard or high-topped shoes and a foot
cradle.
H Provide a low-calorie, high-protein, high-fiber diet.

Monitoring
H Intake and output
H Respiratory status
H Joint mobility
H Muscle weakness
H Complications

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H Difficulty chewing and swallowing

Life-threatening disorder H Jaw hanging open (especially when tired)
H Head bobbing

Myasthenia gravis H Symptoms milder on awakening; worsen as the day

progresses
H Short rest periods that temporarily restore muscle
function
Overview H Symptoms that become more intense during menses,
after emotional stress, after prolonged exposure to
Description sunlight or cold, and with infections
H An acquired autoimmune disorder characterized by
abnormal fatigability of striated (skeletal) muscles Physical findings
H Sporadic but progressive weakness H Sleepy, masklike expression
H Muscle weakness exacerbated by exercise and repeti- H Drooping jaw
tive movement H Ptosis
H Initial symptoms related to cranial nerves H Decreased breath sounds
H With respiratory system involvement, may be life- H Decreased tidal volume
threatening H Respiratory distress and myasthenic crisis
H Spontaneous remissions in about 25% of patients
Test results
Pathophysiology Laboratory
H Blood cells and thymus gland produce antibodies H Serum acetylcholine receptor antibodies are
that block, destroy, or weaken neuroreceptors elevated.
(which transmit nerve impulses). Imaging
H The result is failure in transmission of nerve impuls- H Chest X-rays or computed tomography scan shows
es at the neuromuscular junction. thymoma.
Other
Causes H Positive Tensilon test shows temporary improved
H Autoimmune disorder associated with the thymus muscle function and confirms the diagnosis.
gland H Electrodiagnostic testing shows a rapid reduction
H Accompanies other immune and thyroid disorders of more than 10% in the amplitude of evoked
responses.
Incidence
H Occurs at any age
H Three times more common in females than males Treatment
H Highest in females ages 18 to 25
H Highest in males ages 50 to 60 General
H Transient myasthenia in about 20% of infants born to H Plasmapheresis
myasthenic mothers H Emergency airway and ventilation management
H Diet, as tolerated
Common characteristics H Activity, as tolerated (exercise possibly exacerbating
H Weak eye closure; ptosis symptoms; planned rest periods possibly retarding
H Diplopia symptoms)
H Skeletal muscle weakness; paralysis
Medications
Complications H Anticholinesterase drugs, such as neostigmine and
H Respiratory distress pyridostigmine
H Pneumonia H Corticosteroids such as prednisone
H Aspiration H I.V. immune globulin
H Immunosuppressants such as cyclosporine

Assessment Surgery
H Thymectomy
History
H Varying assessment findings
H Progressive muscle weakness Nursing considerations
H Extreme muscle weakness and fatigue (cardinal
symptoms) Key outcomes
H Ptosis and diplopia (the most common sign and The patient will:
symptom) H maintain a patent airway and adequate ventilation

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H maintain respiratory rate within 5 breaths/minute of

baseline
H perform activities of daily living
H maintain range of motion and joint mobility
H express positive feelings about self.

Nursing interventions
H Provide psychological support.
H Provide frequent rest periods.
H Maintain nutritional management program.
H Maintain social activity.
H Administer prescribed drugs.

Monitoring
H Neurologic and respiratory function
H Response to medications

ALERT
Monitor patient for signs of impending myasthenic
crisis, including increased muscle weakness, respi-
ratory distress, and difficulty talking or chewing.

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H surgery (preoperative and postoperative teaching)
H energy conservation techniques
H medication administration, dosage, and possible ad-
verse effects
H avoidance of strenuous exercise, stress, infection,
needless exposure to the sun or cold weather
H nutritional management program
H swallowing therapy program.

Discharge planning
H Refer the patient to the Myasthenia Gravis Founda-
tion.

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Complications
Life-threatening disorder H Arrhythmias
H Cardiogenic shock

Myocardial infarction H Heart failure causing pulmonary edema

Overview
Description
H Reduced blood flow through one or more coronary
arteries causing myocardial ischemia and necrosis
H Infarction site depends on the vessels involved
H Also called MI and heart attack
Pathophysiology
H One or more coronary arteries become occluded.
H If coronary occlusion causes ischemia lasting longer
than 30 to 45 minutes, irreversible myocardial cell
damage and muscle death occur.
H Every MI has a central area of necrosis surrounded
by an area of hypoxic injury. This injured tissue is
potentially viable and may be salvaged if circulation
is restored, or it may progress to necrosis.
Causes
H Atherosclerosis
H Thrombosis
H Platelet aggregation
H Coronary artery stenosis or spasm
Risk factors
H Increased age (40 to 70)
H Diabetes mellitus
H Elevated serum triglyceride, low-density lipoprotein,
and cholesterol levels, and decreased serum high-
density lipoprotein levels
H Excessive intake of saturated fats, carbohydrates, or
salt
H Hypertension
H Obesity
H Positive family history of coronary artery disease
(CAD)
H Sedentary lifestyle
H Smoking
H Stress or a type A personality
H Use of drugs, such as amphetamines or cocaine
Incidence
H Males more susceptible than premenopausal females
H Increasing among females who smoke and take hor-
monal contraceptives
H In postmenopausal females, similar to incidence in
males
Common characteristics
H Substernal chest pain or pressure with radiation
H Shoulder or jaw pain
H Dyspnea
H Atypical symptoms such as nausea
H Pericarditis
H Rupture of the atrial or ventricular septum, ventricu-
lar wall
H Ventricular aneurysm
H Cerebral or pulmonary emboli
H Extensions of the original infarction
H Mitral insufficiency
Assessment
History
H Possible CAD with increasing anginal frequency,
severity, or duration
H Cardinal symptom of MI: persistent, crushing sub-
sternal pain or pressure possibly radiating to the left
arm, jaw, neck, and shoulder blades, and possibly
persisting for 12 or more hours
H In elderly patient or one with diabetes, pain possibly
absent; in others, pain possibly mild and confused
with indigestion
H A feeling of impending doom, fatigue, nausea, vomit-
ing, and shortness of breath
H Sudden death (may be the first and only indication
of MI)
Physical findings
H Extreme anxiety and restlessness
H Dyspnea
H Diaphoresis
H Tachycardia
H Hypertension
H Bradycardia and hypotension, in inferior MI
H An S4, an S3, and paradoxical splitting of S2 with ven-
tricular dysfunction
H Systolic murmur of mitral insufficiency
H Pericardial friction rub with transmural MI or peri-
carditis
H Low-grade fever during the next few days
Test results
Laboratory
H Serum creatine kinase (CK) level is elevated, espe-
cially the CK-MB isoenzyme.
H Serum lactate dehydrogenase (LD) level is elevated;
higher LD1 isoenzyme (found in cardiac tissue) than
LD2 (in serum).
H Elevated white blood cell count usually appears on
the second day and lasts 1 week.
H Myoglobin (the hemoprotein found in cardiac and
skeletal muscle) thats released with muscle damage
as soon as 2 hours after MI is detected.
H Troponin levels increase within 4 to 6 hours of myo-
cardial injury and may remain elevated for 5 to 11
days.
H Complete blood count may show amenia.
H Serum C-reactive protein level is elevated.

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H Chemistry profile may show abnormal electrolyte
levels.
Imaging
H Nuclear medicine scans can identify acutely damaged
muscle by picking up accumulations of radioactive
nucleotide, which appear as a hot spot on the film.
Myocardial perfusion imaging reveals a cold spot
in most patients during the first few hours after a
transmural MI.
H Echocardiography shows ventricular wall dyskinesia
with a transmural MI and helps to evaluate the ejec-
tion fraction.
Diagnostic procedures
H Serial 12-lead electrocardiography readings may be
normal or inconclusive during the first few hours af-
ter an MI. Characteristic abnormalities include serial
ST-segment depression in subendocardial MI and
ST-segment elevation and Q waves, representing scar-
ring and necrosis, in transmural MI.
H Pulmonary artery catheterization may be performed
to detect left- or right-sided heart failure and to mon-
itor response to treatment.
Treatment
General
H For arrhythmias, a pacemaker or electrical car-
dioversion
H Intra-aortic balloon pump for cardiogenic shock
H Low-fat, low-cholesterol diet
H Calorie restriction, if indicated
H Bed rest with bedside commode
H Gradual increase in activity, as tolerated
Medications
H I.V. thrombolytic therapy, such as streptokinase and
alteplase, started within 3 hours of symptom onset
H Vasodilators such as nitroglycerin
H Platelet aggregation inhibitors such as clopidogrel
H Aspirin
H Antiarrhythmics
H Heparin
H Morphine I.V.
H Inotropic drugs such as dopamine
H Beta-adrenergic blockers such as metoprolol
H Angiotensin-converting inhibitors such as captopril
H Stool softeners
H Oxygen
Surgery
H Surgical revascularization
H Percutaneous revascularization
Nursing considerations
Key outcomes
The patient will:
H maintain hemodynamic stability
H develop no arrhythmia
H develop no complications of fluid volume excess
H express feelings of increased comfort and decreased
pain
H exhibit adequate coping skills.
Nursing interventions
H Assess pain and administer prescribed analgesics.
Record the severity, location, type, and duration of
pain. Avoid I.M. injections.
H Check the patients blood pressure before and after
giving nitroglycerin.
H During episodes of chest pain, obtain electrocardio-
gram.
H Organize patient care and activities to provide peri-
ods of uninterrupted rest.
H Provide a low-cholesterol, low-sodium diet with
caffeine-free beverages.
H Assist with range-of-motion exercises.
H Provide emotional support, and help to reduce stress
and anxiety.
H If the patient has undergone percutaneous translumi-
nal coronary angioplasty, sheath care is necessary.
Watch for bleeding. Keep the leg with the sheath in-
sertion site immobile. Maintain strict bed rest. Check
peripheral pulses in the affected leg frequently.
Monitoring
H Serial electrocardiograms
H Vital signs and heart and breath sounds
ALERT
Watch for crackles, cough, tachypnea, and edema,
which may indicate impending left-sided heart
failure.
H Daily weight; intake and output
H Cardiac enzyme levels; coagulation studies
H Cardiac rhythm for reperfusion arrhythmias (treat
according to facility protocol)
Patient teaching
Be sure to cover:
H procedures
H medication administration, dosage, and psosible ad-
verse reactions
H dietary restrictions
H progressive resumption of sexual activity
H appropriate responses to new or recurrent symptoms
H typical or atypical chest pain to report.
Discharge planning
H Refer the patient to a cardiac rehabilitation program.
H Refer the patient to a smoking-cessation program, if
needed.
H Refer the patient to a weight-reduction program, if
needed.
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Myocarditis H Nonspecific symptoms, such as fatigue, dyspnea, pal-

pitations, persistent tachycardia, and persistent fever
H Mild, continuous pressure or soreness in the chest

Overview Physical findings

H S3 and S4 gallops, muffled S1
Description H Pericardial friction rub
H Focal or diffuse inflammation of the myocardium typ- H Crackles
ically uncomplicated and self-limiting H Arrhythmia
H May be acute or chronic
H Recovery usually spontaneous and without residual Test results
defects Laboratory
H Cardiac enzyme levels, including creatine kinase
Pathophysiology (CK), CK-MB, aspartate aminotransferase, and lactate
H An infectious organism triggers an autoimmune, cel- dehydrogenase are elevated.
lular, and humoral reaction. H White blood cell count and erythrocyte sedimentation
H Inflammation may lead to hypertrophy, fibrosis, and rate are elevated.
inflammatory changes of the myocardium and con- H Antibody titers, such as antistreptolysin-O titer in
duction system. rheumatic fever, are elevated.
H Heart muscle weakens, and contractility is reduced. H Cultures of stool, throat, pharyngeal washings, or
other body fluids show the causative bacteria or
Causes virus.
H Viruses Diagnostic procedures
H Bacteria H Endomyocardial biopsy can be used to confirm diag-
H Fungi nosis.
H Ricettsial H Electrocardiography typically shows diffuse ST-
H Hypersensitive immune reactions such as acute segment and T-wave abnormalities as in pericarditis,
rheumatic fever conduction defects (prolonged PR interval), and ven-
H Radiation therapy tricular and supraventricular ectopic arrhythmias.
H Chronic alcoholism
H Parasitic infections
H Helminthic infections such as trichinosis Treatment
Risk factors General
H Recent viral or bacterial infection H For patient with signs and symptoms of heart failure,
H Human immunodeficiency syndrome hospitalization until stabilized
H Certain medications H Oxygen therapy, if indicated
H Connective tissue diseases H Avoidance of alcohol
H Low-sodium diet
Incidence H Modified bed rest
H Can occur at any age H Activity, as tolerated

Common characteristics Medications

H Mild, continuous chest soreness or pressure H Anti-infectives as appropriate
H Antiarrhythmics
Complications H Anticoagulants
H Left-sided heart failure H Anti-inflammatory agents, such as steroids and non-
H Cardiomyopathy steroidal anti-inflammatory drugs
H Chronic valvulitis (when it results from rheumatic H Angiotensin-converting enzyme inhibitors such as
fever) captoril
H Arrhythmias H Diuretics
H Thromboembolism H Inotropic agents

Surgery
Assessment H Pacemaker implantation
H Ventricular assist device
History H Heart transplantation
H Possible recent upper respiratory tract infection with
fever, viral pharyngitis, or tonsillitis

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Nursing considerations
Key outcomes
The patient will:
H carry out activities of daily living without weakness
or fatigue
H maintain hemodynamic stability and adequate
cardiac output without arrhythmia
H maintain adequate ventilation.

Nursing interventions
H Stress the importance of bed rest. Provide a bedside
commode.
H Allow the patient to express his concerns about the
effects of activity restrictions on his responsibilities
and routines.
H Administer prescribed oxygen.
H Administer prescribed parenteral anti-infectives and
other drugs.
Monitoring
H Vital signs
H Cardiovascular status
H Intake and output
H Signs and symptoms of heart failure
H Possible digoxin toxicity
H Cardiac rhythm
H Arterial blood gas levels
H Daily weight
H Response to treatment

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medication administration, dosage, and possible ad-
verse effects
H prevention of myocarditis
H signs and symptoms of heart failure
H for a patient taking cardiac glycosides at home, how
to check the pulse for 1 full minute before taking the
dose, and the need to withhold the dose and notify
the physician if the heart rate falls below the prede-
termined rate (usually 60 beats/minute)
H when to notify the physician.

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NOverview
Life-threatening disorder

Near drowning

Description
H Victim survives physiologic effects of submersion
H Primary problems: hypoxemia and acidosis
H Dry near drowning: fluid not aspirated; respiratory
obstruction or asphyxia
H Wet near drowning: fluid aspirated; asphyxia or
Assessment
History
H Victim found in water

Physical findings
H Fever or hypothermia
H Rapid, slow, or absent pulse
H Shallow, gasping, or absent respirations
H Altered LOC
H Seizures
H Cyanosis or pink, frothy sputum or both
H Abdominal distention
H Crackles, rhonchi, wheezing, or apnea
secondary changes from fluid aspiration H Tachycardia
H Secondary near drowning: recurrence of respira- H Irregular heartbeat
tory distress
Test results
Pathophysiology Laboratory
H Immersion stimulates hyperventilation. H Arterial blood gas (ABG) level shows degree of hy-
H Voluntary apnea occurs. poxia, intrapulmonary shunt, and acid-base balance.
H Laryngospasm develops. H Electrolyte levels are imbalanced.
H Hypoxemia develops and can lead to brain damage H Complete blood count shows hemolysis.
and cardiac arrest. H Blood urea nitrogen and creatinine levels reveal
impaired renal function.
Causes H Urinalysis shows signs of impaired renal function.
H Inability to swim Imaging
H Panic H Cervical spine X-ray may show evidence of fracture.
H Boating accident H Serial chest X-rays may show pulmonary edema.
H Sudden acute illness Other
H Seizures H Electrocardiography may show myocardial ischemia
H Blow to the head while in the water or infarct or cardiac arrhythmias.
H Venomous stings from aquatic animals
H Excessive alcohol consumption before swimming
H Decompression sickness from deep-water diving Treatment
H Dangerous water conditions
H Suicide attempt General
H Stabilizing neck
Incidence H Establishing airway and providing ventilation
H Most common cause of injury and death in children H Correcting abnormal laboratory values
ages 1 month to 14 years H Warming measures, if hypothermic
H Incidence greater in males H Nothing by mouth until swallowing ability has re-
turned
Common characteristics H Activity based on extent of injury and success of re-
H Altered vital signs suscitation
H Dyspnea
H Hypoxia Medications
H Altered level of consciousness (LOC) H Bronchodilators such as albuterol
H Cardiopulmonary arrest H Cardiac drug therapy if appropriate

Complications
H Neurologic impairment Nursing considerations
H Seizure disorder
H Pulmonary edema Key outcomes
H Renal damage The patient will:
H Bacterial aspiration H maintain adequate cardiac output
H Pulmonary complications H maintain adequate ventilation
H Cardiac complications H have a patent airway at all times
H maintain a normal body temperature
H develop effective coping mechanisms.

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Nursing interventions Prevention

H Perform cardiopulmonary resuscitation as indicated.
H Perform active external rewarming and passive re-
warming measures for mild hypothermia (93.2 to
96.8 F [34 to 36 C]); for active external rewarm-
ing of truncal areas only and passive rewarming mea-
sures for moderate hypothermia (86 F [30 C] to
93.2 F); for active internal rewarming measures for
severe hypothermia (less than 86 F).
H Protect the cervical spine.
H Administer prescribed drugs.
H Provide emotional support.
Monitoring
H Electrolyte and ABG measurement results
H Cardiac rhythm
H Vital signs
H Neurologic status
H Respiratory status
H Core body temperature
H Psychological state
Preventing near drowning
Near drowning can be prevented by following these guide-
lines:
H Surround swimming pools with adequate fencing.
H Lock all entrances to pool area.
H Constantly supervise children near water, including
areas where water level is only a few inches.
H Dont swim after ingesting drugs or drinking alcohol.
H Monitor adults and children near water if they have a
history of seizures.
H Never swim alone.
H Always wear a life jacket in a boat.
H Dont dive into shallow water.

Patient teaching
Be sure to cover:
H the injury, diagnosis, and treatment
H the need to avoid using alcohol or drugs before
swimming
H water safety measures. (See Preventing near drown-
ing.)
Discharge planning
H Recommend a water safety course given by the Red
Cross, YMCA, or YWCA.
H Refer the patient or family for psychological coun-
seling if appropriate.
H Refer the patient or family to resource and support
services.

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H Myonecrosis
Life-threatening disorder H Amputation

Necrotizing fasciitis Assessment

History
Overview H Associated risk factors
H Pain
Description H Tissue injury
H A progressive, rapidly spreading inflammatory infec-
tion of the deep fascia Physical findings
H Mortality rate: 70% to 80% H Rapidly progressing erythema at the site of insult
H Most commonly called flesh-eating bacteria H Fluid-filled blisters and bullae (indicate rapid pro-
H Also called hemolytic streptococcal gangrene, gression of the necrotizing process)
acute dermal gangrene, suppurative fasciitis, and H By days 4 and 5, large areas of gangrenous skin
synergistic necrotizing cellulitis H By days 7 to 10, extensive necrosis of the subcuta-
neous tissue
Pathophysiology H Fever
H Infecting bacteria enter the host through a local H Sepsis
tissue injury or a breach in a mucous membrane H Hypovolemia
barrier. H Hypotension
H Organisms proliferate in an environment of tissue hy- H Respiratory insufficiency
poxia caused by trauma, recent surgery, or a medical H Deterioration in level of consciousness
condition that compromises the patient. H Signs of sepsis
H Necrosis of the surrounding tissue results, accelerat-
ing the disease process by creating a favorable envi- Test results
ronment for organisms. Laboratory
H The fascia and fat tissues are destroyed, with sec- H Tissue biopsy shows infiltration of the deep dermis,
ondary necrosis of subcutaneous tissue. fascia, and muscular planes with bacteria and poly-
morphonuclear cells, and necrosis of fatty and mus-
Causes cular tissue.
H Group A beta-hemolytic Streptococcus (GAS) and H Cultures of microorganisms from the periphery of
Staphylococcus aureus, alone or together: the most the spreading infection or from deeper tissues during
common primary infecting bacteria (More than 80 surgical debridement identify the causative organism.
types of the causative bacteria, Streptococcus pyo- H Gram stain and culture of biopsied tissue identify the
genes, makes epidemiology of GAS infections com- causative organism.
plex.) Imaging
H Radiographic studies may pinpoint the presence of
Risk factors subcutaneous gases.
H Advanced age H Computed tomography scans may show the anatomic
H Immunocompromised state site of involvement by locating necrosis.
H Chronic illness such as diabetes H Magnetic resonance imaging shows areas of necrosis
H Steroid use and areas that require surgical debridement.
Incidence
H Three times more likely in males than females Treatment
H Rarely occurs in children except in countries with
poor hygiene practices General
H Mean age: 38 to 44 H Wound care
H Hyperbaric oxygen therapy
Common characteristics H High-protein, high-calorie diet
H Pain out of proportion to the size of the wound or H Increased fluid intake
injury H Bed rest until treatment effective
H Rapid deterioration in overall clinical status
Medications
Complications H Antimicrobials, such as penicillin, clindamycin, and
H Renal failure metronidazole
H Septic shock H Analgesics
H Scarring with cosmetic deformities
H Myositis

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Surgery
H Immediate surgical debridement, fasciectomy, or
amputation

Nursing considerations
Key outcomes
The patient will:
H maintain collateral circulation
H attain hemodynamic stability
H maintain adequate cardiac output
H remain afebrile
H maintain adequate fluid volume.

Nursing interventions
H Give prescribed drugs.
H Provide supportive care and supplemental oxygen,
as appropriate.
H Provide emotional support.

Monitoring
H Signs and symptoms of complications
H Vital signs
H Mental status
H Wound status
H Pain control

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H importance of strict sterile technique and proper
hand-washing technique for wound care
H medication administration, dosage, and possible
adverse effects
H importance of recognizing and reporting signs and
symptoms of complications.
Discharge planning
H Refer the patient for follow-up with an infectious dis-
ease specialist and surgeon, as indicated.
H Refer the patient to physical rehabilitation, if indi-
cated.
H For education and support, refer the patient to orga-
nizations such as the National Necrotizing Fasciitis
Foundation.

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Incidence
Nephrotic syndrome H In children, 1 in 50,000 new cases per year
H In adults, 1 or 2 in 50,000 new cases per year
H In children, peak incidence between ages 2 and 3
Overview H Slightly more common in males than in females

Description Common characteristics

H Kidney disorder characterized by marked protein- H Fluid retention
uria, hypoalbuminemia, hyperlipidemia, increased H Anorexia
coagulation, and edema H Hypertension
H Results from a glomerular defect that affects perme- H Decreased urine output
ability, indicating renal damage
H Prognosis highly variable, depending on underlying Complications
cause H Malnutrition
H Some forms possibly progressing to end-stage renal H Infection
failure H Coagulation disorders
H Thromboembolic vascular occlusion
Pathophysiology H Accelerated atherosclerosis
H Glomerular protein permeability increases. H Acute renal failure
H Urinary excretion of protein, especially albumin,
increases.
H Hypoalbuminemia develops and causes decreased Assessment
colloidal oncotic pressure.
H Leakage of fluid into interstitial spaces leads to acute, History
generalized edema. H Lethargy
H Vascular volume loss leads to increased blood vis- H Depression
cosity and coagulation disorders. H Anorexia
H The renin-angiotensin system is triggered, causing H Underlying cause
tubular reabsorption of sodium and water and con- H Presence of risk factor
tributing to edema. H Decreased urination

Causes Physical findings

H Primary (idiopathic) glomerulonephritis (about 75% H Periorbital edema
of cases) H Mild to severe dependent edema
H Lipid nephrosis (main cause in children younger H Orthostatic hypotension
than age 8) H Ascites
H Membranous glomerulonephritis (most common H Swollen external genitalia
lesion in adult idiopathic nephrotic syndrome) H Signs of pleural effusion
H Focal glomerulosclerosis (can develop spontaneous- H Pallor
ly at any age, occur after kidney transplantation, or
result from heroin injection; develops in about 10% Test results
of childhood cases and up to 20% of adult cases) Laboratory
H Membranoproliferative glomerulonephritis (may fol- H Urinalysis reveals an increased number of hyaline,
low infection, particularly streptococcal infection; granular, waxy, fatty casts and oval fat bodies; consis-
occurs primarily in children and young adults) tent, heavy proteinuria (levels greater than 3.5 mg/dl
H Metabolic diseases such as diabetes for 24 hours) strongly suggests nephrotic syndrome.
H Collagen-vascular disorders H Serum cholesterol, serum phospholipid, serum
H Circulatory diseases triglyceride levels are increased; serum albumin
H Certain neoplastic diseases such as multiple myeloma levels are decreased.
H Viral infections Diagnostic procedures
H Drugs, such as nonsteroidal anti-inflammatory drugs H Renal biopsy allows histologic identification of the
and penicillamine lesion.
H Certain allergies such as to bee stings

Risk factors Treatment

H Nephrotoxins
H Infection General
H Allergic reactions H Correction of the underlying cause if possible
H Pregnancy H Diet consisting of 0.6 g of protein per kilogram of
H Hereditary nephritis body weight
H Chronic analgesic abuse

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H Restricted sodium intake

H Frequent rest periods

Medications
H Diuretics
H Antibiotics for infection
H Glucocorticoids
H Possible alkylating agents
H Possible cytotoxic agents

Nursing considerations
Key outcomes
The patient will:
H avoid or have minimal complications
H maintain fluid balance
H identify risk factors that worsen tissue perfusion, and
modify lifestyle appropriately
H maintain hemodynamic stability.

Nursing interventions
H Offer the patient reassurance and support, especially
during the acute phase, when severe edema changes
body image.
H Provide information regarding dietary restrictions
and fluid restriction.
Monitoring
H Urine for protein
H Intake and output
H Daily weight
H Plasma albumin and transferrin levels
H Edema

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H signs of infection that should be reported
H adherence to diet
H medication administration, dosage, and possible
adverse effects.
Discharge planning
H Refer the patient to social services as needed.

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Neural tube defects
Overview
Description
H Birth defects that involve the spine or skull
H Result from neural tubes failure to close approxi-
mately 28 days after conception
H Different forms including spina bifida (50% of cas-
es), anencephaly (40%), and encephalocele (10%)
Pathophysiology
H Spina bifida occulta, the least severe neural tube de-
fect (NTD), is characterized by incomplete closure of
one or more vertebrae without protrusion of the
spinal cord or meninges. More severe forms have in-
complete closure of one or more vertebrae, causing
protrusion of the spinal contents in an external sac
or cystic lesion (spina bifida cystica). (See Types of
spinal cord defects.)
H In anencephaly, the closure defect occurs at the cra-
nial end of the neuroaxis and, as a result, part or the
entire top of the skull is missing, severely damaging
the brain. Portions of the brain stem and spinal cord
may also be missing. This condition is fatal.
H In encephalocele, a saclike portion of the meninges
and brain protrudes through a defective opening in
the skull. Usually it occurs in the occipital area, but it
may also occur in the parietal, nasopharyngeal, or
frontal area.
Causes
H Exposure to a teratogen
H Part of a multiple malformation syndrome such as
trisomy 18 or 13 syndrome
H A combination of genetic and environmental factors;
possibly a lack of folic acid in the mothers diet
Incidence
H Spina bifida occulta most common NTD
H At least twice the incidence in North Carolina and
South Carolina than in the rest of the United States
H More common in Whites than in Blacks
Common characteristics
H Some degree of neurologic dysfunction
Complications
H Paralysis below the level of the defect
H Infection such as meningitis
H Hydrocephalus
H Death
H Urinary tract disorders
H Learning disabilities
H Latex allergy
550 Neural tube defects
Assessment
History
H Maternal history revealing factors that cause defect
Physical findings
Spina bifida
H Possibly a depression or dimple, tuft of hair, soft fatty
deposit, port wine nevi, or a combination of these
abnormalities on the skin over the spinal area
H Saclike protrusion over the spinal cord
H Flaccid or spastic paralysis
Anencephaly
H Part or entire top of skull missing
Encephalocele
H Saclike protrusion through a defective opening in the
skull
H Paralysis
Test results
Laboratory
H Elevated maternal alpha-fetoprotein (AFP), amniotic
fluid AFP, and amniotic fluid acetylcholinesterase
levels indicate further testing is needed.
H Fetal karyotype detects chromosomal abnormalities
(present in 5% to 7% of NTDs).
H Maternal serum AFP screening in combination with
other serum markers, such as human chorionic go-
nadotropin (hCG), free beta-hCG, or unconjugated
estriol (for patients with a lower risk of NTDs and
those who will be younger than age 3412 at the time
of delivery) estimates a fetus risk of NTD as well as
possible increased risk for perinatal complications,
such as premature rupture of membranes, abruptio
placentae, or fetal death.
Imaging
H Prenatal ultrasound reveals defect (performed when
an increased risk of open NTD exists, based on fami-
ly history or abnormal serum screening results; not
conclusive for open NTDs or ventral wall defects).
H Spinal X-rays reveal spina bifida occulta.
H Myelography differentiates spina bifida occulta from
other spinal abnormalities, especially spinal cord tu-
mors.
H Skull X-rays, cephalic measurements, and computed
tomography (CT) scan demonstrate associated hy-
drocephalus.
H X-rays show a basilar bony skull defect (CT scan and
ultrasonography further define the defect [with en-
cephalocele]).
Other
H Transillumination of the protruding sac distinguishes
between myelomeningocele (typically doesnt transil-
luminate) and meningocele (typically transillumi-
nates).
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Types of spinal cord defects

There are three major types of spinal cord defects. Spina bifida occulta is characterized by a depression or raised area and a
tuft of hair over the defect. In myelomeningocele, an external sac contains meninges, cerebrospinal fluid, and a portion of the
spinal cord or nerve roots. In meningocele, an external sac contains only meninges and cerebrospinal fluid.

SPINA BIFIDA OCCULTA MYELOMENINGOCELE MENINGOCELE

Treatment After surgery

H Change the dressing regularly, as ordered, and check
and report signs of drainage, wound rupture, and
General infection.
H Symptomatic according to neurologic effects of H Place the infant in a prone position to protect and
defect assess the site.
H Assessment of growth and development throughout H If leg casts have been applied, watch for signs that
lifetime the child is outgrowing the cast. Regularly check
H Diet, as tolerated distal pulses to ensure adequate circulation.
H Physical therapy
Monitoring
Medications Before surgery
H Antibiotics, as indicated H Neurologic status
H Feeding ability
Surgery H Nutritional status
H Surgical closure of the protruding sac After surgery
H Shunt to relieve associated hydrocephalus H Signs of infection
H Surgery during infancy to place protruding tissues H Signs of increased intracranial pressure
back in the skull, excise the sac, and correct associ- H Intake and output
ated craniofacial abnormalities (encephalocele) H Vital signs

Nursing considerations Patient teaching

Key outcomes Be sure to cover:
The patient will: H the disorder, diagnosis, and treatment
H maintain intact skin H how to prevent contractures, pressure ulcers, and
H maintain joint mobility and range of motion urinary tract infections
H attain age-appropriate growth and development. H prevention; folic acid before and during pregnancy.

Nursing interventions Discharge planning

H Provide psychological support. H When an NTD has been diagnosed prenatally, refer
Before surgery the prospective parents to a genetic counselor.
H Clean the defect gently with sterile saline solution or H Refer the family for psychological and support
other solutions, as ordered. services.
H Handle the infant carefully, and dont apply pressure
to the defect.
H Provide adequate time for parent-child bonding, if
possible.

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Neurogenic bladder H Reflux of urine into kidneys

Overview
Description
H All types of bladder dysfunction caused by an inter-
ruption of normal bladder innervation by the nervous
system
H Can be hyperreflexic (hypertonic, spastic, or auto-
matic) or flaccid (hypotonic, atonic, or autono-
mous)
H Also known as neuromuscular dysfunction of the
lower urinary tract, neurologic bladder dysfunc-
tion, and neuropathic bladder
Pathophysiology
H An upper motor neuron lesion (at or above T12)
causes spastic neurogenic bladder, with spontaneous
contractions of detrusor muscles, increased intraves-
ical voiding pressure, bladder wall hypertrophy with
trabeculation, and urinary sphincter spasms.
H A lower motor neuron lesion (at or below S2 to S4)
affects the spinal reflex that controls micturition. The
result is a flaccid neurogenic bladder with decreased
intravesical pressure, and increased bladder capaci-
ty, residual urine retention, and poor detrusor con-
traction. The bladder may not empty spontaneously.
H Interruption of the efferent nerves at the cortical lev-
el results in loss of voluntary control. Higher centers
also control micturition, and voiding may be incom-
plete. Sensory neuron interruption leads to dribbling
and overflow incontinence. (See Types of neuro-
genic bladder.)
Causes
H Cerebral disorders
H Spinal cord disease
H Trauma
H Metabolic disturbances
H Acute infectious diseases
H Heavy metal toxicity
H Chronic alcoholism
H Collagen diseases
H Vascular diseases
H Herpes zoster
H Sacral agenesis (absence of a completely formed
sacrum)
Incidence
H Based on type of neurogenic bladder disorder
Common characteristics
H Some degree of incontinence
H Changes in initiation or interruption of micturition
H Inability to completely empty the bladder
H Urinary tract infections (UTIs)
H Calculus formation
H Renal failure
Assessment
History
H Frequent UTIs
H Hyperactive autonomic reflexes (autonomic dysre-
flexia) when the bladder is distended and the lesion
is at upper thoracic or cervical level
H Involuntary or frequent, scant urination without a
feeling of bladder fullness
H Overflow incontinence and diminished anal sphincter
tone, due to flaccid neurogenic bladder
Physical findings
H Severe hypertension, bradycardia, and vasodilation
(blotchy skin) above the level of the lesion
H Piloerection and profuse sweating above the level of
the lesion
H Spontaneous spasms (caused by voiding) of the arms
and legs
H Increased anal sphincter tone
H Greatly distended bladder without feeling of bladder
fullness, due to sensory impairment
Test results
Laboratory
H Urine culture is positive for infection.
Imaging
H Retrograde urethrography shows strictures and
diverticula.
Diagnostic procedures
H Voiding cystourethrography evaluates bladder neck
function, vesicoureteral reflux, and continence.
H Urodynamic studies evaluate how urine is stored in
the bladder, how well the bladder empties urine, and
urines movement out of the bladder during voiding.
H Urine flow study (uroflow) shows diminished or im-
paired urine flow.
H Cystometry evaluates bladder nerve supply, detrusor
muscle tone, and intravesical pressures during blad-
der filling and contraction.
H Urethral pressure profile determines urethral func-
tion with respect to the urethras length and outlet
pressure resistance.
H Sphincter electromyelography correlates neuromus-
cular function of the external sphincter with bladder
muscle function during bladder filling and contrac-
tion; it also evaluates how well the bladder and uri-
nary sphincter muscles work together.
H Videourodynamic studies correlate visual documen-
tation of bladder function with pressure studies.

Complications
H Incontinence
H Residual urine retention

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Types of neurogenic bladder

Neural lesion Type Cause
Upper motor Uninhibited Lack of voluntary control in infancy
Multiple sclerosis

Reflex or automatic Spinal cord transaction

Cord tumors
Multiple sclerosis

Lower motor Autonomous Sacral cord trauma

Tumors
Herniated disk
Abdominal surgery with transection of pelvic parasympathetic
nerves

Motor paralysis Lesions at levels S2, S3, S4

Poliomyelitis
Trauma
Tumors

Sensory paralysis Posterior lumbar nerve roots

Diabetes mellitus
Tabes dorsalis

Nursing interventions
Treatment H Catheterize the patient, as appropriate.
H Provide emotional support, as appropriate.
General
H Absorbent products Monitoring
H Urethral occlusive devices H Intake and output
H Catheterization of the bladder H Signs of infection
H Avoidance of dietary stimulants, such as spicy foods,
citrus fruits, and chocolate
H Avoidance of excessive fluid intake Patient teaching
H Avoidance of caffeinated and carbonated products
H Pelvic muscle exercises Be sure to cover:
H Bladder training program H the disorder, diagnosis, and treatment
H dietary adjustments
Medications H pelvic exercises
H Anticholinergics such as darifenacin H bladder evacuation techniques
H Alpha-adrenergic stimulators H medication administration, dosage, and possible ad-
H Antispasmodics such as oxybutynin verse effects.
H Antibiotics as appropriate
Discharge planning
Surgery H Refer the patient to resource and support services.
H External sphincterotomy, urethral dilation, urinary H Refer the patient to rehabilitation program as neces-
diversion, or transurethral resection of the bladder sary.
neck to correct structural impairment
H Possible implantation of an artificial urinary sphinc-
ter if permanent incontinence follows surgery

Nursing considerations
Key outcomes
The patient will:
H regain normal voiding habits
H express positive feelings regarding self-image
H demonstrate effective coping mechanisms
H follow bladder training program, as indicated.

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Nocardiosis H Pericarditis
H Endocarditis
H Peritonitis
H Mediastinitis
Overview H Septic arthritis
H Keratoconjunctivitis
Description H Purulent meningitis
H Acute, subacute, or chronic bacterial infection H Seizures
caused by a weakly gram-positive species of the
genus Nocardia usually Nocardia asteroides
Assessment
Pathophysiology
H Nocardia are aerobic gram-positive bacteria with History
branching filaments resembling fungi. H Immunocompromising condition
H Normally found in soil, these organisms cause occa- H Chills
sional sporadic disease in humans and animals H Night sweats
throughout the world. H Anorexia
H Their incubation period is unknown but probably H Malaise
lasts several weeks. H Weight loss
H The usual mode of transmission is inhalation of or- H Dyspnea
ganisms suspended in dust. Transmission by direct H Pleural pain
inoculation through puncture wounds or abrasions is H Puncture wound or abrasion
less common.
Physical findings
Causes H Fever
H Inhalation or inoculation of Nocardia bacteria H Cellulitis
H Productive cough
Risk factors H Subcutaneous abscesses that lack induration
H Immunocompromised state H Crackles
H Alcoholism
H Pulmonary alveolar proteinosis Test results
H Male gender Laboratory
H Culture of sputum or pleural fluid shows causative
Incidence organism.
H About 500 to 1,000 cases annually in the United Imaging
States H Chest X-rays vary and may show fluffy or interstitial
H More common in males (3:1), especially those with a infiltrates, nodules, or abscesses.
compromised immune system Diagnostic procedures
H In patients with brain infection, mortality exceeds H In brain infection with meningitis, lumbar puncture
80%; in other forms, mortality is 50% shows nonspecific changes such as increased open-
ing pressure; cerebrospinal fluid shows increased
Common characteristics white blood cell count and protein levels and de-
Cutaneous infection creased glucose levels compared to serum glucose.
H Cellulitis
H Erythematous nodule at site of inoculation
Pulmonary infection Treatment
H Cough producing thick, tenacious, purulent,
mucopurulent and, possibly, blood-tinged sputum General
H Fever H Diet, as tolerated
Disseminated infection H Activity, as tolerated (during acute phase, bed rest)
H Confusion and disorientation H Safety measures
H Dizziness and nausea
H Headache Medications
H Seizures H Antimicrobial therapy for at least 6 to 12 months
H Combination drug therapy (sulfonamide, ceftri-
Complications axone) and amikacin
H Pleurisy H Antipyretics
H Intrapleural effusions
H Empyema Surgery
H Tracheitis H Drainage of abscesses and excision of necrotic tissue
H Bronchitis

554 Nocardiosis
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Nursing considerations
Key outcomes
The patient will:
H show no signs of infection
H maintain adequate ventilation
H demonstrate effective coping mechanisms
H cough effectively
H have normal breath sounds.

Nursing interventions
H Encourage coughing and deep-breathing exercises.
H Provide psychological support.
H Administer prescribed antibiotics.
H Provide adequate nourishment.
H Give tepid sponge bath to reduce fever.
H Perform chest physiotherapy.
H Assist with range-of-motion exercises.

Monitoring
H Vital signs
H Respiratory status
H Sputum production and character
H Compliance with treatment
H Allergic reaction to antibiotics

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H need for long-term antibiotic therapy
H signs of worsening infection
H allergic reaction to antibiotics.

Discharge planning
H Encourage follow-up care, as indicated.

Nocardiosis 555
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O Obesity
Overview
Description
H An excess of body fat, generally 20% above ideal
body weight
H BMI of 30 or greater (see BMI measurements)
H Morbid obesity: 50% to 100%; or 100 or more
pounds above ideal weight; or body mass index
(BMI) greater than 40
H Second-leading cause of preventable deaths in the
United States
H Hypertension
H Cardiovascular disease
H Hyperlipidemia
H Stroke
H Breast cancer
H Colon cancer
H Degenerative joint disease
H Sleep apnea
H Diabetes mellitus
H Renal disease
H Gallbladder disease
H Psychosocial difficulties
H Premature death

Assessment
Pathophysiology
H Fat cells increase in size in response to dietary History
intake. H Increasing weight
H When the cells can no longer expand, they increase H Complications of obesity
in number.
H With weight loss, the size of the fat cells decreases, Physical findings
but the number of cells doesnt. H Visible excess weight

Causes Test results

H Excessive caloric intake combined with inadequate Other
energy expenditure H Comparison of height and weight to a standard table
H Theories that explain obesity: shows elevation.
Hypothalamic dysfunction of hunger and satiety H Measurement of the thickness of subcutaneous fat
centers folds with calipers approximates excess total body
Genetic predisposition fat. (See Taking anthropometric arm measure-
Abnormal absorption of nutrients ments.)
Impaired action of GI and growth hormones and H BMI is 30 or greater.
of hormonal regulators such as insulin H Waist to hip ratio: patient is overweight when ratio
Socioeconomic status for males is greater than 1 and females is greater
Environmental factors than 0.8.
Psychological factors
Incidence Treatment
H More than 50% of United States residents overweight
H Obesity affecting one in five children General
H Hypnosis and behavior modification techniques
Common characteristics H Psychological counseling
H BMI of 30 or greater H Reduction in daily caloric intake
H Increase in daily activity level
Complications H Treatment of organic cause
H Respiratory difficulties
Medications
H Appetite suppressants such as sibutramine
BMI measurements H Lipase inhibitors such as orlistat

Use these steps to calculate body mass index (BMI): Surgery

H Multiply weight in pounds by 705.
H Vertical banded gastroplasty
H Divide this number by height in inches.
H Then divide this by height in inches again. H Gastric bypass
H Compare results to these standards:
18.5 to 24.9: normal
25.0 to 29.9: overweight
Nursing considerations
30 to 39.9: obese
40 or greater: morbidly obese. Key outcomes
The patient will:
H reduce BMI to normal level

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Taking anthropometric arm measurements

Follow these steps to determine triceps skinfold thickness, midarm circumference, and midarm muscle circumference.

Triceps skinfold thickness Midarm circumference and midarm muscle

H Use the tape measure to find the midpoint between the
shoulder and the elbow. Grasp the patients skin with
your thumb and forefinger, about 38 (1 cm) above the
midpoint, as shown below.
H Place calipers at the midpoint, and squeeze for 3 sec-
onds.
H Record the measurement to the nearest millimeter.
H Take two more readings, and use the average.
circumference
H At the midpoint, measure the midarm circumference, as
shown below. Record the measurement in centimeters.
H Calculate the midarm muscle circumference by multiply-
ing the triceps skinfold thickness measured in millime-
ters by 3.14.
H Subtract this number from the midarm circumference.

Recording the measurements

Record all three measurements as a percentage of the stan-
dard measurements (see table below), using this formula:

Actual measurement
___________________ 100%
Standard measurement

Remember, a measurement
Measurement Standard 90%
less than 90% of the stan- Triceps skinfold thickness Males: 12.5 mm Males: 11.3 mm
dard indicates caloric depri- Females: 16.5 mm Females : 14.9 mm
vation. A measurement over
90% indicates adequate or Midarm circumference Males: 29.3 cm Males: 26.4 cm
more-than-adequate energy Females : 28.5 cm Females : 25.7 cm
reserves.
Midarm muscle circumfer- Males: 25.3 cm Males: 22. 8 cm
ence Females : 23.3 cm Females : 20.9 cm

H safely reduce weight

H demonstrate effective coping mechanisms to deal
Patient teaching
with long-term compliance. Be sure to cover:
H need for long-term maintenance after desired weight
Nursing interventions is achieved
H Obtain an accurate diet history to identify the pa- H dietary guidelines
tients eating patterns and the importance of food H safe weight loss practices.
to his lifestyle.
H Promote increased physical activity as appropriate. Discharge planning
H Refer the patient to a weight-reduction program.
Monitoring H Refer the patient to a long-term cognitive behavior
H Diet modification program.
H Intake and output
H Vital signs
H Weight and BMI

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Physical findings
Obsessive-compulsive H Formal, reserved manner

disorder H Patient is accurate and complete, carefully qualifying

statements and anticipating every move and gesture
of person to whom he speaks
H Flat and unemotional affect, except for controlled
Overview anxiety
H Self-awareness is intellectual, without accompanying
Description emotion or feeling
H Obsessive thoughts and compulsive behaviors that
impair everyday functioning DSM-IV-TR criteria
H May be simple or complex and ritualized Diagnosis is confirmed when the patient meets these
H Also known as OCD criteria:
Obsessions
Pathophysiology H Patient experiences recurrent and persistent ideas,
H This anatomic-physiologic disturbance is thought to thoughts, impulses, or images as intrusive and sense-
involve an alteration in the frontal-subcortical neural less.
circuitry of the brain. H Patient attempts to ignore or suppress such thoughts
H Dysregulation of serotonin neurotransmission may or impulses or to neutralize them with some other
also be a factor. thought or action.
H Patient recognizes that the obsessions are products
Causes of his mind, not externally imposed.
H Decrease in caudate nucleus volume H Patients obsession is unrelated to another Axis I dis-
order.
Risk factors Compulsions
H Coexisting mental disorder H Patient performs repetitive, purposeful, and inten-
H Tic disorders tional behaviors in response to an obsession or ac-
cording to certain rules or in a stereotypical manner.
Incidence H Behavior is intended to neutralize or prevent discom-
H Affects 1 in 50 U.S. residents fort or some dreaded event or situation, but the be-
H Can occur at any age havior isnt connected in a realistic way with intend-
H More common in males and first-born children ed outcome, or is clearly excessive.
H Patient recognizes that the behavior is excessive or
Common characteristics unreasonable.
H Repetitive behaviors and activities for more than
1 hour per day. Test results
H Activities alleviate anxiety triggered by a core fear. Imaging
H Positron-emission tomography shows abnormal
Complications metabolism of frontal cortex and caudate nuclei.
H Impairment of occupational and social functioning Other
H Endangerment of health and safety H Yale-Brown scale rates severity of obsessive-
H Depression compulsive disorder.
H Maudsley Obsessive-Compulsive Inventory identifies
obsessive thoughts and behaviors.
Assessment
History Treatment
H Presence of obsessive thoughts, words, or mental im-
ages that persistently and involuntarily invade the General
consciousness H Behavioral therapy
H Moderate to severe impairment of social and occupa- H Increasing exposure to stressful situations
tional functioning H Keeping a diary of daily stressors
H Patient usually rigid and conscientious, with great H Substituting new activities for compulsive behavior
aspirations
H Patient who takes responsibility seriously and finds Medications
decision-making difficult H Selective serotonin-reuptake inhibitors, such as flu-
H Patient who lacks creativity and the ability to find voxamine, fluoxetine, and sertraline
alternate solutions to problems H Tricyclic antidepressants such as clomipramine

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Nursing considerations
Key outcomes
The patient will:
H reduce the amount of time spent each day on obsess-
ing and ritualizing
H produce no harmful effects from ritualistic behavior
H express feelings of anxiety as they occur
H cope with stress without excessive obsessive-
compulsive behavior.
Nursing interventions
H Provide an accepting patient atmosphere.
H Allow time for ritualistic behavior (unless its danger-
ous) until distraction occurs.
H Provide for basic needs.
H Make reasonable demands and set reasonable limits;
make the patients purpose clear.
H Explore patterns leading to the behavior or recurring
problems.
H Encourage active diversional resources.
H Assist with individualized problem-solving.
H Identify insight and improved behavior.

Monitoring
H Behavioral changes
H Disturbing topics of conversation
H Effective interventions
H Effects of pharmacologic therapy

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H how to identify progress
H importance of realistic expectations of self and
others
H stress relief by channeling emotional energy
H relaxation and breathing techniques.

Discharge planning
H Refer the patient to social services and support
services.
H Stress the importance of follow-up care.

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Common characteristics
Oral and pharyngeal H A nonhealing sore in the mouth

cancer H Unrelieved pain in the mouth

H A persistent lump or thickening in the cheek or neck
H A persistent white or red patch on the gums, tongue,
tonsil, or lining of the mouth
Overview H A persistent sore throat or a feeling that something is
caught in the throat
Description H Difficulty or pain while chewing or swallowing
H Malignant tumors that start in the mouth or in the H Difficulty moving the jaw or tongue
throat behind the mouth H Numbness of the tongue or other area of the mouth
H Involves several types of tissue and cells, resulting in H Swelling of the jaw causing dentures to fit poorly or
different types of cancers, which influences treatment become uncomfortable
options and prognosis H Loosening of the teeth or pain around the teeth or
H 90% of tumors, squamous cell carcinomas jaw
H Others include: H Voice changes
Lymphomas, melanomas, and adenocarcinomas H Weight loss
originating in the minor salivary glands, tonsils,
and base of the tongue Complications
Sarcomas H Recurrence
H Metastasis to larynx, lymph nodes, and other organs
Pathophysiology H Functional and cosmetic disabilities
H Damage to cell deoxyribonucleic acid causes rapid H Persistent dysphagia secondary to surgery or radia-
growth and repair. tion therapy
H Growth is unrestrained and cells lose characteristics H Persistent problems with articulation
of original tissue type.
Causes Assessment
H Tobacco, alcohol, ultraviolet (UV) light, virus, or oth-
er carcinogen History
H Believed to be a combination of biologic, genetic, H One or more risk factors
and lifestyle factors H Complaints of difficulty or pain when swallowing
H Persistent sore throat
Risk factors H Change in speech patterns
H Use of any tobacco (cigarettes, cigars, pipes, snuff, H Weight loss
or chewing tobacco)
H Excessive alcohol consumption Physical findings
H Exposure to UV light H Mouth sores
H Long-term irritation to the lining of the mouth H Lump or thickening in the cheek or neck, or any-
H Plummer-Vinson syndrome where in the mouth
H Human papillomavirus infection H White or red patch on the gums, tongue, tonsil, or
H Immune system suppression lining of the mouth
H Betel nut or betel leaf chewing H Swollen jaw
H Loose teeth
Incidence
H Account for 4% of all cancers occurring in males and Test results
2% in females Imaging
H About two-thirds of cases occurring in people older H Chest X-ray rules out metastasis to the lungs.
than age 55; rare in children H Bone scans if theres pain in the bones suggest bone
H Males affected more commonly than females metastasis.
H Highest incidence in Asia, related to the habit of H Computed tomography scan or magnetic resonance
chewing betel nut, fresh betel leaf, and habitual re- imaging identifies possible intracranial or liver
verse smoking (lighted end held within the oral metastasis.
cavity) Diagnostic procedures
H Most common sites: H Biopsy confirms diagnosis.
Tongue: 28%
Lip: 23%
Floor of the mouth: 16%
Minor salivary glands: 11%

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H importance of preventing aspiration

Treatment H importance of oral hygiene
H need to report adverse drug effects
General H importance of restricting alcohol use
H Varies depending on location of cancer H importance of not smoking or using smokeless to-
H Unresectable lesions usually treated with radiation bacco
therapy, chemotherapy, or both H importance of follow-up care.
H A soft diet or nasogastric or gastrostomy feedings
possibly needed Discharge planning
H Refer the patient to home care or social services as
Medications appropriate.
H Opioid analgesics for pain H Refer the patient to a dietitian as needed.
H Chemotherapy if indicated

Surgery
H Primary tumor resection
H Wide resection, with or without radiation therapy,
chemotherapy, or a combination of both
H Full or partial mandible or maxilla resection
H Micrographic surgery for lip resections
H Laryngectomy or tracheostomy if necessary

Nursing considerations
Key outcomes
The patient will:
H verbalize understanding of the disease process
H be free from mouth lesions
H be free from signs and symptoms of bleeding
H verbalize reduced or absent pain
H maintain or gain weight
H have clear breath sounds.

Nursing interventions
H Administer prescribed drugs.
H Provide care before and after chemotherapy, radia-
tion therapy, or surgery, as appropriate.
H Take precautions to reduce the risk of aspiration
with oral feedings.
H Provide interventions to reduce the risk of infection.
H Encourage activity as tolerated.

Monitoring
H Response to treatment
H Adverse effects of drugs
H Signs and symptoms of infection
H Signs and symptoms of bleeding
H Breath sounds
H Vital signs

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H signs and symptoms that require prompt medical at-
tention
H importance of adequate nutrition and fluids
H care of the mouth and skin after chemotherapy, radi-
ation therapy, or surgery

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Osgood-Schlatter H Pain that worsens from running, jumping, squatting,

and ascending or descending stairs
disease H Symptoms relieved with rest
H Precipitating trauma

Physical findings
Overview H Soft-tissue swelling
H Localized heat and tenderness
Description H Decreased flexibility and restriction in the ham-
H Partial separation of the epiphysis of the tibial tuber- strings, triceps surae, and quadriceps muscle
cle from the tibial shaft, leading to tendinitis H Pain at 30-degree flexion with tibia starting at
H Affects one or both knees 90 degrees in internal rotation
H Also known as osteochondrosis H Palpable firm mass

Pathophysiology Test results

H Bone growth is faster than soft tissue growth. Imaging
H Muscle tendon tightness occurs across the joint. H X-rays and ultrasound show epiphyseal closings, soft
H Flexibility is decreased. tissue swelling, and bone fragmentation.
H When the large quadricep muscle contracts, the H Bone scan may reveal increased uptake in the area of
patellar tendons pull away from the tibia and fibia the tibial tuberosity.
causing pain.
H Tendinitis of the knee results.
Treatment
Causes
H Traumatic avulsion of the proximal tibial tuberosity at General
the patellar tendon insertion H Ice application for 20 minutes every 2 to 4 hours
H Locally deficient blood supply H Reinforced elastic knee support, plaster cast, or
H Genetic factors splint
H Exercise H Reduction of sports activities or exercise
H Avoidance of exercises that demand quadriceps
Risk factors contraction
H Male gender H In severe cases, immobilization for 6 to 8 weeks
H Age 11 to 18 years H Rehabilitation exercises
H Rapid skeletal growth
H Repetitive jumping sports Medications
H Nonsteroidal anti-inflammatory drugs
Incidence H Analgesics
H Most common in active adolescent boys after under-
going a rapid growth spurt Surgery
H Removal or fixation of the epiphysis
Common characteristics
H Frequent fractures
H Pain at inferior aspect of patella Nursing considerations
Complications Key outcomes
H Irregular growth of the proximal tibial epiphysis The patient will:
H Partial avascular necrosis of the proximal tibial H express feelings of increased comfort and decreased
epiphysis pain
H Chronic pain H maintain joint mobility and range of motion
H Patellar tendon avulsion H perform activities of daily living
H Degenerative arthritis H exhibit developmental milestones
H Chrondromalacia H express positive feelings about self.

Nursing interventions
Assessment H Administer prescribed analgesics and assess re-
sponse.
History H Ensure proper application of knee support or splint.
H Intermittent aching, pain, swelling, and tenderness H Provide the patient with crutches if needed.
below the kneecap H Promote and allow adequate time for self-care.
H Encourage verbalization and provide support.

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Monitoring
H Limitation of movement
H Muscle atrophy
H After surgery: circulation, sensation, and pain
H Excessive bleeding

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H prescribed exercise program
H use of crutches if needed
H protection of the injured knee
H avoidance of activities that require deep knee bend-
ing for 2 to 4 months.
Discharge planning
H Refer the patient for occupational and physical
therapy as appropriate.

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Osteoarthritis Assessment
History
Overview H Predisposing traumatic injury
H Deep, aching joint pain
Description H Pain after exercise or weight bearing
H Chronic degeneration of joint cartilage H Pain possibly relieved by rest
H Most common form of arthritis H Stiffness in morning and after exercise
H Disability from minor limitation to near immobility H Aching during changes in weather
H Most commonly affects the hips and knees H Grating feeling when the joint moves
H Varying progression rates H Limited movement

Pathophysiology Physical findings

H Deterioration of the joint cartilage occurs. H Contractures
H Reactive new bone forms at the margins and sub- H Joint swelling
chondral areas. H Muscle atrophy
H Breakdown of chondrocytes occurs. H Deformity of the involved areas
H Cartilage flakes irritate synovial lining. H Gait abnormalities
H The cartilage lining becomes fibrotic. H Hard nodes that may be red, swollen, and tender on
H Joint movement is limited. the distal and proximal interphalangeal joints (see
H Synovial fluid leaks into bone defects, causing cysts. Signs of osteoarthritis)
H Loss of finger dexterity
Causes H Muscle spasms, limited movement, and joint insta-
H Unknown, may be a combination of factors bility
Risk factors Test results
H Advancing age Laboratory
H Hereditary, possibly H Synovial fluid analysis rules out inflammatory
H Muscle weakness arthritis.
H Traumatic injury Imaging
H Congenital abnormality H X-rays of the affected joint may show a narrowing of
H Endocrine disorders such as diabetes mellitus the joint space or margin, cystlike bony deposits in
H Metabolic disorders such as chondrocalcinosis the joint space and margins, sclerosis of the sub-
chondral space, joint deformity or articular damage,
Incidence bony growths at weight-bearing areas, and possible
H Occurs equally in both sexes joint fusion.
H Occurs after age 40 H Radionuclide bone scan may be used to rule out in-
flammatory arthritis by showing normal uptake of the
Common characteristics radionuclide.
H Deep, aching joint pain H Magnetic resonance imaging shows affected joint, ad-
H Stiffness, especially in morning and after exercise jacent bones, and disease progression.
H Crepitus of the joint during motion Diagnostic procedures
H Heberdens nodes (bony enlargements of distal inter- H Neuromuscular tests may show reduced muscle
phalangeal joints) strength.
H Altered gait Other
H Decreased range of motion (ROM) H Arthroscopy shows internal joint structures and iden-
H Localized headaches tifies soft-tissue swelling.
Complications
H Flexion contractures Treatment
H Subluxation
H Deformity General
H Ankylosis H Relieve pain
H Bony cysts H Improve mobility
H Gross bony overgrowth H Minimize disability
H Central cord syndrome H Activity, as tolerated
H Nerve root compression H Physical therapy
H Cauda equina syndrome H Assistive mobility devices

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Signs of osteoarthritis
Heberdens nodes appear on the dorsolateral aspect of the
distal interphalangeal joints. These bony and cartilaginous
enlargements are usually hard and painless. They typically
occur in middle-aged and elderly patients with osteoarthritis.
Bouchards nodes are similar to Heberdens nodes but are
less common and appear on the proximal interphalangeal
joints.

HEBERDENS NODES BOUCHARDS NODES

Medications H For an affected hip, apply moist heat pads and ad-
H Analgesics minister antispasmodics.
H Nonsteroidal anti-inflammatory drugs H For an affected knee, help with ROM exercises.
H Intra-articular injections with corticosteroids H Apply elastic supports or braces.
H Check crutches, cane, braces, or walker for prop-
Surgery er fit.
H Arthroplasty (partial or total)
H Arthrodesis Monitoring
H Osteoplasty H Pain pattern
H Osteotomy H Response to analgesics
H ROM

Nursing considerations
Patient teaching
Key outcomes
The patient will: Be sure to cover:
H express feelings of increased comfort and decreased H the disorder, diagnosis, and treatment
pain H need for adequate rest during the day, after exertion,
H maintain joint mobility and ROM and at night
H perform activities of daily living within confines of H energy conservation methods
the disease H need to take medications exactly as prescribed
H achieve the highest level of mobility H adverse reactions to drugs
H express positive feelings about self. H wearing support shoes that fit well and repairing
worn heels
Nursing interventions H installation of safety devices at home
H Allow adequate time for self-care. H ROM exercises, performing them as gently as
H Adjust pain medications to allow maximum rest. possible
H Identify techniques that promote rest and relaxation. H need to maintain proper body weight
H Administer prescribed anti-inflammatories. H use of crutches or other orthopedic devices.
H For affected hand joints, use hot soaks and paraffin
dips. Discharge planning
H For affected lumbosacral spinal joints, provide a firm H Refer the patient to occupational or physical thera-
mattress. pist as indicated.
H For affected cervical spinal joints, apply a cervical
collar.

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Complications
Osteogenesis imperfecta H Deafness
H Stillbirth or death within the first year of life
(autosomal-recessive disorder)
Overview H Hyperplastic callus formation
H Repeated respiratory infections
Description H Spinal cord compression
H Genetic disease in which bones are thin, poorly de- H Cerebral hemorrhage caused by birth trauma
veloped, and fracture easily
H Expression varies, depending on whether the defect
is carried as a trait or is clinically obvious Assessment
H Also called brittle bone disease
H Categorized into four main types History
Type I: mild H Fractures early in life
Type II: most severe with multiple fractures, hear- H Hearing loss
ing loss, and may be lethal at birth H Easy bruising
Type III and IV: high survival rate and benefits
from treatment Physical findings
H Blue sclerae, showing that mutation is expressed in
Pathophysiology more than one connective tissue
H The pathogenesis begins when mutations in the genes H Short trunk
change the structure of collagen. H Hearing loss
H Possible mutations in other genes may cause varia- H Fractures
tions in the assembly and maintenance of bone and H Kyphoscoliosis
other connective tissues.
H Collectively or alone, these mutated genes lead to Test results
pathologic fractures and impaired healing. Laboratory
H Serum alkaline phosphatase levels are elevated dur-
Causes ing periods of rapid bone formation and cellular in-
H Genetic disease, typically autosomal dominant (char- jury.
acterized by a defect in the synthesis of connective H Skin culture shows reduced quantity of fibroblasts.
tissue) Imaging
H Autosomal recessive carriage of gene defects produc- H Echocardiography may show mitral insufficiency or
ing osteogenesis imperfecta in homozygotes (osteo- floppy mitral valves.
porosis in some) H Prenatal ultrasound (during second trimester) re-
veals bowing of long bones, fractures, limb shorten-
Incidence ing, and decreased skull echogenicity.
H Affects between 20,000 and 50,000 U.S. residents H Skull, long bone, and pelvis X-rays reveal thin bones,
H Affects males and females equally fractures with deformities, beaded ribs, and osteo-
penia.
Special populations
Age of onset of presentation ranges from in utero Treatment
to infancy.
General
H Prevention of fractures
Common characteristics H Nutritious, well-balanced diet
H Frequent fractures caused by falls as toddler begins H Safety during periods of activity
to walk; poor healing H Physical therapy
H Short stature due to multiple fractures caused by mi- H Pain management
nor physical stress
H Deformed cranial structure and limbs due to multi- Medications
ple fractures H Antibiotics (when infection occurs)
H Thin skin and bluish sclera of the eyes; thin collagen H Biphosphates and calcium supplements for types III
fibers of the sclera allowing the choroid layer to be and IV
seen
H Abnormal tooth and enamel development due to im- Surgery
proper deposition of dentin H Internal fixation of fractures to ensure stabilization
H Middle ear deafness and prevent deformities
H Spinal fusion for scoliosis

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Nursing considerations
Key outcomes
The patient (and his family) will:
H follow safety measures to prevent fractures
H understand the disorder and its treatment
H demonstrate effective coping mechanisms.

Nursing interventions
H Ensure a safe environment.
H Encourage activities based on ability.
H Provide psychological support.

Monitoring
H Environment
H Bone condition

Patient teaching
Be sure to cover:
H safe handling of the infant
H how to recognize fractures and correctly splint them
H how to protect the child during diapering, dressing,
and other activities of daily living
H encouraging interests that dont require strenuous
physical activity
H the importance of good nutrition to heal bones and
promote growth
H use of shock-absorbing footwear
H importance of not letting infants younger than age 1
year sit upright.
Discharge planning
H Refer the child and his parents for genetic counseling
to assess the recurrence risk.
H Instruct the parents to provide their child with med-
ical identification jewelry.

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Osteomalacia and ALERT

rickets Incidence of rickets is highest in children with

darkly pigmented skin who, because of their pig-
mentation, absorb less sunlight.
Overview
Common characteristics
Description H May be asymptomatic until a fracture occurs
H Vitamin D deficiency that doesnt allow bone to cal- H Leg and lower back pain due to vertebral collapse
cify normally H Bowed legs
H Also called rickets in infants and young children; H Knock-knees
osteomalacia in adults H Rachitic rosary (beading of ends of ribs)
H Prognosis good with treatment H Enlarged wrists and ankles
H Possible disappearance of bone deformities in adults; H Pigeon breast (protruding ribs and sternum)
usually persist in children H Delayed closing of fontanels
H Softening skull
Pathophysiology H Bulging forehead
H Vitamin D regulates the absorption of calcium ions H Poorly developed muscles (pot belly)
from the intestine. H Difficulty walking and climbing stairs
H When vitamin D is lacking, falling serum calcium H Kyphoscoliosis
concentration stimulates synthesis and secretion of
parathyroid hormone. Complications
H This causes the release of calcium from bone, de- H Spontaneous multiple fractures
creasing renal calcium excretion and increasing re- H Tetany in infants
nal phosphate excretion. H Bone deformities
H When the concentration of phosphate in the bone de-
creases, osteoid may be produced but mineralization
cant proceed normally. Assessment
H This causes large quantities of osteoid to accumulate,
coating the trabeculae and linings of the haversian History
canals and areas beneath the periosteum. H Poor diet
H When bone matrix mineralization is delayed or inad- H Leg and lower back pain
equate, bone is disorganized in structure and lacks
density. The result is gross deformity of both spongy Physical findings
and compact bone. H Bowed legs
H Knock-knees
Causes H Rachitic rosary (beading of ends of ribs)
H Inadequate dietary intake of vitamin D H Enlarged wrists and ankles
H Malabsorption of vitamin D H Pigeon breast (protruding ribs and sternum)
H Inadequate exposure to sunlight H Bulging forehead
H Inherited impairment of renal tubular reabsorption H Poorly developed muscles (pot belly)
of phosphate (from vitamin D insensitivity) in vitamin H Kyphoscoliosis
Dresistant rickets (refractory rickets, familial
hypophosphatemia) Test results
H Conditions reducing the absorption of fat-soluble vit- Laboratory
amin D H Serum calcium concentration is less than 7.5 mg/dl.
H Hepatic or renal disease H Serum inorganic phosphorus concentration is less
H Malfunctioning parathyroid gland contributing to cal- than 3 mg/dl.
cium deficiency and interfering with vitamin D activa- H Serum citrate level is less than 2.5 mg/dl.
tion in the kidneys H Alkaline phosphatase level is less than 4 Bodansky
units/dl.
Incidence Imaging
H Rare in the United States H X-rays show characteristic bone deformities and ab-
H Does appear occasionally in breast-fed infants not re- normalities such as Loosers transformation zones
ceiving a vitamin D supplement or in infants being (radiolucent bands perpendicular to the surface of
fed a formula with a nonfortified milk base the bones indicating reduced bone ossification con-
H Occurs in overcrowded urban areas where smog lim- firm the diagnosis).
its sunlight penetration

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Treatment
General
H Sufficient sun exposure
H Diet high in vitamin D (fortified milk, fish liver oils,
herring, liver, and egg yolks)
H Treatment of bone deformities or fractures

Medications
H Oral supplements of vitamin D, calcium, and phos-
phorus, depending on underlying cause
H For rickets refractory to vitamin D, or in rickets
accompanied by hepatic or renal disease, 25-
hydroxycholecalciferol, 1,25-dihydroxycholecalci-
ferol, or a synthetic-analogue of active vitamin D
Surgery
H Possible surgical intervention for intestinal disease
H Appropriate repair of bone fractures

Nursing considerations
Key outcomes
The patient will:
H have increased vitamin D intake
H remain free from fractures
H express understanding of the disorder and its treat-
ment.
Nursing interventions
H Obtain a dietary history to assess the patients vitamin
D intake.
H Administer prescribed supplements or medications.

Monitoring
H Dietary intake
H Bone integrity

Patient teaching
Be sure to cover:
H symptoms of vitamin D toxicity (headache, nausea,
constipation and, after prolonged use, renal calculi)
H safety and sun exposure.

Discharge planning
H If the patients vitamin D deficiency appears to be
linked to adverse socioeconomic conditions, refer
him to an appropriate community agency.
H Refer the patient to a weight-bearing exercise pro-
gram.

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Common characteristics
Osteomyelitis H Sudden pain in affected bone
H Tenderness, heat, swelling
H Restricted movement
Overview H Chronic infection

Description Complications
H Pyogenic bone infection H Chronic infection
H Infecting microorganisms invading by indirect or di- H Skeletal deformities
rect entry H Joint deformities
H Chronic or acute H Disturbed bone growth in children
H Good prognosis for acute form (with prompt treat- H Differing leg lengths
ment) H Impaired mobility
H Poor prognosis for chronic form

Pathophysiology Assessment
H Organisms settle in a hematoma or weakened area
and spread directly to bone. History
H Pus is produced and pressure builds within the rigid H Previous injury, surgery, or primary infection
medullary cavity. H Sudden, severe pain in the affected bone
H Pus is forced through the haversian canals. H Pain unrelieved by rest and worse with motion
H Subperiosteal abscess forms. H Related chills, nausea, and malaise
H Bone is deprived of its blood supply. H Refusal to use the affected area
H Necrosis results and new bone formation is stim-
ulated. Physical findings
H Dead bone detaches and exits through an abscess or H Tachycardia and fever
the sinuses. H Swelling and restricted movement over the infection
H Osteomyelitis becomes chronic. site
H Tenderness and warmth over the infection site
Causes H Persistent pus drainage from an old pocket in a sinus
H Traumatic injury tract
H Acute infection originating elsewhere in the body
H Staphylococcus aureus Test results
H Streptococcus pyogenes Laboratory
H Pseudomonas aeruginosa H White blood cell count shows leukocytosis.
H Escherichia coli H Erythrocyte sedimentation rate is increased.
H Proteus vulgaris H Blood culture identifies the pathogen.
H Fungi or viruses H Bone or soft tissue biopsy sample is cultured to iden-
H Salmonella tify the pathogen.
H Open bone injury Imaging
H Diminished blood supply to bone as with atheroscle- H X-rays may show bone involvement.
rosis H Bone scans may detect early infection.
H Computed tomography scan and magnetic resonance
Risk factors imaging can show extent of infection.
H Diabetes
H Hemodialysis
H Immunocompromised state Treatment
H Sickle cell disease
H I.V. drug abuse General
H Advanced age H Decrease internal bone pressure
H Prevent bone necrosis
Incidence H Hyperbaric oxygen therapy
H Incidence of both types declining, except in drug H Free tissue transfers
abusers H I.V. fluids, as needed
H High-protein diet rich in vitamin C
H Bed rest
Special populations
H Immobilization of involved bone and joint with a cast
The acute form affects rapidly growing children, or traction
especially boys.

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Medications
H I.V. antibiotics
H Analgesics
H Intracavitary instillation of antibiotics for open
wounds
Surgery
H Surgical drainage
H Local muscle flaps
H Sequestrectomy
H Amputation for chronic and unrelieved symptoms

Nursing considerations
Key outcomes
The patient will:
H experience increased comfort and decreased pain
H maintain joint mobility and range of motion
H exhibit adequate fluid volume
H exhibit adequate tissue perfusion and pulses distally
H perform activities of daily living.

Nursing interventions
H Control infection.
H Protect the bone from injury.
H Provide emotional support.
H Promote and allow adequate time for self-care.
H Encourage activities that promote rest and relaxation.
H Use strict sterile technique.
H With skeletal traction, cover the pin insertion points
with small, dry dressings.
H Provide firm pillows.
H Provide thorough skin care.
H Provide complete cast care.
H Administer prescribed analgesics.

Monitoring
H Vital signs
H Wound appearance and healing
H Pain control
H Drainage and suctioning equipment
H Sudden malpositioning of the limb

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medication administration, dosage, and possible
adverse effects
H techniques for promoting rest and relaxation
H wound site care
H signs of recurring infection
H importance of follow-up examinations.

Discharge planning
H Refer the patient for occupational therapy, as appro-
priate.
H Refer the patient to home care for I.V. antibiotic ther-
apy as appropriate.

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Common characteristics
Osteoporosis H Sudden pain associated with bending or lifting
H Back pain (if vertebral collapse occurs)
H Increasing deformity
Overview H Kyphosis
H Loss of height
Description H Decreased exercise tolerance
H Loss of calcium and phosphate from bones causing H Spontaneous wedge fractures
increased vulnerability to fractures
H Primary or secondary to underlying disease Complications
H Types of primary osteoporosis: postmenopausal os- H Bone fractures (vertebrae, femoral neck, and distal
teoporosis (type I) and age-associated osteoporosis radius)
(type II)
H Secondary osteoporosis: caused by an identifiable
agent or disease Assessment
Pathophysiology History
H The rate of bone resorption accelerates as the rate of H Postmenopausal patient
bone formation decelerates. H Condition known to cause secondary osteoporosis
H Decreased bone mass results and bones become H Snapping sound or sudden pain in lower back when
porous and brittle. bending down to lift something
H Possible slow development of pain (over several
Causes years)
H Exact cause unknown H With vertebral collapse, backache and pain radiating
H Prolonged therapy with steroids, heparin, or anti- around the trunk
seizure drugs H Pain aggravated by movement or jarring
H Bone immobilization
H Alcoholism Physical findings
H Malnutrition H Humped back
H Rheumatoid arthritis H Markedly aged appearance
H Liver disease H Loss of height
H Malabsorption H Muscle spasm
H Scurvy H Decreased spinal movement with flexion more limit-
H Lactose intolerance ed than extension
H Hyperthyroidism
H Osteogenesis imperfecta Test results
H Sudecks atrophy (localized in hands and feet, with Laboratory
recurring attacks) H Serum calcium, phosphorus, and alkaline levels are
H Low calcium intake normal.
H Parathyroid hormone level is elevated.
Risk factors Imaging
H Mild, prolonged negative calcium balance H X-ray studies show characteristic degeneration in the
H Declining gonadal adrenal function lower thoracolumbar vertebrae.
H Female gender H Computed tomography scan assesses spinal bone
H Increasing age loss.
H Family history H Bone scans show injured or diseased areas.
H European descent Diagnostic procedures
H Early menopause H Bone biopsy shows thin, porous, but otherwise nor-
H Cigarette smoking mal bone.
H Alcoholism Other
H Breast cancer and chemotherapy H Dual or single photon absorptiometry (measurement
H Faulty protein metabolism (caused by estrogen defi- of bone mass) shows loss of bone mass.
ciency)
H Sedentary lifestyle
Treatment
Incidence
H Idiopathic affects children and adults General
H Type I (or postmenopausal): affects women ages 51 H Control bone loss
to 75 H Prevent additional fractures
H Type II (or senile): most common between ages 70 H Control pain
and 85 H Reduction and immobilization of fractures

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H Diet rich in vitamin D, calcium, and protein H sleeping on a firm mattress

H Physical therapy program of gentle exercise and H avoiding excessive bed rest
activity H use of a back brace, if appropriate
H Supportive devices H proper body mechanics
H home safety devices
Medications H diet rich in calcium.
H Estrogen
H Sodium fluoride Discharge planning
H Calcium and vitamin D supplements H Refer the patient for physical and occupational thera-
H Biphosphates, such as alendronate, risedronate, and py, as appropriate.
ibandronate
H Teriparatide
H Strontium ranelate
H Calcitonin
H Analgesics

Surgery
H Open reduction and internal fixation for femur
fractures

Nursing considerations
Key outcomes
The patient will:
H maintain joint mobility and range of motion (ROM)
H experience increased comfort and decreased pain
H demonstrate measures to prevent injury
H perform activities of daily living.

Nursing interventions
H Encourage careful positioning, ambulation, and pre-
scribed exercises.
H Promote self-care while allowing adequate time.
H Encourage mild exercise.
H Assist with walking.
H Perform passive ROM exercises.
H Promote physical therapy sessions.
H Use safety precautions.
H Administer prescribed medications.
H Apply heat.

Monitoring
H Skin for redness, warmth, and new pain sites
H Response to analgesia
H Nutritional status
H Height
H Exercise tolerance
H Joint mobility

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medication administration, dosage, and possible
adverse effects
H performing monthly breast self-examination while
on estrogen therapy
H need to report vaginal bleeding promptly
H need to report new pain sites immediately

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Otitis externa Assessment

History
Overview H Repeated exposure to ear trauma, water, use of ear-
phones, or allergic response to hair spray, dye, or
Description other hair-care products
H Acute or chronic inflammation of the external ear H Mild to severe ear itching or pain aggravated by jaw
canal motion, clenching the teeth, opening the mouth, or
H With treatment, usually subsides within 7 days chewing
H Tends to recur and may become chronic H Fungal otitis externa possibly asymptomatic
H If severe and chronic, may reflect underlying dia-
betes mellitus, hypothyroidism, or nephritis Physical findings
H Also known as external otitis and swimmers ear H Swollen, inflamed ear canal
H Ear discharge that may be foul-smelling and yellow to
Pathophysiology green in color
H External ear canal inflammation results from inva- H Thick red epithelium in canal with chronic otitis
sion by infecting organisms. externa
H Increased pain or itching on palpation or manipula-
Causes tion
H Traumatic injury or excessive moisture that predis-
poses canal to infection Test results
H Bacteria (common) and fungi (less common) Laboratory
H Occasionally, dermatologic conditions, such as seb- H Microscopic examination shows the causative organ-
orrhea or psoriasis ism.
Diagnostic procedures
Risk factors H Audiometric testing may reveal a partial hearing loss.
H Swimming in contaminated water H Otoscopy reveals a swollen external ear canal, peri-
H Cleaning ear canal with cotton-tipped applicator, auricular lymphadenopathy and, occasionally, re-
bobby pin, finger, or other object gional cellulitis.
H Exposure to dust, hair-care products, or other irri-
tants
H Regular use of earphones, earplugs, or earmuffs Treatment
H Chronic drainage from a perforated tympanic mem-
brane General
H Cleaning of debris from canal under direct visualiza-
Incidence tion
H Most common during summer, but can occur any H With mild, chronic otitis externa, use of specially
time of the year fitted earplugs for showering or swimming
Common characteristics Medications
H Swollen, inflamed ear canal H Analgesics
H Mild to severe itching or pain aggravated by jaw H Antibiotic drops
motion, clenching the teeth, opening the mouth, or H Oral antibiotics if lymphadenopathy present, or if
chewing external ear swollen
Complications Surgery
H Complete closure of the ear canal H Excision and abscess drainage
H Significant hearing loss
H Otitis media
H Cellulitis Nursing considerations
H Abscesses
H Disfigurement of the pinna Key outcomes
H Lymphadenopathy The patient will:
H Osteitis H show no signs or symptoms of infection
H Septicemia H express feelings of increased comfort
H Stenosis H express understanding of the disorder and treatment
H regain hearing function or develop other ways to
communicate.

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Prevention
Preventing otitis externa
H To prevent recurrence, tell the patient to avoid potential
irritants, such as hair-care products and earrings.
H Warn against cleaning the ears with cotton-tipped ap-
plicators or other objects.
H Dry ears thoroughly with a towel after swimming,
showering, or bathing.
H Turn head to each side and pull earlobes to help water
run out.
H Use a hair dryer set to the coolest setting and lowest
speed to help dry ears.
H Dont use earplugs.
H Instill alcohol-based over-the-counter ear product ac-
cording to manufacturers directions.

Nursing interventions
H Clean and dry the ear gently and thoroughly.
H Use wet soaks on infected skin.
H Administer prescribed drugs.
With hearing loss
H Encourage discussion of concerns.
H Reassure the patient that hearing loss from an exter-
nal ear infection is temporary.
H Face the patient when speaking.
H Enunciate words clearly, slowly, and in a normal
tone.
H Allow adequate time to grasp what was said.
H Provide a pencil and paper to aid communication.
H Alert staff to the communication problem.

Monitoring
H Vital signs, especially temperature
H Auditory acuity
H Type and amount of aural drainage
H Response to treatment
H Complications

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H proper hand washing and daily ear cleaning
H administration of ear drops, ointment, and ear wash
H antibiotics, as prescribed
H recognizing and reporting adverse reactions
H preventing recurrence. (See Preventing otitis exter-
na.)

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Common characteristics
Otitis media H Severe, deep, throbbing ear pain
H Mild to high fever

Overview Complications
H Spontaneous rupture of the tympanic membrane
Description H Persistent perforation
H Inflammation of the middle ear associated with fluid H Chronic otitis media
accumulation H Mastoiditis
H Acute, chronic, suppurative, or secretory H Meningitis
H Cholesteatomas
Pathophysiology H Abscesses, septicemia
H The disease process differs with otitis media type. H Lymphadenopathy, leukocytosis
Suppurative form H Permanent hearing loss and tympanosclerosis
H Nasopharyngeal flora reflux through the eustachian H Vertigo
tube and colonize the middle ear.
H Respiratory tract infections, allergic reactions, and
position changes allow reflux of nasopharyngeal flora Assessment
through the eustachian tube and colonization in the
middle ear. History
Secretory form H Upper respiratory tract infection
H Obstruction of the eustachian tube promotes transu- H Allergies
dation of sterile serous fluid from blood vessels in H Severe, deep, throbbing ear pain
the middle ear membrane. H Dizziness
H Nausea, vomiting
Causes Acute secretory otitis media
H Suppurative otitis media: bacterial infection with H Sensation of fullness in the ear
pneumococci, group A beta-hemolytic streptococci, H Popping, crackling, or clicking sounds on swallow-
staphylococci, and gram-negative bacteria ing or moving the jaw
H Chronic suppurative otitis media: inadequate treat- H Describes hearing an echo when speaking
ment of acute otitis episodes or infection by resistant Tympanic membrane rupture
strains of bacteria H Pain that suddenly stops
H Secretory otitis media: viral infection, allergy, or H Recent air travel or scuba diving
barotrauma
H Chronic secretory otitis media: adenoidal tissue over- Physical findings
growth, edema, chronic sinus infection, or inade- H Sneezing and coughing with upper respiratory tract
quate treatment of acute suppurative otitis media infection
H Mild to high fever
Risk factors H Painless, purulent discharge in chronic suppurative
H Young age otitis media
H Congenital abnormalities H Obscured or distorted bony landmarks of the tym-
H Immune deficiency panic membrane in acute suppurative otitis media
H Exposure to cigarette smoke H Tympanic membrane retraction in acute secretory
H Family history otitis media
H Recent upper respiratory infection H Clear or amber fluid behind the tympanic membrane
H Allergies H Blue-black tympanic membrane with hemorrhage
into the middle ear
Incidence H Pulsating discharge with tympanic perforation
H Most common in infants and children H Conductive hearing loss (varies with size and type of
tympanic membrane perforation and ossicular de-
Special populations struction)
Chronic otitis media
Acute otitis media is an emergency in an immuno- H Thickening and scarring of tympanic membrane
compromised child. H Decreased or absent tympanic membrane mobility
H Cholesteatoma
H Peaks between ages 6 and 24 months
H Subsides after age 3 years Test results
H Most common during winter months Laboratory
H More common in boys H Culture and sensitivity tests of exudate show the
causative organism.
H Complete blood count shows leukocytosis.

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Imaging
H X-ray studies demonstrate mastoid involvement.
Diagnostic procedures
H Tympanometry detects hearing loss and evaluates the
condition of the middle ear.
H Audiometry shows degree of hearing loss.
H Pneumatic otoscopy may show decreased tympanic
membrane mobility.
ALERT
In adults, unilateral serous otitis media should
always be evaluated for a nasopharyngeal-
obstructing lesion such as carcinoma.
Treatment
General
H In acute secretory otitis media, Valsalvas maneuver
several times per day (may be the only treatment
required)
H Concomitant treatment of the underlying cause
H Elimination of eustachian tube obstruction
Medications
H Antibiotic therapy such as amoxicillin
H Analgesics, such as aspirin or acetaminophen
H Sedatives (small children)
H Nasopharyngeal decongestant therapy
Surgery
H Myringotomy and aspiration of middle ear fluid, fol-
lowed by insertion of a polyethylene tube into the
tympanic membrane
H Myringoplasty
H Tympanoplasty
H Mastoidectomy
H Cholesteatoma excision
H Stapedectomy for otosclerosis
Prevention
Preventing otitis media
For a patient recovering from otitis media at home, in-
struct the patient or his family to follow these guidelines
to help prevent a recurrence:
H Teach the patient how to recognize upper respiratory
tract infections, and encourage early treatment of
them.
H Instruct parents not to feed an infant in a supine posi-
tion and not to put him to bed with a bottle. Explain
that doing so could cause reflux of nasopharyngeal
flora.
H If appropriate, teach the patient to promote eustachian
tube patency by performing Valsalvas maneuver sev-
eral times per day, especially during airplane travel.
H After tympanoplasty, advise the patient not to blow his
nose or get his ear wet when bathing.
H Explain adverse reactions to the prescribed medication,
emphasizing those that require immediate medical at-
tention.
H Allow time for the patient to grasp what was said.
H Provide a pencil and paper to aid communication.
H Alert staff to the patients communication problem.
After myringotomy
H Wash hands before and after ear care.
H Place sterile cotton loosely in the external ear to ab-
sorb drainage and prevent infection. Change the cot-
ton when damp. Avoid placing cotton or plugs deep
in ear canal.
H Administer prescribed analgesics.
H Administer antiemetics after tympanoplasty and re-
inforce dressings.
Monitoring
H Pain level
H Excessive bleeding or discharge
H Auditory acuity
H Response to treatment
H Complications

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort
H exhibit no signs or symptoms of infection
H verbalize understanding of the disorder and treat-
ment regimen
H regain hearing or develop compensatory mechanisms
H experience no injury or harm.
Nursing interventions
H Encourage discussion of concerns about hearing
loss.
With hearing loss
H Offer reassurance, when appropriate, that hearing
loss caused by serious otitis media is temporary.
H Face the patient when speaking and enunciate clearly
and slowly.
Patient teaching
Be sure to cover:
H proper instillation of ointment, drops, and ear wash,
as ordered
H medication administration, dosage, and possible
adverse effects
H importance of taking antibiotics
H adequate fluid intake
H correct instillation of nasopharyngeal decongestants
H use of fitted earplugs for swimming after myringoto-
my and tympanostomy tube insertion
H notification of the physician if tube falls out and for
ear pain, fever, or pus-filled discharge
H preventing recurrence. (See Preventing otitis
media.)

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Test results
Otosclerosis Diagnostic procedures
H Rinne test result shows bone-conducted tone is
heard longer than air-conducted tone.
Overview H Webers test result shows that sound lateralizes to the
more damaged ear.
Description H Audiometric testing reveals hearing loss.
H Bone disease that occurs only in the middle ear and
results in an overgrowth of abnormal bone, usually
involving the stapes Treatment
H Most common cause of conductive hearing loss
H With surgery, prognosis good General
H Also known as hardening of the ear and otospon- H Hearing aids
giosis H Avoidance of activities that provoke dizziness

Pathophysiology Medications
H Normal bone of otic capsule is gradually replaced H Sodium fluoride (may prevent further worsening of
with highly vascular spongy bone. hearing)
H Spongy bone immobilizes the footplate of the nor-
mally mobile stapes. Surgery
H Conduction of vibrations from the tympanic mem- H Stapedectomy
brane to the cochlea is disrupted, and conductive H Prosthesis insertion to restore partial or total hearing
hearing loss results. H Fenestration
H If the inner ear is involved, sensorineural hearing H Stapes mobilization
loss may develop.
Causes Nursing considerations
H Genetic factor transmitted as an autosomal dominant
trait Key outcomes
H Pregnancy (may trigger onset) The patient will:
H show no evidence of infection
Incidence H experience no injury or harm
H Occurs in at least 10% of whites H express needs and feelings
H Twice as common in females as in males H regain hearing or develop other ways of communi-
H Usually occurs between ages 15 and 50 cating
H express understanding of illness and treatment.
Common characteristics
H Slow, progressive hearing loss in one ear, with pro- Nursing interventions
gression to both ears, without middle ear infection H Encourage discussion of concerns about hearing
H Tinnitus loss.
H Offer reassurance with hearing loss, when appro-
Complications priate.
H Bilateral conductive hearing loss H Provide clear, concise explanations.
H Taste disturbance H Face the patient when speaking.
H Enunciate clearly and slowly, in a normal tone.
H Allow adequate time to grasp what was said.
Assessment H Provide a pencil and paper to aid communication.
H Alert the staff to communication problem.
History After surgery
H Family history of hearing loss (excluding presbycu- H Position as ordered.
sis) H Assist with ambulation when indicated.
H Tinnitus H Administer prescribed drugs for pain.
H Ability to hear a conversation better in a noisy envi- H Reassure the patient that taste disturbance is com-
ronment than in a quiet one (paracusis of Willis) mon and usually subsides in a few weeks.
H Vertigo, especially after bending over
Monitoring
Physical findings H For vertigo
H Tympanic membrane that appears normal H Response to medication
H Schwartzes sign (faint pink blush throughout the H Hearing loss
tympanic membrane from vascularity of active oto-
sclerotic bone)

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ALERT
Watch for and report postoperative facial drooping,
which may indicate swelling of or around the fa-
cial nerve.

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H preoperative and postoperative teaching, if indicated
H slow movement to prevent vertigo
H medication administration, dosage, and possible
adverse effects
H importance of protecting ears against the cold
H need to avoid activities that provoke dizziness
H avoidance of anyone with an upper respiratory tract
infection
H changing external ear dressing and incision care
H completion of prescribed drug regimen
H need for follow-up care
H how hearing may be masked by packing, dressing,
and postoperative edema
H why hearing may not be noticeably improved for 1 to
4 weeks after surgery
H avoidance of loud noises and sudden pressure
changes until healing is complete
H avoidance of blowing nose for at least 1 week to pre-
vent contaminated air and bacteria from entering the
eustachian tube
H avoidance of sudden movements
H avoidance of wetting head in shower or swimming
for about 6 weeks
H avoidance of getting water in the ear for an additional
4 weeks
H prevention of constipation and avoidance of straining
while defecating.
Discharge planning
H Refer the patient to an audiologist for hearing aids as
appropriate.
H Refer the patient to a speech and language therapist
as needed.
H Refer the patient for lip reading or sign language
instruction as appropriate.

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Ovarian cancer Assessment

Overview
Description
H Malignancy arising from the ovary; a rapidly pro-
gressing cancer; difficult to diagnose
H Prognosis varying with histologic type and stage
H 90% primary epithelial tumors
H Stromal and germ cell tumors also important tumor
types
Pathophysiology
H Ovarian cancer spreads rapidly intraperitoneally by
local extension or surface seeding and, occasionally,
through the lymphatics and the bloodstream.
H Metastasis to the ovary can occur from breast, colon,
gastric, and pancreatic cancers.
Causes
H Exact cause unknown
Risk factors
H Infertility problems or nulliparity
H Celibacy
H Exposure to asbestos and talc
H History of breast or uterine cancer
H Family history of ovarian cancer
H Diet high in saturated fat
H Gene mutation BRCA1 and BRCA2
Incidence
H After lung, breast, and colon cancer, primary ovarian
cancer is the most common cause of cancer death
among females in the United States (about 40% sur-
vive for 5 years)
H More common after age 50
H Females in industrialized nations at greater risk
H Metastatic ovarian cancer: more common than
cancer at any other site in females with previously
treated breast cancer
Common characteristics
H Bloating
H Pelvic or abdominal pain
H Difficulty eating or feeling full quickly
H Urinary urgency or frequency
Complications
H Fluid and electrolyte imbalance
H Leg edema
H Ascites
H Intestinal obstruction
H Profound cachexia
H Recurrent malignant effusions
History
H Symptoms of bloating, pelvic or abdominal pain, dif-
ficulty eating or feeling full quickly, and urinary
symptoms possibly persistent; a change from normal
H May have lack of obvious signs, or signs and symp-
toms that vary with tumor size and extent of metasta-
sis (disease usually metastasized before diagnosis is
made)
H In later stages: urinary frequency, constipation, pelvic
discomfort, distention, weight loss, abdominal pain
Physical findings
H Gaunt appearance
H Grossly distended abdomen accompanied by ascites
H Palpable abdominal mass with rocky hardness or
rubbery or cystlike quality
Test results
Laboratory
H Deoxyribonucleic acid testing indicates an inherited
gene mutation.
H Laboratory tumor marker studies (such as ovarian
carcinoma antigen, carcinoembryonic antigen, and
human chorionic gonadotropin) show abnormalities
that may indicate complications.
Imaging
H Abdominal ultrasonography, computed tomography
scan, or X-rays delineate tumor size.
Diagnostic procedures
H Aspiration of ascitic fluid can reveal atypical cells.
Other
H Exploratory laparotomy, including lymph node evalu-
ation and tumor resection, is required for accurate
diagnosis and staging.
Treatment
General
H Radiation therapy (not commonly used because it
causes myelosuppression, which limits effectiveness
of chemotherapy)
H Radioisotopes as adjuvant therapy
H High-protein diet
H Small, frequent meals
Medications
H Chemotherapy after surgery
H Immunotherapy
H Hormone replacement therapy in prepubertal girls
who had bilateral salpingo-oophorectomy
Surgery
H Total abdominal hysterectomy and bilateral
salpingo-oophorectomy with tumor resection
H Omentectomy, appendectomy, lymph node palpation
with probable lymphadenectomy, tissue biopsies, and
peritoneal washings

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H Resection of involved ovary

H Biopsies of omentum and uninvolved ovary
H Peritoneal washings for cytologic examination of
pelvic fluid

Nursing considerations
Key outcomes
The patient will:
H show no further evidence of weight loss
H express feelings about the potential loss
H express feelings of increased comfort and decreased
pain
H establish effective coping mechanisms.

Nursing interventions
H Encourage verbalization and provide support.
H Administer prescribed drugs.
H Provide abdominal support, and be alert for abdomi-
nal distention.
H Encourage coughing and deep breathing.

Monitoring
H Vital signs
H Intake and output
H Wound site
H Pain control
H Effects of medication
H Hydration and nutrition status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H dietary needs
H relaxation techniques
H importance of preventing infection, emphasizing
proper hand-washing technique
H medication administration, dosage, and possible
adverse effects.
Discharge planning
H Refer the patient to resource and support services.

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Causes
Ovarian cysts H Granulosa-lutein cysts (excessive accumulation of
blood during menstruation)
H Theca-lutein cysts
Overview H Hydatidiform mole
H Choriocarcinoma
Description H Hormone therapy
H Non-neoplastic sacs on an ovary that contain fluid or
semisolid material Incidence
H Usually small and nonsymptomatic H Can occur at any age, but occurring more commonly
H May be single or multiple (polycystic ovary syn- in females of reproductive age
drome)
H Include follicular cysts, theca-lutein cysts, and cor- Common characteristics
pus luteum cysts H Possibly no symptoms (small ovarian cysts such as
H Can develop any time between puberty and meno- follicular cysts)
pause, including during pregnancy H Mild pelvic discomfort, lower back pain, dyspareu-
H Excellent prognosis for non-neoplastic ovarian cysts nia, or abnormal uterine bleeding, secondary to a
(The risk for ovarian malignancy isnt increased with disturbed ovulatory pattern (large or multiple cysts)
a functional [physiologic] ovarian cyst.) H Acute abdominal pain similar to that of appendicitis
(ovarian cysts with torsion)
Pathophysiology H Unilateral pelvic discomfort (from granulosa-lutein
H Follicular cysts are generally very small and arise cysts appearing early in pregnancy and growing as
from follicles that overdistend, either because they large as 2 to 212 [5 to 6 cm] in diameter)
havent ruptured or have ruptured and resealed be- H Delayed menses, followed by prolonged or irregular
fore their fluid was reabsorbed. (See Follicular bleeding (granulosa-lutein cysts in nonpregnant fe-
cyst.) males)
H Luteal cysts develop if a mature corpus luteum per-
sists abnormally and continues to secrete proges- Complications
terone. They consist of blood or fluid that accumu- H Torsion or rupture of cyst
lates in the cavity of the corpus luteum and are H Infertility
typically more symptomatic than follicular cysts. H Amenorrhea
H When luteal cysts persist into menopause, they se- H Secondary dysmenorrhea
crete excessive amounts of estrogen in response to H Oligomenorrhea
the hypersecretion of follicle-stimulating hormone
and luteinizing hormone that normally occurs during
menopause. Assessment
History
Follicular cyst H Mild pelvic discomfort
A common type of ovarian cyst, a follicular cyst is usually H Urinary urgency
semitransparent and overdistended, with watery fluid visi- H Lower back pain
ble through its thin walls. H Dyspareunia
H Irregular bleeding

Physical findings
H Abdominal tenderness
H Abdominal distention
H Rigid abdomen
H Enlarged ovaries

Test results
Laboratory
H Human chorionic gonadotropin (HCG) titer is elevat-
ed (theca-lutein cyst).
H Urine 17-ketosteroid level is slightly elevated (poly-
cystic ovary syndrome).
Imaging
H Ultrasound reveals cyst.
Other
H Laparoscopy (usually for another condition) reveals
cyst.

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Treatment
General
H Follicular cysts: no treatment because cysts common-
ly disappear spontaneously within one to two men-
strual cycles (excision of persistent cysts to rule out
malignancy)
H Theca-lutein cysts: discontinuation of HCG or
clomiphene citrate therapy
H Ruptured cysts: culdocentesis to drain intraperi-
toneal fluid
H Activity, as tolerated

Medications
H Hormonal contraceptives
H Gonadotropin-releasing hormonal agonists, such as
leuprolide and goserelin
H Analgesics

Surgery
H Laparoscopy or exploratory laparotomy with possible
ovarian cystectomy or oophorectomy for persistent
or suspicious ovarian cyst

Nursing considerations
Nursing interventions
H Provide emotional support.
H Administer prescribed drugs.
After surgery
H Encourage early ambulation.

Monitoring
H Signs of rupture
H Vital signs
H Vaginal bleeding

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H perioperative instructions
H importance of follow-up care
H need to report increased menstrual bleeding
H need to report abdominal mass.

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PPagets disease
Overview
Description
 Bone disorder that causes an irregular bone forma-
tion
 Affects one or several skeletal areas (spine, pelvis,
femur, and skull)
 Slow and progressive
 Causes malignant bone changes in about 5% of
patients
 Can be fatal, particularly when associated with heart
 Kyphosis
 Asymmetrical bowing of the tibia and femur
 Waddling gait
 Pathologic fractures
 Muscle weakness

Complications
 Fractures
 Paraplegia
 Blindness and hearing loss with tinnitus and vertigo
 Osteoarthritis
 Sarcoma
 Hypertension
 Renal calculi
 Hypercalcemia
 Gout
failure, bone sarcoma, or giant cell tumors
 Also known as osteitis deformans  Heart failure

ALERT Assessment
Pagets disease of the breast, a form of breast can-
cer, is a different disorder than Pagets disease. History
(See Pagets disease of the breast.)  Severe, persistent pain
 Impaired mobility
 Pain that worsens with weight bearing
Pathophysiology  Increased hat size
 In the initial phase (osteoclastic phase), excessive  Headaches
bone resorption occurs.
 The second phase (osteoblastic phase) involves Physical findings
excessive abnormal bone formation.  Cranial enlargement over frontal and occipital areas
 Affected bones enlarge and soften.  Kyphosis
 New bone structure is chaotic, fragile, and weak.  Barrel-shaped chest
 Asymmetrical bowing of the tibia and femur
Causes  Warmth and tenderness over affected sites
 Exact cause unknown
 Theory: slow or dormant viral infection (possibly Test results
mumps) Laboratory
 Red blood cell count shows anemia.
Incidence  Serum alkaline phosphatase level is elevated.
 More common after age 40  24-hour urine hydroxyproline level is elevated.
 More common in males Imaging
 More common in people of European, Austrailian,  X-ray studies show bone expansion and increased
and New Zealand descent bone density.
 Familial  Bone scans clearly show early pagetic lesions.
Diagnostic procedures
Common characteristics  Bone biopsy shows a characteristic mosaic pattern of
 Severe, persistent pain bone tissue.
 Pain worsened by weight-bearing activities
 Cranial enlargement
 Barrel-shaped chest Treatment
General
Pagets disease of the breast  Heat therapy
 Massage
Commonly misdiagnosed as a dermatologic problem, this  Well-balanced diet
rare type of breast cancer appears as a red, scaly crust on  Activity, as tolerated
the nipple, causing itchiness and burning. Biopsy con-  Pacing of activities
firms the diagnosis. Treatment should be started to pre-  Use of assistive devices
vent spread of malignancy to the lymph nodes and other
parts of the body.

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Medications
 Calcitonin
 Nonsteroidal anti-inflammatory drugs
 Biphosphonates, such as zoledronic acid,
pamidronate, and edidronate
 Calcium supplements
 Vitamin D

Surgery
 Reduction of pathologic fractures
 Correction of secondary deformities
 Relief of neurologic impairment

Nursing considerations
Key outcomes
The patient will:
 express feelings of increased comfort and decreased
pain
 perform activities of daily living to the extent possible
 maintain adequate skin integrity
 demonstrate measures to prevent self-injury
 maintain joint mobility and range of motion.

Nursing interventions
 Take measures to prevent pressure ulcers.
 Instruct the patient with footdrop to wear high-
topped sneakers or use a footboard.
Monitoring
 Pain level, response to analgesic therapy
 New areas of pain
 New movement restrictions
 Sensory and motor disturbances
 Serum calcium and alkaline phosphatase levels
 Intake and output

Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatment
 pacing of activities
 use of assistive devices
 exercise program
 use of a firm mattress or a bed board
 home safety measures
 how to take prescribed drugs
 adverse reactions to report.

Discharge planning
 Refer the patient to community resource and support
sources, as appropriate.
 Refer the patient to physical and occupational
therapy.

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Pancreatic cancer Assessment

History
Overview  Colicky, dull, or vague intermittent epigastric pain,
which may radiate to the right upper quadrant or
Description dorsolumbar area; unrelated to posture or activity
 Proliferation of cancer cells in the pancreas and aggravated by meals
 Fifth most lethal type of carcinoma  Anorexia, nausea, and vomiting
 Poor prognosis (most patients die within 1 year of  Rapid, profound weight loss
diagnosis)
Physical findings
Pathophysiology  Jaundice
 Pancreatic cancer is almost always adenocarcinoma.  Large, palpable, well-defined mass in the subumbili-
 Nearly two-thirds of tumors appear in the head of the cal or left hypochondrial region
pancreas; islet cell tumors are rare.  Abdominal bruit or pulsation
 Two main tissue types form fibrotic nodes. Cylinder
cells arise in ducts and degenerate into cysts; large, Test results
fatty, granular cells arise in parenchyma. Laboratory
 A high-fat or excessive protein diet induces chronic  Pancreatic enzymes are absent.
hyperplasia of the pancreas, with increased cell  Serum bilirubin level is increased.
turnover.  Serum lipase and amylase levels may be increased.
 Thrombin time is prolonged.
Causes  Aspartate aminotransferase and alanine aminotrans-
 Possible link to inhalation or absorption of carcino- ferase levels are elevated if liver cell necrosis is pres-
gens (such as cigarette smoke, excessive fat and pro- ent.
tein, food additives, and industrial chemicals), which  Alkaline phosphatase level is markedly elevated in
the pancreas then excretes biliary obstruction.
 Serum insulin level is measureable if islet cell tumor
Risk factors is present.
 Chronic pancreatitis  Hypoglycemia or hyperglycemia is present.
 Diabetes  Specific tumor markers for pancreatic cancer,
 Chronic alcohol abuse including carcinoembryonic antigen, pancreatic
 Smoking oncofetal antigen, alpha-fetoprotein, and serum
 Occupational exposure to chemicals immunoreactive elastase I, are elevated.
 Overweight Imaging
 Barium swallow, retroperitoneal insufflation, cholan-
Incidence giography, and scintigraphy locate the neoplasm and
 Three to four times more common in smokers than detect changes in the duodenum or stomach.
nonsmokers  Ultrasonography and computed tomography scan
 Highest in black males ages 35 to 70 identify masses.
 Highest in Israel, United States, Sweden, and Canada;  Magnetic resonance imaging discloses tumor loca-
lowest in Switzerland, Belgium, and Italy tion and size.
 Angiography reveals tumor vascularity.
Common characteristics  Endoscopic retrograde cholangiopancreatography
 Intermittent epigastric pain allows tumor visualization and specimen biopsy.
 Weight loss Diagnostic procedures
 Anorexia, nausea, and vomiting  Percutaneous fine-needle aspiration biopsy may de-
 Jaundice tect tumor cells.
 Laparotomy with biopsy allows definitive diagnosis.
Complications
 Nutrient malabsorption
 Type 1 diabetes Treatment
 Liver and GI problems
 Mental status changes General
 Hemorrhage  Mainly palliative
 Pulmonary congestion  May involve radiation therapy as adjunct to fluo-
rouracil chemotherapy
 Well-balanced diet, as tolerated
 Small, frequent meals

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 Postoperative avoidance of lifting and contact sports  expected postoperative care

 After recovery, no activity restrictions  information about diabetes, including signs and
symptoms of hypoglycemia and hyperglycemia
Medications  adverse effects of radiation therapy and chemo-
 Chemotherapy, such as fluorouracil, gemcitabine, therapy.
and erlotinib
 Antibiotics Discharge planning
 Anticholinergics  Refer the patient to community resource and support
 Antacids services.
 Diuretics  Refer the patient to hospice care, if indicated.
 Insulin  Refer the patient to the American Cancer Society.
 Analgesics
 Pancreatic enzymes, such as pancreatin or pancreli-
pase
Surgery
 Total pancreatectomy
 Cholecystojejunostomy, choledochoduodenostomy,
and choledochojejunostomy
 Gastrojejunostomy
 Whipples operation or radical pancreatoduodenec-
tomy

Nursing considerations
Key outcomes
The patient will:
 maintain an adequate weight
 maintain normal fluid volume status
 maintain skin integrity
 verbalize increased comfort and pain relief
 avoid injury.

