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1
ACUTE BIOLOGIC CRISES (24 HOURS)
COURSE OUTLINE
1. High Risk Adult (8 hours)
A. Respiratory Disorders
i. Pulmonary Embolism
ii. Acute Respiratory Distress Syndrome (ARDS)
iii. Respiratory Failure
a. Acute RF
b. Chronic RF
iv. Mechanical Ventilators
B. Endocrine/ Metabolic Disorders
i. Diabetic Ketoacidosis (DKA)
ii. Hyperosmolar Hyperglycemic Nonketotic Coma (HHNC)
iii. Thyrotoxic Crisis (Thyroid Storm)
iv. Adrenal Crisis (Peochromocytoma)
v. Hepatic Failure (Hepatic Coma)
C. Renal Disorders
i. Renal Failure
a. Acute RF
b. Chronic RF
D. Cardiovascular Disorders
i. Angina Pectoris
ii. Myocardial Infarction
iii. Congestive Heart Failure
a. Right-sided CF
b. Left-sided CF
iv. Cardiogenic Shock
v. Thromboembolism
vi. Pericardial Effusion & Cardiac Tamponade
vii. Cardiac Arrest
viii. Dysrhythmias
a. Sinus Node
1. Sinus Bradycardia
2. Sinus Tachycardia
b. Atrial Dysrhythmias
1. Premature Atrial Complex (PAC)
2. Atrial Flutter
3. Atrial Fibrillation
c. Junctional Dysrhythmias
Amanuel/Pslidasan/Ksjuliano/MRCueno
NCM 104 1st sem S.Y. 2007-2008
2
d. Ventricular Dsyrhythmias
1. Premature ventricular Complex
2. Ventricular Tachycardia
3. Ventricular Fibrillation
4. Ventricular Asystole
E. Burns
2.High Risk Pregnancy (12 Hours)
Part I.
A. Infections
i. STDsa. Cndidiasis
b. Trichomoniasis
c. Bacterial Vaginosis (Gardnerella)
d. Chlamydia Trachomatis
e. Syphilis
f. Gonorrhea
g. HPV
h. Group B Streptococci
i.
HIV
ii. TORCH infections
B. Hematologic Disorders
i. Anemias
a. Iron Deficiency
b. Folic Acid Deficiency
c. Sickle Cell
ii. Coagulation Disorders
a. Idiopathic Thrombocytopenic Purpura
C. Renal and Urinary Disorders
i. UTI
ii. Chronic Renal Disease
D. Respiratory Disorders
i. Acute Nasopharyngitis
ii. Influenza
iii. Pneumonia
iv. Asthma
v. Tuberculosis
vi. Cystic Fibrosis
Amanuel/Pslidasan/Ksjuliano/MRCueno
NCM 104 1st sem S.Y. 2007-2008
3
E. Rheumatic Disorders
i. Juvenile Rheumatoid Arthritis
ii.Systemic Lupus Erythematosus (SLE)
F. Gastrointestinal Disorders
i. Appendicitis
ii. Hiatal Hernia
iii. Cholecystitis & Cholelithiasis
iv. Viral Hepatitis
v. Inflammatory Bowel Disease
G. Neurologic Disorders
i. Siezure
ii. Myasthenia Gravis
iii. Multiple Sclerosis
H. Musculoskeletal Disorders
i. Scoliosis
I. Cardiovascular Disorders
i. Left Sided Heart Failure
ii. Right Sided heart Failure
iii. Peripartal Heart Disease
iv. Artificial valve Prosthesis
v. Chronic hypertensive Vascular Disease
vi. Venous Thromboembolic Disease
J. Endocrine Disorders
i. Thyroid Dysfunction
a. Hypothyroidism
b. Hyperthyroidism
ii. Diabetes Mellitus
iii. Gestational Diabetes
iv. Hyperglycemia
K. Mental Illness
L. Trauma
i. Trauma Care
ii. Open wounds
iii. Battered woman
PART II. COMPLICATIONS OF PREGNANCY
A. Bleeding During Pregnancy
i.