Nursing interventions
 Administer prescribed drugs and blood transfusions.
 Provide small, frequent meals.
 Ensure adequate rest and sleep.
 Assist with range-of-motion and isometric exercises,
as appropriate.
 Perform meticulous skin care.
 Apply antiembolism stockings.
 Encourage verbalization and provide emotional
support.
Monitoring
 Fluid balance and nutrition
 Abdominal girth, metabolic state, and daily weight
 Blood glucose levels
 Complete blood count
 Pain control
 Bleeding

Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatment
 end-of-life issues
 medication administration, dosage, and possible
adverse effects

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Pancreatitis  Atelectasis and pleural effusion

 Pneumonia
 Paralytic ileus
 GI bleeding
Overview  Pancreatic abscess and cancer
 Pseudocysts
Description
 Inflammation of the pancreas
 Occurs in acute and chronic forms; 10% mortality in Assessment
acute form
 Irreversible tissue damage with chronic form, tend- History
ing to progress to significant pancreatic function loss  Intense epigastric pain centered close to the umbili-
 Can be idiopathic but sometimes associated with bil- cus and radiating to the back, between the 10th tho-
iary tract disease, alcoholism, trauma, and certain racic and 6th lumbar vertebrae
drugs  Pain aggravated by fatty foods, alcohol consumption,
or recumbent position
Pathophysiology  Weight loss with nausea and vomiting
 Enzymes normally excreted into the duodenum by  Predisposing factor
the pancreas are activated in the pancreas or its
ducts and start to autodigest pancreatic tissue. Physical findings
 Consequent inflammation causes intense pain, third  Hypotension
spacing of large fluid volumes, pancreatic fat necro-  Tachycardia
sis with consumption of serum calcium and, occa-  Fever
sionally, hemorrhage.  Dyspnea, orthopnea
 Generalized jaundice
Causes  Cullens sign (bluish periumbilical discoloration)
 Biliary tract disease  Turners sign (bluish flank discoloration)
 Alcoholism  Steatorrhea (with chronic pancreatitis)
 Abnormal organ structure  Abdominal tenderness, rigidity, and guarding
 Metabolic or endocrine disorders
 Pancreatic cysts or tumors Test results
 Penetrating peptic ulcers Laboratory
 Penetrating trauma  Serum amylase and lipase levels are elevated.
 Viral or bacterial infection  White blood cell count is elevated.
 Serum bilirubin level is elevated.
Risk factors  Transient hyperglycemia and glycosuria may occur.
 Use of glucocorticoids, sulfonamides, thiazides, and  Urinary amylase level is increased.
hormonal contraceptives  In chronic pancreatitis: serum alkaline phosphatase,
 Renal failure and kidney transplantation amylase, and bilirubin levels are elevated; serum glu-
 Endoscopic retrograde cholangiopancreatography cose level shows transient elevation; and lipid and
(ERCP) trypsin level in stool is elevated.
 Heredity Imaging
 Emotional or neurogenic factors  Abdominal and chest X-rays differentiate pancreatitis
from other diseases that cause similar symptoms;
Incidence they also detect pleural effusions.
 Acute form: 2 of every 10,000 people  Computed tomography scan and ultrasonography
 Chronic form: 2 of every 25,000 people show increased pancreatic diameter, pancreatic
 Affects more males than females cysts, and pseudocysts.
 Affects Blacks four times more than Whites Diagnostic procedures
 ERCP shows pancreatic anatomy, identifies ductal
Common characteristics system abnormalities, and differentiates pancreatitis
 Intense epigastric pain from other disorders.
 History of predisposing factors
 Foul-smelling foamy stools
Treatment
Complications
 Diabetes mellitus General
 Massive hemorrhage  Emergency treatment of shock, as needed; vigorous
 Diabetic acidosis I.V. replacement of fluid, electrolytes, and proteins
 Shock and coma  Blood transfusions (for hemorrhage)
 Acute respiratory distress syndrome  Nasogastric suctioning

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9400P.qxd 8/2/12 4:44 PM Page 589

 Nothing by mouth Discharge planning

 Once crisis starts to resolve, oral low-fat, low-protein  Refer the patient to social services, as needed.
feedings implemented gradually
 Alcohol and caffeine abstention
 Activity, as tolerated

Medications
 Analgesics
 Antacids
 Histamine antagonists
 Antibiotics as appropriate
 Anticholinergics
 Total parenteral nutrition
 Pancreatic enzymes such as pancrelipase
 Insulin
 Albumin

Surgery
 Not indicated in acute pancreatitis unless complica-
tions occur
 For chronic pancreatitis: sphincterotomy
 Pancreaticojejunostomy

Nursing considerations
Key outcomes
The patient will:
 maintain normal fluid volume
 maintain a patent airway
 verbalize feelings of increased comfort
 avoid complications
 maintain skin integrity
 initiate lifestyle changes.

Nursing interventions
 Administer prescribed drugs and I.V. therapy.
 Encourage the patient to express his feelings.
 Provide emotional support.

Monitoring
 Vital signs
 Nasogastric tube function and drainage
 Respiratory status
 Acid-base balance
 Serum glucose level
 Fluid and electrolyte balance
 Daily weight
 Pain control
 Nutritional status and metabolic requirements

Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatment
 identification and avoidance of acute pancreatitis
triggers, such as alcohol abuse and smoking
 dietary needs
 medication administration, dosage, and possible
adverse effects.

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Panic disorder Assessment

History
Overview  Repeated episodes of unexpected apprehension or
fear
Description
 Anxiety in its most severe form, characterized by re- Physical findings
current episodes of intense apprehension, terror,  During a panic attack:
and impending doom Trembling
 May be associated with specific situations or tasks Digestive disturbances
 Commonly exists concurrently with agoraphobia Hyperventilation
 May be triggered by severe separation anxiety experi- Tachycardia
enced during early childhood Profuse sweating
 Can persist for years without treatment, with alternat-
ing exacerbations and remissions DSM-IV-TR criteria
Diagnosis of panic disorder is confirmed when the pa-
Pathophysiology tient meets the following criteria:
 Increased sensitivity to adrenergic central nervous  recurrent, unexpected panic attacks with at least one
system discharges occurs, with hypersensitivity of of the attacks having been followed by 1 month (or
presynaptic alpha-2 receptors. more) of one (or more) of the following:
persistent concern about having additional attacks
Causes worry about the attacks implications or conse-
 Combination of physiologic and psychological factors quences
 Temporal lobe dysfunction significant change in behavior related to the attack
 May develop as a persistent pattern of maladaptive agoraphobia
behavior acquired by learning  attacks not due to the direct physiologic effects of a
 Possible contributing factors: alterations in brain substance or a general medical condition
biochemistry, especially in norepinephrine, sero-  attacks not better accounted for by another mental
tonin, and gamma-aminobutyric acid activity disorder, such as social phobia, specific phobia,
 Possibly related to stressful events or unconscious obsessive-compulsive disorder, posttraumatic stress
conflicts that occur early in childhood disorder, or separation anxiety.
Risk factors Test results
 Close family member with the disorder Laboratory
 Urine and serum toxicology tests may reveal the pres-
Incidence ence of psychoactive substances that can precipitate
 Males and females affected equally panic attacks, including barbiturates, caffeine, and
 Panic disorder with agoraphobia about twice as com- amphetamines.
mon in females than in males Other
 Typical onset in late adolescence or early adulthood,  Various tests may be ordered to rule out an organic
commonly in response to a sudden loss basis for the symptoms.
Common characteristics
 Repeated episodes of unexpected apprehension, fear, Treatment
and intense discomfort that may last for minutes or
hours and leave the patient shaken, fearful, and ex- General
hausted  Behavioral therapy
 Attacks that occur several times a week, sometimes  Supportive psychotherapy
daily
 Hyperventilation Medications
 Tachycardia  Antianxiety agents, such as diazepam and lorazepam
 Trembling  Antidepressants such as paroxetine
 Profuse sweating  Buspirone
 Digestive disturbances
 Chest pain

Complications
 Psychoactive substance use disorder

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Nursing considerations
Key outcomes
The patient will:
 experience reduced anxiety by identifying internal
precipitating situation
 identify current stressors
 set limits and compromises on behavior when ready
 develop effective coping mechanisms.

Nursing interventions
 Stay with the patient until the attack subsides.
 Speak in short, simple sentences and slowly give one
direction at a time. Avoid giving lengthy explanations
and asking too many questions.
 Administer prescribed drugs.

Monitoring
 Response to therapy
 Vital signs during an attack

Patient teaching
Be sure to cover:
 relaxation techniques such as focusing on slow, deep
breathing
 medication administration, dosage, and possible
adverse effects
 the importance of follow-up care.

Discharge planning
 Encourage the patient and his family to use commu-
nity resources such as the Anxiety Disorders Associa-
tion of America.

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Parkinsons disease  Excessive sweating

 Decreased GI motility
 Orthostatic hypotension
 Oily skin
Overview  Eyes fixed upward

Description Complications
 Brain disorder causing progressive deterioration,  Injury from falls
with muscle rigidity, akinesia, and involuntary  Food aspiration
tremors  Urinary tract infections
 Usual cause of death: aspiration pneumonia  Skin breakdown
 One of the most common crippling diseases in the
United States
Assessment
Pathophysiology
 Dopaminergic neurons degenerate, causing loss of History
available dopamine.  Muscle rigidity
 Dopamine deficiency prevents affected brain cells  Akinesia
from performing their normal inhibitory function.  Insidious (unilateral pill-roll) tremor, which increas-
 Excess excitatory acetylcholine occurs at synapses. es during stress or anxiety and decreases with pur-
 Nondopaminergic receptors are also involved. poseful movement and sleep
 Motor neurons are depressed. (See Understanding  Dysphagia
Parkinsons disease.)  Fatigue with activities of daily living (ADLs)
 Muscle cramps of legs, neck, and trunk
Causes  Oily skin
 Usually unknown  Increased perspiration
 Exposure to such toxins as manganese dust and car-  Insomnia
bon monoxide  Mood changes
 Type A encephalitis  Dysarthria
 Drug-induced (Haldol, methyldopa, reserpine)
Physical findings
Risk factors  High-pitched, monotonous voice
 Heredity  Drooling
 Expose to pesticides and herbicides  Masklike facial expression
 Reduced estrogen levels  Difficulty walking
 Lack of parallel motion in gait
Incidence  Loss of posture control with walking
 More common in males than females  Oculogyric crises (eyes fixed upward, with involun-
 Occurs in middle age or later tary tonic movements)
 Rare in blacks  Muscle rigidity causing resistance to passive muscle
stretching
Common characteristics  Difficulty pivoting
 Muscle rigidity  Loss of balance
 Tremor
 Resistance to passive muscle stretching Test results
 Akinesia Imaging
 High-pitched, monotonous voice  Computed tomography scan or magnetic resonance
 Drooling imaging rules out other disorders such as intracra-
 Loss of posture control nial tumors.
 Dysarthria

Understanding Parkinsons disease

Treatment
Research on the pathogenesis of Parkinsons disease fo- General
cuses on damage to the substantia nigra from oxidative  Small, frequent meals
stress. Oxidative stress is believed to:  High-bulk foods
 alter the brains iron content  Physical therapy and occupational therapy
 impair mitochondrial function
 Assistive devices to aid ambulation
 alter antioxidant and protective systems
 reduce glutathione
 damage lipids, proteins, and deoxyribonucleic acid.

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Medications  household safety measures

 Levodopa and carbidopa  importance of daily bathing
 Anticholinergics such as trihexyphenidyl  methods to improve communication
 Antihistamines such as diphenhydramine  swallowing therapy regimen (aspiration precau-
 Antiviral agents such as amantadine tions).
 Tricyclic antidepressants
 Dopamine agonist, such as bromocriptine, apomor- Discharge planning
phine, and pramipexole  Refer the patient for occupational and physical reha-
 Coenzyme Q10 bilitation, as indicated.
 Catechol-O-methyltransferase inhibitors such as tol-
capone
Surgery
 Used when drug therapy fails
 Stereotaxic neurosurgery
 Destruction of ventrolateral nucleus of thalamus

Nursing considerations
Key outcomes
The patient will:
 perform ADLs
 avoid injury
 maintain adequate caloric intake
 express positive feelings about himself
 develop adequate coping behaviors
 seek support resources.

Nursing interventions
 Take measures to prevent aspiration.
 Protect the patient from injury.
 Stress the importance of rest periods between
activities.
 Ensure adequate nutrition.
 Provide frequent warm baths and massage.
 Encourage the patient to enroll in a physical therapy
program.
 Provide emotional and psychological support.
 Encourage the patient to be independent.
 Assist with ambulation and range-of-motion
exercises.
Monitoring
 Vital signs
 Intake and output
 Drug therapy
 Adverse reactions to medications
 Postoperatively: signs of hemorrhage and increased
intracranial pressure
 Swallowing

Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatment
 medication administration, dosage, and possible
adverse effects
 measures to prevent pressure ulcers and contrac-
tures

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Patent ductus arteriosus  Respiratory distress

Overview
Description
 Heart condition in which the lumen of the ductus (fe-
tal blood vessel that connects the pulmonary artery to
the descending aorta) remains open after birth
 Initially may produce no clinical effects, but in time
can precipitate pulmonary vascular disease, causing
symptoms to appear by age 40
 Good prognosis if the shunt is small or surgical re-
pair is effective; otherwise, may advance to in-
tractable heart failure, possibly fatal
Pathophysiology
 The lumen of the ductus remains open after birth
and creates a left-to-right shunt of blood from the
aorta to the pulmonary artery, resulting in recircula-
tion of arterial blood through the lungs.
 Prevalent in premature neonates, probably as a result
of abnormalities in oxygenation or the relaxant ac-
tion of prostaglandin E, which prevents ductal spasm
and contracture necessary for closure.
Causes
 May be a combination of genetics and environmental
factors
 Prematurity
 Rubella syndrome
 Associated with other congenital defects, such as
coarctation of the aorta, ventricular septal defect,
and pulmonary and aortic stenoses
Risk factors
 Poorly controlled maternal diabetes
 Drug or alcohol use during pregnancy
 Exposure to chemicals or radiation during pregnancy
Incidence
 Twice as common in females than in males
 The most common congenital heart defect found in
adults
Common characteristics
Infants
 Respiratory distress
 Signs and symptoms of heart failure
 Heightened susceptibility to respiratory tract infec-
tions
 Slow motor development
 Failure to thrive
Adults
 Pulmonary vascular disease
 Fatigability and dyspnea on exertion
Complications
 Chronic pulmonary hypertension
 Intractable left-sided heart failure
Assessment
History
 Prematurity
 Rubella
 Difficulty breathing
Physical findings
 Gibson murmur during systole and diastole
 Thrill at the left sternal border
 Prominent left ventricular impulse
 Bounding peripheral arterial pulses (Corrigans
pulse)
 Widened pulse pressure
Test results
Imaging
 Chest X-rays may show increased pulmonary vascular
markings, prominent pulmonary arteries, and en-
largement of the left ventricle and aorta.
 Echocardiography detects and helps estimate the size
of a patent ductus arteriosus (PDA). It also reveals
an enlarged left atrium and left ventricle or right ven-
tricular hypertrophy from pulmonary vascular dis-
ease.
Diagnostic procedures
 Electrocardiogram may be normal or may indicate
left atrial or ventricular hypertrophy and, in pul-
monary vascular disease, biventricular hypertrophy.
 Cardiac catheterization shows pulmonary arterial
oxygen content higher than right ventricular content
due to the influx of aortic blood.
Treatment
General
 No immediate treatment (if asymptomatic)
 Fluid restriction
 Activity, as tolerated
Medications
 Diuretics
 Cardiac glycosides
 Antibiotics (preoperatively)
 Nonsteroidal anti-inflammatory drugs such as
ibuprofen for premature neonates
Surgery
 Ligation of the ductus
Special populations
If symptoms are mild, surgical correction is usually
delayed until at least age 1. Before surgery, children
with PDA require antibiotics to protect against in-
fective endocarditis.

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 Cardiac catheterization to deposit a plug in the duc-

tus to stop shunting or for administration of in-
domethacin I.V. (a prostaglandin inhibitor that is an
alternative to surgery in premature neonates) to in-
duce ductus spasm and closure

Nursing considerations
Key outcomes
The patient will:
 maintain adequate ventilation
 maintain hemodynamic stability
 remain free from signs and symptoms of infection
 utilize support groups to help cope effectively.

Nursing interventions
 Administer prescribed drugs.
 Provide emotional support to the patient and family.

Monitoring
 Respiratory status
 Vital signs
 Cardiac rhythm
 Intake and output

Patient teaching
Be sure to cover:
 activity restrictions based on the childs tolerance
and energy levels
 importance of informing any physician who treats the
child about his history of surgery for PDA even if
the child is being treated for an unrelated medical
problem.
Discharge planning
 Stress the need for regular medical follow-up exami-
nations.
 Refer the patient to community resources and social
services.

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Common characteristics
Pediculosis  Nits
 Pruritus
 Skin excoriation
Overview
Complications
Description  Skin excoriation
 Infestation of human parasitic lice, which feed exclu-  Secondary bacterial infections
sively on human blood and lay eggs (nits) on body  Hyperpigmentation or residual scarring
hairs or clothing fibers; after nits hatch, lice must
feed within 24 hours or die (see Types of lice)
 Pediculosis capitis (head lice): confined to scalp Assessment
and, occasionally, eyebrows, eyelashes, and beard
 Pediculosis corporis (body lice): found next to skin History
in clothing seams; move to the host only to feed on  Exposure to causative organism
blood  Headache
 Pediculosis pubis (crab lice): found primarily in pu-  Fever
bic hairs; may extend to eyebrows, eyelashes, and ax-  Malaise
illary or body hair  Pruritus
 Cutaneous changes
Pathophysiology
 Lice crawl and attach superficially to the epidermis Physical findings
and hair. One female louse deposits approximately Pediculosis capitis
60 to 150 nits to hair shafts. Nits survive by ingesting  Visible lice
blood from the human host.  Skin excoriation on the scalp and neck
 A louse bite injects a toxin into the skin. Mild irrita-  Matted, lusterless hair (in severe cases)
tion and a purpuric spot result.  Occipital and cervical lymphadenopathy
 Repeated bites cause sensitization to the toxin, lead-  Oval, gray-white nits visible on hair shafts
ing to more serious inflammation. In severe cases, Pediculosis corporis
sensitization causes wheals or a rash on the trunk.  Red papules or macules, usually on the shoulders,
 Scratching may result in secondary bacterial infec- trunk, or buttocks
tion.  Excoriations from scratching
 Nits on clothing seams
Causes Pediculosis pubis
Pediculosis capitis  Visible brownish-gray lice
 Pediculus humanus var. capitis, P. humanus var.  Erythematous papules
corporis  Small macules on the thighs, buttocks, or lower ab-
 Spreads through shared clothing, hats, combs, and domen
hairbrushes  Coarse, grainy-feeling, white-gray nits attached to
Pediculosis corporis pubic hairs
 P. humanus var. corporis
 Spreads through shared clothing and bedding, espe- Test results
cially with environmental overcrowding, prolonged Diagnostic procedures
wearing of same clothing, or poor personal hygiene  Direct inspection with hand lens shows visible lice or
Pediculosis pubis nits.
 Phthirus pubis  Woods light examination shows fluorescence of live
 Spreads through sexual intercourse or contact with nits (dead nits dont fluoresce).
clothing, bedding, or towels harboring lice
Incidence Treatment
Pediculosis capitis
 More common in children General
 More common in girls  Use of fine-toothed comb dipped in vinegar
 More common in warmer months  Hair-washing with ordinary shampoo
 More common in Whites and Asians, less common in  Laundering of potentially contaminated clothing and
Blacks bed linen
Pediculosis pubis  Bathing with soap and water
 More common in adults  Petroleum jelly applied to eyebrows or eyelashes
 More common in cooler months

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Types of lice
Head louse Body louse Pubic louse
Pediculus humanus var. capitis (head Pediculus humanus var. corporis Phthirus pubis (pubic, or crab, louse)
louse) resembles P. humanus var. cor- (body louse) has a long abdomen, and is slightly translucent. Its first set of
poris (body louse). its legs are all about the same length. legs is shorter than its second and
third sets.

Medications Monitoring
Pediculosis capitis  Adverse reactions to insecticide treatment
 Permethrin or pyrethrins  Complications
Pediculosis corporis  Response to treatment
 Pediculicide cream (for severe infestation)
Pediculosis pubis
 Pediculicide shampoo Patient teaching
Be sure to cover:
Nursing considerations  how to inspect for lice, eggs, and lesions
 how to decontaminate infestation sources
Key outcomes  how to apply insecticidal agents
The patient will:  removal of nits and lice
 exhibit resolution of the infestation  importance of not sharing personal articles
 report feelings of increased comfort  adverse reactions to treatment, including when to no-
 demonstrate understanding of the treatment regimen tify the physician
 verbalize feelings about changed body image.  notification and treatment of sexual contacts within
previous 30 days.
Nursing interventions
 Administer prescribed drugs.
 Use personal protective equipment when administer-
ing delousing treatment.
 Notify the school if infestation occurs in a child.
 Encourage the patient to express feelings about the
infestation.

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Pelvic inflammatory Special populations

disease Adolescents are at high risk for sexually transmit-

ted diseases, including PID.

Overview Common characteristics

 Profuse, purulent vaginal discharge
Description  Lower abdominal pain
 Umbrella term referring to any acute, subacute, re-  Vaginal bleeding
current, or chronic infection of the oviducts and
ovaries, with adjacent tissue involvement Complications
 Includes inflammation of the cervix (cervicitis),  Septicemia (potentially fatal)
uterus (endometritis), fallopian tubes (salpingitis),  Pulmonary embolism
and ovaries (oophoritis)  Infertility
 Possible extension of the inflammation to connective  Peritonitis
tissue lying between the broad ligaments (parame-  Shock
tritis)  Death
 Commonly called PID  Ectopic pregnancy

Pathophysiology
 Various conditions, procedures, or instrumentation Assessment
can alter or destroy the cervical mucus, which nor-
mally serves as a protective barrier. History
 As a result, bacteria enter the uterine cavity, causing  Profuse, purulent vaginal discharge
inflammation of various structures.  Low-grade fever
 Malaise
Causes  Lower abdominal pain
 Aerobic or anaerobic organisms (commonly, over-  Vaginal bleeding
growth of one or more of the bacterial species found
in the cervical mucus) Physical findings
 Sexually transmitted infections (Neisseria gonor-  Pain with cervical movement or adnexal palpation
rhoeae and Chlamydia trachomatis)  Vaginal discharge
 Septicemia  Unilaterally or bilaterally tender adnexal mass
 Infected drainage from a chronically infected fallopi-
an tube Test results
 Ruptured appendix Laboratory
 Diverticulitis of the sigmoid colon  Culture and sensitivity and Gram stain of endocervix
 Pelvic abscess or cul-de-sac secretions show the causative agent.
 Use of intrauterine device  Urethral and rectal secretions show the causative
agent.
Risk factors  C-reactive protein level is elevated.
 Multiple sex partners Imaging
 Conditions or procedures that alter or destroy cervi-  Transvaginal ultrasonography may show the presence
cal mucus of thickened, fluid-filled fallopian tubes.
 Procedures that risk transfer of contaminated cervi-  Computed tomography scan may show complex tubo-
cal mucus into the endometrial cavity by an instru- ovarian abscesses and is useful in diagnosing PID.
ment  Magnetic resonance imaging provides images of soft
 Infection during or after pregnancy tissue; useful not only for establishing the diagnosis
 Cigarette smoking of PID but also for detecting other processes respon-
 Multiparity sible for symptoms.
 Douching Diagnostic procedures
 Intercourse during menses  Culdocentesis obtains peritoneal fluid or pus for cul-
 Therapeutic abortion ture and sensitivity testing.
 Diagnostic laparoscopy identifies cul-de-sac fluid,
Incidence tubal distention, and masses in pelvic abscess.
 Primarily affects females ages 16 to 40

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Prevention
Treatment Preventing PID
General Pelvic inflammatory disease (PID) can be prevented by
following these guidelines:
 Frequent perineal care if vaginal discharge occurs  Use latex condoms.
 Bed rest  Have yearly tests for Chlamydia done for sexually
active females with multiple sex partners.
Medications  Abstain from sexual intercourse.
 Antibiotics  Have partners tested and treated for sexually
 Analgesics transmitted diseases (STDs).
 I.V. fluids, as needed  See a physician as soon as symptoms of PID or STD
appear.
Surgery  Avoid multiple sex partners.
 Avoid douching.
 Drainage of pelvic abscess

ALERT
A ruptured pelvic abscess is a life-threatening con-
dition. The patient may need a total abdominal hys-
terectomy with bilateral salpingo-oophorectomy.
Nursing considerations
Key outcomes
The patient will:
 express feelings of increased comfort
 remain free from signs or symptoms of infection
 exhibit stable vital signs
 maintain fluid balance
 express feelings about having PID.
Nursing interventions
 Administer prescribed antibiotics and analgesics.
 Provide frequent perineal care.
 Use meticulous hand-washing technique.
 Encourage the patient to discuss her feelings, and of-
fer emotional support.
 Help the patient develop effective coping strategies.
 causes of PID, such as dyspareunia and sexual activ-
ity
 signs and symptoms of infection after a minor gyne-
cologic procedure
ALERT
Tell the patient to immediately report fever, in-
creased vaginal discharge, or pain especially
after a minor gynecologic procedure.
 avoidance of douching or intercourse for at least 7
days after a minor gynecologic procedure.
Discharge planning
 Refer the patient to infertility counseling, if indicated.
 Refer the patient to a smoking-cessation program, if
indicated.

Monitoring
 Vital signs
 Fluid intake and output
 Signs and symptoms of dehydration
 Vaginal discharge
 Pain control

ALERT
Watch for and report abdominal rigidity and dis-
tention. These signs may indicate development of
peritonitis.

Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatment
 ways to prevent a recurrence (see Preventing PID)

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Complications
Peptic ulcer  GI hemorrhage
 Abdominal or intestinal infarction
 Ulcer penetration into attached structures
Overview
Description Assessment
 Circumscribed lesion in the mucosal membrane of
the lower esophagus, stomach, duodenum, or je- History
junum  Periods of symptom exacerbation and remission,
 Occurs in two major forms: duodenal ulcer and gas- with remissions lasting longer than exacerbations
tric ulcer (both forms chronic)  History of predisposing factor
 Duodenal ulcers: represent about 80% of peptic ul-  Left epigastric pain described as heartburn or indi-
cers; affect the proximal part of the small intestine gestion, accompanied by feeling of fullness or disten-
and follow a chronic course characterized by remis- tion
sions and exacerbations (about 5% to 10% of pa- Gastric ulcer
tients with duodenal ulcers developing complications  Recent weight or appetite loss
that necessitate surgery)  Nausea or vomiting
 Pain triggered or worsened by eating
Pathophysiology Duodenal ulcer
 Helicobacter pylori releases a toxin that promotes  Pain relieved by eating; may occur 112 to 3 hours af-
mucosal inflammation and ulceration. ter food intake
 In a peptic ulcer resulting from H. pylori, acid isnt  Pain that awakens the patient from sleep
the dominant cause of bacterial infection but con-  Weight gain
tributes to the consequences.
 Ulceration stems from inhibition of prostaglandin Physical findings
synthesis, increased gastric acid and pepsin secre-  Pallor
tion, reduced gastric mucosal blood flow, or de-  Epigastric tenderness
creased cytoprotective mucus production.  Hyperactive bowel sounds

Causes Test results

 H. pylori Laboratory
 Use of nonsteroidal anti-inflammatory drugs  Complete blood count shows anemia.
(NSAIDs) or glucocorticoids  Occult blood is present in stools.
 Pathologic hypersecretory states  Venous blood sample shows H. pylori antibodies.
 White blood cell count is elevated.
Risk factors  Urea breath test shows low levels of exhaled carbon
 Type A blood (for gastric ulcer) 13 (13C).
 Type O blood (for duodenal ulcer)  Fasting serum gastrin level rules out Zollinger-Ellison
 Other genetic factors syndrome.
 Exposure to irritants Imaging
 Cigarette smoking  Barium swallow or upper GI and small-bowel series
 Trauma may reveal the ulcer.
 Psychogenic factors and stress  Upper GI tract X-rays reveal mucosal abnormalities.
 Normal aging Diagnostic procedures
 Excessive alcohol consumption  Upper GI endoscopy or esophagogastroduo-
denoscopy confirm the ulcer and permit cytologic
Incidence studies and biopsy to rule out H. pylori or cancer.
 Gastric ulcers: most common in middle-aged and el-  Gastric secretory studies show hyperchlorhydria.
derly males, especially those who are poor and un-
dernourished; prevalence higher in chronic users
of aspirin or alcohol Treatment
 Duodenal ulcers: most common in males ages 20
to 50 General
 Symptomatic
Common characteristics  Iced saline lavage, possibly containing norepineph-
 Left epigastric or abdominal pain with exacerbations rine
and remissions  Laser or cautery during endoscopy
 History of predisposing factor  Stress reduction
 Smoking cessation

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 Avoidance of dietary irritants

 Nothing by mouth if GI bleeding evident
Medications
For H. pylori
 Amoxicillin and biaxin
 Proton pump inhibitors, such as omeprazole and
lansoprazole
For gastric or duodenal ulcer
 Proton pump inhibitors
 Antacids
 Histamine-receptor antagonists or gastric acid pump
inhibitor, such as cimetidine and famotidine
 Coating agents (for duodenal ulcer) such as sucral-
fate
 Sedatives and tranquilizers (for gastric ulcer)
 Anticholinergics such as dicyclomine (for duodenal
ulcers; usually contraindicated in gastric ulcers)
 Prostaglandin analogs such as misoprostol
Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatment
 medication administration, dosage, and possible
adverse effects
 warnings against over-the-counter medications, espe-
cially aspirin, aspirin-containing products, and
NSAIDs, unless the physician approves
 warnings against caffeine and alcohol intake during
exacerbations
 appropriate lifestyle changes
 dietary modifications.
Discharge planning
 Refer the patient to a smoking-cessation program, if
indicated.

Surgery
 Indicated for perforation, lack of response to conser-
vative treatment, suspected cancer, or other compli-
cations
 Type varies with ulcer location and extent; major
operations: bilateral vagotomy, pyloroplasty, and
gastrectomy

Nursing considerations
Key outcomes
The patient will:
 maintain adequate fluid volume
 express feelings of increased comfort
 verbalize an understanding of the illness
 comply with the treatment regimen.

Nursing interventions
 Administer prescribed drugs.
 Provide six small meals or small hourly meals, as
ordered.
 Offer emotional support.

Monitoring
 Medication effects
 Vital signs
 Signs and symptoms of bleeding
 Pain control
If patient had surgery
 Nasogastric tube function and drainage
 Bowel function
 Fluid and nutritional status
 Wound site
 Signs and symptoms of metabolic alkalosis or perfo-
ration

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Perforated eardrum  Perforated tympanic membrane seen on otoscopic

examination
Test results
Overview Laboratory
 Ear drainage culture identifies causative organism or
Description determines if an infection caused the rupture.
 Rupture of the tympanic membrane Imaging
 May cause hearing loss  Skull and temporal lobe X-rays may reveal an associ-
 Typically heals spontaneously ated fracture, especially when a bad fall caused the
eardrum rupture.
Pathophysiology Diagnostic procedures
 Pressure on the tympanic membrane causes a trau-  Audiometric testing evaluates middle ear function.
matic opening that allows release of pressure.
 The rupture may be central or marginal.
 The hole exposes the middle and inner ear to dam- Treatment
age or infection.
General
Causes  May heal spontaneously
 Bacterial infection (acute or chronic suppurative  No dietary restrictions unless nausea occurs; in that
otitis media) case, clear liquids until nausea passes
 Trauma  Safety precautions if the patient has vertigo
 Puncture
 Skull fracture Medications
 Burns  Analgesics such as acetaminophen
 Excessive change in pressure  Antibiotics if perforation resulted from infection

Incidence Surgery
 More common in children  Myringoplasty
 Tympanoplasty
Common characteristics
 Ear pain
 Ear discharge Nursing considerations
 Vertigo (may be transient)
 Tinnitus Key outcomes
 Hearing loss The patient (or parents) will:
 Fever or chills  express an understanding of hearing changes
 Nausea or vomiting  demonstrate appropriate use of pain relief methods
 express an understanding of the potential causes of
Complications ear injury
 Mastoiditis  remain free from infection.
 Meningitis
 Permanent hearing loss Nursing interventions
 Administer prescribed drugs.
 Insert a sterile wick.
Assessment  When talking, face the patient and speak distinctly
and slowly.
History
 Mild or severe ear trauma Monitoring
 Recent airline flight during an upper respiratory in-  Hearing ability
fection  Ear drainage
 Sudden onset of severe earache and bleeding  Safety
from ear  Signs of complications
 Hearing loss
 Tinnitus
 Vertigo

Physical findings
 Signs of hearing loss
 Outer ear drainage

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Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatment
 importance of avoiding swimming or use of ear plugs
 care during hair washing
 the need to complete the course of antibiotic therapy
as prescribed.
 use of safety equipment in the workplace and at
home to prevent injury to the ear
 prevention techniques. (See Preventing a perforated
eardrum.)
Prevention
Preventing a perforated eardrum
A perforated eardrum can be prevented by following these
guidelines:
 Avoid irrigating the ear or cleaning the middle ear canal
with a cotton-tipped applicator.
 Dont insert a foreign object into the ear.
 Treat ear infections promptly.
 Use safety equipment in the workplace and at home to
prevent ear injury.
 Prevent ear popping from excess pressure during flight
by chewing gum during ascent and descent.
 Dont fly or scuba dive with a cold or active allergies.
 Protect ears from loud noises.

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Complications
Pericarditis  Pericardial effusion
 Cardiac tamponade

Overview
Description
 Inflammation of the pericardium the fibroserous
sac that envelops, supports, and protects the heart
 Occurs in acute and chronic forms
 Acute form: can be fibrinous or effusive; character-
ized by serous, purulent, or hemorrhagic exudate
 Chronic form: characterized by dense fibrous peri-
cardial thickening
 Chronic form called constrictive pericarditis
 Delayed form known as Dresslers syndrome: May
occur weeks after heart attack or heart surgery
Pathophysiology
 Pericardial tissue is damaged by bacteria or other
substance that releases chemical mediators of in-
flammation into surrounding tissue.
 Friction occurs as the inflamed layers rub against
each other.
 Chemical mediators dilate blood vessels and increase
vessel permeability.
 Vessel walls leak fluids and proteins, causing extra-
cellular edema.
 Dresslers syndrome may be caused by autoimmune
response.
Causes
 Bacterial, fungal, or viral infection (in infectious
pericarditis)
 Neoplasms (primary or metastatic)
 High-dose chest radiation
 Uremia
 Hypersensitivity or autoimmune disease
 Drugs, such as hydralazine or procainamide
 Idiopathic factors
 Myocardial infarction (MI)
 Chest trauma
 Aortic aneurysm with pericardial leakage
 Myxedema with cholesterol deposits in pericardium
 Radiation
 Rheumatologic conditions
 Tuberculosis
Incidence
 Affects males more than females
 Most common in males ages 20 to 50
Assessment
History
 Predisposing factor
 Sharp, sudden pain, usually starting over the sternum
and radiating to the neck, shoulders, back, and arms
 Pleuritic pain, increasing with deep inspiration and de-
creasing when the patient sits up and leans forward
 Dyspnea
 Chest pain (may mimic MI pain)
Physical findings
 Pericardial friction rub
 Diminished apical impulse
 Fluid retention, ascites, hepatomegaly (resembling
those of chronic right-sided heart failure)
 With pericardial effusion: tachycardia
 With cardiac tamponade: pallor, clammy skin, hypo-
tension, pulsus paradoxus, jugular vein distention,
and dyspnea
Test results
Laboratory
 White blood cell count is elevated, especially in infec-
tious pericarditis.
 Erythrocyte sedimentation rate is elevated.
 Serum CK-MB levels are slightly elevated with associ-
ated myocarditis.
 Pericardial fluid culture may identify a causative or-
ganism in bacterial or fungal pericarditis.
 Blood urea nitrogen level is elevated in uremia.
 Elevated antistreptolysin-O titers may indicate
rheumatic fever.
 Positive reaction in purified protein derivative skin
test indicates tuberculosis.
Imaging
 Echocardiography showing an echo-free space be-
tween the ventricular wall and the pericardium indi-
cates pericardial effusion.
 High-resolution computed tomography scan and
magnetic resonance imaging reveals pericardial
thickness.
Diagnostic procedures
 Electrocardiography shows initial ST-segment eleva-
tion across the precordium.

Common characteristics Treatment

 Pericardial friction rub
 Chest pain General
 Breathing difficulty in a supine position  Management of rheumatic fever, uremia, tuberculo-
 Fatigue sis, or other underlying disorder
 Dry cough  Dietary restrictions based on underlying disorder
 Abdominal or leg swelling  Bed rest as long as fever and pain persist

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Medications Discharge planning

 Nonsteroidal anti-inflammatory drugs  Refer the patient to home care or social services, as
 Corticosteroids needed.
 Antibiotics as appropriate

Surgery
 Surgical drainage
 Pericardiocentesis
 Partial pericardectomy (for recurrent pericarditis)
 Total pericardectomy (for constrictive pericarditis)

Nursing considerations
Key outcomes
The patient will:
 maintain hemodynamic stability and adequate car-
diac output
 avoid arrhythmias
 maintain adequate ventilation
 verbalize feelings of increased comfort and de-
creased pain.
Nursing interventions
 Administer prescribed analgesics and oxygen.
 Administer prescribed antibiotics on time.
 Stress the importance of bed rest. Provide a bedside
commode.
 Place the patient upright to relieve dyspnea and chest
pain.

ALERT
Keep a pericardiocentesis set readily available
whenever you suspect pericardial effusion.

 Encourage the patient to express concerns about the

effects of activity restrictions on responsibilities and
routines.
 Review the patients allergy history.
 Provide appropriate postoperative care.

Monitoring
 Vital signs
 Heart rhythm
 Heart sounds
 Hemodynamic values

Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatments
 how to perform deep-breathing and coughing exer-
cises
 the need to resume daily activities slowly and to
schedule rest periods in daily routine, as instructed
by the physician.

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Peritonitis With progression

 Increasingly severe and constant abdominal pain that
increases with movement and respirations
 Possible referral of pain to shoulder or thoracic area
Overview  Anorexia, nausea, and vomiting
 Inability to pass stools and flatus
Description  Hiccups
 Inflammation of the peritoneum; may extend
throughout the peritoneum or localize as an abscess Physical findings
 Commonly decreases intestinal motility and causes  Fever
intestinal distention with gas  Tachycardia
 Fatal in 10% of cases, with bowel obstruction the  Hypotension
usual cause of death  Shallow breathing
 Can be acute or chronic  Signs of dehydration
 Positive bowel sounds (early); absent bowel sounds
Pathophysiology (later)
 Bacteria invade the peritoneum after inflammation  Abdominal rigidity
and perforation of the GI tract.  General abdominal tenderness
 Fluid containing protein and electrolytes accumulates  Rebound tenderness
in the peritoneal cavity; normally transparent, the  Typical patient positioning: lying very still with knees
peritoneum becomes opaque, red, inflamed, and flexed
edematous.
 Infection may localize as an abscess rather than dis- Test results
seminate as a generalized infection. Laboratory
 Complete blood count shows leukocytosis.
Causes Imaging
 Bacterial or chemical inflammation  Abdominal X-rays show edematous and gaseous dis-
tention of the small and large bowel. With perfora-
Risk factors tion of a visceral organ, X-rays show air in the ab-
 Peritoneal dialysis dominal cavity.
 History of peritonitis  Chest X-rays may reveal elevation of the diaphragm.
 GI tract perforation (from appendicitis, diverticulitis,  Computed tomography scan reveals fluid and inflam-
peptic ulcer, or ulcerative colitis) mation.
 Ruptured ectopic pregnancy Diagnostic procedures
 Paracentesis shows the exudates nature and permits
Incidence bacterial culture testing.
 More common in males

Common characteristics Treatment

 Abdominal pain
 Fever General
 Rebound tenderness  I.V. fluids
 Nasogastric (NG) intubation
Complications  Nothing by mouth until bowel function returns
 Abscess  Gradual increase in diet
 Septicemia  Parenteral nutrition, if necessary
 Respiratory compromise  Bed rest until condition improves
 Bowel obstruction  Semi-Fowlers position
 Shock  Avoidance of lifting for at least 6 weeks postopera-
tively
Assessment Medications
 Antibiotics, depending on infecting organism
History  Electrolyte replacement
Early phase  Analgesics
 Vague, generalized abdominal pain
 If localized: pain over a specific area (usually the in- Surgery
flammation site)  Treatment of choice; procedure varies with the cause
 If generalized: diffuse pain over the abdomen of peritonitis

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Nursing considerations
Key outcomes
The patient will:
 regain normal vital signs
 express feelings of increased comfort
 maintain normal fluid volume
 show no signs or symptoms of infection.

Nursing interventions
 Administer prescribed drugs.
 Encourage early postoperative ambulation.
 Encourage the patient to express his feelings.
 Provide emotional support.

Monitoring
 Fluid and nutritional status
 Pain control
 Vital signs
 NG tube function and drainage
 Bowel function
 Wound site
 Signs and symptoms of dehiscence

ALERT
Watch for signs and symptoms of abscess forma-
tion, including persistent abdominal tenderness
and fever.

Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatment
 preoperatively, coughing and deep-breathing tech-
niques
 postoperative care procedures
 signs and symptoms of infection
 proper wound care
 medication administration, dosage, and possible
adverse effects
 dietary and activity limitations (depending on type of
surgery).
Discharge planning
 Refer the patient to home care services as needed.

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Risk factors
Pertussis  Incomplete immunization

Incidence
Overview  50% of cases seen in underimmunized children
younger than age 1
Description  Commonly occurs in schools, nursing homes, and
 Highly contagious respiratory infection residential facilities
 Typically causes an irritating cough that becomes  Epidemics occurring every 3 to 5 years without sea-
paroxysmal and ends in a high-pitched, inspiratory sonal variation
whoop
 Follows a 6- to 8-week course that includes three Common characteristics
2-week stages with varying symptoms Catarrhal (first) stage
 Also called whooping cough  Hacking nocturnal cough
 Anorexia
Pathophysiology  Sneezing, lacrimation, and rhinorrhea
 The infecting organism adheres to ciliated epithelial Paroxysmal (second) stage
cells and multiplies.  Spasmodic, recurrent coughing (usually at night)
 The resulting local mucosal damage induces parox- with tenacious mucus; cough typically ends in a loud,
ysmal coughing, which enhances disease transmis- crowing, inspiratory whoop
sion.  Vomiting if the patient chokes on mucus
 Various toxins produced during the infection impair Convalescent (third) stage
local defenses and cause local tissue damage. Toxins  Gradual subsidence of paroxysmal coughing and
may cause direct central nervous system injury. vomiting
Causes Complications
 Nonmotile, gram-negative coccobacillus B. pertussis;  Increased venous pressure
occasionally, B. parapertussis or B. bronchiseptica  Anterior eye chamber hemorrhage
(see Bordetella pertussis)  Detached retina and blindness
 Typically transmitted by direct inhalation of contami-  Rectal prolapse
nated droplets from someone in the acute disease  Inguinal or umbilical hernia
stage  Encephalopathy, seizures
 Spreads indirectly through soiled linen and other ar-  Atelectasis, pneumonitis, or pneumonia
ticles contaminated by respiratory secretions  In infants: apnea, anoxia
 Otitis media
 Pneumonia
Bordetella pertussis
This microscopic enlargement shows Bordetella pertussis, Assessment
the nonmotile, gram-negative coccobacillus that
commonly causes whooping cough. After entering the tra- History
cheobronchial tree, pertussis causes mucus to become in-
 Possible lack of immunization coupled with exposure
creasingly tenacious. The classic 6-week course of
whooping cough follows. to pertussis during previous 3 weeks
Physical findings
 Low or normal body temperature
 Mild conjunctivitis
 Listlessness
 Engorged neck veins
 Epistaxis during paroxysmal coughing
 Exhaustion and cyanosis after coughing spell
 Diminished breath sounds, upper airway wheezing

Test results
Laboratory
 White blood cell count and differential show lympho-
cytosis.
 B. pertussis is found in nasopharyngeal swabs and
sputum culture in early disease stages.
 Direct immunofluorescence shows antigen.

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 importance of immunization and vaccinations and

Treatment the need to notify the physician of adverse reactions
to the vaccine.
General
 For infants and elderly patients: hospitalization with Discharge planning
vigorous supportive therapy and fluid and electrolyte  Refer the patient to a pulmonologist for follow-up
replacement care, as indicated.
 Oxygen therapy, as warranted
 Adequate nutrition with small, frequent meals
 Increased fluid intake
 Rest periods when fatigued

Medications
 Antitussives
 Antibiotics, such as erythromycin, azithromycin, and
clarithromycin

Nursing considerations
Key outcomes
The patient will:
 remain free from adventitious breath sounds
 maintain a patent airway
 regain normal arterial blood gas levels
 show no evidence of pathogens in cultures.

Nursing interventions
 Maintain respiratory isolation (mask only) for 5 to
7 days after antibiotic therapy begins.
 Provide oxygen and moist air, as ordered; if needed,
assist respiration.
 Suction secretions, as necessary. Elevate the head of
the bed to ease breathing.
 Create a quiet environment to decrease coughing
stimulation.
 Assess for complications caused by excessive
coughing.
 Provide emotional support to the patient and parents,
as appropriate.
 Report pertussis cases to local public health authori-
ties.
Monitoring
 Respiratory status
 Acid-base balance
 Fluid and electrolyte balance

Patient teaching
Be sure to cover (with the patient or parents, as appro-
priate):
 the disease process and medical procedures
 need for the patients close contacts to get medical
care
 when to notify the physician

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Physical findings
Pharyngitis  Mild fever
 Fiery red appearance of the posterior pharyngeal
wall
Overview  Swollen, exudate-flecked tonsils
 Lymphoid follicles
Description Bacterial pharyngitis
 Acute or chronic inflammation of the pharynx  Acutely inflamed throat, with patches of white and
 Most common throat disorder yellow follicles
 Usually subsides in 3 to 10 days unless complications  Strawberry-red tongue
occur  Enlarged, tender cervical lymph nodes

Pathophysiology Test results

 Cellular damage caused by a virus or bacteria causes Laboratory
an inflammatory response.  Throat culture identifies the causative organism.
 Hyperemia and fluid exudation result.  Rapid strep test shows group A beta-hemolytic strep-
tococcal infection.
Causes  White blood cell count and differential show atypical
 Viral or bacterial infection lymphocytes.
 Beta-hemolytic streptococci (15% to 20% of acute Imaging
pharyngitis cases)  Computed tomography scan identifies abscesses.
 Mononucleosis
In children
 Streptococcal bacteria infections Treatment
Gonococcal pharyngitis
 Release of a toxin produced by Corynebacterium General
diphtheria  Warm saline gargles
Fungal pharyngitis  Hospitalization for dehydration
 Prolonged antibiotic use (in immunosuppressed  Elimination of the underlying cause
patients)  Adequate humidification
 Adequate fluid intake
Incidence  Avoidance of citrus juices
Widespread among adults who:  Bed rest while febrile
 live or work in dusty or dry environments
 use their voices excessively Medications
 use tobacco or alcohol habitually  Anesthetic throat lozenges
 suffer from chronic sinusitis, persistent coughs, or  Analgesics as needed
allergies  Antibiotics as appropriate
 Antifungal agents (for fungal pharyngitis)
Common characteristics  Equine antitoxins (for diphtherial pharyngitis)
 Sore throat
 Pharyngeal edema Surgery
 Abscess drainage
Complications
 Otitis media
 Sinusitis Nursing considerations
 Mastoiditis
 Rheumatic fever Key outcomes
 Nephritis The patient will:
 maintain intact mucous membranes
 maintain normal fluid volume
Assessment  express feelings of increased comfort
 achieve adequate daily calorie intake.
History
 Sore throat Nursing interventions
 Slight difficulty swallowing (swallowing saliva more  Administer prescribed drugs.
painful than swallowing food)  Obtain throat cultures, as ordered.
 Sensation of a lump in the throat  Instruct the patient to use warm saline gargles.
 Constant, aggravating urge to swallow  Encourage adequate oral fluid intake.
 Headache  Perform meticulous mouth care.
 Muscle and joint pain  Maintain a restful environment.

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Monitoring
 Intake and output
 Signs and symptoms of dehydration

ALERT
Examine the patients skin twice per day for rashes
caused by drug sensitivity or rashes that could in-
dicate a communicable disease.

Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatment
 importance of completing prescribed antibiotic
therapy
 medication administration, dosage, and possible
adverse effects
 preventive measures, such as hand washing and
avoiding close contact with people who are sick
 avoidance of excessive exposure to air conditioning
 smoking cessation
 ways to minimize environmental sources of throat
irritation
 importance of throat cultures for all family members
if the patient has a streptococcal infection.
Discharge planning
 Refer the patient to a smoking-cessation program, if
indicated.

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Pheochromocytoma ALERT
Pheochromocytoma may occur during pregnancy
when uterine pressure on the tumor causes more
Overview frequent hypertensive crises. These crises carry a
high risk for spontaneous abortion and can be fa-
Description tal for both the mother and fetus.
 Catecholamine-producing tumor, typically benign;
usually derived from adrenal medullary cells
 Most common cause of adrenal medullary hyper- Assessment
secretion
 Usually produces norepinephrine; large tumors se- History
crete both epinephrine and norepinephrine  Unpredictable episodes of hypertensive crisis
 Potentially fatal, but with treatment carries a good  Paroxysmal symptoms suggesting a seizure disorder
prognosis or anxiety attack
 Also known as chromaffin tumor  Hypertension that responds poorly to conventional
treatment
Pathophysiology  Hypotension or shock after surgery or diagnostic
 Pheochromocytoma causes excessive catecholamine procedures
production from autonomous tumor functioning. During paroxysms or crises
 The tumor stems from a chromaffin cell tumor of the  Throbbing headache
adrenal medulla or sympathetic ganglia (more com-  Palpitations
monly in the right adrenal gland than in the left).  Visual blurring
 Extra-adrenal pheochromocytomas may occur in the  Nausea and vomiting
abdomen, thorax, urinary bladder, and neck and in  Severe diaphoresis
association with the 9th and 10th cranial nerves.  Feelings of impending doom
 Precordial or abdominal pain
Causes  Moderate weight loss
 May be inherited as an autosomal dominant trait  Dizziness or light-headedness when moving to an
upright position
Incidence
 Rare; seen in about 0.5% of newly diagnosed hyper- Physical findings
tensive patients During paroxysms or crises
 Seen in all races  Hypertension
 Affects both sexes equally  Tachypnea
 Typically familial  Pallor or flushing
 Most common in patients ages 30 to 50  Profuse sweating
 Tremor
Common characteristics  Seizures
 Paroxysmal or sustained hypertension  Tachycardia
 Hypertensive crises triggered by conditions that dis-
place the abdominal contents or by use of opiates, Test results
histamine, glucagon, or corticotropin Laboratory
 Headache  Vanillylmandelic acid and metanephrine levels in a
 Flushing 24-hour urine specimen are increased.
 Diaphoresis  Total plasma catecholamine levels are 10 to 50 times
 Tachycardia higher than normal on direct assay.
 Retinal changes Imaging
 Computed tomography (CT) scan or magnetic reso-
Complications nance imaging of adrenal glands may show intra-
 Stroke adrenal lesions.
 Retinopathy  CT scan, chest X-rays, or abdominal aortography may
 Irreversible kidney damage reveal extra-adrenal pheochromocytoma.
 Acute pulmonary edema
 Cholelithiasis
 Cardiac arrhythmias Treatment
 Heart failure
General
 High-protein diet with adequate calories
 Rest during acute attacks

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Medications After adrenalectomy

 Alpha-adrenergic blockers such as phenoxybenza-  Vital signs
mine  Bowel sounds
 Catecholamine-synthesis antagonists  Wound dressings
 Beta-adrenergic blockers such as atenolol  Incision
 Calcium channel blockers  Signs and symptoms of hemorrhage
 I.V. phentolamine or nitroprusside during paroxysms  Pain
or crises

ALERT
Because severe and occasionally fatal paroxysms
have been induced by opiates, histamines, and oth-
er drugs, all medications should be considered
carefully and administered cautiously in patients
with known or suspected pheochromocytoma.
Surgery
 Removal of pheochromocytoma
Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatment
 medication administration, dosage, and possible
adverse effects
 when to notify the physician
 way to prevent paroxysmal attacks
 signs and symptoms of adrenal insufficiency
 importance of wearing medical identification jewelry
 how to monitor his own blood pressure.

Discharge planning
Nursing considerations  Refer family members for genetic counseling if auto-
somal dominant transmission of pheochromocytoma
Key outcomes is suspected.
The patient will:
 maintain stable vital signs
 maintain fluid balance
 maintain normal cardiac output
 express feelings of increased comfort
 avoid complications.

Nursing interventions
 Take orthostatic blood pressures.
 Administer prescribed drugs.
 Ensure the reliability of urine catecholamine mea-
surements.
 Provide comfort measures.
 Consult a dietitian, as needed.
 Tell the patient to report symptoms of an acute
attack.
 Encourage the patient to express his feelings.
 Help the patient develop effective coping strategies.
After adrenalectomy

ALERT
Be aware that postoperative hypertension is com-
mon because the stress of surgery and adrenal
gland manipulation stimulate catecholamine se-
cretion.

Monitoring
 Vital signs, especially blood pressure
 Serum glucose level
 Daily weight
 Neurologic status
 Renal function
 Cardiovascular status
 Adverse reactions to medications

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Complications
Pituitary tumors  Endocrine abnormalities throughout the body, unless
lost hormones are replaced
 Diabetes insipidus from tumor compression of the
Overview hypothalamus
Description
 Nonmalignant intracranial tumor; accounts for 10% Assessment
of all intracranial neoplasms
 Most common tumor tissue types: chromophobe ade- History
noma (90%), basophil adenoma, and eosinophil  Neurologic and endocrine abnormalities
adenoma  Personality changes or dementia
 Most common site: anterior pituitary (adenohypoph-  Amenorrhea
ysis)  Decreased libido
 Considered a neoplastic condition because of the  Impotence
tumors invasive growth  Lethargy, weakness, increased fatigability
 Carries a fair to good prognosis, depending on how  Sensitivity to cold
far the tumor spreads beyond the sella turcica  Constipation
 Seizures
Pathophysiology  With cranial nerve involvement: diplopia and dizzi-
 As a pituitary adenoma grows, it replaces normal ness
glandular tissue and enlarges the sella turcica (which
houses it). Physical findings
 Chromophobe adenoma may be associated with pro-  Rhinorrhea
duction of corticotropin, melanocyte-stimulating hor-  Head tilting during physical examination
mone, growth hormone, and prolactin.  Skin changes
 Basophil adenoma may be associated with excess  Strabismus
corticotropin production and, consequently, Cush-
ings syndrome. Test results
 Eosinophil adenoma may be associated with exces- Laboratory
sive growth hormone.  Cerebrospinal fluid analysis shows an increased pro-
tein level.
Causes Imaging
 Unknown  Skull X-rays with tomography may show an enlarged
sella turcica or erosion of its floor; if growth hor-
Risk factors mone secretion predominates, X-rays show enlarge-
 Autosomal dominant trait ment of the paranasal sinuses and mandible, thick-
ened cranial bones, and separated teeth.
Incidence  Carotid angiography may identify displacement of the
 Affects adults of both sexes between ages 30 and 50 anterior cerebral and internal carotid arteries from
 Twice as common in females as in males tumor enlargement and may rule out intracerebral
aneurysm.
Common characteristics  Computed tomography scan may confirm an adeno-
 Headache, visual changes, double vision, and droop- ma and accurately depict its size.
ing eyelids  Magnetic resonance imaging scan differentiates
 Nipple discharge healthy, benign, and malignant tissues and blood
 Gynecomastia vessels.
 Menses cessation
 Decreased libido, male impotence
 Cold intolerance Treatment
 Nausea, vomiting, and constipation
 Personality changes General
 Skin changes  Radiation therapy used for small, nonsecretory tu-
 Hair loss mors confined to the sella turcica or for patients
 Fatigue considered poor surgical risks
 Seizures  Individualized diet according to tumor manifesta-
 Hypotension tions; possible sodium or caloric restriction
 In initial postoperative period, avoidance of cough-
ing, sneezing, bending, and other movements that

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may increase intracranial pressure (ICP) or cause  medication administration, dosage, and possible ad-
cerebrospinal fluid leakage verse effects
 importance of immediately reporting persistent post-
Medications nasal drip or constant swallowing.
 Corticosteroids or thyroid or sex hormones
 Electrolyte replacement Discharge planning
 Insulin  Encourage the patient to wear medical identification
 Bromocriptine and cabergoline for prolactin- that indicates his medical condition and its proper
producing tumors treatment.
 Octreotide acetate and pegvisomant for growth hor-
mone producing tumors
Surgery
 Transfrontal removal of a large tumor impinging on
the optic apparatus
 Transsphenoidal resection for a smaller tumor con-
fined to the pituitary fossa
 Cryohypophysectomy

Nursing considerations
Key outcomes
The patient will:
 remain free from injury
 express positive feelings about himself
 report an increased sense of well-being
 exhibit increased energy
 participate in care and prescribed therapies (along
with family members).
Nursing interventions
 Administer prescribed drugs.
 Maintain patient safety.
 Provide rest periods to avoid fatigue.
 Establish a supportive, trusting relationship with the
patient.
Monitoring
After supratentorial or transsphenoidal
hypophysectomy
 Proper positioning (head of the bed elevated 30 de-
grees)
 Intake and output
 Signs and symptoms of infection
 Blood glucose level
After craniotomy
 Vital signs
 Neurologic status
 Signs and symptoms of increased ICP

Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatment
 preoperative instructions on surgery, treatments, and
postoperative course
 avoidance of coughing, sneezing, and bending

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Placenta previa Assessment

History
Overview  Onset of painless, bright red, vaginal bleeding after
20th week of pregnancy
Description  Vaginal bleeding before labor onset, typically episod-
 Placental implantation in the lower uterine segment, ic and stopping spontaneously
encroaching on the internal cervical os  May be asymptomatic
 Common cause of bleeding during the second half of
pregnancy (Among patients who develop placenta Physical findings
previa during the second trimester, less than 15%  Soft, nontender uterus
have persistent previa at term.)  Fetal malpresentation
 Carries good maternal prognosis if hemorrhage can  Minimal descent of fetal presenting part
be controlled  Good fetal heart tones
 Usually necessitates pregnancy termination if bleed-
ing is heavy Test results
 Fetal prognosis dependent on gestational age and Laboratory
amount of blood lost; risk for death greatly reduced  Maternal hemoglobin level is decreased.
by frequent monitoring and prompt management Imaging
 Transvaginal ultrasound scan determines placental
Pathophysiology position.
 The placenta covers all or part of the internal cervi- Diagnostic procedures
cal os. (See Three types of placenta previa.)  Pelvic examination confirms diagnosis.

Causes
ALERT
 Unknown
Pelvic examination isnt commonly performed be-
Risk factors cause it increases maternal bleeding and can dis-
 Defective vascularization of the decidua lodge more of the placenta.
 Multiple pregnancy
 Previous uterine surgery
 Multiparity Treatment
 Advanced maternal age
 Endometriosis General
 Smoking  Control of blood loss, blood replacement
 Delivery of viable neonate
Incidence  Prevention of coagulation disorders
 About 1 in every 200 pregnancies  With premature fetus, careful observation to give fe-
 More common in multigravidas than primigravidas tus more time to mature
 Occurs more commonly after age 35  With complete placenta previa, hospitalization
 Possible vaginal delivery (if bleeding is minimal and
Common characteristics placenta previa is marginal or when labor is rapid)
 Painless, bright red, vaginal bleeding
 Vaginal bleeding after 20th week of pregnancy ALERT
Complications Because of possible fetal blood loss through the pla-
 Anemia centa, a pediatric team should be on hand during
 Hemorrhage delivery to immediately assess and treat neonatal
 Disseminated intravascular coagulation shock, blood loss, and hypoxia.
 Shock
 Renal damage  Nothing by mouth initially, then as guided by clinical
 Cerebral ischemia status
 Maternal or fetal death  Bed rest

Medications
 I.V. fluids, using large-bore catheter

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Three types of placenta previa

The degree of placenta previa depends largely on the extent of cervical dilation at the time of examination because the dilat-
ing cervix gradually uncovers the placenta, as shown below.
Marginal placenta previa Partial placenta previa Total placenta previa
If the placenta covers just a fraction of The patient has the partial, or incom- If the placenta covers all of the internal
the internal cervical os, the patient has plete, form of the disorder if the pla- os, the patient has total, complete, or
marginal, or low-lying, placenta previa. centa caps a larger part of the internal central placenta previa.
os.

Surgery Patient teaching

 Immediate cesarean delivery in case of severe hem-
orrhage or as soon as fetus is sufficiently mature Be sure to cover:
 the disorder, diagnosis, and treatment
 signs and symptoms of placenta previa
Nursing considerations  possibility of emergency cesarean delivery
 possibility of the birth of a premature neonate
Key outcomes  possibility of neonatal death
The patient will:  postpartum physical and emotional changes to
 maintain stable vital signs expect.
 maintain normal fluid volume
 express feelings of increased comfort Discharge planning
 verbalize her feelings about her condition  Refer the patient for professional counseling if neces-
 use available support systems to aid coping. sary.
Nursing interventions
 Obtain blood samples for complete blood count and
blood type and crossmatch.
 Initiate external electronic fetal monitoring.
 Administer prescribed I.V. fluids and blood products.
 If the patient is Rh-negative, give Rho(D) immune
globulin (RhoGAM) after every bleeding episode, as
ordered.
 Offer emotional support during labor.
 Provide information about labor progress and the
condition of the fetus.
 Encourage the patient to express her feelings.
 Help the patient develop effective coping strategies.

Monitoring
 Vital signs
 Vaginal bleeding, including character of blood loss
 Central venous pressure
 Intake and output
 Fetal heart tones
 Signs and symptoms of hemorrhage and shock

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Incidence
Life-threatening disorder  Becoming more prevalent in the United States
 Most common between May and September; in

Plague hunters who skin wild animals, between October and

February
 Affects both sexes equally

Overview Common characteristics

 Fever
Description  Chills
 Acute, febrile, zoonotic infection caused by the gram-  Weakness
negative, nonsporulating bacillus Yersinia pestis  Headache
 Usually transmitted to humans through the bite of a Bubonic plague
flea from an infected rodent host, such as a rat or  Characteristic buboes
squirrel; occasional transmission from handling in-  History of exposure to rodents
fected animals or their tissues (see Bubonic plague
carrier) Complications
 Potential bioterrorism and biological warfare agent  Peritoneal or pleural effusions
Forms of plague  Septicemia
 Bubonic: most common form; causes swollen and  Fulminant pneumonia
sometimes suppurating, lymph glands (buboes)  Pericarditis
 Septicemic: rapid, severe systemic form  Seizures
 Pneumonic: can be primary or secondary to the oth-  Diffuse interstitial myocarditis
er two forms; highly contagious, with secondary  Multifocal hepatic necrosis
spread a serious concern (Primary pneumonic  Diffuse hemorrhagic splenic necrosis
plague is an acutely fulminant form causing acute  Respiratory failure
prostration, respiratory distress, and death, possibly  Cardiovascular collapse
within 2 to 3 days after onset. Secondary pneumonic  Disseminated intravascular coagulation
plague is transmitted by contaminated respiratory  Meningitis
droplets.)  Death
 Without treatment, 60% mortality in bubonic plague
and nearly 100% in septicemic and pneumonic
plague; with treatment, 18% mortality Assessment
Pathophysiology History
 Y. pestis is one of the most invasive bacterium Milder form of bubonic plague
known; mechanisms by which it causes disease  History of exposure to rodents
arent fully understood.  Malaise
 Once inoculated through the skin or mucous mem-  Fever
branes, Y. pestis usually invades cutaneous lymphatic  Excruciatingly painful bubo
vessels and regional lymph nodes; direct blood- Severe form of bubonic plague
stream inoculation may also occur.  Sudden fever of 103 to 106 F (39.4 to 41.1 C)
 Organisms are probably phagocytized by mononu-  Chills, myalgia, and headache
clear phagocytes without being destroyed and are  Restlessness, disorientation
then disseminated to distant sites in the body.  Abdominal pain, nausea, and vomiting
 Plague can involve almost any organ and usually re-  Constipation followed by bloody diarrhea
sults in massive and widespread tissue destruction,
especially if left untreated. Physical findings
Milder form of bubonic plague
Causes  Fever
 Y. pestis  Pain or tenderness in regional lymph nodes
 Painful, inflamed, and possibly suppurative buboes
Risk factors (usually in the axillary, cervical, or inguinal areas)
 Rural areas  Necrotization of hemorrhagic areas
 Urban areas with overcrowding, poor sanitation, and  Moribund state within hours after onset
large rat populations Bubonic plague
 Veterinarians  Fever
 Cat owners  Prostration
 Hunters, campers, and hikers in outbreak areas  Restlessness, disorientation, delirium
 Toxemia

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 Staggering gait Bubonic plague carrier

 Skin mottling, petechiae
Bubonic plague is usually transmitted to humans through
 Circulatory collapse
the bite of an infected flea (Xenopsylla cheopis), shown
 Coma here.
Test results
Laboratory
 Y. pestis is found in capsular antigen testing, Wayson
stain, or fluorescent antibody stain.
 White blood cell count is greater than 20,000/l,
with increased polymorphonuclear leukocytes and
hemoagglutination reaction.
 Y. pestis is present in culture and Gram stain of skin-
lesion needle aspirate or lymph node aspirate, blood,
or sputum.
Imaging
 Chest X-rays show fulminating pneumonia in pneu-
monic plague.

Treatment
General  Maintain a patent airway and adequate oxygenation.
 Supportive management to control fever, shock, and  Apply warm, moist compresses to buboes.
seizures and maintain fluid balance  Provide meticulous skin care.
 Warm, moist compresses on buboes  Prevent further injury to necrotic tissue areas.
 Diet, as tolerated  Institute seizure precautions.
 Tube feedings or total parenteral nutrition, if re-  Report suspected plague cases to local public health
quired department.
 Supplemental I.V. fluids
 Bed rest during the acute phase Monitoring
 Vital signs
Medications  Intake and output
 Antibiotics, such as streptomycin and gentamicin  Skin integrity
 Oxygen  Pulmonary status
 Corticosteroids  Cardiovascular status
 Benzodiazepines  Nutritional status
 Anticonvulsants  Seizures
 Antipyretics  Complications
 Abnormal bleeding
Surgery  Mentation
 Incision and drainage of necrotic buboes

Patient teaching
Nursing considerations
Be sure to cover:
Key outcomes  the disorder, diagnosis, and treatment
The patient will:  medication administration, dosage, and possible ad-
 maintain acceptable tissue perfusion and cellular verse effects
oxygenation  isolation procedures
 maintain effective ventilation  personal protective measures
 maintain fluid balance  avoidance of contact with sick or dead wild animals
 verbalize feelings of fear and anxiety and the need to wear gloves when handling animal
 demonstrate effective coping mechanisms. carcasses
 importance of insect and rodent population control
Nursing interventions  use of repellents, insecticides, and protective cloth-
 Administer drugs, I.V. fluids, and oxygen, as pre- ing when at risk for exposure to rodents fleas
scribed and needed.  elimination of rodent food and habitats
 If pneumonic plague, use standard and droplet pre-  insecticide control of fleas.
cautions.
 Provide adequate nutrition.

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Pleural effusion and Assessment

empyema History
 Underlying pulmonary disease
 Shortness of breath
Overview  Chest pain
 Malaise
Description
 Fluid accumulation in the pleural space; the fluid Physical findings
may be extracellular, pus (empyema), blood (hemo-  Fever
thorax), chyle (chylothorax), or bilious  Trachea deviated away from the affected side
 Effusion classified as transudative or exudative  Dullness and decreased tactile fremitus over the effu-
sion
Pathophysiology  Diminished or absent breath sounds
 Typically, fluid and other blood components migrate  Pleural friction rub
through the walls of intact capillaries bordering the  Bronchial breath sounds
pleura.  In empyema, foul-smelling sputum
 In transudative effusion, fluid is watery and diffuses
out of the capillaries if hydrostatic pressure increases Test results
or capillary oncotic pressure decreases. Laboratory
 In exudative effusion, inflammatory processes in- PLEURAL FLUID ANALYSIS FINDINGS
crease capillary permeability. Exudative effusion is  In transudative effusion: specific gravity is less than
less watery and contains high concentrations of white 1.015 and protein level is less than 3 g/dl.
blood cells and plasma proteins.  In exudative effusion: ratio of protein in pleural fluid
 Empyema occurs when pulmonary lymphatics be- to protein in serum is 0.5 or higher; lactate dehydro-
come blocked, leading to outpouring of contaminat- genase (LD) level is 200 IU or higher; ratio of LD in
ed lymphatic fluid into the pleural space. pleural fluid to LD in serum is 0.6 or higher.
 In empyema: microorganisms are present, white
Causes blood cell count is increased, and glucose level is
Transudative pleural effusion decreased.
 Cardiovascular disease  In esophageal rupture or pancreatitis: pleural fluid
 Hepatic disease amylase levels exceede serum amylase levels.
 Renal disease Imaging
 Hypoproteinemia  Chest X-rays may show pleural effusions; lateral de-
Exudative pleural effusion cubitus films may show loculated pleural effusions or
 Pleural infection small pleural effusions not visible on standard chest
 Pleural inflammation X-rays.
 Pleural malignancy  Computed tomography scan of the thorax shows
Empyema small pleural effusions.
 Pulmonary infection Diagnostic procedures
 Lung abscess  Thoracentesis obtains pleural fluid specimens for
 Infected wound analysis.
 Intra-abdominal infection Other
 Thoracic surgery  Tuberculin skin test may be positive for tuberculosis.
 Pleural biopsy may be positive for carcinoma.
Incidence
 Can occur at any age
 Affects both sexes equally Treatment
Common characteristics General
 Shortness of breath  Thoracentesis to remove fluid
 Chest pain  Possible chest tube insertion
 Malaise  Possible chemical pleurodesis
 Nonproductive cough  High-calorie diet
 Activity, as tolerated
Complications
 Atelectasis Medications
 Infection  Antibiotics
 Hypoxemia  Oxygen

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Surgery
 Removal of thick coating over lung (decortication)

Nursing considerations
Key outcomes
The patient will:
 maintain adequate ventilation
 remain free from signs and symptoms of infection
 consume the specified number of calories daily
 express an understanding of the illness
 demonstrate effective coping mechanisms.

Nursing interventions
 Administer prescribed drugs and oxygen.
 Assist during thoracentesis.
 Encourage the patient to use an incentive spirometer.
 Encourage deep-breathing exercises.
 Provide meticulous chest tube care.
 Ensure chest tube patency.
 Keep petroleum gauze at the bedside.

Monitoring
 Vital signs
 Intake and output
 Respiratory status
 Pulse oximetry
 Signs and symptoms of pneumothorax
 Chest tube drainage

Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatment
 medication administration, dosage, and possible
adverse effects
 how thoracentesis is performed
 chest tube insertion and drainage
 signs and symptoms of infection
 signs and symptoms of pleural fluid reaccumulation
 when to notify the physician.

Discharge planning
 Provide a home health referral for follow-up care.
 Refer the patient to a smoking-cessation program, if
indicated.

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Physical findings
Pleurisy  Characteristic late-inspiration and early-expiration
pleural friction rub
 Coarse vibration on palpation of the affected area
Overview
Test results
Description Imaging
 Inflammation of the visceral and parietal pleurae that  Chest X-rays show absence of pneumonia.
line the inside of the thoracic cage and envelop the Diagnostic procedures
lungs  Electrocardiography shows absence of ischemic
 Also called pleuritis heart disease.
Pathophysiology
 The pleurae become swollen and congested. Treatment
 As a result, pleural fluid transport is hampered, and
friction between the pleural surfaces increases. General
 Symptomatic
Causes  Possible intercostal nerve block
 Pneumonia  Diet, as tolerated
 Tuberculosis  Bed rest
 Viruses
 Systemic lupus erythematosus Medications
 Rheumatoid arthritis  Anti-inflammatories
 Uremia  Analgesics
 Dresslers syndrome
 Cancer Surgery
 Pulmonary infarction  Thoracentesis
 Chest trauma
 Pathologic rib fractures
 Pneumothorax Nursing considerations
 Sickle cell disease
 Radiation therapy Key outcomes
 Human immunodeficiency virus The patient will:
 Certain drugs, such as methotrexate or penicillin  maintain a patent airway
 maintain adequate ventilation
Incidence  express feelings of increased comfort; relief of pain
 Affects both sexes equally  demonstrate energy conservation techniques
 demonstrate effective coping strategies.
Common characteristics
 Sudden dull, aching, burning, or sharp pain that Nursing interventions
worsens on inspiration  Administer prescribed drugs.
 Limited movement on the affected side during  Encourage deep breathing and coughing.
breathing  Encourage the patient to use an incentive spirometer.
 Shortness of breath  Assist the patient in splinting the affected side.
 Fever and chills  Position the patient in high Fowlers position.
 Plan care to allow frequent rest periods.
Complications  Assist with passive range-of-motion (ROM) exercises.
 Adhesions  Encourage active ROM exercises.
 Pleural effusion  Provide comfort measures.
 Chronic pain or shortness of breath  Assist with thoracentesis.
 Encourage verbalization and provide emotional
support.
Assessment
Monitoring
History  Vital signs
 Sudden dull, aching, burning, or sharp pain that  Intake and output
worsens on inspiration  Response to treatment
 Predisposing factor  Pain control
 Cough  Complications
 Shortness of breath  Breath sounds
 Fever  Respiratory status

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Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatment
 medication administration, dosage, and possible
adverse effects
 how to perform splinting and deep-breathing
exercises
 importance of regular rest periods
 signs and symptoms of possible complications
 when to notify the physician.

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Physical findings
Life-threatening disorder  Low-grade, intermittent fever
 Tachypnea

Pneumocystis carinii  Dyspnea

 Accessory muscle use for breathing

pneumonia  Cyanosis (with acute illness)

 Dullness on percussion (with consolidation)
 Crackles
 Decreased breath sounds
Overview
Test results
Description Laboratory
 Communicable, opportunistic lung infection com-  P. carinii is found on histologic sputum specimen
monly associated with human immunodeficiency studies.
virus (HIV)  Hypoxia and increased A-a gradient on arterial blood
 A leading cause of opportunistic infection and death gas (ABG) values are seen.
among patients with acquired immunodeficiency syn- Imaging
drome (AIDS) in industrialized countries  Chest X-rays may show slowly progressing, fluffy infil-
trates, occasional nodular lesions, or spontaneous
Pathophysiology pneumothorax.
 The infecting organism invades the lungs bilaterally,  Gallium scan may show increased uptake over the
multiplies extracellularly, and fills alveoli with organ- lungs.
isms and exudate. Diagnostic procedures
 As a result, gas exchange is impaired.  Fiber-optic bronchoscopy
 Alveoli hypertrophy and thicken, eventually leading to  Transbronchial biopsy
extensive consolidation.  Open lung biopsy

Causes
 P. carinii; spreads mainly through the air (although Treatment
part of the normal flora in most healthy people, this
organism becomes an aggressive pathogen in im- General
munocompromised patients)  Oxygen therapy
 Possible role of B-cell function defects  Mechanical ventilation
 High-calorie, high-protein diet
Risk factors  Nutritional supplements, as needed
 HIV/AIDS  Small, frequent meals
 Immunosuppression  Increased fluid intake
 Immunodeficiency disorders  Rest periods when fatigued

Incidence Medications
 Most common in premature or malnourished infants,  Co-trimoxazole (may be given prophylactically to
children with primary immunodeficiency disease, pa- AIDS and other high-risk patients)
tients receiving immunosuppressive therapy, and  Pentamidine
those with HIV/AIDS
Common characteristics Nursing considerations
 Insidious onset, with increasing shortness of breath
and nonproductive cough Key outcomes
 Hypoxemia and hypercapnia (may not cause signifi- The patient will:
cant clinical symptoms)  maintain normal vital signs
 maintain adequate fluid volume
Complications  maintain normal breath sounds
 Disseminated infection  regain normal ABG values
 Pulmonary insufficiency and death  demonstrate correct bronchial hygiene techniques
 verbalize fears, feelings, and concerns.

Assessment Nursing interventions

 Implement standard precautions.
History  Administer prescribed drugs and oxygen.
 Immunodepression, as from HIV infection, leukemia,  Encourage ambulation, deep-breathing exercises,
lymphoma, or organ transplantation and use of an incentive spirometer.

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 Provide adequate rest periods.

 Encourage the patient to express fears, feelings, and
concerns.
 Provide emotional support.

Monitoring
 Respiratory status
 ABG values
 Fluid and electrolyte status

Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatment
 medication administration, dosage, and possible
adverse effects
 energy conservation techniques
 importance of taking prophylactic drugs to prevent
recurrence (for HIV-infected patients and other
immunocompromised individuals)
 home oxygen therapy, if indicated.

Discharge planning
 Refer the patient to a pulmonologist or an infectious
disease specialist for follow-up care, as needed.
 If the patient has AIDS or HIV, provide information
about resources and support organizations.

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Pneumonia Special populations

Incidence and mortality are highest in elderly
patients.
Overview
Description Common characteristics
 Acute infection of the lung parenchyma impairing gas  Pleuritic chest pain
exchange  Cough
 May be classified by etiology, location, or type  Excessive sputum production
 Chills
Pathophysiology
 A gel-like substance forms as microorganisms and Complications
phagocytic cells break down.  Septic shock
 This substance consolidates within the lower airway  Hypoxemia
structure.  Respiratory failure
 Inflammation involves the alveoli, alveolar ducts, and  Empyema
interstitial spaces surrounding the alveolar walls.  Bacteremia
 In lobar pneumonia, inflammation starts in one area  Endocarditis
and may extend to the entire lobe. In bronchopneu-  Pericarditis
monia, it starts simultaneously in several areas, pro-  Meningitis
ducing patchy, diffuse consolidation. In atypical  Lung abscess
pneumonia, inflammation is confined to the alveolar  Pleural effusion
ducts and interstitial spaces.
Causes Assessment
 Bacterial or viral organism
 Aspiration of foreign matter History
Bacterial pneumonia
Risk factors  Sudden onset of:
Bacterial and viral pneumonia Pleuritic chest pain
 Chronic illness and debilitation Cough
 Cancer Purulent sputum production
 Abdominal and thoracic surgery Chills
 Atelectasis Viral pneumonia
 Bacterial or viral respiratory infections  Nonproductive cough
 Chronic respiratory disease  Constitutional symptoms
 Influenza  Fever
 Smoking Aspiration pneumonia
 Malnutrition  Fever
 Sickle cell disease  Weight loss
 Tracheostomy  Malaise
 Poor oral hygiene
 Immunosuppressive therapy Physical findings
 Endotracheal intubation or mechanical ventilation  Fever
Aspiration pneumonia  Sputum production
 Alcoholism  Dullness over the affected area
 Exposure to noxious gases  Crackles, wheezing, or rhonchi
 Caustic substance entering airway  Decreased breath sounds
 Advanced age  Decreased fremitus
 Debilitation  Tachypnea
 Nasogastric (NG) tube feedings  Use of accessory muscles
 Impaired gag reflex
 Decreased level of consciousness Test results
Laboratory
Incidence  Complete blood count shows leukocytosis.
 Affects both sexes and all ages  Blood cultures are positive for causative organism.
 More than four million cases annually in the United  Arterial blood gas (ABG) values show hypoxemia.
States  Fungal or acid-fast bacilli cultures identify the etio-
logic agent.

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 Assay for legionella soluble antigen in urine detects Prevention

presence of antigen. Preventing pneumonia
 Sputum culture, Gram stain, and smear reveal the
 Urge bedridden and postoperative patients to perform
infecting organism. deep-breathing and coughing exercises frequently. Po-
Imaging sition these patients properly to promote full aeration
 Chest X-rays generally show patchy or lobar infil- and secretion drainage.
trates.  Advise the patient to avoid using antibiotics indiscrimi-
Diagnostic procedures nately for minor infections. Doing so could produce
 Bronchoscopy or transtracheal aspiration specimens upper airway colonization with antibiotic-resistant bac-
identify the etiologic agent. teria. If pneumonia develops, the causative organisms
Other may require treatment with more toxic antibiotics.
 Pulse oximetry may reveal decreased oxygen satura-  Encourage the high-risk patient to ask the physician
tion. about an annual influenza vaccination and pneumococ-
cal pneumonia vaccination. A single dose of pneumo-
coccal vaccine is recommended for most patients age
Treatment 54 and older; certain patients may need one booster
dose after 5 years.
 Discuss ways to avoid spreading the infection to oth-
General
ers. Remind the patient to sneeze and cough into tis-
 Mechanical ventilation (positive end-expiratory pres- sues and to dispose of tissues in a waxed or plastic
sure) for respiratory failure bag. Advise the patient to wash his hands thoroughly
 High-calorie, high-protein diet after handling contaminated tissues.
 Adequate fluids
 Bed rest initially; progress as tolerated

Medications  Dispose of secretions properly.

 Antibiotics  Provide a quiet, calm environment with frequent rest
 Humidified oxygen periods.
 Antitussives  Include the patient in care decisions whenever
 Analgesics possible.
 Bronchodilators
Monitoring
Surgery  Vital signs
 Drainage of parapneumonic pleural effusion or lung  Intake and output
abscess  Daily weight
 Sputum production
 Respiratory status
Nursing considerations  Breath sounds
 Pulse oximetry
Key outcomes  ABG values
The patient will:
 maintain adequate ventilation
 maintain fluid balance Patient teaching
 maintain adequate caloric intake
 express feelings of increased comfort Be sure to cover:
 demonstrate effective coping strategies.  the disorder, diagnosis, and treatment
 medication administration, dosage, and possible
Nursing interventions adverse effects
 Administer prescribed drugs.  need for adequate fluid intake
 Administer prescribed I.V. fluids and electrolyte re-  importance of adequate rest
placement.  deep-breathing and coughing exercises
 Maintain a patent airway and adequate oxygenation.  chest physiotherapy
 Administer prescribed supplemental oxygen. Admin-  avoidance of irritants that stimulate secretions
ister oxygen cautiously if the patient has chronic lung  when to notify the physician
disease.  home oxygen therapy, if required
 Suction the patient, as needed.  ways to prevent pneumonia. (See Preventing pneu-
 Obtain sputum specimens, as needed. monia.)
 Provide a high-calorie, high-protein diet of soft
foods. Discharge planning
 Administer supplemental oral feedings, NG tube feed-  Refer the patient to a smoking-cessation program, if
ings, or parenteral nutrition, if needed. indicated.
 Take steps to prevent aspiration during NG feedings.

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 High positive end-expiratory pressures, causing rup-

Life-threatening disorder ture of alveolar blebs
 Chest tube occlusion or malfunction

Pneumothorax Risk factors

 Male gender
 Smoking
Overview  Lung disease
 History of pneumothorax
Description
 Accumulation of air or gas between the parietal and Incidence
visceral pleurae, leading to lung collapse  Occurs in 9,000 United States residents annually
 Degree of lung collapse determined by amount of
trapped air or gas Common characteristics
 Most common pneumothorax types: open, closed,  Sudden, sharp, pleuritic pain
and tension  Pain exacerbated by chest movement
 Shortness of breath
Pathophysiology
 Air accumulates and separates the visceral and pari- Complications
etal pleurae.  Fatal pulmonary and circulatory impairment
 Negative pressure is eliminated, affecting elastic re-
coil forces.
 The lung recoils and collapses toward the hilus. Assessment
 In open pneumothorax, atmospheric air flows direct-
ly into the pleural cavity, collapsing the lung on the History
affected side.  Possibly asymptomatic (with small pneumothorax)
 In closed pneumothorax, air enters the pleural space  Sudden, sharp, pleuritic pain
from within the lung, increasing pleural pressure and  Pain that worsens with chest movement, breathing,
preventing lung expansion. and coughing
 In tension pneumothorax, air in the pleural space is  Shortness of breath
under higher pressure than air in the adjacent lung.
Air enters the pleural space from a pleural rupture Physical findings
only on inspiration. This air pressure exceeds baro-  Asymmetrical chest wall movement
metric pressure, causing compression atelectasis. In-  Overexpansion and rigidity on the affected side
creased pressure may displace the heart and great  Possible cyanosis
vessels and cause mediastinal shift.  Subcutaneous emphysema
 Hyperresonance on the affected side
Causes  Decreased or absent breath sounds on the affected
Open pneumothorax side
 Penetrating chest injury  Decreased tactile fremitus over the affected side
 Central venous catheter insertion Tension pneumothorax
 Chest surgery  Distended jugular veins
 Transbronchial biopsy  Pallor
 Thoracentesis  Anxiety
 Percutaneous lung biopsy  Tracheal deviation away from the affected side
Closed pneumothorax  Weak, rapid pulse
 Blunt chest trauma  Hypotension
 Rib fracture  Tachypnea
 Clavicle fracture  Cyanosis
 Congenital bleb rupture
 Emphysematous bullae rupture Test results
 Barotrauma Laboratory
 Erosive tubercular or cancerous lesions  Arterial blood gas analysis may show hypoxemia.
 Interstitial lung disease Imaging
Tension pneumothorax  Chest X-rays may show air in the pleural space and,
 Penetrating chest wound possibly, a mediastinal shift.
 Lung or airway puncture from positive-pressure ven- Other
tilation  Pulse oximetry may show decreased oxygen satura-
 Mechanical ventilation after chest injury tion.

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ALERT
Treatment
Watch for signs and symptoms of tension pneu-
General mothorax, which can be fatal. These include
 Conservative treatment of spontaneous pneumotho- anxiety, hypotension, tachycardia, tachypnea,
rax with no signs of increased pleural pressure, less and cyanosis.
than 30% lung collapse, and no obvious physiologic
compromise
 Diet, as tolerated
 Bed rest Patient teaching
 Chest tube insertion
 Needle thoracostomy Be sure to cover:
 the disorder, diagnosis, and treatment
Medications  medication administration, dosage, and possible
 Oxygen adverse effects
 Analgesics  chest tube insertion
 deep-breathing exercises
Surgery  signs and symptoms of recurrent spontaneous pneu-
 Thoracotomy, pleurectomy for recurring sponta- mothorax and when to notify the physician.
neous pneumothorax
 Repair of traumatic pneumothorax Discharge planning
 Doxycycline or talc installation into pleural space  Refer the patient to a smoking-cessation program, if
appropriate.
Nursing considerations
Key outcomes
The patient will:
 maintain adequate ventilation
 remain free from signs and symptoms of infection
 express feelings of increased comfort
 demonstrate effective coping strategies.

Nursing interventions
 Administer prescribed drugs.
 Assist with chest tube insertion.

ALERT
If the chest tube dislodges, immediately place a pe-
troleum gauze dressing over the opening.

 Provide comfort measures.

 Encourage deep-breathing and coughing exercises.
 Offer reassurance, as appropriate.
 Include the patient and his family in care decisions
whenever possible.
Monitoring
 Vital signs
 Intake and output
 Respiratory status
 Breath sounds
 Chest tube system
 Complications
 Pneumothorax recurrence

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Cardiac arrhythmias
Life-threatening disorder Acute renal failure
Liver failure
Poisoning Test results
Laboratory
 Lactate level is either increased or decreased.
Overview  Serum calcium level is increased.
 Serum magnesium level is increased.
Description  Toxicology studies show poison levels in the patients
 Contact with a harmful substance by inhalation, in- mouth, vomitus, urine, feces, or blood, or on the pa-
gestion, injection, or skin contact tients hands or clothing.
 Prognosis varies with the amount of poison ab-  Arterial blood gas values identify hypoxemia or meta-
sorbed, its toxicity, and the time lapse between poi- bolic derangements.
soning and treatment  Imbalanced serum electrolyte levels such as hypo-
kalemia may show anion-gap metabolic acidosis.
Pathophysiology Imaging
 The disorder process varies with the type of poison.  Chest X-rays may show pulmonary infiltrates or ede-
ma in inhalation poisoning; may show aspiration
Causes pneumonia in petroleum distillate inhalation.
 Accidental ingestion of medication  Abdominal X-rays may show the presence of iron
 Improper cooking, canning, or storage of food pills or other radiopaque substances.
 Suicide attempt Diagnostic procedures
 Homicide attempt  Electrocardiography may show arrhythmias or
QRS- and QT-interval prolongation.
Risk factors
 Employment in chemical plant
 Inappropriate storage of medications or chemicals Treatment
 Inappropriate labeling
General
Incidence  Emergency resuscitation, as needed
 Affects 1 million people annually; fatal in about 800  Recommendations of local poison control center
cases  Symptomatic care
 Fourth most common cause of death in children  Airway and ventilation maintenance
 Oxygen administration
Common characteristics  Nothing by mouth until the episode resolves
 Hypotension  Safety measures
 Altered neurologic status
 Changes in skin temperature and color Medications
 Cardiopulmonary arrest  Specific antidote, if available
 Activated charcoal, if appropriate
Complications
 Cardiac arrhythmias
 Seizures Nursing considerations
 Neurogenic shock
 Cardiovascular collapse Key outcomes
 Coma and death The patient will:
 maintain adequate ventilation
 maintain a patent airway
Assessment  maintain orientation to time, place, and person
 express feelings of increased comfort and pain relief
History  identify factors that increase the risk for injury.
 Poison exposure
 Drug overdose Nursing interventions
 Perform cardiopulmonary resuscitation, if needed.
Physical findings  Induce emesis, if recommended.
 Vary with type of poison, possibly including:  Perform gastric lavage and administer a cathartic as
Central nervous system depression or excitability ordered.
Respiratory depression  Provide supplemental oxygen as ordered and
Cardiovascular depression needed.
Cardiovascular excitation  Send vomitus and aspirate for analysis.

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 In severe poisoning, provide peritoneal dialysis or Prevention

hemodialysis. Preventing poisoning
Monitoring Poisoning can be prevented by following these guidelines:
 Read all labels before taking medications or using
 Vital signs
chemicals.
 Level of consciousness  Store medication and chemicals away from children
 Respiratory status and pets.
 Suicidal ideations, if indicated  Dont take medication that has been prescribed for
someone else.
 Dont transfer medications or chemicals from their
Patient teaching original container unless properly labeled.
 Dont tell children that medication is candy.
Be sure to cover:  Use childproof caps on medication containers.
 Always close containers carefully.
 prevention techniques (see Preventing poisoning)
 Use well-marked pill-dispensing system to pre-pour
 importance of keeping poison control telephone
medications for elderly or visually impaired patients
number readily available. who are unable to safely self-administer.
Discharge teaching
 Refer the patient for psychological counseling in case
of suicide attempt.
 Refer the patient to the proper authorities in case of
deliberate poisoning.

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Poliomyelitis  Vomiting
 Lethargy
 Irritability
 Pains in neck, back, arms, legs, and abdomen
Overview  Muscle tenderness, weakness, and spasms in the ex-
tensors of the neck and back and sometimes in the
Description hamstring and other muscles
 An acute communicable disease caused by the polio PARALYTIC
virus  Symptoms similar to those of nonparalytic polio-
 Ranges in severity from inapparent infection to fatal myelitis
paralytic illness (mortality 5% to 10%)  Asymmetrical weakness of various muscles
 Prognosis excellent if central nervous system (CNS)  Loss of superficial and deep reflexes
spared  Paresthesia
 Also called polio or infantile paralysis  Hypersensitivity to touch
 Urine retention
Pathophysiology  Constipation
 The poliovirus has three antigenically distinct sero-  Abdominal distention
types (types I, II, and III) that cause poliomyelitis. BULBAR PARALYTIC
 Incubation period ranges from 3 to 35 days (7 to 14  Respiratory paralysis
days on average).  Symptoms of encephalitis
 The virus usually enters the body through the alimen-  Facial weakness
tary tract, multiplies in the oropharynx and lower in-  Diplopia
testinal tract, and then spreads to regional lymph  Dysphasia
nodes and the blood.  Difficulty chewing
 Factors that increase the risk of paralysis include  Inability to swallow or expel saliva
pregnancy; advanced age; localized trauma, such as a  Regurgitation of food through the nasal passages
recent tonsillectomy, tooth extraction, or inoculation;  Dyspnea
and unusual physical exertion at or just before the
clinical onset of poliomyelitis. Complications
 Hypertension
Causes  Urinary tract infection
 Contraction of the virus from direct contact with in-  Urolithiasis
fected oropharyngeal secretions or feces  Atelectasis
 Pneumonia
Risk factors  Myocarditis
 Travel to polio oubtreak area  Cor pulmonale
 Lack of immunization  Skeletal and soft-tissue deformities
 Compromised immune system  Paralytic ileus
 Poor sanitation
 Pregnancy
Assessment
Incidence
 Minor polio outbreaks, usually among nonimmu- History
nized groups  Exposure to polio virus
 Onset during the summer and fall  Fever
 Mostly occurs in people older than age 15
 Adults and girls at greater risk for infection; boys, for Physical findings
paralysis  Muscle weakness
 Resistance to neck flexion (nonparalytic and paralyt-
Common characteristics ic poliomyelitis)
Abortive infection  Patient tripods (extends his arms behind him for
 Slight fever support) when sitting up
 Malaise  Patients head falls back when supine and shoulders
 Headache are elevated (Hoynes sign)
 Sore throat  Unable to raise legs 90 degrees when in a supine po-
 Inflamed pharynx sition
 Vomiting  Kernigs and Brudzinskis signs (paralytic polio-
Major poliomyelitis myelitis)
NONPARALYTIC
 Moderate fever
 Headache

632 Poliomyelitis
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Test results
Laboratory
 Polio virus is isolated from throat washings early in
the disease, from stools throughout the disease, and
from cerebrospinal fluid cultures in CNS infection.
 Convalescent serum antibody titers are four times
greater than acute titers.
 Tests to rule out coxsackievirus and echovirus infec-
tions must be performed.

Treatment
General
 Supportive
 Moist heat applications
 Well-balanced diet
 Activity, as tolerated
 Physical therapy
 Assistive devices

Medications
 Analgesics
 Antipyretics

Nursing considerations
Key outcomes
The patient will:
 report feelings of increased comfort
 maintain adequate ventilation
 demonstrate effective coping mechanisms
 use available support systems.

Nursing interventions
 Provide emotional support.
 Provide good skin care, reposition the patient often,
and keep the bed dry.
 Maintain contact isolation.

Monitoring
 Signs of paralysis
 Respiratory status
 Vital signs
 Nutritional status

Patient teaching
Be sure to cover:
 physical therapy
 avoiding complications of limited mobility
 proper hand-washing and contact isolation tech-
niques
 vaccination of unimmunized household members.

Discharge planning
 Refer the patient to support services as appropriate.

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Polycystic kidney  Heart failure

 Recurrent hematuria

disease  Life-threatening retroperitoneal bleeding

 Proteinuria

Overview Assessment
Description History
 Growth of multiple, bilateral, grapelike clusters of Adult polycystic disease
fluid-filled cysts in the kidneys  Family history
 May progress slowly even after renal insufficiency  Polyuria
symptoms appear  Urinary tract infections (UTIs)
 Two distinct forms  Headaches
infantile form: causes stillbirth or early neonatal  Pain in back or flank area
death  Gross hematuria
adult form: has insidious onset but usually be-  Abdominal pain, usually worsened on exertion and
comes obvious between ages 30 and 50 eased by lying down
 Usually fatal within 4 years of uremic symptom onset,
unless dialysis begins Physical findings
 Carries a widely varying prognosis in adults Infantile form
 Also known as PKD  Pronounced epicanthal folds
 Pointed nose
Pathophysiology  Small chin
 Cysts enlarge the kidneys, compressing and eventual-  Floppy, low-set ears (Potter facies)
ly replacing functioning renal tissue.  Huge, bilateral, symmetrical flank masses that are
 Renal deterioration results; deterioration is more tense and cant be transilluminated
gradual in adults than in infants.  Signs of respiratory distress, heart failure and, even-
 The condition progresses relentlessly to fatal uremia. tually, uremia and renal failure
 Signs of portal hypertension (bleeding varices)
Causes Adult form
 Familial  Hypertension
 Infantile form: inherited as an autosomal recessive  Signs of an enlarging kidney mass
trait  Grossly enlarged kidneys (in advanced stages)
 Adult form: inherited as an autosomal dominant trait
Test results
Risk factors Laboratory
 If one parent has autosomal dominant PKD: 50%  Urinalysis may show hematuria or bacteria or pro-
chance that the disease will pass to a child tein.
 In autosomal recessive PKD: parents not having the  Creatinine clearance test results may show renal in-
disease possibly having a child with the disease if sufficiency or failure.
both parents carriers of the abnormal gene and both  Sodium loss or retention is possible.
passing the gene to their child (one in four chance) Imaging
 Excretory or retrograde urography reveals enlarged
Incidence kidneys, with pelvic elongation, flattening of the ca-
 Affects both sexes equally lyces, and indentations caused by cysts. In a neonate,
 Infantile form: 1 in 6,000 to 40,000 infants excretory urography shows poor excretion of con-
 Adult form: 1 in 50 to 1,000 adults trast medium.
 Ultrasonography, tomography, and radioisotopic
Common characteristics scans show kidney enlargement and cysts.
 Enlarged kidneys  Tomography, computed tomography scan, and mag-
 Signs and symptoms of renal failure netic resonance imaging show multiple areas of cys-
 Abdominal or flank pain tic damage.
 Hypertension
 Nocturia
Treatment
Complications
 Hepatic failure General
 Renal failure  Monitoring of renal function
 Respiratory failure  Dialysis

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 Low-protein and, possibly, low-sodium diet

 Fluid restriction (in renal failure)
 Avoidance of contact sports

Medications
 Analgesics
 Antibiotics for UTI
 Antihypertensive agents

Surgery
 Kidney transplantation
 Surgical drainage for cystic abscess or retroperi-
toneal bleeding

Nursing considerations
Key outcomes
The patient will:
 maintain fluid balance
 maintain urine specific gravity within designated
limits
 maintain hemodynamic stability
 report feelings of increased comfort
 identify risk factors that worsen decreased tissue per-
fusion, and modify lifestyle appropriately.
Nursing interventions
 Administer prescribed drugs.
 Provide supportive care to minimize symptoms.
 Individualize patient care accordingly.

Monitoring
 Urine (for blood, cloudiness, calculi, and granules)
 Intake and output
 Electrolyte levels
 Vital signs
 Access site for dialysis

Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatment
 medication administration, dosage, and possible
adverse effects
 follow-up with the physician for severe or recurring
headaches
 signs and symptoms of UTI and prompt notification
of the physician
 importance of blood pressure control
 possible need for dialysis or transplantation.

Discharge planning
 Refer a young adult patient or the parents of an infant
with polycystic kidney disease for genetic counseling.

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Polycystic ovary  Increased risk for cardiovascular disease and type 2

diabetes mellitus
syndrome  Secondary amenorrhea
 Oligomenorrhea
 Infertility
 Addisons disease
Overview  Ovarian atrophy

Description
 Metabolic disorder characterized by multiple ovarian Assessment
cysts
 Prognosis good for ovulation and fertility with appro- History
priate treatment  Diabetes
 Mild pelvic discomfort
Pathophysiology  Lower back pain
 A general feature of all anovulation syndromes is a  Dyspareunia
lack of pulsatile release of gonadotropin-releasing  Abnormal uterine bleeding secondary to disturbed
hormone. ovulatory pattern
 Initial ovarian follicle development is normal.
 Many small follicles begin to accumulate because Physical findings
theres no selection of a dominant follicle.  Obesity
 These follicles may respond abnormally to the hor-  Hirsutism
monal stimulation, causing an abnormal pattern of  Acne
estrogen secretion during the menstrual cycle.  Male-pattern hair loss
 Endocrine abnormalities may be the cause of poly-  Hyperpigmentation of the skin
cystic ovary syndrome or cystic abnormalities; mus-
cle and adipose tissue are resistant to the effects of Test results
insulin, and lipid metabolism is abnormal. Laboratory
 Urinary 17-ketosteroid levels are slightly elevated.
Causes  Estrogen action is unopposed during menstrual cycle
 Exact cause unknown; possible theories: due to anovulation.
Abnormal enzyme activity triggering excess andro-  Ratio of luteinizing hormone to follicle-stimulating
gen secretion hormone is elevated (usually 3:1 or greater).
Endocrine abnormalities  Testosterone and androstenedione levels are ele-
vated.
Incidence Imaging
 Occurs in 6% to 10% of females in the United States;  Ultrasound permits visualization of the ovary.
50% to 80% of these females, obese Surgery
 Among females who seek treatment for infertility,  Surgery may confirm the presence of ovarian cysts.
more than 75% having some degree of polycystic  Direct visualization by laparoscopy confirms the
ovary syndrome, usually manifesting by anovulation presence of cysts.
alone
 Affects females of reproductive age
Treatment
Common characteristics
 Mild pelvic discomfort General
 Lower back pain  Lifestyle modifications
 Dyspareunia  Weight-loss diet
 Abnormal uterine bleeding secondary to disturbed  Daily exercise program
ovulatory pattern  Hair removal
 Hirsutism
 Acne Medications
 Male-pattern hair loss  Clomiphene
 Infertility  Medroxyprogesterone
 Obesity  Low-dose hormonal contraceptives
 Impaired glucose tolerance (by age 40)  Metformin
 Antiandrogens (for hirsutism)
Complications
 Malignancy

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Surgery
 Ovarian wedge resection
 Laparoscopic surgery to create focal areas of damage
in the ovarian cortex and stoma

Nursing considerations
Key outcomes
The patient will:
 report feelings of increased comfort
 express understanding of condition and treatment
 demonstrate effective coping mechanisms.

Nursing interventions
 Postoperatively, encourage frequent movement in bed
and early ambulation.
 Provide emotional support .
 Encourage weight reduction, if appropriate.
 Provide guidelines for exercise program.

Monitoring
Preoperatively
 Signs of cyst rupture
Postoperatively
 Vital signs
 Signs of infection

Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatment
 diabetic diet, if appropriate
 low-calorie diet
 importance of regular follow-up care.

Discharge planning
 Refer the patient to a reproductive endocrinologist.
 Refer the patient to supportive services as appro-
priate.

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Polycythemia, secondary Assessment

History
Overview  Emphysema
 Headaches
Description  Lethargy
 Excessive production of circulating red blood cells
(RBCs) due to hypoxia, tumor, or disease Physical findings
 Also called reactive polycythemia  Clubbed fingers
 Ruddy skin
Pathophysiology  Cyanosis
 Secondary polycythemia may result from increased  Splenomegaly
production of the hormone erythropoietin.  Shortness of breath
 Bone marrow is stimulated to produce RBCs (in-  Hypoxemia
creased production of erythropoietin possibly an in-
appropriate pathologic response to renal, central Test results
nervous system, or endocrine disorders or to certain Laboratory
neoplasms).  RBC mass is increased.
 Its a compensatory response to several conditions,  Hematocrit and hemoglobin level are elevated.
such as:  Mean corpuscular volume and mean corpuscular-
hypoxemia hemoglobin level are elevated.
hemoglobin abnormalities  Urinary erythropoietin count is elevated.
heart failure  Blood histamine level is elevated.
right-to-left shunting of blood in the heart  Arterial oxygen saturation level is normal to low.
central or peripheral alveolar hypoventilation Diagnostic procedures
low oxygen content at high altitudes.  Bone marrow biopsy reveals hyperplasia confined to
 It may be an inappropriate (pathologic) response to: the erythroid series.
renal disease
central nervous system disease
neoplasms Treatment
endocrine disorders.
General
Causes  Correction of underlying disease or environmental
 Increased production of erythropoietin condition
 Conditions that cause prolonged tissue hypoxia, such  Therapeutic phlebotomy
as shock or compression of major blood vessels  Plasmapheresis
 Recessive genetic trait  Smoking cessation
 Low-sodium diet
Risk factors  Activity, as tolerated
 Smoking
 Severe heart or lung disease Medications
 Long periods of time at high altitudes  Analgesics
 Occupations such as pilots or mountaineers  Low-flow oxygen therapy

Incidence
 Occurs in 2 of every 100,000 people living at or near Nursing considerations
sea level
 Greater incidence among those living at high altitude Key outcomes
The patient will:
Common characteristics  maintain adequate gas exchange
 Ruddy, cyanotic skin  express understanding of condition and treatment
 Emphysema  report feelings of increased comfort
 Hypoxemia without hepatomegaly or hypertension  maintain normal fluid balance
(in the hypoxic patient)  remain free from signs of infection.
 Clubbing of the fingers (when underlying cause is
cardiovascular) Nursing interventions
 Promote optimal activity.
Complications  Before and after therapeutic phlebotomy, check the
 Hemorrhage patients blood pressure with him lying down. After
 Thromboembolism secondary to hemoconcentration the procedure, have the patient drink approximately

638 Polycythemia, secondary

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24 oz (710 ml) of water or juice. To prevent syn-

cope, have him sit up for about 5 minutes before
walking.
 Encourage verbalization and provide support.
 Administer prescribed drugs.

Monitoring
 Signs of thrombosis
 Respiratory status
 Vital signs

Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatment
 symptoms of recurring polycythemia and the impor-
tance of reporting them promptly
 the importance of regular blood studies (every 2 to
3 months), even after the disease is controlled
 the need for relocation if altitude is a contributing
factor
 dietary restrictions
 using an electric razor
 maintaining a safe environment
 alternating rest periods and activity.

Discharge planning
 Refer the patient to social services as appropriate.

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Polycythemia vera  Night sweats

 Epigastric and joint pain
 Vision alterations, such as scotomas, double vision,
and blurred vision
Overview  Pruritus
 Abdominal fullness
Description
 Chronic, myeloproliferative disorder of increased red Physical findings
blood cell (RBC) mass, leukocytosis, thrombocyto-  Congestion of the conjunctiva, retina, and retinal
sis, and increased hemoglobin concentration veins
 Also called primary polycythemia, erythema, poly-  Oral mucous membrane congestion
cythemia rubra vera, splenomegalic polycythemia,  Hypertension
and Vaquez-Osler disease  Ruddy cyanosis
 Ecchymosis
Pathophysiology  Hepatosplenomegaly
 Uncontrolled and rapid cellular reproduction and
maturation cause proliferation or hyperplasia of all Test results
bone marrow cells. Laboratory
 Increased RBC mass makes the blood abnormally  Uric acid level is increased.
viscous and inhibits blood flow to the microcircula-  Increased RBC mass and normal arterial oxygen sat-
tion. uration confirm diagnosis with splenomegaly or two
 Diminished blood flow and thrombocytosis set the of the following:
stage for intravascular thrombosis. platelet count above 400,000/l (thrombocyto-
penia)
Causes white blood cell count above 10,000/l in adults
 Hyperplasia of all bone marrow cells (panmyelosis) elevated leukocyte alkaline phosphatase level
 Mutation to deoxyribonucleic acid in a single cell in elevated serum vitamin B12 levels or unbound B12-
the bone marrow; mutation in the protein JAK2 binding capacity.
Diagnostic procedures
Risk factors  Bone marrow biopsy shows panmyelosis.
 Male gender
 Older than age 60
 Family member with the disorder Treatment
Incidence General
 Five new cases per million people each year  Therapeutic phlebotomy
 Rare in children and blacks  Pheresis
 90% of patients have mutation JAK2
Medications
Common characteristics  Myelosuppressive agents, such as hydroxyurea and
 Joint pain anagrelide
 Hypertension  Radioactive phosphorus
 Chemotherapy
Complications
 Hemorrhage
 Vascular thromboses Nursing considerations
 Uric acid calculi
 Myelofibrosis Key outcomes
 Acute leukemia The patient will:
 maintain strong peripheral pulses
 maintain normal skin color and temperature
Assessment  remain free from evidence of infection
 express feelings of increased comfort and decreased
History pain.
 Vague feeling of fullness in the head or rushing in the
ears Nursing interventions
 Tinnitus  Keep the patient active and ambulatory.
 Headache  If bed rest is necessary, implement a daily program
 Dizziness, vertigo of active and passive range-of-motion exercises.
 Epistaxis  Encourage additional fluid intake.

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 If the patient has symptomatic splenomegaly, suggest
or provide small, frequent meals followed by a rest
period.
 If the patient has pruritus, administer prescribed
drugs.
 Encourage the patient to express concerns about the
disease and its treatment.
ALERT
 instructions on infection prevention for an outpatient
who develops leukopenia (including avoiding crowds
and watching for infection symptoms)
 radioactive phosphorus administration procedure (if
scheduled) and the possible need for repeated phle-
botomies
 dental care
 use of gloves when outdoors if temperature is below
50 F (10 C).

Report acute abdominal pain immediately. It may Discharge planning

signal splenic infarction, renal calculus formation,  Refer the patient to social services as needed.
or abdominal organ thrombosis.

During and after therapeutic phlebotomy

 Make sure the patient is lying down comfortably. Stay
alert for tachycardia, clamminess, and complaints of
vertigo. If these effects occur, the procedure should
be stopped.
 Immediately after phlebotomy, have the patient sit up
for about 5 minutes before letting him walk. Give
24 oz (710 ml) of juice or water.
During myelosuppressive chemotherapy
 If nausea and vomiting occur, begin antiemetic thera-
py and adjust the patients diet.
 If treating with radioactive phosphorus, obtain a
blood sample for complete blood cell (CBC) count
and platelet count before starting treatment. (Person-
nel who administer radioactive phosphorus should
take radiation precautions to prevent contamina-
tion.)
 Have the patient lie down during I.V. administration
and for 15 to 20 minutes afterward.
Monitoring
 Vital signs
 Adverse reactions to drugs
 CBC and platelet count before and during therapy
 Complications
 Signs and symptoms of impending stroke
 Hypertension
 Signs and symptoms of heart failure
 Signs and symptoms of bleeding

Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatment
 importance of staying as active as possible
 use of an electric razor to prevent accidental cuts
 ways to minimize falls and contusions at home
 avoidance of high altitudes
 common bleeding sites, if the patient has thrombocy-
topenia
 importance of reporting abnormal bleeding promptly
 therapeutic phlebotomy procedure (if scheduled)
and its effects
 symptoms of iron deficiency to report
 possible adverse reactions to myelosuppressive
therapy

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Complications
Polyps, intestinal  Anemia
 Bowel obstruction
 Rectal bleeding
Overview  Intussusception
 Colorectal cancer (villous adenomas and familial
Description polyps)
 A small, tumorlike growth that projects from a mu-  Electrolyte imbalance
cous membrane surface
 May develop in the colon or rectum, where they pro-
trude into the GI tract Assessment
Pathophysiology History
 Masses of tissue resulting from unrestrained cell  Diarrhea
growth in the upper epithelium rise above the mu-  Bloody stools
cosal membrane and protrude into the GI tract.  Painful defecation
 They may be described by their appearance:  Changes in bowel habits
pedunculated: attached by a stalk to the intestinal
wall Physical findings
sessile: attached to the intestinal wall with a broad  Polyp felt during digital rectal examination
base and no stalk.
 Polyps are classified according to tissue type: Test results
adenomatous polyps, such as tubular adenoma, Laboratory
tubulovillous adenoma, and villous adenoma  Occult blood is present in stools.
nonadenomatous polyps, such as hyperplastic  Hemoglobin level is low.
polyps, inflammatory polyps, and juvenile polyps.  Hematocrit is low with anemia.
 Most polyps are benign. However, villous and familial  Serum electrolyte imbalances are evident with villous
polyps show a marked inclination to become malig- adenomas.
nant. Imaging
 Barium enema identifies polyps that are located high
ALERT in the colon.
Diagnostic procedures
Familial polyposis is commonly linked to rectosig-  Sigmoidoscopy, colonoscopy, and rectal biopsy iden-
moid adenocarcinoma. tify polyps.

Causes Treatment
 Unknown
General
Risk factors  Activity, as tolerated
 Heredity  Diet, as tolerated
 Age
 High-fat, low-fiber diet Medications
 Analgesics
Incidence
 Villous adenomas most prevalent in males older than Surgery
age 55  Polypectomy, commonly by fulguration (destruction
 Common polypoid adenomas most prevalent in white by high-frequency electricity) during endoscopy
females between ages 45 and 60  Abdominoperineal resection, low anterior resection,
 Incidence in both sexes increased after age 70 ileostomy, colostomy
 Juvenile polyps most common in children younger  Biopsy
than age 10  Snare removal during colonoscopy

Common characteristics
 Rectal bleeding Nursing considerations
 Painful defecation
 Changes in bowel habits Key outcomes
The patient will:
 return to normal bowel habits
 express increased comfort
 maintain electrolyte balance.

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Nursing interventions
 Observe the amount and character of stools.
 Prepare the patient with precancerous or familial le-
sions for abdominoperineal resection.
 Provide emotional support.

Monitoring
 Electrolyte levels
 Rectal bleeding
 Vital signs
 Intake and output
After surgery
 Signs of bleeding
 Wound condition

Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatment
 wound care, if appropriate
 enterostomal therapy and care.

Discharge planning
 If the patient has benign polyps, stress the need for
routine follow-up studies to check for new polypoid
growth.

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Porphyrias  Darkening of urine left in the light or air

Overview
Description
 Umbrella term for a group of metabolic disorders
that affect the biosynthesis of heme (a hemoglobin
component), resulting in excessive porphyrin pro-
duction
 Classified by the site of excessive porphyrin produc-
tion as erythropoietic, hepatic, or erythrohepatic
porphyria
Pathophysiology
 Various metabolic disorders affect heme biosyn-
thesis.
 This leads to excessive production and excretion of
porphyrins or their precursors.
Causes
 Inherited as an autosomal dominant trait, except
Gnthers disease (inherited as an autosomal reces-
sive trait) and toxic-acquired porphyria (which re-
sults from lead ingestion or exposure)
Incidence
 More common in Whites than Blacks or Asians
Common characteristics
 Neuropsychiatric, dermatologic, and abdominal
symptoms
Precipitating factors
 Certain medications
 Hormonal changes
 Infection
 Malnutrition
Complications
 With hepatic porphyria: neurologic and hepatic dys-
function
 With acute intermittent porphyria: flaccid paralysis,
respiratory paralysis, and death
 With erythropoietic porphyria: hemolytic anemia
 Neurologic signs of wristdrop or footdrop
 Muscle weakness
 Fever (with an acute attack)
 Splenomegaly (if hemolytic anemia present)
 Wheezing and dyspnea (with acute intermittent por-
phyria)
Test results
Laboratory
 The ion-exchange chromatography test shows urine
aminolevulinic acid.
 In acute intermittent porphyria: urine porphobilino-
gen (as shown by the Watson-Schwartz test), leuko-
cytosis, elevated bilirubin and alkaline phosphatase
levels, and hyponatremia are present.
 In variegate porphyria: protoporphyrin and copro-
porphyrin is present in stools.
 In hereditary coproporphyria: abundant copropor-
phyrin is present in stools and, to a lesser extent, in
urine.
 In porphyria cutanea tarda: uroporphyrin excretion
is increased with varying amounts of fecal porphy-
rins.
 In Gnthers disease: urine porphyrins are present.
 In erythropoietic protoporphyria: protoporphyrin is
present in red blood cells.
 In toxic acquired porphyria: urine lead level is
0.2 mg/L or higher.
 In porphyria cutanea tarda: serum iron levels are
increased.
Treatment
General
 High-carbohydrate diet
 Fluid restriction
 Avoidance of direct sun exposure
Medications
 Beta-caotene supplements
 Chlorpromazine I.V.
 Analgesics
 Hemin

Surgery
Assessment  In hemolytic anemia: splenectomy

History
 Mild or severe abdominal pain Nursing considerations
 Photosensitivity
 Paresthesia Key outcomes
 Neuritic pain The patient will:
 maintain adequate ventilation
Physical findings  maintain intact skin integrity
 Wide variation, depending on the type of porphyria  avoid complications
 Psychosis  regain normal bowel movements
 Seizures  express feelings of increased comfort.
 Skin lesions

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Drugs that aggravate porphyria Discharge planning

 For toxic-acquired porphyria, refer the patient and
Make sure the patient with porphyria doesnt receive any
family to resources that can help identify lead
of the following drugs, which are known to trigger signs
and symptoms of porphyria:
sources in the home.
 barbiturates
 carbamazepine
 carisoprodol
 chloramphenicol
 chlordiazepoxide
 danazol
 diazepam
 ergot alkaloids
 estrogens
 glutethimide
 griseofulvin
 imipramine
 meprobamate
 methsuximide
 methyldopa
 pentazocine
 phenytoin
 progesterones
 sulfonamides
 tolbutamide.

Nursing interventions
 Check the patients history for use of medications that
can trigger an acute attack. (See Drugs that aggra-
vate porphyria.)
 Administer prescribed drugs.
 Perform passive and active range-of-motion exer-
cises.
 Encourage the patient to express feelings and con-
cerns about the disease.
 Provide emotional support.

Monitoring
 Respiratory status
 GI motility
 Vital signs
 Response to treatment

Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatment
 avoidance of excessive sun exposure and use of sun
screen
 importance of wearing medical identification
 lead sources (if the patient has toxic-acquired por-
phyria)
 precipitating factors, including crash diets, fasting,
and use of alcohol, estrogens, and barbiturates
 stress-management techniques
 ways to prevent infection
 value of a high-carbohydrate diet.

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Posttraumatic stress  Panic attacks

 Phobic avoidance of situations that arouse memories

disorder of the traumatic event

Overview
Description
 Development of psychological symptoms, such as in-
tense fear and feelings of hopelessness and loss of
control, after exposure to extreme trauma
 Can be acute, chronic, or delayed
Pathophysiology
 The alpha2-adrenergic receptor response that in-
hibits stress-induced release of norepinephrine is
impaired.
 Progressive behavioral sensitization results, with gen-
eralization to stimulus cues from the original trauma.
 Consequently, responses of increased sympathetic ac-
tivity occur.
Causes
 An event that the patient views as traumatic (typically
an event outside the range of usual human experi-
ence)
Risk factors
 History of psychopathology
 Neurotic and extroverted characteristics
 History of child abuse or neglect
Incidence
 Affects 30% of trauma victims
 Occurs in up to 15% of Unites States residents at
some time in their lives
 More common in females than males
Common characteristics
 Detachment and loss of emotional response
 Feelings of depersonalization
 Inability to recall specific aspects of the traumatic
event
 Flashbacks within dreams or thoughts when cues to
the event occur
 Nightmares of the traumatic event
Complications
 Increased risk for other anxiety, mood, and sub-
stance-related disorders
 Substance abuse
 Feelings of detachment or estrangement, which may
damage interpersonal relationships
Assessment
History
 Difficulty falling or staying asleep
 Aggressive outbursts on awakening
 Early life experiences, interpersonal factors, military
experiences, or other incidents that suggest the trau-
matic event
 Symptoms that began immediately or soon after the
trauma (although in some cases, symptoms dont de-
velop until months or years later)
 Pangs of painful emotions and unwelcome thoughts
 Traumatic re-experiencing of the traumatic event
 Chronic anxiety
 Rage and survivor guilt
 Use of violence to solve problems
 Depression and suicidal thoughts
 Fantasies of retaliation
Physical findings
 Emotional numbing (diminished or constricted re-
sponse)
 Memory impairment
 Difficulty concentrating
 Signs of substance abuse
 Physiologic reactivity on exposure to internal or ex-
ternal cues that symbolize or resemble an aspect of
the traumatic event
DSM-IV-TR criteria
Diagnosis is confirmed when the patient meets the fol-
lowing criteria:
 Exposure to a traumatic event that included both of
the following:
actual or threatened death or serious injury or
threat to the physical integrity of self or others
a response of intense fear, helplessness, or horror.
 Persistent reexperiencing of this traumatic event in at
least one of these ways:
recurrent and intrusive distressing recollections of
the event
recurrent distressing dreams of the event
flashbacks of the event
intense psychological distress at exposure to
events
physiologic reactivity on exposure to events.
 Persistent avoidance of stimuli associated with the
trauma, or numbing of general responsiveness not
present before the trauma, as indicated by at least
three of these criteria:
efforts to avoid thoughts or feelings associated
with the traumatic event
efforts to avoid activities or situations that arouse
recollections of the traumatic event
inability to recall an important aspect of the event
sharply decreased interest in significant activities
feeling of detachment or estrangement from others
restricted range of effect
sense of a foreshortened future.
 Persistent symptoms of increased arousal (not previ-
ously present) as indicated by two or more of these
criteria:
difficulty falling or staying asleep

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irritability or outbursts of anger  importance of identifying and avoiding cues that

difficulty concentrating worsen symptoms
hypervigilance  problem-solving skills
exaggerated startle response.  relaxation and breathing techniques
The disturbance must have lasted at least 1 month  medication administration, dosage, and possible
and must cause significant distress or impairment of so- adverse effects.
cial, occupational, or other important areas of func-
tioning. Discharge planning
 Refer the patient to support services.
 Refer the patient for psychotherapy.
Treatment  Refer the patient to physical, social, and occupational
rehabilitation programs, as indicated.
General  Refer the patient to drug treatment programs, as ap-
 Supportive or expressive psychotherapy propriate.
 Behavior therapies
 Support groups
 Rehabilitation programs in physical, social, and oc-
cupational areas
 Treatment of alcohol or drug abuse, as needed
 Active avoidance of stimuli that trigger memories of
the traumatic event
Medications
 Benzodiazepines (short-term use)
 Tricyclic antidepressants
 Monoamine oxidase inhibitors
 Selective serotonin-reuptake inhibitors
 Sedating antidepressants
 Anticonvulsants

Nursing considerations
Key outcomes
The patient will:
 express feelings and fears related to the traumatic
event
 use available support systems
 use effective coping mechanisms
 maintain or reestablish adaptive social interactions
with family members.
Nursing interventions
 Encourage the patient to express feelings of grief,
mourning, and anger.
 Practice crisis intervention techniques, as needed.
 Assume a positive, consistent, honest, and nonjudg-
mental attitude.
 Help the patient evaluate behavior.

Monitoring
 Response to drug therapy

Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatment
 healing process

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Precocious puberty Special populations

Males as young as 7 with true precocious puberty
have fathered children.
Overview
In females
Description  Rapid growth spurt
 Early sexual maturity  Breast development at early age
 True precocious puberty: early maturation of the  Pubic hair
hypothalamic-pituitary-gonadal axis, development of  Early menarche
secondary sex characteristics, gonadal development,
and spermatogenesis Complications
 Pseudoprecocious puberty: development of secon-  Testicular tumor (males)
dary sex characteristics without gonadal development  Ovarian or adrenal malignancy (females)
 For males: physical changes occurring before age 9
and for females, before age 8
Assessment
Pathophysiology
 In males, precocious puberty results from pituitary History
or hypothalamic intracranial lesions that cause ex-  Rapid growth spurt
cessive secretion of gonadotropin.  Early muscle development (males)
 In females, it results from early development and ac-  Early menarche (females)
tivation of the endocrine glands without correspond-
ing abnormality. Physical findings
 Enlarged penis or testicles (males)
Causes  Enlarged breasts (females)
In males  Pubic hair
TRUE PRECOCIOUS PUBERTY
 Idiopathic Test results
 Genetically transmitted as a dominant gene Laboratory
PSEUDOPRECOCIOUS PUBERTY IN MALES WITH TRUE PRECOCIOUS PUBERTY
 Testicular tumors  Plasma testosterone levels are elevated.
 Congenital adrenogenital syndrome  Ejaculate shows live spermatozoa.
In females  Luteinizing and follicle-stimulating hormones and
TRUE PRECOCIOUS PUBERTY corticotropin levels are elevated.
 Idiopathic IN MALES WITH PSEUDOPRECOCIOUS PUBERTY
 Central nervous system (CNS) disorders  Chromosomal karyotype analysis shows abnormal
PSEUDOPRECOCIOUS PUBERTY pattern of autosomes and sex chromosomes.
 Ovarian and adrenocortical tumors  24-hour urinary 17-ketosteroid and other steroid
 Estrogen or androgen ingestion levels are elevated.
 Increased end-organ sensitivity to low levels of circu- IN FEMALES WITH PSEUDOPRECOCIOUS PUBERTY
lating sex hormones  Vaginal smear shows estrogen secretion.
 Urinary tests for gonadotropic activity and excretion
Risk factors of 17-ketosteroids are elevated.
 Obesity  Luteinizing and follicle-stimulating hormone levels
 Exposure to sex hormones are elevated.
 McCune-Albright syndrome or congenital adrenal Imaging
hyperplasia  X-rays of the hands, wrists, knees, and hips deter-
mine bone age and possibly premature epiphyseal
Incidence closure.
 Five times more common in females than in males  Ultrasound verifies suspected abdominal lesion.
 More common in blacks  X-rays possibly show CNS tumors.

Common characteristics
In males Treatment
 Early bone development; initial growth spurt
 Early muscle development General
 Stunted adult stature  Aimed at underlying cause
 Adult hair pattern  Supportive psychological counseling
 Penile growth
 Bilateral enlarged testes

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Medications
 Medroxyprogesterone (females)

Surgery
 Removal of ovarian or adrenal tumors
 Removal of thyroid gland

Nursing considerations
Key outcomes
The patient will:
 express understanding of condition and treatment
 demonstrate effective coping mechanisms
 avoid complications.

Nursing interventions
 Provide emotional support.

Monitoring
 Complications

Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatment
 medication administration, dosage, and possible
adverse effects
 the need to continue social and emotional support.

Discharge planning
 Refer the patient to psychological counseling, as nec-
essary.

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Premenstrual syndrome  Edema

 Diarrhea or constipation
 Appetite changes and food cravings
 Fatigue
Overview  Exacerbations of skin, respiratory, or neurologic
problems
Description
 Group of somatic, behavioral, cognitive, and mood- Physical findings
related symptoms occurring 1 to 14 days before  Possible edema
menses and usually subsiding with menses onset
 Causes effects that range from minimal discomfort to Test results
severe, disruptive symptoms Laboratory
 Also known as PMS and premenstrual dysphoric  Blood studies rule out anemia, thyroid disease, or
disorder (PMDD) other hormonal imbalances.
Other
Pathophysiology  A daily symptom calendar aids diagnosis of PMS.
 PMS may result from a progesterone deficiency dur-  Psychological evaluation may be used to rule out or
ing the luteal phase of the ovarian cycle. detect an underlying psychiatric disorder.
 Hormone levels and patterns in females with PMS
dont differ significantly from those in women who
dont experience PMS. Treatment
Causes General
 Physiologic, psychological, and sociocultural factors  Symptom relief
 Possible progesterone deficiency in the luteal phase  Stress reduction
 Possible serotonin or norepinephrine deficiency  Relaxation techniques
 Possible low vitamin and mineral levels  Diet low in simple sugars, caffeine intake, animal fat,
and sodium
Incidence  Increased calcium and complex carbohydrate intake
 Affects 30% of females in the United States  Aerobic exercise

Medications
Special populations
 Antidepressants such as selective serotonin-reuptake
Moderate to severe symptoms occur in 14% to 88% inhibitors
of adolescent girls  Vitamins such as B complex
 Progestins and estrogens, such as drospirenone and
 Usually occurs between ages 25 and 45 ethinyl estradiol and medroxyprogesterone acetate
 Affects women in their 40s most severely  Prostaglandin inhibitors
 PMS resolving completely at menopause  Monophasic birth control pills
 Nonsteroidal anti-inflammatory drugs
Common characteristics
 Anxiety
 Irritability Nursing considerations
 Depression
 Multiple somatic complaints Key outcomes
The patient will:
Complications  identify effective and ineffective coping techniques
 Psychosocial problems  use available support systems, such as family, friends,
 Reduced self-esteem and groups, to develop and maintain effective coping
 Depression skills
 Inability to function (in PMDD)  express feelings of increased comfort
 express positive feelings about herself.

Assessment Nursing interventions

 Encourage adequate fluid intake.
History  Provide comfort measures.
 Behavioral changes  Offer emotional support and reassurance.
 Breast tenderness or swelling  Encourage the patient to express feelings.
 Abdominal tenderness or bloating  Help the patient develop effective coping strategies.
 Joint pain  Instruct the patient to chart symptoms daily for two
 Headache cycles.

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Monitoring
 Response to treatment
 Coping skills

Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatment
 physiologic basis of PMS
 beneficial lifestyle changes
 relaxation and stress-reduction techniques
 dietary management.

Discharge planning
 Refer the patient to a self-help group for females with
PMS.
 Refer the patient for psychological counseling, as in-
dicated.
 Refer the patient to a dietitian as needed.

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Pressure ulcers Assessment

History
Overview  One or more risk factors

Description Physical findings

 Localized areas of ischemic tissue caused by pres-  Shiny, erythematous superficial lesion (early)
sure, shearing, or friction  Small blisters or erosions with progression of super-
 Most common over bony prominences, especially the ficial erythema
sacrum, ischial tuberosities, greater trochanter,  Possible necrosis and ulceration with deeper ero-
heels, malleoli, and elbows sions and ulcerations
 May be superficial, caused by localized skin irritation  Malodorous, purulent discharge (suggesting sec-
(with subsequent surface maceration), or deep, aris- ondary bacterial infection)
ing in underlying tissue (Deep lesions may go unde-  Black eschar around and over the lesion
tected until they penetrate the skin.)
 Also called decubitus ulcers, pressure sores, or Test results
bedsores Laboratory
 Infecting organism is identified by wound culture and
Pathophysiology sensitivity testing of exudate.
 Impaired skin capillary pressure results in local tis-  Total serum protein level is decreased.
sue anoxia. Other
 Anoxia leads to edema and multiple capillary throm-  Diagnosis is typically made from inspection.
boses.
 An inflammatory reaction results in ulceration and
necrosis of ischemic cells. Treatment
Causes General
 Local tissue compression  Measures to prevent pressure ulcers
 Shearing force  Relief of pressure on the affected area
 Friction  Meticulous skin care
 Devices, such as pads, mattresses, and special beds
Risk factors  Moist wound therapy dressings
 Poor nutrition  Whirlpool baths
 Diabetes mellitus  Diet high in protein, iron, and vitamin C (unless con-
 Immobility or paralysis traindicated)
 Cardiovascular disorders  Activity, as tolerated
 Advanced age  Active and passive range-of-motion (ROM) exercises
 Incontinence  Frequent turning and repositioning
 Obesity
 Edema Medications
 Anemia  Enzymatic ointments
 Poor hygiene  Healing ointments
 Exposure to chemicals  Antibiotics, if indicated
 Steroids
Surgery
Incidence  Debridement of necrotic tissue
 Affect roughly 10% of hospitalized patients and 20%  Skin grafting (in severe cases)
to 40% of patients in long-term care facilities
Common characteristics Nursing considerations
 Vary with the ulcer stage (see Stages of pressure ul-
cers) Key outcomes
The patient will:
Complications  exhibit improved or healed lesions or wounds
 Secondary bacterial infection  maintain adequate daily caloric intake
 Septicemia  maintain joint mobility and ROM
 Gangrene  avoid infection and other complications.

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Stages of pressure ulcers

To protect the patient from pressure ulcer complications, learn to recognize the stages of ulcer formation.

Stage I Stage III

The skin is red and intact and doesnt blanche with external A hole develops and slough may be present. Undermining
pressure. (A black persons skin may look purple.) The skin may or may not be present.
feels warm and firm.

Stage IV
The ulcer destroys tissue from the skin to the bone. Find-
Stage II ings include slough or eschar and deep tunnels that extend
Skin breaks appear and discoloration may occur. Penetrat- from the ulcer.
ing to the subcutaneous fat layer, the sore is painful and vis-
ibly swollen. Thulcer may be characterized as an abrasion,
blister, or shallow crater.

Suspected deep tissue injury

The skin is purple or maroon but intact or a blood-filled blis-
ter may be present.

Unstageable
The ulcer destroys tissue from the skin to possibly the bone.
The base of the ulcer is covered by slough, eschar or both.
Until this is removed, the depth and stage cant be deter-
mined.

Nursing interventions Patient teaching

 Administer prescribed drugs.
 Apply dressings appropriate for the ulcer stage. Be sure to cover:
 Encourage adequate food and fluid intake.  the disorder, diagnosis, and treatment
 Reposition the bedridden patient at least every  techniques for changing positions
2 hours.  active and passive ROM exercises
 Elevate the head of the bed 30 degrees or less.  avoidance of skin-damaging agents
 Perform passive ROM exercises.  debridement procedures
 Encourage active ROM exercises, if possible.  skin graft surgery, if required
 Use pressure-relief aids on the bed.  signs and stages of healing
 Provide meticulous skin care.  importance of a well-balanced diet and adequate
fluid intake
Monitoring  medication administration, dosage, and possible
 Changes in skin color, turgor, temperature, sensa- adverse effects
tion, and drainage  importance of notifying the physician immediately of
 Change in the ulcer stage signs and symptoms of infection.
 Laboratory results
 Complications Discharge planning
 Response to treatment  Refer the patient to a wound care specialist, if indi-
 Intake and output cated.

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Proctitis Assessment
History
Overview  Tenesmus
 Abdominal cramping
Description  Loose stool with or without abdominal pain
 An acute or chronic inflammation of the rectal mu-  Pruritus
cosa  Rectal and anal pain
 Good prognosis unless massive bleeding occurs
Physical findings
Pathophysiology  Bloody or mucoid stools
 Mucosal cell loss occurs along with acute inflamma-  Superficial ulcers
tion of the lamina propria, eosinophilic crypt ab-  Mucosal erythema
scess, and endothelial edema of the arterioles  Painless chancres
 Rectal tissue ischemia occurs  Mucosal friability
 Mucosal friability, ulcers, bleeding, and fistulas result
Test results
Causes Laboratory
 Crohns disease  Complete blood count evaluates blood loss.
 Amebiasis  C-reactive protein may be elevated.
 Immunodeficiency disorders  Rectal swab identifies gonorrhea or chlamydia.
 Neisseria gonorrhoeae  Venereal disease research laboratory test diagnoses
 Chlamydia trachomatis syphilis.
 Herpes simplex virus 1 and 2  Culture of vesicular fluid identifies herpes simplex
 Syphilis virus.
 Radiation therapy Diagnostic procedures
 Papillomavirus  In acute proctitis, sigmoidoscopy shows edematous,
 Ischemia bright-red, or pink rectal mucosa thats thick, shiny,
 Toxins friable and, possibly, ulcerated.
 Vasculitis  In chronic proctitis, sigmoidoscopy shows thickened
mucosa, loss of vascular pattern, and stricture of the
Risk factors rectal lumen.
 High-risk sexual practices  Biopsy rules out carcinoma.
 Homosexuality
 Autoimmune disorders
Treatment
Incidence
 Occurs in 5% to 20% of patients receiving radiation General
therapy  Elimination of the underlying cause
 More common in Jewish people  Increased fluids
 More common in males than females  Activity as tolerated
 Occurs predominantly in adults  Sitz baths

Common characteristics Medications

 Tenesmus  Enemas
 Constipation  Steroid (hydrocortisone) suppositories
 Feeling of rectal fullness  Tranquilizers
 Left-sided abdominal pain  Antibiotics (based on cause)
 Antivirals
Complications
 Ulcerations Surgery
 Crypt abscesses  Diverting colostomy may be necessary.
 Bleeding
 Fissures
 Fistulas
 Ulcerative colitis

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Nursing considerations
Key outcomes
The patient will:
 express feelings of increased comfort
 understand the disease process and treatment
regimen
 exhibit adequate coping mechanisms.

Nursing interventions
 Offer emotional support.
 Administer prescribed drugs.

Monitoring
 Response to treatment
 Rectal bleeding
 Amount and character of stools

Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatment
 importance of watching for and reporting bleeding
and other persistent symptoms.
Discharge planning
 Refer the patient to a colorectal surgeon, if appro-
priate.

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Prostate cancer Assessment

Overview
Description
 Proliferation of cancer cells that usually take the
form of adenocarcinomas and typically originate in
the posterior prostate gland
 May progress to widespread bone metastasis and
death
 Is the leading cause of cancer death in males
Pathophysiology
 Slow-growing prostate cancer seldom causes signs
and symptoms until its well advanced.
 Typically, when a primary prostatic lesion spreads
beyond the prostate gland, it invades the prostatic
capsule and spreads along ejaculatory ducts in the
space between the seminal vesicles or perivesicular
fascia.
 Endocrine factors may play a role, leading re-
searchers to suspect that androgens speed tumor
growth.
 Malignant prostatic tumors seldom result from the
benign hyperplastic enlargement that commonly de-
velops around the prostatic urethra in older men.
Causes
 Unknown
History
 Symptoms rare in early stages
 Later, urinary problems, such as difficulty initiating a
urinary stream, dribbling, and urine retention
Physical findings
 In early stages: nonraised, firm, nodular mass with a
sharp edge
 In advanced disease: edema of the scrotum or leg; a
hard lump in the prostate region
Test results
Laboratory
 Elevated serum prostate-specific antigen (PSA) level
may indicate cancer with or without metastasis.
Imaging
 Transrectal prostatic ultrasonography shows prostate
size and presence of abnormal growths.
 Bone scan and excretory urography determine the
diseases extent.
 Magnetic resonance imaging and computed tomogra-
phy scan define the extent of the tumor.
Other
 Standard screening test: digital rectal examination
and PSA test identify cancer (recommended yearly by
the American Cancer Society for males older than age
40).

Risk factors Treatment

 Older than age 50
 Family history General
 Heavy metal exposure (cadmium)  Varies with cancer stage
 Exposure to androgens  Radiation therapy or internal beam radiation
 High-fat diet  Well-balanced diet

Incidence Medications
 Most common among Blacks; least common among  Hormonal therapy
Asians  Chemotherapy
 Unaffected by socioeconomic status or fertility
 Most common neoplasm in males older than age 50 Surgery
 Prostatectomy
Common characteristics  Orchiectomy
 Urinary problems  Radical prostatectomy
 Transurethral resection of prostate
Complications  Cryosurgical ablation
 Spinal cord compression
 Deep vein thrombosis
 Pulmonary emboli Nursing considerations
 Myelophthisis
 Death Key outcomes
The patient will:
 express feelings of increased comfort
 discuss the diseases impact on self and family
members
 demonstrate effective coping mechanisms.

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Nursing interventions
 Administer prescribed drugs.
 Encourage the patient to express his feelings.
 Provide emotional support.

Monitoring
 Pain level
 Wound site
 Postoperative complications
 Medication effects

Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatment
 perineal exercises that decrease incontinence
 follow-up care
 medication administration, dosage, and possible
adverse effects.
Discharge planning
 Refer the patient to appropriate resources and sup-
port services.

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Complications
Prostatitis  Urinary tract infection
 Prostatic abscess
 Acute urinary retention
Overview  Pyelonephritis
 Epididymitis
Description
 Inflammation of the prostate gland
 Occurs in acute, chronic, and several other forms Assessment
Acute prostatitis
 Easily recognized and treated History
Chronic prostatitis  Sudden fever, chills
 Most common cause of recurrent urinary tract infec-  Lower back pain
tion in males  Perineal fullness
 More difficult to recognize than acute prostatitis  Arthralgia, myalgia
Other prostatitis forms  Urinary urgency and frequency
 Granulomatous prostatitis (also called tuberculous  Dysuria, nocturia
prostatitis)  Transient erectile dysfunction
 Nonbacterial prostatitis Chronic bacterial prostatitis
 Prostatodynia (painful prostate)  May be asymptomatic
 Usually causes same urinary symptoms as the acute
Pathophysiology form, but to a lesser degree
 Infectious organism spreads to the prostate gland by  Hemospermia
the hematogenous route, an ascending urethral in-  Persistent urethral discharge
fection, invasion of rectal bacteria via lymphatic ves-  Painful ejaculation
sels, or reflux of infected bladder urine into prostate Nonbacterial prostatitis
ducts.  Dysuria
 Inflammation results.  Mild perineal or lower back pain
 Frequent nocturia
Causes Prostatodynia
 Bacterial prostatitis: Escherichia coli (80% of cas-  Perineal, lower back, or pelvic pain
es); Klebsiella, Enterobacter, Proteus, Pseudo-
monas, Serratia, Streptococcus, Staphylococcus, Physical findings
and diphtheroids (20% of cases)  Cloudy urine
 Chronic prostatitis: bacterial invasion from urethra  Distended bladder
 Granulomatous prostatitis: miliary spread of My-  Prostatic tenderness, induration, swelling, firmness,
cobacterium tuberculosis and warmth
 Nonbacterial prostatitis: Mycoplasma, Ureaplasma,  Crepitation (if prostatic calculi present)
Chlamydia, or Trichomonas vaginalis, or a virus Chronic bacterial prostatitis
 Prostatodynia: unknown  Stony, hard induration of the prostate

Risk factors Test results

 Invasive urethral procedures
 Infrequent or excessive sexual intercourse
Incidence
Chronic prostatitis
 Affects up to 35% of males older than age 50
 Seen in 5 of every 1,000 outpatient visits
Bacterial prostatitis
 Seen in 2 of every 10,000 outpatient visits
Nonbacterial prostatitis
 Seen in 5 of every 10,000 outpatient visits
Common characteristics
 Urinary frequency and urgency
 Fever
Laboratory
 Urine culture identifies infectious organism.
 In nonbacterial prostatitis: inflammatory cells are
found in smears of prostatic secretion.
 In prostatodynia: urine cultures are negative and
theres an absence of inflammatory cells in smears of
prostatic secretions.
Diagnostic procedures
 In granulomatous prostatitis: prostate tissue biopsy
shows M. tuberculosis.
 Urodynamic evaluation reveals detrusor hyperreflexia
and pelvic floor myalgia (from chronic spasms).

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Treatment Patient teaching

General Be sure to cover:
 Sitz baths  the disorder, diagnosis, and treatment
 Regular, protected sexual intercourse  medication administration, dosage, and possible
 Prostatic massage adverse effects
 Increased oral fluids  importance of increased fluid intake
 Bed rest until the condition improves  benefits of regular sexual activity (with chronic pro-
After surgery statitis)
 Avoidance of lifting, strenuous exercise, and long au-  prescribed activity limits
tomobile rides  importance of getting immediate medical attention
 No sexual activity for several weeks after discharge for fever, inability to void, or bloody urine.
Medications Discharge planning
 Analgesics  Refer the patient to counseling or support group as
 Antipyretics needed.
Acute prostatitis
 Systemic antibiotic therapy
Chronic prostatitis
 Oral antibiotics
Granulomatous prostatitis
 Antitubercular drug combinations
Nonbacterial prostatitis
 Oral antibiotics
 Anticholinergics
Prostatodynia
 Muscle relaxants
 Alpha-adrenergic blockers

Surgery
 Transurethral resection of the prostate or total
prostatectomy, if drug therapy unsuccessful

Nursing considerations
Key outcomes
The patient will:
 express feelings of increased comfort
 demonstrate skill in managing urinary elimination
problems
 express his feelings about potential or actual changes
in sexual function
 use available counseling, referrals, or support
groups.
Nursing interventions
 Administer prescribed drugs.
 Ensure bed rest and adequate hydration.
 Give sitz baths.
 Avoid rectal examinations.

Monitoring
After surgery
 Intake and output
 Catheter function and drainage
 Signs of infection
 Pain control

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Pseudomembranous  Peritonitis
 Toxic megacolon

enterocolitis
Assessment
Overview History
 Current or recent antibiotic treatment
Description  Sudden onset of copious, watery, or bloody diarrhea
 Acute inflammation and necrosis of the small and  Cramping abdominal pain
large intestines  Low-grade fever
 Usually affects the mucosa but may extend into the  Nausea
submucosa and, rarely, into other layers  Vomiting
 Marked by severe diarrhea
 Can be fatal in 1 to 7 days from severe dehydration Physical findings
or from toxicity, peritonitis, or perforation  Abdominal tenderness

Pathophysiology Test results

 Pseudomembranous enterocolitis is associated with Laboratory
antibiotic use.  White blood cell count is elevated.
 Normal intestinal flora balance is altered, and over-  Hypoalbuminemia occurs due to poor protein
growth of certain organisms occurs. absorption.
 Necrotic mucosa is replaced by a pseudomembrane  Stool culture identifies C. difficile.
filled with staphylococci, leukocytes, mucus, fibrin, Imaging
and inflammatory cells.  Abdominal X-ray reveals mucosal edema.
 Computed tomography scan may show distention as
Causes well as diffuse and focal thickening of the colon wall.
 Unknown Diagnostic procedures
 Possible role of Clostridium difficile  Rectal biopsy through sigmoidoscopy confirms
pseudomembranous enterocolitis.
Risk factors  Endoscopy reveals characteristic pseudomembranes.
 Antibiotic therapy
 Recent abdominal surgery
 Cancer chemotherapy Treatment
 Compromised immune system
 Advanced age General
 Bone-marrow transplantation  Discontinuation of offending antibiotics
 Intestinal ischemia  Avoidance of opioids and antidiarrheals
 Uremia  Supportive treatment
 Burns  I.V. fluids (if the condition is severe)
 Nothing by mouth until bowel recovery occurs (if the
Incidence condition is severe)
 Affects both sexes equally  Bed rest until recovery begins
 Most common in nursing home and hospital patients  Enteric precautions
 Affects 6 of every 100,000 people treated with antibi-
otics Medications
 Oral metronidazole or oral vancomycin
Common characteristics  Electrolyte replacement
 Watery, green, foul-smelling diarrhea
 Up to 30 stools per day Surgery
 Diverting ileostomy or bowel resection (with perfora-
Complications tion or toxic megacolon)
 Severe dehydration  Early subtotal colectomy
 Electrolyte imbalance
 Hemorrhage
 Hypotension Nursing considerations
 Hypovolemia
 Sepsis Key outcomes
 Shock The patient will:
 Colonic perforation  express feelings of increased comfort
 maintain normal fluid volume

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 maintain stable vital signs

 maintain adequate caloric intake
 regain normal bowel function
 regain normal laboratory values.

Nursing interventions
 Administer prescribed drugs and I.V. fluids.
 Keep the patient as comfortable as possible.
 Maintain precautions to prevent the infection from
spreading to other patients.
Monitoring
 Vital signs
 Fluid and nutritional status
 Skin integrity
 Bowel function
 Electrolytes

Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatment
 medication administration, dosage, and possible
adverse effects
 signs and symptoms of a recurrence
 importance of cautioning future prescribers (if the
disorder was antibiotic-related).
Discharge planning
 Refer the patient to home care services as indicated.

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Psoriasis  Pruritus and burning

 Arthritic symptoms such as morning joint stiffness
 Remissions and exacerbations

Overview Physical findings

Description
 Hereditary chronic skin disease marked by epider-
mal proliferation
 Causes lesions of erythematous papules and plaques
covered with silvery scales (Lesions vary widely in
severity and distribution.)
 Involves recurring remissions and exacerbations
 Exacerbations unpredictable, but usually controllable
with therapy
Pathophysiology
 Psoriatic skin cells have a shortened maturation time
as they migrate from the basal membrane to the sur-
face or stratum corneum.
 As a result, the stratum corneum develops thick,
scaly plaques (the cardinal manifestation of psoria-
sis).
 Erythematous, well-demarcated papules and plaques
covered with silver scales, typically appearing on the
scalp, chest, elbows, knees, back, and buttocks
 In mild psoriasis: plaques scattered over a small skin
area
 In moderate psoriasis: plaques more numerous and
larger (up to several centimeters in diameter)
 In severe psoriasis: plaques covering at least half the
body
 Friable or adherent scales
 Fine bleeding points or Auspitz sign after attempts to
remove scales
 Thin, erythematous guttate lesions, alone or with
plaques, and with few scales (see Identifying types
of psoriasis)
 Small indentations or pits, and yellow or brown dis-
coloration of fingernails or toenails
 In severe cases, separation of nail from nail bed

Causes Test results

 Genetic predisposition Laboratory
 Possible autoimmune process  Serum uric acid level is elevated.
 Physical trauma  In early-onset familial psoriasis: human leukocyte
 Beta-hemolytic streptococci infection antigens Cw6, B13, and Bw-57 are present.
Diagnostic procedures
Risk factors  Skin biopsy helps rule out other diseases.
 Pregnancy
 Endocrine changes
 Cold weather Treatment
 Emotional stress
General
Incidence  Depends on the psoriasis type, extent, and effect on
 Affects about 2% of the United States population the patients quality of life
 Affects both sexes equally  Lesion management
 Can occur at any age  Lukewarm baths
 More common among whites  Ultraviolet B light or natural sunlight
 Two periods of onset: early (young adulthood) and
late (middle adulthood) Medications
 Topical corticosteroid creams and ointments
Common characteristics  Antihistamines
 Silvery scales on red plaques  Analgesics
 Pruritus  Nonsteroidal anti-inflammatory drugs
 Knee-elbow-scalp distribution  Occlusive ointment bases
 Urea or salicylic acid preparations
Complications  Coal tar preparations
 Infection  Vitamin D analogs
 Altered self-image  Emollients
 Social isolation  Kerolytic agents
 Depression  Methotrexate for severe, unresponsive psoriasis
 Potent retinoic acid derivative for resistant psoriasis
 Cyclosporine for severe, widespread psoriasis
Assessment  Immunomodulators (biologics), such as alefacept,
efalizumab, or etanercept for psoriatic arthritis or
History failed treatment
 Family history of psoriasis
 Risk factors

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Identifying types of psoriasis

Psoriasis occurs in various forms, ranging from one or two localized plaques that seldom require long-term medical atten-
tion to widespread lesions and crippling arthritis.

Erythrodermic psoriasis Psoriasis vulgaris

Erythrodermic psoriasis is marked by extensive flushing all
over the body, which may result in scaling. The rash may
develop rapidly, signaling new psoriasis or gradually in
chronic psoriasis. Sometimes the rash occurs as an ad-
verse drug reaction.
Guttate psoriasis
Guttate psoriasis typically affects children and young
adults. Erupting in drop-size plaques over the trunk, arms,
legs and, sometimes, the scalp, this rash generalizes in
several days. Its commonly associated with upper respira-
tory streptococcal infections.
Inverse psoriasis
Smooth, dry, bright red plaques characterize inverse psori-
asis. Located in skin folds (armpits and groin, for example),
the plaques fissure easily.
Psoriasis vulgaris is the most common. It begins with red,
dotlike lesions that gradually enlarge and produce dry, sil-
very scales. The plaques usually appear symmetrically on
the knees, elbows, extremities, genitalia, scalp, and nails.
Pustular psoriasis
Pustular psoriasis features an eruption of local or extensive
small, raised, pus-filled plaques. Possible triggers include
emotional stress, sweating, infections, and adverse drug
reactions.

Surgery  likelihood of exacerbations and remissions

 Surgical nail removal to treat severely disfigured or  medication administration, dosage, and possible
damaged nails caused by psoriasis adverse effects
 how to apply prescribed ointments, creams, and lo-
tions
Nursing considerations  importance of avoiding scratching plaques
 measures to relieve pruritus
Key outcomes  importance of avoiding sun exposure
The patient will:  stress-reduction techniques
 exhibit improved or healed lesions  safety precautions
 report feelings of increased comfort  relationship between psoriasis and arthritis
 verbalize feelings about changed body image  when to notify the physician.
 demonstrate understanding of proper skin care
 express an understanding of the condition and its Discharge planning
treatment.  Refer the patient to the National Psoriasis Founda-
tion.
Nursing interventions
 Administer prescribed drugs.
 Apply topical medications using a downward motion.
 Encourage the patient to verbalize his feelings.
 Provide emotional support.
 Involve family members in the treatment regimen.

Monitoring
 Response to treatment
 Lipid profile results
 Liver function tests
 Renal function
 Blood pressure
 Signs and symptoms of hepatic or bone marrow
toxicity

Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatment
 risk factors
 incommunicability of psoriasis

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Ptosis Assessment
History
Overview  History of causative factor
 Family history
Description  Trauma or ocular surgery
 Drooping of the upper eyelid
 May be congenital or acquired, unilateral or bilater- Physical findings
al, constant or intermittent  Abnormal eyelid
 If severe, usually responds to treatment; if slight, may  Drooping eyelid (see Recognizing ptosis)
not require treatment  Elevated eyebrow
 Also known as blepharoptosis  Wrinkled forehead
 Fixed, dilated pupil
Pathophysiology
 Ptosis is caused by dysfunction of one or both upper Test results
eyelid levator muscles. Imaging
 Digital subtraction angiography and magnetic reso-
Causes nance imaging (MRI) show aneurysm.
Congenital ptosis  MRI reveals multiple sclerosis.
 Transmitted as an autosomal dominant trait Diagnostic procedures
 Results from a congenital anomaly in which the leva-  Glucose tolerance test detects diabetes.
tor muscles of the eyelids fail to develop  Tensilon test detects myasthenia gravis (in acquired
Acquired ptosis ptosis with no history of trauma).
 Advanced age (involutional ptosis, the most common Other
form, usually seen in older patients following  Physical examination reveals upper lid retraction.
cataract surgery)  Examination with the Hertel exophthalmometer re-
 Mechanical factors that make the eyelid heavy veals the degree of proptosis.
 Myogenic factors
 Neurogenic (paralytic) factors
 Nutritional factors Treatment
 Trauma
 Ocular surgery General
 Treatment of underlying cause
Incidence  Special glasses with an attached suspended crutch on
 Congenital ptosis: occurs at birth the frames to elevate the eyelid
 Acquired ptosis: can occur at any age but mostly  Eye protection with potentially dangerous activities
affects adults
 Affects both sexes equally Medications
 Topical antibiotic ointment (after surgery)
Common characteristics
 An infant with congenital ptosis has a smooth, flat up- Surgery
per eyelid, without the eyelid fold normally caused by  Resection of the weak levator muscles
the pull of the levator muscle; associated weakness of
the superior rectus muscle isnt uncommon.
 Ptosis due to oculomotor nerve damage produces a Nursing considerations
fixed, dilated pupil; divergent strabismus; and slight
depression of the eyeball. Key outcomes
The patient will:
Complications  avoid injury
 Disturbed vision  demonstrate improvement in eyelid function
 Amblyopia  express understanding of the disorder and its treat-
 Infection (after surgery) ment.
 Psychosocial effects
Nursing interventions
 Provide a safe environment.
 Apply ointment to the sutures as prescribed.

Monitoring
 Signs of bleeding (after surgery)
 Visual acuity

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Recognizing ptosis
A drooping upper eyelid typically apparent on visual
examination is the hallmark of ptosis. The disorder
may affect one or both eyelids.

Patient teaching
Be sure to cover:
 the need to report postsurgery bleeding immediately
 the need to prevent accidental trauma to the surgical
site until healing is complete.
Discharge planning
 Refer the patient to a neurologist if myasthenia gravis
or multiple sclerosis is diagnosed.

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 Orthopnea
Life-threatening disorder  Paroxysmal nocturnal dyspnea

Complications
Pulmonary edema  Respiratory and metabolic acidosis
 Cardiac or respiratory arrest
 Death
Overview
Description Assessment
 Accumulation of fluid in the extravascular spaces of
the lung History
 Common complication of cardiovascular disorders  Predisposing factor
 May be chronic or acute  Persistent cough
 Can become fatal rapidly  Dyspnea on exertion
 Paroxysmal nocturnal dyspnea
Pathophysiology  Orthopnea
 Pulmonary edema results from either increased pul-
monary capillary hydrostatic pressure or decreased Physical findings
colloid osmotic pressure. Normally, the two pres-  Restlessness and anxiety
sures are in balance.  Rapid, labored breathing
 If pulmonary capillary hydrostatic pressure increas-  Intense, productive cough
es, the compromised left ventricle needs higher fill-  Frothy, bloody sputum
ing pressures to maintain adequate output; these  Mental status changes
pressures are transmitted to the left atrium, pul-  Jugular vein distention
monary veins, and pulmonary capillary bed. Fluids  Sweaty, cold, clammy skin
and solutes are then forced from the intravascular  Wheezing
compartment into the lung interstitium. With fluid  Crackles
overloading the interstitium, some fluid floods pe-  S3
ripheral alveoli and impairs gas exchange.  Tachycardia
 If colloid osmotic pressure decreases, the pulling  Hypotension
force that contains intravascular fluids is lost, and  Thready pulse
nothing opposes the hydrostatic force. Fluid flows  Peripheral edema
freely into the interstitium and alveoli, causing pul-  Hepatomegaly
monary edema.
Test results
Causes Laboratory
 Left-sided heart failure  Arterial blood gas (ABG) analysis shows hypoxemia,
 Diastolic dysfunction hypercapnia, or acidosis.
 Valvular heart disease Imaging
 Arrhythmias  Chest X-rays show diffuse haziness of the lung fields,
 Fluid overload cardiomegaly, and pleural effusion.
 Acute myocardial ischemia and infarction Diagnostic procedures
 Barbiturate or opiate poisoning  Pulse oximetry may show decreased oxygen satura-
 Impaired pulmonary lymphatic drainage tion.
 Inhalation of irritating gases, smoke inhalation  Pulmonary artery catheterization may reveal in-
 Left atrial myxoma creased pulmonary artery wedge pressures.
 Pneumonia  Electrocardiography may show valvular disease and
 Pulmonary veno-occlusive disease left ventricular hypokinesis or akinesis.
 Acute respiratory distress syndrome
 Kidney disease
 Altitude above 8,000 feet Treatment
 Ascent to high altitudes without becoming acclimated
General
Incidence  Fluid overload reduction
 More common in middle-aged and elderly people  Improved gas exchange and myocardial function
 Affects both sexes equally  Correction of underlying disease
 Sodium-restricted diet
Common characteristics  Fluid restriction
 Persistent cough  Activity, as tolerated
 Dyspnea on exertion

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Medications  medication administration, dosage, and possible

 Supplemental oxygen adverse effects
 Diuretics  fluid and sodium restrictions
 Antiarrhythmics  daily weight
 Morphine  signs and symptoms of fluid overload
 energy conservation strategies
 avoidance of alcohol
ALERT
 when to notify the physician.
Be aware that morphine can further compromise
respirations in a patient with respiratory distress. Discharge planning
Keep resuscitation equipment at hand in case the  Refer the patient to a cardiac rehabilitation program,
patient stops breathing. if indicated
 Refer the patient to a smoking-cessation program, if
 Preload-reducing agents, such as furosemide and indicated.
nitroglycerin
 Afterload-reducing agents, such as nitroprusside and
enalapril
 Bronchodilators
 Positive inotropic agents
 Vasopressors

Surgery
 Valve repair or replacement or myocardial revascu-
larization if appropriate to correct the underlying
cause

Nursing considerations
Key outcomes
The patient will:
 maintain adequate ventilation
 maintain fluid balance
 maintain adequate cardiac output
 verbalize decreased anxiety and fear
 demonstrate adequate coping mechanisms.

Nursing interventions
 Administer prescribed drugs and oxygen.
 Place the patient in high Fowlers position.
 Restrict fluids and sodium intake.
 Promote rest and relaxation.
 Provide emotional support.

Monitoring
 Vital signs
 Intake and output
 Daily weight
 Respiratory status
 Response to treatment
 Complications
 Heart rhythm
 ABG values
 Pulse oximetry values
 Hemodynamic values

Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatment

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Complications
Life-threatening disorder  Pulmonary infarction
 Pulmonary hypertension

Pulmonary embolism  Embolic extension

 Hepatic congestion and necrosis
 Pulmonary abscess
 Shock
Overview  Acute respiratory distress syndrome
 Massive atelectasis
Description  Right-sided heart failure
 Obstruction of the pulmonary arterial bed occurring  Ventilation-perfusion mismatch
when a mass (such as a dislodged thrombus) lodges  Death
in the main pulmonary artery or branch, partially or
completely obstructing it
 Most thrombi originate in deep veins of the leg Assessment
 Can be asymptomatic, but sometimes causes rapid
death from pulmonary infarction History
 Predisposing factor
Pathophysiology  Shortness of breath for no apparent reason
 Thrombus formation results from vascular wall dam-  Pleuritic pain or angina
age, venous stasis, or blood hypercoagulability.
 Trauma, clot dissolution, sudden muscle spasm, in- Physical findings
travascular pressure changes, or peripheral blood  Tachycardia
flow changes can cause the thrombus to loosen or  Low-grade fever
fragmentize.  Weak, rapid pulse
 The thrombus (now an embolus) floats to the hearts  Hypotension
right side and enters the lung through the pulmonary  Productive cough, possibly with blood-tinged sputum
artery. There, the embolus may dissolve, continue to  Warmth, tenderness, and edema of the lower leg
fragmentize, or grow.  Restlessness
 By occluding the pulmonary artery, the embolus pre-  Transient pleural friction rub
vents alveoli from producing enough surfactant to  Crackles
maintain alveolar integrity. Alveoli collapse and at-  S3 and S4 with increased intensity of the pulmonic
electasis develop. component of S2
 If the embolus enlarges, it may occlude most or all of  With a large embolus: cyanosis, syncope, distended
the pulmonary vessels and cause death. neck veins
Causes Test results
 Deep vein thrombosis Laboratory
 Pelvic, renal, and hepatic vein thrombosis  Arterial blood gas (ABG) values show hypoxemia.
 Right heart thrombus  D-dimer level is elevated.
 Upper extremity thrombosis Imaging
 Atrial fibrillation  Lung ventilation-perfusion scan shows a ventilation-
 Valvular heart disease perfusion mismatch.
 Rarely, other types of emboli, such as bone, air, fat,  Pulmonary angiography shows a pulmonary vessel
amniotic fluid, tumor cells, or a foreign body filling defect or an abrupt vessel ending and reveals
the location and extent of pulmonary embolism.
Risk factors  Chest X-rays may show a small infiltrate or effusion.
 Various disorders and treatments (see Whos at risk  Spiral chest computed tomography scan may show
for pulmonary embolism?) central pulmonary emboli.
Diagnostic procedures
Incidence  Electrocardiography may reveal right axis deviation
 600,000 to 700,000 cases annually and right bundle-branch block; it also may show atri-
 Affects both sexes equally al fibrillation.
 More common with advancing age

Common characteristics Treatment

 Shortness of breath for no apparent reason
 Tachycardia General
 Anxiety  Maintenance of adequate cardiovascular and pul-
 Pleuritic or anginal pain monary function
 Mechanical ventilation, if indicated

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Whos at risk for pulmonary embolism?

Many disorders and treatments heighten the risk of pulmonary embolism. At particular risk are surgical patients. The anes-
thetic used during surgery can injure lung vessels, and surgery or prolonged bed rest can promote venous stasis, which
compounds the risk.

Predisposing disorders Venous stasis

 Lung disorders, especially chronic types  Prolonged bed rest or immobilization
 Cardiac disorders  Obesity
 Infection  Older than age 40
 Diabetes mellitus  Burns
 History of thromboembolism, thrombophlebitis, or vas-  Recent childbirth
cular insufficiency  Orthopedic casts
 Sickle cell disease Venous injury
 Autoimmune hemolytic anemia  Surgery, particularly of the legs, pelvis, abdomen, or
 Polycythemia thorax
 Osteomyelitis  Leg or pelvic fractures or injuries
 Long-bone fracture  I.V. drug abuse
 Manipulation or disconnection of central lines  I.V. therapy
Increased blood coagulability
 Cancer
 Use of high-estrogen hormonal contraceptives

 Possible fluid restriction  Assist with ambulation as soon as the patient is

 Bed rest during the acute phase stable.
 Encourage the use of an incentive spirometer.
Medications
 Oxygen therapy Monitoring
 Thrombolytics  Vital signs
 Anticoagulation  Intake and output
 Corticosteroids (controversial)  Respiratory status
 Diuretics  Pulse oximetry
 Antiarrhythmics  ABG values
 Vasopressors (for hypotension)  Signs of deep vein thrombosis
 Antibiotics (for septic embolus)  Complications
 Coagulation study results
Surgery  Abnormal bleeding
 Vena caval interruption  Stools for occult blood
 Vena caval filter placement
 Pulmonary embolectomy
Patient teaching
Nursing considerations Be sure to cover:
 the disease, diagnosis, and treatment
Key outcomes  medication administration, dosage, and possible
The patient will: adverse effects
 maintain adequate ventilation  ways to prevent deep vein thrombosis and pulmonary
 maintain adequate cardiac output embolism
 maintain a patent airway  signs and symptoms of abnormal bleeding
 verbalize feelings of increased comfort  prevention of abnormal bleeding
 demonstrate effective coping mechanisms.  how to monitor anticoagulant effects
 dietary sources of vitamin K
Nursing interventions  when to notify the physician.
 Administer prescribed drugs.
 Avoid I.M. injections. Discharge planning
 Encourage active and passive range-of-motion exer-  Refer the patient to a weight-management program, if
cises, unless contraindicated. indicated.
 Avoid massage of the lower legs.
 Apply antiembolism stockings.
 Provide adequate nutrition.

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Common characteristics
Life-threatening disorder  Dyspnea on exertion
 Weakness, fatigue

Pulmonary  Syncope

Complications
hypertension  Cor pulmonale
 Heart failure
 Cardiac arrest
Overview  Death

Description
 Pulmonary condition exhibiting increased pressure Assessment
in the pulmonary artery
 Occurs in a primary form (rare) and a secondary History
form  Shortness of breath with exertion
 In both forms, resting systolic pulmonary artery pres-  Weakness, fatigue
sure (PAP) above 30 mm Hg and mean PAP above  Pain during breathing
20 mm Hg  Near-syncope
 Primary form also known as PPH
Physical findings
Pathophysiology  Ascites
 In PPH, the intimal lining of the pulmonary arteries  Jugular vein distention
thickens for no apparent reason. This narrows the  Peripheral edema
artery and impairs distensibility, increasing vascular  Restlessness and agitation
resistance.  Mental status changes
 Secondary pulmonary hypertension occurs from hy-  Decreased diaphragmatic excursion
poxemia caused by conditions involving alveolar hy-  Apical impulse displaced beyond mid-clavicular line
poventilation, vascular obstruction, or left-to-right  Right ventricular lift
shunting.  Reduced carotid pulse
 Hepatomegaly
Causes  Tachycardia
Primary pulmonary hypertension  Systolic ejection murmur
 Unknown  Widely split S2
 Possible hereditary factors  S3 and S4
 Possible altered autoimmune mechanisms  Hypotension
 Associated with portal hypertension  Decreased breath sounds
Secondary pulmonary hypertension  Tubular breath sounds
 Chronic obstructive pulmonary disease
 Sarcoidosis Test results
 Diffuse interstitial pneumonia Laboratory
 Malignant metastasis  Arterial blood gas (ABG) values show hypoxemia.
 Scleroderma Imaging
 Use of some diet drugs  Ventilation-perfusion lung scan may show a
 Obesity ventilation-perfusion mismatch.
 Sleep apnea  Pulmonary angiography may reveal filling defects in
 Hypoventilation syndromes the pulmonary vasculature.
 Kyphoscoliosis Diagnostic procedures
 Pulmonary embolism  Electrocardiography may reveal right-axis deviation.
 Vasculitis  Pulmonary artery catheterization shows increased
 Left atrial myxoma PAP, with systolic pressure above 30 mm Hg; in-
 Congenital cardiac defects creased pulmonary artery wedge pressure; decreased
 Mitral stenosis cardiac output; and decreased cardiac index.
 Living at a high altitude  Pulmonary function tests may show decreased flow
rates and increased residual volume or reduced total
Incidence lung capacity.
Primary pulmonary hypertension  Echocardiography may show valvular heart disease
 Most common in females ages 20 to 40 or atrial myxoma.
 More prevalent in people with collagen disease Other
 Lung biopsy may show tumor cells.

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 frequent rest periods

Treatment  signs and symptoms of right-sided heart failure
 when to notify the physician.
General
 Low-sodium diet Discharge planning
 Fluid restriction (in right-sided heart failure)  Refer the patient to a smoking-cessation program, if
 Bed rest during acute phase indicated.
Medications
 Oxygen therapy
 Cardiac glycosides
 Diuretics
 Vasodilators such as treprostinil
 Calcium channel blockers such as amlodipine
 Bronchodilators
 Beta-adrenergic blockers
 Iloprost
 Prostacyclin
 Endothelin receptor antagonists such as bosentan
 Anticoagulants

Surgery
 Heart-lung transplantation, if indicated

Nursing considerations
Key outcomes
The patient will:
 maintain adequate ventilation
 maintain adequate cardiac output
 express an understanding of the disorder
 demonstrate effective coping mechanisms.

Nursing interventions
 Administer prescribed drugs and oxygen.
 Implement comfort measures.
 Provide adequate rest periods.
 Offer emotional support.

Monitoring
 Vital signs
 Intake and output
 Daily weight
 Respiratory status
 Signs and symptoms of right-sided heart failure
 Heart rhythm
 ABG values
 Hemodynamic values

Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatment
 medication administration, dosage, and possible
adverse effects
 dietary restrictions

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Pulmonic insufficiency  Fatigue

 Angina
 Palpitations

Overview Physical findings

 Tachycardia
Description  Crackles in the lungs
 Heart condition in which blood ejected into the pul-  Hepatomegaly (right-sided failure)
monary artery during systole flows back into the right  Jugular vein distention
ventricle during diastole  Palpable right ventricular systolic pulsation at left
 Also called pulmonary regurgitation lower sternal border
 S3 or S4 at left mid-to-lower sternal border
Pathophysiology  Hemoptysis
 Pulmonic valve is incompetent.
 Incompetency is caused by: Test results
dilation of the pulmonic valve ring Imaging
acquired alteration of pulmonic cusp morphology  Chest X-rays reveal cardiomegaly, right-sided heart
congenital absence or malformation. enlargement, and pulmonary hypertension.
 Blood flows back into the right ventricle from the  Echocardiography shows right ventricular hypertro-
pulmonary artery. phy and dilation.
 Fluid overload occurs in the ventricle. Diagnostic procedures
 Chronic backflow causes ventricular hypertrophy and  Electrocardiography may show incomplete right
right-sided heart failure. bundle-branch block and right axis deviation.
 Cardiac catheterization may determine underlying
Causes etiology.
 Pulmonary hypertension
 Infective endocarditis
 Tetralogy of Fallot Treatment
 Rheumatic heart disease
 Carcinoid heart disease General
 Dilated cardiomyopathy  Treatment of underlying cause
 Symptomatic treatment
Incidence  Low-sodium diet
 Variable age of occurrence  Activity, as tolerated
 Affects both males and females; frequency based on
specific cause Medications
 Diuretics
Common characteristics  Inotropic agent
 Dyspnea on exertion  Angiotensin-converting enzyme inhibitors
 Peripheral edema  Oxygen
 Tachycardia  Possible prophylactic antibiotics before and after
 Fatigue surgery or dental care to prevent endocarditis
Complications Surgery
 Heart failure  Annuloplasty or valvuloplasty to reconstruct or repair
 Pulmonary edema the valve
 Thromboembolism  Valve replacement with a prosthetic valve
 Endocarditis
 Arrhythmias
Nursing considerations
Assessment Key outcomes
The patient will:
History  perform activities of daily living without weakness or
 Pulmonary hypertension fatigue
 Infective endocarditis  maintain hemodynamic stability
 Tetralogy of Fallot  maintain adequate ventilation.
 Rheumatic heart disease
 Carcinoid heart disease Nursing interventions
 Orthopnea  Administer prescribed oxygen.
 Dyspnea  Watch for signs of heart failure or pulmonary edema.

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Monitoring
 Vital signs and pulse oximetry
 Cardiac rhythm
 Pulmonary artery catheter readings
 Intake and output
 Adverse effects of drug therapy

Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatment
 dietary restrictions
 medication administration, dosage, and possible
adverse effects.
Discharge planning
 Encourage follow-up care with a cardiologist.

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Physical findings
Pulmonic stenosis  Palpable impulse from the right ventricle along the
left parasternal border
 Peripheral edema
Overview  Split S2
 Systolic ejection click
Description  Crackles in the lungs
 Heart condition in which obstructed right ventricular  Hepatomegaly (right-sided failure)
outflow causes right-ventricular hypertrophy, eventu-  Jugular vein distention
ally resulting in right-sided heart failure
 Also called pulmonary regurgitation Test results
Imaging
Pathophysiology  Chest X-rays reveal prominence of the main, right, or
 Dynamic or fixed obstruction affects blood flow from left pulmonary arteries.
the right ventricle to the pulmonary arteriole vascula-  Echocardiography shows thickening of the valves,
ture. characteristic doming of nondysplastic valves, and
 Chronic obstruction may result in right-sided heart right ventricular hypertrophy.
failure.  Cardiac ultrasound reveals thickening of valves, char-
acteristic doming of nondysplastic valves, and right-
Causes ventricular hypertrophy.
 Congenital defect Diagnostic procedures
 Sinus of Valsalva aneurysm  Electrocardiography may show mild right axis
 Aortic graft aneurysm deviation.
 Rheumatic heart disease
 Carcinoid heart disease
Treatment
Incidence
 Affects females slightly more than males General
 Treatment of underlying cause
Common characteristics  Low-sodium diet
 Dyspnea on exertion  Avoidance of vigorous physical activity
 Peripheral edema
 Cyanosis Medications
 Tachycardia  Diuretics
 Fatigue  Inotropic agents
 Angiotensin-converting enzyme inhibitors
Complications  Oxygen
 Heart failure  Possible prophylactic antibiotics before and after
 Pulmonary edema surgery or dental care to prevent endocarditis
 Thromboembolism
 Endocarditis Surgery
 Arrhythmias  Balloon valvoplasty
 Pulmonary artery balloon angioplasty
 Valvotomy
Assessment
History Nursing considerations
 Congenital defect
 Sinus of Valsalva aneurysm Key outcomes
 Aortic graft aneurysm The patient will:
 Rheumatic heart disease  perform activities of daily living without weakness or
 Carcinoid heart disease fatigue
 Orthopnea  maintain hemodynamic stability
 Exertional dyspnea  maintain adequate ventilation
 Fatigue  state understanding of disorder and treatment.
 Angina
 Palpitations Nursing interventions
 Administer prescribed oxygen.
 Watch for signs of heart failure or pulmonary edema.
 Encourage verbalization and provide support.
 Administer prescribed drugs.

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Monitoring
 Vital signs and pulse oximetry
 Cardiac rhythm
 Pulmonary artery catheter readings
 Intake and output
 Adverse effects of drug therapy

Patient teaching
Be sure to cover:
 the disorder, diagnosis, and treatment
 dietary restrictions
 activity restrictions
 medication administration, dosage, and possible
adverse effects.
Discharge planning
 Encourage follow-up care with a cardiologist.

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Q Q fever
Overview
Description
H Acute systemic disease that affects people exposed to
cattle, sheep, or goats
H Rare human-to-human transmission; possible sexual
transmission
H May be acute or chronic

Pathophysiology
H Coxiella burnetii is excreted in urine, milk, and
feces of infected animals.
Assessment
History
H Exposure to cattle, sheep, or goats
H Headache
H Myalgia
H Chills, fever

Physical findings
H Crackles (pneumonia)
H Hepatomegaly and jaundice (hepatitis)
H Heart murmur, signs of heart failure (endocarditis)

Test results
Laboratory
H Once ingested, it proliferates in macrophages (in the H Patients with the acute form may have an elevated
acidic phagolysosome vacuole) and then gains ac- white blood cell count, transient thrombocytopenia,
cess to the blood, producing a transient bacteremia. and elevated transaminases and alkaline phosphatase
H It may invade many organs, most commonly the levels.
lungs and liver. H Cerebrospinal fluid evaluation reveals lymphocytosis,
H Inflammation occurs, manifested by granulomas in elevated protein level, and normal glucose level.
the liver, spleen, and bone marrow. These classic H Complement fixation reveals antephase II antibody
doughnut granulomas disappear with convalescence. titers of 40 or more (acute disease) and antephase I
antibody titers of 200 of more (chronic disease).
Causes H Microimmunofluorescence reveals immunoglobulin
H Coxiella burnetii (Ig) G antephase II antibody titers of 200 or more
and IgM antephase II antibody titers of 50 or more
Incidence (acute). (The presence of antephase I antibodies in-
H Affects males more than females because males more dicates chronic Q fever; the presence of IgG ante-
likely to be exposed to livestock phase I antibody titers of 800 or more is highly pre-
H Most commonly affects people ages 25 to 40 dictive of endocarditis.)
Imaging
Common characteristics H Chest X-rays may show segmental or lobar opacities,
H Self-limiting, febrile illness with headache, myalgia, multiple round opacities, and pleural effusion.
chills H Echocardiography may show pericardial effusion
H May have symptoms of pneumonia, hepatitis, or en- with pericarditis.
docarditis (chronic) Diagnostic procedures
H May be asymptomatic H Electrocardiography shows T-wave abnormalities
with myocarditis and pericarditis.
Complications
H Chronic fatigue syndrome
H Heart failure Treatment
H Endocarditis (see Treating Q fever endocarditis)
General
H Symptomatic
H Diet as tolerated
Treating Q fever endocarditis H Activity as tolerated

Chronic Q fever endocarditis typically requires the use of Medications

multiple drugs to treat effectively. Two different drug treat-
ment protocols have been evaluated: H Antibiotics such as doxycycline
H doxycycline with quinolones, for at least 4 years H Antimalarials such as hydroxychloroquine
H doxycycline with hydroxychloroquine, for 112 to 3
years. Surgery
The second drug treatment protocol causes fewer re- H Possible valve replacement
lapses but requires routine eye examinations to detect
accumulation of chloroquine.
Some patients with C. burnetii endocarditis require
surgery to remove damaged valves.

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Nursing considerations
Key outcomes
The patient will:
H express understanding of illness and treatment
regimen
H remain hemodynamically stable
H remain free from complications.

Nursing interventions
H Provide emotional support.
H Administer prescribed drugs.

Monitoring
H Vital signs
H Cardiac status
H Respiratory status
H Response to treatment

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the importance of follow-up care and compliance
with long-term therapy
H medication administration, dosage, and possible
adverse effects.

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R Rabies
Overview
Life-threatening disorder

Description
H An acute central nervous system (CNS) infection usu-
ally transmitted by animal bite
H Incubation period varies but usually 1 to 3 months
H 70% of cases in the United States from raccoon,
skunk, fox, or bat bite; vaccinations have reduced
Common characteristics
H Progressive signs and symptoms
H After incubation period, local or radiating pain or
burning and coldness, pruritus, and tingling at the
bite site
H Slight fever (100 to 102 F [37.8 to 38.9 C])
H Malaise
H Nervousness that progresses into agitation and cra-
nial nerve dysfunction, causing ocular palsies
H Hyperesthesia
H Photophobia
H Sensitivity to loud noise
H Pupillary dilation
H Tachycardia
H Shallow respirations
transmission from dogs H Excessive salivation, lacrimation, and perspiration
H Almost always fatal if symptoms occur, although H Hydrophobia, during which forceful, painful pharyn-
prompt treatment may prevent fatal CNS invasion geal muscle spasms expel liquids from the mouth
and cause dehydration
Pathophysiology H After about 3 days, gradual, generalized, flaccid
H The rabies virus is transmitted through the bite of an paralysis that ultimately leads to peripheral vascular
infected animal that introduces the virus through the collapse, coma, and death
skin or mucous membrane.
H The virus begins to replicate in the striated muscle Complications
cells at the bite site. H Paralysis
H It then travels up the nerve to the CNS and replicates H Coma
in the brain. H Death
H Finally, it moves through the nerves into other tis-
sues, including the salivary glands.
Assessment
Causes
H Bite from a rabid animal History
H Occasionally transmitted by airborne droplets and in- H Animal bite
fected tissue transplants H Fever
H Malaise
Incidence
H Can affect anyone at any age Physical findings
H Annually, an estimated 35,000 to 50,000 deaths H Burning at wound site
worldwide H Tachycardia
H Excessive salivation
H Shallow respirations
H Dilated pupils and photophobia

First aid for animal bites Test results

H Immediately wash the bite vigorously with soap and
water for at least 10 minutes to remove the animals
saliva.
H Flush the wound with an antiviral, followed by a clear-
water rinse.
H Apply a sterile dressing.
H If possible, dont suture the wound, and dont immedi-
ately stop the bleeding (unless its massive) because
blood flow helps to clean the wound.
H Question the patient about the bite. Ask whether he
provoked the animal (if so, chances are it isnt rabid)
and whether he can identify it or its owner. (The animal
may be confined for observation.)
H Consult local health authorities for treatment informa-
tion.
Laboratory
H Virus is isolated from the patients saliva or throat;
examination of blood shows fluorescent rabies anti-
body (FRA).
H White blood cell count is elevated with increased
polymorphonuclear and large mononuclear cells.
H Urinary glucose, acetone, and protein levels are ele-
vated.
Other
H Animal should be confined and observed for 10 days
by a veterinarian. (If the animal appears rabid, it
should be killed and its brain tissues tested for FRA
and Negri bodies.)

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Treatment
General
H Immediate wound treatment (see First aid for ani-
mal bites)
Medications
H Tetanus-diphtheria prophylaxis, if needed
H Passive immunization with rabies immune globulin
and active immunization with human diploid cell vac-
cine as soon as possible (if not previously immu-
nized)
H Vaccine booster (if already immunized)

Nursing considerations
Key outcomes
The patient will:
H remain hemodynamically stable
H express understanding of the treatment regimen
H express concerns regarding infection.

Nursing interventions
H When injecting the rabies vaccine, rotate injection
sites on the upper arm or thigh.
H Cooperate with public health authorities to determine
the animals vaccination status. If the animal is
proven rabid, help identify others at risk.
H Provide aggressive supportive care (even after onset
of coma).
H Follow standard precautions.
H Provide emotional support.

Monitoring
H Injection site reactions
H Cardiac and pulmonary function

Patient teaching
Be sure to cover:
H the need for vaccination of household pets that may
be exposed to rabid wild animals
H importance of not touching wild animals, especially if
they appear ill or overly docile (a possible sign of ra-
bies)
H prophylactic rabies vaccine for high-risk people,
such as farm workers, forest rangers, spelunkers
(cave explorers), and veterinarians.

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Radiation exposure Assessment

History
Overview Acute hematopoietic radiation toxicity
H Bleeding from the skin, genitourinary tract, and GI
Description tract
H Exposure to excessive radiation that causes tissue H Nosebleeds
damage H Hemorrhage
H Damage varies with amount of body area exposed, H Increased susceptibility to infection
length of exposure, dosage absorbed, distance from GI radiation toxicity
the source, and presence of protective shielding H Intractable nausea, vomiting, and diarrhea
H Can result from cancer radiotherapy, working in a Cerebral radiation toxicity
radiation facility, or other exposure to radioactive H Nausea, vomiting, and diarrhea
materials H Lethargy
H Can be acute or chronic Cardiovascular radiation toxicity
H Hypotension, shock, and cardiac arrhythmias
Pathophysiology
H Ionization occurs in the molecules of living cells. Physical findings
H Electrons are removed from atoms. Charged atoms Acute hematopoietic radiation toxicity
or ions form and react with other atoms to cause cell H Petechiae
damage. H Pallor
H Rapidly dividing cells are the most susceptible to ra- H Weakness
diation damage. Highly differentiated cells are more H Oropharyngeal abscesses
resistant to radiation. GI radiation toxicity
H Mouth and throat ulcers and infection
Causes H Circulatory collapse and death
H Exposure to radiation through inhalation, ingestion, Cerebral radiation toxicity
or direct contact H Tremors
H Seizures
Risk factors H Confusion
H Cancer treatment H Coma and death
H Employment in a radiation facility Generalized radiation exposure
H Signs of hypothyroidism
Incidence H Cataracts
H Unknown H Skin dryness, erythema, atrophy, and malignant
lesions
Common characteristics H Alopecia
H Nausea H Brittle nails
H Diarrhea
H General weakness Test results
H Immunosuppression Laboratory
H Infections H White blood cell, platelet, and lymphocyte counts are
decreased.
Complications H Serum potassium and chloride levels are decreased.
H Leukemia Imaging
H Thyroid cancer H X-rays may reveal bone necrosis.
H Fetal growth retardation or genetic defects in off- Diagnostic procedures
spring (from exposure during childbearing years) H Bone marrow studies may show blood dyscrasia.
H Decreased fertility Other
H Shortened life span H Geiger counter helps determine if radioactive materi-
H Anemia al was ingested or inhaled and evaluates the amount
H Malignant neoplasms of radiation in open wounds.
H Bone necrosis and fractures

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Treatment Patient teaching

General Be sure to cover:
H Management of life-threatening injuries H the injury process, diagnosis, and treatment
H Symptomatic and supportive treatment H effects of radiation exposure
H Based on the type and extent of radiation injury H how to prevent a recurrence
H High-protein, high-calorie diet H skin care
H Activity as tolerated by clinical status H wound care
H need for follow-up care.
Medications
H Chelating agents Discharge planning
H Potassium iodide H Refer the patient to social services.
H Aluminum phosphate gel H If the patient was exposed to significant amounts of
H Barium sulfate radiation, provide a referral to genetic counseling
resources.
Nursing considerations
Key outcomes
The patient will:
H maintain an acceptable weight
H maintain normal fluid volume
H remain free from signs and symptoms of infection.

Nursing interventions
H Implement appropriate respiratory and cardiac sup-
port measures.
H Administer prescribed I.V. fluids and electrolytes.
H For skin contamination, wash the patients body thor-
oughly with mild soap and water.
H Debride and irrigate open wounds, as ordered.
H For ingested radioactive material, perform gastric
lavage and whole-bowel irrigation, and administer
activated charcoal, as ordered.
H Dispose of contaminated clothing properly.
H Dispose of contaminated excrement and body fluids
according to facility policy.
H Use strict sterile technique.

Monitoring
H Intake and output
H Fluid and electrolyte balance
H Vital signs
H Signs and symptoms of hemorrhage
H Nutritional status

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Rape-trauma syndrome H Late stage

Anxiety
Nightmares
Sleep disturbances
Overview Flashbacks
Depression
Description Anger
H Syndrome that occurs after rape (forced sexual inter- Disinterest in sex
course) or attempted rape and causes varying de- Anorgasmia
grees of physical and psychological trauma Suicidal ideation
H Refers to the victims short- and long-term reactions H Rape or attempted rape
and the methods used to cope with trauma H Time the victim arrived at the facility
H Carries a good prognosis if the victim receives physi- H Date and time of alleged rape
cal and emotional support and counseling to help H Time the victim was examined
deal with feelings H Whether the victim was pregnant at the time of the at-
tack
Pathophysiology H Date of last menstrual period
H Rape causes psychological and physiologic reactions. H Details of obstetric and gynecologic history
H Early stage (short-term) and late stage (long-term) H Victims statements (recorded in the first person, us-
reactions can occur. ing quotation marks)
H Objective information provided by others
Causes
H Rape or attempted rape ALERT
Incidence Be aware that your assessment notes may be used
H Affects all ages (reported victims from ages 2 months as evidence if the rapist goes to trial.
to 97 years)
H Most common in females ages 16 to 19 (about 8%
of American females experience rape or attempted Physical findings
rape) H Sore throat
H Usually perpetrated by family member if victim a H Difficulty swallowing
child H Vaginal pain
H Rectal pain
Common characteristics H Pain from other injuries incurred during the assault
H Signs of physical trauma, depending on length of the H Early stage:
attack and whether additional physical violence oc- Reddened (sore) throat
curred Mouth irritation
H Tearfulness, crying Ecchymoses
H Withdrawal Rectal pain and bleeding
H Anxiousness Lacerations, contusions, and abrasions to vulva,
cervix, and vaginal walls
Complications Lacerations and contusions in a male victim
H Lasting psychiatric problems, such as depression, Outward calm
guilt, anxiety, and suicidal ideation Compliance
H Sexually transmitted disease (STD) Glibness
H Unwanted pregnancy Talkativeness
Test results
Assessment Laboratory
H STD screening tests may reveal positive results.
History H Rapid plasma reagin card test may show positive for
H Early stage syphilis.
Disbelief H Urine pregnancy test may be positive 0 to 3 weeks af-
Panic ter missed period.
Severe anxiety H Serum human chorionic gonadotropin test becomes
Anger positive 24 to 48 hours after implantation.
Self-blame H Drug screen (if symptoms warrant) may be positive.
Humiliation H Serum ethanol level (if symptoms warrant) may be
Depression elevated.

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ALERT Monitoring
H Mental status
If the rape occurred within 7 days, the following H Vital signs
specimens may be obtained for legal purposes: H Signs and symptoms of shock
blood; samples for deoxyribonucleic acid testing
(should be collected within 48 hours); hairs of a
different color than the victims or that are obvi- Patient teaching
ously out of place; fibers; soiled or torn material;
body fluids, such as blood or semen, that dont be- Be sure to cover:
long to the victim; and specimens from the cervical H the disorder, diagnosis, and treatment
canal, throat, or rectum. H verbal and written instructions regarding treatment
H medication administration, dosage, and possible
adverse effects.
Treatment
Discharge planning
General H Encourage the patient to get follow-up care.
H Treatment of physical injuries H Refer the patient to resource and support services.
H Crisis intervention and counseling
H Follow-up gynecologic examination after 7 to
14 days; for male patient, follow-up urologic
examination
H Emergency contraception such as the Copper-T
intrauterine device
H Activity based on injuries

Medications
H Tetanus prophylaxis
H STD prophylaxis
H Emergency contraceptive pills

Nursing considerations
Key outcomes
The patient will:
H remain free from signs and symptoms of infection
H express relief of pain
H report absence of or reduction in anxiety
H discuss feelings related to the rape and its effect on
self-esteem.
Nursing interventions
H Dont leave the patient alone unless requested.
H Place the patients clothing in paper, not plastic,
bags. Label each bag and its contents.
H Collect and label fingernail scrapings and foreign
material obtained by combing the patients pubic
hair.
H Label all specimens with the patients name, physi-
cians name, and site from which the specimen was
obtained.
H Note the name of the person to whom specimens
were given.
H Report the rape if required by state law.
H Encourage the patient to express feelings.
H Provide emotional support.

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Raynauds phenomenon
Overview
Description
H Primary arteriospastic disorder
H Causes episodic vasospasms in the small peripheral
arteries and arterioles in response to cold exposure
or stress
H Typically occurs in three phases
H Diagnosis requires exclusion of secondary causes
H More than half of patients have Raynauds disease
H Also called vasospastic arterial disease
Physical findings
H First stage marked pallor of affected skin areas
H Second stage cyanosis of affected skin areas
H Third stage red, warm skin
H Between attacks normal appearance of affected
areas (occasionally, coolness and excessive perspira-
tion of these areas)
H In long-standing disease trophic changes, such as
sclerodactylia and ulcerations
Test results
Diagnostic procedures
H Arteriography and digital photoplethysmography may
aid diagnosis.

Pathophysiology Treatment
H Blood flow to digits decreases in response to stress
or cold. General
H Proposed explanations for decreased digital blood H Smoking cessation
flow include an antigen-antibody immune response H Biofeedback therapy
(most probable theory), intrinsic vascular wall hy- H Avoidance of activities involving exposure to cold and
peractivity to cold, ineffective basal heat production, mechanical or chemical injury
and increased vasomotor tone from sympathetic
stimulation or stress. Medications
H Phenoxybenzamine
Causes H Nifedipine
Primary causes H Reserpine
H Unknown H Guanethidine combined with prazosin
Secondary causes
H Collagen vascular disease Surgery
H Arterial occlusive disease H Sympathectomy, if conservative treatment fails to pre-
H Neurologic disorders vent ischemic ulcers
H Blood dyscrasias
H Trauma
H Drugs Nursing considerations
H Pulmonary hypertension (see Causes of Raynauds
phenomenon) Key outcomes
The patient will:
Incidence H describe feelings of increased comfort and decreased
H More common in females, particularly between late pain
adolescence and age 40 H maintain adequate skin temperature in affected areas
H maintain adequate collateral circulation
Common characteristics H maintain skin integrity
H Occurs bilaterally H perform normal activities to the extent possible
H Usually affects the hands or, less commonly, the feet; H demonstrate effective coping skills.
rarely, the earlobes and tip of nose
Nursing interventions
Complications H Evaluate the patients occupation and its effect on
H Ischemia symptom occurrence.
H Gangrene H Help the patient identify stress triggers and use effec-
H Amputation tive coping strategies.
H Provide psychological support and reassurance.

Assessment Monitoring
H Response to treatment
History H Signs and symptoms of skin breakdown
H Altered skin color in response to cold or stress H Signs and symptoms of infection
H Numbness and tingling (second stage)
H Throbbing, burning, painful sensation (third stage)

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Causes of Raynauds phenomenon

In primary or idiopathic Raynauds phenomenon, more than half of patients have Raynauds disease. Raynauds phenomenon
may also occur secondary to the following diseases and conditions as well as with the use of certain drugs.

Collagen vascular disease H Myeloproliferative disorders

H Dermatomyositis H Waldenstrms disease
H Polymyositis Trauma
H Rheumatoid arthritis H Cold injury
H Scleroderma H Electric shock
H Systemic lupus erythematosus H Hammering
Arterial occlusive disease H Keyboarding
H Acute arterial occlusion H Piano playing
H Atherosclerosis of the extremities H Vibration injury
H Thoracic outlet syndrome Drugs
H Thromboangiitis obliterans H Beta-adrenergic blockers
Neurologic disorders H Bleomycin
H Carpal tunnel syndrome H Cisplatin
H Stroke H Ergot derivatives such as ergotamine
H Intervertebral disk disease H Methysergide
H Poliomyelitis H Vinblastine
H Spinal cord tumors Other
H Syringomyelia H Pulmonary hypertension
Blood dyscrasias
H Cold agglutinins
H Cryofibrinogenemia

Patient teaching
Be sure to cover:
H prevention of attacks (see Preventing a Raynauds
phenomenon attack)
H need to inspect skin frequently and to seek immedi-
ate care for evidence of skin breakdown or infection
H medication administration, dosage, and possible ad-
verse effects
H importance of follow-up care.

Discharge planning
H Refer the patient to a smoking-cessation program or
a support group, as indicated.

Prevention
Preventing a Raynauds
phenomenon attack
A Raynauds phenomenon attack can be prevented by fol-
lowing these guidelines:
H Avoid exposure to cold.
H Dress warmly in cold weather, including wearing a hat
to reduce heat loss.
H Wear mittens, gloves, or oven mitts when handling
cold items in the kitchen.
H Use insulated drinking glasses.
H Wear mittens and socks to bed during cold weather.
H Warm up the car for a few minutes before driving dur-
ing winter.
H Decrease air conditioner temperature during hot
weather.
H Avoid stress.
H Avoid cigarette smoking.

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Reiters syndrome
Overview
Description
H Self-limiting syndrome associated with polyarthritis,
urethritis, mucocutaneous lesions, and conjunctivitis
(or, less commonly, uveitis)
H Also called reactive arthritis
Pathophysiology
H Infection is thought to trigger an aberrant and hyper-
active immune response that causes inflammation in
involved target organs.
Causes
H Unknown
H Typically follows venereal or enteric infection, espe-
cially with Mycoplasma, Shigella, Campylobacter,
Salmonella, Yersinia, or Chlamydia
H May involve genetic susceptibility
Incidence
H Most common in males ages 20 to 40, especially
those positive for human immunodeficiency virus
H Rare in females and children
Common characteristics
H Polyarthritis (dominant feature)
Complications
H Ankylosing spondylitis
H Persistent joint pain and swelling
H Anterior uveitis, glaucoma, blindness
H Prostatitis and hemorrhagic cystitis
H Cardiomyopathy, pericarditis
H Pulmonary edema
H Vertebral inflammation
H Foot deformity and chronic heel pain
Assessment
History
H Initially, dysuria, hematuria, urinary urgency and fre-
quency, and mucopurulent penile discharge with
swelling and reddening of the urethral meatus
H Possible suprapubic pain, fever, and anorexia with
weight loss
Physical findings
H Small, painless ulcers on glans penis
H Asymmetrical and extremely variable polyarticular
arthritis, usually in weight-bearing joints of the legs
and sometimes in the lower back or sacroiliac joints
H Warm, erythematous, painful joints
H Muscle wasting near affected joints
H Swollen, sausagelike appearance of fingers and toes
686 Reiters syndrome
H Skin lesions (keratoderma blennorrhagicum)
H Thick, opaque, brittle nails with keratic debris accu-
mulation under nails
H Painless, transient ulcerations on the buccal mucosa,
palate, and tongue
H Patches of scaly skin on the palms, soles, scalp, or
trunk
Test results
Laboratory
H Human leukocyte antigen (HLA) test is positive for
HLA B27.
H White blood cell (WBC) count and erythrocyte sedi-
mentation rate are elevated.
H Complete blood count and anemia panel show mild
anemia.
H Many WBCs (mostly polymorphonuclear leukocytes)
appear in urethral discharge and synovial fluid.
H Synovial fluid is grossly purulent with high comple-
ment and protein levels.
H Cultures of urethral discharge and synovial fluid are
used to rule out other possible causes of symptoms.
Imaging
H During the first few weeks of the syndrome, X-rays
are normal. Later they may show osteoporosis in in-
flamed areas. If inflammation persists, X-rays may
show small joint erosion, periosteal proliferation
(new bone formation) of involved joints, and cal-
caneal spurs.
Treatment
General
H Physical therapy
H Padded or supportive shoes
H High-calorie, high-protein diet
H During acute stages, weight-bearing restrictions or
complete bed rest
Medications
H Nonsteroidal anti-inflammatory drugs (NSAIDs)
H Cytotoxic agents such as azathioprine
H Corticosteroids
Surgery
H Surgical reconstruction of joints (if medical manage-
ment doesnt prevent severe joint damage)
Nursing considerations
Key outcomes
The patient will:
H express feelings of increased energy
H express feelings of increased comfort and decreased
pain
H attain the highest degree of mobility possible within
confines of the disease.
9400Q-R.qxd 8/2/12 4:46 PM Page 687

Nursing interventions
H Follow standard precautions.
H Administer prescribed drugs.
H Provide a high-calorie, high-protein diet.
H Provide frequent rest periods.
H Develop an exercise program with the physical
therapist.
H Maintain a nonjudgmental attitude.

Monitoring
H Response to medications
H Complications

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H importance of using condoms and avoiding multiple
sex partners (bacteria that leads to Reiters can be
passed from person to person but Reiters syndrome
cant be passed from person to person)
H how to avoid exposure to enteric pathogens (such as
via anal intercourse)
H medication administration, dosage, and possible ad-
verse effects
H importance of taking NSAIDs with meals or milk
H maintaining normal daily activities and moderate ex-
ercise
H good posture and body mechanics
H use of a firm mattress.

Discharge planning
H If the patient has severe or chronic joint impairment,
arrange for occupational counseling.

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summer, when ticks and their hosts (chipmunks,

Life-threatening disorder goats, and prairie dogs) are most active; occasional
cold-weather outbreaks in people such as campers
Relapsing fever who sleep in tick-infested cabins
Common characteristics
H Incubation period 5 to 15 days (average 7 days)
Overview H Fever 105 F (40.5 C)
H Prostration
Description H Headache
H An acute infectious disease caused by Borrelia spiro- H Severe myalgia
chetes H Arthralgia
H Transmitted to humans by lice or ticks and charac- H Diarrhea
terized by relapses and remissions H Vomiting
H Primary Borrelia reservoirs in rodents and other H Coughing
wild animals H Eye or chest pain
H Secondary reservoir possible in people, requiring no
transmission by ordinary contagion and allowing Complications
possible congenital infection and transmission by H Nephritis
contaminated blood H Bronchitis
H Mortality rate for untreated louseborne relapsing H Pneumonia
fever usually above 10%, possibly up to 50% in an H Endocarditis
epidemic H Seizures
H With treatment, excellent prognosis for both louse- H Cranial nerve lesions
borne and tickborne relapsing fevers H Paralysis
H Also called tick, fowl-nest, cabin, or vagabond H Coma
fever or bilious typhoid H Death

Pathophysiology
H Inoculation occurs when the victim crushes the Assessment
louse, causing its infected blood or body fluid to en-
ter the victims bitten or abraded skin or mucous History
membranes. H Recent travel to an epidemic or louse-infested area
H Because tick bites are virtually painless and most Or- H Recent exposure to tick-infested area
nithodoros ticks feed at night but dont embed them- H Fever
selves in the victims skin, many people are bitten un- H Headache
knowingly. H Malaise
H Arthralgia
Causes H Attacks that subside and recur
H Bite from body louse (Pediculus humanus
corporis) that carries Borrelia spirochete, which Physical findings
typically occurs in epidemics during wars, famines, H Splenomegaly
and mass migrations H Hepatomegaly
H Cold weather and crowded living conditions, which H Lymphadenopathy
favor the spread of body lice H Transient petechial rash over torso during febrile pe-
H Bite from tick that carries one of three species of riods
Borrelia most closely identified with tick carriers:
B. hermsii (associated with Ornithodoros hermsi), Test results
B. turicatae (associated with O. turicata), or Laboratory
B. parkeri (associated with O. parkeri) H During febrile periods, spirochetes may appear in
blood smears using Wrights or Giemsa stain.
Incidence H In severe infection, spirochetes appear in urine and
H Most common in indigent victims already suffering cerebrospinal fluid.
from other infections and malnutrition H White blood cell (WBC) count may reach 25,000/l;
H Louseborne disease most common in North and Cen- lymphocytes and erythrocyte sedimentation rate may
tral Africa, Europe, Asia, and South America; no cas- increase.
es in the United States since 1900 H Syphilis test may show a false-positive result.
H Tickborne disease in the United States most prevalent
in Texas and other western states, usually during the

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Prevention
Treatment Preventing relapsing fever
General Relapsing fever can be prevented by following these
guidelines:
H Supportive therapy H Practice proper hand-washing techniques.
H Activity, as tolerated H In tick-infested areas, wear clothing that covers as
H Diet, as tolerated much skin as possible and tuck pant legs into boots or
socks. Also, wear insect repellent containing DEET or
Medications permethrin and cover clothing with it.
H Antipyretics H Rodent proof buildings and remove nesting materials
H Doxycycline or erythromycin from walls.

ALERT
Antibiotics shouldnt be given at the height of a se-
vere febrile attack because they may cause Jarisch-
Herxheimer reaction, resulting in malaise, rigors,
leukopenia, flushing, fever, tachycardia, rising res-
piratory rate, and hypotension. This reaction,
which is caused by toxic by-products from massive
spirochete destruction, can mimic septic shock and
may prove fatal. Antibiotics should be postponed
until the fever subsides.

Nursing considerations
Key outcomes
The patient will:
H maintain a normal body temperature
H verbalize accurate information about the disease
H express increased comfort and decreased pain
H attain the highest degree of mobility possible.

Nursing interventions
H Give tepid sponge baths and antipyretics.
H Encourage fluid intake.
H Administer antibiotics carefully. Document and re-
port any hypersensitive reactions (rash, fever, ana-
phylaxis), especially a Jarisch-Herxheimer reaction.
H Report all cases of louseborne or tickborne relapsing
fever to the local public health department as re-
quired by law.
Monitoring
H Vital signs
H Level of consciousness

Patient teaching
Be sure to cover:
H symptoms of relapsing fever in family members and
in others who may have been exposed to ticks or lice
along with the victim
H prevention techniques. (See Preventing relapsing
fever.)

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Renal calculi H Pain of fluctuating intensity; may be excruciating at

its peak
H Nausea, vomiting
H Fever, chills
Overview H Anuria (rare)

Description Physical findings

H Formation of calculi (stones) anywhere in the uri- H Hematuria
nary tract H Abdominal distention
H Most common in the renal pelvis or calyces
H Vary in size; may be single or multiple (see Varia- Test results
tions in renal calculi) Laboratory
H Necessitate hospitalization in roughly 1 of every H 24-hour urine collection shows calcium oxalate,
1,000 United States residents phosphorus, and uric acid excretion levels.
H Urinalysis shows increased urine specific gravity,
Pathophysiology hematuria, crystals, casts, and pyuria.
H Calculi form when substances normally dissolved in Imaging
the urine, such as calcium, uric acid, struvite, or cys- H Kidney-ureter-bladder (KUB) radiography reveals
tine. most renal calculi.
H Large, rough calculi may occlude the opening to the H Excretory urography helps confirm the diagnosis and
ureteropelvic junction. determines calculi size and location.
H The frequency and force of peristaltic contractions H Kidney ultrasonography can detect obstructive
increase, causing pain. changes and radiolucent calculi not seen on KUB.
Causes
H Unknown Treatment
Risk factors General
H Dehydration H Percutaneous ultrasonic lithotripsy
H Infection H Extracorporeal shock wave lithotripsy
H Urine pH changes H Vigorous hydration (more than 3 qt [3 L]/day)
H Urinary tract obstruction H Dietary restrictions based on stone composition
H Immobilization
H Metabolic factors Medications
H Antibiotics as appropriate
Incidence H Analgesics
H Affect more males than females H Diuretics
H Rare in blacks and children H Methenamine mandelate
H Allopurinol (for uric acid calculi)
Common characteristics H Ascorbic acid
H Flank pain
H Nausea, vomiting Surgery
H Parathyroidectomy for hyperparathyroidism
Complications H Cystoscopy
H Renal parenchymal damage
H Renal cell necrosis
H Hydronephrosis Nursing considerations
H Complete ureteral obstruction
Key outcomes
The patient will:
Assessment H maintain fluid balance
H report increased comfort
History H identify risk factors that increase calculus formation
H Classic renal colic pain severe pain that travels and modify lifestyle accordingly
from the costovertebral angle to the flank and then to H demonstrate the ability to manage urinary elimina-
the suprapubic region and external genitalia tion problems.
H With calculi in the renal pelvis and calyces rela-
tively constant, dull pain

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Variations in renal calculi

Renal calculi vary in size and type. Small calculi may remain in the renal pelvis or pass down the ureter. A staghorn calculus
(a cast of the calyceal and pelvic collecting system) may develop from a calculus that stays in the kidney.

Multiple Staghorn
small calculi calculus

Nursing interventions Patient teaching

H Provide I.V. fluids, as ordered; encourage fluids as
needed. Be sure to cover:
H Strain all urine and save solid material for analysis. H the disorder, diagnosis, and treatment
H Encourage ambulation to aid spontaneous calculus H prescribed diet and importance of compliance (see
passage. Preventing renal calculi)
H drug therapy
Monitoring H ways to prevent recurrences
H Intake and output H how to strain urine for calculi
H Daily weight H immediate return visit to hospital for fever, uncon-
H Pain control trolled pain, or vomiting.
H Catheter function and drainage
H Signs and symptoms of infection Discharge planning
H Patients who dont meet admission criteria should
arrange for a follow-up with a urologist in 2 to
3 days.

Prevention
Preventing renal calculi
Prevention of renal calculi, or kidney stones, requires
lifestyle and dietary changes as recommended by the
practitioner. The restrictions vary based on the chemical
composition of the calculi. Some recommendation may
include:
H Drink enough fluid, about 312 quartswater pre-
ferredto create 212 quarts of urine per day.
H Take calcium supplement with a meal onlyavoiding
dietary calcium isnt necessary.
H Reduce animal protein intake.
H Avoid chocolate, coffee, tea, and cola.
H Reduce salt intake.
H Avoid rhubarb, star fruit, beets, beet greens, collards,
okra, refried beans, spinach, Swiss chard, sweet pota-
toes, sesame seeds, almonds, and soy products.

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Causes
Renal failure, acute Prerenal failure
H Hypovolemia
H Hemorrhagic blood loss
Overview H Loss of plasma volume
H Water and electrolyte losses
Description H Hypotension or hypoperfusion
H Sudden interruption of renal function resulting from Intrarenal failure
obstruction, reduced circulation, or renal parenchy- H ATN
mal disease H Glomerulopathies
H Classified as prerenal failure, intrarenal failure (also H Malignant hypertension
called intrinsic or parenchymal failure), or postre- H Coagulation defects
nal failure Postrenal failure
H Usually reversible with medical treatment H Obstructive uropathies, usually bilateral
H If not treated, may progress to end-stage renal dis- H Ureteral destruction
ease, uremia, and death H Bladder neck obstruction
H Normally occurs in three distinct phases: oliguric,
diuretic, and recovery Incidence
Oliguric phase H Seen in 5% of hospitalized patients
H May last a few days or several weeks
H Urine output dropping below 400 ml/day Common characteristics
H Fluid volume excess, azotemia, and electrolyte imbal- H Vary with renal failure phase
ance occurring.
H Local mediators that are released, causing intrarenal Complications
vasoconstriction H Renal shutdown
H Medullary hypoxia causing cellular swelling and ad- H Electrolyte imbalance
herence of neutrophils to capillaries and venules H Metabolic acidosis
H Hypoperfusion occurring H Acute pulmonary edema
H Cellular injury and necrosis occurring H Hypertensive crisis
H Reperfusion that causes reactive oxygen species to H Infection
form, leading to further cellular injury
Diuretic phase
H Renal function recovered Assessment
H Urine output gradually increasing
H Glomerular filtration rate improving, although tubu- History
lar transport systems remaining abnormal H Predisposing disorder
Recovery phase H Recent fever, chills, or central nervous system prob-
H May last 3 to 12 months, or longer lem
H The patient gradually returning to normal or near H Recent GI problem
normal renal function
Physical findings
Pathophysiology H Oliguria or anuria, depending on renal failure phase
Prerenal failure H Tachycardia
H Prerenal failure is caused by impaired blood flow. H Bibasilar crackles
H Decrease in filtration pressure causes a decline in H Irritability, drowsiness, or confusion
glomerular filtration rate (GFR). H Altered level of consciousness
H Failure to restore blood volume or blood pressure H Bleeding abnormalities
may cause acute tubular necrosis (ATN) or acute H Dry, pruritic skin
cortical necrosis. H Dry mucous membranes
Intrarenal failure H Uremic breath odor
H A severe episode of hypotension, commonly associat-
ed with hypovolemia, is commonly a significant con- Test results
tributing event. Laboratory
H Cell swelling, injury, and necrosis a form of reper- H Blood urea nitrogen, serum creatinine, and potassi-
fusion injury that may also be caused by nephrotox- um levels are elevated.
ins results from ischemia-generated toxic oxygen- H Hematocrit, blood pH, bicarbonate, and hemoglobin
free radicals and anti-inflammatory mediators. levels are decreased.
Postrenal failure H Urine casts and cellular debris are present, and spe-
H Postrenal failure usually occurs with urinary tract ob- cific gravity is decreased.
struction that affects the kidneys bilaterally such as H In glomerular disease, proteinuria and urine osmo-
prostatic hyperplasia. lality are close to serum osmolality level.

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H Urine sodium level is below 20 mEq/L, caused by Preventing acute tubular necrosis
decreased perfusion in oliguria. Acute tubular necrosis occurs mainly in elderly hospital-
H Urine sodium level is above 40 mEq/L from an intra-
ized patients. Contributing causes include aminoglycoside
renal problem in oliguria. therapy and exposure to industrial chemicals, heavy met-
H Urine creatinine clearance is used to measure GFR als, and contrast media. Patients who have been exposed
and estimate the number of remaining functioning must receive adequate hydration; monitor their urinary
nephrons. output closely.
Imaging To prevent acute tubular necrosis, make sure every pa-
Imaging tests that may show the cause of renal failure tient is well hydrated before surgery or after X-rays that
include: use a contrast medium. Administer mannitol, as ordered,
H kidney ultrasonography to a high-risk patient before and during these procedures.
H kidney-ureter-bladder radiography Carefully monitor a patient receiving a blood transfusion,
and stop the transfusion immediately if signs of transfu-
H excretory urography renal scan
sion reaction (fever, rash, and chills) occur.
H retrograde pyelography
H computed tomography scan
H nephrotomography.
Diagnostic procedures Monitoring
H Electrocardiography shows tall, peaked T waves; a H Intake and output
widening QRS complex; and disappearing P waves if H Daily weight
hyperkalemia is present. H Renal function studies
H Vital signs
H Effects of excess fluid volume
Treatment H Dialysis access site

General
H Hemodialysis or peritoneal dialysis (if appropriate) Patient teaching
H High-calorie, low-protein, low-sodium, and low-
potassium diet Be sure to cover:
H Fluid restriction H the disorder, diagnosis, and treatment
H Rest periods when fatigued H medication administration, dosage, and possible
adverse effects
Medications H recommended fluid allowance
H Supplemental vitamins H compliance with diet and drug regimen
H Diuretics H daily weight and importance of immediately report-
H In hyperkalemia, hypertonic glucose-and-insulin in- ing changes of 3 lb (1.4 kg) or more
fusions, sodium bicarbonate, sodium polystyrene sul- H signs and symptoms of edema and importance of
fonate reporting them to the physician.
Surgery Discharge planning
H Creation of vascular access for hemodialysis H Encourage follow-up care with nephrologist.

Nursing considerations
Key outcomes
The patient will:
H avoid complications
H maintain fluid balance
H maintain hemodynamic stability
H verbalize risk factors for decreased tissue perfusion
and modify lifestyle appropriately
H demonstrate the ability to manage urinary elimina-
tion problems.
Nursing interventions
H Administer prescribed drugs.
H Encourage the patient to express feelings.
H Provide emotional support.
H Identify patients at risk for and take steps to prevent
ATN. (See Preventing acute tubular necrosis.)

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Renal failure, chronic Assessment

History
Overview H Predisposing factor
H Dry mouth
Description H Fatigue
H The end result of gradually progressive loss of renal H Nausea
function H Hiccups
H Symptoms sparse until more than 75% of glomerular H Muscle cramps
filtration lost, worsening as renal function declines H Fasciculations, twitching
H Fatal unless treated; to sustain life, may require H Infertility, decreased libido
maintenance dialysis or kidney transplantation H Amenorrhea
H Impotence
Pathophysiology H Pathologic fractures
H Nephron destruction eventually causes irreversible
renal damage. Physical findings
H Disease may progress through the following stages: H Decreased urine output
reduced renal reserve, renal insufficiency, renal fail- H Hypotension or hypertension
ure, and end-stage renal disease. H Altered level of consciousness
H Peripheral edema
Causes H Cardiac arrhythmias
H Chronic glomerular disease H Bibasilar crackles
H Chronic infections such as chronic pyelonephritis H Pleural friction rub
H Congenital anomalies such as polycystic kidney H Gum ulceration and bleeding
disease H Uremic fetor
H Vascular diseases H Abdominal pain on palpation
H Obstructive processes such as calculi H Poor skin turgor
H Collagen diseases such as systemic lupus erythema- H Pale, yellowish bronze skin color
tosus H Thin, brittle fingernails and dry, brittle hair
H Nephrotoxic agents H Growth retardation (in children)
H Endocrine disease
Test results
Incidence Laboratory
H Affects about 2 of every 100,000 people H Blood urea nitrogen, serum creatinine, sodium, and
H Can occur at all ages but more common in adults potassium levels are elevated.
H Affects more males than females H Arterial blood gas (ABG) analysis shows decreased
H Affects more Blacks than Whites arterial pH and bicarbonate levels.
H Hematocrit and hemoglobin level are low; red blood
Common characteristics cell (RBC) survival time decreases.
H Fatigue H Mild thrombocytopenia and platelet defects appear.
H Decreasing urine output H Aldosterone secretion is increased.
H Increasing edema H Hyperglycemia and hypertriglyceridemia occur.
H Electrolyte imbalance H High-density lipoprotein levels are decreased.
H Fluid overload H ABG analysis shows metabolic acidosis.
H Urine specific gravity is fixed at 1.010.
Complications H Patient has proteinuria, glycosuria, and urinary
H Anemia RBCs, leukocytes, casts, and crystals.
H Peripheral neuropathy Imaging
H Lipid disorders H Kidney-ureter-bladder radiography, excretory urogra-
H Platelet dysfunction phy, nephrotomography, renal scan, and renal
H Pulmonary edema arteriography show reduced kidney size.
H Electrolyte imbalances Diagnostic procedures
H Sexual dysfunction H Renal biopsy allows histologic identification of the
underlying disease process.
H EEG shows changes suggesting metabolic enceph-
alopathy.

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H fluid restrictions
Treatment H dialysis site care, as appropriate
H importance of wearing or carrying medical identifi-
General cation.
H Hemodialysis or peritoneal dialysis
H Low-protein (with peritoneal dialysis, high-protein), Discharge planning
high-calorie, low-sodium, low-phosphorus, and low- H Refer the patient to social services.
potassium diet
H Fluid restriction
H Rest periods when fatigued

Medications
H Loop diuretics
H Cardiac glycosides
H Antihypertensives
H Antiemetics
H Iron and folate supplements
H Erythropoietin
H Antipruritics
H Supplementary vitamins and essential amino acids

Surgery
H Creation of vascular access for dialysis
H Possible kidney transplant

Nursing considerations
Key outcomes
The patient will:
H avoid complications
H maintain fluid balance
H report feelings of increased comfort
H maintain hemodynamic stability
H demonstrate the ability to manage urinary elimina-
tion problems
H perform activities of daily living within confines of
the disease.
Nursing interventions
H Administer prescribed drugs.
H Perform meticulous skin care.
H Encourage the patient to express feelings.
H Provide emotional support.

Monitoring
H Renal function studies
H Vital signs
H Intake and output
H Daily weight
H Signs and symptoms of fluid overload
H Signs and symptoms of bleeding

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H dietary changes

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H Shortness of breath
Life-threatening disorder H Nausea and vomiting

Physical findings
Respiratory acidosis H Diaphoresis
H Bounding pulses
H Rapid, shallow respirations
Overview H Tachycardia
H Hypotension
Description H Papilledema
H Acid-base disturbance characterized by reduced alve- H Mental status changes
olar ventilation, as shown by hypercapnia (partial H Asterixis (tremor)
pressure of arterial carbon dioxide [PaCO2] above H Depressed deep tendon reflexes
45 mm Hg)
H Carries varying prognosis, depending on severity of Test results
underlying disturbance and the patients general clin- Laboratory
ical condition H Arterial blood pH is below 7.35, and PaCO2 is above
H Can be acute or chronic 45 mm Hg (hypercapnia)
Pathophysiology
H Depressed ventilation causes compromised carbon Treatment
dioxide elimination.
H Carbon dioxide is then retained and combines with General
water molecules increasing hydrogen ion concentra- H Correction of the condition causing alveolar hypo-
tion. ventilation
H Respiratory acidosis results. H Possible mechanical ventilation
H Possible dialysis
Causes H I.V. fluid administration
H Central nervous system (CNS) trauma H Possible need for parenteral nutrition
H CNS-depressant drugs H Activity as tolerated
H Chronic metabolic alkalosis
H Neuromuscular disease Medications
H Airway obstruction H Oxygen
H Parenchymal lung disease H Bronchodilators
H Chronic obstructive pulmonary disease H Antibiotics
H Asthma H Sodium bicarbonate
H Severe acute respiratory distress syndrome H Drug therapy for the underlying condition
H Chronic bronchitis
H Large pneumothorax Surgery
H Extensive pneumonia H Bronchoscopy
H Pulmonary edema

Incidence Nursing considerations

H Affects males and females equally
Key outcomes
Common characteristics The patient will:
H Headache H maintain a patent airway
H Shortness of breath H maintain adequate ventilation
H Nausea and vomiting H maintain fluid balance
H maintain adequate cardiac output
Complications H demonstrate effective coping strategies.
H Shock
H Respiratory arrest Nursing interventions
H Cardiac arrest H Administer prescribed drugs and oxygen.
H Provide adequate fluids.
H Maintain a patent airway.
Assessment H Perform tracheal suctioning, as needed.