First Trimester Bleeding
a. Abortion
Amanuel/Pslidasan/Ksjuliano/MRCueno
NCM 104 1st sem S.Y. 2007-2008
4
1. Spontaneous
2. Threatened
3. Imminent
4. Complete
5. Incomplete
6. Missed
7. Recurrent
8. Complications of Abortionb. Ectopic pregnancy
ii.
Second Trimester Bleeding
a. Gestational Trophoblastic Disease (H. Mole)
b. Incompetent Cervix
iii.
Third Trimester Bleeding
a. Placenta Previa
b. Abruptio Placenta
iv.
Preterm labor
v.
Disseminated Intravascular Coagulation (DIC)
vi.
Preterm Rupture of Membrane (PROM)
vii.
Pregnancy Induced Hypertension (PIH)
a. Mild Preeclampsia
b. Severe Preeclampsia
c. Eclampsia
d. HELLP Syndrome
viii.
Multiple Pregnancy
ix.
Polyhydramnios
x.
Post term pregnancy
xi.
Psuedocyesis
xii.
Isoimmunization (RH Incompatibility)
xiii.
Fetal Death
3. High Risk Newborn (4 hours)
A. Part I
i. Small-for-Gestational-Age Infant ii. Large-for-Gestational-Age Infant iii. Pr
eterm Infant
iv. Post Term Infant
B. Part II: Illness of the Newborn
i. Respiratory Distress Syndrome
Amanuel/Pslidasan/Ksjuliano/MRCueno
NCM 104 1st sem S.Y. 2007-2008
5
ii. Transient Tachypnea
iii. Meconium Aspiration Syndrome
iv. Apnea
v. Sudden Infant Death Syndrome (SIDS)
vi. Preventricular Leukomalacia (PVL)
vii. Hyperbilirubinemia
viii. Erythroblastosis Fetalis
a. RH incompatibility
b. ABO incompatibility
ix. Hemorrhagic Disease
x. Twin-to-twin Transfusion
xi. Necrotizing Enterocolitis
C. The Newborn at risk due to:
i. Maternal Infection
a. Group B Hemolytic Streptococcal Infection
b. Congenital Rubella
c. Ophthalmia Neonatorum
d. Hepatitis B
e. Generalized Herpes Virus
ii. Maternal Illness
a. Diabetic Mother
b. Drug Dependent Mother
c. Fetal Alcohol Syndrome (FAS)
Amanuel/Pslidasan/Ksjuliano/MRCueno
NCM 104 1st sem S.Y. 2007-2008
6
ACUTE BIOLOGIC CRISES
HIGH RISK ADULT
RESPIRATORY DISORDERS
PULMONARY EMBOLISM
Occurs when a pulmonary embolus [thrombotic (blood clot) or nonthrombotic (fat)
emboli] lodges in the pulmonary artery system. This
blockage obstructs blood flow to the lung tissue supplied by the affected vessel
. Thrombotic emboli mainly originate from the deep veins of the legs, right vent
ricle of the heart, or pelvis. Nonthrombotic emboli mainly originate from fat re
lease after skeletal injuries, amniotic fluid, air, and foreign bodies.
The Virchow’s Triad
-three conditions and risk factors that can predispose a patient
or that can precipitate the formation of venous thrombi
Venous stasis
eg. atrial fibrillation, heart failure
immobility, polycythemia
pregnancy, varicose veins
Vessel wall injury
Coagulation problems
eg. infection, trauma
Pathophysiologic Changes
embolus
lodge in the pulmonary vasculature
Pulmonary embolism
decreased/nonperfusion of alveoli distal to occlusion
infarction of pulmonary vessel
impaired gas exchange
decreased C02
bronchoconstriction
shunting of blood to ventilated areas of the lungs
increased pulmonary resistance
hypoxia
release of mediators at the injury site
increased right ventricular workload
pulmonary vasoconstriction
right ventricular failure
pulmonary hypertension
left ventricular failure
decreased cardiac output
decreased blood pressure
shock
death
Clinical Manifestations
Shortness of breath and/or tachypnea- a response to the hypoxia that develops fr
om impaired gas exchange
Cough
Hemoptysis – occurs when an infaction at or near the periphery of the lung begin
s to hemorrhage
Chest pain – generally comes from an infarction of the pulmonary vessel near the
area in which the pleural nerves innervate. Usually
worsen when the patient takes a deep breath.