History Monitoring
H Predisposing factor H Vital signs
H Headache H Intake and output

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H Neurologic status
H Respiratory status
H Arterial blood gas values
H Serum electrolyte values
H Mechanical ventilator settings

ALERT
Be aware that pulse oximetry, used to monitor oxy-
gen saturation, wont reveal increasing carbon
dioxide levels.

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H supplemental oxygen
H medication administration, dosage, and possible ad-
verse effects
H how to perform coughing and deep-breathing exer-
cises
H signs and symptoms of acid-base imbalance and
when to notify the physician.
Discharge planning
H Refer the patient for home oxygen therapy if
indicated.

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H Maternal history of diabetes or antepartum hemor-

Life-threatening disorder rhage
Physical findings
Respiratory distress H Rapid, shallow respirations

syndrome H Intercostal, subcostal, or sternal retractions

Overview
Description
H Respiratory disorder that involves widespread alveo-
lar collapse
H Most common cause of neonatal death
H If mild, subsides slowly after about 3 days
H Also called RDS or hyaline membrane disease
Pathophysiology
H In neonates born before the 27th week of gestation,
immaturity of alveoli and capillary blood supply lead
to alveolar collapse from lack of surfactant (a lipo-
protein normally present in alveoli and respiratory
bronchioles).
H Surfactant deficiency causes widespread atelectasis,
resulting in inadequate alveolar ventilation and
shunting of blood through collapsed lung areas.
H Hypoxia and acidosis result.
H Compensatory grunting occurs, producing positive
end-expiratory pressure (PEEP) that helps prevent
further alveolar collapse.
Causes
H Surfactant deficiency stemming from preterm birth
Incidence
H Almost exclusively affects neonates born before the
27th gestational week; occurs in about 60% of those
born before the 28th week
H Most common in neonates of mothers with diabetes,
neonates delivered by cesarean birth, and neonates
delivered suddenly after antepartum hemorrhage
H Nasal flaring
H Audible expiratory grunting
H Pallor
H Frothy sputum
H Low body temperature
H Diminished air entry and crackles
H Possible hypotension, peripheral edema, and oliguria
H Possible apnea, bradycardia, and cyanosis
Test results
Laboratory
H Partial pressure of arterial oxygen (PaO2) is de-
creased; partial pressure of arterial carbon dioxide
may be normal, decreased, or increased; and arterial
pH is decreased.
H Lecithin-sphingomyelin ratio shows prenatal lung
development and RDS risk.
Imaging
H Chest X-rays may show a fine reticulonodular pattern
and dark streaks, indicating air-filled, dilated bron-
chioles.
Treatment
General
H Aggressive management, assisted by mechanical ven-
tilation with PEEP or continuous positive airway pres-
sure (CPAP) administered by a tight-fitting face mask
or, when necessary, an endotracheal tube
H For a neonate who cant maintain adequate gas ex-
change, high-frequency oscillation ventilation
H Radiant warmer or Isolette
H Warm, humidified, oxygen-enriched gases given by
oxygen hood or mechanical ventilation
H Tube feedings or total parenteral nutrition

Common characteristics Medications

H Preterm birth H I.V. fluids and sodium bicarbonate
H Labored breathing within minutes to hours after birth H Pancuronium bromide
H Prophylactic antibiotics
Complications H Diuretics
H Respiratory insufficiency H Surfactant replacement therapy
H Shock H Vitamin E
H Bronchopulmonary dysplasia H Antenatal corticosteroids
H Death
Surgery
H Possible tracheostomy
Assessment
History
H Preterm birth
H Cesarean birth

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ALERT
Nursing considerations
Watch for evidence of complications from oxygen
Key outcomes therapy: lung capillary damage, decreased mucus
The patient will: flow, impaired ciliary functioning, and widespread
H maintain adequate ventilation atelectasis. Also be alert for signs of patent ductus
H maintain a patent airway arteriosus, heart failure, retinopathy, pulmonary
H remain free from infection hypertension, necrotizing enterocolitis, and neuro-
H maintain intact skin integrity. logic abnormalities.
The patients family will:
H identify factors that increase the risk of neonatal
injury.
Patient teaching
Nursing interventions
H Administer prescribed drugs. Be sure to cover (with the parents):
H Check the umbilical catheter for arterial or venous H the disorder, diagnosis, and treatment
hypotension, as appropriate. H medication administration, dosage, and possible ad-
H Suction, as necessary. verse effects
H Change the transcutaneous PaO2 monitor lead place- H explanations of respiratory equipment, alarm
ment site every 2 to 4 hours. sounds, and mechanical noise
H Adjust PEEP or CPAP settings as indicated by arterial H potential complications
blood gas (ABG) values. H when to notify the physician.
H Implement measures to prevent infection.
H Provide mouth care every 2 hours. Discharge planning
H Encourage parents to participate in the infants care. H Refer the parents to counselors and social worker, as
H Encourage parents to ask questions and to express indicated.
their fears and concerns. H Refer the patient for follow-up care with a neonatal
H Advise parents that full recovery may take up to ophthalmologist, as indicated.
12 months.
H Offer emotional support.

ALERT
In a neonate on a mechanical ventilator, watch
carefully for signs of barotrauma and accidental
disconnection from the ventilator. Check ventilator
settings frequently. Be alert for signs of complica-
tions of PEEP or CPAP therapy, such as decreased
cardiac output, pneumothorax, and pneumomedi-
astinum.

Monitoring
H Vital signs
H ABG values
H Intake and output
H Central venous pressure
H Signs and symptoms of infection
H Thrombosis
H Decreased peripheral circulation
H Pulse oximetry
H Daily weight
H Skin color
H Respiratory status
H Skin integrity

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Respiratory syncytial H Sudden infant death syndrome

H Residual lung damage

virus infection
Assessment
Overview History
H Nasal congestion
Description H Coughing
H Virus thats the leading cause of lower respiratory H Wheezing
tract infection in infants and young children and up- H Malaise
per respiratory infections in adults H Sore throat
H Suspected cause of fatal respiratory diseases in in- H Earache
fants H Dyspnea
H Can cause serious illness in immunocompromised H Fever
adults, institutionalized elderly people, and patients
with underlying cardiopulmonary disease Physical findings
H Also known as RSV H Nasal and pharyngeal inflammation
H Otitis media
Pathophysiology H Severe respiratory distress (nasal flaring, retraction,
H The virus attaches to cells, eventually resulting in cyanosis, and tachypnea)
necrosis of the bronchiolar epithelium; in severe in- H Wheezes, rhonchi, and crackles
fection, peribronchiolar infiltrate of lymphocytes and
mononuclear cells occurs. Test results
H Intra-alveolar thickening and filling of the alveolar Laboratory
spaces with fluid results. H Cultures of nasal and pharyngeal secretions show
H Narrowing of the airway passages on expiration pre- respiratory syncytial virus.
vents air from leaving the lungs, causing progressive H Serum respiratory syncytial virus antibody titers are
overinflation. elevated.
H Arterial blood gas analysis shows hypoxemia and
Causes respiratory acidosis.
H Respiratory syncytial virus, a subgroup of myxovirus- H In dehydration, blood urea nitrogen levels are ele-
es resembling paramyxovirus vated.
H Transmitted from person to person by respiratory se-
cretions
H Probably spread to infants and young children by Treatment
school-age children, adolescents, and young adults
with mild reinfections General
H Respiratory support
Incidence H Adequate nutrition
H Almost exclusively affects infants and young children, H Avoidance of overhydration
especially those in day care settings H Rest periods when fatigued
H Highest among infants ages 1 to 6 months, peaking
between ages 2 and 3 months Medications
H Annual epidemics during winter and spring H Ribavirin
H Bronchodilator such as albuterol
Common characteristics
H Rhinorrhea, low-grade fever, and mild systemic Surgery
symptoms accompanied by cough and wheezing H Possible tracheostomy
H Tachypnea, shortness of breath
H Cyanosis
H Apneic episodes Nursing considerations
H Reinfection common; produces milder symptoms
than primary infection Key outcomes
The patient will:
Complications H maintain a respiratory rate within 5 breaths/minute
H Pneumonia and progressive pneumonia of baseline
H Bronchiolitis H express or indicate feelings of increased comfort
H Croup while maintaining adequate air exchange
H Otitis media H cough effectively
H Respiratory failure H maintain adequate fluid volume.

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Nursing interventions
H Institute contact isolation.
H Perform percussion, drainage, and suction when
necessary.
H Administer prescribed oxygen.
H Use a croup tent, as needed.
H Place the patient in semi-Fowlers position.
H Observe for signs and symptoms of dehydration, and
administer I.V. fluids accordingly.
H Promote bed rest.
H Offer diversional activities tailored to the patients
condition and age.
Monitoring
H Respiratory status
H Fluid and electrolyte status

Patient teaching
Be sure to cover (with the parents):
H the disorder, diagnosis, and treatment
H how the infection spreads
H preventive measures (RSV immune globulin)
H medication administration, dosage, and possible ad-
verse effects
H importance of a nonsmoking environment in the
home
H importance of keeping follow-up appointments.

Discharge planning
H Refer the patient to home care services, as necessary.

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Incidence
Retinal detachment H Affects twice as many males as females
H More common with increased age

Overview Common characteristics

H Painless vision loss
Description H Sensation of floaters or of looking through a veil,
H Partial or complete separation of the sensory retina curtain, or cobweb
from the underlying pigment epithelium
H May be primary or secondary Complications
H Commonly occurs spontaneously H Severe vision impairment
H Usually involves only one eye; may occur in the other H Blindness
eye later
H Rarely heals spontaneously; usually can be reat-
tached successfully with surgery Assessment
H Carries varying prognosis depending on the retinal
area affected History
H Sensation of seeing floaters and flashes
Pathophysiology H Painless vision loss, described as sensation of look-
H A hole or tear in the retina allows the liquid vitreous ing through a veil, curtain, or cobweb (which may
to seep between the retinal layers. obscure objects in a particular area of the visual
H Liquid separates the sensory retinal layer from its field)
choroidal blood supply. (See Understanding retinal
detachment.) Physical findings
H Visual field loss
Causes
H Intraocular inflammation Test results
H Trauma Imaging
H Age-related degenerative changes H Ocular ultrasonography may be used to examine the
H Tumors retina if the lens is opaque and shows intraocular
H Systemic disease and intraorbital pathology. It also commonly detects
H Traction placed on the retina by vitreous bands or retinal detachments, characteristically producing a
membranes dense, sheetlike echo on a B-mode scan.
H Hereditary factors, usually related to myopia Diagnostic procedures
H Direct ophthalmoscopy shows folds or discoloration
Special populations in the usually transparent retina.
H Indirect ophthalmoscopy shows retinal tears.
In a child, retinal detachment can result from
retinopathy of prematurity, tumors (retinoblas-
tomas), or trauma. Treatment
General
Risk factors H Varies with location and severity of detachment
H Myopia H Nothing by mouth before surgery
H Cataract surgery H Bed rest before surgery
H Trauma H Restriction of eye movements before surgery by
patching affected eye
H Positioning of the patients head to allow gravity to
Understanding retinal detachment pull the detached retina closer to the choroid
Traumatic injury or degenerative changes cause retinal de- Medications
tachment by allowing the retinas sensory tissue layers to H Antiemetics
separate from the retinal pigment epithelium. This permits
H Analgesics
fluid from the vitreous, for example to seep into the
H Mydriatics
space between the retinal pigment epithelium and the rods
H Cycloplegics
and cones of the tissue layers.
The pressure, which results from the fluid entering the H Steroidal eyedrops
space, balloons the retina into the vitreous cavity away H Antibiotic eyedrops
from choroidal circulation. Separated from its blood sup-
ply, the retina cant function. Without prompt repair, the Surgery
detached retina can cause permanent vision loss. H Cryothermy
H Laser therapy

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H Scleral buckling (may be followed by vitreous

replacement with silicone, oil, air, or gas)
H Diathermy

Nursing considerations
Key outcomes
The patient will:
H avoid harm or injury
H express feelings and concerns
H regain the previous level of visual functioning.

Nursing interventions
H Prepare the patient for surgery.
H Administer prescribed antibiotics and cycloplegic or
mydriatic eyedrops.
H In macular involvement, maintain bed rest to prevent
further retinal detachment.
H Postoperatively, position the patient as directed.
H Administer prescribed drugs.
H Discourage activities that increase intraocular
pressure.
H With retrobulbar injection, apply a protective eye
patch.
H Apply cold compresses.
H Avoid putting pressure on the eye.
H Provide encouragement and emotional support.

Monitoring
H Localized corneal edema and perilimbal congestion
after laser therapy
H Persistent pain
H Vital signs
H Visual acuity
H Response to treatment

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H leg and deep-breathing exercises
H possible persistence of blurred vision for several
days after laser therapy
H importance of avoiding driving, bending, heavy lift-
ing, and other activities that affect intraocular pres-
sure for several days after surgery
H avoidance of activities that could cause eye trauma
H how to instill eyedrops
H importance of wearing sunglasses
H applying cold compresses
H medication administration, dosage, and possible ad-
verse effects
H signs and symptoms of increasing ocular pressure
and infection
H early symptoms of retinal detachment.

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Reyes syndrome Assessment

History
Overview H Viral infection
H Aspirin use
Description H Vomiting
H An acute childhood illness that causes fatty infiltra- H Change in mental status
tion of the liver with concurrent hyperammonemia,
encephalopathy, and increased intracranial pressure Physical findings
(ICP) H Hyperactive reflexes
H Possible fatty infiltration of the kidneys, brain, and H Increased blood pressure
myocardium H Tachycardia
H Variable prognosis depending on the severity of cen- H Lethargy
tral nervous system depression
Test results
Pathophysiology Laboratory
H Damaged hepatic mitochondria disrupt the urea cy- H Low or absent serum salicylate level rules out aspirin
cle, which normally changes ammonia to urea for ex- overdose.
cretion from the body. H Liver-function studies show aspartate aminotrans-
H This results in hyperammonemia, hypoglycemia, and ferase and alanine aminotransferase levels elevated
an increase in serum short-chain fatty acids, leading to twice normal; bilirubin level is usually normal.
to encephalopathy. H Cerebrospinal fluid (CSF) analysis reveals a white
H Simultaneously, fatty infiltration is found in renal blood cell count of less than 10; with coma, CSF
tubular cells, neuronal tissue, and muscle tissue, in- pressure increases.
cluding the heart. H Coagulation studies result in prolonged prothrombin
and partial thromboplastin times.
Causes H Blood values show elevated serum ammonia levels;
H Viral infection normal or, in 15% of cases, low serum glucose lev-
H Associated with aspirin use els; and increased serum fatty acid and lactate levels.
Diagnostic procedures
Incidence H Liver biopsy reveals fatty droplets uniformly distrib-
H Linked to aspirin use uted throughout cells.
H Usually increased during influenza outbreaks Other
H History of a recent viral disorder with typical signs
Special populations and symptoms strongly suggests Reyes syndrome.

Reyes syndrome is most common in children ages

4 to 12, with peak incidence at age 6. Treatment
H Dictated by stage of the syndrome (see Stages of
Common characteristics treatment for Reyes syndrome)
H Five-stage development, signs and symptoms varying
in severity with the degree of encephalopathy and
cerebral edema Nursing considerations
H Possible atypical presentation for infants
H Brief recovery period after initial viral infection, dur- Key outcomes
ing which child doesnt seem seriously ill The patient will:
H A few days later, intractable vomiting, lethargy, rapid- H maintain adequate ventilation
ly changing mental status (mild to severe agitation, H maintain joint mobility and range of motion (ROM)
confusion, irritability, delirium), hyperactive reflexes, H maintain skin integrity
and rising blood pressure, respiratory rate, and H remain hemodynamically stable.
pulse rate
Nursing interventions
Complications H Maintain seizure precautions.
H Increased ICP H Provide skin and mouth care.
H Coma H Perform or assist with ROM exercises.
H Seizures
H Respiratory failure

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Stages of treatment for Reyes syndrome

Signs and symptoms Treatment

Stage I
Vomiting, lethargy, hepatic dysfunction
Start baseline treatment:
To decrease intracranial pressure (ICP) and brain edema, administer
I.V. fluids at two-thirds of the maintenance dose. Also administer an
osmotic diuretic or furosemide.
To treat hypoprothrombinemia, administer vitamin K; if vitamin K
proves unsuccessful, administer fresh frozen plasma.
Monitor serum ammonia and blood glucose levels and plasma os-
molality every 4 to 8 hours to check progress.

Stage II Continue baseline treatment.

Hyperventilation, delirium, hepatic
dysfunction, hyperactive reflexes

Stage III Continue baseline and seizure treatment.

Coma, hyperventilation, decorticate
rigidity, hepatic dysfunction
Monitor ICP with a subarachnoid screw or other invasive device.
Provide endotracheal intubation and mechanical ventilation to control
partial pressure of carbon dioxide. A paralyzing agent, such as pan-
curonium I.V. may help maintain ventilation.
Administer mannitol I.V. or glycerol by nasogastric tube.

Stage IV Continue baseline and supportive care.

Deepening coma; decerebrate rigidity; If all previous measures fail, some pediatric centers use barbiturate
large, fixed pupils; minimal hepatic coma, decompressive craniotomy, hypothermia, or an exchange
dysfunction transfusion.

Stage V Continue baseline and supportive care.

Seizures, loss of deep tendon reflexes,
flaccidity, respiratory arrest, ammonia
level greater than 300 mg/dl

Monitoring
H Vital signs
H Intake and output
H ICP
H Respiratory status
H Cardiovascular status
H Level of consciousness

Patient teaching
Be sure to cover:
H the disorder, diagnosis and treatment
H using a nonsalicylate analgesic and an antipyretic
such as acetaminophen for children.
Discharge planning
H Refer parents to the National Reyes Syndrome Foun-
dation for more information.
H Refer the patient to home care or rehabilitation ser-
vices, as needed.

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Rhabdomyolysis H Excessive muscular activity associated with status

epilepticus, electroconvulsive therapy, or high-
voltage electrical shock
H Alcohol use
Overview H Recent soft tissue compression
H Seizure activity
Description
H Breakdown of muscle tissue, causing myoglobinuria Incidence
H Usually follows major muscle trauma, especially a H Greater occurrence in males than females
muscle crush injury H May occur at any age
H Good prognosis if contributing causes are stopped or
disease is checked before damage is irreversible Common characteristics
H Tenderness, swelling, and muscle weakness caused
Pathophysiology by muscle trauma and pressure
H Muscle trauma that compresses tissue causes ische- H Dark, reddish-brown urine from myoglobin
mia and necrosis.
H The ensuing local edema further increases compart- Complications
ment pressure and tamponade; pressure from severe H Renal failure
swelling causes blood vessels to collapse, leading to H Amputation
tissue hypoxia, muscle infarction, neural damage in
the area of the fracture, and release of myoglobin
from the necrotic muscle fibers into the circulation. Assessment
Causes History
H Disorders that damage skeletal muscle H Muscle trauma or breakdown
H Muscle pain
Risk factors H Presence of any risk factors
H Traumatic injury
H Prescription and nonprescription drugs (see Drugs Physical findings
that may cause rhabdomyolysis) H Dark, reddish-brown urine
H Strenuous exertion such as long-distance running H Tense, tender muscle compartment (compartment
H Infection, especially severe infection with necrosis syndrome)
H Anesthetics that cause intraoperative rigidity
H Heat stroke Test results
H Electrolyte disturbances Laboratory
H Cardiac arrhythmias H Urine myoglobin level exceeds 0.5 mg/dl (evident
with only 200 g of muscle damage).
H Creatinine kinase level is elevated (0.5 to 0.95 mg/dl)
due to muscle damage.
H Serum potassium, phosphate, creatinine, and crea-
Drugs that may cause rhabdomyolysis tine levels are elevated.
H Hypocalcemia occurs in early stages, hypercalcemia
The use of these drugs may cause rhabdomyolysis: in later stages.
H aminocaproic acid
H Intracompartmental venous pressure measurements
H amphetamines
H amphotericin B
(using a wick catheter, needle, or slit catheter insert-
H anesthetic and paralytic agents ed into the muscle) are elevated.
H antihistamines Imaging
H caffeine H Computed tomography scan, magnetic resonance
H cocaine imaging, and bone scintigraphy are used to detect
H corticosteroids muscle necrosis.
H cyclic antidepressants
H fibric acid derivatives
H heroin Treatment
H neuroleptics
H phencyclidine General
H propofol
H For underlying disorder
H quinine
H Prevention of renal failure
H salicylates
H selective serotonin-reuptake inhibitors H Bed rest
H statins
H theophylline.

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Medications
H Anti-inflammatory drugs
H Corticosteroids (in extreme cases)
H Analgesics

Surgery
H Immediate fasciotomy and debridement if compart-
ment venous pressure exceeds 25 mm Hg

Nursing considerations
Key outcomes
The patient will:
H maintain normal renal function
H express increased comfort and decreased pain
H verbalize understanding of the disorder and treat-
ment.
Nursing interventions
H Administer prescribed I.V. fluids and drugs.
H Measure intake and output accurately.
H Promote comfort measures.

Monitoring
H Intake and output
H Urine myoglobins
H Renal studies
H Pain control

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the need for prolonged, low-intensity training as op-
posed to short bursts of intense exercise
H medication administration, dosage, and possible ad-
verse effects.

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Rheumatic fever and Special populations

rheumatic heart disease In children, mitral insufficiency is the major con-

sequence of rheumatic heart disease.

Overview Assessment
Description History
H Systemic inflammatory disease of childhood that oc- H Recent streptococcal infection
curs 2 to 6 weeks after an inadequately treated upper H Recent history of low-grade fever spiking to at least
respiratory tract infection with group A beta-hemolyt- 100.4 F (38 C) in late afternoon, along with unex-
ic streptococci plained epistaxis and abdominal pain
H Principally involves the heart, joints, central nervous H Migratory joint pain (polyarthritis)
system, skin, and subcutaneous tissues
H In rheumatic heart disease, early acute phase that Physical findings
may affect endocardium, myocardium, or pericardi- H Swelling, redness, and signs of effusion, most com-
um, possibly followed later by chronic valvular dis- monly in the knees, ankles, elbows, and hips
ease H With pericarditis: sharp, sudden pain that usually
H Commonly recurs starts over the sternum and radiates to the neck,
shoulders, back, and arms; increases with deep in-
Pathophysiology spiration and decreases when the patient sits up and
H Rheumatic fever appears to be a hypersensitivity re- leans forward
action in which antibodies produced to combat H With heart failure caused by severe rheumatic cardi-
streptococci react and produce lesions at specific tis- tis: dyspnea, right upper quadrant pain, and a hack-
sue sites. ing, nonproductive cough
H Antigens of group A streptococci bind to receptors in H Skin lesions, such as erythema marginatum, typically
the heart, muscle, brain, and synovial joints, causing on the trunk and extremities
an autoimmune response. H Subcutaneous nodules, 3 mm to 2 cm in diameter,
H Because the antigens are similar to the bodys own that are firm, movable, and nontender occurring
cells, antibodies may attack healthy body cells by near tendons or bony prominences of joints, persist-
mistake. ing for several days to weeks
H With left-sided heart failure: edema and tachypnea,
Causes bibasilar crackles, and ventricular or atrial gallop
H Group A beta-hemolytic streptococcal pharyngitis H Transient chorea up to 6 months after original strep-
H Familial tendency tococcal infection
H Pericardial friction rub
Incidence H Heart murmurs and gallops
H In the United States, most common in northern states
H Worldwide, 15 to 20 million new cases each year Test results
H Most common during cool, damp weather in winter Laboratory
and early spring H During acute phase, white blood cell count and ery-
throcyte sedimentation rate are elevated.
Common characteristics H During inflammation, complete blood count shows
H Fever slight anemia.
H Joint pain H C-reactive protein test is positive, especially during
H Rash and skin nodules acute phase.
H Sydenhams chorea H In severe carditis, cardiac enzyme levels are in-
H Nose bleeds creased.
H Cardiac effects H Antistreptolysin-O titer is elevated in 95% of patients
within 2 months of onset.
Complications H Throat cultures show group A beta-hemolytic strepto-
H Destruction of mitral and aortic valves cocci.
H Severe pancarditis Imaging
H Pericardial effusion H Chest X-rays show normal heart size (except with
H Heart failure myocarditis, heart failure, and pericardial effusion).
H Systemic emboli H Echocardiography helps evaluate valvular damage,
chamber size, and ventricular function and detects
pericardial effusion.

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Diagnostic procedures
H Electrocardiography reveals no diagnostic changes,
but 20% of patients show a prolonged PR interval.
H Cardiac catheterization evaluates valvular damage
and left ventricular function in severe cardiac dys-
function.
Treatment
General
H Dietary sodium restriction, if indicated
H Bed rest during acute phase
H Gradual activity increase, as tolerated
Medications
H Antibiotics such as penicillin
H Nonsteroidal anti-inflammatory drugs
H Corticosteroids such as prednisone
Surgery
H Commissurotomy, valvuloplasty, or heart valve
replacement
Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the importance of resuming activities of daily living
slowly and scheduling frequent rest periods as in-
structed by the physician
H what to do if signs of an allergic reaction to penicillin
occur
H the importance of reporting early signs and symp-
toms of left-sided heart failure, such as dyspnea and
a hacking, nonproductive cough, and immediately
reporting signs of recurrent streptococcal infection
H keeping the child away from people with respiratory
tract infections
H transient nature of chorea
H compliance with prolonged antibiotic therapy and
follow-up care
H the possible need for prophylactic antibiotics before
any dental work or invasive procedures
H medication administration, dosage, and possible ad-
verse effects.

Nursing considerations
Key outcomes
The patient will:
H maintain adequate ventilation
H maintain hemodynamic stability
H avoid arrhythmias
H carry out activities of daily living without weakness or
fatigue
H express feelings about diminished capacity to per-
form usual roles.
Nursing interventions
H Find out if the patient has ever had a hypersensitivity
reaction to penicillin. Warn the parents (if appropri-
ate) that such a reaction is possible.
H Administer prescribed antibiotics on time.
H Stress the importance of bed rest. Provide a bedside
commode.
H Position the patient upright.
H Provide analgesics and oxygen, as needed.
H Allow the patient to express feelings and concerns.
H Help the parents overcome any guilt feelings they
may have about their childs illness.
H Encourage the parents and child to vent their frustra-
tions during the long recovery. If the child has severe
carditis, help them prepare for permanent changes
in the childs lifestyle.
Monitoring
H Vital signs
H Heart rhythm
H Heart and breath sounds

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Rheumatoid arthritis H Pain on inspiration

H Shortness of breath

Physical findings
Overview H Joint deformities and contractures
H Painful, red, swollen arms
Description H Foreshortened hands
H Chronic, systemic, symmetrical inflammatory disease H Boggy wrists
H Primarily attacking peripheral joints and surround- H Rheumatoid nodules
ing muscles, tendons, ligaments, and blood vessels H Leg ulcers
H Marked by spontaneous remissions and unpre- H Eye redness
dictable exacerbations H Joints that are warm to the touch
H Potentially crippling H Pericardial friction rub
H Positive Babinskis sign
Pathophysiology
H Cartilage damage resulting from inflammation trig- Test results
gers further immune responses, including comple- Laboratory
ment activation. H Rheumatoid factor test is positive in 75% to 80% of
H Complement, in turn, attracts polymorphonuclear patients, as indicated by a titer of 1:160 or higher.
leukocytes and stimulates release of inflammatory H Synovial fluid analysis shows increased volume and
mediators, which exacerbates joint destruction. turbidity but decreased viscosity and complement
(C3 and C4) levels, with white blood cell count pos-
Causes sibly exceeding 10,000/l.
H Unknown H Serum globulin levels are elevated.
H Possible influence of infection (viral or bacterial), H Erythrocyte sedimentation rate is elevated.
hormonal factors, and lifestyle H Complete blood count shows moderate anemia and
slight leukocytosis. (See Classifying rheumatoid
Incidence arthritis.)
H Strikes three times as many females as males Imaging
H Can occur at any age; peak onset, ages 35 and 50 H In early stages, X-rays show bone demineralization
and soft-tissue swelling. Later, they help determine
Common characteristics the extent of cartilage and bone destruction, erosion,
H Stiff, swollen joints subluxations, and deformities and show the charac-
teristic pattern of these abnormalities.
Complications H Magnetic resonance imaging, computed tomography
H Fibrous or bony ankylosis scan may provide information about damage extent.
H Soft-tissue contractures Other
H Joint deformities H Synovial tissue biopsy shows inflammation.
H Sjgrens syndrome
H Spinal cord compression
H Carpal tunnel syndrome Treatment
H Osteoporosis
H Recurrent infections General
H Hip joint necrosis H Adequate sleep (8 to 10 hours every night)
H Splinting
H Range-of-motion (ROM) exercises and carefully indi-
Assessment vidualized therapeutic exercises
H Moist heat application
History H Frequent rest periods between activities
H Insidious onset of nonspecific symptoms, including
fatigue, malaise, anorexia, persistent low-grade fever, Medications
weight loss, and vague articular symptoms H Salicylates
H Later, more specific localized articular symptoms, H Nonsteroidal anti-inflammatory drugs, such as
commonly in the fingers naproxen, nabumetone, and indomethacin
H Bilateral and symmetrical symptoms, which may H Gold salts such as auranofin
extend to the wrists, elbows, knees, and ankles H Corticosteroids
H Stiff joints H Cox-2 inhibitors such as celecoxib
H Stiff, weak, or painful muscles H Disease-modifying antirheumatic drugs (DMARDS),
H Numbness or tingling in the feet or weakness or loss such as hydroxychloroquine and methotrexate
of sensation in the fingers H Immunosuppressants, such as leflunomide, azathio-
prine, and penicilliamine

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H Tumor necrosis factor blockers (class of DMARDS),
such as etanercept and infliximab
H Interleukin-1 receptor antaognist such as anakinra
H Abatacept
H Rituximab
Surgery
H Metatarsal head and distal ulnar resectional arthro-
plasty; insertion of silastic prosthesis between meta-
carpophalangeal and proximal interphalangeal joints
H Arthrodesis (joint fusion)
H Synovectomy
H Osteotomy
H Repair of ruptured tendon
H In advanced disease, joint reconstruction or total
joint arthroplasty
Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort and decreased
pain
H attain the highest degree of mobility possible
H maintain skin integrity
H verbalize feelings about limitations
H express an increased sense of well-being.
Nursing interventions
H Administer prescribed analgesics; watch for adverse
reactions.
H Perform meticulous skin care.
H Supply adaptive devices, such as a zipper-pull, easy-
to-open beverage cartons, and lightweight cups.
After total knee or hip arthroplasty
H Administer prescribed blood replacement products,
antibiotics, and pain medication.
H Have the patient perform active dorsiflexion; immedi-
ately report inability to do so.
H Supervise isometric exercises every 2 hours.
H After total hip arthroplasty, check traction for pressure
areas; keep head of bed raised 30 to 45 degrees.
H Change or reinforce dressings, as needed.
H Have the patient turn, cough, and breathe deeply
every 2 hours.
H After total knee arthroplasty, keep the leg extended
and slightly elevated.
H After total hip arthroplasty, keep the hip in abduc-
tion. Watch for and immediately report inability to
rotate the hip or bear weight on it, increased pain, or
a leg that appears shorter.
H Assist patient in activities, keeping the weight on the
unaffected side.
Monitoring
H Joint mobility and pain level
H Skin integrity
H Vital signs and daily weight
H Sensory disturbances
Classifying rheumatoid arthritis
A patient who meets four of seven American College of
Rheumatology criteria is classified as having rheumatoid
arthritis. She must experience the first four criteria for at
least 6 weeks, and a physician must observe the second
through fifth criteria.
H Morning stiffness in and around the joints that lasts for
1 hour before full improvement
H Arthritis in three or more joint areas, with at least three
joint areas (as observed by a physician) exhibiting
soft-tissue swelling or joint effusions, not just bony
overgrowth (the 14 possible areas involved include the
right and left proximal interphalangeal, metacarpopha-
langeal, wrist, elbow, knee, ankle, and metatarsopha-
langeal joints)
H Arthritis of hand joints, including the wrist, the metacar-
pophalangeal joint, or the proximal interphalangeal joint
H Arthritis that involves the same joint areas on both
sides of the body
H Subcutaneous rheumatoid nodules over bony promi-
nences
H Demonstration of abnormal amounts of serum rheu-
matoid factor by any method that produces a positive
result in less than 5% of patients without rheumatoid
arthritis
H Radiographic changes, usually on posteroanterior hand
and wrist X-rays, must show erosions or unequivocal
bony decalcification localized in or most noticeable ad-
jacent to the involved joints
H Serum electrolyte and hemoglobin level and hema-
tocrit
H Activity tolerance
H Complications of corticosteroid therapy
Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H chronic nature of rheumatoid arthritis and possible
need for major lifestyle changes
H importance of a balanced diet and weight control
H sexual concerns.
If the patient requires total knee or hip arthroplasty,
be sure to cover:
H preoperative and surgical procedures
H postoperative exercises, with supervision
H deep-breathing and coughing exercises to perform
after surgery
H performing frequent ROM leg exercises after surgery
H use of a constant-passive-motion device after total
knee arthroplasty, or placement of an abduction pil-
low between the legs after total hip arthroplasty
H how to use a trapeze to move about in bed
H medication administration, dosage, and possible ad-
verse effects.
Discharge planning
H Refer the patient for physical and occupational therapy.
H Refer the patient to the Arthritis Foundation.
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Rocky Mountain Assessment

spotted fever
Overview
Description
H Acute infectious, febrile, rash-producing illness asso-
ciated with outdoor activities
H Fatal in about 5% of patients
Pathophysiology
H Infecting organism multiplies in endothelial cells and
spreads via the bloodstream.
H Focal areas of infiltration lead to thrombosis and
leakage of red blood cells into surrounding tissue.
Causes
H Rickettsia rickettsii, transmitted by the wood tick
(Dermacentor andersoni) in the western United
States and by the dog tick (D. variabilis) in the east-
ern United States; enters humans or small animals
with the prolonged bite (4 to 6 hours) of an adult
tick
H Occasionally, inhalation or contact of abraded skin
with tick excreta or tissue juices
Incidence
H Endemic throughout the continental United States,
but most common in southeastern and south-central
regions
H Particularly prevalent in children ages 5 to 9
H Increased occurrence in spring and summer
Common characteristics
H Fever, headache, mental confusion, and myalgia
H Macular papular rash on palms and soles in about
90% of patients
H Rash, evident in about 15% of patients on day 1 and
in nearly half of patients by day 3, starting at the
wrists, ankles, or forehead and spreading to the re-
mainder of the extremities and trunk
H Within 2 days, rash seen over the entire body (in-
cluding scalp, palms, and soles)
Complications
H Lobar pneumonia
H Otitis media
H Parotitis
H Disseminated intravascular coagulation
H Renal failure
H Meningoencephalitis
H Hepatic injury
H Enterocolitis
H Death
History
H Recent exposure to ticks or tick-infested areas, or a
known tick bite
H Abrupt symptom onset, including persistent fever
(temperature of 102 to 104 F [38.9 to 40 C]);
generalized, excruciating headache; and aching in
bones, muscles, joints, and back
Physical findings
H Erythematous macules, 1 to 5 mm in diameter, be-
coming maculopapules that blanch with pressure
H Frank hemorrhage at the center of maculopapules,
creating petechia that dont blanch with pressure
H Bronchial cough
H Tachypnea
H Altered level of consciousness
H Decreased urine output; dark urine
H Tachycardia
H Hypotension
H Hepatomegaly, splenomegaly
H Generalized pitting edema
H Abdominal tenderness
Test results
Laboratory
H Serologic tests may be negative in initial stages.
H Indirect immunofluorescence assay has diagnostic
titer of 64 or greater, detectable between days 7 and
14 of the illness.
H Latex agglutination diagnostic titer is 128 or greater
1 week after onset.
H Platelet count, white blood cell (WBC) count, and
fibrinogen levels are decreased.
H Prothrombin time and partial thromboplastin time
are prolonged.
H Serum protein levels (especially albumin) are de-
creased.
H Hyponatremia and hypochloremia occur, related to
increased aldosterone excretion.
H Serum creatinine, blood urea nitrogen, and potassi-
um levels are elevated.
H Hepatic function is abnormal.
H Cerebrospinal fluid analysis shows mild mononu-
clear pleocytosis with slightly elevated protein con-
tent.
H Immunohistologic examination of cutaneous biopsy
of a rash lesion shows R. rickettsii.
Treatment
General
H Careful tick removal
H Careful fluid administration
H Intubation and mechanical ventilation, if needed
H Hemodialysis, if needed
H Treatment of hemorrhage and thrombocytopenia, if
needed

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H Small, frequent meals

H Parenteral nutrition, if the patient cant receive oral
intake
H Bed rest until condition improves

Medications
H Doxycycline (drug of choice), tetracycline, or chlo-
ramphenicol (in pregnant females)
H Anticonvulsants

Nursing considerations
Key outcomes
The patient will:
H maintain hemodynamic stability
H remain afebrile
H exhibit improved or healed lesions or wounds
H maintain adequate fluid volume
H maintain normal WBC count and differential
H report increased comfort and decreased pain.

Nursing interventions
H Administer prescribed drugs.
H Provide oxygen therapy and assisted ventilation for
pulmonary complications as ordered.
H Offer mentholated lotions if the rash itches.
H Turn the patient frequently.
H Encourage incentive spirometry and deep breathing.
H Plan care to promote adequate rest periods.

Monitoring
H Vital signs
H Fluid and electrolyte status
H Respiratory status
H Neurologic status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H importance of reporting recurrent symptoms imme-
diately
H importance of completing antibiotic course
H preventive strategies, including avoiding tick-infested
areas, whole-body inspection (including scalp) every
3 to 4 hours for attached ticks, protective clothing,
and insect repellent
H correct tick removal technique using tweezers or for-
ceps and steady traction.
Discharge planning
H Refer the patient to an infectious disease specialist if
needed.

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Rosacea With ocular involvement

H Blepharitis
H Conjunctivitis
H Uveitis
Overview H Keratitis

Description
H Chronic adult skin disorder that affects the skin and Assessment
eyes
H Produces flushing and dilation of small blood vessels History
in the face, especially the nose and cheeks H Facial flushing
H May cause papules and pustules, but without the H Gritty feeling in eyes
characteristic comedones of acne vulgaris H Facial edema
H Usually spreads slowly; rarely subsides spontaneously H Predisposing or aggravating factors
H Commonly more severe in males and usually associ- H Complaints of burning or stinging of face
ated with rhinophyma (dilated follicles and thick-
ened, bulbous skin on the nose) Physical findings
H Flushed areas on the cheeks, nose, forehead, and
Pathophysiology chin, usually starting across the central oval of the
H Vascular reactivity leads to varying degrees of pap- face (see Lupoid or granulomatous rosacea)
ules, pustules, and hyperplasia of the sebaceous H Telangiectasia with pustules and papules
glands. H Rhinophyma (thickened and disfigured noses) (in
severe rosacea)
Causes H Dry skin appearance
H Unknown H Facial edema
H Factors that cause flushing: H Ocular rosacea:
Drinking hot beverages Conjunctival infection
Using tobacco or alcohol Chalazion
Eating spicy foods Episcleritis
Engaging in physical activity
Being exposed to extreme heat or cold or to Test results
sunlight H Rosacea is confirmed by observation of typical vascu-
lar and acneiform lesions without comedones.
Incidence Diagnostic procedures
H Most common in white females ages 30 to 50 H Skin biopsy may be done to rule out other diseases
such as lupus erythematosus.
Common characteristics
H Flushed areas on cheeks, nose, forehead, and chin
H Ocular involvement (50% of cases) Treatment
Complications General
H Decreased self-esteem H Identification and avoidance of aggravating factors,
H Rosacea fulminans such as hot beverages, alcohol, and spicy foods
H Avoidance of physical activities involving sunlight or
exposure to extreme heat or cold
H Facial massage
Lupoid or granulomatous rosacea
Medications
Firm yellow, brownish, or reddish cutaneous papules or
H Topical azelaic acid
nodules characterize the variant form called lupoid or
H Topical sodium sulfacetamide
granulomatous rosacea. The lesions are less inflammatory
H Topical metronidazole
that those of rosacea. Typically, the surrounding skin is
relatively normal looking, but sometimes its red and H Oral doxycycline (for ocular involvement)
thickened diffusely. Usually, the lesions are monomorphic H Corticosteroids
in each patient, affecting the cheeks and periorificial areas. H Isotretinoin for severe cases
Other signs or symptoms of rosacea arent needed to
make the diagnosis of this form of rosacea. Diascopy with Surgery
a glass spatula reveals the lupoid character of the infiltra- H Electrosurgery
tions. Lupoid or granulomatous rosacea may scar the H Laser therapy
skin.

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Nursing considerations
Key outcomes
The patient will:
H exhibit improved or healed wounds or lesions
H report feelings of increased comfort
H demonstrate an appropriate skin care regimen
H report feelings of improved self-image.
Nursing interventions
H Administer prescribed drugs.
H Encourage patient to express feelings.
H Offer emotional support and reassurance.
H Assist with identification of triggers.
Monitoring
H Adverse reactions to prescribed drugs
H Complications
H Response to treatment
Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medication administration, dosage, and possible ad-
verse effects
H aggravating factors
H prevention of rosacea flare-ups (see Preventing
rosacea flare-up)
H stress-reduction techniques
H meticulous hand washing and personal hygiene
H ways to prevent infection
H signs and symptoms of infection
H when to notify the physician.
Prevention
Preventing rosacea flare-up
Rosacea flare-ups may be prevented by following these
guidelines:
H Practice proper hand-washing techniques.
H Stay cool in hot weather by staying in air conditioned
areas, drinking cold beverages, and avoiding overexer-
tion.
H Avoid cold wind on face by wearing a scarf or face
mask in cold weather.
H Use moisturizer in cold weather to protect against dry-
ing.
H Practice stress-management techniques.
H Avoid foods that trigger flare-ups, such as spicy foods,
hot beverages, and alcohol.
H Avoid heavy exertion during exercise, exercise in well-
ventilated areas, and exercise in short intervals. Also
apply a cold compress to face during exercise.
H Wash face gently and pat dry. Allow to air dry before
using creams and lotions.
H Avoid hot tubs, hot baths, and saunas.
H Avoid skin care products that burn or sting and use
products labeled fragrance free.
H Use a noncomedogenic, high-factor sunscreen when
exposed to sunlight and wind.

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Roseola infantum Assessment

History
Overview H Abruptly increasing, unexplainable fever that peaks
between 103 and 105 F (39.4 and 40.5 C) for
Description 3 to 5 days and then drops suddenly
H Common acute, benign, presumably viral illness H Anorexia
characterized by fever with subsequent rash (see H Irritability
Incubation and duration of common rash- H Listlessness
producing infections) H Cough
H Also known as exanthema subitum or sixth disease
Physical findings
Pathophysiology H When temperature drops abruptly, maculopapular,
H Human herpesvirus (HHV) type 6B, which causes the nonpruritic rash appears that blanches with pressure
disorder, is similar to cytomegalovirus. H Profuse rash on the trunk, arms, and neck; mild rash
H HHV-6 shows persistent and intermittent or chronic on the face and legs; fades within 24 hours
shedding in the normal population, resulting in the H Nagayama spots (red papules on soft palate and
unusually early infection of children. uvula)
H HHV-6 is thought to be latent in salivary glands and H Periorbital edema
blood.
Test results
Causes H Usually, roseola infantum is diagnosed from clinical
H HHV-6B observation.
H May be transmitted by saliva and possibly by genital Laboratory
secretions H Causative organism is present in saliva.
H HHV-6 is isolated in peripheral blood.
Incidence H Complete blood count shows leukopenia and relative
H Affects infants and young children, typically from age lymphocytosis as temperature increases.
6 months to 3 years H Immunofluorescence or enzyme immunoassays may
H Affects both sexes equally show seroconversion during the convalescent phase.
H Occurs year-round, but most common in spring and
fall
Treatment
Common characteristics
H Incubation period of 10 to 15 days General
H High fever with rash appearing after the fever breaks H Supportive and symptomatic
H Increased fluid intake
Complications H Rest until fever subsides
H Encephalopathy
H Thrombocytopenic purpura Medications
H Febrile seizures H Antipyretics
H Meningitis H Anticonvulsants
H Hepatitis

Nursing considerations
Incubation and duration of common Key outcomes
rash-producing infections The patient will:
H regain a normal body temperature
Infection Incubation Duration H maintain adequate fluid volume
(days) (days) H maintain adequate nutritional intake
Roseola 5 to 15 3 to 6 H exhibit improved or healed lesions or wounds.

Varicella 10 to 14 7 to 14 Nursing interventions

Rubeola 13 to 17 H Give tepid sponge baths and prescribed antipyretics.
5
H Replace fluids and electrolytes, as needed.
Rubella 14 to 21 3 H Institute seizure precautions.
H Provide emotional support to parents.

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Monitoring
H Neurologic status
H Fluid and electrolyte status
H Vital signs, especially temperature

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H methods to reduce fever:
tepid sponge baths
dressing the child in lightweight clothing
keeping a comfortable room temperature
use of antipyretics
H importance of adequate fluid intake
H no need for isolation
H reassurance that brief febrile seizures wont cause
brain damage and will stop as the fever subsides
H medication administration, dosage, and possible ad-
verse effects.

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Rotavirus Assessment
History
Overview H Fever, nausea, and vomiting followed by diarrhea

Description Physical findings

H Self-limiting intestinal illness that causes mild to se- H Diarrhea
vere diarrhea in children H Signs of dehydration, such as:
H Causes hospitalization of about 55,000 children each Tachycardia
year in the United States and kills more than 600,000 Hypotension
children worldwide Dry mucous membranes
Concentrated urine
Pathophysiology Poor tear production
H Rotavirus invades and damages the cells of the in- Poor skin turgor
testinal mucosa. Oliguria
H Damage decreases viable absorptive surface, causing Sunken eyeballs
an imbalance of secretion and absorption that results Sunken anterior fontanel
in diarrhea. H Rectal excoriation

Causes Test results

H Infection with rotavirus, a member of the Reoviridae Laboratory
family H Rapid antigen detection shows rotavirus in stool.
H Transmitted primarily by the fecal-oral route through
ingestion of contaminated water or food or through
contact with contaminated surfaces (see Spreading Treatment
rotavirus infection)
General
Incidence H Small, frequent meals
H Highest among infants and young children; affects H Increased fluid intake
most children in the United States by age 2 H Rest periods when fatigued
H Winter seasonal pattern in the United States and H Skin care
other temperate climate countries, with annual
epidemics from November to April Medications
H None (antibiotics and antimotility drugs contraindi-
Common characteristics cated)
H Vomiting and watery diarrhea for 3 to 8 days
H Fever
H Abdominal pain Nursing considerations
Complications Key outcomes
H Severe dehydration and shock The patient will:
H Skin breakdown H maintain adequate nutritional status
H Worsening of other conditions such as cystic fibrosis H maintain normal electrolyte levels
H maintain adequate fluid volume
H exhibit improved or healed lesions or wounds
H verbalize or demonstrate increased energy.
Spreading rotavirus infection
Nursing interventions
Rotavirus infection is contagious. Rotavirus particles pass
H Institute enteric precautions.
in the stool of infected persons before and after they have
symptoms of the illness. A child can catch a rotavirus in- H Enforce strict hand washing and careful cleaning of
fection if he puts his fingers in his mouth after touching all equipment, including toys.
something that has been contaminated by the stool of an H Implement measures to ensure adequate hydration.
infected person. Usually this happens when the child for- H Clean the patients perineum thoroughly to prevent
gets to wash his hands often enough, especially before skin breakdown.
eating and after using the toilet. Because of the wide- H Be aware that breast-fed infants can continue to
spread nature of rotavirus and the fact that almost 100% breast-feed without restrictions. Bottle-fed infants
of children get rotavirus illness, total prevention of the can use lactose-free soybean formulas.
spread of rotavirus is nearly impossible.

718 Rotavirus
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Monitoring
H Intake and output (including stools)
H Skin integrity

Patient teaching
Be sure to cover (with the parents):
H the disorder, diagnosis, and treatment
H proper hand-washing technique
H instructions on diaper changing and thorough
cleaning of the perineum and all affected surfaces
H the importance of notifying the physician of
increased diarrhea or signs of dehydration
H oral vaccine available for infants only.

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Rubella
Overview
Description
H Acute, mildly contagious viral disease that causes a
distinctive maculopapular rash (resembling measles
or scarlet fever) and lymphadenopathy
H Self-limiting with an excellent prognosis, except for
congenital rubella, which can have disastrous conse-
quences
H Transmitted through contact with blood, urine,
stools, or nasopharyngeal secretions of an infected
person; can also be transmitted transplacentally
H Communicable from about 10 days before until
5 days after rash appears
H Also called German measles
Pathophysiology
H A ribonucleic acid virus enters the bloodstream, usu-
ally through the respiratory route.
H The incubation period lasts 14 to 21 days, with a
duration of 3 days.
H The rash is thought to result from virus dissemina-
tion to the skin.
Causes
H Rubella virus (a togavirus) spread by direct contact
or contaminated airborne respiratory droplets
Incidence
H Occurs worldwide
H Most common among children ages 5 to 9, adoles-
cents, and young adults
H Epidemics seen in institutions, colleges, and military
populations
H Flourishes during spring, with limited outbreaks in
schools and workplaces
Giving the rubella vaccine
Know how to manage rubella immunization before giving
the vaccine. First, ask about allergies, especially to
neomycin. If the person has this allergy or has had a reac-
tion to any immunization in the past, check with the physi-
cian before giving the vaccine.
If the person is a female of childbearing age, ask if shes
pregnant. If she is or thinks she may be, dont give the
vaccine.
Give the vaccine at least 3 months after any administra-
tion of immune globulin or blood. These substances may
have antibodies that could neutralize the vaccine.
Dont vaccinate an immunocompromised person, a per-
son with immunodeficiency disease, or a person receiving
immunosuppressant, radiation, or corticosteroid therapy.
Instead, administer immune serum globulin, as ordered,
to prevent or reduce infection.
720 Rubella
Common characteristics
H Rash covering the trunk and body; begins to fade in
the opposite order in which it appeared by the end of
day 2
H Rash subsiding on the face; on the trunk may be con-
fluent and hard to distinguish from scarlet fever rash
H Rash disappearing on day 3
Complications
H Arthritis
H Postinfectious encephalitis
H Thrombocytopenic purpura
H Congenital rubella
In fetal infection (rare after 20th week
of gestation)
H Intrauterine death
H Spontaneous abortion
H Congenital malformations of major organ systems
Assessment
History
H Inadequate immunization, exposure to a person with
rubella infection within the previous 2 to 3 weeks, or
recent travel to an endemic area without reimmu-
nization
H In a child, absence of prodromal symptoms
H In an adolescent or adult, headache, malaise,
anorexia, coryza, sore throat, and cough preceding
rash onset
H Polyarthralgias and polyarthritis (in some adults)
Physical findings
H Rash accompanied by low-grade fever (99 to 101 F
[37.2 to 38.3 C]) that may reach 104 F (40 C)
H Exanthematous, maculopapular, mildly pruritic rash;
typically beginning on the face, and spreading rapid-
ly, covering the trunk and limbs within hours
H Small, red, petechial macules on the soft palate
(Forschheimer spots) preceding or accompanying
the rash
H Coryza
H Conjunctivitis
H Suboccipital, postauricular, and postcervical lymph
node enlargement
Test results
H Usually, the diagnosis is made from clinical observa-
tion.
Laboratory
H Cultures of throat, blood, urine, and cerebrospinal
fluid isolate the rubella virus; convalescent serum
shows a fourfold increase in antibody titers.
H Enzyme-linked immunosorbent assay for immuno-
globulin (Ig) M antibodies reveals rubella-specific
IgM antibody.
H In congenital rubella, rubella-specific IgM antibody
is present in umbilical cord blood.
9400Q-R.qxd 8/2/12 4:46 PM Page 721

Treatment
General
H Isolation precautions
H Small, frequent meals
H Increased fluid intake
H Rest until fever subsides
H Skin care

Medications
H Antipyretics
H Analgesics

Nursing considerations
Key outcomes
The patient will:
H remain free from signs and symptoms of infection
H exhibit improvement or healing of lesions or wounds
H express or demonstrate feelings of increased comfort
and decreased pain.
Nursing interventions
H Administer prescribed drugs.
H Institute isolation precautions until 5 days after the
rash disappears. Keep an infant with congenital
rubella in isolation for 3 months, until three throat
cultures are negative.
H Keep the patients skin clean and dry.
H Ensure that the patient receives care only from non-
pregnant hospital workers who arent at risk for
rubella. As ordered, administer immune globulin to
nonimmunized people who visit the patient. (See
Giving the rubella vaccine.)
H Report confirmed rubella cases to local public health
officials.
H Refer the patient to an infectious disease specialist if
congenital rubella is confirmed.
H Provide parents of an infant with congenital rubella
with support, counseling, and referrals, as needed.
Monitoring
H Vital signs
H Skin for signs of exanthem
H Auditory impairment in congenital rubella

Patient teaching
Be sure to cover (with the parents):
H the disorder, diagnosis, and treatment
H ways to reduce fever
H devastating effects of rubella on an unborn neonate
H importance of people with rubella avoiding pregnant
females
H avoidance of aspirin in a child receiving rubella
vaccine.

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Rubeola H Coryza
H Hoarseness
H Hacking cough

Overview Physical findings

H Temperature peaking at 103 to 105 F (39.4 C to
Description 40.5 C)
H Acute, highly contagious infection causing a charac- H Periorbital edema
teristic rash H Conjunctivitis
H In the United States, a usually excellent prognosis H Kopliks spots (tiny, bluish gray specks, surrounded
H Can be severe or fatal in patients with impaired cell- by red halo) on oral mucosa opposite the molars,
mediated immunity which may bleed
H Mortality highest in children younger than age 2 and H Pruritic rash starting as faint macules behind the ears
in adults and on the neck and cheeks, becoming papular and
H Also called measles or morbilli erythematous, and rapidly spreading over the face,
neck, eyelids, arms, chest, back, abdomen, and
Pathophysiology thighs
H Virus invades the respiratory epithelium and spreads H Fading of rash when it reaches the feet 2 to 3 days
via the bloodstream to the reticuloendothelial system, later, occurring in the same sequence it appeared,
infecting all types of white blood cells. leaving brown discoloration that disappears in 7 to
H Viremia and viruria develop, leading to infection of 10 days
the entire respiratory tract, which spreads to the in- H Severe cough
tegumentary system. H Rhinorrhea
H In measles encephalitis, focal hemorrhage, conges- H Lymphadenopathy
tion, and perivascular demyelination occur.
Test results
Causes Laboratory
H Rubeola virus H The measles virus appears in blood, nasopharyngeal
H Spread by direct contact or by contaminated air- secretions, and urine during the febrile period.
borne respiratory droplets, with portal of entry in the H Serum antibodies appear within 3 days after rash on-
upper respiratory tract set and reach peak titers 2 to 4 weeks later.
Incidence
H Affects mostly preschool children Treatment
H In temperate zones, most commonly seen in late win-
ter and early spring General
H Respiratory isolation precautions
Common characteristics H Use of vaporizer
H Fever, Kopliks spots, and characteristic red, blotchy, H Warm environment
rash that begins on the face and becomes generalized H Small, frequent meals
H Peak communicability from 1 to 2 days before symp- H Increased fluid intake
tom onset until 4 days after the rash appears H Rest until symptoms improve
H Skin care
Complications
H Secondary bacterial infection Medications
H Autoimmune reaction H Antipyretics
H Bronchitis
H Otitis media
H Pneumonia Nursing considerations
H Encephalitis
Key outcomes
The patient will:
Assessment H remain free from signs and symptoms of infection
H exhibit improved or healed lesions or wounds
History H remain free from complications related to oral mu-
H Inadequate immunization and exposure to someone cous membrane trauma.
with measles in the past 14 days The patients family will:
H Photophobia H communicate an understanding of the patients spe-
H Malaise cial dietary needs.
H Anorexia

722 Rubeola
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Nursing interventions
H Institute respiratory isolation measures for 4 days af-
ter rash onset.
H Follow standard precautions.
H Administer prescribed drugs.
H Encourage bed rest during the acute period.
H If photophobia occurs, darken the room or provide
sunglasses.
H To prevent disease spread, administer measles
vaccine, as ordered and needed.
H Report measles cases to local health authorities.

Monitoring
H Vital signs
H Skin for signs of exanthem
H Eyes for conjunctivitis
H Mental status
H Signs and symptoms of pneumonia
H Ears for otitis media

Patient teaching
Be sure to cover (with the parents):
H the disorder, diagnosis, and treatment
H supportive measures, isolation, bed rest, and in-
creased fluids
H instructions on cleaning a vaporizer (if used) and the
importance of changing the water every 8 hours
H early signs and symptoms of complications that
should be reported.

Rubeola 723
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S Overview
Life-threatening disorder

Saint Louis encephalitis

Description
H Acute inflammatory disease of short duration that in-
volves the brain, spinal cord, and meninges following
the bite of an infected mosquito (mosquitoes infec-
tive for life)
H Usually asymptomatic, but severe infection may have
Common characteristics
H Symptoms usually mild
H In severe infections
Acute onset of headache
High fever
Nausea
Myalgia
Malaise
Meningeal signs of stupor
Coma
Seizures (especially in infants)
Spastic paralysis
Death
H In children, possible urinary tract symptoms

Complications
acute onset
H Incubation period of 4 to 21 days H Acute encephalitis
H No person-to-person transmission H Movement disorders and motor deficits
H No chronic infection or reports of relapsing infection H Seizures and coma
H Also known as SEV, SLEV, mosquito-borne H Cranial nerve palsies
encephalitis, arbovirus, and viral encephalitis H Death

Pathophysiology
ALERT
H The virus is found in common birds, such as spar-
rows, finches, blue jays, robins, and doves. Patients with atherosclerosis, heart disease, and
H Culex mosquitoes feed on these birds, contract the hypertension have an increased risk of death from
virus, and then pass it on to human hosts through a this infection.
bite.
H A primary viremia follows reproduction of the virus
at the site of inoculation. Assessment
H In subclinical disease, the pathogen is cleared by the
liver, spleen, and lymph nodes before invasion of the History
central nervous system. H Exposure to infected insect
H Secondary viremia occurs with continued viral repli- H Onset of encephalitis characterized by:
cation, which overwhelms the liver, spleen, and Malaise
lymph nodes. Fever
H The virus then invades the central nervous system, in- Cough and sore throat, followed by common
cluding the brain and spinal cord. symptoms of headache, nausea, vomiting, confu-
sion, disorientation, irritability, tremors, and pos-
Causes sible seizures
H Transmitted by the bite of an infected mosquito
H Laboratory-acquired infections possible through in- Physical findings
fected blood, cerebrospinal fluid (CSF), urine, and H Temperature elevation
exudates H Normal neurologic examination
H 5% of patients present in a deep coma
Risk factors H Cranial nerve palsies in about 25% of patients
H Human immunodeficiency virus infection H Possibly ataxia
H Age older than 70 (tenfold increased risk of clinical H Possibly seizures (infrequent, but more common in
illness) children)
H Travel to endemic areas
H Participation in outdoor activities Test results
H Low socioeconomic status Laboratory
H Crowded living conditions H One of the following will be present: A fourfold in-
H Outdoor occupations crease in the antivirus antibody titer between the
acute and the convalescent periods; virus isolation
Incidence from tissue, blood, or CSF; or specific immunoglobu-
H Occurs in North, South, and Central America and the lin M antibody.
Caribbean; major health problem in the United Sates H Pyuria or proteinuria occurs.
H Highest incidence in late summer or early fall H Sodium level is decreased.
H Higher incidence in males, probably because of
more outdoor exposure

724 Saint Louis encephalitis

9400S.qxd 8/2/12 4:48 PM Page 725

H CSF pressure is normal to mildly elevated, blood glu- Prevention

cose level is normal, and protein level is normal to Preventing mosquito bites
mildly elevated; CSF white blood cell count usually is
Mosquito bites may be prevented by following these
less than 200/l.. guidelines:
H Stay indoors between dusk and dark.
H Wear long pants and long-sleeved shirts when outside.
Treatment H Wear socks and tuck pants legs into socks.
H Choose light-colored clothing.
General H Spray exposed skin with insect repellent.
H Supportive H Avoid areas of standing water where mosquitoes con-
H Management of seizures or neurologic symptoms gregate.
H Diet as tolerated H Eliminate standing water around home to prevent
H Bed rest breeding, such as:
unclogging gutters
Medications removing old tires
emptying wading pools or change water frequently
H Antipyretics
changing bird bath water frequently
H Analgesics checking flower pots for pooling water and drain.
H Use an electronic bug zapper.
H Change outdoor lights to yellow bug lights.
Nursing considerations
Key outcomes
The patient will:
H remain safe from falls caused by ataxia or seizures
H accept comfort measures
H maintain adequate nutrition and fluid intake.

Nursing interventions
H Administer prescribed drugs.
H Encourage nutritional intake.
H Encourage fluids and lying flat after lumbar punc-
ture.
H Assist with ambulation, as needed.
H Frequently reposition the unconscious patient.
H Encourage range-of-motion (ROM) exercises (pas-
sive ROM exercises if the patient is unconscious).
Monitoring
H Vital signs
H Level of consciousness
H Skin breakdown
H Seizure activity
H Complications of lumbar puncture, if performed

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H mosquito bite prevention. (See Preventing mosquito
bites.)
Discharge planning
H Encourage follow-up appointments, as needed.

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Salmonella infection
Overview
Description
H One of the most common intestinal infections in the
United States
H Occurs as enterocolitis, bacteremia, localized infec-
tion, typhoid fever, or paratyphoid fever
H Nontyphoid forms, usually mild to moderate illness
with low mortality
H Typhoid fever most severe form; usually lasts from
1 to 4 weeks and confers lifelong immunity, although
patient may become a carrier
Pathophysiology
H Invasion occurs across the small intestinal mucosa,
altering the plasma membrane and entering the lami-
na propria.
H Invasion activates cell-signaling pathways, which alter
electrolyte transport, and may cause diarrhea.
H Some salmonella produce a molecule that increases
electrolyte and fluid secretion.
Causes
H Gram-negative bacilli of the genus Salmonella
(member of the Enterobacteriaceae family)
Typhoid fever: S. typhi
Enterocolitis: S. enteritidis
Bacteremia: S. choleresis
H Nontyphoidal infection usually, ingestion of conta-
minated water or food or inadequately processed
food, especially eggs, chicken, turkey, and duck
H Contact with infected person or animal
H Ingestion of contaminated dry milk, chocolate bars,
or pharmaceuticals of animal origin
Special populations
Salmonella infection in children younger than age
5 is usually from fecal-oral spread.
H Typhoid fever usually, drinking water contaminat-
ed by excretions of a carrier
Incidence
H Increasing in the United States due to travel to en-
demic areas, especially the borders of Mexico
H Lifelong immunity after initial attack of typhoid fever,
but patient may become a carrier
H Paratyphoid fever rare in the United States
Common characteristics
H Nontyphoidal forms usually, mild to moderate ill-
ness, with low mortality
H Enterocolitis and bacteremia especially common
(and more virulent) among infants, elderly people,
726 Salmonella infection
and those already weakened by other infections, es-
pecially human immunodeficiency virus infection
Complications
H Dehydration
H Hypovolemic shock
H Abscess formation
H Sepsis
H Toxic megacolon
Assessment
History
H With enterocolitis, possible report of contaminated
food eaten 6 to 48 hours before onset of symptoms
H With bacteremia, patient usually reveals immuno-
compromised condition, especially acquired immun-
odeficiency syndrome
H With typhoid fever, possible ingestion of contaminat-
ed food or water, typically 1 to 2 weeks before symp-
toms develop
Physical findings
H Fever
H Abdominal pain
H With enterocolitis, severe diarrhea
H With typhoidal infection, headache, increasing fever,
and constipation
Test results
Laboratory
H Blood culture in typhoid or paratyphoid fever and
bacteremia shows causative organism in most cases.
H Stool culture in typhoid or paratyphoid fever and en-
terocolitis shows causative organism.
H Other culture specimens (urine, bone marrow, pus,
and vomitus) show causative organism.
H Presence of S. typhi in stools 1 or more years after
treatment indicates that the patient is a carrier
(about 3% of patients).
H Widals test, an agglutination reaction against somatic
and flagellar antigens, suggests typhoid fever with a
fourfold increase in titer.
H Complete blood count (CBC) shows transient leuko-
cytosis during the first week of typhoidal salmonella
infection.
H CBC shows leukopenia during the third week of ty-
phoidal salmonella infection.
H CBC shows leukocytosis with local infection.
Treatment
General
H Supportive therapy
H Possible hospitalization for severe diarrhea
H Fluid and electrolyte replacement
H High-calorie fluids
H Activity as tolerated
9400S.qxd 8/2/12 4:48 PM Page 727

Medications Prevention
H Antimicrobials Preventing recurrence of
H Antidiarrheals
salmonella infection
To prevent salmonella infection from recurring, follow
ALERT these teaching guidelines:
H Explain the causes of salmonella infection.
Dont give antipyretics. They may mask fever and H Show the patient how to wash his hands by wetting
lead to hypothermia. Instead, promote heat loss by them under running water, lathering with soap and
applying tepid, wet towels to the patients groin scrubbing, rinsing under running water with his fingers
and axillae. pointing down, and drying with a clean towel or paper
towel.
H Tell the patient to wash his hands after using the bath-
Surgery room and before eating.
H Tell him to cook foods thoroughly especially eggs
H Surgical drainage of localized abscesses
and chicken and to refrigerate them at once.
H Teach him how to avoid cross-contaminating foods by
Nursing considerations cleaning preparation surfaces with hot, soapy water
and drying them thoroughly after use; cleaning sur-
faces between foods when preparing more than one
Key outcomes food; and washing his hands before and after handling
The patient will: each food.
H regain and maintain fluid and electrolyte balance H Tell the patient with a positive stool culture to avoid
H return to a normal elimination pattern handling food and to use a separate bathroom or clean
H conserve energy while carrying out daily activities the bathroom after each use.
H Tell the patient to report dehydration, bleeding, or re-
H report adequate pain relief
currence of signs of salmonella infection.
H experience no further weight loss.

Nursing interventions
H Follow enteric precautions until three consecutive Discharge planning
stool cultures are negative the first one 48 hours H Arrange for follow-up with an infectious disease
after antibiotic treatment ends, followed by two more specialist or a gastroenterologist as needed.
at 24-hour intervals.
H Watch closely for signs of bowel perforation.
H Maintain adequate I.V. fluid and electrolyte therapy,
as ordered.
H Provide good skin and mouth care.
H Apply mild heat to relieve abdominal cramps.
H Report salmonella cases to public health officials.

Monitoring
H Fluid and electrolyte status
H Vital signs
H Daily weight

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the need for close contacts to obtain a medical exam-
ination and treatment if cultures are positive
H how to prevent salmonella infections (see Prevent-
ing recurrence of salmonella infection)
H the need to be vaccinated (for those at high risk for
contracting typhoid fever, such as laboratory workers
and travelers)
H the importance of proper hand washing
H the need to avoid preparing food or pouring water
for others until salmonella infection is eliminated.

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Sarcoidosis Assessment
History
Overview H Pain in the wrists, ankles, and elbows
H General fatigue and malaise
Description H Unexplained weight loss
H A multisystemic, granulomatous disorder that char- H Breathlessness and dyspnea
acteristically produces lymphadenopathy, pulmonary H Nonproductive cough
infiltration, and skeletal, liver, eye, or skin lesions H Substernal pain
H May be acute (usually resolves within 2 years) or
chronic Physical findings
H Chronic, progressive sarcoidosis (uncommon) asso- H Erythema nodosum
ciated with pulmonary fibrosis and progressive pul- H Punched out lesions on the fingers and toes
monary disability H Cranial or peripheral nerve palsies
H Extensive nasal mucosal lesions
Pathophysiology H Anterior uveitis
H An excessive inflammatory process begins in the alve- H Glaucoma and blindness occasionally in advanced
oli, bronchioles, and blood vessels of the lungs. disease
H Monocyte-macrophages accumulate in the target tis- H Bilateral hilar and paratracheal lymphadenopathy
sue where they induce the inflammatory process. H Splenomegaly
H CD4+ T-lymphocytes and sensitized immune cells H Arrhythmias
form a ring around the inflamed area.
H Fibroblasts, mast cells, collagen fibers, and proteo- Test results
glycans encase the inflammatory and immune cells, Laboratory
causing granuloma formation. H Arterial blood gas (ABG) analysis shows a decreased
partial pressure of arterial oxygen and increased car-
Causes bon dioxide levels.
H Exact cause unknown Imaging
H Possible causes: H Chest X-rays show bilateral hilar and right paratra-
Hypersensitivity response to atypical mycobacteria, cheal adenopathy, with or without diffuse interstitial
fungi, and pine pollen infiltrates.
Chemicals Diagnostic procedures
T-cell abnormalities H Kveim-Siltzbach skin test shows granuloma develop-
Lymphokine production abnormalities ment at the injection site in 2 to 4 weeks when posi-
tive.
Incidence H Lymph node, skin, or lung biopsy shows noncaseat-
H Most common in people ages 20 to 40 ing granulomas with negative cultures for mycobacte-
H In the United States, predominant occurrence among ria and fungi.
blacks H Pulmonary function tests show decreased total lung
H Affects twice as many females as males capacity and compliance and reduced diffusing ca-
H Incidence slightly higher in families, suggesting pacity.
genetic predisposition
Common characteristics Treatment
H Pain in the wrists, ankles, and elbows
H Malaise General
H Unexplained weight loss H None needed for asymptomatic sarcoidosis
H Shortness of breath on exertion H Protection from sunlight
H Substernal pain H Low-calcium diet for hypercalcemia
H Reduced-sodium, high-calorie diet
Complications H Adequate fluids
H Pulmonary fibrosis H Activity as tolerated
H Pulmonary hypertension
H Cor pulmonale Medications
H Corticosteroids such as prednisone

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Discharge planning
Nursing considerations H Refer a patient with failing vision to community sup-
port and resource groups such as the American
Key outcomes Foundation for the Blind, if necessary.
The patient will:
H maintain adequate ventilation
H demonstrate effective coping mechanisms
H express an understanding of the illness
H perform activities of daily living within confines of
the illness
H remain free from signs and symptoms of infection.

Nursing interventions
H Administer prescribed drugs.
H Administer supplemental oxygen.
H Provide a nutritious, high-calorie diet.
H Encourage oral fluid intake.
H Provide a low-calcium diet for hypercalcemia.
H Provide emotional support.
H Provide comfort measures.
H Include the patient in care decisions whenever
possible.
Monitoring
H Vital signs
H Intake and output
H Daily weight
H Respiratory status
H Chest X-ray results
H Sputum production
H ABG results
H Cardiac rhythm

ALERT
Because corticosteroids may induce or worsen dia-
betes mellitus, test the patients blood by finger-
sticks for glucose and acetone at least every
12 hours at the beginning of corticosteroid therapy.
Also, watch for other adverse effects, such as fluid
retention, electrolyte imbalance (especially hypo-
kalemia), moon face, hypertension, and personali-
ty changes.

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medication administration, dosage, and possible ad-
verse effects
H when to notify the physician
H steroid therapy
H the need for regular follow-up examinations
H the importance of wearing medical identification
jewelry
H infection prevention.

Sarcoidosis 729
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Scabies H Occurs worldwide

H Can be endemic

Common characteristics
Overview H Burrows
H Severe pruritus
Description H Excoriations
H Transmissible skin infestation with Sarcoptes scabiei
var. hominis (itch mite) Complications
H Characterized by burrows, severe pruritus, and exco- H Secondary bacterial infection
riations H Abscess formation
H Septicemia
Pathophysiology
H Mites burrow into the skin on contact, progressing
2 to 3 mm per day. Assessment
H Females live about 4 to 6 weeks and lay about 40 to
50 eggs, which hatch in 3 to 4 days. History
H Pruritus occurs only after sensitization to the mite H Predisposing factors
develops. With initial infestation, sensitization re- H May be asymptomatic initially
quires several weeks. With reinfestation, sensitization H Intense pruritus being more severe at night
develops within 24 hours.
H Dead mites, eggs, larvae, and their excrement trigger Physical findings
an inflammatory eruption of the skin in infested H Characteristic gray-brown, threadlike burrows (0.5
areas. to 1 cm long) with tiny papule or vesicle at one end
H Common sites: flexor surfaces of wrists, elbows, axil-
Causes lary folds, waistline, nipples in females, and genitalia
H Direct (skin to skin) contact or contact with contam-
inated articles for up to 48 hours (see Scabies: Special populations
Cause and effect)
In infants, the burrows may appear on the head
Risk factors and neck.
H Overcrowded living conditions
H Poor hygiene H Papules, vesicles, crusting, abscess formation, and
H Multiple sex partners cellulites with secondary infection
H Day-care or institutional settings
Test results
Incidence Laboratory
H Common in children and young adults H Wound culture demonstrates secondary bacterial in-
H Common in elderly and debilitated patients fection.
Diagnostic procedures
H Mineral oil burrow-scraping reveals mites, nits, or
Scabies: Cause and effect eggs, and feces or scybala.
H Punch biopsy may help confirm the diagnosis.
Infestation with Sarcoptes scabiei the itch mite Other
causes scabies. This mite (shown enlarged below) has a H Resolution of infestation with therapeutic trial of a
hard shell and measures a microscopic 0.1 mm.
pediculicide confirms the diagnosis.

Treatment
General
H Bathing with soap and water

Medications
H Topical scabicides
H Topical 6% to 10% sulfur solution
H Systemic antibiotics
H Antipruritics

730 Scabies
9400S.qxd 8/2/12 4:48 PM Page 731

ALERT Prevention
Preventing scabies transmission
Avoid the use of topical steroids, which may poten- and recurrence
tiate the infection.
Scabies transmission and recurrence may be prevented
by following these guidelines:
Special populations H Avoid sharing towels, linen, and clothing.
H Wash all infested items with hot, soapy water and dry
When treating infants, include the head in treat- on high heat in the dryer.
ment. H Place items you cant wash in a plastic bag and leave
for 1 week. Mites die within 48 to 72 hours away from
the human body.
Nursing considerations H Practice good personal hygiene.

Key outcomes
The patient will:
H exhibit resolution of infestation H prevention of transmission and recurrence (see Pre-
H report relief of pruritus venting scabies transmission and recurrence)
H avoid complications H proper application of the prescribed scabicide.
H demonstrate understanding of proper skin care
regimen.
Nursing interventions
H Trim patients fingernails short.
H Administer prescribed drugs.
H Isolate the patient until treatment is completed.
H Practice meticulous hand washing.
H Sterilize blood pressure cuffs in a gas autoclave
before using on other patients.
H Decontaminate linens, towels, clothing, and personal
articles.
H Disinfect the patients room after discharge.
H If the patient is a child, notify his school of the infes-
tation.
H Encourage verbalization of feelings.
H Observe wound and skin precautions for 24 hours
after treatment with a scabicide.
Monitoring
H Response to treatment
H Complications
H Neurologic status

ALERT
Prolonged use of scabicides may lead to excessive
central nervous system stimulation and seizures.

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H identification of characteristic lesions
H modes of transmission
H mite resistance to scabicides
H assessment of close personal contacts for infestation
H successful treatment for infestation with good hy-
giene and scabicides

Scabies 731
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Scarlet fever H Malaise

H Likely high temperature (100 to 103 F [37.8 to
39.4 C])
H Characteristic rash 12 to 48 hours after onset of fever
Overview
Physical findings
Description H Inflamed and heavily coated tongue, progressing to
H A hypersensitivity reaction that usually follows strep- strawberry-like tongue
tococcal pharyngitis H Tongue that peels and becomes beefy red, returning
H May follow other streptococcal infections, such as to normal by the end of the second week
wound infections, urosepsis, and puerperal sepsis H Red and edematous uvula, tonsils, and posterior
H Also known as scarlatina oropharynx, with mucopurulent exudate
H Fine, erythematous rash, appears first on the upper
Pathophysiology chest and back, spreading to the neck, abdomen,
H After infection, an erythrogenic toxin is produced, legs, and arms
resulting in a hypersensitivity reaction. H Rash resembling sunburn with goose bumps; blanch-
H Replication site is the tonsils and pharynx. es with pressure
H Inflammatory reaction occurs. H Flushed face; circumoral pallor
H Tachycardia
Causes
H Group A beta-hemolytic streptococci transmitted by Test results
direct contact with infected person or droplet Laboratory
spread; indirectly by contact with contaminated arti- H Pharyngeal culture is positive for group A beta-
cles or ingestion of contaminated food hemolytic streptococci.
H Complete blood count reveals increased white blood
Incidence cell count and eosinophilia during the second week.
H Most common in children ages 3 to 15; peak inci-
dence ages 4 to 8
H Infection rate increased in overcrowded situations Treatment
H Males and females affected equally
General
Common characteristics H Increased fluid intake
H Incubation period typically lasting 2 to 4 days, may H Rest periods when fatigued
last 1 to 7 days H Appropriate skin care
H High fever
H Pharyngitis Medications
H Rash H Antibiotics, such as penicillin and erythromycin
H Antipyretics
Complications
H Severe disseminated toxic illness
H Septicemia Nursing considerations
H Rheumatic heart disease
H Liver damage Key outcomes
H Otitis media The patient will:
H Peritonsillar and retropharyngeal abscess H have moist, pink mucous membranes without lesions
H Sinusitus H chew and swallow without discomfort
H Glomerulonephritis H have no signs or symptoms of infection
H Meningitis H express feelings of increased comfort or absence of
H Brain abscess pain at rest.
Nursing interventions
Assessment H Implement respiratory secretion precautions for
24 hours after starting antibiotic therapy.
History H Offer frequent oral fluids and oral hygiene.
H Possible contact with person with a sore throat H Administer prescribed drugs.
H Sore throat H Provide skin care to relieve discomfort from the
H Headache rash.
H Chills H Provide warm liquids or cold foods to ease sore
H Anorexia throat pain.
H Abdominal pain

732 Scarlet fever

9400S.qxd 8/2/12 4:48 PM Page 733

H Use a cool mist humidifier to keep the air moist and

prevent the throat from getting too dry and more
sore.
Monitoring
H Adverse drug reactions
H Response to treatment
H Complications
H Body temperature
H Rash
H Nutritional status
H Signs and symptoms of dehydration

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the need to take oral antibiotics for the prescribed
length of time to prevent serious complications
H proper disposal of purulent discharge
H follow-up care
H when to notify the physician
H medication administration, dosage, and possible ad-
verse effects
H prevention of scarlet fever and strep throat by wash-
ing hands and avoiding others with the disease.

Scarlet fever 733

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Incidence
Schistosomiasis H Uncommon in the United States
H Most prevalent in children and adolescents

Overview Common characteristics

H Initially, a transient, pruritic rash at the site of cer-
Description cariae penetration, along with fever, myalgia, and
H A slowly progressive disease caused by blood flukes cough
of the class Trematoda H Later, hepatomegaly, splenomegaly, and lymphade-
H Three major types: Schistosoma mansoni and S. nopathy
japonicum that infect intestinal tract; S. haematobi-
um that infects urinary tract (see Types of schisto- Complications
somes) H Portal hypertension
H Degree of infection determines intensity of illness H Pulmonary hypertension
H Also known as bilharziasis H Heart failure
H Ascites
Pathophysiology H Hematemesis from ruptured esophageal varices
H Larvae penetrate the skin or mucous membranes and H Renal failure
eventually work their way to the livers venous portal H Flaccid paralysis
circulation. They mature in 1 to 3 months and mi- H Seizures
grate to other parts of the body. H Skin abscesses
H The female cercariae (the final larval stage) lay spiny
eggs in blood vessels surrounding the large intestine
or bladder. Assessment
H After penetrating the mucosa of these organs, the
eggs are excreted in feces or urine. History
H If the eggs hatch in fresh water, the first-stage larvae H Recent travel to endemic areas
(miracidia) penetrate freshwater snails, which act as H Fever
passive intermediate hosts. Cercariae produced in H Myalgia
snails escape into water and begin a new life cycle. H Cough

Causes Physical findings

H Contamination with Schistosoma larvae transmitted H Rash at site of contamination
by bathing, swimming, wading, or working in water H Hepatomegaly
H Splenomegaly
H Lymphadenopathy

Types of schistosomes Test results

Laboratory
Species and Signs and H Ova appear in the urine or stool.
incidence symptoms
H White blood cell count shows eosinophilia.
Schistosoma mansoni Irregular fever, malaise, Diagnostic procedures
Western hemisphere, weakness, abdominal dis- H Mucosal lesion biopsy confirms infection.
particularly Puerto Rico, tress, weight loss, diarrhea,
Lesser Antilles, Brazil, ascites, hepatosplenomegaly,
and Venezuela; also Nile portal hypertension, fistulas,
delta, Sudan, and central and intestinal stricture Treatment
Africa

Schistosoma japonicum Irregular fever, malaise,

General
Affects males more than weakness, abdominal dis- H Supportive
females; particularly tress, weight loss, diarrhea, H Fluid replacement
prevalent among farmers ascites, hepatosplenomegaly,
H Diet as tolerated
in Japan, China, and the portal hypertension, fistulas,
Philippines. and intestinal stricture H Activity as tolerated

Schistosoma Terminal hematuria, dysuria, Medications

haematobium uretal colic; with secondary
Africa, Cyprus, Greece, infection colicky pain, in- H Praziquantel
and India termittent flank pain, vague
GI complaints, and complete
renal failure

734 Schistosomiasis
9400S.qxd 8/2/12 4:48 PM Page 735

Schistosomal dermatitis
Nursing considerations
Schistosomal dermatitis, also known as swimmers itch or
Key outcomes clam diggers itch, affects those who bathe in and camp
along freshwater lakes in the eastern and western United
The patient will: States. Its caused by schistosomal cercariae that are har-
H remain hemodynamically stable bored by migratory birds and penetrate the skin, causing
H avoid complications a pruritus papular rash. Initially mild, the reaction grows
H express an understanding of the disorder and more severe with repeated exposure. Treatment consists
treatment. of 5% copper sulfate solution as an antipruritic and 2%
methylene blue as an antibacterial agent.
Nursing interventions
H Encourage fluid intake.
H Provide support.
H Encourage activity.

Monitoring
H Vital signs
H Comfort level
H Response to treatment

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H avoiding possibly contaminated water or, if the pa-
tient must enter the water, the need to wear protec-
tive clothing and dry off thoroughly after leaving the
water. (See Schistosomal dermatitis.)
Discharge planning
H Before discharge, tell the patient to schedule a
follow-up visit between 3 and 6 months after treat-
ment. (If this checkup reveals any living eggs, treat-
ment may be resumed.)

Schistosomiasis 735
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Schizophrenia Special populations

The onset of schizophrenia usually occurs during
late adolescence.
Overview
Description Common characteristics
H Disturbances in thought content and form, percep- H Change in emotional expression
tion, affect, language, social activity, sense of self, vo- H Inappropriate behavior
lition, interpersonal relationships, and psychomotor H Inaccurate interpretation of events
behavior H Ineffective communication
H Five types recognized by the Diagnostic and Statisti-
cal Manual of Mental Disorders, Fourth Edition, Complications
Text Revision (DSM-IV-TR): catatonic, paranoid, H Suicide (about 10%)
disorganized, residual, and undifferentiated H Impairment of health
H Insidious onset and poor outcome H Impairment of social functioning
H Can progress to social withdrawal, perceptual distor-
tions, chronic delusions, and hallucinations
H Up to one-third of patients having only one psychotic Assessment
episode
H Some patients having no disability between periods of History
exacerbation; others needing continuous institutional H Possible long-standing psychiatric illness with repeat-
care ed episodes
H Worsening prognosis with each acute episode H Decreased social functioning

Pathophysiology Physical findings

H A biochemical hypothesis holds that schizophrenia
results from excessive activity at dopaminergic
synapses.
H Other neurotransmitter alterations may also con-
tribute to schizophrenic symptoms.
H Structural abnormalities of the intraventricular sys-
tem, temporal lobe abnormalities, decreased volume
of the amygdala and hippocampus of the limbic sys-
tem, structural changes in prefrontal white matter,
and increased volume of the basal ganglia have been
found.
Causes
H Exact cause unknown
H May result from a combination of genetic, biological,
cultural, environmental, and psychological factors
Risk factors
H Familial history
H Gestational and birth complications
H Prenatal nutritional deficiencies
H In utero exposure to viruses or malnutrition
H Stressful environment
H Decreased emotional expression
H Impaired concentration
DSM-IV-TR criteria
Diagnosis depends on identifying two or more of the
following signs and symptoms for a significant portion
of time during a 1-month period (or only one symptom
if delusions are bizarre, hallucinations consist of a
voice issuing a running commentary, or hallucinations
consist of two or more voices conversing with each
other):
H delusions
H prominent hallucinations
H disorganized speech
H grossly disorganized or catatonic behavior
H negative symptoms (flat affect or inability to make
decisions or speak).
In addition, one or more major areas of functioning
(work, relationships, and self-care) are markedly be-
low previous level, and the disturbance isnt due to a
substance, medical condition, or schizoaffective or
mood disorder.

Incidence Treatment
H Affects about 1% of the United States population
H Close relatives of patients up to 50 times more likely General
to develop schizophrenia; the closer the degree of H Psychotherapy
biological relatedness, the higher the risk H Social skills training
H Higher incidence among lower socioeconomic H Family therapy
groups H Vocational counseling

736 Schizophrenia
9400S.qxd 8/2/12 4:48 PM Page 737

Medications
H Antipsychotic drugs (neuroleptic drugs), such as
chlorpromazine and haloperidol
H Antidepressants
H Anxiolytics
H Atypical antipsychotics, such as clozapine and
risperidone

Nursing considerations
Key outcomes
The patient will:
H identify internal and external factors that trigger
delusional episodes
H identify and perform activities that decrease delu-
sions
H remain free from injury
H participate with his family in care and prescribed
therapies
H demonstrate effective social interaction skills.

Nursing interventions
H Evaluate the patients ability to carry out activities of
daily living.
H Maintain a safe environment, minimizing stimuli.
H Administer prescribed drugs.
H Adopt an accepting and consistent approach.
H Avoid promoting dependence.
H Reward positive behavior.
H Provide reality-based explanations for distorted body
images or hypochondriacal complaints.
H Set limits on inappropriate behavior.
H Offer simple and matter-of-fact explanations about
environmental safeguards, drugs, and policies.
H Build trust; be honest and dependable. Dont threat-
en, and dont promise what you cant fulfill.
Monitoring
H Suicidal ideation
H Homicidal ideation
H Effects of drug regimen
H Weight

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medication administration, dosage, and possible
adverse effects
H how family members can recognize an impending
relapse, and ways to manage symptoms.
Discharge planning
H Refer the patient to appropriate community re-
sources and support services.

Schizophrenia 737
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Scleroderma
Overview
Description
H Connective tissue disease characterized by inflamma-
tory, degenerative, and fibrotic changes in skin,
blood vessels, synovial membranes, skeletal muscles,
and internal organs; thickening of tissues
H May affect the visceral organs or remain localized to
the skin when the connective tissues of many organs,
including the heart, kidney, GI tract, and lungs, are
involved
H Cutaneous lesions usually on the face, hands, neck,
and upper chest
H Also known as systemic sclerosis
Pathophysiology
H The skin atrophies, and infiltrates containing CD4+
T cells surround the blood vessels; inflamed collagen
fibers become edematous, losing strength and elas-
ticity.
H The dermis becomes tightly bound to the underlying
structures, resulting in atrophy of the affected dermal
appendages and destruction of the distal phalanges
by osteoporosis.
H As the disease progresses, atrophy can affect other
areas.
Causes
H Unknown
H Possible causes:
Systemic exposure to silica dust, polyvinyl chlo-
ride, or organic solvents
Anticancer agents such as bleomycin or nonopioid
analgesics such as pentazocine
Fibrosis due to an abnormal immune system re-
sponse
Underlying vascular cause with tissue changes ini-
tiated by inconsistent perfusion
Asymptomatic or common viral infections
Incidence
H Rarely occurs in children or males younger than
age 35
H Affects females three to four times more commonly
than males, especially between ages 30 and 50
H Peak incidence from ages 50 to 60
Common characteristics
H Skin thickening in face and fingers
Complications
H Related to thickening of tissues:
Slowly healing ulcerations on fingertips or toes
leading to gangrene
Decreased food intake and weight loss due to GI
symptoms
Arrhythmias and dyspnea
738 Scleroderma
Malignant hypertension
Respiratory failure
Renal failure
Esophageal or intestinal obstruction or perforation
H Raynauds phenomenon
H Pulmonary fibrosis
Assessment
History
H Pain, stiffness, and swelling of fingers and joints (lat-
er symptoms)
H Frequent reflux, heartburn, dysphagia, and bloating
after meals due to GI dysfunction
H Diarrhea, constipation, and malodorous floating
stool
Physical findings
H Skin thickening, commonly limited to the distal ex-
tremities and face, but possibly involving internal or-
gans
H CREST syndrome (a benign subtype of limited sys-
temic sclerosis): calcinosis, Raynauds phenomenon,
esophageal dysfunction, sclerodactyly, and telangiec-
tasia
H Patchy skin changes with a teardrop-like appearance
known as morphea (localized scleroderma)
H Band of thickened skin on the face or extremities
that severely damages underlying tissues, causing at-
rophy and deformity (linear scleroderma)
H Raynauds phenomenon (blanching, cyanosis, and
erythema of the fingers and toes); progressive pha-
langeal resorption that may shorten the fingers (early
symptoms)
H Taut, shiny skin over the entire hand and forearm
due to skin thickening
H Tight and inelastic facial skin, causing a masklike ap-
pearance and pinching of the mouth
H Thickened skin over proximal limbs and trunk (dif-
fuse systemic sclerosis)
H Abdominal distention
Test results
Laboratory
H Erythrocyte sedimentation rate is slightly elevated,
rheumatoid factor is positive in 25% to 35% of pa-
tients, and antinuclear antibody is positive.
H Urinalysis shows proteinuria, microscopic hema-
turia, and casts.
Imaging
H Hand X-rays show terminal phalangeal tuft resorp-
tion, subcutaneous calcification, and joint space nar-
rowing and erosion.
H Chest X-rays show bilateral basilar pulmonary fi-
brosis.
H GI X-rays show distal esophageal hypomotility and
stricture, duodenal loop dilation, small-bowel malab-
sorption pattern, and large diverticula.
9400S.qxd 8/2/12 4:48 PM Page 739

Diagnostic procedures H Administer oxygen, as ordered, for pulmonary com-

H Pulmonary function studies show decreased diffusion plications.
and vital capacity.
H Electrocardiography shows nonspecific abnormali- Monitoring
ties related to myocardial fibrosis and possible H Intake and output
arrhythmias. H Possible adverse reactions to prescribed drugs
H Skin biopsy shows changes consistent with disease H Daily weight
progression, such as marked thickening of the der- H End organ damage such as renal failure
mis and occlusive vessel changes. H Skin integrity
H Nutritional status
H Vital signs, especially blood pressure
Treatment H Renal function
H Electrocardiograms
General H Pulmonary function
H Physical therapy H Abdominal distention
H Heat therapy
H Hemodialysis
H Lanolin emollients Patient teaching
H Soft, bland foods
H Possible enteral feedings Be sure to cover:
H Regular exercise, as tolerated H the disorder, diagnosis, and treatment
H Frequent rest periods H how to assess skin for changes
H avoiding cold weather and cigarette smoking
Medications H reporting abnormal bleeding or bruising and any
H Immunosuppressants nonhealing abrasions
H Vasodilators H the importance of staying as active as possible, with
H Antihypertensives frequent rest periods
H Antacids H follow-up care
H Histamine-2 receptor antagonist or proton pump in- H medication administration, dosage, and possible ad-
hibitor verse effects.
H Broad-spectrum antibiotics
H Angiotensin-converting enzyme inhibitor Discharge planning
H Refer the patient to physical therapy and occupation-
Surgery al therapy as needed.
H Digital sympathectomy or, rarely, cervical sympathet- H Refer the patient to a smoking-cessation program, if
ic blockade needed.
H Digital plaster cast H Refer the patient to the Scleroderma Foundation.
H Possible surgical debridement
H Kidney transplant

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort and decreased
pain
H attain the highest degree of mobility possible within
the confines of disease
H state feelings about limitations
H express an increased sense of well-being
H regain and maintain skin integrity.

Nursing interventions
H Avoid using fingersticks for blood tests.
H Provide heat therapy to relieve joint stiffness.
H Elevate the head of the bed to help relieve GI symp-
toms.
H Provide meticulous skin care.
H Encourage oral fluid intake.
H Provide a soft, bland diet with frequent small meals.

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Common characteristics
Scoliosis H Fatigue
H Backache
H Dyspnea
Overview H Change in appearance
H Kyphosis
Description
H Lateral curvature of the spine thats apparent on Complications
frontal projection, measures greater than 10 degrees, H Debilitating back pain
and is associated with vertebral rotation H Severe deformity
H Right thoracic curve most common H With thoracic curve exceeding 60 degrees, possible
H Classified as nonstructural (flexible spinal curve, reduced pulmonary function
with temporary straightening when patient leans side- H With thoracic curve exceeding 80 degrees, increased
ways) or structural (fixed deformity) risk of cor pulmonale in middle age
Pathophysiology
H The vertebrae rotate, forming the convex part of the Assessment
curve.
H The rotation causes rib prominence along the tho- History
racic spine and waistline asymmetry in the lumbar H Familial history
spine. H Detected during community or school scoliosis
H Severity of spinal deformity dictates physiological screening
impairment. H Hemlines look uneven
H Pant legs appear unequal in length
Causes H One hip higher than the other
H Nonstructural scoliosis: H Backache, fatigue, and dyspnea
Leg-length discrepancies
Poor posture Physical findings
Paraspinal inflammation H Signs of scoliosis (see Testing for scoliosis)
Acute disk disease
H Structural scoliosis: no known cause Test results
H Neuromuscular scoliosis: may be caused by muscu- Imaging
lar dystrophy, polio, cerebral palsy, or spinal muscu- H Spinal X-ray studies confirm scoliosis and determine
lar atrophy the degree of curvature and flexibility of the spine;
H Neurofibromatosis (Recklinghausens disease) they also determine skeletal maturity, predict remain-
H Traumatic scoliosis: may result from vertebral frac- ing bone growth, and differentiate nonstructural
tures or disk disease from structural scoliosis.
H Local inflammation and infection Other
H Bone growth studies may help determine skeletal
Special populations maturity.

Degenerative scoliosis may develop in older pa-

tients with osteoporosis and degenerative joint Treatment
disease of the spine.
General
H Close observation
Risk factors H Brace
H Congenital or neuromuscular problem H Spinal orthoses
H Functional strengthening program
Incidence H Gradually increased activity
H Idiopathic H No vigorous sports
H Less than 1% of school-age children affected H Prescribed exercise regimen
H Seen at growth spurts between ages 10 and 13 H Swimming, but no diving
H Affects females seven times more than males
H Infantile scoliosis: most common in boys ages 1 to 3 Surgery
H Juvenile scoliosis: affects boys and girls ages 3 to 10 H Posterior spinal fusion and internal stabilization
about equally (rods and spinal hardware)
H Adolescent scoliosis: occurs after age 10 and during
adolescence

740 Scoliosis
9400S.qxd 8/2/12 4:48 PM Page 741

Testing for scoliosis

When assessing the patient for an abnormal spinal curve,
use this screening test for scoliosis. Have the patient remove
her shirt and stand as straight as she can with her back to Rib hump
you. Instruct her to distribute her weight evenly on each
foot. While the patient does this, observe both sides of her
back from neck to buttocks. Look for these signs: Asymmetrical
H uneven shoulder height and shoulder blade prominence thoracic spine
H unequal distance between the arms and the body
H asymmetrical waistline
Asymmetrical
H uneven hip height
waistline
H a sideways lean.
With the patients back still facing you, ask the patient to do
the forward-bend test. In this test, the patient places her
palms together and slowly bends forward, remembering to
keep her head down. As she complies, check for these signs:
H asymmetrical thoracic spine or prominent rib cage (rib
hump) on either side
H asymmetrical waistline.

Nursing considerations Patient teaching

Key outcomes Be sure to cover:
The patient will: H the disorder, diagnosis, and treatment
H experience feelings of increased comfort and de- H brace care
creased pain H skin care
H maintain joint mobility and range of motion (ROM) H safe body mechanics
H achieve the highest level of mobility possible H cast care, if needed
H express positive feelings about self H signs of cast syndrome
H demonstrate measures to prevent injury to self. H medication administration, dosage, and possible ad-
verse effects
Nursing interventions H relaxation techniques.
H Promote self-care while allowing adequate time.
H Administer prescribed drugs.
H Encourage deep-breathing exercises.
H Promote active ROM arm exercises.

Monitoring
H Response to analgesia
H Skin around the cast edge daily
H Sensation, movement, color, and pulses
H Intake and output
H Urine specific gravity
H Abdominal distention and bowel sounds
H Skin breakdown

ALERT
Watch for signs of cast syndrome (nausea, abdomi-
nal pressure, and vague abdominal pain), which
may result from hyperextension of the spine.

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Complications
Septic arthritis H Osteomyelitis
H Loss of joint cartilage
H Ankylosis
Overview H Fatal septicemia

Description
H Inflammation of a synovial membrane Assessment
H Usually caused by bacteria
H Usually affects a single joint History
H May have sudden onset H Abrupt onset of intense pain in the affected joint
H Also known as infectious arthritis H Fever and chills

Pathophysiology Physical findings

H Bacteria invade a joint, and inflammation of the syn- H Affected joint kept in a flexed position
ovial lining results. H Redness and edema over the affected joint
H Organisms invade the joint cavity, and effusion and H Severely reduced range of motion (ROM)
pyogenesis follow. H Warmth and extreme tenderness over the involved
H Eventual bone and cartilage destruction result. joint
H Chills
Causes
H Bacteria spread from a primary site of infection Test results
H Gram-positive cocci Laboratory
H Staphylococcus aureus H Synovial fluid analysis shows pus or watery, cloudy
H Streptococcus pyogenes fluid of decreased viscosity, typically with 50,000/l
H Streptococcus pneumoniae or more white blood cells (WBCs) containing pri-
H Streptococcus viridans marily neutrophils; also a low glucose level.
H Gram-negative cocci H Gram stain or culture of the fluid identifies the
H Neisseria gonorrhoeae causative organism.
H Haemophilus influenzae H Countercurrent immunoelectrophoresis measures
H Gram-negative bacilli bacterial antigens in body fluids and guides treat-
H Escherichia coli ment.
H Salmonella H Positive blood cultures confirm the diagnosis even
H Pseudomonas with negative synovial culture.
H Fungi or mycobacteria (rare cause) H WBC count is elevated with many polymorphonuclear
cells.
Risk factors H Erythrocyte sedimentation rate is increased.
H Concurrent bacterial infection H C-reactive protein level is elevated.
H Serious chronic illness H Lactic assay distinguishes septic from nonseptic
H Alcoholism arthritis.
H Advanced age Imaging
H Immune system depression H X-rays may show distention of the joint capsule, nar-
H History of immunosuppressive therapy rowing of the joint space, and erosion of bone.
H I.V. drug abuse H Radioisotope joint scan may show infection or in-
H Recent articular trauma flammation, especially in less accessible joints.
H Arthroscopy and joint surgery Diagnostic procedures
H Intra-articular injections H Arthrocentesis allows collection of a synovial fluid
H Local joint abnormalities specimen for analysis.
H Biopsy of the synovial membrane confirms the diag-
Incidence nosis and identifies the causative organism.
H Gram-positive cocci more common in children age 2
and older and adults
H H. influenzae most common in children younger Treatment
than age 2
General
Common characteristics H Based on antimicrobial susceptibilities and the pa-
H Joint inflammation tients age
H Severe pain H Drainage by repeated closed-needle aspiration,
H Pseudoparalysis of affected area arthroscopy, or arthrotomy
H Warmth and erythema of affected area H Exercise, as tolerated
H Joint immobilization

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Medications
H Analgesics
H Appropriate parenteral antibiotic for 3 to 4 weeks

Surgery
H Reconstructive surgery for severe joint damage
H Possible open surgical drainage

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort and decreased
pain
H maintain joint mobility and ROM
H perform activities of daily living within confines of
the disorder.
Nursing interventions
H Practice strict sterile technique.
H Check splints or traction regularly.
H Maintain proper alignment.
H Assist with ROM exercises.
H Administer prescribed drugs.
H Allow adequate time for and promote self-care.

Monitoring
H Signs and symptoms of joint inflammation
H Vital signs and fever pattern
H Pain levels
H Response to pain medications
H Condition after joint aspiration

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the etiology of the disease
H the role of I.V. drug use
H the prevention of recurrence
H medication administration, dosage, and possible ad-
verse effects
H the exercise regimen
H rest periods
H home I.V. therapy, if required
H avoiding aggravating factors.

Discharge planning
H Refer the patient to drug counseling, if appropriate.
H Refer the patient to Alcoholics Anonymous, if appro-
priate.

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Complications
Life-threatening disorder H Respiratory difficulties
H Severe thrombocytopenia (low platelet count)

Severe acute respiratory H Death

syndrome Assessment
History
Overview H Contact with a person known to have SARS
H Travel to an endemic area
Description
H Severe viral infection that may progress to pneu- Physical findings
monia H Nonproductive cough
H Believed to be less infectious than influenza H Rash
H Incubation period estimated to range from 2 to H High fever
7 days (average, 3 to 5 days) H Diarrhea
H Not highly contagious when protective measures are H Respiratory distress in later stages
used
H Also known as SARS Test results
Laboratory
Pathophysiology H SARS-specific polymerase chain reaction test detects
H Coronaviruses cause diseases in pigs, birds, and oth- SARS-CoV ribonucleic acid.
er animals. H Antibodies to coronavirus are detected by enzyme-
H A theory suggests that a coronavirus may have mutat- linked immunosorbent assay.
ed, allowing transmission to and infection of hu- H Sputum Grams stain and culture isolates corona-
mans. virus.
H Platelet count may be low.
Causes Imaging
H A new type of coronavirus known as SARS- H Changes in chest X-rays indicate pneumonia (infil-
associated coronavirus (SARS-CoV) trates).
Risk factors
H Close contact with an infected person Treatment
H Contact with aerosolized (exhaled) droplets and
bodily secretions from an infected person General
H Travel to endemic areas H Symptomatic treatment
H Isolation for hospitalized patients
Incidence H Strict respiratory and mucosal barrier precautions
H More common in adults than children H Quarantine of exposed people to prevent spread
H Outbreaks in China, Hong Kong, Toronto, Singapore, H Diet as tolerated
Taiwan, and Vietnam, with many other countries re- H Activity as tolerated
porting smaller numbers of cases H Global surveillance and reporting of suspected cases
H Affects all races to national health authorities
H Affects both sexes equally
Medications
Common characteristics The following medications may be beneficial:
H Fever greater than 100.4 F (38 C) H Lopinavir-ritanavir with ribavirin
H Dry cough H Combination of steroids and antimicrobials
H Shortness of breath or other respiratory difficulties H Antipyretics
H Headache
H Muscle stiffness
H Loss of appetite Nursing considerations
H Malaise
H Confusion Key outcomes
H Rash The patient will:
H Diarrhea H remain in isolation as recommended
H Sore throat H practice good hygiene to prevent further transmis-
sion

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H maintain good nutritional status Prevention

H maintain a patent airway. Preventing transmission of SARS
Nursing interventions
Severe acute respiratory syndrome (SARS) transmission
H Administer prescribed drugs.
may be prevented by following these guidelines:
H Encourage adequate nutritional intake. H Wash hands frequently.
H Observe, record, and report nature of rash. H Cover mouth and nose when coughing or sneezing.
H Maintain proper isolation technique. H Avoid close personal contact with friends and family.
H Collect laboratory specimens, as needed. H Avoid going to work, school, or other public places un-
til 10 days after fever and respiratory symptoms re-
Monitoring solve.
H Vital signs H Wear a surgical mask when around other people or, if
H Nutritional status the patient cant wear one, a mask should be worn by
H Respiratory status those in contact with the patient.
H Avoid sharing silverware, towels, or bedding until they
H Complications
have been washed in soap and hot water.
H Use disposable gloves and household disinfectant to
Patient teaching clean any surface that might have been exposed to the
patients body fluids.

Be sure to cover:
H the disorder and treatment
H prevention of transmission (see Preventing trans-
mission of SARS)
H good nutrition, hydration, and rest during recovery
H medication administration, dosage, and possible ad-
verse effects.
Discharge planning
H Refer the patient for follow-up, as needed.

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Life-threatening disorder Assessment

History
Severe combined H Extreme susceptibility to infection within the first few

immunodeficiency months after birth, but probably no sign of gram-

disease
Overview
Description
H Disorder that involves deficient or absent cell-
mediated (T-cell) and humoral (B-cell) immunity
H Predisposes patient to infection from all classes of
microorganisms during infancy
H Also known as SCID
Pathophysiology
H Three types of SCID have been identified:
Reticular dysgenesis, the most severe type, in
which the hematopoietic stem cell fails to differen-
tiate into lymphocytes and granulocytes
Swiss-type agammaglobulinemia, in which the
hematopoietic stem cell fails to differentiate into
lymphocytes alone
Enzyme deficiency, such as adenosine deaminase
deficiency, in which the buildup of toxic products
in the lymphoid tissue causes damage and subse-
quent dysfunction.
Causes
H Transmitted as autosomal recessive trait but may be
X-linked
H Possible enzyme deficiency
H Failure of thymus or bursa equivalent to develop nor-
mally or possible defect in thymus and bone marrow
(responsible for T- and B-cell development)
negative infection until about age 6 months because
of protection by maternal immunoglobulin G
Physical findings
H Emaciated appearance and failure to thrive
H Assessment findings dependant on the type and site
of infection
H Signs of chronic otitis media and sepsis
H Signs of the usual childhood diseases such as chick-
enpox
Test results
H Defective humoral immunity is difficult to detect
before an infant reaches age 5 months.
Laboratory
H Tests show a severely diminished or absent T-cell
number and function.
Imaging
H A chest X-ray characteristically shows bilateral pul-
monary infiltrates.
Diagnostic procedures
H Lymph node biopsy that shows an absence of lym-
phocytes can be used to confirm diagnosis.
Treatment
General
H Strict protective isolation (germ-free environment)
H Gene therapy (experimental)
Medications
H Immunoglobulin
H Antibiotic therapy as appropriate

Incidence Surgery
H Affects more males than females H Histocompatible bone marrow transplantation
H Occurs in 1 of every 100,000 to 500,000 births H Fetal thymus and liver transplantation

Common characteristics
H Frequent infections in the first few months after birth Nursing considerations
Complications Key outcomes
H Without treatment, infection within 1 year of birth The patient will:
causes death H demonstrate age-appropriate skills and behaviors
H Pneumonia H not experience chills, fever, and other signs of ill-
H Oral ulcers ness.
H Failure to thrive The parents will:
H Dermatitis H establish eye, physical, and verbal contact with the
infant or child
H develop adequate coping mechanisms and support
systems.

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Nursing interventions
H If infection develops, provide prompt and aggressive
drug therapy and supportive care, as ordered.
H Watch for adverse effects of any drugs given.
H Avoid vaccinations, and give only irradiated blood
products if a transfusion is ordered.

Special populations
Although SCID infants must remain in strict pro-
tective isolation, try to provide a stimulating at-
mosphere to promote growth and development.

H Encourage parents to visit their child often, to hold

him, and to bring him toys that can be easily steril-
ized.
H Maintain a normal day and night routine, and talk to
the child as much as possible.
H If parents cant visit, call them often to report on the
childs condition.
H Provide emotional support for the family.

Monitoring
H Signs and symptoms of infection
H Growth and development
H Skin integrity
H Respiratory status
H Response to treatment
H Complications
H Signs and symptoms of transplant rejection
H Social interaction

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the proper technique for strict protective isolation
H the signs and symptoms of infection and the need to
notify a physician promptly
H medication administration, dosage, and possible ad-
verse effects.
Discharge planning
H Encourage the parents to seek genetic counseling.

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Shigellosis Assessment
History
Overview H Crowded living conditions
H Close contact with someone who has acute diarrhea
Description H Fever
H An acute intestinal infection caused by the bacteria H Diarrhea
Shigella, a short, nonmotile, gram-negative rod H Tenesmus
H Can be classified into four groups:
Group A caused by S. dysenteriae: most common Physical findings
in Central America; causes particularly severe in- H Pus in stools
fection and septicemia H Signs of dehydration
Group B caused by S. flexneri together with Group H Decreased blood pressure
D: responsible for 90% of shigellosis cases H Hyperactive bowel sounds
Group C caused by S. boydii: occurs internation- H Abdominal tenderness
ally H Abdominal distention
Group D caused by S. sonnei H Rapid, thready pulse
H Also known as bacillary dysentery
Test results
Pathophysiology Laboratory
H Highly contagious aerobic, nonmotile, glucose- H Microscopic examination of stools reveals mucus,
fermenting, gram-negative rods cause diarrhea after red blood cells, and polymorphonuclear leukocytes.
ingestion of as few as 180 organisms. H Direct immunofluorescence with specific antisera
H Rods invade the colonic epithelium and produce en- may reveal Shigella.
terotoxin, which enhances virulence. Diagnostic procedures
H Sigmoidoscopy or proctoscopy may reveal typical su-
Causes perficial ulcerations.
H Transmission of Shigella bacteria through the fecal-
oral route, by direct contact with contaminated ob-
jects, or through ingestion of contaminated food or Treatment
water
H Occasional transmission by housefly vector General
H Enteric precautions
Incidence H Low-residue diet
H Most common in children ages 1 to 4; many adults H Replacement of fluids and electrolytes with I.V. infu-
acquire illness from children sions of normal saline solution (with electrolytes)
H Endemic in North America, Europe, and the tropics;
in the United States, about 23,000 cases annually, Medications
usually in children or elderly, debilitated, or mal- H Antibiotics (questionable value, but may be used)
nourished people
H Commonly occurs among confined populations such ALERT
as those in mental institutions; also common in hos-
pitals Antidiarrheals that slow intestinal motility are
contraindicated in shigellosis because they delay
Common characteristics fecal excretion of Shigella and prolong fever and
H High fever (especially in children) diarrhea.
H Acute self-limiting diarrhea with tenesmus (ineffectu-
al straining at stool) ALERT
H Electrolyte imbalance and dehydration
A vaccine to help prevent shigellosis is currently
Complications under development.
H Electrolyte imbalance (especially hypokalemia)
H Metabolic acidosis
H Shock

748 Shigellosis
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Nursing considerations
Key outcomes
The patient will:
H maintain hemodynamic stability
H regain and maintain normal fluid and electrolyte
balance
H experience no further weight loss.

Nursing interventions
H Administer prescribed I.V. fluids.
H Maintain enteric precautions until microscopic bac-
teriologic studies confirm that the stool specimen is
negative.
Monitoring
H Vital signs
H Comfort level
H Intake and output

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H prevention of infecting others, through proper hand
washing after using the toilet and before preparing
food.

Shigellosis 749
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Life-threatening disorder Assessment

Shock, cardiogenic
Overview
Description
H A condition of diminished cardiac output that severe-
ly impairs tissue perfusion
H The most lethal form of shock
H Sometimes called pump failure
Pathophysiology
H Left ventricular dysfunction initiates a series of com-
pensatory mechanisms that attempt to increase car-
diac output.
H As cardiac output decreases, aortic and carotid
baroreceptors activate sympathetic nervous re-
sponses.
H Responses increase heart rate, left ventricular filling
pressure, and peripheral resistance to flow to en-
hance venous return to the heart.
H This action initially stabilizes the patient but later
causes deterioration with increasing oxygen demands
on the already compromised myocardium.
H These events consist of a cycle of low cardiac output,
sympathetic compensation, myocardial ischemia, and
even lower cardiac output.
Causes
H Myocardial infarction (MI) (most common)
H Myocardial ischemia
H Papillary muscle dysfunction
H End-stage cardiomyopathy
H Myocarditis
H Acute mitral or aortic insufficiency
H Ventricular septal defect
H Ventricular aneurysm
Incidence
H Typically affects patients in whom area of MI involves
40% or more of left ventricular muscle mass (a
group in which mortality may exceed 85%)
Common characteristics
H Previous disorder that decreases left ventricular
function
Complications
H Multiple organ dysfunction
H Death
History
H Disorder, such as MI or cardiomyopathy, that severe-
ly decreases left ventricular function
H Anginal pain
Physical findings
H Urine output less than 20 ml/hour
H Pale, cold, clammy skin
H Decreased sensorium
H Rapid, shallow respirations
H Rapid, thready pulse
H Mean arterial pressure of less than 60 mm Hg in
adults
H Gallop rhythm, faint heart sounds and, possibly, a
holosystolic murmur
H Jugular vein distention
H Severe anxiety
H Decreased level of consciousness (LOC)
H Pulmonary crackles
Test results
Laboratory
H Serum enzyme measurements show elevated levels of
creatine kinase, lactate dehydrogenase, aspartate
aminotransferase, and alanine aminotransferase.
H Troponin levels are elevated.
Imaging
H Cardiac catheterization and echocardiography may
reveal other conditions that can lead to pump dys-
function and failure, such as cardiac tamponade,
papillary muscle infarct or rupture, ventricular septal
rupture, pulmonary emboli, venous pooling, and hy-
povolemia.
Diagnostic procedures
H Pulmonary artery pressure monitoring reveals in-
creased pulmonary artery pressure and pulmonary
artery wedge pressure, reflecting an increase in left
ventricular end-diastolic pressure (preload) and
heightened resistance to left ventricular emptying (af-
terload) caused by ineffective pumping and in-
creased peripheral vascular resistance.
H Invasive arterial pressure monitoring shows systolic
arterial pressure less than 80 mm Hg caused by im-
paired ventricular ejection.
H Arterial blood gas (ABG) analysis may show metabol-
ic and respiratory acidosis and hypoxia.
H Electrocardiography demonstrates possible evidence
of acute MI, ischemia, or ventricular aneurysm.
Treatment
General
H Intra-aortic balloon pump (IABP)
H Possible parenteral nutrition or tube feedings
H Bed rest

750 Shock, cardiogenic

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Medications H Cardiac status

H Vasopressors such as dopamine H Hemodynamics
H Inotropics such as milrinone H Intake and output
H Vasoconstrictors H Respiratory status
H Analgesics; sedatives H LOC
H Osmotic diuretics
H Vasodilators such as nitroglycerin to treat cause
H Oxygen Patient teaching
Surgery Be sure to cover:
H Possible ventricular assist device H the disorder, diagnosis, and treatment
H Possible heart transplant H explanations and reassurance for patient and his
H Possible catheter-based procedure such as angio- family
plasty to treat coronary artery occlusion H the possibly fatal outcome.

Nursing considerations
Key outcomes
The patient will:
H maintain adequate cardiac output and hemodynamic
stability
H develop no complications of fluid volume excess
H maintain adequate ventilation
H express feelings and develop adequate coping mech-
anisms.
Nursing interventions
H Administer oxygen therapy.
H Administer prescribed drugs.
H Follow IABP protocols and policies.

ALERT
When a patient is on an IABP, move him as little as
possible. Never place the patient in a sitting posi-
tion higher than 45 degrees (including for chest
X-rays) because the balloon may tear through the
aorta and cause immediate death. Assess pedal
pulses and skin temperature and color. Check the
dressing on the insertion site frequently for bleed-
ing, and change it according to facility protocol.
Also check the site for hematoma or signs of infec-
tion, and culture any drainage.

H Monitor the patient for cardiac arrhythmias.

H Plan your care to allow frequent rest periods, and
provide as much privacy as possible. Allow the pa-
tients family to visit and comfort him as much as
possible.
H Provide explanations and reassurance for the patient
and his family as appropriate.
H Prepare the patient and his family for a possibly fatal
outcome, and help them find effective coping strate-
gies.
Monitoring
H ABG levels (acid-base balance) and pulse oximetry
H Complete blood count and electrolyte levels
H Vital signs and peripheral pulses

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Incidence
Life-threatening disorder H Depends on cause
H Affects all ages

Shock, hypovolemic H More frequent and less tolerated in elderly patients

H Affects males and females equally

Overview
Description
H Reduced intravascular blood volume causing circula-
tory dysfunction and inadequate tissue perfusion re-
sulting from loss of blood, plasma, or fluids
H Potentially life-threatening
Pathophysiology
H When fluid is lost from the intravascular space,
venous return to the heart is reduced.
H This decreases ventricular filling, which leads to a
drop in stroke volume.
H Cardiac output falls, causing reduced perfusion to
tissues and organs.
H Tissue anoxia prompts a shift in cellular metabolism
from aerobic to anaerobic pathways.
H This produces an accumulation of lactic acid, result-
ing in metabolic acidosis.
Causes
H Acute blood loss (about one-fifth of total volume)
H Intestinal obstruction
H Burns
H Peritonitis
H Acute pancreatitis
H Ascites
H Dehydration, as from excessive perspiration, severe
diarrhea, protracted vomiting, diabetes insipidus, di-
uresis, or inadequate fluid intake
H Diuretic abuse
Checking for early hypovolemic shock
Orthostatic vital signs and tilt test results can help in as-
sessing for the possibility of impending hypovolemic
shock.
Orthostatic vital signs
Measure the patients blood pressure and pulse rate while
hes lying in a supine position, sitting, and standing. Wait
at least 1 minute between each position change. A systolic
blood pressure decrease of 10 mm Hg or more between
positions or a pulse rate increase of 10 beats/minute or
more is a sign of volume depletion and impending hypo-
volemic shock.
Tilt test
With the patient lying in a supine position, raise his legs
above heart level. If his blood pressure increases signifi-
cantly, the test is positive, indicating volume depletion and
impending hypovolemic shock.
Common characteristics
H Pallor, tachycardia, hypotension
H Cool skin
H Altered level of consciousness
Complications
H Acute respiratory distress syndrome
H Acute tubular necrosis and renal failure
H Disseminated intravascular coagulation
H Multiple organ dysfunction
Assessment
History
H Disorders or conditions that reduce blood volume,
such as GI hemorrhage, trauma, and severe diarrhea
and vomiting
H Patient with cardiac disease: possible anginal pain
due to decreased myocardial perfusion and oxygena-
tion
Physical findings
H Pale, cool, clammy skin
H Decreased sensorium
H Rapid, shallow respirations
H Urine output usually less than 20 ml/hour
H Rapid, thready pulse
H Mean arterial pressure less than 60 mm Hg in adults
(in chronic hypotension, mean pressure may fall be-
low 50 mm Hg before signs of shock)
H Orthostatic vital signs and tilt test results consistent
with hypovolemic shock (see Checking for early hy-
povolemic shock)
Test results
Laboratory
H Hematocrit is low, and hemoglobin levels and red
blood cell and platelet counts are decreased.
H Serum potassium, sodium, lactate dehydrogenase,
creatinine, and blood urea nitrogen levels are ele-
vated.
H Urine specific gravity (greater than 1.020) and urine
osmolality are increased.
H The pH and partial pressure of arterial oxygen are
decreased, and partial pressure of arterial carbon
dioxide is increased.
H Aspiration of gastric contents through a nasogastric
tube identifies internal bleeding.
H Occult blood tests are positive.
H Coagulation studies show coagulopathy due to dis-
seminated intravascular coagulation.

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Imaging H Coagulation studies for signs of impending coagu-

H X-rays (chest or abdominal) help to identify internal lopathy
bleeding sites. H Complete blood count and electrolyte measurements
Diagnostic procedures H Arterial blood gas levels
H Gastroscopy helps identify internal bleeding sites. H Intake and output
H Invasive hemodynamic monitoring shows reduced H Hemodynamics
central venous pressure, right atrial pressure, pul-
monary artery pressure, pulmonary artery wedge
pressure, and cardiac output. Patient teaching
Be sure to cover:
Treatment H the disorder, diagnosis, and treatment
H all procedures and their purpose
General H the risks associated with blood transfusions
H In severe cases, an intra-aortic balloon pump, ven- H the purpose of all equipment such as mechanical
tricular assist device, or pneumatic antishock gar- ventilation
ment H dietary restrictions
H Oxygen administration H medication administration, dosage, and possible ad-
H Bleeding control by direct application of pressure verse effects.
and related measures
H Possible parenteral nutrition or tube feedings
H Bed rest
H Fluid replacement
H Blood infusion

Medications
H Positive inotropes
H Possibly diuretics

Surgery
H Possibly, to correct underlying problem

Nursing considerations
Key outcomes
The patient will:
H maintain adequate cardiac output
H maintain hemodynamic stability
H maintain adequate ventilation
H express feelings and develop adequate coping mech-
anisms
H regain adequate fluid volume.

Nursing interventions
H Check for a patent airway and adequate circulation.
If blood pressure and heart rate are absent, start car-
diopulmonary resuscitation.
H Obtain type and crossmatch, as ordered.
H Administer prescribed I.V. solutions or blood
products.
H Administer prescribed drugs.
H Insert an indwelling urinary catheter.
H Administer prescribed oxygen.
H Provide emotional support to the patient and family.

Monitoring
H Vital signs and peripheral pulses
H Cardiac rhythm

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Life-threatening disorder Assessment

History
Shock, septic H Disorder or treatment that can cause immunosup-
pression
H Previous invasive tests or treatments, surgery, or
Overview trauma
H Fever and chills (although 20% of patients possibly
Description hypothermic)
H Low systemic vascular resistance and an elevated car-
diac output (initially) Physical findings
H Probably a response to infections that release mi- Hyperdynamic or warm phase
crobes or an immune mediator H Peripheral vasodilation
H Skin possibly pink and flushed or warm and dry
Pathophysiology H Altered level of consciousness (LOC) reflected in agi-
H Initially, the bodys defenses activate chemical media- tation, anxiety, irritability, and shortened attention
tors in response to the invading organisms. span
H The release of these mediators results in low sys- H Respirations rapid and shallow
temic vascular resistance and increased cardiac H Urine output below normal
output. H Rapid, full, bounding pulse
H Blood flow is unevenly distributed in the microcircu- H Blood pressure normal or slightly elevated
lation, and plasma leaking from capillaries causes Hypodynamic or cold phase
functional hypovolemia. H Peripheral vasoconstriction and inadequate tissue
H Diffuse increase in capillary permeability occurs. perfusion
H Eventually, cardiac output decreases, and poor tissue H Pale skin and possible cyanosis
perfusion and hypotension cause multisystem dys- H Decreased LOC; possible obtundation and coma
function syndrome and death. H Respirations possibly rapid and shallow
H Urine output possibly less than 25 ml/hour or absent
Causes H Rapid, weak, thready pulse
H Any pathogenic organism H Irregular pulse if arrhythmias present
H Gram-negative bacteria, such as Escherichia coli, H Cold, clammy skin
Klebsiella pneumoniae, Serratia, Enterobacter, and H Hypotension
Pseudomonas, most common causes (up to 70% of H Crackles or rhonchi if pulmonary congestion present
cases)
Test results
Incidence Laboratory
H Possible in any person with impaired immunity H Blood cultures are positive for the causative organ-
ism.
H Complete blood count shows the presence or ab-
Special populations
sence of anemia and leukopenia, severe or absent
Neonates and elderly people are at greatest risk for neutropenia, and usually the presence of thrombocy-
septic shock. topenia.
H Blood urea nitrogen and creatinine levels are in-
H About two-thirds of cases in hospitalized patients creased, and creatinine clearance is decreased.
(most have underlying diseases) H Prothrombin time and partial thromboplastin time
are abnormal.
Common characteristics H Serum lactate dehydrogenase levels are elevated, with
H Hyperdynamic or warm phase metabolic acidosis.
H Hypodynamic or cold phase H Urine studies show increased specific gravity (more
than 1.02), increased osmolality, and decreased
Complications sodium levels.
H Disseminated intravascular coagulation H Arterial blood gas (ABG) analysis demonstrates in-
H Renal failure creased blood pH and partial pressure of arterial
H Heart failure oxygen and decreased partial pressure of arterial
H GI ulcers carbon dioxide with respiratory alkalosis in early
H Abnormal liver function stages.
H Death

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9400S.qxd 8/2/12 4:48 PM Page 755

Diagnostic procedures H Administer prescribed oxygen.

H Invasive hemodynamic monitoring shows: H Provide emotional support to the patient and his
increased cardiac output and decreased systemic family.
vascular resistance in warm phase H Document the occurrence of a nosocomial infection,
decreased cardiac output and increased systemic and report it to the infection-control practitioner.
vascular resistance in cold phase.
Monitoring
H ABG levels and pulse oximetry
Treatment H Intake and output
H Vital signs and peripheral pulses
General H Hemodynamics
H Removal of I.V., intra-arterial, or urinary drainage H Cardiac rhythm
catheters as infection source whenever possible H Heart and breath sounds
H In patients immunosuppressed from drug therapy,
drugs discontinued or reduced, if possible
H Mechanical ventilation if respiratory failure occurs Patient teaching
H Fluid volume replacement
H Possible parenteral nutrition or tube feedings Be sure to cover:
H Bed rest H the disorder, diagnosis, and treatment
H all procedures and their purpose (to ease the pa-
Medications tients anxiety)
H Antimicrobial H risks associated with blood transfusions
H Granulocyte transfusions H all equipment and its purpose
H Colloid or crystalloid infusions H medication administration, dosage, and possible ad-
H Oxygen verse effects
H Diuretics H possible complications.
H Vasopressors
H Antipyretics

Nursing considerations
Key outcomes
The patient will:
H maintain adequate cardiac output
H maintain hemodynamic stability
H maintain adequate ventilation
H show no signs of infection
H express feelings and develop adequate coping mech-
anisms
H maintain adequate fluid volume.

Nursing interventions
H Remove any I.V., intra-arterial, or urinary drainage
catheters, and send them to the laboratory to culture
for the presence of the causative organism.
H Administer prescribed I.V. fluids and blood products.

ALERT
A progressive drop in blood pressure accompanied
by a thready pulse generally signals inadequate
cardiac output from reduced intravascular volume.
Notify the physician immediately and increase the
infusion rate.

H Administer prescribed drugs.

H Notify the physician if urine output is less than
30 ml/hour.

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Complications
Silicosis H Pulmonary fibrosis
H Cor pulmonale
H Cardiac or respiratory failure
Overview H Pulmonary tuberculosis
H Lung infection
Description H Pneumothorax
H Progressive pneumonoconiosis disease characterized
by nodular lesions, commonly leading to fibrosis
H Classified according to severity of pulmonary disease Assessment
and rapidity of onset and progression
H Usually a simple, asymptomatic illness History
H Considered an industrial disease H Long-term exposure to silica dust
H Prognosis good unless complications occur H Dyspnea on exertion
H Dry cough, especially in the morning
Pathophysiology
H Small particles of mineral dust are inhaled and de- Physical findings
posited in the respiratory bronchioles, alveolar H Decreased chest expansion
ducts, and alveoli. H Tachypnea
H The surface of these particles generates silicon-based H Lethargy
radicals that lead to the production of hydroxy, hy- H Decreased mentation
drogen peroxide, and other oxygen radicals that H Areas of increased and decreased resonance
damage cell membranes and inactivate essential cell H Medium crackles, wheezing
proteins. H Diminished breath sounds
H Alveolar macrophages ingest the particles, become
activated, and release cytokines, such as tumor ALERT
necrosis factor and others that attract other inflam-
matory cells. Assess patient for the presence of an intensified
H The inflammation damages resident cells and the ventricular gallop on inspiration, which is a hall-
extracellular matrix. mark of cor pulmonale.
H Fibroblasts are stimulated to produce collagen,
resulting in fibrosis. H Hemoptysis

Causes Test results

H Silica dust due to:
manufacture of ceramics (flint) and building ma-
terials (sandstone)
mixed form in construction materials (cement)
powder form (silica flour), in paints, porcelain,
scouring soaps, and wood fillers
mining of gold, lead, zinc, and iron
Incidence
H Highest incidence in those who work around silica
dust, such as foundry workers, boiler scalers, and
stone cutters
H Acute silicosis possible after 1 to 3 years in sand
blasters, tunnel workers, and others exposed to high
concentrations of respirable silica
H Accelerated silicosis possible in those exposed to
lower concentrations of free silica, usually after
about 10 years of exposure
H More common in those ages 40 to 75
H More common in males than in females
Common characteristics
H Dyspnea on exertion
H Dry cough, especially in the morning
Laboratory
H Arterial blood gas analysis shows:
normal partial pressure of oxygen in simple silico-
sis (may be significantly decreased in late stages
or complicated disease)
normal partial pressure of carbon dioxide in early
stages of the disease. (Hyperventilation may cause
it to decrease; partial pressure of carbon dioxide
may increase if restrictive lung disease develops.)
Imaging
H Chest X-rays in simple silicosis show small, discrete,
nodular lesions distributed throughout both lung
fields, although they typically concentrate in the up-
per lobes.
H Lung nodes may appear enlarged and show eggshell
calcification.
H Chest X-rays in complicated silicosis show one or
more conglomerate masses of dense tissue.
Diagnostic procedures
H Pulmonary function tests show:
reduced forced vital capacity (FVC) in complicated
silicosis
reduced forced expiratory volume in 1 second
(FEV1) with obstructive disease
reduced FEV1 with a normal or high ratio of FEV1
to FVC in complicated silicosis

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reduced diffusing capacity for carbon monoxide H Changes in mentation

when fibrosis destroys alveolar walls and obliter- H Sputum production
ates pulmonary capillaries or when it thickens the H Breath sounds
alveocapillary membrane.
Patient teaching
Treatment
Be sure to cover:
General H the disorder, diagnosis, and treatment
H Relief of respiratory symptoms H medication administration, dosage, and possible ad-
H Management of hypoxia and cor pulmonale verse effects
H Prevention of respiratory tract infections H when to notify a physician
H Steam inhalation and chest physiotherapy H the need to avoid crowds and people with known
H Increased fluid intake infections
H High-calorie, high-protein diet H home oxygen therapy, if needed
H Regular exercise program, as tolerated H transtracheal catheter care, if needed
H postural drainage and chest percussion
Medications H coughing and deep-breathing exercises
H Bronchodilators H the need to consume a high-calorie, high-protein diet
H Oxygen H adequate hydration
H Antibiotics H the risk of tuberculosis
H Anti-inflammatory drugs H energy conservation techniques.

Surgery Discharge planning

H Possible tracheostomy H Refer the patient for influenza and pneumococcus
H Possible lung transplantation immunizations, as needed.
H Whole lung lavage H Refer the patient to a smoking-cessation program, if
indicated.
H Refer the patient for tuberculosis testing, if indicated.
Nursing considerations
Key outcomes
The patient will:
H maintain adequate ventilation
H use energy conservation techniques
H express an understanding of the illness
H demonstrate effective coping mechanisms
H maintain adequate caloric intake.

Nursing interventions
H Administer prescribed drugs and oxygen
H Perform chest physiotherapy.
H Provide a high-calorie, high-protein diet.
H Provide small, frequent meals.
H Provide frequent mouth care.
H Ensure adequate hydration.
H Encourage daily exercise as tolerated.
H Provide diversional activities as appropriate.
H Provide frequent rest periods.
H Help with adjustment to the lifestyle changes associ-
ated with a chronic illness.
H Include the patient and family in care decisions
whenever possible.
Monitoring
H Vital signs
H Intake and output
H Daily weight
H Respiratory status
H Activity tolerance
H Complications

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Sinusitis Assessment
History
Overview H Nasal congestion
H Nasal discharge, clear turning purulent
Description H Sore throat
H Inflammation of the paranasal sinuses H Localized headache
H Usually follows upper respiratory infections H Generalized malaise; fatigue
H May be acute, subacute, chronic, allergic, or hyper- H Pain specific to the affected sinus (see Locating the
plastic paranasal sinuses)
H In hyperplastic sinusitis, a combination of purulent H Vague facial discomfort
acute sinusitis and allergic sinusitis or rhinitis H Nonproductive cough
H For all types, prognosis good
Physical findings
Pathophysiology H Edematous nasal mucosa
H Impairment in drainage of sinuses and retention of H Low-grade fever
secretions result in inflammation. H Edema over sinuses
H Enlarged turbinates
Causes H Mucosal lining thickening
H Bacterial infections (common) H Mucosal polyps (hyperplastic sinusitis)
H Viral infections H Pain and pressure over affected sinus areas with pal-
H Fungal infections (uncommon) pation
H Any condition that interferes with sinus drainage and
ventilation Test results
H Swimming in contaminated conditions Laboratory
H Immunocompromised states H Culture and sensitivity testing of purulent nasal
H Diabetes drainage shows the causative bacterial organism.
H Blood dyscrasias Imaging
H Allergic rhinitis H Sinus X-rays show cloudiness in affected sinus, air-
H Orofacial trauma fluid levels, or thickened mucosal lining.
H Endotracheal intubation H Ultrasonography and computed tomography scan
show recurrent or chronic sinusitis, unresolved si-
Risk factors nusitis.
H Anatomic abnormalities Diagnostic procedures
H Viral upper respiratory infection H Transillumination of sinuses may be diminished.
H Allergies H Sinus endoscopy shows purulent nasal drainage,
H Overuse of topical decongestants nasal edema, and obstruction of ostia.
H Asthma

Incidence Treatment
H Affects 16% of population annually
H Affects all ages General
H Affects both sexes equally H Depends on type of sinusitis
H Indirect drainage of ethmoid and sphenoid sinuses
Common characteristics H Steam inhalation
H Nasal congestion H Local heat applications
H Purulent nasal discharge H Adequate rest periods
H Facial pain specific to affected sinus
H Fever Medications
H Antibiotics
Complications H Analgesics
H Meningitis H Vasoconstrictors
H Cavernous and sinus thrombosis H Nasal corticosteroids
H Bacteremia or septicemia H Antihistamines
H Brain abscess
H Osteomyelitis Surgery
H Mucocele H Antral puncture to remove purulent material
H Orbital cellulitis or abscess H Sinus irrigation

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Locating the paranasal sinuses

Nursing considerations
The location of a patients sinusitis pain indicates the af-
Key outcomes fected sinus. For example, an infected maxillary sinus can
cause tooth pain. (Note: The sphenoid sinus, which lies
The patient will: under the eye and above the soft palate, isnt depicted
H express feelings of increased comfort here.)
H exhibit an adequate breathing pattern
H show no signs of infection
H express understanding of condition and treatment
H develop no complications.

Nursing interventions
H Encourage oral fluid intake. Frontal
H Elevate the head of the bed no more than 30 degrees. sinuses
H Encourage expression of concerns. Ethmoid
H Apply warm compresses. sinuses
H Administer prescribed drugs. Maxillary
H Encourage use of a humidifier. sinuses

ALERT
Watch for and report vomiting, chills, fever, edema
of the forehead or eyelids, blurred or double vision,
and personality changes.

After surgery
H Place the patient in semi-Fowlers position.
H Apply ice compresses over the nose and iced saline
gauze over the eyes for 24 hours.
H Frequently change the mustache dressing or
drip pad.
H Provide meticulous and frequent mouth care.
H importance of medical follow-up
H proper hand-washing technique
H avoidance of bending and stooping during the acute
phase
H avoidance of contact with an infected person.

Monitoring Discharge planning

H Complications H Refer the patient to a smoking-cessation program.
H Response to treatment
H Pain control
H Nasal discharge
After surgery
H Excessive drainage or bleeding
H Consistency, amount, and color of drainage
H Vital signs

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medication administration, dosage, and possible ad-
verse effects
H cautions against driving a motor vehicle or consum-
ing alcohol while taking antihistamines or analgesics
H the need to complete the full course of prescribed
antibiotics
H the need to leave nasal packing in place for 12 to
24 hours after surgery
H the need to breathe through the mouth and refrain
from blowing the nose and sneezing
H the need to refrain from smoking for at least 2 or
3 days after surgery
H signs and symptoms of complications

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Sjgrens syndrome H Possible epistaxis, hoarseness, chronic nonproduc-

tive cough, recurrent otitis media, and frequent res-
piratory tract infections
Overview H Possible dyspareunia
H Generalized itching, fatigue, recurrent low-grade
Description fever, and arthralgia or myalgia

H Connective tissue disease: the most common autoim- Physical findings

mune disorder after rheumatoid arthritis H Mouth ulcers, dental caries and, possibly, enlarged
H May be primary disorder or associated with other in- salivary glands
flammatory connective tissue disorders H Palpable purpura
H Palpable lymph node enlargement
Pathophysiology H Dry, sticky, erythematous oral mucosa
H Lymphocytic infiltration of exocrine glands causes
tissue damage resulting in xerostomia and dry eyes. Test results
H Immunologic activation occurs. Laboratory
H Erythrocyte sedimentation rate is elevated in more
Causes than 90% of patients.
H Unknown H Complete blood count shows mild anemia and
H Possible genetic and environmental factors leukopenia in about 30% of patients.
H Immunologic activation H Serum protein electrophoresis shows hypergamma-
globulinemia in about 50% of patients.
Incidence H Typically, 75% to 90% of patients test positive for
H Affects more females (about 90%) than males rheumatoid factor, and between 50% and 80% of pa-
H Mean age of occurrence: 50 tients test positive for antinuclear antibodies.
Diagnostic procedures
Common characteristics H For a diagnosis of Sjgrens syndrome, symptoms
H Dry eyes and mouth must meet specific criteria. (See Diagnosing Sj-
grens syndrome.)
Complications H Tests supporting the diagnosis include measuring eye
H Corneal ulceration or perforation involvement with the Schirmers test and a slit-lamp
H Epistaxis examination with rose bengal dye.
H Deafness H Labial salivary gland biopsy (to detect lymphoid foci)
H Otitis media is the only specific diagnostic technique.
H Splenomegaly H Salivary gland involvement may be evaluated by mea-
H Renal tubular necrosis suring the volume of parotid saliva, by secretory
sialography, and by salivary scintigraphy.
H Salivary gland biopsy results typically show lympho-
Assessment cytic infiltration in Sjgrens syndrome; lower lip
biopsy findings show salivary gland infiltration by
History lymphocytes.
H Xerophthalmia or xerostomia
H Gritty, sandy eye along with redness, burning, photo-
sensitivity, eye fatigue, itching, and mucoid discharge Treatment
H Difficulty swallowing and talking; an abnormal taste
or smell sensation (or both); thirst; ulcers of the General
tongue, mouth, and lips (especially at the corners of H Meticulous oral hygiene
the mouth); and severe dental caries H Humidifier
H Unscented skin lotions
H Frequent dental care
Diagnosing Sjgrens syndrome H Avoidance of sugar, tobacco, alcohol, and spicy, salty,
or highly acidic foods
For a diagnosis of Sjgrens syndrome, the patient must H Increased oral fluid intake for mouth dryness
have the following:
H keratoconjunctivitis sicca Medications
H diminished salivary gland flow
H Pilocarpine and cevimeline
H a positive salivary gland biopsy, showing mononuclear
H Preservative-free artificial tears and sustained-release
cell infiltration
H the presence of autoantibodies in a serum sample, indi- cellulose capsules
cating a systemic autoimmune process. H Artificial salivas

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H Glucocorticoids or other immunosuppressive agents

for extraglandular manifestations such as systemic
vasculitis
H Saline nasal sprays
H Vaginal lubricants
H Nonsteroidal anti-inflammatory drugs
H Antifungal agents
H Ophthalmic lubricants

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort
H have pink, moist oral mucosa
H demonstrate thorough oral hygiene practices
H acknowledge problems in sexual function.

Nursing interventions
H Instill artificial tears as often as every 30 minutes to
prevent eye damage, and instill an eye ointment at
bedtime.
H Provide plenty of fluids, especially water, for the pa-
tient to drink, and sugarless chewing gum or candy.
Monitoring
H Response to treatment
H Extraglandular manifestations
H Complications

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the instillation of eye drops and ointments
H the need to wear sunglasses to protect the eyes
H the need to keep the face clean and to avoid rubbing
the eyes
H avoidance of saliva-decreasing drugs, such as atro-
pine derivatives, antihistamines, anticholinergics,
and antidepressants
H meticulous oral hygiene and regular dental visits
H high-calorie, protein-rich liquid supplements to
prevent malnutrition if mouth lesions make eating
painful
H the need to consume a nutritious diet
H avoidance of sugar, tobacco, alcohol, and spicy, salty,
or highly acidic foods
H the need to humidify the home and work environ-
ments
H use of normal saline solution, in drop or spray form,
to relieve nasal dryness
H avoidance of prolonged hot showers and baths and
the use of moisturizing lotions on dry skin. (Suggest
use of a water-soluble gel such as a vaginal lubri-
cant.)

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Skull fracture deep tendon reflexes, and altered pupillary and mo-
tor response
In sphenoidal fracture
H Blindness
Overview In temporal fracture
H Unilateral deafness or facial paralysis
Description In basilar fracture
H Break in the integrity of the skull bone H Hemorrhage from the nose, pharynx, or ears
H May be simple (closed) or compound (open) H Blood under the periorbital skin (raccoon eyes) and
H May displace bone fragments conjunctiva
H May be linear (common hairline break, without dis- H Battles sign (supramastoid ecchymosis)
placement of structures), comminuted (splintering H Cerebrospinal fluid (CSF) or brain tissue leakage
or crushing the bone into several fragments), or de- from the nose or ears
pressed (a fracture that pushes the bone toward the
brain) Complications
H Epilepsy
H Hydrocephalus
ALERT
H Organic brain syndrome
Because possible damage to the brain is the first H Headaches, giddiness, fatigability, neuroses, and be-
concern, rather than the fracture itself, a skull havior disorders
fracture is considered a neurosurgical condition.

H Classified according to location, such as cranial vault Assessment

fracture and basilar fractures
History
H Head trauma
ALERT
H Headache
Because of the danger of grave cranial complica- H Loss of consciousness
tions and meningitis, basilar fractures are usually
far more serious than vault fractures. Physical findings
H Decreased pulse and respirations
H Altered level of consciousness (LOC)
Pathophysiology H Scalp wound
H Trauma to the head causes a fracture at certain H Bleeding in the periorbital area, nose, pharynx, ears,
anatomic sites, such as: or under the conjunctivae
parietal bone H CSF leakage from the nose or ears; halo sign on pil-
squama of temporal bone lowcase (a blood-tinged spot surrounded by a lighter
foramen magnum ring)
petrous temporal ridge
inner parts of the sphenoid wings at the skull base Test results
middle cranial fossa Laboratory
cribriform plate H Reagent strips turn blue if CSF is present.
roof of orbits in the anterior cranial fossa Imaging
bony areas between the mastoid and dural sinuses H Computed tomography scan and magnetic resonance
in the posterior cranial fossa. imaging show fracture, intracranial hemorrhage
from ruptured blood vessels, and swelling.
Causes
H Head trauma
Treatment
Incidence
H Simple linear fracture most common, especially in General
children younger than age 5 H Depends on type and severity of fracture
H May occur at any age H Supportive
H Cleaning and debridement of wounds
Common characteristics H Diet as tolerated; nothing by mouth if surgery is nec-
H Persistent, localized headache essary
H Scalp wounds abrasions, contusions, lacerations, H Limited activity
or avulsions
H Signs of brain injury agitation and irritability, loss
of consciousness, labored respirations, abnormal

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Medications
H Mild analgesics
H Prophylactic antibiotics
H Dexamethasone (basilar and vault fractures)

ALERT
Dont give the patient opioids or sedatives because
they may depress respirations, increase carbon
dioxide levels, lead to increased intracranial pres-
sure, and mask changes in neurologic status.

Surgery
H Craniotomy to elevate or remove fragments that have
been driven into the brain and to extract foreign bod-
ies and necrotic tissue, thereby reducing the risk of
infection and further brain damage (severe injury)

Nursing considerations
Key outcomes
The patient will:
H remain neurologically and hemodynamically stable
H express increased comfort and decreased pain
H relate fears and feelings related to traumatic event.

Nursing interventions
H Establish and maintain a patent airway.

ALERT
Nasal airways are contraindicated in patients with
possible basilar skull fractures. Intubation may be
necessary.

H Suction through the mouth, not the nose, to prevent

the introduction of bacteria.
H Position the patient with a head injury for proper se-
cretion drainage. Elevate the head of the bed 30 de-
grees if intracerebral injury is suspected.
H Apply appropriate dressings; control bleeding as nec-
essary.
H Institute seizure precautions.

Monitoring
H Vital signs
H Neurologic status
H Comfort level

Patient teaching
Be sure to cover:
H the injury, diagnosis, and treatment
H preoperative and postoperative care, if appropriate
H need to watch closely for changes in mental status,
LOC, or respirations
H use of mild analgesics as opposed to opioids
H wound care.

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Sleep apnea Alcohol or sedative intake before bedtime

Smoking
H Central
Neurologic conditions affecting respiratory center
Overview Heart disease
Description Incidence
H Breathing that stops or gets very shallow during sleep H Predominantly middle-age males
H Pause typically lasts 10 to 20 seconds or more H Increases with age
H Can occur 20 to 30 times or more per hour H 90% of cases, obstructive; 10%, central
H Most common type: obstructive (insufficient air flow
into the lungs) Common characteristics
H Rare type: central H Obstructive
H Blood oxygen levels that drop Excessive daytime sleepiness
H Breaths that resume with a loud snort or gasping Loud snoring
sound Snort or gasp that arouses patient from sleep
H Repetitive apneas that produce sleep disruption, H Central
leading to excessive daytime sleepiness Typically no snoring
H Usually chronic Difficulty staying asleep
Abrupt awakenings accompanied by shortness of
Pathophysiology breath
H Obstructive Daytime sleepiness
Nasopharynx or oropharynx briefly narrows or
collapses during inspiration. Complications
This occurs because throat muscles and tongue H Respiratory arrest
relax more than normal, tonsils and adenoids are H Increases risk of hypertension, stroke, myocardial
large, anatomic abnormalities create smaller air- infarction, diabetes, and cardiovascular disease
way, or excess weight makes it harder to keep the H Work-related and driving accidents due to sleepiness
throat area open.
H Central
Theres no breathing effort for brief periods. Assessment
Malfunction of respiratory control center in brain
doesnt send correct signals to respiratory mus- History
cles. H One or more risk factors for either type
H Witnessed apneic episodes at night
Causes H Progression of daytime sleepiness from mild (occur-
H Upper airway narrowing possibly caused by: ring during quiet activities) to severe (occurring dur-
Obesity ing dynamic activities, such as work or driving)
Enlarged tonsils or uvula H Complaints of poor concentration, memory prob-
Low soft palate lems, irritability, and mood changes
Redundant tissue in soft palate or tonsillar pillars H Morning headaches
Large or posteriorly located tongue
Craniofacial abnormalities Physical findings
Alcohol or sedative use before bedtime H Most patients have a normal physical examination
H Central form: primarily caused by heart disease, H May have hypertension, obesity, or appear sleepy
sleeping at high altitudes, and neurologic conditions, H Possible findings with obstructive type:
such as stroke and brain tumors Narrowing of the lateral airway wall
Tonsillar hypertrophy
Risk factors Long or thick uvula
H Obstructive High, arched hard palate
Obesity Soft palate edema
Male gender Macroglossia
Postmenopausal female Deviated nasal septum
Older than age 40 Poor nasal airflow
Nasal obstruction (such as polyps, rhinitis, or de- Short neck with large circumference
viated septum) H Central type may cause cardiac and neurologic symp-
Anatomic narrowing (such as tonsillar hypertro- toms
phy, macroglossia, craniofacial abnormalities)
Hypothyroidism
Neurologic syndromes (such as muscular dystro-
phy, cerebral palsy)

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Test results
Laboratory Nursing considerations
H Thyroid studies, such as triiodothyronine, thyroid-
stimulating hormone, or free thyroxine rule out hy- Key outcomes
pothyroidism. The patient will:
H Elevated hematocrit shows polycythemia, which can H regulate sleep patterns
occur in nocturnal hypoxemia. H maintain a patent airway
H Arterial blood gas analysis evaluates daytime hyper- H demonstrate effective breathing pattern while sleep-
capnia. ing.
Imaging
H Head measurements and neck X-rays are used as Nursing interventions
aids during surgical treatments. H Place the patient in semi-Fowlers position for sleep.
Diagnostic procedures H Maintain pulse oximetry while patient sleeps.
H Polysomnogram, or PSG, records brain activity, eye H Provide emotional support.
movement, muscle activity, breathing, and heart rate; H Administer oxygen via appropriate method, as or-
how much air moves in and out of the lungs during dered.
sleep; and percentage of oxygen in the blood.
H Multiple sleep latency testing provides an objective Monitoring
measurement of daytime sleepiness. H Breathing pattern
Other H Pulse oximetry (during sleep)
H Apnea-hypopnea index determines severity and is de- H Sleep patterns
fined as the total number of apneas and hypopneas
divided by the total sleep time.
Mild: apnea-hypopnea index 5 to 15 Patient teaching
Moderate: apnea-hypopnea index 15 to 30
Severe: apnea-hypopnea index greater than 30 Be sure to cover:
H the disorder, diagnosis, and treatment
H the use of CPAP, BiPAP, or ASV if indicated
Treatment H positioning for sleep for optimum oxygenation
H diet modification for weight control (if appropriate)
General H avoidance of driving or operating equipment when
H Continuous positive airway pressure, also known as drowsy
CPAP, most effective treatment H avoidance of alcohol intake
H Bilevel positive airway pressure, also known as Bi- H necessity of follow-up appointments.
PAP, (boosts the weak breathing pattern of central
sleep apnea; can be set to automatically deliver a Discharge planning
breath if the patient hasnt taken a breath after a cer- H Refer the patient for home respiratory supplies and
tain number of seconds) support.
H Adaptive servo-ventilation, also known as ASV, for
central sleep apnea; (monitors the patients normal
breathing patterns and stores the information in a
built-in computer; then, as needed, uses pressure to
regulate the breathing to the patients normal pat-
tern)
H Treatment for associated medical problems
H Supplemental oxygen
H Weight loss
H Modification of activities or habits

Medications
H Generally not effective in treating this disorder

Surgery
H Surgical correction of the upper airway may be indi-
cated, depending on the cause of the apnea
H Experimental treatments, such as the Pillar proce-
dure, that involves placement of three tiny polyester
rods in the soft palate; recommended for some peo-
ple with mild to moderate obstructive sleep apnea

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H In temperate zones, incidence highest during winter

Life-threatening disorder H In tropics, incidence highest during hot, dry months

Common characteristics
Smallpox H Fever
H Maculopapular rash

Overview Complications
H Secondary bacterial infections
Description H Encephalitis
H Acute, highly contagious infectious disease caused by H Bleeding abnormalities
the poxvirus variola H Death
H Associated with tremendous morbidity and mortality
H Two related viruses:
Variola major (classic smallpox), with a case Assessment
mortality of 20% to 50%
Variola minor (alastrim), a clinically milder form History
with mortality less than 1% H Influenza-type symptoms
H Eliminated worldwide in 1980 (World Health Organi- H High fever, chills
zation declaration) as a result of a global vaccination H Rash
and eradication program; routine smallpox vaccina- H Malaise
tion stopped; variola virus, preserved in two research H Headache, backache
laboratories, remains unlikely but potential source of H Abdominal pain
infection; humans were sole reservoir of infection; H Nausea, vomiting
no carrier state
H Potential for use in bioterrorism and biological war- Physical findings
fare; classified as category-A biological disease, H After average incubation period of 12 days:
transmitted human to human with no known treat- Fever
ment Macular rash
H Also known as variola Progression to typical vesicular and pustular le-
sions, and then crusted scabs
Pathophysiology Centrifugal distribution to rash; starts on the face
H Poxviruses are characterized by a large double- and extremities; moves to the trunk
stranded deoxyribonucleic acid (DNA) genome and a
brick-shaped morphology. Test results
H Poxviruses are the only DNA viruses that replicate in Laboratory
cytoplasm. H Culture of aspirate from vesicles and pustules shows
H The virus is spread through direct contact or inhala- presence of variola.
tion of respiratory droplets. H Electron microscopy of vesicular scrapings shows
H The incubation period is 7 to 19 days. Illness onset is presence of variola.
in 10 to 14 days, with onset of the characteristic rash
in 2 to 4 days. Fever and macular rash appear after
an average incubation period of 12 days, with a pro- Treatment
gression to typical vesicular and pustular lesions over
1 or 2 weeks. General
H Its most contagious during the first week of illness H Home treatment if possible to reduce spread
(before the eruptive period) and during the time be- H No current treatment other than supportive
tween lesion development and scab disappearance. H Strict isolation
H Diet as tolerated
Causes H I.V. fluids
H Poxvirus variolae H Activity as tolerated

Incidence Medications
H Last known case in the United States reported in H Cidofovir possibly given within 1 to 2 days of expo-
1949 sure
H Last case of endemic smallpox reported in Africa in H Smallpox vaccine given within 4 days of exposure
1977 H Antibiotics for secondary infection
H Affected people of all ages H Antipruritics

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H Antihistamines
H Analgesics

Nursing considerations
Key outcomes
The patient will:
H maintain adequate nutrition
H verbalize feelings of fear and anxiety
H demonstrate effective coping mechanisms
H maintain tissue perfusion and cellular oxygenation
H maintain balanced fluid status
H maintain skin integrity.

Nursing interventions
H Administer prescribed drugs.
H Report any case of smallpox to the appropriate pub-
lic health office.
H Institute strict exposure precautions, including isola-
tion and airborne, contact, and standard precau-
tions.
H Autoclave all laundry and hospital waste before laun-
dering or incinerating.
H Provide meticulous skin care.
H Encourage verbalization of fears and concerns.
H Provide adequate hydration.
H Provide a well-balanced diet.
H Assist in the development of effective coping mecha-
nisms.
H Provide adequate rest periods.

Monitoring
H Vital signs
H Intake and output
H Complications
H Fluid and electrolyte status
H Signs and symptoms of secondary bacterial infection

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medication administration, dosage, and possible ad-
verse effects
H when to notify the physician
H isolation precautions
H hydration
H skin lesion care.

Discharge planning
H Refer those in direct contact with an infected person
for pre-exposure and postexposure vaccination if
more than 3 years have passed since last vaccination.

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Physical findings
Spinal injury H Level of injury and any spinal cord damage located
by neurologic assessment
H Limited movement and activities that cause pain
Overview H Surface wounds
H Pain location
Description H Loss of sensation below the level of injury
H Fractures, contusions, or compressions of the spine H Deformity
H Most common sites: C5, C6, C7, T12, and L1 verte-
brae Test results
Imaging
Pathophysiology H Spinal X-rays, myelography, computed tomography
H Injury causes microscopic hemorrhages. scan, and magnetic resonance imaging can indicate
H All of the gray matter is filled with blood. the location of the fracture and the site of the com-
H Necrosis results. pression.
H Edema causes spinal cord compression.
H Blood supply is further decreased.
H Long-term scarring and meningeal thickening occur. Treatment
H Nerves are blocked or tangled.
H Sensory and motor deficits occur. General
H Stabilization of spine and prevention of cord damage
Causes H Hemodynamic support
Serious injury H Application of a hard cervical collar
H Motor vehicle accident H Wound care (if appropriate)
H Fall H Chemotherapy and radiation for neoplastic lesion
H Diving into shallow water H Aspiration precautions
H Gunshot and related wound H Skeletal traction with skull tongs
Less serious injury H Bed rest on a firm surface
H Improper lifting of heavy object H Rotation bed with cervical traction (if appropriate)
H Minor fall H Splinting: thoracic lumbar sacral orthotics
H Neoplastic lesion
H Osteoporosis Medications
H Corticosteroids
Incidence H Analgesics
H Most common between ages 15 and 35 H Muscle relaxants
H Chemotherapy for neoplastic lesion
Common characteristics
H Based on severity and location of injury: Surgery
Muscle spasm or back pain (worsens with move- H Decompression of spinal cord
ment) H Stabilization of spinal column
Mild paresthesia to quadriplegia
Shock
Loss of motor function, muscle flaccidity Nursing considerations
Bladder and bowel atony
Loss of perspiration below the level of the injury Key outcomes
Respiratory impairment The patient will:
H express feelings of increased comfort and decreased
Complications pain
H Paralysis H develop effective coping mechanisms
H Death H attain the highest degree of mobility
H Autonomic dysreflexia H maintain a patent airway and adequate ventilation
H Spinal shock H show no signs of aspiration.
H Neurogenic shock
Nursing interventions
H Apply a hard cervical collar.
Assessment H Immobilize the patient.
H Comfort and reassure the patient.
History H Administer prescribed drugs.
H Muscle spasm H Provide wound care, if appropriate.
H Back or neck pain H Provide diversionary activities.
H In cervical fractures, point tenderness H Provide proper skin care.

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Monitoring
H Neurologic changes
H Respiratory status
H Changes in skin sensation and loss of muscle
strength
H Skin integrity
H Hydration and nutritional status
H Pain control

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H traction methods used
H exercises to maintain physical mobility
H medication administration, dosage, and possible
adverse effects
H the prescribed home care regimen
H the importance of follow-up examinations.

Discharge planning
H Refer the patient to the appropriate rehabilitation
center.
H Refer the patient to resource and support services.

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Incidence
Sprains and strains H More common in athletes (occurs in 80% of ath-
letes)
H More common in males than in females
Overview
Common characteristics
Description Sprain
H Sprain complete or incomplete tear in supporting H Localized pain
ligaments surrounding a joint H Swelling and warmth
H Strain acute or chronic injury to a muscle or H Progressive loss of motion
tendinous attachment H Ecchymosis
H Classified as mild, moderate, or severe (see Classify- Strain
ing sprains and strains) H Pain
H Inflammation
Pathophysiology H Erythema
Sprain H Ecchymosis
H A ligament tear causes bleeding. H Elevated skin temperature
H A hematoma forms.
H Inflammatory exudates follow. Complications
H Granulation tissue develops. Sprain
H Collagen forms. H Avulsion fracture
H Swelling or stretching of nerves or vessels occurs. Strain
H Persistent laxity and chronic joint instability result. H Complete rupture of muscle tendon unit
Strain H Deep vein thrombosis
H Strains result from the same process as sprains.
H New tendon or muscle eventually becomes strong
enough to withstand normal muscle strain. Assessment
Causes History
H Fall H Physical activity
H Motor vehicle accident H Similar past injury
H Trauma H Systemic disease with high risk factors
H Excessive or new exercise H Local pain that worsens during joint movement
H Sports injury H Loss of mobility
H Sharp, transient pain and rapid swelling
Risk factors H Stiffness, soreness, and generalized tenderness
H Participation in sports
Physical findings
H Ecchymosis
H Swelling
H Point tenderness
Classifying sprains and strains
Test results
The guide below will help you classify the severity of
sprains and strains.
Imaging
H X-ray results are used to rule out fractures and con-
Sprains
H Grade 1 (mild): minor or partial ligament tear with nor- firm damage to ligaments.
mal joint stability and function
H Grade 2 (moderate): partial tear with mild joint laxity
and some function loss
Treatment
H Grade 3 (severe): complete tear or incomplete separa-
tion of ligament from bone, causing total joint laxity General
and function loss H RICE rest, ice, compression (wrapping in an elas-
Strains tic bandage), and elevation to affected area
H Grade 1 (mild): microscopic muscle or tendon tear (or H Rehabilitation or exercise program
both) with no loss of strength
H Nothing by mouth if surgery scheduled
H Grade 2 (moderate): incomplete tear with bleeding into
H Limited activity and weight bearing to injured area,
muscle tissue and some loss of strength
H Grade 3 (severe): complete rupture, usually resulting based on extent of injury
from separation of muscle from muscle, muscle from H Elevation of affected joint above the level of the heart
tendon, or tendon from bone (usually stems from sud- for 48 to 72 hours
den, violent movement or direct injury) H Range-of-motion (ROM) exercises

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Medications
H Vitamin C supplements
H Nonsteroidal anti-inflammatory drugs
H Analgesics
H Cox-2 inhibitors

Surgery
H Based on extent of injury

Nursing considerations
Key outcomes
The patient will:
H attain the highest possible level of mobility
H express feelings of increased comfort and decreased
pain
H identify factors that increase the potential for injury.

Nursing interventions
H Apply ice intermittently.
H Apply an elastic bandage or air cast.
H Administer prescribed drugs.
H Elevate the extremity.

Monitoring
H Edema
H Response to treatment
H Pain control
H Complications
H Adverse effects of drugs
H ROM

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H how to apply ice intermittently for the first 12 to
48 hours
H how to reapply elastic bandage or air cast
H crutch-gait training
H avoidance of further injury to the joint
H medication administration, dosage, and possible
adverse effects.

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Spurious polycythemia Assessment

History
Overview H Headaches
H Dizziness
Description H Cardiac or pulmonary disease
H Blood disorder characterized by increased hemat- H Fatigue
ocrit and a normal or low red blood cell (RBC) total H Diaphoresis
mass H Dyspnea
H Results from diminished plasma volume and subse- H Claudication
quent hemoconcentration
H Also known as relative polycythemia, stress ery- Physical findings
throcytosis, stress polycythemia, benign poly- H Ruddy appearance
cythemia, Gaisbcks disease, or pseudopoly- H Short neck
cythemia H Hepatosplenomegaly
H Slight hypertension
Pathophysiology H Hypoventilation when recumbent
H Conditions that promote severe fluid loss decrease
plasma volume and lead to hemoconcentration. Test results
H Nervous stress causes hemoconcentration by an un- Laboratory
known mechanism. This form of erythrocytosis H Hemoglobin level and hematocrit are increased.
(chronically elevated hematocrit) is particularly H RBC count is increased.
common in the middle-aged male whos a chronic H RBC mass is normal or decreased
smoker and has a type A personality (tense, hard dri- H Arterial oxygen saturation is normal.
ving, and anxious). H Bone marrow is normal.
H In many patients, an increased hematocrit merely re- H Plasma volume is decreased or normal.
flects a normally high RBC mass and low plasma vol- H Hyperlipidemia may be present.
ume. This is particularly common in patients who H Uricosuria may be present.
dont smoke, arent obese, and have no history of hy-
pertension.
Treatment
Causes
H Dehydration General
H Hemoconcentration from stress H Appropriate fluids and electrolytes to correct dehy-
H High-normal RBC mass and low-normal plasma dration
volume H Cessation of dietary diuretics such as caffeine
H Hypertension H Low-cholesterol, low-fat diet
H Thromboembolic disease H Adequate hydration
H Elevated serum cholesterol and uric acid H Adequate exercise
H Familial tendency
H Pregnancy Medications
H Antidiarrheals, if needed
Incidence
H Usually affects middle-aged people
H More common in males than in females Nursing considerations
Common characteristics Key outcomes
H Headaches or dizziness The patient will:
H Ruddy appearance H express feelings of increased energy
H Slight hypertension H exhibit adequate ventilation
H Tendency to hyperventilate when recumbent H express feelings of increased comfort
H Cardiac or pulmonary disease H maintain normal fluid volume.

Complications Nursing interventions

H Thromboemboli H Administer prescribed I.V. fluids.
H Encourage adequate fluid intake.
H Encourage activity.

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H Provide emotional support.

H Provide dietary counseling if appropriate.

Monitoring
H Intake and output
H Blood studies
H Response to treatment

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H changing the patients work habits, if appropriate
H the need for proper relaxation
H dietary restrictions
H importance of proper hydration
H recognizing and reporting of signs and symptoms of
increasing polycythemia and thromboembolism.
Discharge planning
H Refer the patient to a smoking-cessation program, if
necessary.
H Emphasize the need for follow-up examinations every
3 to 4 months after leaving the hospital.

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Squamous cell H Presence of premalignant lesions (such as actinic

keratosis or Bowens disease)
carcinoma H Rarely, develops on site of smallpox vaccination, pso-
riasis, or chronic discoid hippus erythematosus
Incidence
Overview H Most common in fair-skinned, light-eyed, and light-
haired people
Description H Risk greatly increased by outdoor employment and
H Invasive tumor arising from keratinizing epidermal residence in sunny, warm climate
cells
Common characteristics
Pathophysiology H Chronic skin ulceration
H Transformation from a premalignant lesion to squa-
mous cell carcinoma may begin with induration and Complications
inflammation of an existing lesion. H Lymph node involvement
H When squamous cell carcinoma arises from normal H Visceral metastasis
skin, the nodule grows slowly on a firm, indurated
base. If untreated, this nodule eventually ulcerates
and invades underlying tissues. (See Squamous cell Assessment
carcinoma nodule.)
History
Causes H Areas of chronic ulceration, especially on
H Unknown sun-damaged skin
H Actinic damage from solar ultraviolet radiation H Pain, malaise, anorexia, fatigue, and weakness
H Ionizing radiation
H Chemical carcinogens Physical findings
H Burns, scars H Lesions on the face, ears, or dorsa of the hands and
H Ulcerations forearms, and on other sun-damaged skin areas (le-
sions possibly scaly and keratotic with raised, irregu-
Risk factors lar borders; in late disease, lesions growing outward
H Overexposure to the suns ultraviolet rays or exophytic and friable and tending toward chronic
H Radiation therapy crusting)
H Ingestion of herbicides containing arsenic
H Chronic skin irritation and inflammation Test results
H Exposure to local carcinogens (such as tar and oil) Diagnostic procedures
H Hereditary diseases (such as xeroderma pigmento- H Excisional biopsy allows a definitive diagnosis.
sum and albinism)
Treatment
Squamous cell carcinoma nodule General
H Determined by size, shape, location, and invasiveness
An ulcerated nodule with an indurated base and a raised,
irregular border is a typical lesion in squamous cell carci- of tumor and condition of underlying tissue
noma. H Radiation therapy for older or debilitated patients
H High-protein, high-calorie diet

Medications
H Chemotherapy
H Topical corticosteroids

Surgery
H Wide surgical excision, curettage, and electrodesic-
cation
H Cryosurgery
H Mohs micrographic surgery

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Nursing considerations
Key outcomes
The patient will:
H express positive feelings about self
H experience feelings of increased energy
H exhibit improved or healed lesions or wounds
H express feelings of increased comfort.

Nursing interventions
H Encourage verbalization and provide emotional sup-
port.
H Provide appropriate wound care.
H Provide periods of rest between procedures if the
patient fatigues easily.
H Provide small, frequent meals and a high-protein,
high-calorie diet.
Monitoring
H Wound site
H Adverse effects of radiation therapy, such as nausea,
vomiting, hair loss, malaise, and diarrhea
H Pain control

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medication administration, dosage, and possible
adverse effects
H information about skin examination
H the importance of follow-up skin surveillance
H avoidance of excessive sun exposure to prevent re-
currence; the need to use strong sunscreen.
Discharge planning
H Refer the patient to resource and support services.

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Incidence
Stomatitis Acute herpetic stomatitis
H Common in children ages 1 to 3
Aphthous stomatitis
Overview H Common in young girls and female adolescents

Description Common characteristics

H Inflammation of oral mucosa; may extend to the buc- H Painful gums
cal mucosa, lips, palate, and tongue H Ulcers on gum papillae
H Common infection occurring alone or as part of sys-
temic disease Complications
H Two main types: acute herpetic stomatitis and aph- H Dysphagia
thous stomatitis H Sepsis (in immunocompromised patient)
H Usually heals spontaneously, without scarring, in 10 H Ocular or central nervous system involvement (her-
to 14 days petic stomatitis)
Pathophysiology
H Stomatitis is an inflammatory reaction that may cause Assessment
loss of the oral epithelium as a protective barrier.
History
Causes H Burning mouth pain
Acute herpetic stomatitis H Malaise
H Herpes simplex virus H Lethargy
Aphthous stomatitis H Anorexia
H Unknown (autoimmune and psychosomatic causes H Irritability
under investigation) H Fever
H Extreme tenderness of the oral mucosa
Risk factors
H Smoking Physical findings
H Poor oral hygiene Herpetic stomatitis
H Stress H Bleeding and swollen gums
H Poor nutrition H Papulovesicular ulcers in the mouth and throat
H Chemotherapy H Submaxillary lymphadenitis
H Immunosuppression Aphthous stomatitis
H Slight swelling of the mucous membrane
H Single or multiple shallow ulcers with whitish centers
and red borders, about 2 to 5 mm in diameter (see
Looking at aphthous stomatitis Looking at aphthous stomatitis)
In aphthous stomatitis, numerous small, round vesicles Test results
appear. They soon break and leave shallow ulcers with red
Laboratory
areolae.
H Smear of ulcer exudate identifies the causative organ-
ism in Vincents angina (painful pseudomembranous
ulceration of gums, oral mucous membranes, phar-
ynx, and tonsils).
H Viral cultures performed on fluid and herpetic vesi-
cles in acute herpetic stomatitis identify the virus.

Treatment
General
H Symptom relief
H Nonantiseptic warm-water mouth rinses
H Ice
H Soft-bristled toothbrush
H Smoking cessation
H Soft, pureed, or liquid diet, as tolerated; avoidance of
salty, spicy foods
H Activity as tolerated

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Medications
H I.V. fluids (severe cases)
Acute herpetic stomatitis
H Topical anesthetic solutions
H Topical corticosteroids
H Acyclovir
Aphthous stomatitis
H Topical anesthetic coating agent

Nursing considerations
Key outcomes
The patient will:
H show improvement or complete healing of lesions or
wounds
H avoid complications
H express feelings of increased comfort and decreased
pain
H demonstrate good oral hygiene practices.

Nursing interventions
H Advise using a sponge instead of a toothbrush for
brushing teeth.
H Suggest rinsing with hydrogen peroxide or normal
saline mouthwash.
H Administer prescribed drugs.
H Develop a meal plan based on soft, liquid, or pureed
foods.
H Offer iced drinks.

Monitoring
H Lesion state
H Response to treatment
H Complications

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the infection and expected course
H the importance of good oral hygiene
H the proper application of topical drugs
H recommended dietary changes
H medication administration, dosage, and possible ad-
verse effects
H (with aphthous stomatitis) the need to avoid such
precipitating factors as stress and fatigue.
Discharge planning
H Refer the patient to a smoking-cessation program, if
appropriate.

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Incidence
Life-threatening disorder H 3% to 35% of pneumococcal illness due to drug-
resistant strains
Streptococcus Common characteristics
pneumoniae infection, H DRSP possibly causing:
Bacteremia
drug-resistant

Meningitis
Otitis media
Peritonitis
Pneumonia
Overview Sinusitis
Description Complications
H Infections caused by Streptococcus pneumoniae H Colonized people not commonly detected or treated
among leading causes of illness and death among H Treatment failures, prolonged hospitalization, recur-
young, elderly, and debilitated people rent disease, and increased cost
H Also known as DRSP H Death in 14% of adults with invasive disease
H Seven serotypes (6A, 6B, 9V, 14, 19A, 19F, and 23F) H Neurologic sequelae after meningitis
accounting for most DRSP H Hearing impairment from recurrent otitis media
H Vaccine available for the 23 most common serotypes H Developmental delay in children with recurrent otitis
H Commonly resistant to penicillin; also resistant to media
erythromycin, co-trimoxazole, vancomycin, tetracy-
cline, chloramphenicol, and ofloxacin
H In pneumonias caused by resistant strains, death rate Assessment
twice as high as in those sensitive to antibiotics
History
Pathophysiology H Member of high-risk population
H DRSP can affect people by colonization or infection. H Recent exposure to respiratory secretions of infected
H People who carry S. pneumoniae as part of their person
normal flora but remain asymptomatic may unknow- H Recent antimicrobial use
ingly spread the infection.
H Disease results when bacteria multiply locally (otitis Physical findings
media), multiply after aspiration (pneumonia), or In meningitis
invade a sterile site (central nervous system or H Fever
blood). H Stiff neck
H Drowsiness
Causes H Rash
H Abuse of antimicrobial agents H Seizures
H Increasing prevalence of strains resistant to multiple H Increased white blood cells in cerebrospinal fluid
drug classes (CSF)
In otitis media
Risk factors H High fever (101.3 F [38.5 C])
H Contact with infected respiratory droplets or direct H Irritability
or indirect contact with objects freshly soiled with H Possibly effusion
respiratory discharge H Bulging tympanic membrane thats red, opaque,
H Populations at risk: white, yellow, or purple and immobile on pneumatic
Elderly people otoscope
Children age 2 and older In pneumonia
Blacks H Fluid-filled tissue and lobes
Native Americans H Shaking chills
People with autoimmune disorders H Cough
Nursing home residents H Rust- or green-colored mucus
Child-care workers H High fever
H Diaphoresis
H Elevated pulse and respirations
Special populations
H Bluish lips and nailbeds
The Advisory Committee on Immunization Prac- H Confusion or delirium
tices recommends the S. pneumoniae vaccine be
given to people age 2 and older with certain med-
ical conditions and to all people age 65 and older.

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Test results Discharge planning

Laboratory H Refer the patient for follow-up, as needed.
H Bacteria are isolated from a fluid sample (blood, CSF, H Recommend to the patient that close contacts receive
sputum, respiratory drops, ear). the S. pneumoniae vaccine.
Imaging
H Chest X-rays display pneumonia.
Diagnostic procedures
H Lumbar puncture is performed for suspected menin-
gitis.

Treatment
General
H Supportive, symptomatic care
H Activity as tolerated
H Diet as tolerated

Medications
H Analgesics
H Antibiotics (type depending on resistance patterns in
community)
H Vancomycin (meningitis)

Nursing considerations
Key outcomes
The patient will:
H report resolution of symptoms
H have normal vital signs
H have adequate oxygen levels
H have normal laboratory values.

Nursing interventions
H Administer prescribed drugs.
H Provide rest periods as needed.
H Provide emotional support.

Monitoring
H Seizures
H Vital signs
H Intake and output
H Complications after lumbar puncture

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the importance of covering the mouth and nose when
sneezing or coughing
H regular hand washing
H taking the entire prescription of antibiotic for any
infection
H never giving a prescribed antibiotic to anyone else
H importance of reporting a change in symptoms to the
physician.

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H Use of hormonal contraceptives in conjunction with

Life-threatening disorder smoking and hypertension
H Elevated cholesterol and triglyceride levels

Stroke Incidence
H Mostly affects older adults but can strike at any age
H More common in males than in females
Overview H Affects Blacks and Hispanics more commonly than
other groups
Description
H Sudden impairment of blood circulation to the brain Common characteristics
H Third most common cause of death in the United H Sudden unilateral weakness or numbness in limb
States H Sudden speech difficulties
H Affects 500,000 people each year, causing death in H Sudden vision disturbances
half H Sudden ataxia, gait disturbance
H Most common cause of neurologic disability H Sudden altered level of consciousness (LOC)
H About 50% of stroke survivors permanently disabled H Sudden severe headache
H Recurrences possible within weeks, months, or years
H Also known as cerebrovascular accident or brain Complications
attack H Unstable blood pressure from loss of vasomotor con-
trol
Pathophysiology H Fluid and electrolyte imbalances
H The oxygen supply to the brain is interrupted or di- H Malnutrition
minished. H Infections
H In thrombotic or embolic stroke, neurons die from H Sensory impairment
lack of oxygen. H Altered LOC
H In hemorrhagic stroke, impaired cerebral perfusion H Aspiration
causes infarction. H Contractures
H Skin breakdown
Causes H Deep vein thrombosis
Cerebral thrombosis H Pulmonary emboli
H Most common cause of stroke H Depression
H Obstruction of a blood vessel in the extracerebral
vessels
H Site possibly intracerebral Assessment
Cerebral embolism
H Second most common cause of stroke History
H History of rheumatic heart disease H Varying clinical features, depending on:
H Endocarditis artery affected
H Posttraumatic valvular disease severity of damage
H Cardiac arrhythmias extent of collateral circulation
H Post open-heart surgery H One or more risk factors present
Cerebral hemorrhage H Sudden onset of hemiparesis or hemiplegia
H Third most common cause of stroke H Gradual onset of dizziness, mental disturbances, or
H Chronic hypertension seizures
H Cerebral aneurysms H Loss of consciousness or sudden aphasia
H Arteriovenous malformation
Physical findings
Risk factors H With stroke in left hemisphere, signs and symptoms
H History of transient ischemic attack on right side
H Heart disease H With stroke in right hemisphere, signs and symptoms
H Smoking on left side
H Familial history of cerebrovascular disease H With stroke that causes cranial nerve damage, signs
H Obesity and symptoms on same side
H Alcohol use H Change in LOC
H High red blood cell count H With conscious patient, anxiety along with communi-
H Cardiac arrhythmias cation and mobility difficulties
H Diabetes mellitus H Urinary incontinence
H Gout H Hemiparesis or hemiplegia on one side of the body
H High serum triglyceride levels H Decreased deep tendon reflexes
H Hemianopsia on the affected side of the body

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H With left-sided hemiplegia, problems with visuospa- Prevention

tial relations Preventing stroke
H Sensory losses
Risk of stroke may be reduced by following these guide-
Test results lines:
H Stop smoking through a smoking-cessation program.
Laboratory H Maintain ideal body weight.
H Laboratory tests including anticardiolipin antibod- H Control diabetes and hypertension.
ies, antiphospholipid, factor V (Leiden) mutation, H Follow a low-cholesterol, low-sodium diet.
antithrombin III, protein S, and protein C may H Take prescribed medications as ordered, especially an-
show increased thrombotic risk. ticoagulants or platelet aggregation inhibitors.
Imaging H Perform physical exercise regularly.
H Magnetic resonance imaging and magnetic reso- H Avoid prolonged bedrest.
nance angiography allow for evaluation of the loca- H Minimize stress.
H Seek prompt treatment if experiencing signs and
tion and size of the lesion.
symptoms of stroke.
H Cerebral angiography details the disruption of cere-
bral circulation and is the test of choice for examin-
ing the entire cerebral blood flow.
H Computed tomography scan detects structural abnor-
malities. Nursing considerations
H Positron-emission tomography provides data on
cerebral metabolism and on cerebral blood flow Key outcomes
changes. The patient will:
Other H maintain adequate ventilation
H Transcranial Doppler studies evaluate the velocity of H remain free from injury
blood flow. H achieve maximal independence
H Carotid Doppler measures flow through the carotid H maintain joint mobility and range of motion.
arteries.
H Two-dimensional echocardiogram evaluates the heart Nursing interventions
for dysfunction. H Maintain a patent airway and oxygenation.
H Cerebral blood flow studies measure blood flow to H Offer the urinal or bedpan every 2 hours.
the brain. H Insert an indwelling urinary catheter, if necessary.
H Electrocardiography evaluates electrical activity in an H Ensure adequate nutrition.
area of cortical infarction. H Provide careful mouth and eye care.
H Follow the physical therapy program.
H Establish and maintain patient communication.
Treatment H Provide psychological support.
H Protect the patient from injury and complications.
General H Position to prevent aspiration and contractures.
H Careful blood pressure management H Administer prescribed drugs.
H Pureed dysphagia diet or tube feedings, if indicated
H Physical, speech, and occupational rehabilitation Monitoring
H Helping patient adapt to specific deficits H Neurologic, GI, and respiratory status
H Vital signs
Medications H Fluid, electrolyte, and nutritional intake
H Tissue plasminogen activator when the cause isnt he- H Development of deep vein thrombosis and pul-
morrhagic (emergency care within 3 hours of onset) monary embolus
H Anticonvulsants
H Stool softeners
H Anticoagulants or antiplatelets Patient teaching
H Analgesics
H Antidepressants Be sure to cover:
H Lipid-lowering agents H the disorder, diagnosis, and treatment
H Antihypertensives H the dietary regimens
H medication administration, dosage, and possible ad-
Surgery verse effects
H Craniotomy H stroke prevention. (See Preventing stroke.)
H Endarterectomy
H Extracranial-intracranial bypass Discharge planning
H Ventricular shunts H Refer the patient to home care services, outpatient
services, and speech and occupational rehabilitation
programs as needed.

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Strongyloidiasis Assessment
History
Overview H Institutionalization
H Autoimmune susceptibility
Description H Cough
H A parasitic intestinal infection caused by the helminth H Abdominal pain and diarrhea
Strongyloides stercoralis H Recent travel to endemic area
H Doesnt confer immunity; in people with autoimmune
disorders, possibly overwhelming disseminated in- Physical findings
fection H Erythematous, pruritic rash at entrance site
H Because threadworms reproductive cycle may con- H Normal or hyperactive bowel sounds
tinue in untreated host for up to 45 years, autoinfec- H Crackles
tion highly probable
H Most patients recover, but death resulting from debil- Test results
itating protein loss possible Laboratory
H Also called threadworm infection H S. stercoralis larvae can be observed in a fresh stool
specimen (2 hours after excretion, look like hook-
Pathophysiology worm larvae).
H Larvae develop from noninfective rhabdoid larvae in H Eosinophils and larvae may appear in sputum, with
human feces. marked eosinophilia in disseminated strongyloidiasis
H The filariform larvae penetrate the human skin, usu- (pulmonary phase).
ally at the feet, and then migrate by way of the lym- H Hemoglobin level is decreased.
phatic system to the bloodstream and the lungs. H In white blood cell count with differential, eosinophil
H Once they enter into pulmonary circulation, the filar- count is 450 to 700/l.
iform larvae break through the alveoli and migrate Imaging
upward to the pharynx, where they are swallowed. H Chest X-rays show alveolar or interstitial infiltrates or
H Larvae then lodge in the small intestine, where they pulmonary effusions (pulmonary phase).
deposit eggs that mature into noninfectious rhabdoid
larvae.
H These larvae migrate into the large intestine and are Treatment
excreted in feces, starting the cycle again.
H In autoinfection, rhabdoid larvae mature in the intes- General
tine to become infective filariform larvae. H High-protein diet
H I.V. fluids
Causes H Blood transfusion
H Contact with soil that contains infective S. stercoralis
filariform larvae Medications
H Thiabendazole
Incidence
H Endemic to the tropics and subtropics
H Universal susceptibility Nursing considerations
Common characteristics Key outcomes
H Erythematous maculopapular rash at the site of pene- The patient will:
tration producing swelling and pruritus H experience no further weight loss
H Pulmonary signs including minor hemorrhage, pneu- H maintain normal fluid and electrolyte balance
monitis, and pneumonia H express feelings of increased comfort and decreased
H Intestinal infection producing frequent, watery, and pain.
bloody diarrhea, accompanied by intermittent ab-
dominal pain Nursing interventions
H Encourage high-protein diet.
Complications H Wear gloves when handling bedpans or giving per-
H Malnutrition ineal care, and dispose of feces promptly.
H Anemia H In pulmonary infection, reposition the patient fre-
H Secondary bacterial infection quently, encourage coughing and deep breathing,
H Perforated intestine and administer oxygen, as ordered.
H Septicemia

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Monitoring
H Intake and output
H Response to treatment
H Respiratory status
H Amount and character of stools

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the possibility that thiabendazole may cause mild
nausea, vomiting, drowsiness, and giddiness
H proper hand-washing technique, stressing the impor-
tance of washing hands before eating and after defe-
cating
H the need to wear shoes when in endemic areas.

Discharge planning
H Check the patients family and close contacts for
signs of infection.
H Emphasize the need for follow-up stool examination,
continuing for several weeks after treatment.

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Incidence
Subarachnoid H About 30,000 people a year in the United States have

hemorrhage a nontraumatic subarachnoid hemorrhage

H Predominant between ages 40 and 70
H More common in females then in males
H Ruptured saccular aneurysms: account for about
Overview 80% of nontraumatic cases
H AVMs: account for about 10% of cases
Description H Estimated 23% to 39% occurring due to severe head
H Bleeding into subarachnoid space injury
Subarachnoid space located between the pia mater
and the arachnoid layer of the meninges that sur- Common characteristics
round the brain and spinal cord; normally filled H Vary with location, duration and amount of va-
with clear, colorless cerebrospinal fluid (CSF) and sospasm, and the degree of increased ICP
a network of arteries and veins H Typically, change in level of consciousness occurring
Blood also entering the CSF pathways H Sudden onset of severe headache
H Two types H Neck pain and nuchal rigidity
Traumatic: more common H Nausea and vomiting
Spontaneous (nontraumatic) H Photophobia
H Seizures
Pathophysiology H Possible prodromal headaches caused by minor
H Bleeding occurs into the subarachnoid space. blood leakage, also called sentinel headaches: oc-
H Blood spreads through the CSF, across the surface of cur in 30% to 50% of cases with aneurysm as the
the brain, collecting and clotting in the ventricles, cause; may occur a few hours to a few months before
cisterns, and foramen. the rupture
H Intracranial pressure (ICP) increases due to the
pressure exerted within a closed system. Complications
H Perfusion distal to the rupture is decreased as well as H Rebleeding
cerebral perfusion. H Hyponatremia
H Veins are compressed and venous outflow is re- H Severe neurologic damage
duced. H Paralysis
H Vasospasm occurs from irritation of the meninges, H Coma
further decreasing perfusion. H Death
H Subacute or chronic hydrocephalus and brain infarc-
tions can result.
Assessment
Causes
H Head trauma History
H Rupture of intracranial saccular aneurysm H Traumatic head injury
H Intracranial arteriovenous malformation (AVM) H Headaches
H Hypertension H Recent onset of seizures
H Rarely, tumors and blood dyscrasias H Symptoms of meningeal irritation
H Arterial dissection H Photophobia and visual changes
H Extension from intracerebral hemorrhage H Loss of consciousness
H Iatrogenic during surgery or intervention
H Meningitis Physical findings
All or none of these findings may be present:
Risk factors H Global or focal neurologic abnormalities
H Congenital weakness in arterial wall H Symptoms of cranial nerve compression
H Degenerative weakening in the arterial wall from ath- H Vision loss
erosclerosis H Motor deficits
H Cerebral aneurysms (associated with genetic abnor- H Retinal hemorrhage
malities, such as polycystic kidney disease and fibro- H Papilledema
muscular dysplasia) H Mild-to-moderate blood pressure elevation
H Hypertension H Tachycardia
H Pregnancy H Weakness, paralysis, or numbness on one side of
H Smoking body
H Drug and alcohol abuse H Difficulty speaking

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Test results
Laboratory
H Complete blood count may show decreased hemo-
globin level and hematocrit.
H Prothrombin time and partial thromboplastin time
may be increased.
H Blood typing and crossmatching is done for possible
transfusion.
Imaging
H Computed tomography (CT) scan, initially without
contrast, establishes diagnosis.
H Cerebral angiography assesses vascular anatomy and
bleeding site also assists in surgical planning.
H Magnetic resonance imaging is done if other testing
is negative.
Diagnostic procedures
H Lumbar puncture, only if contrast CT scan shows
negative results and there are no signs of increased
ICP; may detect blood in CSF; contraindicated with
increased ICP because brain stem herniation may re-
sult.
H Electrocardiography detects myocardial ischemia
caused by the increased circulation of cate-
cholamines.
Treatment
General
H Establishing and maintaining airway, breathing, and
circulation as necessary; providing supplemental
oxygen
H Directed at preventing complications, including re-
bleeding, hydrocephalus, and cerebral vasospasm
H Vasospasm treated with generous volume expansion
and hypertension to promote cerebral perfusion, af-
ter aneurysm obliterated
H Providing a darkened, quiet, private room to mini-
mize stimuli
H Elevating the head of the bed 30 degrees to facilitate
intracranial venous drainage
H Vigorous rehabilitation program
Medications
H Analgesics to reduce pain
H Calcium channel blockers, such as nimodipine for
21 days to prevent vasospasm and to enhance collat-
eral blood flow
H Osmotic agent, such as mannitol, or loop diuretic
such as furosemide to reduce ICP
H Antihypertensive agents and vasopressors (possibly
indicated)
H Possibly, antiemetics for nausea or vomiting and
stool softeners to prevent constipation and straining
to defecate
Surgery
H Hydrocephalus: cerebral spinal fluid drainage or
permanent shunting procedures
H AVMs and certain aneurysms: possibly obliterated
with embolization; cranial surgery possibly necessary
H Radiosurgery possibly used to treat small, deep AVMs
H Endovascular obliteration of aneurysms
Nursing considerations
Key outcomes
The patient will:
H express relief from or decrease in pain
H achieve optimum functioning
H demonstrate improvement in orientation
H maintain optimal gas exchange and ventilation
H maintain adequate cerebral perfusion
H verbalize decrease in or relief from nausea
H remain free from injury.
Nursing interventions
H Administer prescribed medications.
H Establish and maintain a patent airway.
H Provide supplemental oxygen and mechanical venti-
lation, as needed.
H Evaluate fluid and electrolyte status.
H Avoid overhydration with I.V. fluids to prevent in-
creases in intracranial pressure.
H Turn patient often, one movement at a time, and use
antiembolism stockings.
H Institute measures to prevent skin breakdown.
H Institute seizure precautions, as indicated.
H Prepare the patient for surgery, as appropriate.
Monitoring
H Neurologic status (hourly)
H Signs of increased ICP
H Cerebral perfusion pressure
H Signs of decreased level of consciousness
H Vital signs
H Respiratory and cardiac status
H Seizure activity
H Laboratory test results
Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H importance of preventing Valsalvas maneuver
(straining at stool, coughing)
H medication regimen
H tests, neurologic examinations, treatments, and pro-
cedures
H avoidance of unnecessary physical activity for pa-
tients receiving conservative treatment
H need to report adverse reactions to prescribed med-
ications
H need to report signs of rebleeding
H importance of follow-up care.
Discharge planning
H Refer the patient to physical therapy, occupational
therapy, and speech therapy as appropriate.
H Refer the patient to social services as appropriate.
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H Dilated, nonreactive pupil ipsilateral to the

Life-threatening disorder hematoma
H Hemiparesis contralateral to the hematoma

Subdural hematoma Complications

H Neurologic impairment
H Coma
Overview H Death

Description
H Meningeal hemorrhage resulting from accumulation Assessment
of blood in subdural space
H May be acute (less than 72 hours old), subacute (3 History
to 20 days old), or chronic (older than 20 days) H Head trauma
H May be unilateral or bilateral H Headache
H Change in level of consciousness (LOC)
Pathophysiology
Acute Physical findings
H Blunt impact to the skull may cause a tear in con- H Dilated, nonreactive pupil ipsilateral to the
necting veins (rarely, arteries) in the cerebral cortex. hematoma
Chronic H Hemiparesis contralateral to the hematoma
H Chronic subdural hematoma begins as a separation H Balance problems
in the dura-arachnoid interface, which is then filled H Altered LOC
by cerebrospinal fluid (CSF).
H Dural border cells proliferate around this CSF collec- Test results
tion to produce a neomembrane. Laboratory
H Fragile new vessels grow into the membrane and H CSF is yellow with relatively low protein (chronic
hemorrhage. subdural hematoma).
H Coagulation studies may be abnormal.
Causes Imaging
H Head trauma H Computed tomography scan, X-rays, and arteriogra-
phy reveal mass and altered blood flow in the area.
Risk factors
Acute
H Anticoagulant therapy Treatment
H Age
Chronic General
H Alcoholism H Supportive treatment
H Epilepsy H Wound care
H Coagulopathy H Fresh frozen plasma (to correct coagulation)
H Arachnoid cysts H Adequate hydration
H Anticoagulant therapy (including aspirin) H Diet based on extent of injury
H Cardiovascular disease (hypertension, arteriosclero- H Nothing by mouth if surgery necessary
sis) H Bed rest initially, then activity as tolerated
H Thrombocytopenia H Flat bed after evacuation of hematoma
H Diabetes
Medications
Incidence H Vitamin K, fresh frozen plasma, platelets, or clotting
H Acute type: occurs in 5% to 25% of patients with products (if coagulation studies are abnormal)
severe head injuries. H Analgesics (after extent of injury is determined)
Most common in people older than age 40 H Osmotic diuretics
H Chronic type: most common in people older than H Anticonvulsants
age 50 H Prophylactic antibiotics (with surgery)
H Both types occurring more commonly in males than
in females Surgery
H Burr holes
Common characteristics H Craniotomy
H Headache
H Deteriorating mental status

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Nursing considerations
Key outcomes
The patient will:
H remain neurologically stable
H express feelings of increased comfort and decreased
pain
H express an understanding of the disorder and treat-
ment regimen.
Nursing interventions
H Provide appropriate wound care.
H Administer prescribed drugs.
H Provide emotional support.
H Institute seizure precautions.

Monitoring
H Vital signs
H Neurologic status
H Wound healing
H Seizure activity
H Respiratory status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, anad treatment
H importance of reporting changes in neurologic status
H avoiding aspirin as a pain treatment
H observing for CSF drainage and signs of infection.

Discharge planning
H Refer the patient to physical therapy, occupational
therapy, and speech therapy, as appropriate.
H Refer the patient to social services, as appropriate.

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Substance abuse and H Hepatitis

H Cirrhosis

dependence H Vasculitis
H Septicemia
H Thrombophlebitis
H Pulmonary emboli
Overview H Gangrene
H Malnutrition and GI disturbances
Description H Respiratory infections
H Use of a legal or an illegal substance that causes H Musculoskeletal dysfunction
physical, mental, emotional, or social harm, such as H Trauma
opioids, stimulants, depressants, antianxiety agents, H Depression and increased risk of suicide
and hallucinogens H Psychosis
H Number one health problem in the United States H Toxic or allergic reactions
H Impaired social and occupational functioning
Pathophysiology
H Tolerance develops when a drug is administered
long-term (such as an opioid for a cancer patient), Assessment
with cross-tolerance developing.
H Withdrawal occurs with abrupt discontinuation or History
administration of an antagonist due to rebound nora- H Abdominal pain, nausea, or vomiting
drenergic activity in the central nervous system H Painful injury or chronic illness
(CNS). H Feigned illnesses
H Overdose
Causes H High tolerance to potentially addictive drugs
H Combination of low self-esteem, peer pressure, inad- H Amenorrhea
equate coping skills, and curiosity H Suggestive behavior patterns or the presence of
H May follow the use of prescribed drugs to relieve known risk factors
physical pain H Mood swings, anxiety, impaired memory, sleep dis-
turbances, flashbacks, slurred speech, depression,
Risk factors and thought disorders
H Male gender
H History of depression Physical findings
H History of other substance abuse disorders H Lacrimation (with opiate withdrawal)
H Familial history H Nystagmus (with CNS depressants and phencyclidine
H Peer pressure intoxication)
H Low socioeconomic status H Drooping eyelids (with opiate or CNS depressant
use)
Incidence H Constricted pupils (with opiate use or withdrawal)
H Can occur at any age H Dilated pupils (with hallucinogens or ampheta-
H Experimentation common beginning in adolescence mines)
and preadolescence H Rhinorrhea (with opiate withdrawal or cocaine
H Affects more than 18 million United States residents abuse)
who use alcohol and 5 million who use illicit drugs H Inflammation, atrophy, or perforation of the nasal
(fewer than one-fourth treated) mucosa (with drug sniffing)
H Sweating (with opiates or CNS stimulants or drug
Common characteristics withdrawal)
H Nutritional deficiency H Sensation of bugs crawling on the skin (with alcohol
H Mood swings, anxiety, impaired memory, sleep dis- withdrawal)
turbances, flashbacks, slurred speech, depression, H Excoriated skin
and thought disorders H Needle marks or tracks
H Physical signs of substance abuse (based on sub- H Cellulitis or abscesses
stance) H Thrombophlebitis
H Withdrawal signs when substance not used H Fascial infection
H Bilateral crackles and rhonchi (with smoking and in-
Complications haling drugs or by opiate overdose)
H Cardiac and respiratory arrest H Cardiopulmonary signs of overdose (respiratory de-
H Intracranial hemorrhage pression and hypotension)
H Acquired immunodeficiency syndrome H Acute-onset hypertension
H Subacute bacterial endocarditis H Cardiac arrhythmias

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H Hemorrhoids Medications
H Tremors, hyperreflexia, hyporeflexia, and seizures H Detoxification with the same drug or a pharmacolog-
H Uncooperative, disruptive, or violent behavior ically similar drug
H Sedatives
DSM-IV-TR criteria H Anticholinergics
H Diagnosis is confirmed with at least three of the fol- H Antidiarrheal agents
lowing criteria (some symptoms must have persisted H Antianxiety drugs
for at least 1 month or have occurred repeatedly over H Anticonvulsants
a longer time): H Nutritional and vitamin supplements
substance usually taken in larger amounts or for a
longer time than the patient intended
persistent desire or one or more unsuccessful ef- Nursing considerations
forts to cut down or control substance use
excessive time devoted to activities necessary to Key outcomes
obtain the substance The patient will:
frequent intoxication or withdrawal symptoms H express his feelings related to self-esteem
when expected to fulfill major obligations at work, H join gradually in self-care and the decision-making
school, or home or when substance use is physi- process
cally hazardous H engage in social interactions with others
impaired social, occupational, or recreational ac- H participate with his family to identify and use support
tivities systems.
continued substance use despite the recognition of
a persistent or recurrent social, psychological, or Nursing interventions
physical problem thats caused or exacerbated by H Maintain a quiet, safe environment.
the use of the substance H Institute seizure precautions.
marked tolerance H Set limits for dealing with demanding, manipulative
characteristic withdrawal symptoms behavior.
substance commonly taken to relieve or avoid
withdrawal symptoms. Monitoring
H Vital signs
Test results H Suicide ideation
Laboratory H Visitors
H Serum or urine drug screen reveals the substance. H Signs of complications
H Serum protein electrophoresis shows elevated serum H Nutrition
globulin levels. H Effects of pharmacologic therapy
H Serum glucose measurement shows hypoglycemia.
H Complete blood count (CBC) shows leukocytosis.
H Liver function is abnormal. Patient teaching
H CBC shows elevated mean corpuscular hemoglobin
levels. Be sure to cover:
H Uric acid levels are elevated. H the disorder, diagnosis, and treatment
H Blood urea nitrogen levels are decreased. H detoxification and rehabilitation, as appropriate
H measures for preventing human immunodeficiency
virus infection and hepatitis
Treatment H measures for safer sex and birth control.

General Discharge planning

H Symptomatic treatment based on the drug ingested H Recommend participation in a drug-oriented
H Fluid replacement therapy self-help group.
H Symptomatic treatment for complications H Refer the patient to support services.
H Gastric lavage, induced emesis, activated charcoal in-
stillation, forced diuresis and, possibly, hemoperfu-
sion or hemodialysis
H Detoxification (inpatient or outpatient)
H Psychotherapy
H Exercise
H Relaxation techniques
H Rehabilitation
H Well-balanced diet
H Monitored activity for safety

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Complications
Life-threatening disorder H Always fatal

Sudden infant death Assessment

syndrome
Overview
Description
H Sudden death of an infant younger than age 1 year
without identifiable cause
H Also known as SIDS and crib death
Pathophysiology
Hypotheses
H The infant may have damage to the respiratory con-
trol center in the brain from chronic hypoxemia.
H The infant may not respond to increasing carbon
dioxide levels. During an episode of apnea, carbon
dioxide levels increase, but the child isnt stimulated
to breathe. As apnea continues, high levels of carbon
dioxide further suppress the ventilatory effort until
the infant stops breathing.
H The infant may have periods of sleep apnea and even-
tually die during one of these episodes.
Causes
H Possibly viral
H Hypoxia theory
H Apnea theory
H Possible Clostridium botulinum toxin
H Possibly associated with diphtheria, tetanus, and per-
tussis vaccines
Incidence
H About 7,000 SIDS deaths annually in United States
H 2 in every 1,000 live births; about 60% male
Special populations
SIDS occurs mostly between ages 1 and 4 months.
Incidence declines rapidly between ages 4 and
12 months.
H Increased incidence in nonbreast-fed infants
H Occurs most commonly in fall and winter
H Slightly higher incidence in:
Preterm neonates
Inuit neonates
Disadvantaged black neonates
Neonates of mothers younger than age 20
Neonates of multiple births
Common characteristics
H Respiratory tract infections
H Apnea
History
H Occasionally, respiratory tract infection
H Possible abnormal hepatic or pancreatic function
H Previous near-miss respiratory event in 60% of cases
H With infant wedged in a crib corner or with blankets
wrapped around head, suffocation ruled out by au-
topsy as the cause of death
H With frothy, blood-tinged sputum found around in-
fants mouth or on crib sheets revealing a patent air-
way, aspiration of vomitus ruled out by autopsy as
cause of death
H No crying or signs of disturbed sleep by infant
Physical findings
H Postmortem examination possibly showing:
Changes indicating chronic hypoxia, hypoxemia,
and large airway obstruction
Bruising; possible fractured ribs
Blood in the infants mouth, nose, or ears
Mottled complexion; extremely cyanotic lips and
fingertips
Pooled blood in legs and feet
Diaper possibly wet and full of stool
Test results
Diagnostic procedures
H Autopsy may show:
small or normal adrenal glands
enlarged thymus
petechiae over the visceral surfaces of the pleura,
within the thymus, and in the epicardium
well-preserved lymphoid structures
signs of chronic hypoxemia
increased pulmonary artery smooth muscle
edematous, congestive, and fully expanded lungs
liquid blood in the heart
stomach curd inside the trachea.
Treatment
General
H Emotional support for the family
H Prevention for any surviving infant found apneic and
any sibling with apnea; assessment with home apnea
monitor until the at-risk infant passes age of vulnera-
bility
Nursing considerations
Key outcomes
The family will:
H use available support systems to assist in coping
H share feelings about the event

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H identify feelings of hopelessness regarding the cur-

rent situation
H use effective coping strategies to ease spiritual dis-
comfort.
Nursing interventions
H Ensure that both parents are present when the childs
death is confirmed.
H Stay calm and allow the parents to express their feel-
ings.
H Reassure the parents that they arent to blame.
H Allow the parents to see the infant in a private room
and to express their grief. Stay in the room with
them, if appropriate.
H Offer to call clergy, friends, or relatives.
H Return the infants belongings to the parents.
H Ensure that the parents receive the autopsy report
promptly.
Monitoring
H Parents reactions and coping mechanisms

Patient teaching
Be sure to cover:
H the need for an autopsy to confirm the diagnosis
H basic facts about SIDS
H information to help parents cope with pregnancy and
the first year of a new infants life, if they decide to
have another child.
Discharge planning
H Refer the parents and family to community and
health care facility support services.
H Refer the parents to a local SIDS parents group.
H Advise the parents to contact the SIDS hot line
(1-800-221-SIDS).
H Refer the parents to cardiopulmonary resuscitation
classes, if appropriate.
H Refer the family to a home health nurse for contin-
ued support, if indicated.

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H Cerebrovascular disease
Life-threatening disorder H Cancer
H Pulmonary disease

Syndrome of H Recent head injury

H Anorexia, nausea, vomiting

inappropriate H Weight gain

H Lethargy, headaches, emotional and behavioral

antidiuretic hormone changes

Physical findings
H Tachycardia
Overview H Disorientation
H Seizures and coma
Description H Sluggish deep tendon reflexes
H Disease of the posterior pituitary marked by exces- H Muscle weakness
sive release of antidiuretic hormone (ADH) (vaso-
pressin) Test results
H Potentially life-threatening Laboratory
H Prognosis depends on underlying disorder and re- H Serum osmolality levels are less than 280 mOsm/kg.
sponse to treatment H Serum sodium levels are less than 123 mEq/L.
H Also known as SIADH H Urine sodium levels are greater than 20 mEq/L with-
out diuretics.
Pathophysiology H Renal function tests are normal.
H Excessive ADH secretion occurs in the absence of
normal physiologic stimuli for its release.
H Excessive water reabsorption from the distal convo- Treatment
luted tubule and collecting ducts results in hypona-
tremia and normal to slightly increased extracellular General
fluid volume. (See Understanding SIADH.) H Based primarily on symptoms
H Correction of the underlying cause
Causes H Restricted water intake (500 to 1,000 ml/day)
H Oat cell carcinoma of the lung H High-sodium, high-protein diet or urea supplements
H Neoplastic diseases to enhance water excretion
H Central nervous system disorders H Activity as tolerated
H Pulmonary disorders
H Drugs Medications
H Miscellaneous conditions, such as myxedema and H Demeclocycline or lithium for long-term treatment
psychosis H Loop diuretics if fluid overload, history of heart fail-
ure, or resistance to treatment
Incidence H 3% sodium chloride solution if serum sodium level
H Common cause of hospital-acquired hyponatremia less than 120 or if the patient seizing
Common characteristics Surgery
H Increased water retention H To treat underlying cause such as cancer
H Fluid and electrolyte imbalance
H Hyponatremia
Nursing considerations
Complications
H Water intoxication Key outcomes
H Cerebral edema The patient will:
H Severe hyponatremia H develop no complications
H Heart failure H remain alert and oriented to the environment
H Seizures H verbalize understanding of the disorder and treat-
H Coma ment regimen
H Death H maintain adequate fluid balance.

Nursing interventions
Assessment H Restrict fluids.
H Provide comfort measures for thirst.
History H Reduce unnecessary environmental stimuli.
H Possible clue to the cause H Orient as needed.

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Understanding SIADH
The events that produce the syndrome of inappropriate antidiuretic hormone (SIADH) secretion are depicted in this
flowchart.

Excessive antidiuretic hormone secretion

Increased renal tubule permeability

Increased water retention and expanded extracellular fluid volume

Reduced plasma Dilutional Diminished Elevated glomerular

osmolality hyponatremia aldosterone secretion filtration rate

Decreased sodium
Intracellular
reabsorption in
fluid shift
proximal tubule

Increased sodium
excretion

Cerebral edema Hyponatremia

H Provide a safe environment. Patient teaching

H Institute seizure precautions as needed.
H Administer prescribed drugs. Be sure to cover:
H the disorder, diagnosis, and treatment
Monitoring H fluid restriction
H Intake and output H methods to decrease discomfort from thirst
H Vital signs H medication administration, dosage, and possible ad-
H Daily weight verse effects
H Serum electrolytes, especially sodium H self-monitoring techniques for fluid retention such as
H Response to treatment daily weight
H Breath sounds H signs and symptoms that require immediate medical
H Heart sounds intervention.
H Neurologic checks
H Changes in level of consciousness

ALERT
Watch closely for signs and symptoms of heart fail-
ure, which may occur due to fluid overload.

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Syphilis Secondary syphilis

Overview
Description
H Chronic, infectious, sexually transmitted disease
H Untreated, progresses in four stages: primary, sec-
ondary, latent, and late (formerly called tertiary)
Pathophysiology
H The infecting organism penetrates intact mucous
membranes or abrasions in the skin, entering lym-
phatics and blood.
H Systemic infection and systemic foci precede primary
lesion development at the site of inoculation.
H Organ involvement occurs from dissemination.
Causes
H The spirochete Treponema pallidum
H Transmission primarily through sexual contact dur-
ing the primary, secondary, and early latent stages of
infection
H Prenatal transmission possible
H Transmission by way of fresh blood transfusion
(rare)
Incidence
H In the United States, incidence highest in urban pop-
ulations, especially in people between ages 15 and
39, drug users, and those infected with human im-
munodeficiency virus (HIV)
H About 34,000 cases, in primary and secondary
stages, reported in the United States annually
Complications
H Cardiovascular disease
H Irreversible neurologic disease
H Irreversible organ damage
H Membranous glomerulonephritis
H With fetal infection:
Spontaneous abortion
Stillbirth
Low birth weight
Deafness
Assessment
History
H Unprotected sexual contact with an infected person
Physical findings
Primary syphilis
H One or more chancres (small, fluid-filled lesions) on
the genitalia; others on the anus, fingers, lips,
tongue, nipples, tonsils, or eyelids
H In female patient, possible chancres on cervix or
vaginal wall
H Unilateral or bilateral adenopathy
H Headache, malaise
H Nausea, vomiting
H Anorexia, weight loss
H Sore throat, slight fever
H Symmetrical mucocutaneous lesions
H Rash possibly macular, papular, pustular, or nodular
H Lesions uniform, well defined, and generalized
H Macules typically erupting between rolls of fat on the
trunk and proximally on the arms, palms, soles, face,
and scalp
H In warm, moist body areas, lesions enlarged and
eroding, producing highly contagious, pink or gray-
ish white lesions (condylomata lata)
H Alopecia
H Brittle and pitted nails
H Generalized lymphadenopathy
Latent syphilis
H Physical signs and symptoms absent except for possi-
ble recurrence of mucocutaneous lesions that resem-
ble those of secondary syphilis
Late syphilis
H Findings that vary with the involved organ
H Three subtypes:
Neurosyphilis affecting meningovascular tissues:
headache, vertigo, insomnia, hemiplegia, seizures,
and psychological difficulties; if parenchymal tis-
sue affected: paresis, alteration in intellect, para-
noia, illusions, and hallucinations; in addition, Ar-
gyll Robertson pupil (a small, irregular pupil
thats nonreactive to light but accommodates for
vision), ataxia, slurred speech, trophic joint
changes, positive Rombergs sign, and a facial
tremor
Late benign: gummas (lesions that develop be-
tween 1 and 10 years after infection and may be a
chronic, superficial nodule or a deep, granuloma-
tous lesion thats solitary, asymmetrical, painless,
indurated, and large or small) visible on the skin
and mucocutaneous tissues; commonly affect
bones and can develop in any organ
Cardiovascular: decreased cardiac output that may
cause decreased urine output and decreased sen-
sorium related to hypoxia, pulmonary congestion
Test results
Laboratory
H Dark-field microscopy identifies T. pallidum from le-
sion exudate to provide an immediate syphilis diag-
nosis. (See Identifying syphilis by dark-field mi-
croscopy.)
H Non-treponemal serologic tests include the Venereal
Disease Research Laboratory (VDRL) slide test, the
rapid plasma reagin (RPR) test, and the automated
reagin test, detecting nonspecific antibodies.
H Treponemal serologic studies include the fluorescent
treponemal antibody absorption test, the T. pallidum
hemagglutination assay, and the microhemagglutina-
tion assay, detecting the specific antitreponemal anti-
body and confirming positive screening results.

794 Syphilis
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H Cerebrospinal fluid examination identifies neu- Identifying syphilis by dark-field

rosyphilis when the total protein level is above microscopy
40 mg/dl, the VDRL slide test is reactive, and the The presence of spiral-shaped bacteria (Treponema pal-
white blood cell count exceeds 5 mononuclear lidum) on dark-field examination confirms the diagnosis
cells/l. of syphilis.

Treatment
General
H Immediate examination of all sexual contacts
H Avoidance of pregnancy until a good response to
therapy is demonstrated
H Hospitalization for symptomatic late syphilis
H No sexual activity until cured

Medications
H Antibiotics (penicillin being the treatment of choice)

Nursing considerations
H risks to the fetus if the patient is contemplating preg-
Key outcomes nancy
The patient will: H following safer sex practices.
H voice feelings about changes in sexual activity
H express concern about self-concept, self-esteem, and Discharge planning
body image H As needed, obtain a physical or occupational therapy
H state infection risk factors consultation.
H exhibit improved or healed lesions or wounds H Refer the patient for contact tracing.
H report feelings of increased comfort. H Refer the patient to a specialist if congenital syphilis
is suspected.
Nursing interventions H Consult a social worker to determine home care
H Follow standard precautions. needs.
H Administer prescribed drugs.
H Promote rest and adequate nutrition.
H In secondary syphilis, keep lesions clean and dry;
dispose of contaminated materials properly.
H Report all syphilis cases to the appropriate health au-
thorities.
Monitoring
H Neurologic status
H Cardiovascular status
H Complications
H Response to treatment
H Compliance with treatment

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the importance of completing the prescribed course
of therapy even after symptoms subside
H the importance of informing, testing, and treating
sexual partners
H the need to refrain from sexual activity until treat-
ment is completed and follow-up VDRL/RPR test re-
sults are normal
H information for patient and sexual partners about
HIV infection

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Systemic lupus Assessment

erythematosus History
H Onset acute or insidious; no characteristic clinical
pattern
Overview H Possible fever, anorexia, weight loss, malaise, fatigue,
abdominal pain, nausea, vomiting, diarrhea, consti-
Description pation, rash, and polyarthralgia
H A chronic inflammatory autoimmune disorder that H Possible drug history with one of 25 drugs that can
affects connective tissues cause SLE-like reaction
H Two forms: discoid lupus erythematosus (DLE) and H Irregular menstruation or amenorrhea, particularly
systemic lupus erythematosus (SLE) during flare-ups
H Only the skin affected by DLE H Chest pain and dyspnea
H Emotional instability, psychosis, organic brain syn-
Pathophysiology drome, headaches, irritability, and depression
H The body produces antibodies, such as antinuclear H Oliguria, urinary frequency, dysuria, and bladder
antibodies (ANAs), against its own cells. spasms
H The formed antigen-antibody complexes suppress the
bodys normal immunity and damage tissues. Physical findings
H Patients with SLE produce antibodies against many H Joint involvement that resembles rheumatoid arthritis
different tissue components, such as red blood cells H Raynauds phenomenon
(RBCs), neutrophils, platelets, lymphocytes, and al- H Skin eruptions provoked or aggravated by sunlight or
most any organ or tissue in the body. UV light
H Tachycardia, central cyanosis, and hypotension
Causes H Altered level of consciousness, weakness of the ex-
H Unknown tremities, and speech disturbances
H Predisposing factors: H Skin lesions
Stress H Butterfly rash over nose and cheeks
Streptococcal or viral infections H Patchy alopecia (common)
Exposure to sunlight or ultraviolet (UV) light H Vasculitis
Injury H Lymph node enlargement (diffuse or local and non-
Surgery tender)
Exhaustion H Pericardial friction rub
Emotional upsets
Immunization, pregnancy Test results
Abnormal estrogen metabolism Laboratory
H Complete blood count with differential shows anemia
Incidence and a reduced white blood cell (WBC) count, de-
H Affects females eight times more commonly than creased platelet count, and elevated erythrocyte sedi-
males (15 times more common during childbearing mentation rate; serum electrophoresis shows hyper-
years) gammaglobulinemia.
H Occurs worldwide; most prevalent among Asians and H ANA, anti-deoxyribonucleic acid, and lupus erythe-
Blacks matosus cell test findings are positive in most pa-
tients with active SLE, but these are only slightly use-
Common characteristics ful in diagnosing the disease. (ANA test is sensitive
H Recurrent seasonal remissions and exacerbations, but not specific for SLE.)
especially during spring and summer H Urine studies show RBCs, WBCs, urine casts, sedi-
ment, and significant protein loss (more than 3.5 g
Complications in 24 hours).
H Pleurisy H Blood studies demonstrate decreased serum comple-
H Pleural effusions ment (C3 and C4) levels, indicating active disease.
H Pericarditis, myocarditis, endocarditis (Leukopenia, mild thrombocytopenia, and anemia
H Coronary atherosclerosis are also seen during active disease.)
H Renal failure H C-reactive protein level is increased during flare-ups.
H Seizures and mental dysfunction H Rheumatoid factor is positive in 30% to 40% of pa-
tients.
Imaging
H Chest X-rays may disclose pleurisy or lupus pneu-
monitis.

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Diagnostic procedures H Institute seizure precautions if you suspect CNS in-

H Central nervous system (CNS) involvement may ac- volvement.
count for abnormal EEG results in about 70% of pa- H Warm and protect the patients hands and feet if she
tients, but brain scans and magnetic resonance imag- has Raynauds phenomenon.
ing may be normal in patients with SLE despite CNS H Support the patients self-image.
disease.
H Electrocardiography may show a conduction defect Monitoring
with cardiac involvement or pericarditis. H Signs and symptoms of organ involvement
H Renal biopsy shows progression of SLE and the ex- H Urine, stools, and GI secretions for blood
tent of renal involvement. H Scalp for hair loss and skin and mucous membranes
H Skin biopsy shows immunoglobulin and complement for petechiae, bleeding, ulceration, pallor, and
deposition in the dermal-epidermal junction in 90% bruising
of patients. H Response to treatment
H Complications
H Nutritional status
Treatment H Joint mobility
H Seizure activity
General
H Use of sunscreen with sun protection factor of at
least 15 Patient teaching
H No dietary restrictions unless renal failure occurs
H Regular exercise program Be sure to cover:
H the disorder, diagnosis, and treatment
Medications H ROM exercises and body alignment and postural
H Nonsteroidal anti-inflammatory drugs techniques
H Topical corticosteroid creams H ways to avoid infection, such as avoiding crowds and
H Fluorinated steroids people with known infections
H Antimalarials H the need to notify the physician if fever, cough, or
H Corticosteroids rash occurs or if chest, abdominal, muscle, or joint
H Cytotoxic drugs pain worsens
H Antihypertensives H the importance of eating a balanced diet
H Immunosuppressants, such as azathioprine and H medication administration, dosage, and possible ad-
cyclophosphamide verse effects
H the importance of good skin care
Surgery H the benefits of exercise
H Possible joint replacement H the importance of keeping regular follow-up appoint-
ments and contacting the physician if flare-ups occur
H the need to wear protective clothing and use a sun-
Nursing considerations screen
H how to perform meticulous mouth care.
Key outcomes
The patient will: Discharge planning
H express feelings of increased comfort and decreased H Arrange for a physical therapy and occupational ther-
pain apy consultation if musculoskeletal involvement com-
H express feelings of increased energy promises mobility.
H maintain joint mobility and range of motion (ROM) H Refer the patient to a rheumatology specialist if she
H maintain skin integrity becomes pregnant.
H maintain fluid balance.