Tachycardia – a response to the decrease in oxygenation and impaired gas exchang
e
Jugular vein distention – a result of pulmonary hypertension and the decreased e
ffectiveness of the right ventricle
Amanuel/Pslidasan/Ksjuliano/MRCueno
NCM 104 1st sem S.Y. 2007-2008
7
Hypotension – observed with large pulmonary embolism and is related to the decre
ase in cardiac output after ventricular dysfunction
Diagnosis
Chest radiograph – excludes other reasons that may cause the same clinical manif
estations. May show pulmonary artery distention, an
elevation of the diaphragm, and small infiltrates or pleural effusions.
ABG analysis – can reveal respiratory alkalosis, low partial pressure of oxygen,
and low partial pressure of carbon dioxide
Electrocardiogram – involve transient nonspecific ST segment and T wave changes
Management
The best treatment for pulmonary embolism is PREVENTION. When patients are at ri
sk for developing pulmonary embolism, prophylactic
measures should be instituted such as intravenous or subcutaneous heparin (Loven
ox) or oral anticoagulants such as warfarin (Coumadin). The
goal of therapy is to prevent thrombi formation, limit thrombi growth, and encou
rage breakdown of existing thrombi.
Management of hypoxia may require supplemental oxygen, intubation and mechanical
ventilation.
Heparin Therapy
-
started with a bolus (usually based on patient’s weight) and a continuous infusi
on adjusted every 4-6 hours, depending on the
institution’s protocol. Activated partial thromboplastin time (apt) should be ma
intained at 1.5-2.0 times the normal value.
-
generally continued for 7-14 days while the patient is on bedrest
-
reversal agent (antidote) is protamine sulfate
The reversal agent for warfarin (Coumadin) is vitamin K or fresh frozen plasma.
Surgical intervention is rarely used and is considered a last resort.Pulmonary e
mbolectomy is the removal of a clot from the larger vessel of the
pulmonary vasculature. This surgery carries a high risk of death and is only use
d in those patients who do not respond or have contraindications to
other interventions.
Nursing Responsibilities
The main nursing goal is to prevent the development of deep venous thrombosis (D
VT) that may lead to a thrombotic pulmonary embolism.
Interventions should include early ambulation, use of pneumatic stockings, suppo
rt hose, and passive range-of-motion exercises. All of these
improve venous blood flow and increase circulation.
Other nursing interventions include the following:
Signs and symptoms of DVT are monitored in the lower extremities (calf pain or t
enderness, redness, swelling, warmth, pain on
dorsiflexion of foot [Homan’s sign]). If Homan’s sign is positive, DO NOT retest
it; doing so may dislodge the clot.
Prescribed oxygen therapy is maintained, and the patient is asked to cough and d
eep breath every 2 hours
Signs and symptoms of respiratory distress or a worsening of pulmonary status (h
eart failure, pulmonary edema) are monitored, and the
physician is notified of any developments.
ABG analysis is monitored and pulse oximetry is continuously taken
Patient is positioned for comfort and maximal oxygenation, as well as to promote
the expulsion of secretions.
Signs and symptoms of bleeding are monitored when anticoagulant or thrombolytic
therapy is in progress. (eg. blood in stool or urine,
pale mucous membranes, petechiae, echymosis, complaints of back or flank pain).
ACUTE RESPIRATORY DISTRESS SYNDROME
A clinical syndrome characterized by a sudden and progressive pulmonary edema,
increasing bilateral infiltrates, hypoxemia refractory to
oxygen supplementation and reduced lung compliance
A syndrome with inflammation and increased permeability of the alveollocapillar
y membrane that occurs as a result of an injury to the lungs.