Nursing interventions
H Provide a balanced diet.
H Provide bland, cool foods if the patient has a sore
mouth.
H Provide a mouth rinse of normal saline solution after
meals to assist healing of oral lesions.
H Apply heat packs to relieve joint pain and stiffness.
H Encourage regular exercise to maintain full ROM.
H Explain the expected benefit of prescribed drugs, and
watch for adverse effects.

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T Taeniasis
Overview
Description
H A parasitic infestation by Taenia saginata (beef tape-
worm), T. solium (pork tapeworm), Diphylloboth-
rium latum (fish tapeworm), or Hymenolepis nana
(dwarf tapeworm)
H Although usually a chronic, benign intestinal disease,
dangerous systemic and central nervous system
(CNS) symptoms possible if T. solium larvae invade
the brain or striated muscle of vital organs
H Particularly prevalent among institutionalized mental-
ly retarded children and in underdeveloped coun-
tries
Common characteristics
T. saginata
H Crawling sensation in the perianal area caused by
worm segments that have passed rectally
T. solium
H Seizures
H Headaches
H Personality changes
D. latum
H Anemia
H. nana
H Also called tapeworm disease and cestodiasis H Dependent on patients nutritional status and number
of parasites
Pathophysiology H Commonly no symptoms with mild infestation
H Gastric acid activates larvae, allowing them to ma- H With severe infestation, anorexia, diarrhea, restless-
ture, after ingestion of undercooked, bacteria- ness, dizziness, and apathy
infested beef or pork.
H Mature tapeworms fasten to the intestinal wall and Complications
produce ova that are passed in the feces. H Appendicitis
H A single tapeworm produces an average of 50,000 H Obstruction of bile ducts and pancreatic duct
eggs per day and may live 25 years.
Causes Assessment
T. saginata
H Uncooked or undercooked beef History
T. solium H Ingestion of raw or undercooked beef or pork
H Uncooked or undercooked pork H Occasionally, worm segments exiting through the
D. latum anus and appearing on bed clothes
H Uncooked or undercooked freshwater fish, such as H Increased hunger
pike, trout, salmon, and turbot H Weight loss
H. nana H Nausea
H No intermediate host H Abdominal pain (usually in the morning) relieved by
H Person-to-person transmission via ova passed in eating
stool H Pruritus ani

Risk factors Physical findings

H Handling or eating contaminated food H Weight loss
H Poor hygiene H Intraocular larvae
H Inadequate hand-washing facilities
Test results
Incidence Laboratory
T. saginata H Tapeworm ova or body segments are seen in feces
H Worldwide, but most prevalent in Europe and East (may require multiple specimens).
Africa
T. solium
H Incidence highest in Mexico and Latin America Treatment
H Lowest incidence among Muslims and Jews
D. latum General
H Most prevalent in Finland, parts of Russia, Japan, H Diet as tolerated
Alaska, Australia, the Great Lakes region of the Unit- H Activity as tolerated
ed States, Switzerland, Chile, and Argentina
H. nana Medications
H Most common tapeworm in humans H Anthelmintics
H High-dose glucocorticosteroids

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ALERT
During treatment for T. solium, other health-related
measures, such as laxative use and induced vomit-
ing, are contraindicated because of the danger of
autoinfection and systemic disease.

Surgery
H Possible if complications develop

Nursing considerations
Key outcomes
The patient will:
H express understanding of illness
H exhibit no signs of infection
H regain or maintain optimal weight.

Nursing interventions
H Dispose of the patients excretions carefully. Wear
gloves when giving personal care and handling fecal
excretions, bedpans, and bed linens; wash your
hands thoroughly and instruct the patient to do the
same.
H Tell the patient not to consume anything after mid-
night on the day niclosamide therapy begins because
the drug must be taken on an empty stomach. After
administering the drug, document passage of strobi-
lae.
Monitoring
H Stool specimens
H Daily weight
H Response to treatment

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H expected response to treatment
H preventing reinfection by washing hands thoroughly
and cooking meat and fish thoroughly.
Discharge planning
H After drug treatment, all types of tapeworm infesta-
tion require a follow-up laboratory examination of
stool specimens during the next 3 to 5 weeks to
check for any remaining ova or worm segments.
H Persistent infestation typically requires a second
course of medication.

Taeniasis 799
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Life-threatening disorder Assessment

History
Tay-Sachs disease H Familial history of Tay-Sachs disease
H Normal appearance at birth (but with possible exag-
gerated Moros reflex)
Overview H Onset of clinical signs and symptoms between ages 5
and 6 months
Description H Progressive deterioration
H Lipid storage disease that results from a congenital H Psychomotor retardation
enzyme deficiency H Blindness
H Leads to progressive mental and motor deterioration H Dementia
H Always fatal, usually before age 5
H Rare form occurs in patients between ages 20 and 30 Physical findings
H No known cure H In 3- to 6-month-old infant:
Apathetic appearance
Pathophysiology Augmented response to loud sounds
H In this autosomal recessive disorder, the enzyme hex- Progressive weakness of the neck, trunk, arm, and
osaminidase A is absent or deficient. leg muscles that prevents child from sitting up or
H Without hexosaminidase A, lipid pigments (ganglio- lifting head
side GM2) accumulate and progressively destroy and Difficulty turning over
demyelinate central nervous system cells. Inability to grasp objects
H The juvenile form typically appears between ages 2 Progressive vision loss
and 5 as a progressive deterioration of psychomotor H By age 18 months:
skills and gait. Possible seizures
Generalized paralysis
Causes Spasticity
H Autosomal recessive disorder Blindness
Holding eyes wide open and rolling eyeballs
Incidence Pupils always dilated
H Affects fewer than 100 infants born yearly in the Unit- Decerebrate rigidity
ed States Complete vegetative state
H About 100 times more common (about 1 in 3,600 Head circumference possibly showing enlarge-
live births) in those with Ashkenazic Jewish ancestry ment
than in the general population Pupils nonreactive to light
H About 1 in 30 Ashkenazi Jews, French Canadians, and Ophthalmoscopic examination possibly showing
American Cajuns heterozygous carriers of gene for optic nerve atrophy and a distinctive cherry-red
this disorder spot on the retina
H In a child who survives bouts of recurrent broncho-
Common characteristics pneumonia: possible ataxia and progressive motor
H Progressive mental and motor deterioration retardation between ages 2 and 8 years
H Blindness
H Deafness Test results
H Inability to swallow Laboratory
H Cherry-red spot on the retina H Serum analysis shows deficient hexosaminidase A.
H Amniocentesis or chorionic villus sampling allows
Complications prenatal diagnosis of hexosaminidase A deficiency.
H Recurrent bronchopneumonia
H Dementia
H Blindness Treatment
H Seizures
H Paralysis General
H Death, usually before age 5 H Supportive care
H Suctioning
H Postural drainage to remove secretions
H Meticulous skin care
H Tube feedings with nutritional supplements

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H Activity as tolerated
H Active and passive range-of-motion exercises

Medications
H Mild laxatives
H Anticonvulsants

Nursing considerations
Key outcomes
The patient (or family, if appropriate) will:
H avoid complications
H maintain a patent airway
H express understanding of the disease process and
treatment regimen
H seek outside sources to assist with coping and adjust-
ing to the patients situation.
Nursing interventions
H Help the patients family deal with progressive illness
and death.
H Prevent skin breakdown.
H Provide adequate nutrition.
H Maintain a patent airway.
H Implement seizure precautions.
H Administer prescribed drugs.
H Stress the importance of amniocentesis in future
pregnancies.
Monitoring
H Vital signs
H Intake and output
H Respiratory status
H Nutritional status
H Neurologic status
H Response to treatment

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H how to perform suctioning when needed
H how to perform postural drainage
H how to give tube feedings
H need for proper skin care to prevent breakdown.

Discharge planning
H Refer the parents for genetic counseling.
H Refer the parents to the National Tay-Sachs and Allied
Diseases Association.
H Refer the parents for psychological counseling if in-
dicated.
H Refer the siblings for screening to determine whether
theyre carriers.
H If the siblings are adult carriers, refer them for ge-
netic counseling; stress that the disease isnt trans-
mitted to offspring unless both parents are carriers.

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Common characteristics
Temporomandibular H Pain, stiffness, and tenderness in jaw muscles, face,

joint disease or neck

H Headache
H Earache
H Painful clicking or popping over the TMJ
Overview H Limitation of mandibular movement or locking of jaw
H Malalignment of upper and lower teeth
Description
H Disorder of the temporomandibular joint (TMJ), Complications
which connects the jaw to the skull H Secondary degenerative joint disease
H Includes several conditions that cause tenderness H Chronic TMJ dislocation
and pain in the TMJ, including: H Loss of joint range of motion
Muscle tension and spasm H Depression
Psychological stress H Chronic pain syndromes
Degenerative joint disease
Internal joint derangement
Assessment
Pathophysiology
H Lower jaw has rounded ends called condyles that History
glide in and out of the joint socket with movement of H Complaints of jaw pain
the jaw. H Jaw injury
H Surfaces of the condyles and socket of the temporal H Recent dental treatments
bone are covered with cartilage and separated by a H Psychological stress
small disk, which absorbs shock and keeps the
movement smooth. Physical findings
H Displacement of the disc causes pressure on and H Pain or tenderness without jaw movement; worsens
stretching of sensory nerves, especially the trigeminal with jaw movement
nerve, causing pain. H Limited jaw opening
H Popping or clicking occurs when the disk snaps into H Facial muscle spasm
place with jaw movement. H Unilateral facial swelling
H Chronic malposition of the disc and persistent wear H Clicking or popping in the TMJ
on the cartilage lining causes further damage. H Tenderness to palpation
H Crepitus over joint
Causes H Excessive wear patterns on teeth
H Synovitis
H Disc derangement Test results
H Hypermobile TMJ Imaging
H Bruxism H Videoarthrography shows abnormal jaw motion.
H Muscle spasm H Panoramic dental X-rays show abnormal wear.
H Trauma H Computed tomography scan shows altered bone
H Poorly fitting dentures structure.
H Poor posture of the head, neck and shoulders H Magnetic resonance imaging aids in treatment op-
H Hereditary conditions affecting the structures of the tions.
joint
Risk factors Treatment
H Chronic oral habits, such as clenching or grinding
the teeth General
H Osteoarthritis and rheumatoid arthritis H Jaw rest
H Dental malocclusion H Heat therapy
H Fibrositis H Correction of malocclusion with orthodontic appli-
H Psychosocial stress ance
H Stress reduction
Incidence H Behavior modification to eliminate tension-relieving
H Estimated that over 10 million Americans affected oral habits
H More common in females than in males H Soft diet to reduce chewing
H Most common between ages 30 and 50

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Medications
H Anti-inflammatories
H Muscle relaxants
H Analgesics
H Botulinum toxin

Surgery
H Possibly, a procedure to correct disc displacement or
replace a damaged disc

Nursing considerations
Key outcomes
The patient will:
H experience relief or decrease in pain
H verbalize an understanding of the condition
H express understanding of measures for relief of
symptoms
H comply with the treatment plan.

Nursing interventions
H Help identify the underlying cause.
H Help the patient identify risk factors.
H Assist the patient with the proper use of malocclusion
orthodontic appliances.
H Help the patient identify triggers for stress.
H Refer the patient to a behavior-modification program
for stress.
H Incorporate stress-reduction techniques.
H Encourage the patient to frequently rest the jaw.
H Apply heat to affected area.

Monitoring
H Compliance with therapeutic plan
H Response to treatment

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medication administration, dosage, and possible ad-
verse effects
H use of orthodontic appliances
H stress management
H avoidance of clenching or grinding teeth
H diagnostic studies
H consumption of a soft diet to reduce chewing
H avoidance of wide yawning.

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Incidence
Tendinitis and bursitis H More common in elderly people
H Common in those performing activities that over-
stress a tendon or repeatedly stress a joint
Overview
Common characteristics
Description H Localized pain
Tendinitis H Interrupted sleep
H Inflammation affecting the tendons and tendon- H Limited movement
muscle attachments H Crepitus over involved area
H Most common sites: H Swelling over involved area
Shoulder rotator cuff
Hip Complications
Achilles tendon H Scar tissue with subsequent disability
Hamstring
Elbow
Bursitis Assessment
H Painful inflammation of one or more bursae
H Most common sites: History
Subdeltoid Tendinitis
Subacromial H Traumatic injury or strain from athletic activity
Olecranon H Concurrent musculoskeletal disorder
Trochanteric H Palpable tenderness over the affected site
Calcaneal H Referred tenderness in the related segment
Prepatellar H Shoulder:
H May be septic, calcific, acute, or chronic Localized pain; most severe at night
Pain usually interfering with sleep
Pathophysiology Pain aggravated by heat
Tendinitis H Elbow: pain when grasping objects or twisting the
H Inflammation causes localized pain around the elbow
affected area. H Hamstring: pain in the posterolateral aspect of the
H Joint movement is restricted. knee
H Swelling results from fluid accumulation. H Foot: pain over the Achilles tendon and on dorsi-
H Calcium deposits form in and around the tendon. flexion
H Further swelling and immobility result. Bursitis
Bursitis H Unusual strain or injury 2 to 3 days before pain
H Bursae sacs hold lubricating synovial fluid. began
H Inflammation causes gradual pain and limits joint H Pain that develops suddenly or gradually
motion. H Pain that may limit movement
H Work or leisure activity that may involve repetitive
Causes action
Tendinitis
H Trauma (such as a strain during sports activity) Physical findings
H Musculoskeletal disorders (rheumatic diseases and Tendinitis
congenital defects) H Shoulder: restricted shoulder movement (especially
H Postural malalignment abduction)
H Abnormal body development H Elbow: tenderness over the lateral epicondyle
H Hypermobility in calcific tendinitis H Hamstring: palpable tenderness when knee flexed at
Bursitis a 90-degree angle
H Recurring trauma from an inflammatory joint disease H Foot: crepitus when the patient moves his foot
H Common stressors: Bursitis
Repetitive kneeling H Tenderness over the affected site
Jogging in worn-out shoes on hard asphalt sur- H Swelling with severe bursitis
faces
Prolonged sitting with crossed legs on hard sur- Test results
faces Laboratory
H Septic bursitis: wound infection or bacterial invasion H Various serum and urine test results rule out other
(see Anatomy of tendons and bursae) disorders.
Imaging
H X-rays in tendinitis may show bony fragments, osteo-
phyte sclerosis, or calcium deposits.

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Anatomy of tendons and bursae

Tendons, like stiff rubber bands, hold the muscles in place and enable them to move the bones. Bursae are located at friction
points around joints and between tendons, cartilage, or bone. Bursae keep these body parts lubricated so they move freely.

SHOULDER JOINT

Clavicle

Acromioclavicular joint

Subacromial bursa

Humerus

Subscapularis muscle
Biceps tendons

H X-rays in calcific bursitis may show calcium deposits Nursing interventions

in the joint. H Apply cold or heat therapies, as ordered.
H Arthrography is usually normal in tendinitis with mi- H Promote self-care.
nor irregularities on the tendon under the surface. H Administer drug therapy.
Diagnostic procedures H Encourage use of active ROM exercises.
H Arthrocentesis may identify causative microorgan-
isms and other causes of inflammation. Monitoring
H Severity and pattern of pain
H Response to treatment
Treatment H ROM

General
H Cold, heat, or ultrasound applications Patient teaching
H No dietary restrictions
H Resting the affected joint Be sure to cover:
H Range-of-motion (ROM) exercises H the disorder, diagnosis, and treatment
H how to minimize GI distress caused by NSAIDs
Medications H medication administration, dosage, and possible
H Nonsteroidal anti-inflammatory drugs (NSAIDs) adverse effects
H Local anesthetics H activities that promote rest and relaxation
H Corticosteroids H strengthening exercises
H Oral anti-inflammatories H the prescribed exercise regimen
H Short-term analgesics H need for proper sports equipment, shoes, and play-
ing surfaces
H use of cushioned shoes
Nursing considerations H application of cold packs
H proper body mechanics.
Key outcomes
The patient will: Discharge planning
H have increased comfort and decreased pain H Refer the patient to a weight-management program,
H maintain joint mobility and ROM as appropriate.
H perform activities of daily living
H express understanding of the treatment regimen and
disease process.

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Testicular cancer H Metastasis

H Ureteral obstruction

Overview Assessment
Description History
H Proliferation of cancerous cells in the testicles H Previous injury to the scrotum
H Most originating from germinal cells and about 40% H Viral infection (such as mumps)
becoming seminomas H Use of DES or other estrogen-progestin drugs by the
H Prognosis dependent on cancer cell type and stage patients mother during pregnancy
(with treatment, a more than 5-year survival rate) H Feeling of heaviness or a dragging sensation in the
scrotum
Pathophysiology H Weight loss (late sign)
H Testicular cancer spreads through the lymphatic sys- H Fatigue and weakness (late sign)
tem to the iliac, para-aortic, and mediastinal nodes.
H Metastasis affect the lungs, liver, viscera, and bone. Physical findings
H Enlarged testes
Causes H Gynecomastia
H Exact cause unknown H Lethargic, thin, and pallid appearance (later stages)
H Palpable firm, smooth testicular mass
Risk factors H Enlarged lymph nodes in surrounding areas
H Cryptorchidism (see Cryptorchidism and testicular
cancer) Test results
H Mumps orchitis Laboratory
H Inguinal hernia in childhood H Elevated levels of the proteins (tumor markers)
H Maternal use of diethylstilbestrol (DES) or other human chorionic gonadotropin (HCG) and alpha-
estrogen-progestin combinations during pregnancy fetoprotein (AFP) suggest testicular cancer and
can differentiate a seminoma from a nonseminoma.
Incidence H Elevated HCG and AFP levels indicate a nonsemi-
H Most common in males ages 20 to 40 noma.
H Rare in nonwhite males H Elevated HCG and normal AFP levels indicate a semi-
H Accounts for less than 1% of all male cancer deaths noma.
H Rare in children Diagnostic procedures
H Biopsy confirms the diagnosis and can be used to
Common characteristics stage the disease.
H Fullness of testes H Scrotal ultrasound shows the tumor.
H Lump in testes

Complications Treatment
H Back or abdominal pain from retroperitoneal
adenopathy General
H Varies with tumor cell type and stage
H Radiation therapy
Cryptorchidism and testicular cancer H Autologous bone marrow transplantation for patients
In males with cryptorchidism (the failure of a testicle to nonresponsive to standard therapy
descend into the scrotum), testicular tumors are about 50 H Well-balanced diet
times more common than in males with normal anatomic
structure. A simple surgical procedure, called orchiopexy,
Medications
can bring the testicle to its normal position in the scrotum H Chemotherapy
and reduce the testicular cancer risk. Nevertheless, testic- H Hormonal therapy
ular tumors occur more commonly in a surgically de-
scended testicle than in a naturally descended one. Surgery
What happens in orchiopexy H Orchiectomy and retroperitoneal node dissection
In orchiopexy, the surgeon incises the groin area and sep-
arates the testicle and its blood supply from surrounding
abdominal structures. Then he creates a tunnel into the
scrotum to accommodate the descent of the testicle.
Reducing the risk further
After orchiopexy, urge the patient to examine his testicles
monthly to detect a tumor at its earliest stage.

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Nursing considerations
Key outcomes
The patient will:
H express positive feelings about himself
H report feeling less tension or pain
H avoid or minimize complications
H voice understanding of treatment
H express feelings and perceptions about change in
sexual performance.
Nursing interventions
H Encourage verbalization and provide support.
H Administer drug therapy.
H Apply an ice pack to the scrotum.

Monitoring
H Wound site
H Vital signs
H Hydration and nutritional status
H Pain control
H Effects of medication
H Postoperative complications

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H reassurance that infertility and impotence usually
dont follow unilateral orchiectomy
H sperm-banking procedures before the patient begins
treatment, especially if infertility and impotence may
result from surgery
H testicular self-examination.

Discharge planning
H Refer the patient to available resource and support
services.

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Incidence
Testicular torsion H Most common between ages 12 and 18, but may oc-
cur at any age
H Occurs in 1 in 4,000 males younger than age 25
Overview
Common characteristics
Description H Excruciating pain in the affected testis or iliac fossa
H An abnormal twisting of the spermatic cord caused
by rotation of a testis or the mesorchium (a fold in Complications
the area between the testis and epididymis) H Loss of testicle
H Causes strangulation and eventual infarction of the H Infarction of testicle
testis if untreated H Infection
H 90% of cases unilateral H Infertility

Pathophysiology
H Normally, the tunica vaginalis envelops the testis and Assessment
attaches to the epididymis and spermatic cord.
H In intravaginal torsion (the most common type of tes- History
ticular torsion in adolescents), testicular twisting H Previous episodes of intermittent testicular pain that
may result from an abnormality of the tunica, in resolved spontaneously
which the testis is abnormally positioned, or from a H Sudden scrotal pain
narrowing of the mesentery support. H Nausea and vomiting
H In extravaginal torsion (most common in neonates), H Abdominal pain
loose attachment of the tunica vaginalis to the scrotal H Fever
lining causes spermatic cord rotation above the
testis. A sudden forceful contraction of the cremaster Physical findings
muscle may precipitate this condition. (See Extra- H Scrotal swelling
vaginal torsion.) H Painful testicle
H Horizontal lie of the testicle
Causes H Scrotal erythema
H Congenital anomaly H Ipsilateral loss of the cremasteric reflex
H Trauma
H Sexual activity Test results
H Undescended testicle Diagnostic procedures
H Exercise H Doppler ultrasonography helps distinguish testicular
torsion from strangulated hernia, undescended
testes, or epididymitis.
Extravaginal torsion
In extravaginal torsion, rotation of the spermatic cord
above the testis causes strangulation and, eventually,
Treatment
infarction of the testis.
General
H Manual detorsion
H Nothing by mouth before surgery; diet as tolerated
after surgery
H Activity as tolerated after surgery

Spermatic Medications
cord rotation
H Analgesics

Surgery
H Immediate surgical repair by orchiopexy (fixation of
a viable testis to the scrotum) or orchiectomy (exci-
Mesorchium
sion of a nonviable testis); as with ovarian torsion in
the female, preservation of the organ preferred
Testis

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Nursing considerations
Key outcomes
The patient will:
H report increased comfort and decreased pain
H express understanding of condition and treatment
H develop no complications.

Nursing interventions
H Promote the patients comfort before and after
surgery.
H After surgery, administer drugs for pain.
H Apply an ice bag with a cover to reduce edema.
H Protect the wound from contamination.

Monitoring
H Voiding
H Scrotal swelling
H Pain control

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H wound care.

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H Cardiac arrhythmias
Life-threatening disorder H Rhabdomyolysis
H Death

Tetanus
Overview
Description
H An acute exotoxin-mediated infection
H Usually systemic, but possibly localized
H Up to 60% fatal in unimmunized patients
H Also known as lockjaw
Pathophysiology
H After the organism enters the body, local infection
and tissue necrosis result.
H Toxins enter the bloodstream and lymphatics, eventu-
ally spreading to central nervous system tissue.
H The incubation period is 3 to 21 days.
Causes
H Anaerobic, spore-forming, gram-positive bacillus
Clostridium tetani
H Transmission through puncture wounds, burns, or
minor wounds contaminated by soil, dust, or animal
excreta containing C. tetani
Assessment
History
H Inadequate immunization
H Recent wound or burn
H Pain or paresthesia at the site of injury
H Complaints of difficulty chewing or swallowing food,
drooling
Physical findings
H Spasm and increased muscle tone near the wound
(local infection)
H Irregular heartbeat and tachycardia
H Marked muscle hypertonicity
H Hyperactive deep tendon reflexes
H Profuse sweating, low-grade fever
H Painful, involuntary muscle contractions
H Rigid neck and facial muscles, resulting in lockjaw
(trismus) and a grotesque, grinning expression (ris-
us sardonicus)
H Rigid somatic muscles causing arched-back rigidity
(opisthotonos)
H Intermittent tonic seizures

Risk factors Test results

H Participating in outdoor sports or occupations Laboratory
H Exposure to animal feces H Blood cultures and tetanus antibody tests are nega-
H Gardening tive.
H Wound culture is positive in one-third of patients.
Incidence H Cerebrospinal fluid (CSF) pressure is increased.
H Occurs worldwide, but more prevalent in agricultural Diagnostic procedures
regions and developing countries that lack mass im- H Lumbar puncture (spinal tap) may show elevated CSF
munization programs pressure.
H One of the most common causes of neonatal deaths
in developing countries
H In the United States, about 110 cases each year, all Treatment
in patients not immunized or whose immunization
expired General
H About 75% of cases between April and September H Airway maintenance
H Enteral or parenteral feeding
Common characteristics H Bed rest until recovery
H Usually, a normal body temperature or a slight fever
in the early stages; fever possibly increasing as the Medications
disease progresses H Tetanus immune globulin
H Despite pronounced neuromuscular symptoms, nor- H Tetanus antitoxin
mal cerebral and sensory function H Tetanus toxoid immunization
H Muscle relaxants
Complications H Neuromuscular blockers
H Pneumonia H Antibiotics
H Airway obstruction
H Respiratory arrest
H Heart failure
H Fractures

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Nursing considerations
Key outcomes
The patient will:
H maintain adequate fluid balance
H express feelings of increased comfort and decreased
pain
H maintain tissue perfusion and cellular oxygenation
H have a patent airway and adequate ventilation
H show no signs of neurologic compromise.

Nursing interventions
H Debride and clean the injury site.
H Check the immunization history.
H Maintain an adequate airway and ventilation.
H Keep emergency airway equipment on standby.
H Administer I.V. therapy as prescribed.
H Minimize stimulation.
H Perform range-of-motion exercises.

Monitoring
H Response to treatment
H Fluid and electrolyte status
H Respiratory status
H Cardiovascular status
H Injury site
H Complications
H Deep tendon reflexes
H Muscle tone

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the importance of getting a booster dose of tetanus
toxoid every 10 years
H the need for tetanus prophylaxis in case of a skin
injury or burn
H the need to avoid external stimulation (evokes
muscle spasms) and to keep the room dark and
quiet.

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Tetralogy of Fallot Assessment

History
Overview H Blue spells
H Diminished exercise tolerance
Description H Increasing dyspnea on exertion
H A combination of four cardiac defects: ventricular H Growth retardation
septal defect (VSD); right ventricular outflow tract H Eating difficulties
obstruction (pulmonary stenosis); right ventricular
hypertrophy; and dextroposition of the aorta, with Physical findings
overriding of the VSD H Clubbing
H Cyanosis
Pathophysiology H Dyspnea on exertion
H Blood shunts right to left through the VSD, permitting H Loud systolic heart murmur (best heard along the
unoxygenated blood to mix with oxygenated blood, left sternal border), which may diminish or obscure
resulting in cyanosis. the pulmonic component of S2
H Condition sometimes coexists with other congenital H Cardiac thrill at the left sternal border and an obvi-
heart defects, such as patent ductus arteriosus or ous right ventricular impulse
atrial septal defect. H Prominent inferior sternum

Causes Test results

H Unknown Laboratory
H Associated with fetal alcohol syndrome and thalido- H Arterial oxygen saturation is diminished.
mide use during pregnancy H Polycythemia is present. (Hematocrit may be more
than 60%.)
Risk factors Imaging
H Maternal viral illness during pregnancy H Chest X-rays may demonstrate decreased pulmonary
H Poor prenatal nutrition vascular marking, depending on the severity of the
H Maternal age older than 40 pulmonary obstruction, and a boot-shaped cardiac
H History of tetralogy of Fallot in parent silhouette.
H Down syndrome H Echocardiography identifies septal overriding of the
aorta, the VSD, and pulmonary stenosis, and detects
Incidence the hypertrophied walls of the right ventricle.
H Accounts for about 10% of all congenital heart Diagnostic procedures
diseases H Electrocardiography shows right ventricular hyper-
H Occurs equally in males and females trophy, right axis deviation and, possibly, right atrial
hypertrophy.
Common characteristics H Cardiac catheterization confirms the diagnosis by
H Cyanosis showing pulmonary stenosis, the VSD, and the over-
H Blue spells, which are characterized by dyspnea; riding aorta and ruling out other cyanotic heart
deep, sighing respirations; bradycardia; fainting; defects.
seizures; and loss of consciousness
H Children squat following exertion (increases blood
flow to lungs) Treatment
Complications General
H Cerebral abscesses H Prevention and treatment of complications
H Pulmonary thrombosis H During cyanotic spells, knee-chest position and ad-
H Venous thrombosis ministration of oxygen and morphine to improve
H Cerebral embolism oxygenation
H Infective endocarditis
H In females with tetralogy of Fallot living to childbear- Medications
ing age, increased risk of spontaneous abortion, pre- H Beta-adrenergic blockers
mature births, and low birth weight H Prophylactic antibiotics

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Surgery
H Palliative surgery: performed on infants with poten-
tially fatal hypoxic spells (The goal of surgery is to
enhance blood flow to the lungs to reduce hypoxia;
this is commonly accomplished by joining the sub-
clavian artery to the pulmonary artery [Blalock-
Taussig procedure].)
H Complete corrective surgery: relieves pulmonary
stenosis and closes the VSD, directing left ventricular
outflow to the aorta

Nursing considerations
Key outcomes
The patient and family will:
H maintain hemodynamic stability
H foster improved cardiac blood flow
H express understanding of condition and treatment.

Nursing interventions
H Provide postoperative care.
H Administer drug therapy.
H Explain the disorder and its treatment to the patients
parents. Inform them that their child will set his own
exercise limits and will know when to rest.
Monitoring
H Vital signs
H Blue spells
H Oxygenation levels
H Intake and output

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H how to recognize serious hypoxic spells, which can
cause dramatically increased cyanosis; deep, sighing
respirations; and loss of consciousness
H preventing infective endocarditis and other infec-
tions, and keeping the child away from people with
infections
H following good dental hygiene, and watching for ear,
nose, and throat infections and dental caries, all of
which require immediate treatment
H medication administration, dosage, and possible
adverse effects.
Discharge planning
H Refer the patient and family to support and social
services.
H Refer parents to genetic counseling as needed.

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Thalassemia In alpha-thalassemia
H Four forms exist:
Alpha trait (the carrier trait), in which a single
alpha-chain-forming gene is defective
Overview Alpha-thalassemia minor, in which two genes are
defective
Description Hemoglobin H disease, in which three genes are
H A group of genetic disorders characterized by defec- defective
tive synthesis in one or more of the polypeptide Alpha-thalassemia major, in which all four alpha-
chains needed for hemoglobin production chain-forming genes are defective; death is in-
H Most commonly occurring as a result of reduced or evitable because alpha chains are absent and
absent production of alpha or beta chains oxygen cant be released to the tissues
H Affects hemoglobin production and impairs red
blood cell (RBC) synthesis Causes
H Inherited autosomal recessive disorder
Pathophysiology
In beta-thalassemia Incidence
H The fundamental defect is the uncoupling of alpha- H Second most common cause of microcytic anemia
and beta-chain synthesis. H Alpha-thalassemia more common in Blacks and
H Beta-chain production is depressed moderately in Asians
beta-thalassemia minor and severely in beta- H Beta-thalassemia more common in Mediterranean
thalassemia major (also called Cooleys anemia). populations
H Depression of beta-chain synthesis results in erythro-
cytes with reduced hemoglobin and accumulations of Common characteristics
free-alpha chains. H Anemia
H The free-alpha chains are unstable and easily precip-
itate in the cell; most erythroblasts that contain pre- Complications
cipitates are destroyed by mononuclear phagocytes H Iron overload from RBC transfusions
in the marrow, resulting in ineffective erythropoiesis H Pathologic fractures
and anemia. H Cardiac arrhythmias
H Some precipitate-carrying cells mature and enter the H Liver failure
bloodstream but are destroyed prematurely in the H Heart failure
spleen, resulting in mild hemolytic anemia. H Death

Assessment
Skull changes in thalassemia major
History
This illustration of an X-ray shows a characteristic skull
H Severity of anemia and symptoms range from mild to
abnormality in thalassemia major: diploetic fibers extend-
ing from internal lamina and resembling hair standing on severe:
end. Fatigue
Shortness of breath
Headache
Angina
Physical findings
H Pallor or bronze appearance
H Dyspnea on exertion
H Splenomegaly
H Hepatomegaly
H Tachycardia
H Systolic murmur (in moderate or severe anemia)

Test results
Laboratory
H Complete blood count shows decreased hemoglobin,
hematocrit, and mean corpuscular volume.
H Serum iron level is normal or increased.
H Serum ferritin level is normal or increased.
H Total iron-binding capacity is normal.

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H Reticulocyte count is normal or increased.

H Hemoglobin electrophoresis shows decreased alpha-
or beta-hemoglobulin chains.
Imaging
H In thalassemia major, X-rays of the skull and long
bones show thinning and widening of the marrow
space because of overactive bone marrow. Long
bones may show areas of osteoporosis. The pha-
langes may also be deformed (rectangular or bicon-
vex). The bones of the skull and vertebrae may ap-
pear granular. (See Skull changes in thalassemia
major.)
Treatment
General
H No treatment for mild or moderate forms
H Iron supplements contraindicated in all forms
H Avoidance of iron-rich foods
H Avoidance of strenuous activities
Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the importance of good nutrition
H signs and symptoms of iron overload
H follow-up care
H with the parents of a young patient, various options
for healthy physical and creative outlets. Such a child
must avoid strenuous athletic activity. Reassure the
parents that the child may be allowed to participate
in less stressful activities.
Discharge planning
H Refer the patient to a hematologist.
H Refer the patient for genetic counseling.

Medications
H Transfusions of packed RBCs
H Chelation therapy, such as desferal and exjade

Surgery
H Splenectomy
H Bone marrow transplantation

Nursing considerations
Key outcomes
The patient will:
H develop no arrhythmias
H remain hemodynamically stable
H demonstrate age-appropriate skills and behaviors to
the extent possible.
Nursing interventions
H Administer blood transfusions, and watch for adverse
reactions.
H Provide an adequate diet, and encourage oral fluid
intake.
H Provide emotional support to help the patient and
family cope with the chronic nature of the illness and
the need for lifelong transfusions.
Monitoring
H Transfusion reaction
H Signs and symptoms of iron overload
H Complications
H Cardiac arrhythmias
H Anemia symptom severity
H Response to treatment

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Physical findings
Thrombocytopenia H Petechiae and ecchymoses, along with slow, continu-
ous bleeding from any injuries or wounds
H In adults, blood-filled bullae in the mouth
Overview
Test results
Description Laboratory
H A deficient number of circulating platelets H Platelet count is diminished to less than 100,000/l
H The most common cause of hemorrhagic disorders in adults.
H Bleeding time is prolonged.
Pathophysiology H Prothrombin and partial thromboplastin times are
H Lack of platelets can cause inadequate hemostasis. normal.
H Four mechanisms are responsible: decreased platelet Diagnostic procedures
production, decreased platelet survival, pooling of H In severe thrombocytopenia, a bone marrow study
blood in the spleen, and intravascular dilation of cir- shows the number, size, and cytoplasmic maturity of
culating platelets. the megakaryocytes (bone marrow cells that release
H Megakaryocytes are giant cells in bone marrow that mature platelets); study may show ineffective platelet
produce the marrow. Platelet production decreases production as the cause of thrombocytopenia and be
when the number of megakaryocytes is reduced or used to rule out a malignant disease process.
when platelet production becomes dysfunctional.
Causes Treatment
H May be congenital or acquired
H Decreased or defective platelet production in the General
bone marrow H Removal of the offending agents in drug-induced
H Increased platelet destruction outside the marrow thrombocytopenia
caused by an underlying disorder (such as cirrhosis H Well-balanced diet
of the liver, disseminated intravascular coagulation, H Rest periods between activities
or severe infection) H During active bleeding, strict bed rest
H Sequestration (hypersplenism, hypothermia) or
platelet loss Medications
H Transient occurrence after a viral infection (such as H Platelet transfusions
Epstein-Barr virus) or infectious mononucleosis H Corticosteroids
H Immune globulin
Incidence H Immunosuppressants, such as cyclophosphamide
H Acquired form more common and azathioprine
Common characteristics Surgery
H Sudden onset of petechiae or ecchymoses on skin H Splenectomy
H Bleeding into any mucous membrane

Complications Nursing considerations

In severe thrombocytopenia
H Hemorrhage Key outcomes
H Death The patient will:
H incur no injury
H experience no fever, chills, or other signs or symp-
Assessment toms of illness
H demonstrate use of protective measures, energy con-
History servation, a balanced diet, and adequate rest
H Sudden onset of petechiae and ecchymoses or bleed- H demonstrate effective coping skills.
ing into mucous membranes (GI, urinary, vaginal, or
respiratory) Nursing interventions
H Malaise, fatigue, and general weakness (with or with- H Provide emotional support.
out accompanying blood loss) H Provide rest periods between activities.
H In acquired thrombocytopenia, possible use of one H Provide a stool softener if necessary.
or several offending drugs H Protect all areas of ecchymosis and petechiae from
H Menorrhagia further injury.
H Take precautions against bleeding; protect the patient
from trauma.

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9400T.qxd 8/2/12 4:50 PM Page 817

H Avoid invasive procedures.

H During active bleeding, maintain strict bed rest; keep
the head of the bed elevated.
Monitoring
H Daily platelet count
H Bleeding
H Ecchymoses and petechiae
H Occult blood in stool, urine, and emesis
H During corticosteroid therapy, fluid and electrolyte
balance and signs and symptoms of infection, patho-
logic fractures, and mood changes

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H how to recognize and report signs of intracranial
bleeding and other signs of bleeding
H avoidance of straining with stools and coughing, both
of which can lead to increased intracranial pressure
H the function of platelets
H in severe thrombocytopenia, an understanding that
even minor bumps or scrapes may result in bleeding
H how to control local bleeding
H if thrombocytopenia is drug-induced, the importance
of avoiding the offending drug
H if the patient must receive long-term corticosteroid
therapy, the need to watch for and report cushingoid
symptoms and to discontinue corticosteroids gradu-
ally
H avoidance of aspirin in any form as well as other
drugs that impair coagulation
H if the patient experiences frequent nosebleeds, using
a humidifier at night
H how to examine the skin for ecchymoses and pe-
techiae
H how to test stools for occult blood
H the importance of wearing medical identification
jewelry.

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Causes
Thrombophlebitis H Inflammation due to a blood clot

Risk factors
Overview H May be idiopathic
H Prolonged bed rest
Description H Trauma
H Development of a thrombus that may cause vessel oc- H Surgery
clusion or embolization H Pregnancy and childbirth
H An acute condition characterized by inflammation H Hormonal contraceptives or replacement therapy
and thrombus formation such as estrogens
H May occur in deep or superficial veins (see Major H Neoplasms
venous pathways of the leg) H Fracture of the spine, pelvis, femur, or tibia
H Typically occurs at the valve cusps because venous H Venous stasis
stasis encourages accumulation and adherence of H Venulitis
platelet and fibrin H Family history of clotting disorder
H Smoking
Pathophysiology H Obesity
H Alteration in epithelial lining causes platelet aggrega-
tion and fibrin entrapment of red blood cells, white Incidence
blood cells, and additional platelets. H Increasing with the use of subclavian vein catheters
H The thrombus initiates a chemical inflammatory H Risk for developing deep vein thrombophlebitis dra-
process in the vessel epithelium that leads to fibrosis, matically increased after age 40
which may occlude the vessel lumen or embolize.
Common characteristics
H Tenderness, erythema, and warmth over affected area
H Swelling of affected leg
Major venous pathways of the leg
Thrombophlebitis can occur in any leg vein. It most com-
Complications
monly occurs at valve sites. H Pulmonary embolism
H Chronic venous insufficiency
Inferior vena cava
Common iliac
Assessment
External iliac

Common femoral
History
Internal iliac
H Asymptomatic in up to 50% of patients with deep vein
Deep femoral thrombophlebitis
Superficial femoral H Possible tenderness, aching, or severe pain in the af-
Greater saphenous
fected leg or arm; fever, chills, and malaise
Popliteal Physical findings
H Redness, swelling, and tenderness of the affected leg
Lesser saphenous
or arm
Communicating H Possible positive Homans sign
(perforator) H Positive cuff sign
H Possible warm feeling in affected leg or arm
H Lymphadenitis in case of extensive vein involvement

Test results
Posterior tibial
Diagnostic procedures
H Doppler ultrasonography shows reduced blood flow
to a specific area and any obstruction to venous flow,
Anterior tibial
particularly in iliofemoral deep vein thrombophle-
bitis.
H Plethysmography shows decreased circulation distal
to the affected area and is more sensitive than ultra-
sonography in detecting deep vein thrombophlebitis.
H Phlebography confirms the diagnosis and shows fill-
ing defects and diverted blood flow.

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9400T.qxd 8/2/12 4:50 PM Page 819

Treatment Patient teaching

General Be sure to cover:
H Application of warm, moist compresses to the affect- H the disorder, diagnosis, and treatment
ed area H the importance of follow-up blood studies to monitor
H Antiembolism stockings anticoagulant therapy
H Bed rest, with elevation of the affected extremity H how to give injections (if the patient is being dis-
charged on subcutaneous anticoagulation therapy)
Medications H the need to avoid prolonged sitting or standing to
H Anticoagulants help prevent a recurrence
H Thrombolytics H proper application and use of antiembolism stock-
H Analgesics ings
H the importance of adequate hydration
Surgery H use of an electric razor and avoidance of products
H Simple ligation to vein plication, or clipping that contain aspirin.
H Embolectomy
H Caval interruption with transvenous placement of a
vena cava filter

Nursing considerations
Key outcomes
The patient will:
H maintain collateral circulation
H express feelings of increased comfort and decreased
pain
H maintain tissue perfusion and cellular oxygenation
H develop no signs or symptoms of infection.

Nursing interventions
H Enforce bed rest and elevate the patients affected
arm or leg, but avoid compressing the popliteal
space.
H Apply warm compresses or a covered aquathermia
pad.
H Administer prescribed analgesics.
H Mark, measure, and record the circumference of the
affected arm or leg daily, and compare this measure-
ment with that of the other arm or leg.
H Administer prescribed anticoagulants.
H Perform or encourage range-of-motion exercises.
H Use pneumatic compression devices.
H Apply antiembolism stockings.
H Encourage early ambulation.

Monitoring
H Signs and symptoms of bleeding
H Vital signs
H Partial thromboplastin time for patient on heparin
therapy
H Prothrombin time for patient on warfarin
H Signs and symptoms of heparin-induced thrombocy-
topenia
H Signs and symptoms of pulmonary embolism
H Response to treatment

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Thyroid cancer H Palpable lymph nodes with an enlarged thyroid

H Hoarseness
H Dysphagia

Overview Complications
H Dysphagia
Description H Stridor
H Proliferation of cancer cells in the thyroid gland H Hormone alterations
H The most common endocrine malignancy H Distant metastasis
H Papillary carcinomas: nearly 70% of all cases
H Medullary cancer: may be associated with pheochro-
mocytoma; curable when detected before it causes Assessment
symptoms
History
Pathophysiology H Sensitivity to cold and mental apathy (hypothy-
H Papillary cancer is usually multifocal and bilateral. It roidism)
metastasizes slowly into regional nodes of the neck, H Sensitivity to heat, restlessness, and overactivity
mediastinum, lungs, and other distant organs. Its the (hyperthyroidism)
least virulent form of thyroid cancer. H Diarrhea
H Follicular cancer is less common but is more likely H Dysphagia
to recur and metastasize to the regional lymph nodes H Anorexia
and spread through blood vessels into the bones, liv- H Irritability
er, and lungs. H Ear pain
H Medullary (solid) carcinoma originates in the para-
follicular cells derived from the last branchial pouch Physical findings
and contains amyloid and calcium deposits. It can H Hard, painless nodule in an enlarged thyroid gland
produce calcitonin, histaminase, corticotropin (pro- or palpable lymph nodes with thyroid enlargement
ducing Cushings syndrome), and prostaglandin E2 H Hoarseness and vocal stridor
and F3 (producing diarrhea). Untreated medullary H Disfiguring thyroid mass
cancer grows rapidly, commonly metastasizing to H Bruits
bones, liver, and kidneys.
H Anaplastic carcinoma (giant and spindly cell cancer) Test results
resists radiation and is almost never curable by re- Laboratory
section. This cancer metastasizes rapidly, causing H Calcitonin assay identifies silent medullary carcino-
death by invading the trachea and compressing adja- ma. Measuring calcitonin level in a resting state and
cent structures. during calcium infusion (15 mg/kg over 4 hours)
shows an elevated fasting calcitonin level and an ab-
Causes normal response to calcium stimulation a higher
H Previous exposure to radiation treatment in the neck release of calcitonin from the node than from the
area rest of the gland indicating medullary cancer.
H Prolonged secretion of thyroid-stimulating hormone Imaging
(radiation or heredity) H Thyroid scan differentiates functional nodes, which
are rarely malignant, from hypofunctional nodes,
Risk factors which are commonly malignant.
H Familial predisposition (possibly inherited as an au- H Ultrasonography shows changes in the size of thyroid
tosomal dominant trait) nodules after thyroxine suppression therapy and is
H Chronic goiter used to guide fine-needle aspiration and to detect re-
current disease.
Incidence H Magnetic resonance imaging and computed tomogra-
H 1.2 to 2.6 per 100,000 cases in males phy scans provide a basis for treatment planning be-
H 2.0 to 3.8 per 100,000 cases in females cause they show the extent of disease in the thyroid
H Nearly two times the number of cases in Iceland and and surrounding structures.
Hawaii compared to Canada and the U.S. mainland Diagnostic procedures
H Particularly common among Chinese males and Fil- H Fine-needle aspiration biopsy differentiates benign
ipino females from malignant thyroid nodules.
H Rare in children H Histologic analysis stages the disease and thereby
guides treatment plans.
Common characteristics
H Painless nodule; hard nodule in an enlarged thyroid
gland

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9400T.qxd 8/2/12 4:50 PM Page 821

H treatments and home care

Treatment H medication administration, dosage, and possible
adverse effects.
General
H Radioisotope (131I) therapy with external radiation Discharge planning
(sometimes postoperatively in lieu of radical neck H Refer the patient to available resource and support
excision) or alone (for metastasis) services.
H Soft diet with small frequent meals (if dysphagia
occurs)
Medications
H Suppressive thyroid hormone therapy
H Chemotherapy

Surgery
H Total or subtotal thyroidectomy with modified node
dissection (bilateral or homolateral) on the side of
the primary cancer (for papillary or follicular can-
cer)
H Total thyroidectomy and radical neck excision (for
medullary or anaplastic cancer)

Nursing considerations
Key outcomes
The patient will:
H maintain current weight without further loss
H express positive feelings about self
H not aspirate
H express feelings of increased comfort and decreased
pain.
Nursing interventions
H Encourage verbalization and provide support.
Before surgery
H Prepare the patient for scheduled surgery.
H Establish a way to communicate postoperatively.
After surgery
H Keep the patient in semi-Fowlers position, with ade-
quate neck support.
H Keep a tracheotomy set and oxygen equipment near-
by in case of respiratory obstruction.
Monitoring
H Vital signs
H Wound site
H Pain control
H Serum calcium levels (if the parathyroid glands were
removed)
H Postoperative complications
H Hydration and nutritional status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H (before surgery) the operation and postoperative
procedures and positioning

Thyroid cancer 821

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Thyroiditis
Overview
Description
H Several disorders that involve inflammation of the
thyroid gland
H Autoimmune (Hashimotos) thyroiditis: the most
common chronic inflammatory disease of the thyroid
gland
H Postpartum thyroiditis: a form of autoimmune thy-
roiditis that occurs within 1 year of delivery
H Subacute thyroiditis: a transient inflammation of the
thyroid gland thats probably viral in origin
H Riedels thyroiditis: a rare condition with unknown
etiology possibly a variant of Hashimotos thyroiditis
H Supportive thyroiditis: an uncommon bacterial or
fungal infection of the thyroid thats potentially very
serious
H Silent thyroiditis: a transient hyperthyroid condition
characterized by a small painless goiter and may be
autoimmune in origin
Pathophysiology
H The inflammatory process has varying effects on thy-
roid hormone levels (may be low, normal, or high).
Also, lymphocytes and leukocytes may infiltrate thy-
roid tissue.
H Hashimotos thyroiditis is thought to result from lym-
phocytic infiltration of the thyroid gland and forma-
tion of antibodies to thyroid antigens in the blood.
H Riedels thyroiditis causes intense fibrosis of the thy-
roid and surrounding structures.
Causes
H Mumps
H Influenza, coxsackievirus, or adenovirus infections
H Tuberculosis
H Syphilis
H Actinomycosis
H Bacterial infection
H Sarcoidosis and amyloidosis
Incidence
H More common in females than in males
H Autoimmune thyroiditis most common in middle-age
females; most common cause of sporadic goiter in
children
Common characteristics
H Signs and symptoms of hyperthyroidism or hypothy-
roidism
Complications
H Depending on type of inflammation:
Non-Hodgkins lymphoma of the thyroid gland
Permanent hypothyroid or hyperthyroid condition
Abscess formation and rupture
822 Thyroiditis
Tracheal or esophageal compression, necrosis,
and hemorrhage
Assessment
History
H Recent viral or bacterial infection
H Disorder, such as systemic lupus erythematosus,
rheumatoid arthritis, pernicious anemia, or Graves
disease
H Gradual onset of hypothyroid-like symptoms
H Occasionally, symptoms of hyperthyroidism
H Local pain or pain referred to the lower jaw, ear, or
occiput
H Dysphagia
H Dyspnea
H Asthenia, malaise
Physical findings
H Enlargement of the thyroid gland (goiter)
H Reddened skin over the thyroid gland
H Indurated neck tissues
H Small, firm, and finely nodular thyroid gland with a
characteristic bandlike depression circling the gland
H A small lymph node in the midline above the isthmus
H Nodularity
H Swelling and warmth of the overlying skin
H Woody, hard enlargement that feels anchored to
surrounding structures
H Stridor
Test results
Laboratory
H In autoimmune processes, serum thyroglobulin and
microsomal antibody levels are increased.
HASHIMOTOS THYROIDITIS
H Thyroid-stimulating hormone (TSH) level is in-
creased.
H Triiodothyronine and thyroxine levels are normal or
decreased.
H Antimicrosomal and antithyroglobulin antibodies are
increased.
SUBACUTE THYROIDITIS
H Thyroid hormone levels may be elevated, suppressed,
or normal depending on the phase of the disorder.
H Protein-bound iodine levels are increased.
H TSH levels are decreased in the thyrotoxic phase, fail-
ing to respond to thyrotropin-releasing hormone; in
the hypothyroid phase, TSH levels are increased.
H Radioactive iodine (131I) uptake is decreased.
H Erythrocyte sedimentation rate, white blood cell
count, and hepatic enzyme levels are increased.
H Thyroid antibody levels are transiently low.
H Thyroglobin levels are increased.
RIEDELS THYROIDITIS
H 131I uptake is normal or decreased.
H Antimicrosomal antibody levels are increased.
Imaging
H Thyroid scan may show isolated areas of function or
total failure to visualize the gland.
9400T.qxd 8/2/12 4:50 PM Page 823

Diagnostic procedures Monitoring

H Fine-needle thyroid gland biopsy offers histologic H Vital signs
confirmation. H Intake and output
H Daily weight
H Respiratory status
Treatment H Signs and symptoms of hyperthyroidism or hypothy-
roidism
General H Neck circumference
H Varies with the type of thyroiditis
H Activity, as tolerated
Patient teaching
Medications
H Thyroid hormone Be sure to cover:
H Analgesics H the disorder, diagnosis, and treatment
H Anti-inflammatories H medication administration, dosage, and possible
H Beta-adrenergic blockers adverse effects
H Corticosteroids H when to notify the physician
H Antibiotics H signs and symptoms of respiratory distress
H signs and symptoms of hyperthyroidism and hypo-
Surgery thyroidism
H Partial thyroidectomy H long-term hormone replacement therapy after
thyroidectomy
H the importance of wearing or carrying medical
Nursing considerations identification.
Key outcomes Discharge planning
The patient will: H Refer the patient to a mental health professional for
H maintain a patent airway additional counseling if indicated.
H express feelings of increased comfort
H consume adequate calories daily
H express positive feelings about self
H avoid complications.

Nursing interventions
H Administer prescribed drugs.
H Elevate the head of the bed 90 degrees during meal-
times and for 30 minutes afterward.
H Keep suction equipment readily available.
H Consult a dietitian.
H Provide frequent mouth care.
H Provide meticulous skin care.
H Provide comfort measures.
H Encourage oral fluid intake.
H Encourage verbalization of feelings.
H Offer emotional support.
H Help develop effective coping strategies.

ALERT
After thyroidectomy, watch for signs of tetany sec-
ondary to accidental parathyroid injury during
surgery. Keep 10% calcium gluconate available for
I.V. use if needed. Check dressings frequently for
excessive bleeding. Watch for signs of airway ob-
struction, such as difficulty talking or increased
swallowing, and keep tracheotomy equipment
handy.

Thyroiditis 823
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Common characteristics
Tobacco abuse H Female smokers: generally have earlier menopause
H Important events given up because of restrictions of
tobacco use
Overview H Continued tobacco use despite negative conse-
quences
Description H Cravings of tobacco
H Addiction to nicotine, the drug in tobacco H Large amounts of time spent using tobacco
H Effects on the brain similar to heroin, morphine, and H Tolerance to nicotine effects
cocaine H Withdrawal symptoms: increased anger, hostility, and
H Includes cigarettes, cigars, pipe tobacco, snuff, and aggression; disturbed emotional equilibrium follow-
chewing tobacco ing stress; impairment across a wide range of psy-
H Results in withdrawal symptoms when a person tries chomotor and cognitive functions such as difficulty
to stop using tobacco with concentration
H Harmful effects of tobacco products dose-dependent
Complications
Pathophysiology H Cardiovascular diseases: coronary artery disease, pe-
H Rapid absorption of nicotine through the lungs of ripheral vascular disease, and stroke
cigarette smokers; bolus of nicotine reaches the H Cancers of the head and neck, lung, and GI tract
brain within 10 to 16 seconds. H Chronic lung disease
H Equally fast absorption through the oral mucosa of H Hypertension
cigar, pipe, and smokeless tobacco users. H Oral cancer
H In the brain, nicotine activates nicotinic acetylcholine H Oral leukoplakia
receptors, leading to the release of dopamine and a H Nicotine palatinus stomatitis
discharge of epinephrine from the adrenal cortex. H Smokeless tobacco keratosis
H Stimulation of the central nervous system and en- H Gingivitis
docrine glands causes a sudden release of glucose, H Periodontitis
followed by depression and fatigue; leads the user to H Sinusitis
seek more nicotine.
Causes Assessment
H Physiologic and psychological dependence
H Pervasive media messages about tobacco use History
H Minimization of risks of smoking H Use of tobacco products
H Perception that smoking helps with relaxation H Inability to successfully stop using tobacco
H Other drug or alcohol use
H Mental illnesses, such as depression or anxiety Physical findings
H Elevated blood pressure
Risk factors H Increased pulse rate
H Addictive personality H Cough
H A friend who was a substance abuser
H Family members who smoke or with other addictions Test results
H In adolescents, average to below average school per- Imaging
formance and divorce or family conflict H Chest X-ray shows chronic changes related to smok-
ing.
Incidence Other
H 25% to 33% of adult males and females smoking H Nicotine dependence assessment tool, such as the
H Numbers expected to diminish to 15% to 20% over Nicotine Dependence Syndrome Scale, shows the
the next 30 years level of addiction.
H Rates in adolescents showing a gradual increase
since 1987
H About 5 million smokers in the United States: be- Treatment
tween ages 12 and 17; more than 500,000: between
ages 8 and 11 General
H During the past 40 years: cigarette smoking caused H Motivation to stop using tobacco
an estimated 12 million deaths, including 4.1 million H Behavioral counseling
deaths from cancer, 5.5 million deaths from cardio- H Skills training to overcome high-risk situations
vascular diseases, 2.1 million deaths from respirato- H Psychological support
ry diseases, and 94,000 infant deaths related to H Alternative rewards and reinforcers
mothers smoking during pregnancy

824 Tobacco abuse

9400T.qxd 8/2/12 4:50 PM Page 825

Medications
H Nicotine replacement therapy in the form of nicotine
gum, lozenges, patches, nasal sprays, and inhalers
H Antidepressants
H Bupropion (Zyban)
H Clonidine (Catapres)
H Nortriptyline (Pamelor)

Nursing considerations
Key outcomes
The patient will:
H express a desire to stop abusing tobacco
H identify risks associated with tobacco abuse
H demonstrate improved physical health and function
H verbalize an improved sense of well-being and men-
tal health
H develop a plan to stop abusing tobacco.

Nursing interventions
H Assess the patients attitude toward tobacco abuse.
H Be supportive and remain nonjudgmental.
H Advise the patient about health risks and effective
cessation methods.
H Assist the patient in developing a plan to quit.
H Suggest motivational strategies for quitting.
H Help the patient identify ways to avoid weight gain af-
ter stopping smoking.
H Refer the patient to available resources and support
groups.
H Arrange for follow-up care.

Monitoring
H Prescribed medications and possible adverse effects
H Vital signs
H Psychological and emotional response

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medication administration, dosage, and possible ad-
verse effects
H the risks of second-hand smoke
H withdrawal symptoms and ways to reduce their ef-
fects
H strategies to improve chance of successful quitting
H where to obtain support.

Tobacco abuse 825

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Tonsillitis H Headache
H Pain, commonly referred to the ears
H Constant urge to swallow
H Constricted feeling in the back of the throat
Overview
Physical findings
Description H Fever
H Inflammation of the tonsils H Swollen, tender submandibular lymph nodes
H May be acute or chronic H Generalized inflammation of pharyngeal wall
H Typical viral infection: mild and of limited duration H Swollen tonsils projecting from between the pillars
of the fauces and exuding white or yellow follicles
Pathophysiology H Purulent drainage with application of pressure to
H The inflammatory response to cell damage by viruses tonsillar pillars
or bacteria results in hyperemia and fluid exudation. H Uvula possibly edematous and inflamed

Causes Test results

H Bacterial infection (group A beta-hemolytic strepto- Laboratory
cocci) H Throat culture reveals the infecting organism.
H Viral infection H Serum white blood cell count usually reveals leu-
kocytosis.
Risk factors
H Close contact with others in school or child care
facility Treatment
Incidence General
H Symptom relief
Special populations H Adequate fluid intake
H Rest periods as needed
Commonly affects children between ages 5 and 10
Medications
H Tonsils tending to hypertrophy during childhood and H Aspirin or acetaminophen
atrophy after puberty H Antibiotics

Common characteristics Surgery

H Sore throat H Possible tonsillectomy
H Enlarged tonsils

Complications Nursing considerations

H Chronic upper airway obstruction
H Sleep disturbance, sleep apnea Key outcomes
H Cor pulmonale The patient will:
H Failure to thrive H express feelings of increased comfort
H Eating or swallowing disorders H show no signs of aspiration
H Speech abnormalities H maintain effective breathing pattern
H Febrile seizures H have balanced intake and output.
H Otitis media
H Cardiac valvular disease Nursing interventions
H Peritonsillar abscesses H Encourage oral fluids.
H Glomerulonephritis H Offer a child ice cream and flavored drinks and ices.
H Bacterial endocarditis H Provide humidification.
H Cervical lymph node abscesses H Encourage gargling to soothe the throat and remove
debris from tonsillar crypts.
After surgery
Assessment H Maintain a patent airway.
H Watch for signs of airway obstruction or bleeding,
History such as difficulty talking or increased swallowing.
H Mild to severe sore throat H Prevent aspiration by side positioning.
H Young child possibly stops eating H Keep suction equipment readily available.
H Muscle and joint pain H Provide water after gag reflex returns.
H Chills H Later, encourage nonirritating oral fluids.
H Malaise H Avoid milk products and salty or irritating foods.

826 Tonsillitis
9400T.qxd 8/2/12 4:50 PM Page 827

H Provide analgesics for pain relief.

H Encourage deep-breathing exercises.

Monitoring
H Hydration status
H Effect of pain medication
Before surgery
H Bleeding abnormalities
After surgery
H Vital signs
H Signs and symptoms of bleeding
H Respiratory status

ALERT
Immediately report excessive bleeding, increased
pulse rate, or decreasing blood pressure.

ALERT
The greatest risk of bleeding is 7 to 10 days after
surgery.

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the importance of completing the entire course of
antibiotics
H avoidance of irritants
H the need for soft foods for about 3 weeks after
surgery to decrease risk of rebleeding
H medication administration, dosage, and possible
adverse effects
H the possibility of throat discomfort and some bleed-
ing after surgery
H expectation of a white scab to form in the throat 5 to
10 days after surgery
H the need to report bleeding, ear discomfort, or a
fever that lasts 3 days or more.

Tonsillitis 827
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H Half of all cases in settings other than menstruation

Life-threatening disorder H Affects both sexes and all ages

Common characteristics
Toxic shock syndrome H In the early convalescent period: fever, hypotension,
rash, multiorgan dysfunction, and desquamation
H Menstruation (the most common setting for TSS)
Overview H Bacteremia (in about 60% of patients)

Description Complications
H An inflammatory response syndrome linked to bacte- H Septic abortion
rial infections H Musculoskeletal and respiratory infections
H An acute and life-threatening condition H Staphylococcal bacteremia
H Also called TSS H Renal and myocardial dysfunction
H Acute respiratory distress syndrome
Pathophysiology H Desquamation of the skin
H Toxic exoproteins are produced by infecting organ- H Peripheral gangrene
isms. H Muscle weakness
H TSST-1 is the most common toxin; staphylococcal H Neuropsychiatric dysfunction
enterotoxin B is the second most common.
H For illness to develop, the patient must be infected
with a toxigenic strain of Staphylococcus aureus and Assessment
lack antibodies to that strain.
History
Causes H Possible recent streptococcal infection
H Penicillin-resistant S. aureus H Possible tampon use or menstruation
H Intense myalgia, headache
Risk factors H Nausea, vomiting, and diarrhea
H Tampon use H Sore throat
H Varicella infection H Dizziness
H Streptococcal pharyngitis
Physical findings
Incidence H Fever (104 F [40 C] or higher)
H Affects 1 in 100,000 H Pharyngeal infection, strawberry tongue
H Primarily affects young people H Hypotension
H Altered mental status
H Macular erythroderma (generalized or local)
Guidelines for diagnosing toxic shock H Peripheral edema
syndrome H Vaginal hyperemia, purulent vaginal discharge

Toxic shock syndrome is typically diagnosed based on the Test results

following criteria.
H Fever 102 F (38.9 C) or higher
H Diffuse macular erythrodermal rash (sunburn rash)
H Hypotension (systolic blood pressure 90 mm Hg or
less in adults or below the 5th percentile for age)
H Involvement of at least three organ systems:
GI (vomiting, diarrhea)
Muscular (myalgias or liver function test at least
twice normal upper limit)
Mucous membrane hyperemia (conjunctiva, vagina,
oropharyngeal)
Renal (blood urea nitrogen or creatinine level at least
twice normal upper limit, or pyuria)
Hepatic (total serum bilirubin or aminotransferase
level twice normal level)
Hematologic (thrombocytopenia)
Central nervous system (disorientation or change in
level of consciousness)
H Desquamation, especially of palms and soles, 1 or 2
weeks after onset of illness
H Other conditions ruled out
Laboratory
H Isolation of S. aureus from vaginal discharge or in-
fection site supports the diagnosis. (See Guidelines
for diagnosing toxic shock syndrome.)
H Blood urea nitrogen examination shows azotemia.
H Urinalysis shows pyuria.
H Serum albumin levels reveal hypoalbuminemia.
H Serum calcium levels reveal hypocalcemia.
H Serum phosphorus levels reveal hypophosphatemia.
H Complete blood count shows leukocytosis or
leukopenia.
H Platelet count shows thrombocytopenia.
H Serum creatinine level is increased.
Treatment
General
H Aggressive fluid resuscitation
H Correction of electrolyte imbalances

828 Toxic shock syndrome

9400T.qxd 8/2/12 4:50 PM Page 829

H Supportive treatment such as possible ventilatory Prevention

support Preventing TSS
H Identification and decontamination of toxin produc-
Toxic shock syndrome (TSS) may be prevented by follow-
tion site ing these guidelines:
H Bed rest until acute phase resolved H Wash your hands before inserting a tampon.
H Change tampons every 4 to 8 hours.
Medications H Use the lowest absorbency tampon necessary for your
H Antibiotics menstrual flow.
H Inotropics H Alternate between tampons and sanitary napkins.
H Vasopressors H Dont use tampons if you have had TSS because of the
H I.V. immunoglobulin risk of recurrence.

Surgery
H Examination and irrigation of recent surgical wounds

Nursing considerations
Key outcomes
The patient will:
H maintain collateral circulation
H attain and maintain hemodynamic stability
H maintain adequate cardiac output
H remain afebrile
H have an adequate fluid volume.

Nursing interventions
H Administer prescribed drugs.
H Assess fluid balance and replace fluids I.V., as
needed.
H Reorient as needed.
H Use appropriate safety measures to prevent injury.
H Use standard precautions for any vaginal discharge
and lesion drainage.
Monitoring
H Cardiovascular status
H Fluid and electrolyte status
H Neurologic status
H Vital signs
H Pulmonary status
H Response to treatment
H Complications

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H TSS prevention. (See Preventing TSS.)

Toxic shock syndrome 829

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Toxoplasmosis H Chemotherapy
H Steroid use
H Pregnancy

Overview Incidence
H Up to 70% of people in United States infected
Description H Occurs worldwide; less common in cold or hot, arid
H One of the most common parasitic infectious dis- climates and at high elevations
eases
H Usually causes localized infection Common characteristics
H May produce significant generalized infection, espe- H Fever
cially in an immunodeficient patient H Rash
H Once infected, organism carried for life and acute in- H Constitutional symptoms
fection can reactivate
H Congenital type characterized by lesions in the cen- Complications
tral nervous system (CNS); may result in stillbirth or H Seizure disorder
serious birth defects H Vision loss (see Ocular toxoplasmosis)
H Mental retardation
Pathophysiology H Deafness
H After ingestion, parasites are released from latent H Generalized infection
cysts by the digestive process; they then invade the GI H Stillbirth
tract and multiply. H Congenital toxoplasmosis
H Parasites disseminate to various organs, especially H Death
lymphatic tissue, skeletal muscle, myocardium, reti-
na, placenta, and the CNS (most commonly).
H The parasite infects host cells, replicates, and then Assessment
invades adjoining cells, resulting in cell death and fo-
cal necrosis surrounded by an acute inflammatory History
response. H Possible immunocompromised state, exposure to cat
feces, or ingestion of poorly cooked meat
Causes H Malaise
H The protozoan Toxoplasma gondii, which exists in H Fatigue
trophozoite forms in the acute stages of infection and H Myalgia
in cystic forms (tissue cysts and oocysts) in latent H Headache
stages H Sore throat
H Transmitted by ingestion of tissue cysts in raw or un- H Vomiting
dercooked meat or by fecal-oral contamination from
infected cats Physical findings
H Congenital toxoplasmosis from transplacental trans- H Fever (if generalized, possibly 106 F [41.1 C])
mission H Cough
H Dyspnea
Risk factors H Cyanosis
H Human immunodeficiency virus and acquired H Coarse crackles
immunodeficiency syndrome H Delirium, seizures
H Immunosuppression H Diffuse maculopapular rash (except on the palms,
soles, and scalp)
H In an infant with congenital toxoplasmosis:
Ocular toxoplasmosis Hydrocephalus or microcephalus
Ocular toxoplasmosis (active chorioretinitis) is character- Jaundice, purpura, rash
ized by focal necrotizing retinitis. It accounts for about Strabismus, blindness
25% of all cases of granulomatous uveitis. Although usu- Epilepsy, mental retardation
ally the result of a congenital infection, it may not appear Lymphadenopathy, splenomegaly, and hepato-
until adolescence or young adulthood, when infection is megaly
reactivated.
Symptoms include blurred vision, scotoma, pain, photo- Test results
phobia, and impairment or loss of central vision. Vision Laboratory
improves as inflammation subsides but usually without H Specimens (such as bronchoalveolar lavage material
recovery of lost visual acuity. Ocular toxoplasmosis may
from immunocompromised patients or lymph node
subside after treatment with prednisone.
biopsy) contain parasites.

830 Toxoplasmosis
9400T.qxd 8/2/12 4:50 PM Page 831

H Intraperitoneal inoculation with blood or other body Prevention

fluids into mice or tissue cultures shows isolation of Preventing toxoplasmosis
parasites.
Toxoplasmosis may be prevented by following these
H Polymerase chain reaction detects parasites genetic
guidelines:
material (especially in detecting congenital infections H Wash your hands after working with soil or uncooked
in utero). meat.
H Cook meat thoroughly before eating.
H Freeze uncooked meat if not using promptly.
Treatment H Protect childrens play areas from cat and dog feces.
H Cover childrens sandboxes.
General H Keep flies away from food because flies transport
H No treatment in otherwise healthy patient who isnt oocysts.
pregnant H Pregnant women should avoid cleaning and handling
H Rest periods when fatigued cat litter boxes or wear gloves.
H Seizure precautions

Medications H ways to prevent the spread of toxoplasmosis. (See

H Pyrimethamine plus sulfadiazine with leucovorin Preventing toxoplasmosis.)
Discharge planning
Nursing considerations H Refer the patient for follow-up with a neurologist or
infectious disease specialist if needed.
Key outcomes
The patient will:
H have normal vital signs
H have an adequate fluid volume
H report an increased energy level
H develop no complications
H maintain respiratory rate within 5 breaths/minute of
baseline.
Nursing interventions
H Give tepid sponge baths to reduce fever.
H Administer prescribed drugs.
H Provide chest physiotherapy, and administer oxygen,
as needed. Assist ventilations if needed.
H Institute seizure precautions.

ALERT
Dont palpate the patients abdomen vigorously;
this could lead to a ruptured spleen. For the same
reason, discourage vigorous activity.

H Report all cases of toxoplasmosis to the local public

health department.
Monitoring
H Neurologic status
H Response to treatment
H Complications

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H necessary drugs, including the need for frequent
blood tests
H the importance of regularly scheduled follow-up care

Toxoplasmosis 831
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Life-threatening disorder
Tracheoesophageal
fistula and
esophageal atresia
Overview
Description
H Tracheoesophageal fistula: a developmental anomaly
characterized by an abnormal connection between
the trachea and the esophagus; usually accompanies
esophageal atresia, in which the esophagus is closed
off at some point
H Malformations have numerous anatomic variations,
most commonly, esophageal atresia with fistula to
the distal segment
H Two of the most serious surgical emergencies in
neonates; requires immediate diagnosis and
correction
Pathophysiology
H Tracheoesophageal fistula and esophageal atresia re-
sult from failure of the embryonic esophagus and tra-
chea to develop and separate correctly.
H Respiratory system development begins at about day
26 of gestation.
H Abnormal development of the septum during this
time can lead to tracheoesophageal fistula.
H The most common abnormality is type C tracheo-
esophageal fistula with esophageal atresia, in which
the upper section of the esophagus terminates in a
blind pouch, and the lower section ascends from the
stomach and connects with the trachea by a short
fistulous tract.
H In type A atresia, both esophageal segments are blind
pouches, and neither is connected to the airway.
H In types B and D, the upper portion of the esopha-
gus opens into the trachea; infants with this anomaly
may experience life-threatening aspiration of saliva
or food.
H In type E (or H-type) tracheoesophageal fistula with-
out atresia, the fistula may occur anywhere between
the level of the cricoid cartilage and the midesopha-
gus but is usually higher in the trachea than in the
esophagus. Such a fistula may be as small as a pin-
point.
Causes
H Congenital anomalies
Risk factors
H Commonly found in infants with other anomalies,
such as:
Congenital heart disease
Imperforate anus
832 Tracheoesophageal fistula and esophageal atresia
Genitourinary abnormalities
Intestinal atresia
Incidence
H Esophageal atresia in about 1 of 4,000 live births;
about one-third of these neonates born prematurely
Common characteristics
Tracheoesophageal fistula
H Type B (proximal fistula) and Type D (fistula to both
segments): immediate aspiration of saliva into the
airway and bacterial pneumonitis
H Type E (or H-type): suspected with repeated episodes
of pneumonitis, pulmonary infection, and abdominal
infection; choking followed by cyanosis
Esophageal atresia
H Type A: normal swallowing, excessive drooling, pos-
sible respiratory distress
H Type C: seemingly normal swallowing followed short-
ly afterward by coughing, struggling, cyanosis, lack of
breathing
Complications
H Aspiration of secretions into the lungs leading to res-
piratory distress, pneumonia, or cessation of breath-
ing
H Death if untreated
After surgery
H Abnormal esophageal motility
H Recurrent fistulas
H Pneumothorax
H Esophageal stricture
Assessment
History
H Coughing and choking after eating
Physical findings
H Respiratory distress
H Drooling
Test results
Imaging
H Chest X-rays demonstrate the position of the catheter
and can also show a dilated, air-filled upper esoph-
ageal pouch, pneumonia in the right upper lobe, or
bilateral pneumonitis. Both pneumonia and pneu-
monitis suggest aspiration.
H Abdominal X-rays show gas in the bowel in a distal
fistula (type C) but none in a proximal fistula (type
B) or in atresia without fistula (type A).
H Cinefluorography allows visualization on a fluoro-
scopic screen. After a size 10 or 12 French catheter
is passed through the patients nostril into the esoph-
agus, a small amount of contrast medium is instilled
to define the tip of the upper pouch and to differenti-
ate between overflow aspiration from a blind end
(atresia) and aspiration from passage of liquids
through a tracheoesophageal fistula.
9400T.qxd 8/2/12 4:50 PM Page 833

Other H Administer antibiotics and parenteral fluids.

H A size 6 or 8 French catheter passed through the H Maintain gastrostomy tube feedings.
nose meets an obstruction (esophageal atresia) H Offer the parents support and guidance in dealing
about 4 to 5 (10 to 12.5 cm) distal to the nostrils. with their infants acute illness. Encourage them to
Aspirate of gastric contents is less acidic than nor- participate in care and to hold and touch the infant
mal. as much as possible to facilitate bonding.
Monitoring
Treatment H Respiratory status
H Intake and output
General After surgery
H I.V. fluids H Chest tubes
H Supine position with the head low to facilitate H Signs of complications
drainage or with the head elevated to prevent aspira-
tion
H After surgery: placement of a suction catheter in the Patient teaching
upper esophageal pouch to control secretions and
prevent aspiration Be sure to cover:
H the disorder, diagnosis, and treatment
Medications H feeding procedures
H Antibiotics for superimposed infection H recognizing and reporting complications
H proper positioning.
Surgery
Tracheoesophageal fistula and esophageal atresia re- Discharge planning
quire surgical correction and are usually surgical emer- H Instruct the parents that X-rays are required about 10
gencies. The type and timing of the surgical procedure days after surgery, and again 1 and 3 months later, to
depend on the nature of the anomaly, the patients gen- evaluate the effectiveness of surgical repair.
eral condition, and the presence of coexisting congeni-
tal defects.
H In premature neonates (nearly 33% of infants with
this anomaly) who are poor surgical risks: correc-
tion of combined tracheoesophageal fistula and
esophageal atresia done in two stages: first, gastros-
tomy (for gastric decompression, prevention of re-
flux, and feeding) and closure of the fistula; then, 1
to 2 months later, anastomosis of the esophagus
H Correction of esophageal atresia alone requiring
anastomosis of the proximal and distal esophageal
segments in one or two stages; end-to-end anastomo-
sis commonly producing postoperative stricture;
end-to-side anastomosis less likely to do so
H If the esophageal ends widely separated: treatment
possibly including a colonic interposition (grafting a
piece of the colon) or elongation of the proximal
segment of the esophagus by bougienage

Nursing considerations
Key outcomes
The patient will:
H develop no respiratory complications
H remain hemodynamically stable.
The parents or family will:
H express understanding of disorder and treatment.

Nursing interventions
H Administer oxygen as needed.
H Perform pulmonary physiotherapy and suctioning, as
needed.
H Provide a humid environment.

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Transient ischemic H Headaches

H Confusion

attack H Vertigo
H Ataxia
H Facial paresis
H Nausea or vomiting
Overview
Complications
Description H Stroke
H Sudden onset of focal and transient neurologic deficit H Seizure
due to brain ischemia H Bleeding as a result of anticoagulants
H Vascular (occlusive) in origin H Trauma (if patient experiences a sudden fall)
H Rapid in onset; typically reaching maximum effect in
less than 5 minutes
H Variable duration; usually lasting 2 to 15 minutes; Assessment
possibly lasting as long as 24 hours
H Also known as TIA History
H Include family members, coworkers, witnesses, and
Pathophysiology emergency medical services personnel in question-
H Cerebral blood flow is temporarily reduced or ing, if possible
stopped. H Reports of changes in behavior, speech, gait, memo-
H This affects neuronal function in cortical, subcorti- ry, movement, and vision
cal, and nuclear regions of the central nervous sys- H Symptoms lasting only several minutes
tem. H Recent surgery
H Previous strokes
Causes H Use of illicit drugs
H Carotid and vertebral artery atherosclerosis H Complete medication regimen
H Hypertension H May have vague complaints of feeling short of breath;
H Embolism possibly preceded by palpitations or slight chest
H Arterial dissection pain; followed by inability to speak properly and fa-
H Arteritis cial droop
H Mitral valve disease H History of arteritis
H Acute anterior myocardial infarction
H Congestive cardiomyopathy Physical findings
H Cardiac arrhythmia H Low-grade fever
H Hypercoagulable states H Elevated blood pressure
H Sympathomimetic drugs such as cocaine H Decreased peripheral pulses compared to the apical
pulse
Risk factors H Carotid bruit
H Hypertension H Possibly poor language and memory skills
H Cardiac disease H Unequal pupil reaction to direct and consensual light
H Smoking exposure
H Diabetes H Diminished cranial nerve response
H Obesity H Decreased somatic motor strength
H Family history H Forehead wrinkling asymmetry
H Hypercholesterolemia H Incomplete eyelid closure
H Atrial fibrillation H Asymmetrical mouth retraction
H Hormonal contraceptives H Swallowing difficulty
H Pregnancy and parturition H Lateral tongue movement
H Weak shoulder shrugging
Incidence H Visual field deficits
H From 83 to 200 cases per 100,000
H Significantly higher in Blacks than in Whites Test results
H Affects males at higher rates than females Laboratory
H Uncommon in people younger than age 60 H Partial thromboplastin time may be decreased.
H Antiphospholipid antibodies are elevated.
Common characteristics H Platelet count may be elevated.
H Vision changes H Cholesterol levels are elevated.
H Hemiplegia H Elevated D-dimer shows hypercoagulability.
H Hemianesthesia H Drug screens show illicit drug use.
H Aphasia

834 Transient ischemic attack

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Imaging H Assess motor function.

H Duplex carotid ultrasonography shows narrowed ar- H Maintain a safe environment.
teries. H Assess the impact of TIAs on all systems and func-
H Angiography shows cerebral or carotid artery steno- tions of the body.
sis. H Assess the impact of TIAs on psychosocial issues,
H Transthoracic echocardiogram shows thrombus or body image, and self-esteem.
structural defect. H If swallowing ability is impaired, avoid giving thin liq-
H Computed tomography scan of head identifies cause uids.
of TIA.
H Brain magnetic resonance imaging identifies cause of Monitoring
TIA. H Vital signs
H Magnetic resonance angiography of the brain or H Adverse reaction to medication
blood vessels shows cause of TIA. H Coagulation studies
Diagnostic procedures H Hemodynamic status
H Electrocardiography identifies underlying arrhyth- H Signs and symptoms of complications
mia. H Neurologic status
H Ophthalmoscopic examination shows retinal choles-
terol emboli.
Patient teaching
Treatment Be sure to cover:
H the disorder, diagnosis, and treatment
General H medication administration, dosage, and possible ad-
H Maintaining patent airway and providing supplemen- verse effects, and the need to report them
tal oxygen H antiplatelet therapy, if indicated
H control of risk factors (see Preventing TIAs)
Medications H dietary modification
H Aspirin or other antithrombotic therapy, such as H measures to maintain a safe environment
clopidogrel and dipyridamole H importance of reporting a change in neurologic sta-
H Angiotensin-converting enzyme inhibitors tus.
H Statins
H Anticoagulants

Surgery
H Carotid endarterectomy

Nursing considerations
Key outcomes
The patient will:
H verbalize understanding of the condition, diagnostic
studies, treatment, and risk factors
H demonstrate effective ways to cope with sensory limi-
tations
H achieve the maximum visual ability possible
H maintain optimum cerebral tissue perfusion
H remain free from injury and falls
H remain free from peripheral neurovascular impair-
ment.
Nursing interventions
H Evaluate using a stroke scale such as National Insti-
tutes of Health Stroke Scale.
H Administer prescribed drugs.
H Assess level of consciousness, mental status, and cog-
nition.
H Assess speech, facial symmetry, and sensory function.
H If speech is affected, provide alternative methods for
communication.
H Assess pupil reaction to light.
Prevention
Preventing TIAs
Transient ischemic attack (TIA) risk factors may be re-
duced by following these guidelines:
H Stop smoking.
H Avoid cholesterol and fat.
H Eat fruits and vegetables that contain potassium, folate
and antioxidants, which may protect against TIA.
H Avoid salt if you have hypertension.
H Exercise regularly.
H Drink alcohol moderately or not at all.
H Maintain a healthy weight.
H Manage diabetes and hypertension.
H Dont use cocaine or other illicit drugs that will in-
crease your risk of TIA.

Transient ischemic attack 835

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Transposition of the
great arteries
Overview
Description
H Congenital heart defect in which the great arteries
are reversed: aorta arising from right ventricle and
pulmonary artery from left ventricle, producing two
noncommunicating circulatory systems (pulmonary
and systemic)
H Commonly coexists with other congenital heart de-
fects, such as ventricular septal defect (VSD), VSD
with pulmonary stenosis (PS), atrial septal defect
(ASD), and patent ductus arteriosus (PDA)
Pathophysiology
H In transposition, oxygenated blood returning to the
left side of the heart is carried back to the lungs by a
transposed pulmonary artery; unoxygenated blood
returning to the right side of the heart is carried to
the systemic circulation by a transposed aorta.
H Communication between the pulmonary and systemic
circulations is necessary for survival. In infants with
isolated transposition, blood mixes only at the patent
foramen ovale and at the patent ductus arteriosus,
resulting in slight mixing of unoxygenated systemic
blood and oxygenated pulmonary blood.
H In infants with concurrent cardiac defects, greater
mixing of blood occurs.
Causes
H Faulty embryonic development
Risk factors
H Maternal rubella or other viral illness during preg-
nancy
H Parent with transposition of the great arteries or oth-
er congenital heart defect
H Poor prenatal nutrition
H Prenatal alcohol exposure
H Maternal age older than 40
H Maternal diabetes
Incidence
H Accounts for about 5% of all congenital heart defects
H Affects males two to three times more than females
Common characteristics
H Within the first few hours after birth, neonates with
transposition of the great arteries generally show
cyanosis and tachypnea, which worsen with crying.
H After several days or weeks, such neonates usually
develop signs of heart failure (gallop rhythm, tachy-
cardia, dyspnea, hepatomegaly, and cardiomegaly).
S2 is louder than normal because the anteriorly
transposed aorta is directly behind the sternum; in
836 Transposition of the great arteries
many cases, however, no murmur can be heard dur-
ing the first few days of life.
Complications
H Heart failure
H Cardiac arrhythmia
H Eisenmengers syndrome (irreversible and progres-
sive pulmonary vascular obstructive disease)
Assessment
History
H Diminished exercise tolerance
H Fatigability
H Coughing
Physical findings
H Cyanosis
H Clubbing of nailbeds
H Pronounced murmurs if ASD, VSD, PDA, or PS
present
Test results
Laboratory
H Arterial blood gas (ABG) values indicate hypoxia and
secondary metabolic acidosis.
Imaging
H Chest X-rays are normal in the first days of life. With-
in days to weeks, right atrial and right ventricular en-
largement characteristically cause the heart to ap-
pear oblong. X-rays also show increased pulmonary
vascular markings, except when pulmonary stenosis
coexists.
H Echocardiography demonstrates the reversed posi-
tion of the aorta and pulmonary artery and records
echoes from both semilunar valves simultaneously,
due to aortic valve displacement. It also detects other
cardiac defects.
Diagnostic procedures
H Electrocardiography typically reveals right axis devia-
tion and right ventricular hypertrophy; it may be nor-
mal in a neonate.
H Cardiac catheterization reveals decreased oxygen sat-
uration in left ventricular blood and aortic blood; in-
creased right atrial, right ventricular, and pulmonary
artery oxygen saturation; and right ventricular sys-
tolic pressure equal to systemic pressure. Dye injec-
tion reveals the transposed vessels and the presence
of any other cardiac defects.
Treatment
General
H Atrial balloon septostomy (Rashkind procedure)
during cardiac catheterization
H Increased caloric density before correction; no di-
etary restrictions after correction
H Activity, as tolerated
9400T.qxd 8/2/12 4:50 PM Page 837

Medications Discharge planning

H Inotropic agents H Refer the patient and family to support and social
H Loop diuretics services as needed.
H Prostaglandin E1
H Prophylactic antibiotics

Surgery
One of three surgical procedures can correct transposi-
tion, depending on the defects physiology:
H Mustard procedure: replaces the atrial septum with a
Dacron or pericardial partition that allows systemic
venous blood to be channeled to the pulmonary
artery, which carries the blood to the lungs for oxy-
genation and oxygenated blood returning to the heart
to be channeled from the pulmonary veins into the
aorta
H Senning procedure: accomplishes the same result us-
ing the atrial septum to create partitions to redirect
blood flow
H Arterial switch, or Jatene procedure: transposed ar-
teries surgically anastomosed to the correct ventricle;
for this procedure to be successful, the left ventricle
must be used to pump at systemic pressure, as it
does in neonates or in children with a left ventricular
outflow obstruction or large VSD; surgery also cor-
recting other heart defects

Nursing considerations
Key outcomes
The patient will:
H maintain hemodynamic stability
H improve oxygenation
H have no signs of heart failure.

Nursing interventions
H Offer emotional support.
H Give digoxin and I.V. fluids, being careful to avoid
fluid overload.
H After Mustard or Senning procedures, watch for signs
of baffle obstruction such as marked facial edema.
Monitoring
H Vital signs
H ABG values
H Intake and output
H Central venous pressure
H Signs of heart failure

Patient teaching
Be sure to cover (with the parents):
H the disorder, diagnosis, and treatment
H how to recognize signs of heart failure and digoxin
toxicity (poor feeding and vomiting)
H the importance of regular checkups to monitor car-
diovascular status
H protecting the infant from infection and giving antibi-
otics.

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Trichinosis Stage 2 (dissemination)

H Occurs 7 to 10 days after ingestion
H Penetrates the intestinal mucosa and begins to mi-
grate to striated muscle
Overview H Signs and symptoms:
Edema, especially of the eyelids or face
Description Muscle pain, particularly in limbs
H An infection caused by larvae of the intestinal round- Occasionally, itching and burning skin, sweating,
worm Trichinella spiralis skin lesions, a temperature of 102 to 104 F
H May produce multiple symptoms, such as respiratory, (38.9 to 40 C), and delirium
central nervous system (CNS), cardiovascular com- In severe respiratory, cardiovascular, or CNS infec-
plications and, rarely, death tions, palpitations and lethargy
H Also known as trichiniasis or trichinellosis Stage 3 (encystment)
H Occurs during convalescence, generally 1 week later
Pathophysiology H Invades muscle fiber and becomes encysted
H T. spiralis cysts are found primarily in swine, less
commonly in dogs, cats, bears, foxes, wolves, and Complications
marine animals. These cysts result from the animals H Meningitis
ingestion of similarly contaminated flesh. In swine, H Subcortical infarcts
such infection results from eating table scraps or raw H Encephalitis
garbage. H Myocarditis with heart failure
H After gastric juices free the worm from the cyst cap- H Nephritis
sule, it reaches sexual maturity in a few days. H Glomerulonephritis
H The female roundworm burrows into the intestinal H Sinusitis
mucosa and reproduces. H Pneumonia
H Larvae are then transported through the lymphatic
system and the bloodstream. They become embed-
ded as cysts in striated muscle, especially in the di- Assessment
aphragm, chest, arms, and legs.
H Human-to-human transmission doesnt take place. History
H Ingestion of raw or improperly cooked pork or pork
Causes products
H Ingestion of uncooked or undercooked meat that H Myalgia
contains T. spiralis cysts H Abdominal discomfort
H Diarrhea
Risk factors H Constipation
H Residing in a rural area H Anorexia
H Eating wild or noncommercial meats H Nausea
H Improper food preparation
Physical findings
Incidence H Diffuse weakness
H Occurs worldwide, especially in populations that eat H Dyspnea on exertion
pork or bear meat H Hoarseness
H Affects both sexes equally H Cough
H Abdominal distention
Common characteristics H Macular or petechial rash
H Usually mild and seldom produces symptoms; when H Periorbital edema
symptoms occur, vary with the stage and degree of
infection Test results
Stage 1 (invasion) Laboratory
H Occurs 1 week after ingestion H Stools contain mature worms and larvae during the
H Release of larvae and reproduction of adult T. spi- invasion stage.
ralis causing: H Diagnosis is confirmed by elevated acute and conva-
Anorexia lescent antibody titers (determined by flocculation
Nausea tests 3 to 4 weeks after infection).
Vomiting H Aspartate aminotransferase, alanine aminotrans-
Diarrhea ferase, creatine kinase, and lactate dehydrogenase
Abdominal pain levels are increased during the acute stages, and
Cramps eosinophil count is increased (up to 15,000/l).

838 Trichinosis
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H Cerebrospinal fluid lymphocyte level (to 300/l) H for travelers to foreign countries or poor areas of the
is normal or increased, and protein levels are in- United States, the importance of avoiding pork con-
creased, indicating CNS involvement. sumption; swine in these areas are commonly fed
Diagnostic procedures raw garbage.
H Skeletal muscle biopsies can show encysted larvae 10
days after ingestion; if available, analyses of contami-
nated meat also show larvae.
H Skin testing may show a positive histamine-like reac-
tivity 15 minutes after intradermal injection of the
antigen (within 17 to 20 days after ingestion); how-
ever, such a result may remain positive for up to 5
years after exposure.

Treatment
General
H Supportive care as indicated
H Diet as tolerated
H Initially, bed rest with increased activity as tolerated

Medications
H Antipyretics
H Anthelmintics, such as albendazole and mebendazole
H Glucocorticoids
H Analgesics

Nursing considerations
Key outcomes
The patient will:
H report increased comfort and decreased pain
H express an understanding of the disorder and its
treatment
H maintain adequate ventilation
H maintain hemodynamic stability.

Nursing interventions
H Reduce fever with alcohol rubs, tepid baths, hypo-
thermia blankets, or antipyretics.
H Relieve muscle pain with analgesics, enforced bed
rest, and proper body alignment.
H Frequently reposition the patient, and gently massage
bony prominences to prevent pressure ulcers.
H Report all cases of trichinosis to local public health
authorities.
Monitoring
H Response to treatment
H Vital signs
H Respiratory status

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H proper cooking (cooking to an internal temperature
of 150 F) and storing methods for all meat from
carnivores

Trichinosis 839
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Trichomoniasis Assessment
History
Overview H Severe itching
H Dyspareunia
Description H Dysuria
H A protozoal infection of the lower genitourinary tract H Urinary frequency
H May be acute or chronic in females H Postcoital spotting, menorrhagia, or dysmenorrhea
H Risk of recurrence minimized when sexual partners
treated concurrently Physical findings
H Vaginal erythema, edema, and frank excoriation
Pathophysiology H Frothy, malodorous, greenish yellow vaginal dis-
H Trichomonas vaginalis a tetraflagellated, motile charge
protozoan causes trichomoniasis in females by in- H Rarely, a thin, gray pseudomembrane over the vagina
fecting the vagina, the urethra and, possibly, the en-
docervix, bladder, Bartholins glands, or Skenes Test results
glands; in males, it infects the lower urethra and, Laboratory
possibly, the prostate gland, seminal vesicles, or epi- H Direct microscopic examination of vaginal or semi-
didymis. nal discharge is decisive when it reveals T. vaginalis,
H T. vaginalis grows best when the vaginal mucosa is a motile, pear-shaped organism. Examination of
more alkaline than normal (pH about 5.5 to 5.8). clear urine specimens may also reveal T. vaginalis.
Other
Causes H Cervical examination demonstrates punctate cervical
H Usually transmitted by sexual intercourse; less com- hemorrhages, giving the cervix a strawberry appear-
monly, by contaminated douche equipment or moist ance thats almost pathognomonic for this disorder.
washcloths
Risk factors Treatment
H Factors that raise the vaginal pH, such as the follow-
ing: General
Use of hormonal contraceptives H Abstinence from sexual intercourse until cured
Pregnancy H Sitz baths to help relieve symptoms
Bacterial overgrowth
Exudative cervical or vaginal lesions Medications
Frequent douching, which disturbs lactobacilli that H Single 2-g dose of oral metronidazole given to both
normally live in the vagina and maintain acidity sex partners
Incidence
H Affects about 15% of sexually active females and 10% Nursing considerations
of sexually active males
Key outcomes
Common characteristics The patient will:
H About 70% of females and most males asymptomatic H express feelings of increased comfort and decreased
H In females: gray or greenish yellow and possibly pro- pain
fuse and frothy, malodorous vaginal discharge H express understanding of the condition and treat-
H In males: mild to severe transient urethritis, possibly ment
with dysuria and urinary frequency H discuss the impact of the disorder on self and signifi-
cant others.
Complications
H With pregnant women: preterm or low-birth-weight Nursing interventions
infant H Instruct the patient to avoid using tampons.
H Prostatitis H Provide emotional support.
H Epididymitis H Practice standard precautions.
H Urethral stricture disease
H Infertility Monitoring
H Response to treatment

840 Trichomoniasis
9400T.qxd 8/2/12 4:50 PM Page 841

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the need to refer sex partners for treatment
H the need to avoid alcohol while taking metronidazole
because alcohol may provoke a disulfiram-type reac-
tion (confusion, headache, cramps, vomiting, and
seizures)
H the possibility that metronidazole may turn urine
dark brown
H the need to avoid over-the-counter douches and vagi-
nal sprays because they can alter vaginal pH
H the benefits of wearing loose-fitting, cotton under-
wear, which reduce the risk of genitourinary bacteri-
al growth by allowing ventilation; bacteria flourish in
a warm, dark, moist environment
H prevention of a sexually transmitted disease by using
a condom.

Trichomoniasis 841
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Tricuspid insufficiency Assessment

History
Overview H Occurrence of one of listed causes
H Orthopnea, dyspnea
Description H Fatigue
H Heart condition in which the tricuspid valve doesnt H Angina
function properly H Palpitations
H Also called tricuspid regurgitation
Physical findings
Pathophysiology H Tachycardia
H The tricuspid valve is incompetent. H Crackles in the lungs
H Blood flows back into the right atrium. H Hepatomegaly (right-sided failure)
H Fluid overload occurs in the atrium. H Jugular vein distention
H Congestive failure occurs, and impedance to the H S3
pulmonary vasculature may result in hypoxemia, H Diminished peripheral pulses
cyanosis, and polycythemia. H Ascites
H Atrial fibrillation
Causes H Peripheral edema
H Rheumatic heart disease H Pansystolic murmur (see Identifying the murmur
H Endocarditis of tricuspid insufficiency)
H Epsteins anomaly
H Prolapse Test results
H Carcinoid heart disease Imaging
H Papillary muscle dysfunction H Chest X-rays show right atrial and ventricular en-
H Trauma largement.
H Connective tissue disease H Echocardiography shows right ventricular dilation
and prolapse or flailing of the tricuspid leaflets.
Incidence Diagnostic procedures
H Affects both sexes equally H Electrocardiography shows right atrial hypertrophy,
H Usually occurs in childhood right or left ventricular hypertrophy, atrial fibrilla-
tion, and incomplete right bundle-branch block.
Common characteristics H Right-sided heart catheterization shows high atrial
H Dyspnea on exertion pressure, tricuspid insufficiency, and decreased or
H Peripheral edema normal output.
H Tachycardia
H Fatigue
Treatment
Complications
H Heart failure General
H Pulmonary edema H Underlying cause
H Thromboembolism H Low-sodium diet
H Endocarditis H Fluid restriction
H Arrhythmias H Activity as tolerated

Medications
Identifying the murmur of tricuspid H Diuretics
insufficiency H Cardiac glycoside
H Anticoagulants
A high-pitched, blowing pansystolic murmur in the tricus-
H Angiotensin-converting enzyme inhibitors
pid area characterizes tricuspid insufficiency.
H Oxygen
H Prophylactic antibiotics in some patients before and
SYSTOLE DIASTOLE SYSTOLE
after surgery or dental care to prevent endocarditis
S1 S2 S1 S2
Surgery
H Annuloplasty or valvuloplasty to reconstruct or repair
the valve
H Valve replacement with a prosthetic valve

842 Tricuspid insufficiency

9400T.qxd 8/2/12 4:50 PM Page 843

Nursing considerations
Key outcomes
The patient will:
H carry out activities of daily living without weakness
or fatigue
H maintain hemodynamic stability
H maintain adequate ventilation.

Nursing interventions
H Administer oxygen.
H Watch for signs of heart failure or pulmonary edema.
H Alternate periods of activity and rest.
H Keep patients legs elevated to improve venous return
to the heart.
Monitoring
H Vital signs and pulse oximetry
H Cardiac rhythm
H Pulmonary artery catheter readings
H Intake and output
H Adverse effects of drug therapy

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H dietary restrictions and medications
H signs and symptoms that should be reported
H the importance of consistent follow-up care
H the need to elevate his legs when sitting.

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Tricuspid stenosis Assessment

History
Overview H Orthopnea
H Dyspnea
Description H Fatigue
H Heart condition in which the tricuspid valve improp- H Angina
erly functions, allowing backflow of blood into the H Palpitations
right atrium and causing right atrial enlargement
Physical findings
Pathophysiology H Diastolic murmur (see Identifying the murmur of
H Alterations in the structure of the tricuspid valve tricuspid stenosis)
cause incompetence of the valve. H Split S1
H Restriction of blood flow into the right ventricle and, H Crackles in the lungs
subsequently, to the pulmonary vasculature occurs. H Hepatomegaly (with right-sided failure)
H Obstructed venous return results in hepatic enlarge- H Ascites
ment, decreased pulmonary blood flow, peripheral
edema, and right atrial enlargement. Test results
Imaging
Causes H Chest X-ray reveals cardiomegaly.
H Mitral and aortic valve disorders H Echocardiography shows structure of the valves.
H Rheumatic heart disease Diagnostic procedures
H Carcinoid heart disease H Electrocardiography may show atrial fibrillation.
H Infective endocarditis
H Endomyocardial fibrosis
H Systemic lupus erythematosus Treatment
H Tricuspid atresia
General
Incidence H Underlying cause
H Affects females slightly more commonly than males H Low-sodium diet
H Fluid restriction
Common characteristics H Activity as tolerated
H Dyspnea on exertion
H Peripheral edema Medications
H Fatigue H Diuretics
H Ascites H Inotropic agent
H Angiotensin-converting enzyme inhibitors
Complications H Oxygen
H Heart failure H Antibiotics before and after dental procedures or
H Pulmonary edema surgery in some patients or if infection present
H Thromboembolism
H Endocarditis Surgery
H Arrhythmias H Balloon valvoplasty
H Pulmonary artery balloon angioplasty
H Valvotomy

Identifying the murmur of tricuspid

stenosis Nursing considerations
A low, rumbling crescendo-decrescendo murmur in the Key outcomes
tricuspid area characterizes tricuspid stenosis.
The patient will:
H carry out activities of daily living without weakness or
SYSTOLE DIASTOLE SYSTOLE
fatigue
S1 S2 S1 S2
H maintain hemodynamic stability
H maintain adequate ventilation.

Nursing interventions
H Administer oxygen.
H Watch for signs of heart failure or pulmonary edema.
H Alternate periods of activity and rest.

844 Tricuspid stenosis

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H When sitting in a chair, elevate legs to improve

venous return to the heart.
H Elevate the head of the bed.
H Keep the patient on a low-sodium diet.
H If the patient has surgery, watch for hypotension,
arrhythmias, and thrombus formation.
Monitoring
H Vital signs and pulse oximetry
H Cardiac rhythm
H Pulmonary artery catheter readings
H Intake and output
H Adverse effects of drug therapy

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H dietary restrictions
H medication administration, dosage, and possible
adverse effects
H signs and symptoms that should be reported
H avoidance of triggers.

Discharge planning
H Refer the patient to support services as needed.

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Incidence
Trigeminal neuralgia H Affects people older than age 40
H Affects more females than males

Overview Common characteristics

H Sudden onset of severe, throbbing pain
Description H Contortion of affected side of the face
H Painful disorder of the 5th cranial (trigeminal) nerve
H Right side of face affected more commonly than left Complications
H Can subside spontaneously H Excessive weight loss
H Remissions last from several months to years H Depression
H Also known as tic douloureux H Social isolation

Pathophysiology
H The trigeminal nerve has multiple branches. This Assessment
nerve affects chewing movements and sensations of
the face, scalp, and teeth. (See Trigeminal nerve History
function and distribution.) H Searing or burning facial pain occurring in lightning-
H A trigger zone is stimulated, and interaction or like jabs
short-circuiting of touch and pain fibers occurs. Lasts from 1 to 15 minutes (usually 1 or 2 min-
H Paroxysmal attacks of excruciating facial pain result. utes)
Localized in an area innervated by the trigeminal
Causes nerve
H Afferent reflex phenomenon Initiated by a light touch to a hypersensitive area
H Compression of the nerve root by: H Attacks possibly following:
Posterior fossa tumors Draft of air
Middle fossa tumors Exposure to heat or cold
Vascular lesions Eating, smiling, and talking
H Multiple sclerosis Drinking hot or cold beverages
H Herpes zoster A pain-free period
H Stroke
Physical findings
H Favoring (splinting) of affected area
Trigeminal nerve function and H Affected side of the face unwashed and unshaven
distribution H Patient never touches affected area
H No impairment of sensory or motor function
Function
H Motor: chewing movements
H Sensory: sensations of face, scalp, and teeth (mouth
Test results
and nasal chamber) Imaging
Distribution H Skull X-rays, computed tomography scan, and mag-
I ophthalmic netic resonance imaging results rule out sinus or
II maxillary tooth infections and tumors.
III mandibular

Treatment
I
General
H No dietary restrictions
H No activity restrictions

Medications
H Anticonvulsants, such as carbamazepine, gabapentin,
II and phenytoin
H Antidepressants such as nortriptyline
H Baclofen

III Surgery
H Microvascular decompression
H Radiosurgery with stereotactic technique
H Partial sensory rhizotomy to sever the nerve

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H Percutaneous balloon compression of the trigeminal

nerve
H Alcohol or glycerol injection

Other
H Radiation therapy
H Acupuncture
H Biofeedback
H Electrical stimulation of nerves

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort and decreased
pain
H perform activities of daily living within confines of
the disorder
H consume required caloric intake daily
H express feelings of increased energy and decreased
fatigue
H perform routine roles.

Nursing interventions
H Provide emotional support.
H Provide nutritional management.
H Administer prescribed drugs.
H After microsurgery, provide postcraniotomy care.

Monitoring
H Characteristics of each attack
H Precipitating factors of each attack
H Response to medications
H Postoperatively, neurologic function and vital signs

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H preoperative teaching if indicated
H medication administration, dosage, and possible
adverse effects
H nutritional management
H avoidance of triggers.

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Complications
Trisomy 13 syndrome H Congenital heart defects (common), especially hy-
poplastic left heart, ventricular septal defect, patent
ductus arteriosus, or dextroposition, which may sig-
Overview nificantly contribute to the cause of death
H Musculoskeletal abnormalities
Description H Microphthalmia, cataracts, and other eye abnormali-
H Third most common multiple malformation syn- ties
drome
H In most affected infants, full trisomy 13 at birth;
rarely, mosaic partial trisomy 13 syndrome (with Assessment
varying phenotypes) or translocation types
H Brain and facial abnormalities as well as major car- History
diac, GI, and limb malformations typical H Failure to thrive
H Full trisomy 13 syndrome fatal H Seizures
H Also known as Pataus syndrome H Apnea
H Feeding difficulties
Pathophysiology
H About 75% of all cases result from chromosomal Physical findings
nondisjunction. H Sloping forehead with wide sutures and fontanel
H About 20% of cases result from chromosomal H Scalp defect at the vertex
translocation, involving a rearrangement of chromo- H Bilateral cleft lip with associated cleft palate
somes 13 and 14. H Flat, broad nose
H About 5% of cases are estimated to be mosaics; the H Low-set ears and inner ear abnormalities
clinical effects in these cases may be less severe. H Polydactyl hands and feet
H Club feet
Causes H Omphaloceles
H Chromosomal abnormality H Neural tube defects
H Cystic hygroma
Risk factors H Genital abnormalities
H Advanced maternal age (mean maternal age
about 31) Test results
Laboratory
Incidence H Karyotype, done either prenatally or on peripheral
H Many trisomic zygotes spontaneously aborted (50% blood lymphocytes or skin fibroblasts in a neonate or
to 70% die within 1 month after birth and 85% by the an aborted fetus, is diagnostic.
first year) H Results are abnormal (but not diagnostic) in
H Only isolated cases of survival beyond 5 years in full multiple-marker maternal serum screening tests in-
trisomy 13 patients; in all survivors, profound mental volving different combinations of alpha-fetoprotein,
retardation human chorionic gonadotropin (HCG) or free beta-
H Estimated to affect 1 in 4,000 to 10,000 neonates HCG in some laboratories, and unconjugated estriol.
Imaging
Common characteristics H Ultrasonography usually reveals multiple abnormali-
H Microcephaly ties in the fetus.
H Varying degrees of holoprosencephaly
H Sloping forehead with wide sutures and fontanel
H Scalp defect at the vertex Treatment
H Bilateral cleft lip with associated cleft palate
H Flat, broad nose General
H Low-set ears and inner ear abnormalities H Supportive care
H Polydactyl hands and feet
H Club feet
H Omphaloceles Nursing considerations
H Neural tube defects
H Cystic hygroma Key outcomes
H Genital abnormalities The patient will:
H Cystic kidneys H function at the highest level possible
H Hydronephrosis H appear comfortable.

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Nursing interventions
H Maintain the infants fluid balance.
H Position the infant comfortably.
H Allow adequate time for the parents to bond with and
hold their child.
H Provide emotional support to the family.

Monitoring
H Intake and output
H Safety
H Growth

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H activities that can be carried out with the child
H safety factors.

Discharge planning
H Refer the parents of an affected infant for genetic
counseling to explore the cause of the disorder and
to discuss the risk of recurrence in future pregnan-
cies.
H Refer the parents to a social worker or grief coun-
selor for additional support if needed.
H Refer the parents to the Support Organization for
Trisomy 18, 13, and Related Disorders (S.O.F.T.)
national support program to allow them to interact
with other parents of infants with trisomy 18 and
trisomy 13.