This inflammation causes noncardiogenic pulmonary edema with severely impaired g
as exchange.
Etiologic Factors Related to ARDS :
1. Aspiration (gastric secretions, drowning, hydrocarbons)
2. Drug ingestion and overdose
3. Hematologic disorders
4. Prolonged inhalation of high concentrations of oxygen, smoke, or corrosive su
bstances
5. Localized infection (bacterial, fungal, viral pneumonia)
6. Metabolic disorders ( pancreatitis, uremia)
7. Shock (any cause)
8. Trauma ( pulmonary contusion, multiple fractures, head injury)
9. Fat or air embolism
10. Systemic sepsis
Pathophysiology
lung injury
immune system initiates an inflammatory response
activation of neutrophils, macrophages, and endotoxins into the lungs
and the release of mediators
increased alveolomembrane permeability
fluid enters into the lung tissue
Acute Respiratory Distress Syndrome
alveolar collapse
narrowing of airways
pulmonary vasoconstriction
hypoxia
pulmonary hypertension
hyperventilation
right ventricular dysfunction
Amanuel/Pslidasan/Ksjuliano/MRCueno
NCM 104 1st sem S.Y. 2007-2008
8
respiratory failure
decreased cardiac output
Clinical Manifestations:
1. Rapid onset of severe dyspnea
2. Anxiety
3. Labored breathing and tachypnea
Assessment: Intercostal retractions and crackles
In patients with ARDS, PaO2 will be low, despite oxygen administration, pCO2 wil
l decrease as a result of hyperventilation.
Medical Management: The main goals in the treatment of ARDS include improving an
d maintaining oxygenation, maintaining fluid and electrolyte
imbalances, providing adequate nitrition, and preventing respiratory and metabol
ic complications.
1. Primary focus of management includes identification and treatment of the cond
ition.
2. Supportive Therapy: Intubation and mechanical ventilation to maintain adequat
e gas exchange
3. Circulatory support, adequate fluid volume and nutritional support. Fluid res
triction is generally observed to prevent further leakage of fluid into
the alveoli and to decrease pulmonary edema, but fluid restriction can also caus
e a decrease in cardiac output and blood pressure.
4. Supplemental oxygen is used as the patient begins the initial spiral of hypox
emia. Oxygen toxicity may develop if high concentrations of oxygen
are used for longer than 24-48 hours.
5. Positive end-expiratory pressure (PEEP)- generally leads to improved gas exch
ange and allows for lower concentrations of oxygen to be used
6. Hypovolemia must be carefully treated
7. Intravenous crystalloid solutions are administered
8. Pulmonary artery pressure catheters are used to monitor patients fluid status
Nursing Management:
1. Positioning is important. Nurse should turn the patient frequently to improve
ventilation and perfusion in the lungs and enhance secretion
drainage.Prone positioning is an intervention that may improve oxygenation by de
creasing edema and atelectasis, thereby providing an
improved distribution of oxygen throughout the lungs.
2. Nurse must closely monitor rapid changes in oxygenation with changes in posit
ion
3. The nurse should explain all procedures and deliver care in a calm, reassurin
g manner
4. Rest is essential to reduce oxygen consumption
Nursing Diagnosis: Impaired gas exchange r/t inadequate respiratory center activ
ity, chest wall movement, airway obstruction, fluids in the lungs
RESPIRATORY FAILURE
Respiratory failure is a sudden and life-threatening deterioration of the gas e
xchange function of the lung.
Exists when the exchange of oxygen for carbon dioxide in the lungs can not keep
up with the rate of oxygen consumption and carbon dioxide
production by the cells of the body.
ACUTE RESPIRATORY FAILURE (ARF)
Defined as a fall in arterial oxygen tension and a rise in arterial carbon diox
ide tension.
The ventilation and/or perfusion mechanisms in the lung are impaired.