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Life-threatening disorder
Trisomy 18 syndrome
Overview
Description
H Second most common multiple malformation syn-
drome
H In most affected infants, full trisomy 18, involving an
extra (third) copy of chromosome 18 in each cell;
partial trisomy 18 (with varying phenotypes) and
translocation types also reported
H Intrauterine growth retardation, congenital heart de-
fects, microcephaly, and other malformations in most
infants with this disorder
H Full trisomy 18 syndrome generally fatal or extremely
poor prognosis (30% to 50% of infants die within the
first 2 months and 90% die within the first year; most
surviving patients are profoundly mentally retarded.)
H Also known as Edwards syndrome
Pathophysiology
H Most cases of trisomy 18 result from spontaneous
meitotic nondisjunction, effecting an extra copy of
chromosome 18 in each cell.
Causes
H Chromosomal abnormality
Risk factors
H Typically increases with maternal age (mean mater-
nal age 3212)
Incidence
H Incidence ranges from 1 in 3,000 to 8,000 neonates;
three to four females affected for every male
Common characteristics
H Growth retardation, which begins in utero and re-
mains significant after birth
H Initial hypotonia that may soon give way to hyper-
tonia
H Microcephaly and dolichocephaly
H Micrognathia
H Short, narrow nose with upturned nares
H Unilateral or bilateral cleft lip and palate
H Low-set, slightly pointed ears
H Short neck
H Conspicuous clenched hand with overlapping fingers
(commonly seen on ultrasound)
H Cystic hygroma
H Choroid plexus cysts (also seen in some normal in-
fants)
Complications
H Congenital heart defects, such as ventricular septal
defect, tetralogy of Fallot, transposition of the great
vessels, and coarctation of the aorta (in 80% to 90%
of patients), which may be the cause of death in
many cases
H Other congenital anomalies, such as diaphragmatic
hernia, various renal defects, omphalocele, neural
tube defects, genital and perineal abnormalities (in-
cluding imperforate anus), and oligohydramnios
Assessment
History
H Growth retardation, which begins in utero and re-
mains significant after birth
Physical findings
H Short, narrow nose with upturned nares
H Unilateral or bilateral cleft lip and palate
H Low-set, slightly pointed ears
H Short neck
H Conspicuous clenched hand with overlapping fingers
(commonly seen on ultrasound)
H Cystic hygroma
H Choroid plexus cysts (also seen in some normal in-
fants)
Test results
Laboratory
H Karyotype, done either prenatally or on peripheral
blood lymphocytes or skin fibroblasts in a neonate or
an aborted fetus, is diagnostic.
H Results are abnormal (but not diagnostic) in
multiple-marker maternal serum screening tests in-
volving different combinations of alpha-fetoprotein,
human chorionic gonadotropin, and unconjugated
estriol.
Imaging
H Ultrasonography commonly reveals variable abnor-
malities in the fetus.
Treatment
General
H Emotional support for the family
H Nutrition maintenance using gavage feedings
Nursing considerations
Key outcomes
The patient will:
H function at the highest level possible
H appear comfortable.

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Nursing interventions
H Allow adequate time for the parents to bond with and
hold their child.
H Provide emotional support to the family.

Monitoring
H Intake and output
H Growth

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H home care and feeding techniques.

Discharge planning
H Refer the parents of a child affected with trisomy 18
syndrome for genetic counseling to explore the cause
of the disorder and discuss the risk of recurrence in
a future pregnancy.
H Refer the parents to a social worker or grief coun-
selor for additional support if needed.
H Refer the parents to the Support Organization for
Trisomy 18, 13, and Related Disorders (S.O.F.T.)
national support program to allow them to interact
with other parents of infants with trisomy 18 and tri-
somy 13.

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Common characteristics
Tuberculosis H Weakness and fatigue
H Anorexia, weight loss
H Low-grade fever
Overview H Night sweats

Description Complications
H Acute or chronic lung infection characterized by pul- H Massive pulmonary tissue damage
monary infiltrates and the formation of granulomas H Respiratory failure
with caseation, fibrosis, and cavitation H Bronchopleural fistulas
H Prognosis excellent with proper treatment and com- H Pneumothorax
pliance H Pleural effusion
H Also known as TB H Pneumonia
H Infection of other body organs by small mycobacteri-
Pathophysiology al foci
H Multiplication of the bacillus Mycobacterium tuber- H Liver disease involvement secondary to drug therapy
culosis causes an inflammatory process where de-
posited.
H A cell-mediated immune response follows, usually Assessment
containing the infection within 4 to 6 weeks.
H The T-cell response results in the formation of granu- History
lomas around the bacilli, making them dormant. This In primary infection
confers immunity to subsequent infection. H May be asymptomatic after a 4- to 8-week incubation
H Bacilli within granulomas may remain viable for period
many years, resulting in a positive purified protein H Weakness and fatigue
derivative or other skin test for TB. H Anorexia, weight loss
H Active disease develops in 5% to 15% of those H Low-grade fever
infected. H Night sweats
H Transmission occurs when an infected person In reactivated infection
coughs or sneezes. H Chest pain
H Productive cough for blood, or mucopurulent or
Causes blood-tinged sputum
H Exposure to M. tuberculosis H Low-grade fever
H Sometimes, exposure to other strains of mycobac-
teria Physical findings
H Dullness over the affected area
Risk factors H Crepitant crackles
H Close contact with newly diagnosed TB patient H Bronchial breath sounds
H History of prior TB exposure H Wheezes
H Multiple sexual partners H Whispered pectoriloquy
H Recent immigration from Africa, Asia, Mexico, or
South America Test results
H Gastrectomy Laboratory
H History of silicosis, diabetes, malnutrition, cancer, H Tuberculin skin test is positive in both active and in-
Hodgkins disease, or leukemia active TB.
H Drug and alcohol abuse H Stains and cultures of sputum, cerebrospinal fluid,
H Residence in nursing home, mental health facility, or urine, abscess drainage, or pleural fluid show
prison heat-sensitive, nonmotile, aerobic, acid-fast bacilli.
H Immunosuppression and use of corticosteroids Imaging
H Homelessness H Chest X-rays show nodular lesions, patchy infiltrates,
cavity formation, scar tissue, and calcium deposits.
Incidence H Computed tomography scan or magnetic resonance
H Overall decrease in TB but greater among high-risk imaging shows presence and extent of lung damage.
populations Diagnostic procedures
H Twice as common in males as in females H Bronchoscopy specimens show heat-sensitive, non-
H Four times as common in nonwhites as in whites motile, aerobic, acid-fast bacilli in specimens.
H Higher incidence in Black and Hispanic males
between ages 25 and 44
H Highest incidence in people who live in crowded,
poorly ventilated, unsanitary conditions

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Treatment
General
H After 2 to 4 weeks, when disease is no longer infec-
tious, resumption of normal activities while continu-
ing to take medication
H Well-balanced, high-calorie diet
H Rest, initially; activity as tolerated
Medications
H Antitubercular therapy for at least 6 months with dai-
ly oral doses of the following:
Isoniazid
Rifampin
Pyrazinamide
Ethambutol, added in some cases
H Second-line drugs include the following:
Capreomycin
Streptomycin
Aminosalicylic acid (para-aminosalicylic acid)
Pyrazinamide
Cycloserine
Surgery
H For some complications
Nursing considerations
Key outcomes
The patient will:
H maintain adequate ventilation
H use support systems to assist with coping
H identify measures to prevent or reduce fatigue
H express an understanding of the illness
H comply with treatment regimen.
Nursing interventions
H Administer prescribed drugs.
H Isolate the patient in a quiet, properly ventilated
room, and maintain TB precautions.
H Provide diversional activities.
H Properly dispose of secretions.
H Provide adequate rest periods.
H Provide well-balanced, high-calorie foods.
H Provide small, frequent meals.
H Consult with a dietitian if oral supplements are
needed.
H Perform chest physiotherapy.
H Provide supportive care.
H Include the patient in care decisions.
Prevention
Preventing tuberculosis
The spread of tuberculosis (TB) can be prevented by fol-
lowing these guidelines:
H Hospitalized patients should follow respiratory and
standard precautions.
H A discharged patient should wear a mask around oth-
ers until hes no longer contagious.
H Tell all health care providers, including dentists and op-
tometrists about TB diagnosis so they can use infec-
tion control precautions.
H Cough and sneeze into a tissue and dispose of prop-
erly.
H Practice thorough hand washing with hot soapy water
after handling secretions.
H Wash eating utensils separately in hot, soapy water.
Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medication administration, dosage, and possible ad-
verse effects
H when to notify the physician
H need for isolation
H postural drainage and chest percussion
H coughing and deep-breathing exercises
H regular follow-up examinations
H signs and symptoms of recurring TB
H possible decreased hormonal contraceptive effective-
ness while taking rifampin
H need for a high-calorie, high-protein, balanced diet
H TB prevention. (See Preventing tuberculosis.)
Discharge planning
H Refer anyone exposed to an infected patient for test-
ing and follow-up.
H Refer the patient to a support group such as the
American Lung Association.
H Refer the patient to a smoking-cessation program
if indicated.

Monitoring
H Vital signs
H Intake and output
H Daily weight
H Complications
H Adverse reactions
H Visual acuity if taking ethambutol
H Liver and kidney function tests

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Tularemia Assessment
History
Overview H Tick bite
H Exposure to contaminated food or water
Description H Exposure to contaminated blood
H Francisella tularensis organism, a gram-negative H Abrupt onset of fever, chills, headache, and malaise
pleomorphic bacterium, causing disease in humans H Contact with an infected carcass
and animals
H As few as 10 organisms able to cause disease Physical findings
H Incubation period 3 to 4 days Ulceroglandular
H Six forms: H Ulcers at the site of inoculation
Ulceroglandular form H Swollen regional lymph nodes
Glandular form Glandular
Oculoglandular form H Swollen regional lymph nodes
Oropharyngeal form Oculoglandular
Pneumonic form H Painful
Septicemic form H Red eye
H Purulent exudates
Pathophysiology H Swollen submandibular, preauricular, or cervical
H The organism gains access to the host by skin or mu- lymph nodes
cous membrane inoculation, inhalation, or ingestion. Oropharyngeal
H After inoculation a papule (that eventually evolves H Sore throat
into an ulcer) and high fever develop. H Abdominal pain
H Nausea
Causes H Vomiting
H Bites of ticks and deerflies H Diarrhea
H Eating or drinking contaminated food or water H Occasionally, GI bleeding
H Contact with the blood of an infected animal, espe- Pneumonic
cially rabbits H Dry cough
H Breathing in the bacteria F. tularensis H Dyspnea
H Pleuritic chest pain
Risk factors Septicemic
H Participating in hunting and trapping H Fever, chills, myalgia, malaise, and weight loss
H Gardening H Absence of ulcer
H Participating in outdoor sports or occupations
Test results
Incidence Laboratory
H About 200 cases in humans annually H White blood cell count is normal or elevated.
H Occurs more commonly in the south-central and H Blood or sputum cultures are positive for F. tularen-
western United States sis.
H Serology is positive for antibodies to tularemia.
Common characteristics Imaging
H Ulcer and fever H Chest X-ray shows pneumonia.

Complications
H Pneumonia Treatment
H Lung abscess
H Respiratory failure General
H Rhabdomyolysis H Proper skin care
H Meningitis H Increased fluid intake
H Pericarditis
H Osteomyelitis Medications
H Antibiotics, such as streptomycin, gentamicin, and
tetracycline
H Antipyretics

854 Tularemia
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Nursing considerations
Key outcomes
The patient will:
H regain normal temperature
H regain or maintain normal fluid balance.

Nursing interventions
H Administer prescribed drugs.
H Replace lost fluids through diet or I.V. fluids.

Monitoring
H Intake and output
H Vital signs
H Signs of dehydration

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medication administratiion, dosage, and possible
adverse effects
H complications and when to notify the physician
H preventive measures, such as using insect repellent
containing DEET on skin, or treating clothing with
repellent containing permethrin.

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U Ulcerative colitis
Overview
Description
H Episodic inflammatory chronic disease causing ul-
cerations of the mucosa in the colon
H Condition beginning in the rectum and sigmoid colon
and possibly extending upward into the entire colon
H Rarely affecting the small intestine, except for the ter-
minal ileum
H Produces congestion, edema (leading to mucosal
friability), and ulcerations
H Coagulation defects
H Erythema nodosum on the face and arms
H Pyoderma gangrenosum on the legs and ankles
H Uveitis
H Pericholangitis, sclerosing cholangitis
H Cirrhosis
H Cholangiocarcinoma
H Ankylosing spondylitis
H Strictures
H Pseudopolyps, stenosis, and perforated colon leading
to peritonitis and toxemia
H Arthritis

Assessment
H Range of severity from mild, localized disorder to
fulminant disease causing many complications History
H Remission and exacerbation of symptoms
Pathophysiology H Mild cramping and lower abdominal pain
H The disorder primarily involves the mucosa and the H Recurrent bloody diarrhea as often as 10 to 25 times
submucosa of the bowel. daily
H Crypt abscesses and mucosal ulceration may occur. H Nocturnal diarrhea
H The mucosa typically appears granular and friable. H Fatigue and weakness
H The colon becomes a rigid, foreshortened tube. H Anorexia and weight loss
H In severe ulcerative colitis, areas of hyperplastic H Nausea and vomiting
growth occur, with swollen mucosa surrounded by
inflamed mucosa with shallow ulcers. Physical findings
H Submucosa and the circular and longitudinal mus- H Liquid stools with visible pus, mucus, and blood
cles may be involved. H Possible abdominal distention
H Abdominal tenderness
Causes H Perianal irritation, hemorrhoids, and fissures
H Cause unknown H Jaundice
H May be related to an abnormal immune response in H Joint pain
the GI tract, possibly associated with genetic factors
Test results
Risk factors Laboratory
H Stress (may increase severity of an attack) H Stool specimen analysis reveals blood, pus, and mu-
H Family history cus, but no pathogenic organisms.
H Jewish ancestry H Other supportive laboratory tests show decreased
serum levels of potassium, magnesium, hemoglobin,
Incidence and albumin as well as leukocytosis and increased
H Primarily young adults, especially females prothrombin time; an elevated erythrocyte sedimen-
H More prevalent among Jews and higher socioeco- tation rate correlates with the severity of the attack.
nomic groups Imaging
H About 1 in 1,000 persons affected H Barium enema discloses the extent of disease and
H Onset of symptoms commonly peaking between ages complications, such as strictures and carcinoma.
15 and 30 and again between ages 50 and 70 This study isnt performed in a patient with active
signs and symptoms.
Common characteristics Diagnostic procedures
H Crampy lower abdominal pain H Sigmoidoscopy confirms rectal involvement in most
H Recurrent bloody diarrhea cases by showing increased mucosal friability, de-
creased mucosal detail, and thick inflammatory exu-
Complications dates, edema, and erosions.
H Nutritional deficiencies H Colonoscopy may be used to determine the extent of
H Perineal sepsis the disease and to evaluate the areas of stricture and
H Anal fissure, anal fistula pseudopolyps. This test isnt performed when the pa-
H Perirectal abscess tient has active signs and symptoms.
H Perforation of the colon H Biopsy, performed during colonoscopy, helps to con-
H Hemorrhage, anemia firm the diagnosis.
H Toxic megacolon
H Cancer

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Treatment Patient teaching

General Be sure to cover:
H I.V. fluid replacement H the disorder, diagnosis, and treatment
H Blood transfusions (if needed) H prescribed dietary changes
H Nothing by mouth (if severe) H need to avoid GI stimulants, such as caffeine, alco-
H Parenteral nutrition (with severe disease) hol, and smoking
H Supplemental feedings H medication administration, dosage, and possible
H Rest periods during exacerbations adverse effects
H after a proctocolectomy and ileostomy, stoma care
Medications H after a pouch ileostomy, procedures to insert the
H Corticotropin and adrenal corticosteroids catheter and care for the stoma
H Sulfasalazine H the need for regular physical examinations because
H Mesalamine of the increased risk of colorectal cancer.
H Antispasmodics and antidiarrheals
H Fiber supplements Discharge planning
H Immune modifiers, such as azathioprine, 6-MP and H Refer the patient to a smoking-cessation program if
methotrexate indicated.
H Antibiotics H Refer the patient to an enterostomal therapist if
appropriate.
Surgery
H Treatment of last resort
H Proctocolectomy with ileostomy
H Pouch ileostomy
H Ileoanal reservoir with loop ileostomy
H Colectomy

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort and decreased
pain
H have normal fluid volume
H have intact skin
H exhibit no evidence of infection
H avoid or have only minimal complications
H maintain adequate caloric intake.

Nursing interventions
H Encourage verbalization and provide support.
H Provide diet therapy.
H Administer drug therapy.
H Administer blood transfusions.
H Schedule care to allow for frequent rest periods.

Monitoring
H Response to treatment
H Fluid and electrolyte status
H Hemoglobin level and hematocrit
H Complications
After surgery
H Vital signs
H Wound site
H Pain level
H Bowel function
H Nasogastric tube function and drainage
H Skin integrity

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Incidence
Urinary tract infection, H Nearly 10 times more common in females than in

lower males (except elderly males), probably because

natural anatomic features facilitate infection
H Affects 10% to 20% of all females at least once

Overview Common characteristics

H Urinary urgency and frequency
Description H Dysuria
H Bacterial infection of the lower urinary tract system H Cloudy, foul-smelling urine
H Two forms: H Mild fever
Cystitis (infection of the bladder)
Urethritis (infection of the urethra) Complications
H Usually a ready response to treatment H Damage to the urinary tract lining
H Possible recurring and resistant bacterial flare-ups H Infection of adjacent organs and structures
during therapy H Kidney infections and damage
H Also known as lower UTI
Special populations
Special populations
Elderly people and young children have the greatest
In adult males and children, lower UTIs are typical- risk for kidney damage because they may lack the
ly associated with anatomic or physiologic abnor- typical symptoms, thereby delaying diagnosis.
malities and require close evaluation.
Assessment
Pathophysiology
H Local defense mechanisms in the bladder break History
down. H Urinary urgency and frequency
H Bacteria invade the bladder mucosa and multiply. H Bladder cramps or spasms
H Bacteria cant be readily eliminated by normal urina- H Pruritus
tion. H Feeling of warmth during urination
H The pathogens resistance to prescribed antimicro- H Nocturia or dysuria
bial therapy usually causes bacterial flare-up during H Urethral discharge (in males)
treatment. H Lower back or flank pain
H Recurrent lower UTIs result from reinfection by the H Malaise and chills
same organism or a new pathogen. H Nausea and vomiting

Causes Physical findings

H Ascending infection by a single gram-negative, en- H Pain or tenderness over the bladder
teric bacterium, such as Escherichia coli, Klebsiella, H Hematuria
Proteus, Enterobacter, Pseudomonas, and Serratia H Fever
H Simultaneous infection with multiple pathogens H Cloudy, foul-smelling urine

Risk factors Test results

H Natural anatomical variations Laboratory
H Inadequate fluid consumption H Microscopic urinalysis shows red blood cell and
H Trauma or invasive procedures white blood cell counts greater than 10 per high-
H Urinary catheter power field, suggesting lower UTI.
H Urinary tract obstructions H Urinalysis shows bacterial count of more than
H Vesicourethral reflux 100,000/ml, confirming UTI.
H Urinary stasis H Sensitivity testing determines appropriate antimi-
H Diabetes crobial drug.
H Bowel incontinence H If the patient history and physical examination war-
H Immobility rant, a blood test or a stained smear of urethral dis-
H Sexual intercourse (females) charge rules out sexually transmitted disease.
Imaging
H Voiding cystourethrography or excretory urography
may demonstrate congenital anomalies, predisposing
the patient to recurrent UTIs.

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Prevention
Treatment Preventing UTIs
General Urinary tract infections (UTIs) can be prevented by follow-
ing these guidelines:
H Increased fruit juice intake, especially cranberry H Practice proper cleaning after toileting by wiping from
H Increased fluid intake front to back.
H Empty your bladder after intercourse and drink a full
Medications glass of water.
H Antimicrobials H Drink plenty of water each day.
H Urinate when you feel the urge, dont hold it in.
Surgery H Avoid irritating feminine products with deodorants,
H In case of recurrent infections from infected renal such as douches and powders.
calculi, chronic prostatitis, or structural abnor-
malities

Nursing considerations
Key outcomes
The patient will:
H report increased comfort
H identify risk factors that worsen the condition, and
modify her lifestyle accordingly
H demonstrate skill in managing the urinary elimina-
tion problem
H complete the prescribed course of treatment.

Nursing interventions
H Collect all urine specimens appropriately.
H Administer drug therapy.
H Encourage oral fluid intake unless contraindicated.
H Apply warm compresses to lower abdomen for com-
fort as needed.
Monitoring
H Intake and output
H Urine characteristics
H Voiding patterns
H Vital signs
H Adverse effects of antimicrobial therapy

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H completing the prescribed course of antibiotic
therapy
H medication administration, dosage, and possible
adverse effects
H prevention. (See Preventing UTIs.)

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Urticaria Assessment
and angioedema History
H Drug history, including nonprescription prepara-
tions, such as vitamins, aspirin, and antacids
Overview H Reported commonly troublesome foods and environ-
mental factors
Description H Exposure to physical factors, such as cold, sunlight,
H Common allergic reactions exercise, and trauma (dermatographism)
H Occur separately or simultaneously H Adverse reaction to iodinated contrast media used
H Urticaria: may be acute (present less than 6 weeks) for diagnostic radiologic studies
or chronic (present at least 6 weeks)
H Also known as hives Physical findings
H Distinct, raised, evanescent dermal wheals surround-
Pathophysiology ed by a reddened flare
H Urticaria is an episodic, rapidly occurring, usually H Nonpitting swelling of deep subcutaneous tissue on
self-limiting skin reaction. It involves only the super- the eyelids, lips, genitalia, and mucous membranes
ficial portion of the dermis, which erupts with local that doesnt itch but may burn and tingle
wheals surrounded by an erythematous flare. H Respiratory stridor and hoarseness
H Angioedema involves additional skin layers and pro- H Anxiety, gasping for breath, and difficulty speaking
duces deeper, larger wheals (usually on the hands, H Abdominal colic with or without nausea and vomiting
feet, lips, genitalia, and eyelids). It causes diffuse H Signs of anaphylaxis: hypotension, respiratory dis-
swelling of loose subcutaneous tissue and may affect tress, stridor
the upper respiratory and GI tracts.
H Several mechanisms and disorders may provoke ur- Test results
ticaria and angioedema. They include immunoglobu- Laboratory
lin (Ig) E-induced release of mediators from cuta- H Decreased serum levels of C1, C2, and C4 inhibitors
neous mast cells and binding of IgG or IgM to confirm the diagnosis.
antigen, resulting in complement activation. Diagnostic procedures
H Diagnosis can be confirmed through careful skin
Causes testing with the suspected offending substance to see
H Unknown if a local wheal and flare result.
H Drug allergy
H Food allergy
H Insect bite Treatment
H Occupational skin exposure
H Inhalant allergens (animal dander, cosmetics) General
H Viral infection H Emergency measures if signs of anaphylaxis
H Hormones H Limited contact with triggering factors
H Thyroid abnormality H Desensitization to the triggering antigen
H Rheumatological disease H Avoidance of food allergens
H Cholinergic trigger (heat, exercise, stress)
Medications
Incidence H Antihistamines
H Affect about 20% of general population at some time H Systemic glucocorticoids
H More common after adolescence, with highest inci-
dence in the 30s
H Affect females more commonly than males Nursing considerations
Common characteristics Key outcomes
H Raised, red wheals The patient will:
H Diffuse edema H maintain a patent airway
H Pruritus H express feelings of increased comfort and decreased
pain
Complications H exhibit improved or healed lesions or wounds
H Skin abrasion and secondary infection H avoid or have only minimal complications
H Laryngeal edema H correlate precipitating factors with appropriate skin
H Respiratory arrest care regimen.
H Severe abdominal colic

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Nursing interventions
H Maintain a patent airway.
H Reduce or minimize environmental exposure to
offending allergens and irritants, such as wool
and harsh detergents.
H If food is a suspected cause, gradually eliminate
foods from the diet, and watch for improvement.
H Administer drug therapy.

Monitoring
H Vital signs, with attention to respiratory status
H Skin, for signs of secondary infection caused by
scratching
H Response to treatment

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H how to identify the cause by keeping a diary to
record exposure to suspected offending substances
and signs and symptoms that appear after exposure
H how to monitor nutritional status and food replace-
ments for nutrients lost by excluding allergy-
provoking foods and beverages
H the need to keep fingernails short to avoid abrading
the skin when scratching
H signs and symptoms that indicate a skin infection
H use of an epinephrine emergency kit if anaphylaxis
occurs
H use of medical identification jewelry.

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Common characteristics
Uterine bleeding, H Metrorrhagia (episodes of vaginal bleeding between

dysfunctional menses)
H Hypermenorrhea (heavy or prolonged menses,
longer than 8 days, also incorrectly termed menor-
rhagia)
Overview H Chronic polymenorrhea (menstrual cycle less than
18 days) or oligomenorrhea (infrequent menses)
Description H Fatigue from anemia
H Abnormal endometrial bleeding without recognizable H Oligomenorrhea and infertility from anovulation
organic lesions
H The indication for almost 25% of gynecologic surgi- Complications
cal procedures H Iron deficiency anemia (blood loss of more than
H Prognosis varies with cause, but good prognosis with 1.6 L over a short time)
correction of hormonal imbalance or structural H Hemorrhagic shock
abnormality H Right-sided heart failure (rare)
H Also known as DUB H Endometrial adenocarcinoma from chronic estrogen
stimulation
Pathophysiology
H Irregular bleeding is associated with hormonal im-
balance and anovulation (failure of ovulation to oc- Assessment
cur).
H When progesterone secretion is absent but estrogen History
secretion continues, the endometrium proliferates H Abnormal uterine bleeding
and becomes hypervascular. H Fatigue
H When ovulation doesnt occur, the endometrium is H Infertility
randomly broken down, and exposed vascular chan- H Bleeding in response to a brief course of proges-
nels cause prolonged and excessive bleeding. terone
H In most cases of abnormal uterine bleeding, the en- H Absence of body temperature changes during ovula-
dometrium shows no pathologic changes; however, tory cycle
in chronic unopposed estrogen stimulation (as from
a hormone-producing ovarian tumor), the endo- Physical findings
metrium may show hyperplastic or malignant H Pallor
changes. H Signs of underlying disorder
H Pelvic examination revealing uterine abnormality
Causes
H Usually an imbalance in the hormonal-endometrial Test results
relationship involving persistent and unopposed Laboratory
stimulation of the endometrium by estrogen H Hemoglobin levels and hematocrit determine the
H Disorders causing sustained high estrogen levels: need for blood transfusion or iron supplementation.
Polycystic ovary syndrome H Serum progesterone levels are decreased.
Obesity (because enzymes present in peripheral Diagnostic procedures
adipose tissue convert the androgen androstene- H Dilatation and curettage (D&C) or office endometrial
dione to estrogen precursors) biopsy rules out endometrial hyperplasia and cancer
Immaturity of the hypothalamic-pituitary-ovarian in females older than age 35.
mechanism (postpubertal teenagers)
Anovulation (females in their late 30s or early
40s) Treatment
H Trauma (foreign object insertion or direct trauma)
H Endometriosis General
H Coagulopathy, such as thrombocytopenia or leukemia H Monitoring of bleeding episodes
(rare) H Emotional support
H Drug-induced coagulopathy H Balanced diet
H Rest periods when fatigued
Incidence
H About 10% of females with normal ovulatory cycles Medications
H More episodes of abnormal bleeding among black H High-dose estrogen-progestogen combination thera-
females, possibly secondary to a higher incidence py (hormonal contraceptives); maintenance therapy
of leiomyomas and higher levels of estrogen with lower dose combination hormonal contracep-
H Most common in puberty and perimenopause tives

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H Progestogen therapy
H I.V. estrogen followed by progesterone or combina-
tion hormonal contraceptives if the patient is young
(more likely to be anovulatory) and severely anemic
(if oral drug therapy is ineffective)
H Iron supplementation or transfusions of packed cells
or whole blood
Surgery
H Endometrial biopsy to rule out endometrial adeno-
carcinoma (patients age 35 and older)
H D&C (short-lived treatment and not clinically useful,
but an important diagnostic tool) with hysteroscopy
as an adjunct

Nursing considerations
Key outcomes
The patient will:
H maintain hemodynamic stability
H have normal menstrual cycles
H express understanding of the disorder and its treat-
ment.
Nursing interventions
H Tell the patient to record the dates of the bleeding
and the number of pads she saturates per day. In-
struct the patient not to use tampons.
H Offer reassurance and support.
H Suggest to the patient that she minimize blood flow
by avoiding strenuous activity and by lying down with
her feet elevated.
Monitoring
H Vital signs
H Amount of bleeding
H Hemoglobin levels
H Response to treatment

Patient teaching
Be sure to cover:
H the importance of following the prescribed hormonal
therapy
H the purpose and procedures of D&C or endometrial
biopsy procedure if ordered
H the need for regular checkups to assess the effective-
ness of treatment
H the importance of reporting abnormal bleeding im-
mediately to help rule out major hemorrhagic disor-
ders such as those that occur in abnormal pregnancy
H having a Papanicolaou test and a pelvic examination
annually.

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Uterine cancer Assessment

History
Overview H Presence of risk factors
H Spotting and protracted, heavy menses (in younger
Description patient)
H Proliferation of cancer cells in the endometrium H In postmenopausal woman, possible bleeding begin-
H Most common gynecologic cancer ning 12 or more months after menses stopped
H Also known as endometrial cancer H Vaginal discharge, initially watery, then increasingly
blood streaked
Pathophysiology
H Uterine cancer is usually adenocarcinoma. Physical findings
H Metastasis occurs late (usually from the endometri- H Palpable enlarged uterus (advanced disease)
um to the cervix, ovaries, fallopian tubes, and other H Abdominal tenderness
peritoneal structures). It may spread to distant or-
gans, such as the lungs and the brain, by way of the Test results
blood or the lymphatic system; lymph node involve- Diagnostic procedures
ment can also occur. H Endometrial, cervical, or endocervical biopsy con-
H Less common uterine tumors include adenoacan- firms the presence of cancer cells.
thoma, endometrial stromal sarcoma, lymphosar- H Fractional dilatation and curettage are used to identi-
coma, mixed mesodermal tumors (including carci- fy the problem when the disease is suspected but the
nosarcoma), and leiomyosarcoma. endometrial biopsy result is negative.
H Multiple cervical biopsies and endocervical curettage
Causes pinpoint cervical involvement.
H Exact cause unknown H Papanicolaou test result may be normal or show
abnormal cells.
Risk factors Other
H Low fertility index and anovulation H Schillers test involves staining the cervix and vagina
H History of infertility or failure of ovulation with an iodine solution that turns healthy tissues
H Abnormal uterine bleeding brown. (Cancerous tissues resist the stain.)
H Obesity
H Hypertension
H Diabetes Treatment
H Nulliparity
H Familial tendency General
H History of uterine polyps or endometrial hyperplasia H Radiation therapy
H Prolonged estrogen therapy with exposure unop- H Well-balanced diet
posed by progesterone
H Tamoxifen therapy Medications
H Hormonal therapy such as progestin
Incidence H Chemotherapy
H Most common in postmenopausal females between
ages 60 and 70 (uncommon between ages 30 and 40 Surgery
and rare before age 30) H Total abdominal hysterectomy, bilateral salpingo-
H Most premenopausal patients having history of oophorectomy or, possibly, omentectomy with or
anovulatory menstrual cycles or other hormonal without pelvic or para-aortic lymphadenectomy
imbalances H Total pelvic exenteration
H Annually about 33,000 new cases reported; about
5,500 eventually fatal
Nursing considerations
Common characteristics
H Abnormal vaginal bleeding Key outcomes
H Lower abdominal bleeding The patient will:
H express positive feelings about self
Complications H report feeling increased comfort and decreased pain
H Anemia H (with partner) express feelings and perceptions
H Intestinal obstruction about change in sexual performance
H Ascites H experience no signs or symptoms of infection.
H Increasing pain
H Hemorrhage

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Nursing interventions
H Encourage verbalization and provide support.
H Administer drug therapy.
H Encourage the patient to breathe deeply and cough.

Monitoring
After surgery
H Wound site and drainage system
H Vital signs
H Postoperative complications
H Pain control
Internal radiation therapy
H Safety precautions (time, distance, and shielding)
H Movement (limited while source is in place)
H Vital signs
H Complications from radiation therapy, such as skin
reaction, vaginal bleeding, abdominal discomfort,
and dehydration

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H preoperative and postoperative care
H (if the patient is premenopausal) that removal of her
ovaries will induce menopause
H safety measures involved in internal radiation therapy
H dietary modifications
H medication administration, dosage, and possible
adverse effects
H importance of follow-up examinations with a gyne-
cologist.
Discharge planning
H Refer the patient to available resource and support
services.

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Uterine leiomyomas H Malposition of the fetus

Overview
Description
H Most common benign uterine tumors in females
H Tumors composed of smooth muscle that usually oc-
cur in the uterine corpus, although they may appear
on the cervix or on the round or broad ligament
H Malignant (leiomyosarcoma) in less than 0.1% of
patients
H Also known as myomas, fibromyomas, or fibroids
Pathophysiology
H Classified according to location, tumors may be lo-
cated within the uterine wall (intramural) or pro-
trude into the endometrial cavity (submucous) or
from the serosal surface of the uterus (subserous).
H Size varies greatly.
H Tumors are usually firm and surrounded by a pseu-
docapsule composed of compressed but otherwise
normal uterine myometrium.
H The uterine cavity may become larger, increasing the
endometrial surface area. This can cause increased
uterine bleeding.
Causes
H Unknown, but some factors implicated as regulators
of leiomyoma growth include the following:
Several growth factors including epidermal growth
factor
Steroid hormones, including estrogen and proges-
terone (typically arise after menarche and regress
after menopause, implicating estrogen as a pro-
moter of leiomyoma growth)
Risk factors
H Females of reproductive age
H Family member with uterine leiomyomas
H Anemia secondary to excessive bleeding
H Bladder compression
H Infection (if tumor protrudes out of the vaginal
opening)
H Secondary infertility (rare)
H Bowel obstruction
Assessment
History
H Abnormal menstrual bleeding
H Urinary frequency, urgency, or incontinence
H Abdominal cramping during menstruation
Physical findings
H Pelvic pressure
H Abdominal distention
Test results
Laboratory
H Blood studies show anemia caused by abnormal
bleeding (may support diagnosis).
Imaging
H Ultrasonography allows accurate assessment of the
dimension, number, and location of tumors.
H Magnetic resonance imaging reveals calcified
fibroids.
Diagnostic procedures
H Hysterosalpingography detects myomas.
Other
H Patient history reveals evidence.
H Bimanual examination shows enlarged, firm, non-
tender, and irregularly contoured uterus (also seen
with adenomyosis and other pelvic abnormalities).
H Endometrial biopsy rules out endometrial cancer
in patients older than age 35 with abnormal uterine
bleeding.
H Laparoscopy corroborates other testing.

Incidence Treatment
H May affect three times as many Blacks as Whites; true
incidence in either population unknown General
H May occur at any age, but most common in females H Blood transfusions
older than age 30 H Activity as tolerated

Common characteristics Medications

H Abnormal bleeding, typically menorrhagia with dis-
rupted submucosal vessels (most common symptom)
H Pain only associated with torsion of a pedunculated
(stemmed) subserous tumor or leiomyomas under-
going degeneration
H Pelvic pressure and impingement on adjacent viscera
(indications for treatment, depending on severity)
resulting in mild hydronephrosis
Complications
H Recurrent spontaneous abortion
H Preterm labor
H Gonadotropin-releasing hormone agonists to rapidly
suppress pituitary gonadotropin release
H Nonsteroidal anti-inflammatory drugs
Surgery
H Abdominal, laparoscopic, or hysteroscopic myomec-
tomy
H Myolysis
H Uterine artery embolization (radiologic procedure)
to block uterine arteries using small pieces of
polyvinyl chloride
H Hysterectomy

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Nursing considerations
Key outcomes
The patient will:
H report increased comfort and decreased pain
H relate understanding of the disorder and treatment
and state feelings
H return to normal menstrual periods.

Nursing interventions
H Reassure the patient that she wont experience pre-
mature menopause if her ovaries are left intact.
H In a patient with severe anemia from excessive bleed-
ing, give iron supplements and blood transfusions.
H Encourage the patient to verbalize her feelings and
concerns related to the disease process and its ef-
fects on her lifestyle.
Monitoring
H Comfort level
H Amount of bleeding
H Response to treatment

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the importance of reporting abnormal bleeding or
pelvic pain immediately
H the importance of regular gynecologic examinations.

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V Vaginal cancer
Overview
Description
H Proliferation of cancer cells in the vagina
H Rarest gynecologic cancer
H Usually appears as squamous cell carcinoma, but
occasionally as melanoma, sarcoma, or adenocar-
cinoma
Pathophysiology
H Because the vagina is a thin-walled structure with
Physical findings
H Ulcerated lesion in any area of the vagina

Test results
Laboratory
H Papanicolaou test shows abnormal cells.
Diagnostic procedures
H Biopsy identifies cancerous cells. Biopsy of the cervix
and vulva may also be performed to rule out these
areas as primary cancer sites.
H Colposcopy is used to locate lesions that may have
been missed during the pelvic examination.
Other
H Lugols solution painted on the suspected area helps
to identify malignant areas by staining glycogen-
rich lymphatic drainage, vaginal cancer varies in containing normal tissue. (Abnormal tissue resists
severity, depending on its exact location and effect on staining.)
lymphatic drainage.
H It may progress from an intraepithelial tumor to an
invasive cancer. Treatment
H The upper third of the vagina is the most common
site of vaginal cancer. General
H Radiation therapy (preferred treatment for all stages
Causes of vaginal cancer)
H Exact cause unknown H Well-balanced diet
H Limited activity with internal radiation therapy
Risk factors
H Advanced age (most likely risk factor) combined Medications
with the following: H Topical chemotherapy with fluorouracil and laser
Trauma surgery
Chronic pessary use
Use of chemical carcinogens (such as those in Surgery
some sprays and douches) H May be recommended when tumor is so extensive
Use of diethylstilbestrol (DES) by the patients that vaginas close proximity to the bladder and rec-
mother during pregnancy tum allows only minimal tissue margins around re-
Previous cancer of the endometrium, vulva, or sected vaginal tissue
cervix
History of human papilloma virus
Nursing considerations
Incidence
H Usually occurs in females in their early to middle 50s Key outcomes
H Rarely, rhabdomyosarcoma in children The patient will:
H express positive feelings about self
Common characteristics H experience feelings of increased comfort and de-
H Bloody vaginal drainage creased pain
H Urine retention H express feelings and perceptions about change in
sexual performance (with partner)
Complications H exhibit no signs or symptoms of infection.
H Metastasis possibly affecting the cervix, uterus, and
rectum Nursing interventions
H Encourage verbalization and provide support.
H Administer prescribed drugs.
Assessment
Monitoring
History H Response to treatment
H Presence of risk factors H Vaginal discharge
H Bloody vaginal discharge Internal radiation therapy
H Irregular or postmenopausal bleeding H Safety measures (time, distance, and shielding)
H Urine retention or urinary frequency (if the lesion is H Limited movement
close to the neck of the bladder) H Complications caused by radiation therapy

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Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H safety measures (for internal radiation therapy)
H importance of follow-up care
H importance of regular gynecologic check-ups
H potential adverse reactions to chemotherapy and
ways to manage them
H signs and symptoms of infection and the need to re-
port them to a physician immediately
H ways to avoid infection.

Discharge planning
H Refer the patient (and family) to American Cancer
Society for resources and support services.

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Complications
Vancomycin H Sepsis

intermediate-resistant H Multisystem organ involvement

H Death in the immunocompromised patient

Staphylococcus aureus
Assessment
Overview History
H Possible breach in the immune system, surgery, or
Description condition predisposing the patient to the infection
H Staphylococci infection that has decreased suscepti- H Multiple antibiotic use
bility to vancomycin
H Common in chronically ill patients; most likely devel- Physical findings
oping in health care setting H The carrier patient commonly asymptomatic but pos-
H Patient with methicillin-resistant Staphylococcus au- sibly exhibiting signs and symptoms related to the
reus (MRSA) normally most reliably and effectively primary diagnosis
treated with vancomycin; MRSA with decreased sus- H The patient possibly exhibiting cardiac, respiratory,
ceptibility to vancomycin possibly a sign that van- or other major symptoms
comycin-resistant strains are emerging
H Also called VISA, VRSA (more severe form) and gly- Test results
copeptide intermediate-resistant Staphylococcus Laboratory
aureus H Culture shows staphylococci with decreased suscepti-
bility to vancomycin after 24-hour incubation.
Pathophysiology
H Genes encode resistance and are carried on plasmids
that transfer themselves from cell to cell. Treatment
H Resistance is mediated by enzymes that substitute a
different molecule for the terminal amino acid so General
that vancomycin cant bind. H With an infection, possibly no treatment (Stop all an-
tibiotics and simply wait for normal bacteria to re-
Causes populate and replace the strain.)
H Colonized patient: more than 10 times as likely to be- H Colonized patient in contact isolation until culture-
come infected with the organism as uncolonized pa- negative or discharged
tient such as through a breach in the immune system H Antimicrobial drugs (VISA isolates not susceptible to
H VISA that enters a health care facility through an in- vancomycin generally are susceptible to other
fected or colonized patient or a colonized health care drugs.)
worker H No dietary restrictions
H Spread during direct contact between the patient and H Rest periods when fatigued
caregiver or patient and patient; possibly being
spread through patient contact with a contaminated Medications
surface such as an overbed table H Antimicrobials

Risk factors
H Diabetes Nursing considerations
H Kidney disease
H Previous MRSA infection Key outcomes
H Recent hospitalization The patient will:
H Recent antimicrobial therapy H maintain collateral circulation
H attain hemodynamic stability
Incidence H maintain adequate cardiac output
H First discovered in mid-1996 H remain afebrile
H Incidence rare, about 16 cases reported in the Unit- H have an adequate fluid volume.
ed States
H Noted in patients receiving multiple courses of van- Nursing interventions
comycin for MSRA infections H Consider grouping infected patients together and
having the same nursing staff care for them.
Common characteristics H Institute contact isolation precautions.
H Causative organism possibly living for weeks on such H Ensure judicious and careful use of antibiotics. En-
surfaces as patient gowns, bed linens, and handrails courage physicians to limit the use of antibiotics.
H No specific symptoms; cultures found incidentally

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H Use infection-control practices, such as wearing Prevention

gloves before and after contact with infectious body Preventing the transmission
tissues and proper hand washing, to reduce the of VISA
spread of VISA. The transmission of vancomycin-intermediate resistant
Monitoring Staphylococcus aureus (VISA) can be prevented by fol-
lowing these guidelines:
H Vital signs H Practice proper hand-washing techniques using soap
H Response to treatment and water.
H Complications H Avoid contact with open wounds or contaminated
dressings.
H Dispose of contaminated articles, including items used
Patient teaching for dressing change and protective equipment, prop-
erly.
H Family and friends should wear protective equipment
Be sure to cover:
when visiting a patient with VISA.
H the disorder, diagnosis, and treatment
H medication administration, dosage, and possible
adverse effects
H how to prevent the spread of VISA. (See Preventing
the transmission of VISA.)

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Vancomycin-resistant Assessment
enterococcus History
H Possible breach in the immune system, surgery, or
condition predisposing the patient to the infection
Overview H Multiple antibiotic use

Description Physical findings

H Mutation of a common bacterium H Carrier commonly asymptomatic
H Easily spread by direct person-to-person contact
H Also called VRE Test results
Laboratory
Pathophysiology H VRE is isolated from stool or a rectal swab.
H Genes encode resistance and are carried on plasmids
that transfer themselves from cell to cell.
H Resistance is mediated by enzymes that substitute a Treatment
different molecule for the terminal amino acid so
that vancomycin cant bind. General
H With an infection, possibly no treatment
Causes H Colonized patient placed in contact isolation until
H Enters health care facility through infected or colo- culture-negative or discharged
nized patient or colonized health care worker H Rest periods when fatigued
H Spread through direct contact between patient and
caregiver, between patients, or through contact with Medications
contaminated surfaces H Antimicrobials (VRE isolates not susceptible to van-
comycin generally susceptible to other antimicrobial
Risk factors drugs)
H Immunocompromised condition
H Advanced age
H Indwelling catheter Nursing considerations
H Major surgery
H Open wounds Key outcomes
H History of taking vancomycin or a third-generation The patient will:
cephalosporin H remain afebrile
H History of enterococcal bacteremia, commonly H have adequate fluid volume.
linked to endocarditis
H Organ transplantation Nursing interventions
H Prolonged or repeated hospital admissions H Consider grouping infected patients together and
H Chronic renal failure having the same nursing staff care for them.
H Exposure to contaminated equipment or a VRE- H Institute contact isolation precautions.
positive patient. H Ensure judicious and careful use of antibiotics. En-
courage physicians to limit the use of antibiotics.
Incidence H Use infection-control practices, such as wearing
H Reported in facilities in more than 40 states gloves and proper hand-washing techniques, to re-
H Rates as high as 14% in oncology units duce the spread of VRE.
Common characteristics Monitoring
H No specific signs and symptoms H Vital signs
H May be found incidentally when culture results show H Response to treatment
the organism H Complications

Complications
H Sepsis

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Prevention
Preventing the spread of
VRE at home
The transmission of VRE can be prevented by following
these guidelines:
H Wash hands with soap and water after physical contact
with the patient and before leaving the home.
H Use towels only once when drying hands after contact.
H Wear disposable gloves if you expect to come in con-
tact with the patients body fluids and wash hands after
removing the gloves.
H Change linens routinely and whenever they become
soiled.
H Clean the patients environment routinely and when it
becomes soiled with body fluids with a household dis-
infectant or a mixture of 14 cup of bleach and 1 qt of
water.
H Tell physicians and other health care personnel caring
for the patient that the patient is infected with an or-
ganism resistant to multiple drugs.

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment (see Prevent-
ing the spread of VRE at home)
H the need for family and friends to wear personal pro-
tective equipment when visiting the patient
H how to dispose of protective equipment
H medication administration, dosage, and possible
adverse effects.
Discharge planning
H Refer the patient and family to support and social
services.

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Complications
Varicella H With scratching due to severe pruritus: infection,
scarring, impetigo, furuncles, and cellulitis
H Reyes syndrome
Overview H Pneumonia
H Myocarditis
Description H Bleeding disorders
H An acute, highly contagious viral infection H Arthritis
H The same virus that causes chickenpox, thought to H Nephritis
become latent until the sixth decade of life or later, H Hepatitis
causing herpes zoster (shingles) H Acute myositis
H Transmission through direct contact (primarily with H Congenital varicella-caused hypoplastic deformity,
respiratory secretions, less commonly with skin le- limb scarring, retarded growth, and central nervous
sions) and indirect contact (airborne) system and eye problems
H Commonly known as chickenpox

Pathophysiology Assessment
H Localized replication of the virus occurs (probably in
the nasopharynx), leading to seeding of the reticu- History
loendothelial system and development of viremia. H Recent exposure to someone with chickenpox
H Diffuse and scattered skin lesions result with vesicles H Malaise
involving the corium and dermis with degenerative H Headache
changes (ballooning) and infection of localized H Anorexia
blood vessels.
H Necrosis and epidermal hemorrhage result; vesicles Physical findings
eventually rupture and release fluid or are reab- H Temperature 101 to 103 F (38.3 to 39.4 C)
sorbed. H Crops of small, erythematous macules on the trunk
H Incubation period lasts 13 to 17 days. or scalp
H Infection is communicable from 48 hours before le- H Macules progressing to papules and then clear vesi-
sions erupt until after vesicles are crusted over. cles on an erythematous base (so-called dewdrops
on rose petals)
Causes H Vesicles becoming cloudy and breaking easily; then
H Varicella-zoster herpesvirus scabs forming
H Rash that spreads to face and, rarely, to extremities
Risk factors H Rash containing a combination of red papules, vesi-
H Close contact with others at home, school, or child cles, and scabs in various stages
care facility H Ulcers on mucous membranes of the mouth, con-
H Lack of immunization junctivae, and genitalia
Incidence Test results
H Most common in children ages 5 to 9, but can occur Laboratory
at any age H Virus can be isolated from vesicular fluid within the
H Congenital varicella possibly in infants whose moth- first 3 to 4 days of the rash.
ers had acute infections in first or early second H Giemsa stain distinguishes the varicella-zoster virus
trimester from the vaccinia-variola virus.
H Neonatal infection rare, probably because of tran- H Serum samples contain antibodies 7 days after onset
sient maternal immunity of symptoms.
H Occurs worldwide; endemic in large cities with out- H Serologic testing differentiates rickettsial pox from
breaks occurring sporadically varicella.
H Equally affects all races and both sexes
H Seasonal distribution varies; in temperate areas, inci-
dence higher during late winter and spring Treatment
Common characteristics General
H Malaise H Strict isolation until all vesicles have crusted over; for
H Crops of macules progressing to vesicles congenital chickenpox, no isolation
H Pruritus H Increased fluid intake
H Rest periods when fatigued

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Medications
H Antipruritics
H Antibiotics
H Analgesic and antipyretic
H Acyclovir
H Varicella-zoster immune globulin

Nursing considerations
Key outcomes
The patient will:
H report or demonstrate an increased energy level
H exhibit improved or healed lesions or wounds
H interact with family and peers to decrease feelings of
isolation
H express or demonstrate increased comfort.

Nursing interventions
H Observe an immunocompromised patient for mani-
festations of complications, such as pneumonitis and
meningitis, and report them immediately.
H Provide skin care comfort measures (calamine lo-
tion, cornstarch, sponge baths, or showers).
H Administer varicella-zoster immune globulin if or-
dered to lessen the severity of the disease.
H Institute strict isolation measures until all skin le-
sions have crusted.
H Prevent exposure to pregnant women.

Monitoring
H Response to treatment
H Complications
H Skin integrity
H Signs and symptoms of dehydration
H Signs and symptoms of infection
H Adverse drug reactions

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medication administration, dosage, and possible
adverse effects
H how to correctly apply topical antipruritic medica-
tions
H the importance of good hygiene and keeping the
childs fingernails trimmed
H the need for the child to avoid scratching the lesions
H the parents need to watch for and immediately re-
port signs of complications (severe skin pain and
burning that may indicate a serious secondary infec-
tion and require prompt medical attention)
H the need for parents to refrain from giving the child
aspirin because of its association with Reyes syn-
drome
H signs and symptoms of Reyes syndrome and the need
to immediately report them to a physician.

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Incidence
Varicocele H Present in 30% of all males diagnosed with infertility
H Occurs in the left spermatic cord 95% of the time
H Highest in males between ages 15 and 25
Overview
Common characteristics
Description H Asymptomatic
H A mass of dilated and tortuous varicose veins in the H Feeling of heaviness on the affected side
spermatic cord H Testicular pain and tenderness on palpation
H Commonly described as a bag of worms (see Tak-
ing a close look at a varicocele) Complications
H Infertility
Pathophysiology H Hydrocele
H Because of a valvular disorder in the spermatic vein,
blood pools in the pampiniform venous plexus.
H One function of the pampiniform plexus is to keep Assessment
the testes slightly cooler than body temperature,
which is the optimal temperature for sperm produc- History
tion. H Infertility
H Incomplete blood flow through the testes thus inter- H Feeling of heaviness on affected side
feres with spermatogenesis.
H Testicular atrophy may also occur because of the re- Physical findings
duced blood flow. H Palpation of bag of worms when patient upright
H Drained, cant be felt when patient recumbent
Causes H Testicular tenderness
H Incompetent or congenitally absent valves in the
spermatic veins Test results
H Tumor or thrombus obstructing the inferior vena Other
cava (unilateral left-sided varicocele) H Physical examination confirms varicocele.

Treatment
Taking a close look at a varicocele
General
Varicocele, an abnormal dilation of the veins of the sper- H Scrotal support to relieve discomfort
matic cord, is asymptomatic, but its important to identify
and correct this condition in adolescent boys because it Surgery
causes infertility.
H Surgical repair or removal involving ligation of the
spermatic cord at the internal inguinal ring (if infer-
tility is an issue)

Nursing considerations
Key outcomes
The patient will:
H express understanding of the disorder and its treat-
ment
H express feelings regarding effect on fertility
H express feelings of increased comfort.

Nursing interventions
H Promote the patients comfort before and after
surgery.
H After surgery, administer prescribed drugs.
H Apply an ice bag with a cover to reduce edema.
H Protect the wound from contamination.

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H Allow the patient to perform as many normal daily

activities as possible.
Monitoring
H Intake and output
H Comfort level
H Wound healing

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H wound care.

From Pillitte
Philadelphia

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Varicose veins Assessment

History
Overview H May be asymptomatic
H Feeling of heaviness in the legs that worsens in the
Description evening and in warm weather
H Dilated, tortuous veins, engorged with blood result- H Leg cramps at night
ing from improper venous valve function H Diffuse, dull, aching leg pain after prolonged stand-
H Primary varicose veins originating in superficial veins ing or walking
(the saphenous veins and branches) H Aching legs during menses
H Secondary varicose veins occurring in deep and H Fatigue
perforating veins H Exercise possibly relieving symptoms because venous
return improves
Pathophysiology
H A weakened valve allows backflow of blood to the Physical findings
previous valve in a vein. H Dilated, purplish, ropelike veins, especially in the
H If the valve cant hold the pooling blood, it becomes calf
incompetent, allowing even more blood to flow back- H Orthostatic edema and stasis of the calves and ankles
ward. H Nodules along affected veins and valve incompetence
H As the volume of venous blood builds, pressure in H In chronic condition, venous stasis ulcers, which
the vein increases and the vein becomes distended. must be differentiated from arterial and diabetic
H As the vein stretches, it loses elasticity, enlarges, and ulcerations
becomes tortuous.
H Hydrostatic pressure increases, plasma is forced Test results
out into surrounding tissue, and edema results. Imaging
H Ascending and descending venography demonstrate
Causes venous occlusion and patterns of collateral flow.
H Congenital weakness of the valves or venous wall Diagnostic procedures
H Pregnancy H Photoplethysmography, a noninvasive test, character-
H Tight clothing izes venous blood flow by showing changes in the
H Occupations that necessitate standing for an extend- skins circulation.
ed period H Doppler ultrasonography quickly and accurately
H Deep vein thrombosis shows the presence or absence of venous backflow
H Trauma in deep or superficial veins.
H Venous outflow and reflux plethysmography can be
Risk factors used to detect deep venous occlusion.
H Polonged standing or time on feet
H Obesity
H Heavy lifting Treatment
H Pregnancy
General
Incidence H Wearing elastic stockings
H Common in middle adulthood H Avoiding tight clothing
H Primary varicose veins: Family tendency, affect both H For moderate varicose veins: wearing antiembolism
legs, twice as common in females as males stockings or elastic bandages
H Secondary varicose veins: usually in only one leg H For severe varicose veins: custom-fitted, surgical-
weight stockings with graduated pressure
Common characteristics H Avoidance of prolonged standing
H Dilated, purple, ropelike veins H Routine exercise
H Edema of calves and ankles H Elevation of the legs
H Venous stasis ulcers
Medications
Complications H Sclerotherapy
H Venous insufficiency
H Venous stasis ulcers Surgery
H Stripping and ligation
H Laser surgery

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H Catheter-assisted procedures Prevention

H Phlebectomy Preventing varicose veins
H Endoscopic vein surgery
Individuals with risk factors for varicose veins may pre-
vent them by following these guidelines:
Nursing considerations H Rest your legs and elevate them periodically if standing
is prolonged.
H Wear supportive stockings.
Key outcomes H Avoid wearing high heels and panty leg girdles.
The patient will: H Drink 2 to 3 qt (2 to 3 L) of fluid per day.
H express understanding of disorder and treatment H Eat plenty of fiber and avoid salt to decrease swelling
H maintain adequate distal and collateral circulation caused by fluid retention and constipation.
H express feelings of increased comfort and decreased H Avoid crossing your legs when sitting.
pain H Exercise regularly
H Maintain a healthy weight.
H carry out activities of daily living without excess
fatigue or discomfort.
Nursing interventions
H After stripping and ligation or after injection of a
sclerosing agent, administer analgesics as ordered
to relieve pain.
H Frequently check circulation in toes and observe
elastic bandages for bleeding. When ordered, rewrap
bandages at least once per shift, wrapping from toe
to thigh, with the leg elevated. (See Preventing vari-
cose veins.)
Monitoring

ALERT
Watch for signs and symptoms of complications,
such as sensory loss in the leg, calf pain, and fever.

H Response to treatment
H Skin integrity
H Pain control

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the need to avoid wearing constrictive clothing
H elevating the legs above heart level when possible
and avoiding prolonged standing or sitting
H how to put on the elastic, antiembolism, or compres-
sion stockings before getting out of bed in the morn-
ing (or lying with the legs raised for 1 minute before
putting on the stockings)
H how to avoid injury to the lower legs, ankles, and feet
and the need to observe for altered skin integrity of
those areas and to report any problems to the physi-
cian as soon as possible.

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Vascular retinopathies Central retinal vein occlusion

H Reduced visual acuity, allowing perception of only
hand movement and light within 3 to 4 months after
occlusion
Overview Diabetic retinopathy
NONPROLIFERATIVE DIABETIC RETINOPATHY
Description H Changes in the lining of the retinal blood vessels that
H Noninflammatory retinal disorders that result from cause the vessels to leak plasma or fatty substances,
interference with the blood supply to the eyes which decrease or block blood flow (nonperfusion)
H Five distinct types: central retinal artery occlusion, within the retina
central retinal vein occlusion, diabetic retinopathy, H Microaneurysms and small hemorrhages
hypertensive retinopathy, and sickle cell retinopathy H Significant loss of central visual acuity (necessary for
reading and driving)
Pathophysiology H Diminished night vision
H When one of the arteries maintaining blood circula- PROLIFERATIVE DIABETIC RETINOPATHY
tion in the retina becomes obstructed, the dimin- H Fragile new blood vessels on the disk and elsewhere
ished blood flow causes visual deficits. in the fundus (neovascularization)
Hypertensive retinopathy
Causes H Based on the location of retinopathy, mild visual dis-
Central retinal artery occlusion turbances such as blurred vision resulting from
H Idiopathic retinopathy located near the macula
H Embolism Sickle cell retinopathy
H Atherosclerosis H Optic disc changes
H Infection H Macular changes
H Conditions that retard blood flow, such as carotid
occlusion and heart valve vegetations Complications
Central retinal vein occlusion Central retinal artery occlusion
H External compression of the retinal vein H Permanent vision loss
H Trauma Central retinal vein occlusion
H Diabetes H Secondary glaucoma
H Thrombosis Diabetic retinopathy
H Granulomatous diseases PROLIFERATIVE DIABETIC RETINOPATHY
H Generalized and localized infections H Vitreous hemorrhage with corresponding sudden
H Glaucoma vision loss
H Atherosclerosis H Macular distortion
Diabetic retinopathy H Retinal detachment
H Juvenile or adult diabetes Hypertensive retinopathy
Hypertensive retinopathy H Blindness
H Prolonged hypertensive disease H Mild, prolonged disease
Sickle cell retinopathy H Visual defects
H Impaired ability of the sickled cell to pass through Sickle cell retinopathy
the microvasculature, producing vasocclusion H Optic nerve neovascularization
H Sickling crisis
Incidence H Optic nerve and macular infarction
Central retinal vein occlusion
H Most prevalent in elderly patients
Diabetic retinopathy Assessment
H About 75% of patients with juvenile diabetes develop-
ing retinopathy within 20 years of onset of diabetes History
H In adults with diabetes, incidence increasing with the H Changes in visual acuity
duration of diabetes; 80% of patients who have had H Causative factors
diabetes for 20 to 25 years developing retinopathy, a
leading cause of acquired adult blindness Physical findings
Sickle cell retinopathy H Decreased visual acuity
H Occurs in 1% to 6% of sickle-cell patients H Abnormal opthalmic examination

Common characteristics Test results

Central retinal artery occlusion H Appropriate diagnostic tests depend on the type of
H Sudden, painless, unilateral loss of vision (partial or vascular retinopathy. (See Diagnostic tests for vas-
complete) cular retinopathies.)

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Diagnostic tests for vascular

Treatment retinopathies
Central retinal artery occlusion Central retinal artery occlusion
H Ophthalmoscopy (direct or indirect): shows blockage
General of retinal arterioles during transient attack.
H Immediate ocular massage H Retinal examination: within 2 hours of onset, shows
H Anterior chamber paracentesis clumps or segmentation in artery; later, milky white
Medications retina around disk caused by swelling and necrosis of
H Heparin (if the cause of the occlusion is the heart) ganglion cells caused by reduced blood supply; also
shows cherry-red spot in macula that subsides after
Central retinal vein occlusion several weeks.
General H Color Doppler tests: evaluates carotid occlusion with
H Laser photocoagulation no need for arteriography.
Central retinal vein occlusion
Medications H Ophthalmoscopy (direct or indirect): shows flame-
H Aspirin
shaped hemorrhages, retinal vein engorgement, white
patches among hemorrhages, edema around the disk.
Diabetic retinopathy H Color Doppler tests: confirm or rule out occlusion of
General blood vessels.
H Careful control of blood glucose levels Diabetic retinopathy
H Eye examinations 3 to 4 times per year; annually for H Indirect ophthalmoscopic examination: shows retinal
children with diabetes changes, such as microaneurysms (earliest change),
H Laser photocoagulation (proliferative diabetic retinal hemorrhages and edema, venous dilation and
retinopathy) beading, lipid exudates, fibrous bands in the vitreous,
H Diabetic diet and growth of new blood vessels. Infarcts of the nerve
H Regular exercise fiber layer are observed.
H Fluorescein angiography: shows leakage of flourescein
Medications from weak-walled vessels and lights up microaneu-
H Antidiabetic drugs or insulin as appropriate
rysms, differentiating them from true hemorrhages.
Surgery Hypertensive retinopathy
H Vitrectomy for vitreous hemorrhage to restore vision H Ophthalmoscopy (direct or indirect): in early stages,
shows hard, shiny deposits; flame-shaped hemor-
Hypertensive retinopathy rhages; silver wire appearance of narrowed arterioles;
General and nicking of veins where arteries cross them (arterio-
H Control of blood pressure with appropriate drugs venous nicking). In late stages, shows cotton wool
H Low-sodium, low-cholesterol diet patches, lipid exudates, retinal edema, papilledema
H Regular exercise caused by ischemia and capillary insufficiency, hemor-
rhages, and microaneurysms in both eyes.
Sickle cell retinopathy Sickle cell retinopathy
H Ocular examination and dilated retinal evaluation:
General shows staged ocular symptoms.
H Treatment of disease
Stage 1: peripheral retinal arteriolar occlusion
Surgery Stage 2: peripheral arteriovenous anastamoses
H Laser retinal photocoagulation Stage 3: neovascular fronds known as seafans
H Retinal cryotherapy Stage 4: vitreous hemorrhage and tearing of neovascu-
H Vitrectomy or membranectomy lar membranes
Stage 5: severe vitreous traction and retinal detach-
ment
Nursing considerations
Key outcomes
The patient will: Monitoring
H maintain current health status H Vital signs
H regain visual function H Visual acuity
H express understanding of condition and its treatment.

Nursing interventions Patient teaching

H Arrange for immediate ophthalmologic evaluation
when a patient complains of sudden, unilateral loss
of vision.
H Encourage a patient with diabetes to comply with the
prescribed regimen.
Be sure to cover:
H the disorder, diagnosis, and treatment
H complying with therapy for underlying condition
H obtaining recommended follow-up care.

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Vasculitis Assessment
History
Overview H Varied findings, depending on blood vessels involved
Polyarteritis nodosa
Description H Fever
H Autoimmune condition that includes a broad spec- H Weight loss
trum of disorders characterized by blood vessel in- H Malaise
flammation and necrosis H Headache
H Clinical effects dependent on the vessels involved and H Abdominal pain
reflective of tissue ischemia caused by blood flow ob- H Myalgias
struction
Physical findings
Pathophysiology Polyarteritis nodosa (depends on body
H The process is initiated by excessive circulating anti- system)
gen, which triggers the formation of soluble antigen- H Hypertension (renal)
antibody complexes. The reticuloendothelial system H Arthritic changes (musculoskeletal)
cant effectively clear these complexes, which are de- H Rash, purpura, nodules, and cutaneous infarcts
posited in blood vessel walls. (skin)
H Increased vascular permeability (associated with the H Altered mental status and seizures (central nervous
release of vasoactive amines by platelets and baso- system)
phils) enhances this deposition. The deposited com- H Respiratory distress, peripheral edema, hepatomeg-
plexes activate the complement cascade and result in aly, peripheral vasoconstriction (cardiovascular)
chemotaxis of neutrophils, which release lysosomal
enzymes. Test results
H Vessel damage and necrosis result. Diagnostic procedures
H Not all vasculitis disorders can be diagnosed defini-
Causes tively through specific tests. The most useful general
H Several theories: diagnostic procedure is biopsy of the affected vessel.
Follows serious infectious disease and may be re-
lated to high doses of antibiotics
Formation of autoantibodies directed at the bodys Treatment
own cellular and extracellular proteins, which can
lead to the activation of inflammatory cells or cyto- General
toxicity H Avoidance of antigenic drugs
Cell-mediated (T-cell) immune response H Avoidance of antigenic foods
In atopic individuals, exposure to allergens H Avoidance of offending environmental substances

Risk factors Medications

H Hepatitis B or C H Corticosteroids
H Rheumatoid arthritis H Antihypertensives
H Sjgrens syndrome H Analgesics
H Other immune system disorders H Immunosuppressive agents
H Drug allergy H Antineoplastics

Incidence
H Can affect a person at any age (except mucocuta- Nursing considerations
neous lymph node syndrome, which affects only chil-
dren) Key outcomes
The patient will:
Common characteristics H express feelings of increased comfort and decreased
H Based on affected blood vessel pain
H express positive feelings about self
Complications H attain hemodynamic stability
H Renal failure, renal hypertension, glomerulitis H demonstrate adequate ventilation
H Fibrous scarring of the lung tissue H avoid complications.
H Stroke
H GI bleeding, intestinal obstruction
H Myocardial infarction and pericarditis
H Rupture of mesenteric aneurysms

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Nursing interventions
H Assess for dry nasal mucosa. Instill nose drops to lu-
bricate the mucosa and minimize crusting; irrigate
nasal passages with warm normal saline solution.
H Keep the patient well hydrated (about 3 qt [3 L] of
fluid daily).
H Make sure that a patient with decreased visual acuity
has a safe environment.
H Regulate environmental temperature to prevent addi-
tional vasoconstriction caused by cold temperatures.
H Provide emotional support to the patient and family.

Monitoring
H Vital signs and neurologic status
H Signs and symptoms of organ involvement
H Laboratory values
H GI disturbances and renal function tests
H Intake and output
H Daily weight

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medication administration, dosage, and possible
adverse effects
H watch for signs of bleeding and report adverse effects
to the physician
H the importance of wearing warm clothes and gloves
when going outside in cold weather.
Discharge planning
H Refer the patient to a smoking-cessation program if
appropriate.

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Ventricular septal defect
Overview
Description
H Heart condition in which an opening in the septum
between the ventricles allows blood to shunt between
the left and right ventricles
H Most common congenital heart disorder
H Also known as VSD
Pathophysiology
H The ventricular septum fails to close completely by
the 8th week of gestation, as it would normally.
H VSDs are located in the membranous or muscular
portion of the ventricular septum and vary in size.
H Some defects close spontaneously; in other defects,
the entire septum is absent, creating a single ventri-
cle.
H VSD isnt readily apparent at birth because right and
left ventricular pressures are approximately equal, so
blood doesnt shunt through the defect.
H As the pulmonary vasculature gradually relaxes, be-
tween 4 and 8 weeks after birth, right ventricular
pressure decreases, allowing blood to shunt from the
left to the right ventricle.
Causes
H Congenital
Risk factors
H Fetal alcohol syndrome
H Coexists with additional birth defects, especially
Down syndrome and other autosomal trisomies, re-
nal anomalies, and cardiac defects, such as patent
ductus arteriosus and coarctation of the aorta
Incidence
H Affects 2% to 7% of live births
H Slightly more common in females
Common characteristics
H Clinical features of VSD varying with the size of the
defect, the effect of the shunting on the pulmonary
vasculature, and the infants age
H A small VSD possibly closing spontaneously without
ever causing symptoms
H Large VSD shunts eventually causing biventricular
heart failure and cyanosis
Complications
H Heart failure
H Pneumonia
884 Ventricular septal defect
Assessment
History
H Dyspnea
H Cyanosis
H Slow weight gain
H Feeding difficulties
H Rapid grunting respirations
Physical findings
H Prominent anterior chest wall
H Clubbing
H Cyanosis
H With a large VSD, audible murmurs (at least a grade
3 pansystolic), loudest at the fourth intercostal
space, usually with a thrill; pulmonic component of
S2 loud and widely split
H With fixed pulmonary hypertension, diastolic mur-
mur possibly audible on auscultation, systolic mur-
mur becoming quieter, and S2 greatly accentuated
H Displacement of the point of maximal impulse to the
left
H Typical murmur associated with a VSD, blowing or
rumbling and varying in frequency
H In the neonate, moderately loud early systolic mur-
mur along the lower left sternal border, possibly be-
coming louder and longer about the second or third
day after birth
H In infants, murmur possibly loudest near the base of
the heart, which may suggest pulmonary stenosis
H In small VSD, functional murmur or characteristic
loud, harsh systolic murmur
Test results
Imaging
H Chest X-rays are normal in small defects; in large
VSDs, they show cardiomegaly, left atrial and left ven-
tricular enlargement, and prominent pulmonary vas-
cular markings.
H Echocardiography may detect a large VSD and its lo-
cation in the septum, estimate the size of a left-to-
right shunt, suggest pulmonary hypertension, and
identify associated lesions and complications.
Diagnostic procedures
H Electrocardiogram is normal in children with small
VSDs; in large VSDs, it shows left and right ventricu-
lar hypertrophy, suggesting pulmonary hypertension.
H Cardiac catheterization determines the size and exact
location of the VSD, calculates the degree of shunting
by comparing the blood oxygen saturation in each
ventricle, determines the extent of pulmonary hyper-
tension, and detects associated defects.
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H watching for signs of heart failure, such as poor

Treatment feeding, sweating, and heavy breathing
H medication administration, dosage, and possible
General adverse effects
H If the child has other defects and will benefit from H letting the child engage in normal activities
delaying surgery, pulmonary artery banding to nor- H the importance of prophylactic antibiotics before
malize pressures and flow distal to the band and pre- and after surgery.
vent pulmonary vascular disease
H Low-sodium diet Discharge planning
H Fluid restriction H Refer the patient and family to support and social
H Activity as tolerated services.
Medications
H Digoxin
H Diuretics
H Antibiotics
After surgery
H Analgesics
H Antibiotics
H Vasopressors

Surgery
H For small defects, simple suture closure
H For moderate to large defects, insertion of a patch
graft using cardiopulmonary bypass
H Mesh patch or plug placement during cardiac
catheterization (investigational)

Nursing considerations
Key outcomes
The patient will:
H maintain adequate ventilation
H maintain hemodynamic stability
H remain free from signs and symptoms of infection.

Nursing interventions
H Provide emotional support.
H Adminster prescribed drugs.

Monitoring
H Vital signs
H Signs of heart failure
H Intake and output
H Respiratory status
After surgery
H Hemodynamics
H Cardiac rhythm
H Oxygenation

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H preventing complications until the child is scheduled
for surgery or the defect closes

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Vesicoureteral reflux
Overview
Description
H A genitourinary condition in which urine flows from
the bladder back into the ureters and eventually into
the renal pelvis or the parenchyma
H Because the bladder empties poorly, possible urinary
tract infection (UTI), which may lead to acute or
chronic pyelonephritis with renal damage
Pathophysiology
H Incompetence of the ureterovesical junction and
shortening of intravesical ureteral musculature allow
backflow of urine into the ureter when the bladder
contracts during voiding.
Causes
H Congenital anomalies of the ureters or bladder
H Inadequate detrusor muscle buttress in the bladder,
stemming from congenital paraureteral bladder di-
verticulum
H Acquired diverticulum (from outlet obstruction)
H Flaccid neurogenic bladder
H High intravesical pressure from outlet obstruction
H Cystitis
H Sometimes unknown
Incidence
Special populations
Most common during infancy in boys and during
early childhood (ages 3 to 7) in girls
H Primary vesicoureteral reflux resulting from congeni-
tal anomalies most prevalent in females and rare in
blacks
H Also shown in up to 25% of asymptomatic siblings
of children with diagnosed primary vesicoureteral
reflux
Common characteristics
H Signs and symptoms of UTI
H Dark, concentrated urine
H With upper urinary tract involvement: high fever,
chills, flank pain, vomiting, and malaise
ALERT
In children, fever, nonspecific abdominal pain, and
diarrhea may be the only clinical effects. Rarely,
children with minimal symptoms remain undiag-
nosed until puberty or later, when they begin to ex-
hibit clear signs of renal impairment (anemia, hy-
pertension, and lethargy).
886 Vesicoureteral reflux
Complications
H Renal impairment
H UTIs
Assessment
History
H Urinary frequency and urgency
H Burning on urination
Physical findings
H In infants, hematuria or strong-smelling urine
H Hard, thickened bladder (hard mass deep in the
pelvis) if posterior urethral valves are causing an
obstruction in male infants
Test results
Laboratory
H Clean-catch urinalysis shows a bacterial count
greater than 100,000/l.
H Microscopic examination may reveal white blood
cells, red blood cells, and an increased urine pH in
the presence of infection. Specific gravity less than
1.010 demonstrates inability to concentrate urine.
H Elevated creatinine levels (more than 1.2 mg/dl) and
elevated blood urea nitrogen levels (more than
18 mg/dl) indicate advanced renal dysfunction.
Diagnostic procedures
H Cystoscopy, with instillation of a solution containing
methylene blue or indigo carmine dye, may confirm
the diagnosis.
H Excretory urography may show dilated lower ureter,
ureter visible for its entire length, hydronephrosis,
calyceal distortion, and renal scarring.
H Voiding cystourethrography (either fluoroscopic or
radionuclide) identifies and determines the degree of
reflux and shows when reflux occurs. It may also
pinpoint the causative anomaly.
H Nuclear cystography and renal ultrasound may detect
reflux.
Other
H Catheterization of the bladder after the patient voids
determines the amount of residual urine.
Treatment
General
H Increased fluid intake
Medications
H Antibiotics
Surgery
H Vesicoureteral reimplantation (if UTI recurs despite
adequate prophylactic antibiotic therapy)
H Bladder outlet obstruction in neurogenic bladder re-
quiring surgery only if renal dysfunction present
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Nursing considerations
Key outcomes
The patient will:
H return to normal urinary function
H remain free from infection
H develop no complications of the disorder.

Nursing interventions
H Encourage one of the parents to stay with the patient
during all procedures.
H Explain the procedures to the parents and to the
child, if hes old enough to understand.
H Administer prescribed drugs.
H Make sure catheters are patent and draining well.
Maintain sterile technique during catheter care.
Monitoring
H Intake and output
H Comfort level
H Vital signs

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H utilizing the vesicoureteral reflux to double void
(void once and then try to void again in a few
minutes)
H voiding every 2 to 3 hours whether or not the urge
exists
H recognizing and reporting recurring signs of UTI
(painful, frequent, burning urination; foul-smelling
urine)
H the importance of completing the prescribed therapy
or maintaining low-dose antibiotic prophylaxis.
Discharge planning
H After surgery, close medical follow-up is necessary
even if symptoms havent recurred.

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Common characteristics
Vitamin A deficiency H Night blindness (nyctalopia)
H Dry, scaly skin
H Follicular hyperkeratosis
Overview H Shrinking and hardening of the mucous membranes
H Failure to thrive and apathy
Description H Corneal changes, which can lead to ulceration and
H Deficiency of vitamin A in the body possibly resulting rapid destruction of the cornea (severe deficiency)
in night blindness, decreased color adjustment, kera-
tinization of epithelial tissue, and poor bone growth Complications
H With therapy, excellent chance of reversing symptoms H Blindness
of night blindness and milder conjunctival changes; H Infections of the eyes and the respiratory or geni-
with corneal damage, emergency treatment necessary tourinary tract
Pathophysiology
H A fat-soluble vitamin absorbed in the GI tract, vitamin Assessment
A maintains epithelial tissue and retinal function.
H Healthy adults have adequate vitamin A reserves to History
last up to 1 year; children typically dont. H Night blindness (nyctalopia)
H Failure to thrive
Causes H Apathy
H Inadequate dietary intake of foods high in vitamin A
(liver, kidney, butter, milk, cream, cheese, and forti- Physical findings
fied margarine) or carotene, a precursor of vitamin H Dry, scaly skin
A found in dark green, leafy vegetables, and yellow or H Follicular hyperkeratosis
orange fruits and vegetables H Conjunctival changes
H Malabsorption caused by: H Shrinking and hardening of the mucous membranes
Celiac disease
Sprue Test results
Obstructive jaundice Laboratory
Cystic fibrosis H Carotene levels below 40 mcg/dl suggest vitamin A
Giardiasis deficiency, but vary with seasonal ingestion of fruits
Habitual use of mineral oil as a laxative and vegetables.
H Massive urinary excretion caused by: H Serum levels of vitamin A below 20 mcg/dl are diag-
Cancer nostic.
Tuberculosis Other
Pneumonia H Dietary history and typical ocular lesions suggest vita-
Nephritis min A deficiency.
Urinary tract infection
H Decreased storage and transport of vitamin A from
hepatic disease Treatment
Incidence General
H Affects more than 80,000 people annually world- H Increased dietary intake of vitamin A
wide mostly children in underdeveloped countries H Cream-based or petroleum-based products for dry
H Rare in the United States, although many disadvan- skin
taged children have substandard levels of vitamin A H Control of underlying condition

Medications
Foods that contain vitamin A H Vitamin A replacement
H Bile salts with biliary obstruction
The following foods contain significant amounts of
vitamin A. H Pancreatin with pancreatic insufficiency
H Butternut squash
H Cantaloupe
H Carrots
H Dandelion
H Kale
H Mangoes
H Red peppers
H Sweet potatoes

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Nursing considerations
Key outcomes
The patient will:
H improve vitamin levels
H express understanding of dietary changes needed to
improve nutritional status
H express understanding of diet high in vitamin A.

Nursing interventions
H Administer prescribed oral vitamin A supplements
with or after meals or parenterally.
H Provide information on foods high in vitamin A. (See
Foods that contain vitamin A.)
Monitoring
H Signs of hypercarotenemia (orange coloration of the
skin and eyes)
H Signs of hypervitaminosis A (children):
Rash
Hair loss
Anorexia
Transient hydrocephalus
Vomiting
H Signs of hypervitaminosis A (adults):
Bone pain
Hepatosplenomegaly
Diplopia
Irritability

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H signs of hypercarotenemia and hypervitaminosis
H dietary counseling on foods high in vitamin A.

Discharge planning
H Refer the patient for nutritional counseling and, if
necessary, to an appropriate community agency.

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Vitamin B deficiency Pyridoxine deficiency

H Can occur at any age
H Rare
Cobalamin deficiency
Overview H Most common in people older than age 40

Description Common characteristics

H Deficiency of vitamin B in the body Thiamine deficiency
H Most common deficiencies: thiamine (B1), riboflavin H Polyneuritis
(B2), niacin (B3), pyridoxine (B6), cobalamin (B12) H Wernickes encephalopathy
H Korsakoffs psychosis
Pathophysiology H Palpitations
H Vitamin B complex is a group of water-soluble vita- H Tachycardia
mins essential to normal metabolism, cell growth, H Dyspnea
and blood formation. (See Recommended daily H Constipation and indigestion
allowance of B-complex vitamins.) Riboflavin deficiency
H Cheilosis (cracking of the lips and corners of the
Causes mouth)
Thiamine deficiency H Sore throat
H Malabsorption H Glossitis
H Inadequate dietary intake of vitamin B1 H Dermatitis
Riboflavin deficiency H Eye disturbances
H Diet deficient in milk, meat, fish, green leafy vegeta- Niacin deficiency
bles, and legumes H Fatigue
Niacin deficiency H Anorexia
H Corn as a dominant staple food H Muscle weakness
H Carcinoid syndrome H Headache
H Hartnup disease H Indigestion
Pyridoxine deficiency H Mild skin eruptions
H Destruction of pyridoxine in infant formulas by auto- H Weight loss
claving H Dermatitis
H Pyridoxine antagonists, such as isoniazid and penicil- Pyridoxine deficiency
lamine H Dermatitis
Cobalamin deficiency H Occasional cheilosis or glossitis unresponsive to
H Absence of intrinsic factor in gastric secretions riboflavin therapy
H Absence of receptor sites after ileal resection H Abdominal pain
H Malabsorption syndromes associated with sprue, in- H Vomiting
testinal worm infestation, regional ileitis, and gluten H Ataxia
enteropathy H Seizures
H Diet low in animal protein Cobalamin deficiency
H Pernicious anemia H Pernicious anemia, anorexia, weight loss, abdominal
H Medication discomfort, constipation, diarrhea, and glossitis
H Peripheral neuropathy
Risk factors H Ataxia, spasticity, and hyperreflexia
H Chronic alcoholism
H Prolonged diarrhea Complications
H Exposure of milk to sunlight H Cardiomegaly
H Treatment of legumes with baking soda H Circulatory collapse
H Beriberi
Incidence H Pellagra
Thiamine deficiency
H Affects males and females equally ALERT
H Can occur at any age
Riboflavin deficiency Because of a triad of symptoms, pellagra is some-
H Most common nutrient deficiency in the United States times called a 3-D syndrome dementia, der-
Niacin deficiency matitis, and diarrhea. If not reversed by therapeu-
H Usually affects adults tic doses of niacin, pellagra can be fatal.

H Central nervous system disturbances

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Recommended daily allowance of B-complex vitamins

Vitamin Men Women Infants Children
(23 to 50) (23 to 50) (1 to 10)
B1* 1.4 mg 1.4 mg 0.4 mg 0.7 to 12 mg

B2* 1.6 mg 1.6 mg 0.5 mg 0.8 to 1.4 mg

Niacin* 18 mg 18 mg 5 to 8 mg 9 to 16 mg

B6 2.2 mg 2.2 mg 0.4 mg 0.9 to 1.6 mg

B12 3 mcg 3 mcg 0.3 mcg 2 to 3 mcg

*requirements per 1,000 kilocalories of dietary intake

Niacin deficiency
Assessment H Dark, scaly dermatitis, especially on exposed parts of
the body, that makes the patient appear to be severely
History sunburned
Thiamine deficiency H Red mouth, tongue, and lips
H Palpitations Pyridoxine deficiency
H Dyspnea H Weakness
H Constipation and indigestion H Confusion
Riboflavin deficiency H Glossitis
H Burning, itching, light sensitivity, and tearing of the H Seborrheic dermatitis
eyes Cobalamin deficiency
H Neuropathy H Abdominal discomfort
H Signs of mild anemia H Peripheral neuropathy
H Growth retardation H Ataxia, spasticity, and hyperreflexia
Niacin deficiency
H Backache Test results
H Sore mouth, tongue, and lips Laboratory
H Nausea, vomiting, and diarrhea THIAMINE DEFICIENCY
H Confusion, disorientation, and neuritis may be- H 24-hour urine collection (commonly measured as
come severe enough to induce hallucinations and micrograms per deciliter [mcg/dl]) shows the fol-
paranoia lowing age-related deficiency levels.
Pyridoxine deficiency
H Presence of risk factors Special populations
H Fatigue
H Distal limb numbness Ages 1 to 3, less than 120 mcg/dl
H Depression Ages 4 to 6, less than 85 mcg/dl
Cobalamin deficiency Ages 7 to 9, less than 70 mcg/dl
H Pernicious anemia Ages 10 to 12, less than 60 mcg/dl
H Anorexia Ages 13 to 15, less than 50 mcg/dl
H Weight loss Adults, less than 27 mcg/dl
H Constipation, diarrhea
H Glossitis H In pregnant females, the 24-hour urine collection
H Peripheral neuropathy results show:
less than 23 mcg/dl (second trimester)
Physical findings less than 21 mcg/dl (third trimester).
Thiamine deficiency RIBOFLAVIN DEFICIENCY
H Tachycardia H 24-hour urine collection (measured as micrograms
H Ataxia, nystagmus, and ophthalmoplegia per gram [mcg/g]of creatinine) shows the following
Riboflavin deficiency age-related deficiency levels.
H Seborrheic dermatitis in the nasolabial folds, scro-
tum, and vulva and, possibly, generalized dermatitis
involving the arms, legs, and trunk

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Special populations Riboflavin deficiency

General
Ages 1 to 3, less than 150 mcg/g H Diet high in riboflavin foods (meats; enriched flour;
Ages 4 to 6, less than 100 mcg/g milk and dairy products; green, leafy vegetables;
Ages 7 to 9, less than 85 mcg/g eggs; and cereal)
Ages 10 to 15, less than 70 mcg/g Medications
Adults, less than 27 mcg/g H Supplemental riboflavin

H In pregnant females, the 24-hour urine collection Niacin deficiency

results show: General
less than 39 mcg/g (second trimester) H Dietary enrichment (meats, fish, peanuts, brewers
less than 30 mcg/g (third trimester). yeast, enriched breads, and cereals rich in niacin;
NIACIN DEFICIENCY milk and eggs, in tryptophan)
H Deficiency is measured by N-methyl nicotinamide in Medications
a 24-hour urine collection as micrograms per gram H Supplemental B-complex vitamins
(mcg/g) of creatinine. H Niacinamide
H Adult deficiency levels are less than 0.5 mcg/g.
H In pregnant females, the 24-hour urine collection Pyridoxine deficiency
results show: General
less than 0.5 mcg/g (first trimester) H Symptomatic
less than 0.6 mcg/g (second trimester) H Dietary adjustments
less than 0.8 mcg/g (third trimester). H Increased carbohydrate intake before vigorous exer-
PYRIDOXINE DEFICIENCY cise
H Xanthurenic acid is more than 50 mg/day in 24-hour Medications
urine collection after administration of 10 g of H Prophylactic pyridoxine therapy in infants and in
L-tryptophan. children with seizure disorder
H Serum and red blood cell transaminases levels are H Supplemental B-complex vitamins
decreased.
H Pyridoxic acid excretion in urine is reduced. Cobalamin deficiency
COBALAMIN DEFICIENCY General
H Cobalamin serum levels are less than 150 pg/ml. H Blood transfusion if severe
H Schilling test measures absorption of radioactive H Diet high in folate
cobalamin with and without intrinsic factor. Medications
H Gastric analysis and hemoglobin studies uncover H Parenteral cyanocobalamin in patients with reduced
causation. gastric secretion of hydrochloric acid, lack of intrin-
sic factor, some malabsorption syndromes, or ileum
resections
Treatment H Folate

Thiamine deficiency
General Nursing considerations
H High-protein diet, with adequate calorie intake and
thiamine rich foods (pork, peas, wheat bran, oat- Key outcomes
meal, and liver) The patient will:
Medications H improve vitamin levels
H B-complex vitamins H express understanding of dietary adjustments needed
H Thiamine supplements or thiamine hydrochloride as to improve nutritional status.
part of a B-complex concentrate (with alcoholic
beriberi) Nursing interventions
H Administer prescribed supplements.
H Explain all tests and procedures.

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Monitoring
H Adverse effects from large doses of niacinamide, in
patients with niacin deficiency
H Dietary intake
H Response to therapy

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H keeping an accurate dietary history
H that prognosis is good with treatment
H importance of adhering strictly to their prescribed
treatment for the rest of their lives
H dietary adjustments.

Discharge planning
H Refer the patient to appropriate assistance agencies if
his diet is inadequate due to adverse socioeconomic
conditions.

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Vitamin C deficiency weaned from breast milk to cows milk without a vit-
amin C supplement
H Also known as scurvy

Overview Pathophysiology
H Deficiency of vitamin C can lead to scurvy or inade-
Description quate production of collagen, an extracellular sub-
H Deficiency of vitamin C in the body stance that binds the cells of the teeth, bones, and
H Historically common among sailors and others de- capillaries.
prived of fresh fruits and vegetables for long periods; H Because the body cant store this water-soluble vita-
uncommon today in the United States, except in alco- min in large amounts, the supply needs to be replen-
holics, people on restricted-residue diets, and infants ished daily.
Causes
Scurvys effect on gums and legs H Diet lacking foods rich in vitamin C, such as citrus
fruits, tomatoes, cabbage, broccoli, spinach, and
In adults, scurvy causes swollen or bleeding gums and
loose teeth.
berries
H Destruction of vitamin C in foods by overexposure to
air or by overcooking
H Excessive ingestion of vitamin C during pregnancy,
which causes the neonate to require large amounts
of the vitamin after birth
H Marginal intake of vitamin C during periods of physi-
ologic stress
Risk factors
H Hyperthyroidism
H Acquired immunodeficiency syndrome
H Cancer
H Smoking
H Hemodialysis
H Alcoholism
H Economic hardship

Incidence
It also causes follicular hyperkeratosis, usually on the H Rare in the United States
legs. H Can occur at any age
H Can affect males and females

Common characteristics
H Petechiae
H Ecchymoses
H Follicular hyperkeratosis (especially on the buttocks
and legs)
H Signs of anemia
H Anorexia
H Limb and joint pain (especially in the knees)
H Swollen or bleeding gums (see Scurvys effect on
gums and legs)
H Loose teeth
H Insomnia
H Poor wound healing
H Ocular hemorrhages in the bulbar conjunctivae
H Beading, fractures of the costochondral junctions of
the ribs or epiphysis
H Psychological disturbances, such as irritability, de-
pression, hysteria, and hypochondriasis

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Complications Foods that contain vitamin C

H Sudden death
The following foods contain significant amounts of
vitamin C.
H Blackberries H Kiwi
Assessment H Broccoli H Lemons
H Brussels sprouts H Oranges
History H Cantaloupe H Papaya
H Anorexia H Green and red peppers H Strawberries
H Limb and joint pain (especially in the knees) H Guava H Peas
H Insomnia H Kale H Tomatoes
H Poor wound healing
H Irritability
H Depression
H Hysteria H Avoid moving the patient unnecessarily to avoid irri-
H Hypochondriasis tating painful joints and muscles.
H Fatigue H Encourage the patient to consume foods high in vita-
min C. (See Foods that contain vitamin C.)
Physical findings
H Pallor Monitoring
H Petechiae H Dietary intake
H Ecchymoses
H Follicular hyperkeratosis (especially on the buttocks
and legs) Patient teaching
H Swollen or bleeding gums
H Loose teeth Be sure to cover:
H Ocular hemorrhages in the bulbar conjunctivae H the disorder, diagnosis, and treatment
H Beading, fractures of the costochondral junctions of H the importance of supplemental ascorbic acid
the ribs or epiphysis H good dietary sources of vitamin C
H not taking too much vitamin C because excessive
Test results doses of ascorbic acid may cause nausea, diarrhea,
Laboratory and renal calculi formation and may also interfere
H Serum ascorbic acid levels are less than 0.2 mg/dl. with anticoagulant therapy.
H White blood cell ascorbic acid levels are less than
30 mg/dl.
Other
H Dietary history revealing an inadequate intake of
ascorbic acid suggests vitamin C deficiency.

Treatment
General
H Diet high in foods rich in vitamin C

Medications
H Vitamin C supplements

Nursing considerations
Key outcomes
The patient will:
H improve vitamin levels
H express understanding of dietary adjustments needed
to improve nutritional status.
Nursing interventions
H Adminster prescribed ascorbic acid orally or by slow
I.V. infusion.

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Incidence
Vitamin D deficiency H Once a common childhood disease, now rare in the
United States
H Occasionally appears in breast-fed infants not receiv-
Overview ing vitamin D supplementation and in infants receiv-
ing a formula with a nonfortified milk base
Description H May also occur in overcrowded, urban areas where
H Deficiency of vitamin D in the body smog limits sunlight penetration
H Also known as rickets H Highest incidence in black children who, because of
their skin color, absorb less sunlight (solar ultravio-
Pathophysiology let rays irradiate 7-dehydrocholesterol, a precursor
H Deficiency of vitamin D causes failure of normal of vitamin D, to form calciferol)
bone calcification, which results in rickets in infants
and young children and osteomalacia in adults. Common characteristics
H With treatment, the prognosis is good; however, in H Profuse sweating
rickets, bone deformities usually persist, while in H Restlessness
osteomalacia, such deformities may disappear. H Irritability
H Numerous bone malformations
Causes
H Inadequate dietary intake of preformed vitamin D Complications
H Malabsorption of vitamin D H Spontaneous fractures
H Too little exposure to sunlight H Abnormal gait
H Vitamin D-resistant rickets (refractory rickets, famil- H Short stature
ial hypophosphatemia) from an inherited impair-
ment of renal tubular reabsorption of phosphate
(from vitamin D insensitivity) Assessment
H Hepatic or renal disease
H Malfunctioning parathyroid gland (decreased secre- History
tion of parathyroid hormone), which contributes to H Spontaneous multiple fractures
calcium deficiency (normally, absorption of calcium H Pain in the legs and lower back
and phosphorus through the intestine controlled by
vitamin D) and interferes with activation of vitamin D Physical findings
in the kidneys H Bowlegs (see Recognizing bowlegs)
H Knock-knees
H Rachitic rosary (beading of ends of ribs)
Recognizing bowlegs H Enlargement of wrists and ankles
H Pigeon breast
This infant with rickets shows characteristic bowing of the H Delayed closing of the fontanels
legs.
H Softening of the skull
H Bulging of the forehead

Test results
Laboratory
H Plasma calcium serum levels are less than 7.5 mg/dl.
H Serum inorganic phosphorus levels are less than
3 mg/dl.
H Serum citrate levels are less than 2.5 mg/dl.
H Alkaline phosphatase levels are less than 4 Bodansky
units/dl.
Imaging
H X-rays show characteristic bone deformities and ab-
normalities such as Loosers zones (pseudofrac-
tures).

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Treatment
General
H Sunlight exposure

Medications
H For osteomalacia and rickets (except when caused
by malabsorption), massive oral doses of vitamin D
or cod liver oil
H For rickets refractory to vitamin D or in rickets ac-
companied by hepatic or renal disease, 25-hydroxy-
cholecalciferol, 1,25-dihydroxycholecalciferol, or a
synthetic analogue of active vitamin D

Nursing considerations
Key outcomes
The patient will:
H improve vitamin levels
H express understanding of dietary adjustments needed
to improve nutritional status.
Nursing interventions
H Obtain a dietary history to assess the patients current
vitamin D intake.
H Administer supplementary aqueous preparations of
vitamin D for chronic fat malabsorption, hydroxylat-
ed cholecalciferol for refractory rickets, and supple-
mental vitamin D for breast-fed infants.
Monitoring
H Dietary intake
H Comfort level

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H watching for signs of vitamin D toxicity (headache,
nausea, constipation and, after prolonged use, renal
calculi).
Discharge planning
H If deficiency is due to socioeconomic conditions, re-
fer the patient to an appropriate community agency.

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Common characteristics
Vitamin E deficiency Infants
H Edema
H Skin lesions
Overview Adults
H Intermittent claudication
Description
H Deficiency of vitamin E in the body Complications
H Disorders of reproduction
Pathophysiology H Abnormalities of muscle, liver, bone marrow, and
H Vitamin E (tocopherol) appears to act primarily as brain function
an antioxidant, preventing intracellular oxidation of H Hemolysis of RBC
polyunsaturated fatty acids and other lipids. H Skeletal muscle dystrophy
H Deficiency of vitamin E usually manifests as hemolytic
anemia in low-birth-weight or premature neonates.
With treatment, prognosis is good. Assessment
Causes History
H In infants, usually results from consuming formulas H Intermittent claudication
high in polyunsaturated fatty acids that are fortified
with iron but not vitamin E (Such formulas increase Physical findings
the need for vitamin E because the iron supplement H Edema
catalyzes the oxidation of red blood cell [RBC] H Skin lesions
lipids.)
H Conditions associated with fat malabsorption Test results
Laboratory
Incidence H Serum alpha-tocopherol levels are below 0.5 mg/dl
H Uncommon in adults but possible in people whose in adults and below 0.2 mg/dl in infants.
diets are high in polyunsaturated fatty acids, which H Creatinuria, increased creatine kinase levels, hemo-
increase vitamin E requirements, and in people with lytic anemia, and an elevated platelet count support
vitamin E malabsorption, which impairs RBC survival the diagnosis.
Other
H Dietary and medical histories suggest vitamin E defi-
ciency.

Foods that contain vitamin E

Treatment
The following foods contain significant amounts of General
vitamin E. H Diet high in foods rich in vitamin E, such as vegetable
H Almonds oils, whole grains, dark green leafy vegetables, nuts,
H Almond oil
and legumes
H Asparagus
H Avocadoes Medications
H Canola oil
H Corn H Vitamin E supplementation
H Corn oil
H Cottonseed oil
H Hazelnuts
Nursing considerations
H Kiwi
H Mangoes Key outcomes
H Nuts The patient will:
H Olives H improve vitamin levels
H Safflower oil H express understanding of dietary adjustments needed
H Soybeans
to improve nutritional status.
H Soybean oil
H Sunflower seeds Nursing interventions
H Wheat germ
H Wheat germ oil H Encourage patient to consume foods high in vitamin
E. (See Foods that contain vitamin E.)

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Monitoring
H Dietary intake

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H preventing deficiency by providing vitamin E supple-
ments for low-birth-weight infants receiving formulas
not fortified with vitamin E and for adults with vita-
min E malabsorption
H dietary changes
H that food manufacturers fortify many products
with vitamins and minerals (Read the nutrition facts
panel of food labels to find out if a food contains
vitamin E.)
H that most adults in the United States get enough vita-
min E from their normal diets to meet current rec-
ommendations. (Caution those on low-fat diets that
low-fat intake can substantially decrease vitamin E
intake if appropriate food choices arent made.)
Discharge planning
H If vitamin E deficiency is related to socioeconomic
conditions, refer the patient to appropriate commu-
nity agencies.

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Incidence
Vitamin K deficiency H Vitamin K deficiency is common among neonates in
the first few days postpartum due to poor placental
transfer of vitamin K and inadequate production of
Overview vitamin K-producing intestinal flora.
Description Common characteristics
H Deficiency of vitamin K in the body H Abnormal bleeding tendency

Pathophysiology Complications
H Vitamin K is an element necessary for formation of H Bleeding
prothrombin and other clotting factors in the liver;
deficiency produces abnormal bleeding.
H If the deficiency is corrected, the prognosis is excel- Assessment
lent.
H Vitamin K is found in specific foods and is also made History
by the bacteria that line the GI tract. H Prolonged or easy bleeding

Causes Physical findings

H Prolonged use of drugs, such as the anticoagulant H Ecchymosis
dicumarol and antibiotics that destroy normal intesti- H Petechiae
nal bacteria
H Obstruction of the bile duct or bile fistula Test results
H Malabsorption of vitamin K due to sprue, pellagra, Laboratory
bowel resection, ileitis, or ulcerative colitis H Prothrombin time (PT) 25% longer than the normal
H Chronic hepatic disease range of 10 to 20 seconds confirms the diagnosis of
H Cystic fibrosis vitamin K deficiency after other causes of prolonged
PT (such as anticoagulant therapy or hepatic dis-
ease) have been ruled out.

Foods that contain vitamin K Treatment

The following foods contain significant amounts of
vitamin K. General
Breads, cereals, rice, and pasta H Diet rich in foods high in vitamin K, such as green
H Oats leafy vegetables, cereals, soybeans, and other vegeta-
H Wheat bran bles. (See Foods that contain vitamin K.)
H Whole wheat flour
Fruits Medications
H Avocados
H Vitamin K
Vegetables
H Broccoli
H Cabbage
H Cauliflower
Nursing considerations
H Endive
H Kale Key outcomes
H Lentils (dry) The patient will:
H Lettuce (iceberg) H improve vitamin levels
H Soybeans H show less tendency to bleed easily
H Spinach H show improved laboratory values.
H Swiss chard
H Turnip greens Nursing interventions
H Watercress
H Encourage the patient to consume foods high in vita-
Organ meats
H Beef liver min K.
H Chicken liver H Administer vitamin K to neonates and patients with fat
H Pork liver malabsorption or with prolonged diarrhea caused by
Fats, oils, sugars colitis, ileitis, or long-term antibiotic therapy.
H Corn oil
H Soybean oil Monitoring
H PT
H Signs of bleeding

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Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H warning against self-medication with or overuse of
antibiotics, which destroy the intestinal bacteria nec-
essary to generate significant amounts of vitamin K
H dietary counseling
H warning the patient to take safety precautions be-
cause vitamin K deficiency can cause an increased
risk of bruising and bleeding.

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Vitiligo H About 50% of cases beginning between ages 10 and

30
H No racial predilection
H Males and females about equally affected (Females
Overview tend to seek treatment more than males.)
Description Common characteristics
H Hypopigmentation condition of the skin H Loss of pigment
H May cause a serious cosmetic problem H Locally increased sunburn
H Concurrent risk of other diseases, especially thyroid
Complications
Pathophysiology H Extreme photosensitivity in depigmented areas
H Destruction of melanocytes and circulating antibod- H Hypersensitivity reactions to therapeutic agents and
ies results in hypopigmented areas. to dyes or cosmetics used to camouflage lesions
Causes
H Unknown; may have both genetic and environmental Assessment
components
History
Risk factors H Familial history of vitiligo
H In about 30% of patients, first-degree relative with
the same disorder Physical findings
H Precipitating factors: H Depigmented or stark-white skin patches; almost im-
Stressful physical or psychological events perceptible on fair-skinned whites
Chemical agents, such as phenols and catechols H Patches usually bilaterally symmetrical, with distinct
H Associated concurrent diseases: borders that may be raised and hyperpigmented (see
Thyroid dysfunction Recognizing vitiligo)
Pernicious anemia H Patches most likely over bony prominences, around
Addisons disease orifices, within body folds, and at sites of traumatic
Aseptic meningitis injury
Diabetes mellitus H Hair within lesions also possibly white
H Prematurely gray hair
Incidence H Ocular pigment changes
H Affects about 1% of U.S. population
H Onset at any age Test results
Diagnostic procedures
H Woods light examination in a darkened room shows
Recognizing vitiligo vitiliginous patches in fair-skinned patients.
H Skin biopsy result confirms the diagnosis.
This illustration shows characteristic depigmented skin
patches in vitiligo. These patches are usually bilaterally
symmetrical, with distinct borders. Treatment
General
H Sunscreens
H Cosmetics and skin dyes as cover-ups

Medications
H Repigmentation compounds, such as topical corti-
costeroids or calcipotriene
H Depigmentation creams
H Oral psoralen photochemical therapy

Surgery
H Skin grafting
H Tattooing (micropigmentation)

Other
H Narrow-band ultraviolent B therapy

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9400V.qxd 8/2/12 4:53 PM Page 903

Nursing considerations
Key outcomes
The patient will:
H verbalize understanding of the disorder and treat-
ment
H verbalize feelings about changed body image
H avoid complications.

Nursing interventions
H Encourage expression of feelings about appearance.
H Offer emotional support and reassurance.
H Reinforce treatment goals.

Monitoring
H Response to treatment
H Complications

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H that exposure to sunlight also darkens normal skin in
patients undergoing repigmentation therapy
H the use of sunscreen, sunglasses, and protective
clothing
H that results of depigmentation are permanent
H adverse effects of sunlight.

Discharge planning
H Refer the patient to the National Vitiligo Foundation.

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Risk factors
Volvulus H Straining at stool
H Pregnancy
H Intestinal malignancy
Overview H Hernia
H High-bulk diet
Description H History of previous attacks
H Twisting of the intestine at least 180 degrees on itself H Use of chronic neuropsychotropic drugs
H Marked by sudden onset of severe abdominal pain H Chronic constipation and laxative abuse
H Results in blood vessel compression
H Causes obstruction both proximal and distal to the Incidence
twisted loop H Varies worldwide in cases of volvulus of the large
H Occurs in a bowel segment long enough to twist, bowel
most commonly the sigmoid colon (small bowel a H Accounts for 1% to 5% of all large-bowel obstruc-
common site in children) tions in advanced Western populations
H Other common sites: the stomach and cecum H Most common sites: sigmoid colon (80%), cecum
(15%), transverse colon (3%), and splenic flexure
Pathophysiology (2%)
H The colon twists on its mesentery. H Common in regions of Africa, Southern Asia, and
H A closed loop obstruction occurs, affecting venous South America
drainage and arterial inflow. H About 50% of large-bowel obstructions caused by
H Cecal volvulus is a congenital defect in the peri- volvulus occurring in the volvulus belt of Africa
toneum with inadequate fixation of the cecum. (See and the Middle East
What happens in volvulus.) H Affects males and females equally

Causes Common characteristics

H Anomaly of bowel rotation in utero H Severe abdominal pain and distention
H Ingested foreign body H Vomiting
H Adhesions H Constipation
H Meconium ileus (in patients with cystic fibrosis)

What happens in volvulus

Although volvulus may occur anywhere in a bowel segment long enough to twist, the most common site, as this illustration
depicts, is the sigmoid colon, causing edema within the closed loop and obstruction at its proximal and distal ends.

NORMAL BOWEL SEGMENT VOLVULUS

Sigmoid colon Edematous intestine

Counter-
clockwise
twist

904 Volvulus
9400V.qxd 8/2/12 4:53 PM Page 905

Complications H regain normal bowel function

H Strangulation of the twisted bowel loop H express an understanding of the disorder and treat-
H Bowel ischemia and infarction ment regimen.
H Bowel perforation
Nursing interventions
H Encourage verbalization and provide support.
Assessment H Adminster prescribed drugs.
H Adminster prescribed I.V. fluids.
History
H Severe abdominal pain Monitoring
H Bilious vomiting H Pain control
H Constipation H Bowel function
H Vital signs
Physical findings H Fluid and electrolyte balance
H Abdominal distention H Nasogastric tube function and drainage
H Palpable abdominal mass H Wound site

Test results
Laboratory
H White blood cell count, in strangulation, is greater
than 15,000/ml; in bowel infarction, its greater than
20,000/ml.
Imaging
H Abdominal X-rays may show multiple distended bow-
el loops and a large bowel without gas. In midgut
volvulus, abdominal X-rays may be normal.
H Barium enema, in cecal volvulus, shows barium fill-
ing the colon distal to the affected section of cecum;
in sigmoid volvulus, barium may twist to a point and,
in adults, take on an ace of spades configuration.
Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H preoperative teaching
H medication administration, dosage, and possible
adverse effects
H the signs and symptoms of infection
H the importance of follow-up care.
Discharge planning
H Refer the patient to support services.