Respiratory system mechanisms leading to ARF include:
1. Alveolar hypoventilation
2. Diffusion abnormalities
3. Ventilation-perfusion mismatching
4. Shunting
Pathophysiology:
Common Causes of Acute Respiratory Failure:
Decreased Respiratory Drive
May occur with severe brain injury, large lesions of the brain stem (multiple s
clerosis), use of sedative medications, and metabolic disorders
such as hyperthyroidism. This disorders impair the normal response of chemorecep
tors in the brain to normal respiratory stimulation
Dysfunction Of The Chest Wall
The impulses arising in the respiratory center travel through nerves that exten
d from the brain stem down the spinal cord to receptors in the
muscles of respiration. Thus, any disease of the nerves, spinal cord, muscles or
neuromuscular junction involved in respiration seriously
affects ventilation and may lead to ARF
Dysfunction Of Lung Parenchyma
Pleural effusion, hemothorax, pneumothorax, and upper airway obstruction are co
nditions that interfere with ventilation by preventing
expansion of the lung. These conditions, which may cause respiratory failure, us
ually are produced by an underlying lung disease, pleural
disease, trauma and injury.
Other diseases and conditions of the lung that lead to ARF include pneumonia, s
tatus asthmaticus, lobar atelectasis, pulmonary embolism and
pulmonary edema
Other Factors
In the postoperative period, esp. after major thoracic or abdominal surgery, in
adequate ventilation and respiratory failure may occur. Causes of
ARF during this period include the effects of anesthetic agents, analgesics, and
sedatives; they may depress respiration and lead to
hypoventilation
Clinical Manifestations:
Early signs are those associated with impaired oxygenation
Restlessness, fatigue, headache, dyspnea, air hunger, tachycardia, tachypnea, c
entral cyanosis, diaphoresis and finally, respiratory arrest
Physical findings: use of accessory muscles, decreased breath sounds
Medical Management:
Objectives of treatment are to correct the underlying cause and to restore adeq
uate gas exchange in the lung
Intubation and mechanical ventilation
Nursing Management:
Assist with intubation
Assess respiratory status by monitoring patient’s level of response, arterial b
lood gases, pulse oximetry and vital signs
Implement strategies to prevent complications: turning schedule, mouth care, sk
in care, ROM
CHRONIC RESPIRATORY FAILURE
Defined as a deterioration in the gas exchange function of the lung that has de
veloped insidiously or has persisted for a long period after an
episode of ARF
Amanuel/Pslidasan/Ksjuliano/MRCueno
NCM 104 1st sem S.Y. 2007-2008
9
Patients develop a tolerance to the worsening hypoxemia and hypercapnia
Patient with chronic respiratory failure may develop Acute respiratory failure
– seen in COPD patients who develops an exacerbation or
infection that causes additional deterioration of the gas exchange mechanism
2 Causes of Chronic Respiratory Failure:
1. COPD
2. Neuromuscular Diseases
What is Mechanical Ventilation?
Mechanical ventilation is a form of artificial ventilation that takes over all o
r part of the work performed by the respiratory muscles and organs. It is initia
ted when the patient’s ability to oxygenate and exchange carbon dioxide is impai
red. Mechanical ventilation may be indicated for the following reasons:•
Hypoxemia
•
Respiratory Distress
•
Atelectasis
•
To reduce intracranial pressure
•
Aspiration
•
Pulmonary Edema
•
Pulmonary Embolism
•
To stabilize the chest wall
•
Respiratory Muscle Fatigue
•
Acute Respiratory Distress
Syndrome
•
Over sedation
The main goal of mechanical ventilation is to support gas exchange until the dis
ease process or condition is resolved.
Positive –pressure ventilation is the most common form of mechanical ventilation
used in the acute care setting. This form of ventilation forces
oxygen into the lungs, either through an endotracheal tube or a tracheostomy tub
e, mimicking respiration.
Modes of Ventilation
There are various modes of ventilation that may be used to ventilate and oxygena
te the patient. Essentially, these modes are ways in which
ventilation is triggered; they allow the patient some or all control over his or
her breathing.
1.Controlled ventilation (CV) delivers a preset volume or pressure at a preset r
ate. This mode takes away all control of breathing from
the patient; it is primarily used for patients who have no respiratory effort at
all.