Treatment
General
H For adults with sigmoid volvulus, nonsurgical treat-
ment: proctoscopy to check for infarction and reduc-
tion by careful insertion of a flexible sigmoidoscope
to deflate the bowel
H I.V. therapy
H Nothing by mouth until condition resolves
H Bed rest until condition resolves

Medications
H Antibiotics
H Analgesics

Surgery
H For children with midgut volvulus
H Detorsion (untwisting)
H Resection and anastomosis

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort and decreased
pain
H have stable vital signs
H avoid complications

Volvulus 905
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von Willebrands
disease
Overview
Description
H Hereditary bleeding disorder characterized by pro-
longed bleeding time, moderate deficiency of clotting
factor VIII (antihemophilic factor), and impaired
platelet function
H Also known as angiohemophilia, pseudohemophil-
ia, and vascular hemophilia
Pathophysiology
H Mild to moderate deficiency of factor VIII and defec-
tive platelet adhesion prolong coagulation time.
H This disease results from a deficiency of von Wille-
brands factor (factor VIIIVWF), which appears to oc-
cupy the factor VIII molecule and may be necessary
for the production of factor VIII and proper platelet
function.
H Defective platelet function is characterized by de-
creased agglutination and adhesion at the bleeding
site, reduced platelet retention when filtered through
a column of packed glass beads, and diminished
ristocetin-induced platelet aggregation.
Causes
H Inherited as an autosomal dominant trait
H Acquired form identified in patients with cancer and
immune disorders
Incidence
H Affects males and females; tends to be more common
in males
Common characteristics
H Bleeding from the skin or mucosal surfaces
H In females, excessive uterine bleeding
Complications
H Hemorrhage
Assessment
History
H Possible familial history of the disease
H Easy bruising and frequent bleeding from the nose or
gums (petechiae rare)
H Menorrhagia
H Hemorrhage after a laceration or surgery
H Possible episodes of GI bleeding
Physical findings
H Bruises
H Abnormal bleeding
H Rash
Test results
Laboratory
H Bleeding time is prolonged to more than 6 minutes.
H Partial thromboplastin time is slightly prolonged to
more than 45 seconds.
H Factor VIII-related antigen levels are absent or re-
duced, and factor VIII activity level is low.
H In vitro platelet aggregation is defective using the ris-
tocetin coagulation factor assay test.
H Platelet count and clot retraction are normal.
H Urinalysis is positive for blood cells.
H Stool sample is heme-positive.
Treatment
General
H Depends on the symptoms and underlying type of
disease
H Decreasing bleeding time by local measures and re-
placing factor VIII and, consequently, factor VIIIVWF
H Avoidance of aspirin
H Alternation of activities and rest periods (if patient is
fatigued after a bleeding episode)
Medications
H Cryoprecipitate (cryoprecipitated antihemophilic fac-
tor)
H Vasopressin analogue such as desmopressin
H Factor VIII concentrates
Nursing considerations
Key outcomes
The patient will:
H experience hemodynamic stability
H have palpable peripheral pulses
H maintain normal fluid volume
H incur no injury
H exhibit adequate coping skills.
Nursing interventions
H Provide emotional support as necessary.
H During a bleeding episode, elevate the area if possi-
ble, and apply cold compresses and gentle pressure
to the bleeding site. (Pressure is usually the only
treatment necessary.)
H Adminster prescribed drugs or transfusions.
H Prevent potential injury by using an electric razor,
keeping the room free from clutter, and providing a
cushioned sitting and sleeping surface (such as a
convoluted foam mattress).
Monitoring
H Signs and symptoms of decreased tissue perfusion
H Vital signs
H Frequently, for bleeding from the skin, mucous mem-
branes, and wounds

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H After surgery, bleeding time or other clotting proce-

dure for 24 to 48 hours and for signs of new bleed-
ing
H Adverse reactions to blood products

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the need to notify a physician after even minor trau-
ma and before all surgery, including dental proce-
dures, to determine whether replacement of blood
components is necessary
H warnings against using aspirin and other drugs that
impair platelet function (how to recognize over-
the-counter medications that contain aspirin)
H special precautions to prevent bleeding episodes
H the importance of wearing or carrying medical iden-
tification
H measures to control bleeding and how to prevent
bleeding, unnecessary trauma, and complications.
Discharge planning
H Refer parents of an affected child for genetic coun-
seling.

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Vulvovaginitis Assessment
History
Overview Trichomonal vaginitis
H Vaginal irritation and itching
Description H Urinary symptoms, such as burning and frequency
H Inflammation of the vulva (vulvitis) and vagina Candidal vaginitis
(vaginitis) H Intense vaginal itching
H Prognosis good with treatment H Thick, white, cottage cheese-like discharge
Bacterial vaginosis
Pathophysiology H Fishy-smelling discharge
H Because of the proximity of the vulva and vagina, in- H May be asymptomatic
flammation of one usually precipitates inflammation Gonorrhea
of the other. H Possibly no symptoms
H Dysuria
Causes Acute vulvitis
Vaginitis H Vulvar burning, pruritus
H Protozoan infection (Trichomonas vaginalis) H Severe dysuria
H Fungal infection (Candida albicans) H Dyspareunia
H Bacterial infection (bacterial vaginosis)
H Venereal infection (Neisseria gonorrhoeae) Physical findings
H Viral infection with venereal warts or herpes simplex Trichomonal vaginitis
virus Type 2 H Thin, bubbly, green-tinged, and malodorous vaginal
Vulvitis discharge
H Parasitic infection (Phthirus pubis, crab louse) Candidal vaginitis
H Traumatic injury H Thick, white, cottage cheese-like discharge
H Poor personal hygiene H Red, edematous mucous membranes with white
H Chemical irritations flecks on vaginal wall
H Allergic reactions, such as to douches or toilet paper Bacterial vaginosis
H Retention of a foreign body such as a tampon H Gray, foul, fishy-smelling discharge
Gonorrhea
Risk factors H Profuse and purulent discharge
H Pregnancy Acute vulvitis
H Hormonal contraceptives H Vulvar edema and erythema
H Diabetes mellitus Herpesvirus infection
H Systemic broad-spectrum antibiotics H Ulceration or vesicle formation on the perineum (ac-
H Vaginal mucosa and vulval atrophy in menopausal tive phase)
women H Severe edema that may involve entire perineum
(chronic infection)
Incidence
H Occurs at any age Test results
H Affects most females at some time Laboratory
H Wet slide preparation and microscopic examination
Common characteristics of vaginal exudates are used in obtaining various test
H Vaginal itching in most cases results:
H Vaginal discharge in many cases Vaginitis diagnosis requires identification of the in-
fectious organism.
Complications In trichomonal infections, the presence of motile,
H Inflammation of the perineum flagellated trichomonads confirms the diagnosis.
H Skin breakdown In monilial vaginitis, 10% potassium hydroxide is
H Secondary infection added to the slide; diagnosis requires identifica-
H Dyspareunia tion of C. albicans fungus.
H Dysuria In bacterial vaginosis, saline wet mount shows the
presence of clue cells, giving it a stippled appear-
ance.
Gonorrhea requires a culture of vaginal exudate to
confirm the diagnosis.
H Diagnosis of vulvitis or a suspected sexually transmit-
ted disease (STD) may require a complete blood

908 Vulvovaginitis
9400V.qxd 8/2/12 4:53 PM Page 909

count, urinalysis, cytology screening, biopsy of H proper application of vaginal ointments and supposi-
chronic lesions to rule out cancer, and culture of tories
exudate from acute lesions. H the need for meticulous hand washing before and af-
ter drug administration
H preventing skin breakdown and secondary infections
Treatment H good hygiene practices
H wearing all-cotton, white underpants and avoiding
General tight-fitting pants and panty hose
H Cold compresses or cool sitz baths to relieve pruritus H abstaining from alcoholic beverages with metronida-
H Warm compresses for severe inflammation zole therapy
H Avoidance of drying soaps H that metronidazole therapy may turn the urine dark
H Loose clothing to promote air circulation brown.
H For chronic vulvitis, changing problematic environ-
mental factors
Medications
H Antibacterials
H Antiprotozoal agents
H Topical corticosteroids
H Antipruritics
H Topical estrogen ointments
H Antivirals

Nursing considerations
Key outcomes
The patient will:
H express feelings of increased comfort
H exhibit no signs of infection
H express concerns about self-concept, self-esteem,
and body image
H use available counseling or a support group.

Nursing interventions
H Encourage expression of feelings.
H Help the patient develop effective coping strategies.
H Provide comfort measures.
H Use meticulous hand-washing technique.
H Report cases of STDs to the public health authorities.
H Administer drug therapy.

Monitoring
H Response to treatment
H Vaginal discharge
H Signs and symptoms of secondary infection

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H the correlation between sexual contact and spread of
vaginal infections
H using condoms to prevent or decrease the spread of
sexually transmitted infections
H notifying sexual partners of the need for treatment
H abstaining from sexual intercourse until the infection
resolves
H completing prescribed drugs, even if symptoms sub-
side

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W Warts
Overview
Description
H Common, benign, skin growths
H Prognosis varies, some disappearing readily with
treatment, others necessitating more vigorous and
prolonged treatment
H Also known as verrucae

Pathophysiology
H Warts are small harmless tumors of the skin caused
Plantar
H Slightly elevated or flat
H Occur singly or in large clusters (mosaic warts), pri-
marily at pressure points of the feet
Digitate
H Fingerlike, horny projection arising from a pea-
shaped base
H On scalp or near hairline
Condyloma acuminatum (moist wart)
H Usually small, pink to red, moist, and soft
H Single or in large cauliflower-like clusters on the
penis, scrotum, vulva, or anus
H May be transmitted through sexual contact; not
always venereal in origin
Complications
by a virus.
H Most are well-defined. H Scarring
H Mode of transmission is probably through direct H Recurrence of wart
contact, but autoinoculation is possible. H Formation of keloid
H Warts are categorized by location and appearance.

Causes Assessment
H Infection with the human papillomavirus, a group of
ether-resistant, deoxyribonucleic acid-containing pa- History
povaviruses H Based on type and location
H Contact with someone having warts
Risk factors
H Breaks in skin Physical findings
H Nail biting H Small, hard, flat-to-raised lump or lesion on the skin
H Small, flat lesion on forehead, cheeks, arms, or legs
Incidence H Rough, round, painful lesion on sole
H Highest in children and young adults, but may occur H Rough growth around fingernails or toenails
at any age
Test results
Common characteristics Diagnostic procedures
H Clinical manifestations dependent on the type of wart H Recurrent anal warts require sigmoidoscopy to rule
and its location. out internal involvement, which may necessitate
Common (verruca vulgaris) surgery.
H Rough, elevated, rounded surface H Skin biopsy may confirm diagnosis in some cases.
H Appears most commonly on limbs, particularly hands Other
and fingers H Visual examination usually confirms the diagnosis.
H Most prevalent in children and young adults
Filiform
H Single, thin, threadlike projection Treatment
H Commonly occurs around the face and neck
Periungual General
H Rough, irregularly shaped, elevated surface H Cryotherapy
H Occurs around edges of fingernails and toenails
H When severe, may extend under the nail and lift it off Medications
the nail bed, causing pain H Acid therapy (primary or adjunctive)
Flat (juvenile) H 25% podophyllin in compound benzoin tincture (for
H Multiple groupings of up to several hundred slightly venereal warts)
raised lesions with smooth, flat, or slightly rounded H Imiquimod cream
tops H Bleomycin injection
H Common on the face, neck, chest, knees, dorsa of
hands, wrists, and flexor surfaces of the forearms Surgery
H Usually in children but can affect adults H Electrodesiccation and curettage (see Removing
H Distribution usually linear because spreading possi- warts by electrosurgery)
ble from scratching or shaving H Carbon dioxide laser therapy

910 Warts
9400WXYZ.qxd 8/2/12 4:54 PM Page 911

Removing warts by electrosurgery

1. Injection of 1% to 2% lidocaine under and around the 2. Electrodesiccation of the wart
wart, avoiding the wart itself

3. Removal of the wart tissue with a curette and 4. Light desiccation of the area to control bleeding and
curved scissors prevent recurrence

Nursing considerations H Bleeding

H Lesion healing
Key outcomes
The patient will:
H express understanding of disorder and treatment Patient teaching
H express feelings about change in body image
H exhibit improved or healed lesions. Be sure to cover:
H the disorder, diagnosis, and treatment
Nursing interventions H that conscientious adherence to prescribed therapy
H During acid or podophyllin therapy, protect the sur- is essential
rounding area with petroleum jelly or sodium bicar- H that the patients sex partner may also need treatment
bonate (baking soda). H need to avoid direct contact with warts.

Monitoring
H Response to treatment

Warts 911
9400WXYZ.qxd 8/2/12 4:54 PM Page 912

West Nile encephalitis Assessment

History
Overview H Headache
H Myalgia
Description H Neck stiffness
H An infectious disease, part of a family of vector-borne H Possible recent exposure to bodies of water, dead
diseases that also includes malaria, yellow fever, and birds, or recent mosquito bites
Lyme disease H Decreased appetite
H Mortality rate from 3% to 15%; higher in elderly H Nausea
population H Vomiting
H Ticks infected with the virus found in Africa and Asia H Diarrhea
only; role of ticks in transmission and maintenance
of the virus uncertain Physical findings
H Also called West Nile virus H Fever
H Rash
Pathophysiology H Swollen lymph glands
H Virus has an incubation period of 5 to 15 days after H Stupor and disorientation
exposure. H Stiff neck
H Mosquitoes become infected by feeding on birds H Change in mental status
contaminated with the virus.
H The virus is transmitted to a human by the bite of an Test results
infected mosquito (mostly the Culex species). Laboratory
H Disease primarily causes inflammation or encephali- H White blood cell (WBC) count is normal or in-
tis of the brain. creased.
H Enzyme-linked immunosorbent assay (ELISA), the
Causes MAC-ELISA, allows a rapid and definitive diagnosis.
H A flavivirus commonly found in humans, birds, and H Accurate diagnosis is possible only when serum or
other vertebrates in Africa, West Asia, and the Middle cerebrospinal fluid specimens are obtained while the
East patient is still hospitalized with acute illness and they
show an elevated WBC count and protein levels.
Risk factors Imaging
H Recent chemotherapy H Magnetic resonance imaging may show inflamma-
H Recent organ transplantation tion.
H Immunocompromised state
H Pregnancy
H Advanced age Treatment
H Breast-feeding
General
Incidence H No specific treatment
H In temperate areas, occurs mainly in late summer or H Respiratory support
early fall H Increased fluid intake
H In milder climates, can occur year-round H Rest periods when fatigued
H Risk greater in areas with active cases
H Greatest risk in those older than age 50 and those Medications
with compromised immune systems H Antipyretics

Common characteristics
H Incubation period 5 to 15 days after exposure Nursing considerations
H No symptoms in most patients bitten by infected mos-
quito; only 1 in 300 getting sick Key outcomes
H Fever The patient will:
H Headache H maintain collateral circulation
H Myalgia H maintain hemodynamic stability
H have adequate cardiac output
Complications H remain afebrile
H Neurologic impairment H have an adequate fluid volume.
H Seizures
H Death

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Nursing interventions Prevention

H Maintain adequate hydration with I.V. fluids. Preventing West Nile
H Adminster prescribed medications. encephalitis
H Provide respiratory support measures when needed.
To reduce the risk of infection with West Nile encephalitis,
H Follow standard precautions when handling blood or
advise patients to follow these guidelines:
other body fluids. H Stay indoors at dawn and dusk and in early evening
H Report any suspected cases of West Nile encephalitis when mosquitoes are biting.
to the state department of health. H Wear long-sleeved shirts and long pants when out-
doors.
Monitoring H Apply insect repellent sparingly to exposed skin. Effec-
H Fluid and electrolyte status tive repellents contain 20% to 30% DEET (N,N-diethyl-
H Neurologic status toluamide). DEET in high concentrations (greater than
H Vital signs 30%) can cause adverse effects, particularly in chil-
dren, and should be avoided; adults should apply re-
pellent on children with no more than 10% DEET.
Patient teaching H Dont place repellent under clothing.
H Dont apply repellent over cuts, wounds, sunburn, or
irritated skin.
Be sure to cover: H Wash repellent off daily and reapply as needed.
H the disorder, diagnosis, and treatment
H the proper use of insect repellants, which can irritate
the eyes and mouth, and to avoid applying repellant
to the hands of children (shouldnt be applied to
children younger than age 3) (see Preventing West
Nile encephalitis)
H the expected course and outcomes of the illness
H the need to drink fluids to avoid dehydration
H how to stop mosquitoes from breeding by:
cleaning out birdbaths and wading pools at least
once per week
cleaning roof gutters and downspout screens
eliminating any standing water
not allowing water to collect in trash cans
turning over or removing containers in yards
where rainwater collects, such as toys and old
tires.
Discharge planning
H Refer the patient to an infectious disease specialist.

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X
X-linked
infantile hypogamma-
globulinemia
Overview
Description
Y
H A congenital disorder in which all five immunoglobu-
lins (Ig) IgM, IgG, IgA, IgD, and IgE and circu-
lating B cells absent or deficient but T cells intact
H Good prognosis with early treatment, except in in-
H Abnormal dental caries
H Polyarthritis resembling rheumatoid arthritis

Physical findings
H Retarded growth
H Lymphadenopathy and splenomegaly usually absent,
despite recurrent infections
Test results
Laboratory
H Immunoelectrophoresis confirms decreased levels or
a total absence of IgM, IgA, and IgG in the serum;
however, diagnosis by this method usually isnt possi-
ble until the infant is age 9 months.
H Antigenic stimulation confirms an inability to pro-
fants developing polio or persistent viral infection; duce specific antibodies, although cellular immunity
usually causing some permanent damage, especially remains intact.
in the neurologic or respiratory system
H Also called Brutons agammaglobulinemia or XLA
Treatment
Pathophysiology
H B cells and B-cell precursors may be present in the General
bone marrow and peripheral blood, but a mutation H Prevention or control of infections
in the B-cell protein tyrosine kinase causes failure of H Fresh frozen plasma
the B cells to mature and to secrete immunoglobulin. H Well-balanced diet

Causes Medications
H Congenital H Immune globulin
H Antibiotics
Incidence
H Affects males almost exclusively
H Occurs in 1 in 50,000 to 100,000 births Nursing considerations
Common characteristics Key outcomes
H Asymptomatic until age 6 months, when transplacen- The patient will:
tal maternal immunoglobulins that provided immuni- H demonstrate an understanding of the disorder
ty have been depleted H prevent infections by limiting exposure
H Recurrent infections such as bacterial otitis media H report signs and symptoms of infection promptly.

Complications Nursing interventions

H Hepatitis H Maintain adequate nutrition and hydration.
H Enteroviral infections H Perform chest physiotherapy if required.
H Poliovirus
Monitoring
H Vital signs
Assessment H Intake and output

History
H Recurrent infections: Patient teaching
Otitis media
Pneumonia Be sure to cover:
Dermatitis H the disorder, diagnosis, and treatment
Bronchitis H recognizing early signs of infection and reporting
Meningitis them promptly
Conjunctivitis H cleaning cuts and scrapes immediately

914 X-linked infantile hypogammaglobulinemia

9400WXYZ.qxd 8/2/12 4:54 PM Page 915

H avoiding crowds and people who have active infec-

tions
H how to meet nutritional and fluid needs during acute
infection.
Discharge planning
H Suggest genetic counseling if parents have questions
about the vulnerability of future offspring.

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ZZinc deficiency
Overview
Description
H Insufficient amounts of zinc, an essential trace ele-
ment thats a vital component of many enzymes and
present in the bones, teeth, hair, skin, testes, liver,
and muscles
H Good prognosis with correction of the deficiency

Pathophysiology
H Zinc deficiency causes impairment of synthesis of de-
H Dysgeusia (unpleasant taste)
H Hyposmia (decreased odor acuity)
H Dysosmia (unpleasant odor in nasopharynx)
H Severe iron deficiency anemia
H Bone deformities

Complications
H Hypogonadism
H Dwarfism
H Hyperpigmentation

Assessment
History
oxyribonucleic acid, ribonucleic acid and, ultimately, H Weight loss
protein, and alters normal blood concentrations of H Poor appetite
vitamin A by mobilizing it from the liver. H Growth retardation
H About 90% of zinc stores are in bone and skeletal H Short stature
muscle. H Mental lethargy
H Diarrhea
Causes H Intercurrent infections
H Excessive intake of foods (containing iron, calcium,
vitamin D, and the fiber and phytates in cereals) that Physical findings
bind zinc to form insoluble chelates that prevent its H Sparse hair growth
absorption H Rough skin
H Blood loss from parasitism H Poor wound healing
H Low dietary intake of foods containing zinc H Striae
H White spots on fingernails
Risk factors H Acne
H Alcohol consumption
H Corticosteroids Test results
H Celiac disease Laboratory
H Fasting serum zinc levels are below 70 mcg/dl.
Incidence
H Most common in people from underdeveloped coun-
tries, especially in the Middle East Treatment
H Children most susceptible to this deficiency during
periods of rapid growth General
H Correction of the underlying cause
Common characteristics H Diet high in zinc
H Hepatosplenomegaly
H Sparse hair growth Medications
H Soft, misshapen nails H Zinc supplementation
H Poor wound healing
H Anorexia
H Hypogeusesthesia (decreased taste acuity) Nursing considerations
Key outcomes
Foods that contain zinc The patient will:
H express understanding of dietary needs
The following foods contain significant amounts of zinc. H improve zinc levels
H Beans
H maintain or improve weight
H Dairy products
H Fortified breakfast cereals H experience improved skin condition.
H Nuts
H Oysters
Nursing interventions
H Poultry H Administer prescribed drugs.
H Red meat H Provide information about dietary sources of zinc.
H Seafood (See Foods that contain zinc.)
H Whole grains

916 Zinc deficiency

9400WXYZ.qxd 8/2/12 4:54 PM Page 917

Monitoring
H Response to treatment

Patient teaching
Be sure to cover:
H taking zinc supplements with milk or meals to pre-
vent gastric distress and vomiting
H following a balanced diet that includes foods high
in zinc
H correct use of calcium and iron supplements.

Zinc deficiency 917

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Zollinger-Ellison H GI bleeding
H Steatorrhea

syndrome H Duodenal ulceration

Complications
H Metastatic disease
Overview H Hemorrhage
H Perforation
Description H Obstruction
H Rare disease characterized by: H Production of other substances, such as corti-
Markedly elevated gastric acid secretion cotropin, with resulting Cushings syndrome
Peptic ulcer disease H Decrease in vitamin B12 levels possible due to med-
A gastrinoma or non-beta islet cell tumor of the ication effects
pancreas or duodenal wall that produces the hor-
mone gastrin
H Gastrinomas, may be single or multiple, large or Assessment
small, and benign or malignant.
H More than two-thirds of gastrinomas malignant; History
about one-third metastasized to the liver at the time H Numerous ulcers resistant to treatment
of diagnosis H Presence of peptic ulcer disease without evidence of
H Causes numerous ulcers in unusual areas of the bacterial etiology
stomach or intestine, more resistant to treatment H Signs and symptoms of disorder
than other ulcers; ulcers commonly returning after H Anemia
treatment
Physical findings
Pathophysiology H Weight loss
H Tumors that produce excess gastrin form in the pan- H Abdominal pain
creas, stomach, and duodenum. H Hematemesis
H Hypergastrinemia causes hypertrophy of the gastric
mucosa, leading to increased numbers of parietal Test results
cells and increased acid output. Laboratory
H Gastrin also stimulates acid secretion, resulting in in- H Gastrin secretion studies are elevated.
creased basal acid secretion. H Fasting serum gastrin level is elevated.
H This leads to GI mucosal ulceration. H Basal gastric acid output is elevated.
H Decreased gastric pH shows high acidity.
Causes H Serum calcium, phosphorus, cortisol, and prolactin
H Unknown levels rule out MEN I.
H May be hereditary or associated with some cancers Imaging
H May be associated with multiple endocrine neoplasia, H Computed tomography scans locate tumors.
type I (MEN I); about 25% of people having gastrino- H Magnetic resonance imaging locates tumors.
mas have them as part of MEN I H Upper GI endoscopy shows ulcers.
H Endoscopic ultrasound locates tumors and allows a
Risk factors biopsy to be obtained.
H MEN I H Somatostatin receptor scintigraphy determines tumor
H Family history of ulcer disease metastasis.
Diagnostic procedures
Incidence H Portal vein sampling
H Fewer than three out of every one million people in
the United States
H Average age at diagnosis: 50 Treatment
H Slightly higher in males than in females
General
Common characteristics H Blood transfusions, if necessary
H Gnawing, burning abdominal pain H Surgical removal of tumors generally unsuccessful
H Reflux esophagitis because gastrinomas usually small, numerous, and
H Diarrhea difficult to locate; regrowth common
H Nausea
H Vomiting Medications
H Fatigue and weakness H Proton pump inhibitors to suppress acid production
H Weight loss and promote healing

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H Histamine blockers to reduce the amount of hy-

drochloric acid released into the digestive tract
H Chemotherapy to treat malignant tumors

Surgery
H To stop hemorrhaging from bleeding ulcers, relieve
an obstruction, or close a perforation
H Sympathectomy of nerves that promote acid secretion
H Laparotomy to remove resectable tumors

Nursing considerations
Key outcomes
The patient will:
H experience increased comfort and decreased pain
H maintain balanced fluid volume
H verbalize understanding of disorder and treatment
H return to normal bowel elimination
H maintain appropriate weight.

Nursing interventions
H Administer prescribed drugs.
H Assist with dietary choices.
H Provide preoperative and postoperative care, as ap-
propriate.
H Provide emotional support.

Monitoring
H Intake and output
H Daily weight
H Pain control
H Wound healing (if surgery is performed)

Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H medication administration, dosage, and possible ad-
verse effects
H diet modifications
H importance of follow-up care.

Zollinger-Ellison syndrome 919

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9400_BM.qxd 8/2/12 4:17 PM Page 921

Less common diseases

Selected references
Web resources
Index

921
9400_BM.qxd 8/2/12 4:17 PM Page 922
Less common diseases
Names Description
Achilles tendon Shortening of the Achilles tendon that results
contracture in foot pain and strain with limited ankle dor-
siflexion; may be due to a congenital abnor-
mality, reaction to chronic poor posture, or a
paralytic condition
Actinomycosis Infection caused by gram-positive anaerobic
(lumpy jaw) bacillus Actinomyces israelii, resulting in
painful swellings of granulomatous, suppura-
tive lesions with abscesses commonly on the
head, neck, thorax, or abdomen
Adenovirus Acute, self-limiting febrile infection resulting
infection in inflammation of the respiratory or ocular
mucous membranes, or both; 35 serotypes
cause five major infections; transmitted by di-
rect inoculation into the eye, oral-fecal route,
or inhalation of droplets; highly contagious
Alpha1-antitrypsin Autosomal recessive inherited disorder result-
deficiency ing in emphysema and liver dysfunction prob-
lems
Alports syndrome Hereditary nephritis characterized by recur-
rent gross or microscopic hematuria; associ-
ated with deafness, eye defects, albuminuria,
and progressive azotemia
American Febrile parasitic illness prevalent in Central
trypanosomiasis and South America; cardiomyopathy may oc-
(Chagas disease) cur; megaesophagus and megacolon may de-
velop many years later; can be severe in chil-
dren
922 Less common diseases
Treatment
Conservative treatment includes raising the
inside heel of the shoe, lowering the heels
of shoes, stretching exercises, support
braces, casting, and analgesics.
Tenectomy may be performed for patients
with fixed footdrop.
High-dose I.V. penicillin cycline is adminis-
tered for 1 to 2 months, followed by oral
penicillin for 1 to 6 months.
Lesions are surgically excised and drained.
Bed rest, antipyretics, and analgesics may
be prescribed as needed.
Ocular infections may require corticosteroid
therapy and supervision by an ophthalmolo-
gist.
Hospitalization is required for infants with
pneumonia and in epidemic keratoconjunc-
tivitis.
Enzyme replacement therapy is given
weekly.
Smoking cessation and asthma control are
promoted to prevent infection and lung
problems.
Vaccination against hepatitis B is given pro-
phylactically.
Liver and lung function are monitored.
Antihypertensives are given for hyperten-
sion.
Hearing aids, learning sign language, and
corrective eyewear or surgical repair of
cataracts are employed.
Dialysis or kidney transplantation may be
required for end-stage renal failure.
Nifurtimox or benznidazole is given during
the acute phase.
Supportive treatment is given for symptoms
caused by heart and intestinal complica-
tions during the chronic phase.
9400_BM.qxd 8/2/12 4:17 PM Page 923
Names Description
Amyloidosis A chronic disease resulting in the accumula-
tion of an abnormal fibrillar scleroprotein,
which infiltrates body organs and soft tissues,
resulting in permanent and usually life-
threatening organ damage
Anal stricture Develops when the lumen of the anus de-
(anal stenosis or creases and stenosis prevents dilation of the
contracture) sphincter and defecation; can result from
scarring after surgery, inflammation, laxative
abuse, surgical trauma, or congenital abnor-
mality
Angiofibroma, Highly vascular nasopharyngeal tumor made
juvenile up of fibrous tissue with thin-walled blood
vessels that may grow to completely fill the
nasopharynx, nose, paranasal sinuses, and
the orbit
Barometer-makers Soreness of gums, loosening of teeth, hyper-
disease salivation, fetid breath, abdominal cramping
(chronic mercury and diarrhea, weakness, peripheral neuropa-
poisoning) thy, ataxia, intention tremors, irritability and
depression, tachycardia, hypertension, repro-
ductive failures, birth defects (especially de-
velopmental neurologic damage), and death
Berylliosis A form of pneumoconiosis resulting from in-
halation of beryllium or from its absorption
through the skin; characterized by systemic
granulomatous disorder with predominant
respiratory symptoms that can lead to respi-
ratory failure, cor pulmonale, and death
Treatment
Kidney transplantation is used for renal fail-
ure, although the new organ may also de-
velop amyloidosis.
If the heart is affected, diuretics, digoxin,
antiarrhythmics, pacemakers, or heart
transplantation may be necessary.
In end-stage GI involvement, total parenter-
al nutrition is used as needed for malnutri-
tion.
Conservative treatment includes laxatives,
suppositories, and enemas.
A dilator is used daily.
Anoplasty or excision of eschar is em-
ployed with lateral internal sphincterotomy.
Surgery or cryosurgical techniques after
embolization decreases vascularization.
Chelation therapy with dimercaprol is initi-
ated.
Neurologic toxicity generally isnt consid-
ered reversible.
Supportive therapy is given for chronic ef-
fects.
Beryllium ulcer requires excision or curet-
tage. Acute berylliosis requires cortico-
steroid therapy.
Hypoxia may require oxygen; respiratory
failure, mechanical ventilation. Other respi-
ratory symptoms may be treated with bron-
chodilators and chest physiotherapy.
Chronic forms are treated with cortico-
steroids and immunosuppressants.
Less common diseases 923
9400_BM.qxd 8/2/12 4:17 PM Page 924
Names Description
Blastocystis hominis Parasitic infection resulting in watery or loose
infection stools, diarrhea, abdominal pain, anal itching,
(blastocystosis) weight loss, and flatus; conversely, no symp-
toms may be present
Bouillauds syndrome Manifests as a heart murmur of either mitral
(rheumatic endo- or aortic insufficiency; pericarditis and heart
carditis) failure are seen in severe cases
Budd-Chiari Hepatic vein obstruction that impairs blood
syndrome flow out of the liver, producing massive as-
cites and hepatomegaly; may be acute or
chronic
Cat-scratch fever Subacute self-limiting disease characterized
(cat-scratch disease) by a primary local lesion and regional lym-
phadenopathy; more common in children and
young adults in contact with cats (90% of
cases); disseminated form, bacillary an-
giomatosis, found in immunocompromised
people such as those infected with the human
immunodeficiency virus
Celiac disease Poor food absorption and gluten intolerance
(sprue, nontropical from environmental and genetic factors; re-
sprue, gluten current diarrhea, steatorrhea, abdominal dis-
intolerance) tention, and anorexia, resulting in malnutri-
tion; hematologic (anemia), musculoskeletal
(from vitamin D deficiency), neurologic, der-
matologic, and endocrine systems affected
Choriocarcinoma Rapidly metastasizing malignant tumor of pla-
cental tissue that typically causes profuse
vaginal and intra-abdominal bleeding
Chronic An inherited disorder in which abnormal neu-
granulomatous trophil metabolism impairs phagocytosis, re-
disease sulting in increased susceptibility to low viru-
lent or nonpathogenic organisms; infections
of the skin, lymph nodes, lungs, liver, and
bone occur
924 Less common diseases
Treatment
Drug therapy includes ketoconazole or itra-
conazole.
Amphotericin B is required for severe dis-
ease.
Provide nutritional support.
Monitor for fluid and electrolyte imbal-
ances.
Although no specific cure is available, a
course of penicillin should still be given to
eliminate group A streptococci.
Supportive therapy is provided to reduce
morbidity and mortality.
Surgery is performed to shunt hepatic
blood flow and remove obstruction.
If cause is congenital, transcardiac mem-
branectomy or percutaneous stent place-
ment is performed for patients with inferior
vena cava web.
Liver transplantation may be recommended
for patients with marked hepatocellular
dysfunction.
Symptomatic treatment is given.
If patient is ill, ciprofloxacin, doxycycline,
co-trimoxazole, erythromycin, cefoxitin, ce-
fotaxime, mezlocillin, aminoglycosides, or
antimycobacterials may be administered.
Gluten (wheat, rye, barley, and oat prod-
ucts, vegetable protein, malt, soy sauce,
grain vinegar) should be excluded from the
patients diet for life.
Supplements may be given to correct defi-
ciencies.
Corticosteroids may be required.
Chemotherapy is initiated.
Uterine contents are evacuated.
A hysterectomy is rarely needed.
B-hCG levels are monitored to detect pro-
gressively decreasing levels.
Antibiotics are used for early, aggressive
treatment.
9400_BM.qxd 8/2/12 4:17 PM Page 925
Names Description
Chronic Inherited defect in cell-mediated (T-cell) im-
mucocutaneous mune responses leading to recurrent infec-
candidiasis tions with Candida albicans and potential for
autoimmune-mediated endocrinopathies;
usually begins in early childhood with chronic
candidal infections; endocrinopathies include
hypoparathyroidism (and severe hypocalce-
mia), hypothyroidism, Addisons disease, dia-
betes, pernicious anemia; hepatitis
Colorado tick fever A benign infection from the bite of a wood
(mountain tick fever, tick infected with Dermacentor andersoni
mountain fever, (Fever begins abruptly after a 3- to 6-day in-
American mountain cubation; severe aching of the back, arms,
fever) and legs; lethargy; headache with eye move-
ment; photophobia; abdominal pain; nausea;
and vomiting.)
Conversion disorder A disorder that allows a patient to resolve a
(hysterical neurosis) psychological conflict through the loss of a
specific physical function, such as paralysis
or blindness
Cryptosporidiosis Watery diarrhea, stomach cramps, upset
stomach, and slight fever caused by a one-
celled parasite, Cryptosporidium parvum; life
threatening to those with weakened immune
systems and transplant recipients
Cystinuria Autosomal recessive disorder resulting from
an inborn error of amino acid transport in the
kidneys and intestine that allows excessive
urinary excretion of cystine and other dibasic
amino acids; resulting in recurrent cystine re-
nal calculi
Depersonalization Recurrent episodes of detachment in which
disorder self-awareness is temporarily altered or lost
in the entire body or only in a limb; usually
caused by severe stress
Dientamoeba fragilis Loose stools, diarrhea, and abdominal
infection cramping caused by contact with or ingestion
of stool, food, or water infected with the
parasite Dientamoeba fragilis
DiGeorges syndrome Fetal thymus fails to develop, leading to par-
(congenital thymic tial or total absence of T lymphocytes and
hypoplasia or cell-mediated immunity; may be linked with
aplasia) maternal alcoholism and fetal alcohol syn-
drome; increased susceptibility to infections;
hypoparathyroidism and cardiac anomalies
may also occur
Treatment
Topical or oral antifungal agents (micona-
zole, nystatin, fluconazole) control chronic
infection.
Therapy for endocrinopathy is organ-
directed, depending on the system affected.
Remove the tick and keep it for identifica-
tion.
Administer tetanus-diphtheria booster.
Monitor fluid and electrolyte balance.
Antipyretics are given to reduce fever.
Psychotherapy, family therapy, relaxation
therapy, behavioral therapy, or hypnosis
may be used alone or in combination.
Supportive therapy for affected body part is
used to prevent complications.
Theres no cure, but paromomycin, ato-
vaquone, nitazoxaine, and azithromycin
may reduce symptoms.
Reverse dehydration is used.
Immune status improves with antiviral
agents.
Theres no cure, but treatment can reduce
the risk of calculi formation.
Increase fluid intake to 3 L/day.
Sodium bicarbonate or sodium citrate help
alkalinize the urine.
Penicillamine is used to increase cystine
solubility.
Calculi are removed surgically or through
lithotripsy.
Prevent and treat urinary tract infections.
Psychotherapy and reality-based coping
strategies may be helpful.
Infection can be prevented by prudent hand
washing.
Antimicrobial agents are available to treat
Dientamoeba fragilis.
Monitor for fluid and electrolyte imbal-
ances.
Early development of life-threatening
hypocalcemia is treated immediately with
I.V. 10% calcium gluconate infusion.
Fetal thymic transplantation may be re-
quired to restore normal cell-mediated im-
munity.
Less common diseases 925
9400_BM.qxd 8/2/12 4:17 PM Page 926
Names Description
Dissociative amnesia Sudden inability to recall important personal
information that cant be explained by ordi-
nary forgetfulness; usually caused by severe
psychological stress
Dissociative fugue Wandering or traveling while mentally block-
ing out a traumatic event; a different person-
ality may be assumed and later cant recall
what happened; may be related to dissocia-
tive identity disorder, narcissistic personality
disorder, and sleepwalking
Dissociative identity Existence of two or more distinct, fully inte-
disorder (multiple grated personalities in the same person;
personality disorder) cause unknown but some type of abuse may
have been experienced
Duhrings disease Chronic inflammatory disease marked by ery-
(dermatitis herpeti- thematous, papular, vesicular, bulbous, or
formis) pustular lesions, with tendency toward group-
ing and associated with itching and burning;
usually symmetrical, with eruptions in el-
bows, knees, sacrum, buttocks, and occiput
Epidermolysis Blisters occur in response to normally harm-
bullosa (EB) less heat and friction and may result in scar-
ring with disfigurement; prognosis depends
on severity; may be inherited as an autoso-
mal dominant or recessive disorder and
cause multiple complications because skin
and mucous membranes are affected
Epstein-Barr virus Classic heterophil-positive infectious
(mononucleosis) mononucleosis, occasionally complicated by
neurologic diseases, such as encephalitis or
transverse myelitis
Fallopian tube cancer Cancer that usually produces a palpable
mass, vague abdominal or pelvic complaints,
bloating, or pain in the early stages; over
time, excessive menstrual bleeding may oc-
cur; causes appear to be linked with nullipari-
ty and infertility; more than half of the pa-
tients have never given birth
Fanconis syndrome Hereditary renal disorder producing malfunc-
(de Toni-Fanconi tions of the proximal renal tubules, leading to
syndrome) electrolyte losses and, eventually, retarded
growth and development and rickets
Fever, relapsing An acute infectious disease caused by spiro-
(tick, fowl-nest, chetes of the genus Borrelia transmitted by
cabin, or vagabond lice or ticks; presents with recurring high
fever or bilious fever, prostration, headache, severe myalgia,
typhoid) arthralgia, diarrhea, vomiting, coughing, eye
or chest pain, splenomegaly, hepatomegaly,
lymphadenopathy, and macular rash
926 Less common diseases
Treatment
Psychotherapy is necessary.
Hypnosis may be beneficial.
Antianxiety drugs may be ordered.
Psychotherapy is necessary.
Hypnosis may be beneficial.
Antianxiety drugs may be ordered.
Psychotherapy may be helpful.
Safety precautions may be needed.
Antipsychotic drugs may be ordered.
Sulfa-based antibiotics are administered.
A strict gluten-free diet should be followed.
Avoid skin trauma. sun exposure, and high
environmental temperatures.
Severe forms may need constant medical
attention.
Supportive treatment includes protection of
the skin.
Diet therapy helps combat malnutrition and
promote healing.
Generally, symptomatic treatment because
the disease has a benign course.
Total abdominal hysterectomy, bilateral
salpingo-oophorectomy, or omentectomy is
performed, followed by chemotherapy.
The patient receives external radiation for 5
to 6 weeks.
Symptomatic treatment may be given to
replace the patients specific deficiencies.
(Wilsons disease is treated with D-penicil-
lamine; cystinosis is treated with cyste-
amine.)
Supportive therapy is given by replacing
electrolytes, normalizing pH, and giving di-
etary supplements.
Tetracycline or erythromycin is given for
4 to 5 days, except during a severe febrile
attack because it may cause Jarisch-
Herxheimer reaction.
Symptomatic treatment is given; for exam-
ple, parenteral fluids and electrolytes.
9400_BM.qxd 8/2/12 4:17 PM Page 927
Names Description
Gauchers disease Genetic enzyme deficiency that causes abnor-
(glucosylceramide mal accumulation of glucocerebrosides in
storage disease, reticuloendothelial cells; signs include hepa-
GSDI) tosplenomegaly and bone lesions
Gender identity Persistent feelings of gender discomfort and
disorder (trans- dissatisfaction from a combination of predis-
sexualism) posing factors (chromosomal anomaly, hor-
monal imbalance, impaired parent-child
bonding, and child-rearing practices)
Hallux valgus Lateral deviation of the great toe at the
metatarsophalangeal joint, with medial en-
largement of the first metatarsal head and
painful bunion formation; may be congenital
or familial, but is usually acquired from de-
generative arthritis or prolonged pressure on
the foot, especially from narrow-toed, high-
heeled shoes
Hand, foot, and Common disease of infants and children
mouth disease characterized by fever, mouth sores, and a
(HFMD) rash with blisters on the hands and soles;
caused by coxsackievirus; highly contagious
Herpangina Acute infection caused by group A coxsack-
ieviruses transmitted by the fecal-oral route,
resulting in sore throat, pain on swallowing,
headache, and fever that persist for 1 to 4
days and may cause seizures, anorexia, vom-
iting, malaise, diarrhea, and pain; grayish
white papulovesicles appear on the soft
palate
Hydatidiform mole Chorionic tumor of the placenta that occurs
early in pregnancy; may follow death of the
embryo and loss of fetal circulation, although
in many cases, there is no fetus
Hypochondriasis The unrealistic misinterpretation of the sever-
(Hypochondria) ity and significance of physical signs or sen-
sations as abnormal and preoccupation with
the fear of having a serious disease, which
persists despite medical reassurance to the
contrary; unlinked to cause, although stress
increases the risk; frequently develops in
people who have experienced an organic dis-
ease or have a relative who has experienced
one
Iodine deficiency Insufficient iodine from inadequate intake or
thyroid dysfunction; complications range
from dental caries to cretinism
Treatment
Long-term therapy includes I.V. replace-
ment of the missing enzyme every 2 weeks.
Gene therapy is an experimental approach,
as well as N-butyldeoxynojirimycin
(OGT918) to inhibit production of gluco-
cerebroside.
The patient is referred for psychotherapy to
resolve conflict. Individual and family coun-
seling is recommended.
Sex reassignment through surgery and hor-
monal therapy may be used.
In the early stage, proper shoes and good
foot care such as felt pads to protect the
bunion, devices to separate the toes at
night, and a supportive pad and exercises
to strengthen the metatarsal arch may
eliminate the need for bunionectomy.
Surgery to realign the toe or bunionectomy
may be ordered.
Treatment is symptomatic only because
disease is self-limiting.
Acetaminophen and salt water mouth rins-
es (12 teaspoon salt to 1 glass warm water)
are used to provide soothing relief.
Symptomatic treatment emphasizes mea-
sures to prevent seizures (such as anti-
pyretics and and tepid sponge baths), fluids
to prevent dehydration, and bed rest.
Provide topical anesthetics for the mouth
(benzocaine and xylocaine) as needed.
Provide a non-irritating diet.
Increase fluid intake.
Uterus is evacuated by suction curettage or
abdominal hysterectomy.
Supportive treatment is given for postoper-
ative hypovolemia and anemia.
The goal is to help the patient lead a pro-
ductive life, despite distressing symptoms
and fears. Outpatient psychotherapy with
behavior modification is the first line of
treatment.
Symptoms must be evaluated to rule out
medical causes first.
Routine psychiatric appointments, regard-
less of new symptoms, help as part of psy-
chotherapy.
Iodine supplements (potassium iodide
[SSKI]) are administered to correct the de-
ficiency.
Increase iodine intake with iodized table salt
and iodine-rich foods.
Less common diseases 927
9400_BM.qxd 8/2/12 4:17 PM Page 928
Names Description
Lassa fever Epidemic hemorrhagic fever caused by the
Lassa virus; transmitted to humans by con-
tact with infected rodent urine, feces, and
saliva; fever persists for 2 to 3 weeks with
exudative pharyngitis, oral ulcers, lymphade-
nopathy and swelling of the face and neck,
purpura, conjunctivitis, and bradycardia;
shock and peripheral vascular collapse can
occur
Leprosy Chronic, systemic infection with progressive
(Hansens disease) cutaneous lesions caused by Mycobacterium
leprae; attacks the peripheral nervous system
Leptospirosis Infectious disease that causes meningitis, he-
patitis, nephritis, or febrile disease; may be
mild (anicteric) or severe (icteric or Weils
disease)
Lichen planus Benign, pruritic skin eruption producing scal-
ing, purple papules with white lines or spots;
cause unknown
Maple syrup urine Enzyme defect in the metabolism of the
disease branched chain amino acids, resulting in
mental and physical retardation, reflex
changes, feeding difficulties, characteristic
odor of urine and perspiration, seizures, and
death; four clinical phenotypes: classic, inter-
mediate, intermittent, and thiamine-respon-
sive
Marfan syndrome Rare inherited, degenerative generalized dis-
ease of the connective tissue that causes oc-
ular, skeletal, and cardiovascular anomalies
Mastoiditis Bacterial infection and inflammation of the air
cells of the mastoid antrum resulting in dull
ache and tenderness in the area of the mas-
toid process, low-grade fever, headache, and
thick, purulent drainage; meningitis, facial
paralysis, brain abscess, and suppurative
labyrinthitis may occur
928 Less common diseases
Treatment
Strict isolation is imposed for at least 3
weeks.
Drug therapy includes antiviral (I.V. rib-
avirin), I.V. colloids for shock, analgesics
for pain, and antipyretics for fever.
Immune plasma from patients who have re-
covered from Lassa fever is infused.
Drug regimen includes antimicrobial thera-
py with dapsone, rifampin, clofazimine, or
ethionamide.
Supportive care with aspirin, prednisone, or
thalidomide to control inflammation may be
used.
Doxycycline or ampicillin is administered.
Supportive treatment of other symptoms is
provided.
Relieve inflammation with topical steroids
and suppress immune response.
Antihistamines are used to reduce discom-
fort.
Viscous lidocaine is used for mouth le-
sions.
Corticosteroids may be injected into a le-
sion.
Topical retinoic (vitamin A) cream and other
anti-inflammatory or anti-pruritic ointments
or creams are used to reduce itching and
inflammation.
Ultraviolet light therapy may be used.
Supportive treatment is provided.
Intake of protein is controlled.
Branched chain amino acids are eliminated
from the diet.
Peritoneal dialysis or hemodialysis is per-
formed to reduce amino acid level.
One form is responsive to early initiation of
thiamine.
Treatment is aimed at relieving the symp-
toms such as surgical repair of aneurysms
and ocular deformities.
Preventive antibiotics are given before den-
tal procedures.
Children shouldnt be involved in maximal
exercise programs because of concern of
aortic aneurysm.
Intense antibiotic therapy is administered
parenterally.
Myringotomy is performed if bone damage
is minimal.
Mastoidectomy is performed if the mastoid
is chronically inflamed.
9400_BM.qxd 8/2/12 4:17 PM Page 929
Names Description
Medullary sponge Inherited disorder, possibly where collecting
kidney ducts in renal pyramids dilate and cavities,
clefts, and cysts form, producing complica-
tions of calcium oxylate stones and infections
Monkeypox Rare viral disease caused by the monkeypox
virus; occurs mainly in the rainforest areas of
central and western Africa; symptoms include
fever, headache, muscle aches, backache,
swollen lymph nodes, and exhaustion; a
papular rash develops within 1 to 3 days of
the onset of fever (In June 2003, monkeypox
was reported in prairie dogs and humans in
the United States.)
Multiple endocrine A hereditary disorder in which two or more
neoplasia endocrine glands develop hyperplasia, adeno-
ma, or carcinoma concurrently or consecu-
tively; symptoms depend on glands affected
Neurofibromatosis Group of inherited developmental disorders
of the nervous system, muscles, bones, and
skin that cause formation of multiple, pedun-
culated, soft tumors and caf-au-lait spots
Nocardiosis Bacterial infection caused by gram-positive
species of the genus Nocardia and transmit-
ted by inhalation; causes cough, mucopuru-
lent sputum, high fever, chills, night sweats,
anorexia, malaise, and weight loss
Orbital cellulitis Acute infection of the orbital tissues and eye-
lids that can spread to the cavernous sinus or
meninges; produces unilateral eyelid edema,
hyperemia, reddened eyelids, and matted
lashes
Parainfluenza Group of respiratory illnesses caused by the
parainfluenza virus that affect the upper and
lower respiratory tracts; transmitted by direct
contact or inhalation of airborne droplets
Paroxysmal Red cell breakdown with release of hemoglo-
nocturnal bin in the urine, resulting in dark-colored
hemoglobinuria urine in the morning; symptoms include he-
molytic anemia, thrombosis of large vessels,
and a deficiency of hematopoiesis resulting in
anemia (pancytopenia)
Treatment
Supportive care focuses on preventing or
treating complications caused by stones
and infection. Includes increasing fluid in-
take and monitoring renal function.
Surgery may be required to remove stones
during acute obstruction. Nephrectomy is
required if serious, uncontrollable infection
or hemorrhage occur.
Theres no specific treatment for monkey-
pox.
Persons caring for infected individuals
should receive a smallpox vaccination.
Provide analgesics, antipyretics, and anti-
histamines as needed.
Supportive treatment is dependent on the
affected glands.
Tumors are eradicated; subsequent treat-
ment controls symptoms.
Intracerebral or intraspinal tumors are re-
moved and kyphoscoliosis is corrected.
Disfiguring or disabling growths are treated
with cosmetic surgery.
Annual eye examinations are strongly rec-
ommended.
Long-term antibiotic treatment with sulfon-
amides is given.
Abscesses are surgically drained and
necrotic tissue is excised.
Bed rest and supportive treatment are or-
dered.
Hospitalization is required.
Appropriate antibiotics are given.
Supportive therapy includes administration
of fluids, application of warm moist com-
presses, and bed rest.
Surgical drainage may be necessary.
Treatment regimen includes bed rest, anti-
pyretics for fever, analgesics for pain, and
antitussives for cough.
Specific treatments are available for croup
and bronchiolitis.
Symptomatic treatment with corticosteroids
is provided.
Androgen therapy is administered.
Oral iron supplements and folic acid are
given as needed.
Transfusions are administered to treat
severe anemia.
Thrombotic complications are treated.
Less common diseases 929
9400_BM.qxd 8/2/12 4:17 PM Page 930
Names Description
Penile cancer Malignant, ulcerative or papillary (wartlike,
nodular) lesions, which may become quite
large before spreading beyond the penis, po-
tentially destroying the glans prepuce and in-
vading the corpora; generally associated with
poor personal hygiene and phimosis in uncir-
cumcised men, although the exact cause is
unknown
Pilonidal disease Coccygeal cyst forms in the intergluteal cleft
on the posterior surface of the lower sacrum,
often becoming infected or developing a fis-
tula; may be congenital or caused by irritation
from exercise, heat, perspiration, or constric-
tive clothing
Polymyalgia An inflammatory syndrome characterized by
rheumatica significant stiffness and dull aching pain of
the proximal muscle groups, weight loss,
malaise, and fever; cause unknown, but it
predominantly involves whites, tends to run
in families, and is possibly associated with
HLA-DR4 antigens, all of which suggest a
possible genetic predisposition
Puerperal infection Inflammation of the birth canal during the
postpartum period or after abortion; caused
by streptococci, coagulase-negative staphylo-
cocci, Clostridium perfringens, Bacteroides
fragilis, and Escherichia coli
Rectal polyps Mass lesions that result from unrestrained
cell growth in the upper epithelium and pro-
trude into the intestinal lumen; varying in
appearance; include common polypoid ade-
nomas, villous adenomas, polyposis syn-
dromes, juvenile polyps, and focal polypoid
hyperplasia; predisposing factors include
heredity, age, infection, and diet
930 Less common diseases
Treatment
Depending on the stage of progression,
treatment includes surgical resection of the
primary tumor and, possibly, chemotherapy
(bleomycin) and radiation.
Invasive tumors require partial penectomy
(unless contraindicated because of the pa-
tients young age); tumors of the base of
the penile shaft require total penectomy and
inguinal node dissection.
Radiation therapy may improve treatment
effectiveness after resection of localized le-
sions without metastasis; it may also re-
duce the size of lymph nodes before nodal
resection.
Psychotherapy is recommended for related
emotional issues.
Abscesses are incised and drained, pro-
truding hairs are extracted, and sitz baths
are ordered.
Entire affected area is excised if infections
persist.
Corticosteroids, such as prednisone or
prednisolone, are the treatment of choice to
help relieve discomfort and stiffness.
I.V. broad-spectrum antibiotics are ordered
to combat infection.
Supportive therapy includes analgesics, an-
ticoagulants, antiemetics, bed rest, admin-
istration of I.V. fluids, and prevention of
thrombophlebitis (antiembolism stockings).
Specific treatment varies according to type
and size of the polyps and their location in
the colon.
Common polypoid adenomas less than
1 cm require polypectomy, frequently by
fulguration (destruction by high-frequency
electricity) during endoscopy. For common
polypoid adenomas over 4 cm and all inva-
sive villous adenomas, treatment usually
consists of abdominoperineal resection or
low anterior resection. Transanal excision is
performed to remove an adenoma from the
rectum.
Depending on large-bowel involvement,
hereditary polyposis necessitate restorative
proctolectomy, ileoanal anastomosis with
temporary ileostomy.
Focal polypoid hyperplasia can be obliterat-
ed by a biopsy.
Increase fluid intake and provide stool soft-
eners to reduce risk of constipation.
9400_BM.qxd 8/2/12 4:17 PM Page 931
Names Description
Rectal prolapse Circumferential protrusion of one or more
layers of the rectum through the anus caused
by straining or conditions that affect the
pelvic floor or rectum; patient may also have
a feeling of rectal fullness, bloody diarrhea,
and pain
Retinitis pigmentosa Genetically induced progressive destruction
of the retinal rods resulting in visual field
constriction, cataracts, edema, atrophic mac-
ulopathy, and blindness
Throat abscess Either peritonsillar (quinsy) abscess that
forms in the connective tissue space between
the tonsil capsule and constrictor muscle of
the pharynx or retropharyngeal abscess that
forms between the posterior pharyngeal wall
and prevertebral fascia (Peritonsillar abscess
is a complication of acute tonsillitis, usually
after streptococcal or staphylococcal infec-
tion. Acute retropharyngeal abscess results
from infection in the retropharyngeal lymph
glands, which may follow an upper respirato-
ry tract bacterial infection. Chronic retropha-
ryngeal abscess may result from tuberculosis
of the cervical spine [Potts disease].)
Tinea versicolor Chronic, superficial fungal (yeast) infection
(pityriasis versicolor) producing a multicolored rash or macular or
raised scaly lesions, commonly on the upper
trunk and caused by Pityrosporum orbiculare
Toxocariasis Infection caused by parasitic roundworms in
(ocular larva dogs and cats spread by the fecal-oral route
migrans, visceral and resulting in eye infections that can cause
larva migrans) blindness or visceral (rare) symptoms with
swelling of body organs or central nervous
system
Trachoma (granular Infection by Chlamydia trachomatis that af-
conjunctivitis, fects the eye but can also localize in the ure-
Egyptian ophthalmia) thra; may cause permanent damage to the
cornea and conjunctiva
Uveitis (iritis) Inflammation of one uveal tract producing
moderate to severe eye pain, severe ciliary in-
jection, photophobia, tearing, a small nonre-
active pupil, and blurred vision; results from
allergy, infection, chemicals, trauma, surgery,
or systemic diseases or may be idiopathic
Vaginismus Involuntary spastic constriction of the lower
vaginal muscles with pain on insertion of any
object into the vagina; cause may be physical
or psychological
Treatment
Treat the underlying cause and eliminate
predisposing factors (straining, coughing,
nutritional disorders).
Manual return of the rectal mucosa may be
necessary.
Surgical repair is performed in severe or
chronic cases.
No cure exists.
Vitamin A supplementation may be given to
slow degeneration.
Advise the use of sunglasses to protect
from ultraviolet light.
For early-stage peritonsillar abscess, large
doses of a broad-spectrum antibiotic are
given.
For late-stage peritonsillar abscess with cel-
lulitis of the tonsillar space, primary treat-
ment is incision and drainage under a local
anesthetic, followed by antibiotic therapy
for 7 to 10 days.
For both stages of peritonsillar abscess,
tonsillectomy is recommended after several
episodes. It must be scheduled at least 1
month after acute infection.
Incision and drainage of abcesses.
Treat with topical antifungals, such as
clotrimazole, ketoconazole, and miconal-
zole.
Over-the-counter dandruff shampoos ap-
plied to the skin for 10 minutes each day in
the shower may also eliminate it.
Infection is treated with mebendazole, al-
bendazole, or diethylcarbamazine.
Preventive measures include treating ani-
mals and thorough hand washing.
Topical or systemic antibiotic therapy with
erythromycin or doxycycline is given.
Surgical correction is necessary if severe
entropion occurs.
Underlying cause is diagnosed and treated.
Topical cycloplegic and topical cortico-
steroids are given.
Steroid drops or ointment may be needed.
Oral systemic corticosteroids are given in
severe cases.
Maladaptive muscle constriction is elimi-
nated with dilators.
Education, counseling, and behavioral exer-
cises are given.
Kegel exercises to improve voluntary con-
trol are ordered.
Less common diseases 931
9400_BM.qxd 8/2/12 4:17 PM Page 932

Names Description Treatment

Whipples disease GI malabsorption disorder characterized by Appropriate antibiotic therapy is initiated.

(intestinal lipodystro- chronic diarrhea and progressive wasting, Supportive therapy with fluid and elec-
phy, lipophagia with skin pigmentation and polyarthralgia trolyte replacement is provided.
granulomatosis) Iron, folate, vitamin D, and magnesium
supplementation is administered.

Wilsons disease Rare, inherited metabolic disorder character-
(hepatolenticular ized by excessive copper retention in the
degeneration) liver, brain, kidneys, and corneas; Kayser-
Fleischer rings of the eye are produced, and
deposits may lead to tissue necrosis and fi-
brosis.
Treatment with pyridoxine in conjunction
with penicillamine, a copper-chelating agent
that mobilizes copper from the tissues and
promotes its excretion in the urine, is life-
long.
Copper-containing foods should be avoided
as well as tap water (because of copper
pipes) and copper cooking utensils.
The patient and his family should receive
genetic counseling.

Wiskott-Aldrich X-linked recessive inherited disease charac-
syndrome terized by defective B- and T-cell functions
(immunodeficiency (increased susceptibility to infections) and
with eczema and metabolic defects in platelet synthesis
thrombocytopenia) (thrombocytopenia) (Male infants develop
early bleeding complications [bloody stools,
petechiae, and purpura] and by age 6 months
develop recurrent systemic infections; by age
1 year, eczema develops, leading to scratch-
ing and skin infections; high susceptibility to
neoplastic diseases, such as lymphoma and
leukemia, occurs. Average life span is 4
years.)
Bleeding is controlled with platelet transfu-
sions.
Prophylactic or early aggressive therapy
with antibiotics is indicated for infections.
Topical steroids help control eczema symp-
toms.
Bone marrow transplantation may be effec-
tive in some patients.

932 Less common diseases

9400_BM.qxd 8/2/12 4:17 PM Page 933
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934 Selected references

9400_BM.qxd 8/2/12 4:17 PM Page 935

Web resources

Aetna Intelihealth Autism Society of America

www.intelihealth.com www.autism-society.org
Alateen Center for AIDS Prevention Studies
www.al-anon.alateen.org www.caps.ucsf.edu
Alcoholics Anonymous Centers for Disease Control and Prevention
www.alcoholics-anonymous.org www.cdc.gov
Al-Anon Centers for Disease Control and Prevention Injury Center
www.al-anon.org www.cdc.gov/ncipc
ALS Association Centers for Disease Control and Prevention Sexually
www.alsa.org Transmitted Diseases
American Academy of Allergy, Asthma, and Immunology www.cdc.gov/std
www.aaaai.org Dermatology Foundation
American Academy of Dermatology www.dermfnd.org
www.aad.org Digestive Disease National Coalition
American Academy of Neurology www.ddnc.org
www.aan.com eMedicine
American Academy of Ophthalmology www.emedicine.com
www.aao.org EndocrineWeb.com
American Academy of Pediatrics www.endocrineweb.com
www.aap.org Epilepsy.com
American Association of Kidney Patients www.epilepsy.com
www.aakp.org Hereditary Hemorrhagic Telangiectasia Foundation
American Burn Association www.hht.org
www.ameriburn.org Huntingtons Disease Society of America
American Cancer Society www.hdsa.org
www.cancer.org Iron Disorders Institute
American College of Obstetricians and Gynecologists www.irondisorders.org
www.acog.org iVillage Total Health
American Heart Association www.totalhealth.ivillage.com
www.americanheart.com KidsHealth
American Lung Association www.kidshealth.org
www.lungusa.org Mayo Clinic
American Psychological Association Help Center www.mayoclinic.com
www.apahelpcenter.org Mental Health America
American Society for Reproductive Medicine www.nmha.org
www.asrm.org Myasthenia Gravis Foundation of America
American Sudden Infant Death Syndrome Institute www.myasthenia.org
www.sids.org NARAL Pro-Choice America (formerly the National
Arthritis Foundation Abortion and Reproductive Rights Action League)
www.arthritis.org www.naral.org
Arthritis Society Narcotics Anonymous
www.arthritis.ca www.na.org
Asthma and Allergy Foundation of America National Abortion Federation
www.aafa.org www.prochoice.org

Web resources 935

9400_BM.qxd 8/2/12 4:17 PM Page 936

National Association for Children of Alcoholics

www.nacoa.net
National Association of Anorexia Nervosa and Associated
Disorders
www.anad.org
National Asthma Education and Prevention Program
www.nhlbi.nih.gov/about/naepp
National Cancer Institute
www.cancer.gov
National Center for Infectious Disease
www.cdc.gov/ncidod
National Center for Learning Disabilities
www.ncld.org
National Cervical Cancer Coalition
www.nccc-online.org
National Council on Alcoholism and Drug Dependence
www.ncadd.org
National Down Syndrome Society
www.ndss.org
National Eye Institute
www.nei.nih.gov
National Fragile X Foundation
www.fragilex.org
National Health Information Center
www.health.gov/nhic
National Heart, Lung, and Blood Institute
www.nhlbi.nih.gov
National Institute for Occupational Safety and Health
www.cdc.gov/niosh
National Institute of Allergy and Infectious Diseases
www3.niaid.nih.gov
National Institute of Arthritis and Musculoskeletal and
Skin Diseases
www.niams.nih.gov
National Institute of Diabetes and Digestive and Kidney
Diseases
www2.niddk.nih.gov
National Institute of Neurological Disorders and Stroke
www.ninds.nih.gov
National Lung Health Education Program
www.nlhep.org
National Multiple Sclerosis Society
www.nationalmssociety.org
National Organization for Rare Disorders
www.rarediseases.org
National Right to Life
www.nrlc.org
National Womens Health Information Center
www.4woman.gov
Nephrology Channel
www.nephrologychannel.com
Overeaters Anonymous
www.oa.org
Sickle Cell Disease Association of America
www.sicklecelldisease.org
U.S. Food and Drug Administration
www.fda.gov

936 Web resources

9400_INDEX.qxd 8/2/12 4:19 PM Page 937

Index

A Allergic purpura, 30-31

Abdominal aortic aneurysm, 58-59 lesions of, 30i
endovascular grafting for, 59i Allergic rhinitis, 32-33
Abdominal obesity, 519 Alopecia, 34-35
ABO incompatibility, 276-277 cancer drugs causing, 35t
Abortion, spontaneous, 2-3 Alpha1-antitrypsin deficiency, 922t
Abruptio placentae, 4-5 Alports syndrome, 922t
degrees of separation in, 5i Alzheimers disease, 36-37
Acceleration-deceleration injuries, 6-7 Amebiasis (amebic dysentery), 38-39
cervical collar for, 7i Amenorrhea, 40-41
Achilles tendon contracture, 922t American mountain fever, 925t
Acidosis American trypanosomiasis, 922t
metabolic, 394 Amnesia, dissociative, 926t
respiratory, 696-697 Amyloidosis, 923t
Acne vulgaris, 8-9 Amyotrophic lateral sclerosis, 42-43
Acquired immunodeficiency syndrome, 10-11 modifying home for, 43
Acromegaly, 408 Anal stricture, 923t
Actinomycosis, 922t Anaphylaxis, 44-45
Acute infective tubulointerstitial nephritis, 14-15 Anemia
Acute leukemia, 482-483 aplastic, 46-47
Acute poststreptococcal glomerulonephritis, 12-13, folic acid deficiency, 48-49
316-317 iron deficiency, 50-51
Acute pyelonephritis, 14-15 pernicious, 52-53
Acute respiratory distress syndrome, 16-17 sickle cell, 54-55
Acute respiratory failure, 18-19 sideroblastic, 56-57, 57i
Acute tubular necrosis, 20-21, 693 Anencephaly, 550
Addisons anemia, 52-53 Aneurysm
Addisons disease, 22-23 abdominal aortic, 58-59, 59i
Adenovirus infection, 922t femoral and popliteal, 60-61
Adrenal (addisonian) crisis, 22-23 intracranial, 62-63
Adrenal hypofunction, 22-23 thoracic aortic, 64-65
Adrenogenital syndrome, 24-25 ventricular, 66-67
Adult chorea, 380-381 Angioedema, 860-861
Adult respiratory distress syndrome, 16-17 Angiofibroma, juvenile, 923t
Age-related macular degeneration, 26-27 Angiohemophilia, 906-907
central vision in, 26i Animal bites, first aid for, 678
Airway crisis in epiglottiditis, 270 Anion gap, 394
Alcoholism, 28-29 Ankylosing spondylitis, 68-69
Allens test, 139i Anorexia nervosa, 70-71
i refers to an illustration; t refers to a table.

Index 937
9400_INDEX.qxd 8/2/12 4:19 PM Page 938

Anthrax, 72-73 Beckers muscular dystrophy, 536

Anthropometric arm measurements, 557i Bedsores, 652-653, 653i
Antimalarial drugs, 508, 509 Bee sting, 446-447
Anxiety disorder, generalized, 304-305 Bells palsy, 110-111
Aorta, coarctation of, 190-191, 191i facial paralysis in, 110i
Aortic aneurysm Benign polycythemia, 772-773
abdominal, 58-59, 59i Benign prostatic hyperplasia, 112-113
thoracic, 64-65 Berylliosis, 923t
Aortic insufficiency, 74-75 Bilharziasis, 734-735, 734t
murmur of, 75i Bilious typhoid, 688-689, 926t
Aortic stenosis, 76-77 Bipolar disorder, 114-115
murmur of, 77i Bites
muscular, 151t, 152-153, 152i animal, first aid for, 678
Aphthous stomatitis, 776-777 insect, 446-447
lesions of, 776i mosquito, preventing, 725, 913
Aplastic anemia, 46-47 Black widow spider bite, 446-447
Apnea, sleep, 764-765 Bladder, neurogenic, 552-553, 553t
Appalachian Mountain disease, 372-373 Bladder cancer, 116-117
Appendicitis, 78-79 Blastocystis hominis infection (blastocystosis), 924t
Arbovirus, 724-725 Blastomycosis, 118-119
Arterial occlusive disease, 80-81 European, 216-217
Arteries of leg, 61i Blepharitis, 120-121
Arteriovenous malformations, 82-83 Blepharoptosis, 664-665, 665i
Arthritis Blood transfusion reaction, 122-123
juvenile rheumatoid, 454-455 Body lice, 596, 597i
osteo-, 564-565, 565i Body mass index measurement, 556
reactive, 686-687 Bone tumors, primary malignant, 124-125
rheumatoid, 710-711 types of, 125t
septic, 742-743 Bordetella pertussis, 608i
Asbestosis, 84-85 Botulism, 126-127
Ascariasis, 86-87 Bouchards nodes, 565i
Aspergillosis, 88-89 Bouillauds syndrome, 924t
Asphyxia, 90-91 Bowlegs, 896i
Aspiration pneumonia, 626 Brain attack, 780-781
Asthma, 92-93 Brain tumor, 128-129
Atelectasis, 94-95 Breast cancer, 130-131
Atopic dermatitis, 96-97 sources and sites of, 131i
signs of, 97i Brittle bone disease, 566-567
Atopy, factors contributing to, 96 Bronchiectasis, 132-133
Atrial fibrillation, 98-99 Bronchitis, chronic, 134-135
recognizing, 98i pathophysiology of, 135i
Atrial septal defect, 100-101 Brown recluse spider bite, 446-447
Attention deficit hyperactivity disorder, 102-103 Brucellosis, 136-137
Autistic disorder, 104-105 Brutons agammaglobulinemia, 914-915
Autotransfusion for chest wounds, 351i Bubonic plague, 618-619
Avian influenza, 106-107 carrier of, 619i
Budd-Chiari syndrome, 924t
B Buergers disease, 138-139
Bacillary dysentery, 748-749 Allens test for, 139i
Bangs disease, 136-137 Bulimia nervosa, 140-141
Barometer-makers disease, 923t Bullous impetigo, 438
Basal cell carcinoma, 108-109 Burns, 142-143
identifying, 108i

i refers to an illustration; t refers to a table.

938 Index
9400_INDEX.qxd 8/2/12 4:19 PM Page 939

Bursae, 805i Cellulitis, 162-163

Bursitis, 804-805 orbital, 929t
synergistic necrotizing, 546-547
C Central Mississippi Valley disease, 372-373
Cabin fever, 688-689, 926t Central retinal artery or vein occlusion, 880-881
Calculi Cerebral contusion, 164-165
gallbladder, 176-177 intracranial pressure in, 165i
renal, 690-691, 691i Cerebral palsy, 166-167
Campylobacteriosis, 144-145 Cerebrovascular accident. See Stroke.
Cancer. See also Tumors; specific type. Cervical cancer, 168-169
basal cell, 108-109, 108i preventing, 168
bladder, 116-117 testing for, 169
breast, 130-131, 131i, 584 Cervical collar, applying, 7i
cervical, 168-169 Cestodiasis, 798-799
colorectal, 194-195 Chagas disease, 922t
esophageal, 278-279 Chalazion, 170-171
fallopian tube, 926t eye patch for, 171i
gastric, 296-297 recognizing, 170i
laryngeal, 470-471 Chancroid, 172-173
liver, 490-491 lesion in, 172i
lung, 494-495 Chest wounds, autotransfusion for, 351i
oral and pharyngeal, 560-561 Chickenpox, 716t, 874-875
ovarian, 580-581 Chlamydial infections, 174-175, 175i
pancreatic, 586-587 Chlamydia trachomatis, 175i
penile, 930t Chloride, dietary sources of, 418
prostatic, 656-657 Chloroquine, 508, 509
renal, 462-463, 462i Cholangitis, 176
squamous cell, 774-775, 774i Cholecystitis, 176-177
testicular, 806-807 Choledocholithiasis, 176
thyroid, 820-821 Cholelithiasis, 176-177
uterine, 864-865 Cholera, 178-179
vaginal, 868-869 Chondrosarcoma, 125t
Cancer drugs causing alopecia, 35t Chordoma, 125t
Candidiasis, 146-147 Chorea, Huntingtons, 380-381
chronic mucocutaneous, 925t Choriocarcinoma, 924t
oropharyngeal, 146i Choriomeningitis, lymphocytic, 500-501
Carbunculosis, 288-289 Chorioretinitis, active, 830
hair follicles in, 288i Chromaffin tumor, 612-613
Cardiac tamponade, 148-149 Chronic bronchitis, 134-135, 135i
pathophysiology of, 149i Chronic dermatitis, 230t
Cardiogenic shock, 750-751 Chronic fatigue and immune dysfunction syndrome,
Cardiomyopathies 180-181
assessment findings in, 151t Chronic granulomatous disease, 924t
dilated, 150-151, 150i Chronic leukemia
hypertrophic, 152-153, 152i granulocytic (myelogenous), 484-485
restrictive, 154-155, 154i lymphocytic, 486-487
Carpal tunnel, 156i Chronic mucocutaneous candidiasis, 925t
Carpal tunnel syndrome, 156-157 Chronic progressive chorea, 380-381
Cataract, 158-159 Chvosteks sign, 417i
removal methods for, 159i Cirrhosis, 182-183
Cat-scratch fever, 924t Clam diggers itch, 735
Causalgia, 198-199, 199t Cleft lip and cleft palate, 184-185
Celiac disease, 160-161, 506, 924t types of, 185i

i refers to an illustration; t refers to a table.

Index 939
9400_INDEX.qxd 8/2/12 4:19 PM Page 940

Clostridium difficile infection, 186-187 Cyclothymic disorder, 114, 115

Clostridium perfringens, 294i Cystic fibrosis, 222-223
Clubfoot, 188-189 Cystinuria, 925t
recognizing, 188i Cysts
Coarctation of aorta, 190-191 ovarian, 582-583, 582i, 636-637
recognizing, 191i renal, 634-635
Cobalamin. See Vitamin B12. Cytomegalovirus infection, 224-225
Coccidioidomycosis, 192-193
Cold, common, 196-197, 197i D
Colitis Dacryocystitis, 226-227
spastic or mucous, 452-453 Da Nang lung, 16-17
ulcerative, 856-857 Dark-field microscopy for syphilis, 795i
Colorado tick fever, 925t Darlings disease, 372-373
Colorectal cancer, 194-195 Decubitus ulcers. See Pressure ulcers.
Common cold, 196-197 Defibrination syndrome, 242-243
pathophysiology of, 197i Depersonalization disorder, 925t
Complete abortion, 3 Depression, major, 504-505
Complex regional pain syndrome, 198-199 Dermal gangrene, acute, 546-547
stages of, 199t Dermatitis, 228-229
Concussion, 200-201 atopic, 96-97, 97i
Condylomata acuminata, 308-309, 308i schistosomal, 735
Congenital (aganglionic) megacolon, 370-371 types of, 230-231t
Congestive cardiomyopathy, 150-151, 150i, 151t Dermatitis herpetiformis, 926t
Conjunctival papillae, 202i de Toni-Fanconi syndrome, 926t
Conjunctivitis, 202-203 Developmental dysplasia of hip, 232-233
granular, 931t degrees of, 232i
papillae in, 202i signs of, 233
Conns syndrome, 388 Diabetes insipidus, 234-235
Constrictive pericarditis, 604 Diabetes mellitus, 236-237
Consumption coagulopathy, 242-243 Diabetic retinopathy, 880-881
Contact dermatitis, 230t Dientamoeba fragilis infection, 925t
Contact precautions, 144 DiGeorges syndrome, 925t
Conversion disorder, 925t Dilated cardiomyopathy, 150-151
Corneal abrasion, 204-205 assessment findings in, 151t
eye irrigation for, 205i pathophysiology of, 150i
Coronary artery disease, 206-207 Diphtheria, 238-239
Cor pulmonale, 208-209, 342 Discoid lupus erythematosus, 496, 796
pathophysiology of, 208i Dislocations, 240-241
Corticotropin deficiency, 430, 431 elbow, 240i
Coxa plana, 478-479 hip, 232i
Crab lice, 596, 597i Disseminated intravascular coagulation, 242-243
Creutzfeldt-Jakob disease, 210-211 Dissociative amnesia, 926t
variant, 210 Dissociative fugue, 926t
Crib death, 790-791 Dissociative identity disorder, 926t
Crohns disease, 212-213 Diverticular disease, 244-245
Croup, 214-215 Down syndrome, 246-247
upper airway in, 215i Droplet precautions, 238
Cryptococcosis, 216-217 Drowning, near, 544-545
Cryptorchidism, 218-219 Drugs
testicular cancer and, 806 causing alopecia, 35t
varieties of, 218i causing gynecomastia, 332
Cryptosporidiosis, 925t causing hypercalcemia, 392
Cushings syndrome, 220-221 causing hyperchloremia, 394

i refers to an illustration; t refers to a table.

940 Index
9400_INDEX.qxd 8/2/12 4:19 PM Page 941

Drugs (continued) Enterobacteriaceae infections, 264-265

causing hyperkalemia, 396 Enterococcus, vancomycin-resistant, 872-873
causing hypermagnesemia, 400 Enterocolitis, pseudomembranous, 660-661
causing hypernatremia, 402 Epidermolysis bullosa, 926t
causing hyperphosphatemia, 406 Epididymitis, 266-267
causing hypochloremia, 418 Epidural hematoma, 268-269
causing hypokalemia, 420 Epiglottiditis, 270-271
causing hypomagnesemia, 422 airway crisis in, 270
causing hyponatremia, 424 Haemophilus influenzae, 334
causing hypophosphatemia, 428 Epilepsy, 272-273
aggravating porphyria, 645 Epstein-Barr virus, 926t
causing rhabdomyolysis, 706 chronic, 180-181
3-D syndrome, 890 Erbs muscular dystrophy, 536
Duchennes muscular dystrophy, 536 Erectile dysfunction, 274-275
Duhrings disease, 926t Erythema, 640-641
Duodenal ulcer, 600-601 Erythroblastosis fetalis, 276-277
Dysentery Rh isoimmunization in, 276i
amebic, 38-39 Erythrodermic psoriasis, 663
bacillary, 748-749 Escherichia coli infection, 264-265
Dysfunctional uterine bleeding, 862-863 Esophageal atresia, 832-833
Dysmenorrhea, 248-249 Esophageal cancer, 278-279
Dysmetabolic syndrome, 518-519 European blastomycosis, 216-217
Ewings sarcoma, 124, 125t
E Exanthema subitum, 716-717, 716t
Ear, hardening of, 578-579 Exfoliative dermatitis, 230t
Eardrum, perforated, 576, 602-603 Exophthalmos, 280-281
Ebola virus infection, 250-251 detecting unilateral, 281i
Eclampsia, 310-311 recognizing, 280i
Ecthyma versus impetigo, 439 External otitis, 574-575
Ectopic pregnancy, 252-253 Extracapsular cataract extraction, 159i
implantation sites of, 252i Extravaginal torsion, 808i
Eczema, immunodeficiency with, 932t Eye examination with slit lamp, 460
Edwards syndrome, 850-851 Eye irrigation, 205i
Egyptian ophthalmia, 931t Eye patch, applying, 171i
Elbow dislocation, 240i
Electric shock, 254-255 F
Electrosurgery for warts, 911i Facial paralysis in Bells palsy, 110i
Emphysema, 256-257 Failure to thrive, 282-283
pathophysiology of, 257i Fallopian tube cancer, 926t
Empyema, 620-621 Fanconis syndrome, 926t
Encephalitis, 258-259 Fasciitis, necrotizing, 546-547
St. Louis, 724-725 Femoral aneurysm, 60-61
West Nile, 912-913 Femoral hernia, 445i
Encephalocele, 550 Fibrocystic breast disease, 284-285
Encephalopathy, hepatic, 352-353, 492 Fibroids, uterine, 866-867
Endocarditis, 260-261 Fibromyalgia syndrome, 286-287
degenerative changes in, 261i tender points in, 287i
Q fever, treating, 676 Fibromyomas, uterine, 866-867
rheumatic, 924t Fibrosarcoma, 125t
Endolymphatic hydrops, 514-515 Fire ant sting, 446-447
Endometrial cancer, 864-865 Flesh-eating bacteria, 546-547
Endometriosis, 262-263 Flu. See Influenza.
Endovascular grafting for abdominal aortic aneurysm, 59i Folic acid, foods high in, 49t

i refers to an illustration; t refers to a table.

Index 941
9400_INDEX.qxd 8/2/12 4:19 PM Page 942

Folic acid deficiency anemia, 48-49 Goiter, 318-319

Follicular cysts, 582i, 583 simple, 318
Follicular hyperkeratosis, 894i toxic diffuse, 414-415
Folliculitis, 288-289 Gonadotropin deficiency, 320-321, 430-431
hair follicles in, 288i Gonorrhea, 322-323
Food poisoning, Vibrio parahaemolyticus, 178 Goodpastures syndrome, 316, 324-325
Fowl-nest fever, 688-689, 926t Gout, 326-327
Fractures tophi in, 327i
hip, 368-369 Graft rejection syndrome, 328-329
skull, 762-763 Granular conjunctivitis, 931t
Fragile X syndrome, 290-291 Granulomatous disease, chronic, 924t
Frostbite, 292-293 Granulomatous rosacea, 714
Fugue, dissociative, 926t Graves disease, 414-415
Furunculosis, 288-289 Grawitzs tumor, 462-463, 462i
hair follicles in, 288i Grippe. See Influenza.
Ground itch, 376-377
G Growth hormone excess, 408-409
Gaisbcks disease, 772-773 Guillain-Barr syndrome, 330-331
Gallstone ileus, 176 Guttate psoriasis, 663
Gallstones, 176-177 Gynecomastia, 332-333
Gangrene
gas, 294-295, 294i H
hemolytic streptococcal, 546-547 Habitual abortion, 3
Gas gangrene, 294-295 Haemophilus influenzae infection, 334-335
pathophysiology of, 294i Hair follicles, bacterial infection of, 288i
Gastric cancer, 296-297 Hair loss, 34-35, 35t
Gastric ulcer, 600-601 Hallux valgus, 927t
Gastritis, 298-299 Hand, foot, and mouth disease, 927t
Gastroenteritis, 300-301 Hansens disease, 928t
Gastroesophageal reflux disease, 302-303 Hantavirus pulmonary syndrome, 336-337
Gauchers disease, 927t Sin Nombre virus in, 336i
Gender identity disorder, 927t Hashimotos thyroiditis, 822
Generalized anxiety disorder, 304-305 Headache, 338-339
Generalized salivary gland disease, 224-225 Head lice, 596, 597i
Genital herpes, 306-307 Hearing loss, 340-341
cycle in, 306i, 365i Heart attack, 540-541
primary, 364 Heartburn, 302-303
Genital warts, 308-309 Heart failure, 342-343
recognizing, 308i right-sided, 208-209, 208i
German measles, 716t, 720-721 Heat syndrome, 344-345
Gestational hypertension, 310-311 Heberdens nodes, 565i
Giant cell tumor, malignant, 125t HELLP syndrome, 310
Giardiasis, 312-313 Hematoma
Gigantism, 408 epidural, 268-269
Gilchrists disease, 118-119 subdural, 786-787
Glaucoma, 314-315 Hemoglobinuria, paroxysmal nocturnal, 929t
optic disk changes in, 314i Hemolytic disease of newborn, 276-277, 276i
Glomerulonephritis, 316-317 Hemolytic streptococcal gangrene, 546-547
acute poststreptococcal, 12-13 Hemophilia, 346-347
Glucosylceramide storage disease, 927t vascular, 906-907
Gluten intolerance, 160-161, 506, 924t Hemorrhoids, 348-349
Glycopeptide intermediate-resistant Staphylococcus types of, 348i
aureus, 870-871

i refers to an illustration; t refers to a table.

942 Index
9400_INDEX.qxd 8/2/12 4:19 PM Page 943

Hemothorax, 350-351 Hypernatremia, 402-403

autotransfusion for, 351i clinical effects of, 402t
Hepatic encephalopathy, 352-353, 492 Hypernephroma, 462-463, 462i
Hepatitis Hyperparathyroidism, 404-405
nonviral, 354-355 Hyperphosphatemia, 406-407
viral, 356-357 Hyperpituitarism, 408-409
Hepatolenticular degeneration, 932t Hypersplenism, 410-411
Hepatorenal syndrome, 492 Hypertension, 412-413
Hereditary chorea, 380-381 gestational, 310-311
Hereditary hemorrhagic telangiectasia, 358-359 pulmonary, 670-671
lesions of, 358i Hypertensive retinopathy, 880-881
Hernias Hyperthyroidism, 414-415
hiatal, 360-361 Hypertrophic cardiomyopathy, 152-153
identifying, 444 assessment findings in, 151t
inguinal, 444-445 pathophysiology of, 152i
sites of, 445i Hypocalcemia, 416-417
Herniated intervertebral disk, 362-363 clinical effects of, 416t
Herpangina, 927t signs of, 417i
Herpes simplex, 364-365 Hypochloremia, 418-419
genital, 306-307, 306i, 365i Hypochondriasis, 927t
Herpes zoster, 366-367 Hypogammaglobulinemia, X-linked infantile, 914-915
lesions in, 366i Hypokalemia, 420-421
Herpetic stomatitis, acute, 776-777 clinical effects of, 420t
Hiatal hernia, 360-361 Hypomagnesemia, 422-423
Hip dysplasia, 232-233 clinical effects of, 422t
degrees of, 232i Hyponatremia, 424-425
Hip fracture, 368-369 clinical effects of, 424t
Hirschsprungs disease, 370-371 Hypoparathyroidism, 426-427
Histoplasmosis, 372-373 Hypophosphatemia, 428-429
Hives, 860-861 Hypopituitarism, 430-431
Hodgkins disease, 374-375 Hypothermia, 432-433
Hookworm disease, 376-377 Hypothyroidism, 434-435
Human immunodeficiency virus, 10-11 Hypovolemic shock, 752-753
Human papillomavirus, 378-379 Hysterical neurosis, 925t
Huntingtons disease, 380-381
Hyaline membrane disease, 698-699 I
Hydatidiform mole, 927t Idiopathic hypertrophic subaortic stenosis, 151t,
Hydrocele, 382-383 152-153, 152i
Hydrocephalus, 384-385 Idiopathic thrombocytopenic purpura, 436-437
Hydronephrosis, 386-387 Immunodeficiency with eczema and thrombo-
Hyperaldosteronism, 388-389 cytopenia, 932t
Hyperbilirubinemia, unconjugated, 390-391 Impetigo, 438-439
Hypercalcemia, 392-393 ecthyma versus, 439
clinical effects of, 392t recognizing, 438i
Hyperchloremia, 394-395 Impotence, 274-275
Hyperkalemia, 396-397 Incisional hernia, 445i
clinical effects of, 396t Incomplete abortion, 3
false test results in, 397 Inevitable abortion, 3
Hyperlipoproteinemia, 398-399 Infant botulism, 126
Hypermagnesemia, 400-401 Infantile paralysis, 632-633
clinical effects of, 400t Infantile polyarteritis, 458-459
patellar reflex test for, 401i Infectious arthritis, 742-743
Infectious mononucleosis, 440-441

i refers to an illustration; t refers to a table.

Index 943
9400_INDEX.qxd 8/2/12 4:19 PM Page 944

Influenza, 442-443 Latex allergy, 474-475

avian, 106-107 Laubensteins stages in Kaposis sarcoma, 456
preventing spread of, 443 Lead poisoning, 476-477
Inguinal hernia, 444-445 Left-sided heart failure, 342
identifying, 444 Legg-Calv-Perthes disease, 478-479
site of, 445i Legionnaires disease, 480-481
Insect bites and stings, 446-447 Leiomyomas, uterine, 866-867
Insulin resistance syndrome, 518-519 Leprosy, 928t
Intervertebral disk, herniated, 362-363 Leptospirosis, 928t
Intestinal lipodystrophy, 932t Leukemia
Intestinal obstruction, 448-449 acute, 482-483
Intestinal polyps, 642-643 chronic granulocytic, 484-485
Intracapsular cataract extraction, 159i chronic lymphocytic, 486-487
Intracranial aneurysm, 62-63 Lice, 596-597
Intracranial pressure, increased, 165i types of, 597i
Intussusception, 450-451 Lichen planus, 928t
bowel in, 450i Lichen simplex chronicus, 230t
Inverse psoriasis, 663 Lipophagia granulomatosis, 932t
Iodine deficiency, 927t Listeriosis, 488-489
Iritis, 931t Liver, functions of, 492
Iron Liver cancer, 490-491
absorption and storage of, 50 Liver failure, 492-493
overdose of, 51 Lockjaw, 810-811
Iron deficiency anemia, 50-51 Lou Gehrig disease, 42-43
Irritable bowel syndrome, 452-453 Lower esophageal sphincter pressure, 303
Lumpy jaw, 922t
J Lung cancer, 494-495
Jarisch-Herxheimer reaction, 689 Lupoid rosacea, 714
Jaundice, neonatal, 390-391 Lupus erythematosus, 496-497
Juvenile rheumatoid arthritis, 454-455 systemic, 497, 796-797
Lyme disease, 498-499
K Lymphocytic choriomeningitis, 500-501
Kanners autism, 104-105 Lymphoma, non-Hodgkins (lymphosarcoma), 502-503
Kaposis sarcoma, 456-457
Kawasaki syndrome, 458-459 M
Keratitis, 460-461 Macular degeneration, age-related, 26-27, 26i
Kidney cancer, 462-463 Major depression, 504-505
unilateral, 462i Malabsorption, 506-507
Kidney stones, 690-691, 691i Malaria, 508-509
Klinefelter syndrome, 464-465 Malignant giant cell tumor, 125t
Malignant hypertension, 412
L Malignant lymphoma, 502-503
Labyrinthitis, 466-467 Malignant melanoma, 512-513
Lactase insufficiency, 468i, 506 Malignant plasmacytoma, 530-531
Lactose intolerance, 468-469 Malta fever, 136-137
pathophysiology of, 468i Mantle zone lymphoma, 502
Lambliasis, 312-313 Maple syrup urine disease, 928t
Landouzy-Dejerine muscular dystrophy, 536 Marfan syndrome, 928t
Laryngeal cancer, 470-471 Marginal zone lymphoma, 502
Laryngitis, 214-215, 215i, 472-473 Marie-Strmpell disease, 68-69
Laryngotracheobronchitis, 214-215, 215i Mastitis, 510-511
Lassa fever, 928t Mastoiditis, 928t
Latex, products containing, 474

i refers to an illustration; t refers to a table.

944 Index
9400_INDEX.qxd 8/2/12 4:19 PM Page 945

Measles, 722-723 Myasthenia gravis, 538-539

German, 720-721 Myelomatosis, 530-531
incubation and duration of, 716t Myelomeningocele, 551i
Medullary sponge kidney, 929t Myocardial infarction, 540-541
Megacolon, congenital, 370-371 Myocarditis, 542-543
Melanoma, malignant, 512-513 Myomas, uterine, 866-867
Mnires disease, 514-515 Myxedema, 434
Meningitis, 516-517
Haemophilus influenzae, 334 N
lymphocytic, 500-501 Near drowning, 544-545
Meningocele, 551i Necrotizing fasciitis, 546-547
Mercury poisoning, chronic, 923t Neonatal jaundice, 390-391
Mesothelioma, 84-85 Nephritis
Metabolic acidosis, 394 acute infective tubulointerstitial, 14-15
Metabolic syndrome, 518-519 acute tubulointerstitial, 20-21, 693
Methicillin-resistant Staphylococcus aureus, 520-521 Nephrocarcinoma, 462-463, 462i
Midarm circumference, 557i Nephrotic syndrome, 548-549
Migraine, 338-339 Neural tube defects, 550-551
Miscarriage, 2-3 spinal, 551i
Missed abortion, 3 Neurodermatitis, localized, 230t
Mitral stenosis, 522-523 Neurofibromatosis, 929t
murmur of, 522i Neurogenic bladder, 552-553
Mitral valve insufficiency, 524-525 types of, 553t
murmur of, 524i Niacin, recommended daily allowance of, 891t
Mitral valve prolapse, 526-527 Niacin deficiency, 890-893
Mongolism, 246-247 Nocardiosis, 554-555, 929t
Moniliasis, 146-147, 146i Non-Hodgkins lymphoma, 502-503
Monkeypox, 929t Nucleus pulposus, herniated, 362-363
Mononucleosis, infectious, 440-441, 926t Nummular dermatitis, 231t
Morbilli, 716t, 722-723
Mosquito bites, preventing, 725, 913 O
Mosquito-borne encephalitis, 724-725 Obesity, 556-557
Motion sickness, 528-529 abdominal, 519
Mountain (tick) fever, 925t anthropometric measurements in, 557i
Mucocutaneous lymph node syndrome, 458-459 body mass index in, 556
Mucous colitis, 452-453 Obsessive-compulsive disorder, 558-559
Multiple endocrine neoplasia, 929t Ocular larva migrans, 931t
Multiple metabolic syndrome, 518-519 Ocular toxoplasmosis, 830
Multiple myeloma, 530-531 Ohio Valley disease, 372-373
Multiple personality disorder, 926t Ophthalmic ointment, applying, 121
Multiple sclerosis, 532-533 Optic disk in glaucoma, 314i
Mumps, 534-535 Oral cancer, 560-561
parotid inflammation in, 535i Orbital cellulitis, 929t
Murmurs Orchiopexy, 806
of aortic insufficiency, 75i Orchitis, 267
of aortic stenosis, 77i Orthostatic vital signs, 752
of mitral insufficiency, 524i Ortolanis sign, 233
of mitral stenosis, 522i Osgood-Schlatter disease, 562-563
of tricuspid insufficiency, 842i Osler-Weber-Rendu disease, 358-359, 358i
of tricuspid stenosis, 844i Osteitis deformans, 584-585
Muscular aortic stenosis, 151t, 152-153, 152i Osteoarthritis, 564-565
Muscular dystrophy, 536-537 signs of, 565i
Myalgic encephalomyelitis, 180-181 Osteoblastoma, 124-125, 125t

i refers to an illustration; t refers to a table.

Index 945
9400_INDEX.qxd 8/2/12 4:19 PM Page 946

Osteochondrosis, 562-563 Pityriasis versicolor, 931t

Osteogenesis imperfecta, 566-567 Placental abruption, 4-5, 5i
Osteogenic sarcoma, 124, 125t Placenta previa, 616-617
Osteomalacia, 568-569 types of, 617i
Osteomyelitis, 570-571 Plague, 618-619
Osteoporosis, 572-573 carrier of, 619i
Osteosarcoma, 124-125, 125t Plasma cell myeloma, 530-531
Otitis externa, 574-575 Pleural effusion, 620-621
Otitis media, 576-577 Pleurisy (pleuritis), 622-623
Otosclerosis (otospongiosis), 578-579 Pneumocystis carinii pneumonia, 624-625
Ovarian cancer, 580-581 Pneumonia, 626-627
Ovarian cysts, 582-583 Haemophilus influenzae, 334
follicular, 582i Pneumocystis carinii, 624-625
multiple, 636-637 preventing, 627
Pneumothorax, 628-629
P Poisoning, 630-631
Pagets disease, 584-585 lead, 476-477
Pain syndrome, complex regional, 198-199, 199t mercury, 923t
Pancreatic cancer, 586-587 preventing, 631
Pancreatitis, 588-589 Poliomyelitis, 632-633
Panhypopituitarism, 430, 431 Polyarteritis, infantile, 458-459
Panic disorder, 590-591 Polyarteritis nodosa, 882
Paraesophageal hernia, 360 Polycystic kidney disease, 634-635
Parainfluenza, 929t Polycystic ovary syndrome, 636-637
Paralysis, infantile, 632-633 Polycythemia
Paranasal sinuses, 759i secondary, 638-639
Parkinsons disease, 592-593 spurious, 772-773
Parosteal osteogenic sarcoma, 125t Polycythemia (rubra) vera, 640-641
Parotid inflammation, 535i Polymyalgia rheumatica, 930t
Parotitis, epidemic or infectious, 534-535 Polyps
Paroxysmal nocturnal hemoglobinuria, 929t intestinal, 642-643
Pataus syndrome, 848-849 rectal, 930t
Patellar reflex, testing, 401i Popliteal aneurysm, 60-61
Patent ductus arteriosus, 594-595 Porphyrias, 644-645
Pediculosis, 596-597 Poststreptococcal glomerulonephritis, 12-13, 316-317
types of, 597i Posttraumatic stress disorder, 646-647
Pellagra, 890 Potassium, dietary sources of, 421
Pelvic inflammatory disease, 598-599 Precocious puberty, 648-649
Pelvic pain, causes of, 248 Preeclampsia, 310-311
Penile cancer, 930t Pregnancy, ectopic, 252-253, 252i
Peptic ulcer, 600-601 Premenstrual syndrome, 650-651
Perforated eardrum, 576, 602-603 Pressure ulcers, 652-653
Pericarditis, 604-605 stages of, 653i
Peritonitis, 606-607 Primaquine, 508, 509
Pernicious anemia, 52-53 Primary polycythemia, 640-641
Pertussis, 608-609 Proctitis, 654-655
pathogen in, 608i Prolactin deficiency, 430, 431
Pharyngeal cancer, 560-561 Prostate cancer, 656-657
Pharyngitis, 610-611 Prostatic hyperplasia, benign, 112-113
Pheochromocytoma, 612-613 Prostatitis, 658-659
Phosphorus, foods high in, 407 Prostatodynia, 658, 659
Pilonidal disease, 930t Pruritus, essential, 230t
Pituitary tumors, 614-615 Pseudohemophilia, 906-907

i refers to an illustration; t refers to a table.

946 Index
9400_INDEX.qxd 8/2/12 4:19 PM Page 947

Pseudomembranous enterocolitis, 660-661 Respiratory distress syndrome

Pseudopolycythemia, 772-773 acute or adult, 16-17
Pseudoprecocious puberty, 648 neonatal, 698-699
Psoriasis, 662-663 Respiratory failure, acute, 18-19
Psoriasis vulgaris, 663 Respiratory syncytial virus infection, 700-701
Ptosis, 664-665 Restrictive cardiomyopathy, 154-155
recognizing, 665i assessment findings in, 151t
Puberty, precocious, 648-649 pathophysiology of, 154i
Pubic lice, 596, 597i Retinal detachment, 702-703
Puerperal infection, 930t Retinitis pigmentosa, 931t
Pulmonary edema, 666-667 Retinopathies, vascular, 880-881
Pulmonary embolism, 668-669 Reyes syndrome, 704-705
Pulmonary hypertension, 670-671 stages of treatment for, 705t
Pulmonic insufficiency, 672-673 Rhabdomyolysis, 706-707
Pulmonic stenosis, 674-675 Rheumatic endocarditis, 924t
Pump failure, 750-751 Rheumatic fever and rheumatic heart disease, 708-709
Purpura Rheumatoid arthritis, 710-711
allergic, 30-31, 30i classifying, 711
idiopathic thrombocytopenic, 436-437 juvenile, 454-455
Purpuric lesions, 30i Rheumatoid spondylitis, 68-69
Pustular psoriasis, 663 Rh incompatibility, 276-277
Pyelonephritis, acute, 14-15 Rhinitis, allergic, 32-33
Pyridoxine, recommended daily allowance of, 891t Rh isoimmunization, 276i
Pyridoxine deficiency, 890-892 Rh system, 122
Pyrimethamine, 508, 509 Riboflavin, recommended daily allowance of, 891t
Riboflavin deficiency, 890-892
Q Rickets, 568-569, 896-897
Q fever, 676-677 bowlegs in, 896i
Quinine, 508, 509 Riedels thyroiditis, 822
Right-sided heart failure, 208-209, 208i, 342
R Ringed sideroblast, 57i
Rabies, 678-679 Robin sequence, 184, 185
Radiation exposure, 680-681 Rocky Mountain spotted fever, 712-713
Rape-trauma syndrome, 682-683 Rosacea, 714-715
Rash-producing infections, incubation and duration of, 716t Roseola infantum, 716-717
Raynauds phenomenon, 684-685 incubation and duration of, 716t
Reactive arthritis, 686-687 Rotavirus, 718-719
Reactive polycythemia, 638-639 Roundworm infection, 86-87
Rectal polyps, 930t Rubella, 720-721
Rectal prolapse, 931t incubation and duration of, 716t
Reflex sympathetic dystrophy, 198-199, 199t Rubella vaccine, giving, 720
Reiters syndrome, 686-687 Rubeola, 722-723
Relapsing fever, 688-689, 926t incubation and duration of, 716t
Relative polycythemia, 772-773 Ruptured disk, 362-363
Renal calculi, 690-691 Ruptures. See Hernias.
preventing, 691
variations in, 691i S
Renal carcinoma, 462-463, 462i Salmonella infection, 726-727
Renal failure San Joaquin Valley fever, 192-193
acute, 692-693 Sarcoidosis, 728-729
chronic, 694-695 Scabies, 730-731
Respiratory acidosis, 696-697 cause and effect of, 730i
preventing, 731

i refers to an illustration; t refers to a table.

Index 947
9400_INDEX.qxd 8/2/12 4:19 PM Page 948

Scarlet fever (scarlatina), 732-733 Sprue, celiac or nontropical, 160-161, 506, 924t
Schistosomal dermatitis, 735 Spurious polycythemia, 772-773
Schistosomes, 734t Squamous cell carcinoma, 774-775
Schistosomiasis, 734-735 nodule in, 774i
Schizophrenia, 736-737 St. Louis encephalitis, 724-725
Scleroderma, 738-739 Staphylococcus aureus
Scoliosis, 740-741 methicillin-resistant, 520-521
testing for, 741i vancomycin intermediate-resistant, 870-871
Scurvy, 894-895 Stasis dermatitis, 231t
gums and legs in, 894i Steatorrhea, idiopathic, 160-161
Seborrheic dermatitis, 231t Stiff lung, 16-17
Seizure disorder, 272-273 Stings, insect, 446-447
Sensorimotor nerve degeneration, 331 Stomatitis, 776-777
Septic abortion, 3 aphthous, 776i
Septic arthritis, 742-743 Strains, 770-771
Septic shock, 754-755 Streptococcus pneumoniae infection, drug-resistant,
Severe acute respiratory syndrome, 744-745 778-779
Severe combined immunodeficiency disease, 746-747 Stress erythrocytosis or polycythemia, 772-773
Shigellosis, 748-749 Stroke, 780-781
Shingles, 366-367, 366i Strongyloidiasis, 782-783
Shock Subarachnoid hemorrhage, 784-785
cardiogenic, 750-751 Subdural hematoma, 786-787
electric, 254-255 Subluxations, 240-241
hypovolemic, 752-753 hip, 232i
septic, 754-755 Substance abuse and dependence, 788-789
Shock lung, 16-17 Sudden infant death syndrome, 790-791
Sickle cell anemia, 54-55 Suicide prevention guidelines, 505
Sickle cell retinopathy, 880-881 Suppurative fasciitis, 546-547
Sideroblastic anemia, 56-57 Swimmers ear, 574-575
ringed sideroblast in, 57i Swimmers itch, 735
Silicosis, 756-757 Syndrome of inappropriate antidiuretic hormone, 792-793
Sin Nombre virus, 336i pathophysiology of, 793i
Sinuses, paranasal, 759i Syndrome X, 518-519
Sinusitis, 758-759 Synergistic necrotizing cellulitis, 546-547
Sixth disease, 716-717, 716t Syphilis, 794-795
Sjgrens syndrome, 760-761 identifying, 795i
Skull fracture, 762-763 Systemic lupus erythematosus, 496, 497, 796-797
Skull in thalassemia major, 814i Systemic sclerosis, 738-739
Sleep apnea, 764-765
Sliding hiatal hernia, 360 T
Slipped disk, 362-363 Taeniasis (tapeworm disease), 798-799
Slit-lamp examination of eye, 460 Talipes, 188-189, 188i
Smallpox, 766-767 Tay-Sachs disease, 800-801
Spastic colon or colitis, 452-453 Tears, drainage of, 226i
Spider bite, 446-447 Telangiectasia, hereditary hemorrhagic, 358-359, 358i
Spina bifida, 550 Temporomandibular joint disease, 802-803
Spina bifida occulta, 550, 551i Tendinitis, 804-805
Spinal cord defects, 550 Tendons, 805i
types of, 551i Testicular cancer, 806-807
Spinal injury, 768-769 Testicular torsion, 808-809, 808i
Splenomegalic polycythemia, 640-641 Tetanus, 810-811
Splenomegaly, causes of, 410 Tetralogy of Fallot, 812-813
Sprains, 770-771

i refers to an illustration; t refers to a table.

948 Index
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Thalassemia, 814-815 Trypanosomiasis, American, 922t

skull changes in, 814i Tuberculosis, 852-853
Thiamine, recommended daily allowance of, 891t Tularemia, 854-855
Thiamine deficiency, 890-892 Tumors. See also Cancer; specific type.
Thoracic aortic aneurysm, 64-65 bone, 124-125, 125t
Threadworm infection, 782-783 brain, 128-129
Threatened abortion, 3 chromaffin, 612-613
Throat abscess, 931t pituitary, 614-615
Thromboangiitis obliterans, 138-139, 139i renal, 462i
Thrombocytopenia, 816-817 Turners syndrome, 464
immunodeficiency with, 932t Tympanic membrane rupture, 576, 602-603
Thrombocytopenic purpura, idiopathic, 436-437 Typhoid, bilious, 688-689, 926t
Thrombophlebitis, 818-819
sites of, 818i U
Thrush, 146i Ulcerative colitis, 856-857
Thymic hypoplasia or aplasia, congenital, 925t Ulcers
Thyroid cancer, 820-821 peptic, 600-601
Thyroiditis, 822-823 pressure, 652-653, 653i
Thyroid-stimulating hormone deficiency, 430, 431 Umbilical hernia, 445i
Thyrotoxicosis, 414-415 Uncinariasis, 376-377
Tic douloureux, 846-847 Undulant fever, 136-137
Tick bite, 446-447 Urinary tract, neuromuscular dysfunction of lower,
Tick fever, 688-689, 926t 552-553, 553t
Tilt test, 752 Urinary tract infection, lower, 858-859
Tinea versicolor, 931t Urticaria, 860-861
Tobacco abuse, 824-825 Uterine bleeding dysfunctional, 862-863
Tonsillitis, 826-827 Uterine cancer, 864-865
Tophi, gouty, 327i Uterine leiomyomas, 866-867
Torulosis, 216-217 Uveitis, 931t
Toxic diffuse goiter, 414-415
Toxic shock syndrome, 828-829 V
Toxocariasis, 931t Vagabond fever, 688-689, 926t
Toxoplasmosis, 830-831 Vaginal cancer, 868-869
Tracheoesophageal fistula, 832-833 Vaginismus, 931t
Trachoma, 931t Vaginitis, 908-909
Transient ischemic attack, 834-835 Vagus nerve stimulation for epilepsy, 273
Transposition of great arteries, 836-837 Valley fever, 192-193
Transsexualism, 927t Vancomycin intermediate-resistant Staphylococcus aureus,
Travelers diarrhea, preventing, 300 870-871
Trendelenburgs sign, 233 Vancomycin-resistant enterococcus, 872-873
Triceps skinfold thickness, 557i Vaquez-Osler disease, 640-641
Trichinosis, 838-839 Varicella, 874-875
Trichomoniasis, 840-841 incubation and duration of, 716t
Tricuspid insufficiency, 842-843 Varicocele, 876-877
murmur of, 842i identifying, 876i
Tricuspid stenosis, 844-845 Varicose veins, 878-879
murmur of, 844i Variola, 766-767
Trigeminal nerve, 846i Vascular hemophilia, 906-907
Trigeminal neuralgia, 846-847 Vascular retinopathies, 880-881
Trisomy 13 syndrome, 848-849 diagnostic tests for, 881
Trisomy 18 syndrome, 850-851 Vasculitis, 882-883
Trisomy 21 syndrome, 246-247 Vasospastic arterial disease, 684-685
Trousseaus sign, 417i Venereal warts, 308-309, 308i

i refers to an illustration; t refers to a table.

Index 949
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Venous pathways of leg, 818i Z

Ventricular aneurysm, 66-67 Zinc, foods containing, 916
Ventricular septal defect, 884-885 Zinc deficiency, 916-917
Verrucae. See Warts. Zollinger-Ellison syndrome, 506, 918-919
Vesicoureteral reflux, 886-887
Vestibular function, normal, 514
Vibrio parahaemolyticus food poisoning, 178
Viral encephalitis, 724-725
Viral hepatitis, 356-357
Viral pneumonia, 626
Visceral larva migrans, 931t
Vitamin A, foods containing, 888
Vitamin A deficiency, 888-889
Vitamin B complex, recommended daily allowance of, 891t
Vitamin B deficiency, 890-893
Vitamin B12
dietary sources of, 53
recommended daily allowance of, 891t
Vitamin B12 deficiency, 52-53, 890-892
Vitamin C, foods containing, 895
Vitamin C deficiency, 894-895
Vitamin D deficiency, 896-897, 896i
Vitamin E, foods containing, 898
Vitamin E deficiency, 898-899
Vitamin K, foods containing, 900
Vitamin K deficiency, 900-901
Vitiligo, 902-903
recognizing, 902i
Volvulus, 904-905
pathophysiology of, 904i
von Willebrands disease, 906-907
Vulvovaginitis, 908-909

W
Warts, 910-911
genital, 308-309, 308i
removing, 911i
Wasp sting, 446-447
West Nile encephalitis, 912-913
Wet or white lung, 16-17
Whiplash, 6-7, 7i
Whipples disease, 932t
Whooping cough, 608-609, 608i
Wilsons disease, 932t
Wiskott-Aldrich syndrome, 932t

X
X-linked infantile hypogammaglobulinemia, 914-915

Y
Yellow jacket sting, 446-447
Yuppie flu, 180-181

i refers to an illustration; t refers to a table.

950 Index