2.Assist-control ventilation (ACV) delivers a preset volume or pressure whenever
the patient initiates a breath. If the patient does not
initiate a breath by a preset time, the ventilator will give one. This mode is u
sed primarily for the patient with normal breathing but who
has weak respiratory muscles or who cannot achieve an adequate volume on his or
her own.
3.Synchronized intermittent mandatory ventilation (SIMV) delivers a preset volum
e at a preset rate and is synchronized with patient’s
effort. This mode allows for spontaneous breathing between ventilated breaths an
d prevents competition between the patient and the ventilator. When a spontaneou
s breath occurs, it is at the patient’s own rate and tidal volume. SIMV is the m
ost common mode used and allows for weaning from the ventilator.
4.Pressure-controlled ventiation (PCV) delivers a positive pressure breath until
a maximum amount of pressure is reached; then the
breath stops. The maximum pressure limit is preset and helps prevent barotraumas
(damage from the pressure) to the lungs. The
amount of volume that is delivered varies, based on airway resistance and lung c
ompliance. Usually the maximal pressure limit is set to
achieve a goal tidal volume that is designed by the physician.
5.Inverse-ratio ventilation (IRV) is used when the inspiratory time is increased
and the expiratory time is decreased. With IRV the
inspiration-expiration (I/E) ratios used most are 1:1 and 2:1. This mode of vent
ilation allows for a longer period for gas exchange to
improve oxygenation. This mode is generally used in patients with ARDS. This typ
e of ventilatory mode creates an abnormal breathing
pattern for the patient; consequently the patient may become uncomfortable and a
nxious.
6.Constant positive airway pressure (CPAP) provided positive pressure during spo
ntaneous breaths; the ventilator will not initiate any
breaths. This mode increases oxygenation by opening any closed alveoli that may
occur at end-expiration. CPAP generally ranges from 5-10 cm water pressure. Grea
ter than 10 cm water pressure may increase intrathoracic pressure to the point t
hat it affects the patient’s venous return, decreasing cardiac output and blood
pressure. CPAP at this level may also cause a pneumothorax to occur
7.Positive end-expiratory pressure (PEEP) adds positive pressure during expirati
on of each ventilated breath.
Ventilator settings must be individualized to each patient to allow for optimal
gas exchange. Settings are generally based on arterial blood gas
(ABG) measurements and arterial oxygen saturation level.
Amanuel/Pslidasan/Ksjuliano/MRCueno
NCM 104 1st sem S.Y. 2007-2008
10
Ventilator Setting
Description
Ranges
VT (Tidal Volume)
Amount of oxygen delivered to patient
with each preset ventilated breath
5-15 ml/kg (average 10ml/kg)
Respiratory rate
Number of breaths per minute that
ventilator is set to deliver
4-20 breaths/min
FiO2 (Fraction of Inspired Oxygen)
Percentage of oxygen delivered by
ventilator with each breath
21%-100%
I/E Ratio ( inspiratory to expiratory)
Duration of I/E time
1:2 (unless IRV is used)
Sensitivity
Determines amount of effort patient
must generate before ventilator will
give a breath
Too low – patient will have to work
harder to obtain a breath
Too high – patient may fight ventilator
Flow rate
Determines how fast VT will be
delivered during inspiration
High – increase airway pressure
Low – decrease airway pressure
Pressure limits
Regulates maximum amount of
pressure the ventilator will generate to
deliver preset VT
Ventilated breath is stopped when
pressure limit is reached
Barotrauma occurs when high airway pressures cause overdistention of the alveoli
, rupture and leakage of air. Barotrauma can cause
pneumothorax, subcutaneous emphysema, or crepitus. Air can leak under the medias
tinum or into the pericardium or peritoneum, causing
problems with organs located in these areas.
A patient needing long-term ventilatory management will need a tracheostomy plac
ed at some point. Endotracheal tubes (oral or nasal) are not intended for long-t
erm management and may lead to other problems such as mucosal breakdown, skin ul
cerations (lips), sinusitis, and vocal cord paralysis or damage (or both).
The following are practices performed for patients receiving mechanical ventilat
ion.
•
The respiratory status is assessed every 4 hours and more frequently when a chan
ge in condition occurs. Close attention is paid to
breathing sounds and the amount of patient effort.
•
Signs of hypoxia are assessed. These signs include restlessness, anxiety, increa
sed heart rate and blood pressure, increased
respiratory rate, and oxygen saturation via pulse oximetry less than 90%.
•
Endotracheal or tracheostomy tube placement is maintained by properly securing t
he tube and preventing inadvertent extubation by staff
or patient. Placement is maintained until extubation.
•
The endotracheal tube is repositioned per institutional policy to prevent pressu
re sores.
•
Secretions are suctioned to maintain an open airway. Amount, color, and consiste
ncy of the secretions are noted, as well as how the
patient tolerated the procedure.
•
Ventilator settings and alarms are verified once a shift or when any changes occ
ur.
•
Continuous pulse oximetry and ABGs are monitored for assessing the oxygenation s
tatus; the physician is notified of any changes in
parameters.
•
The patient is frequently positioned to allow for optimal ventilation, to preven
t complications, to mobilize secretions, and to promote
comfort.
•
Ventilator circuit is monitored for moisture or water trapping in tubing and emp
tied when necessary. Moisture may impede the flow of
oxygen and may provide a medium for bacterial growth.
•
A functioning manual resuscitation bag is maintained at bedside at all times in
case of malfunctioning equipment.
•
The patient is medicated as needed to decrease anxiety and facilitate oxygenatio
n.
•
Alternative methods of communication are provided for patients to decrease anxie
ty and maintain some control over their environment.
•
Mouth and lip care is provided at least once very shift to keep mucous membranes
moist.
Amanuel/Pslidasan/Ksjuliano/MRCueno
NCM 104 1st sem S.Y. 2007-2008
11
ENDOCRINE/METABOLIC DISORDERS
DIABETIC KETOACIDOSIS
DKA is caused by an absence or markedly inadequate amount of insulin. First, be
cause the beta cells in the pancreas have the inability to
produce insulin, the ensuing hyperglycemia causes a hyperosmolar state. This hyp
erosmolarity results in fluid shifting from inside the cell to the serum; eventu
ally this fluid is lost in the urine, causing electrolyte shifts and total body
dehydration. Other metabolic derangements occur because no insulin exists to all
ow glucose to enter the cells; therefore cells begin to break down fats and prot
eins to use for fuel. This process causes the formation of ketones. Ketones decr
ease the blood pH and the bicarbonate concentration causing a ketosis. DKA is on
e of the more serious metabolic crises that can result from hyperglycemia in pat
ients with uncontrolled diabetes mellitus.
Three Main Clinical Features of DKA:
1. Hyperglycemia
2. Dehydration and electrolyte loss
3. Acidosis
Three Main Causes of DKA:
1. Decreased or missed dose of insulin
2. Illness or infection
3. Undiagnosed and untreated diabetes
Clinical Manifestations:
1. Acetone breath
2. Poor appetite or anorexia
3. Nausea and vomiting
4. Abdominal pain
5. Blurred vision
6. Weakness
7. Headache
8. Dehydration
9. Thirst or polydipsia
10. Orthostatic hypotension
11. Hyperventilation (Kussmaul respirations)
12. Mental status changes in DKA vary from patient to patient
Assessment and Diagnostic Findings :
1. Blood glucose levels may vary from300 to 800 mg/dl
2. The severity of DKA is not necessarily related to the blood glucose level
3. Evidence of DKA is reflected in low serum bicarbonate and low pH values
Prevention :
1. Patients must be taught “sick day “rules for maintaining their diabetes when
ill.
2. The most important issue is not to eliminate insulin doses when nausea and vo
miting occur and then attempt to consume frequent small portions
of carbohydrates
3. Drinking fluids every hour is important to prevent dehydration
4. Patients are taught to have available foods for use on sick days.
5. Supply of urine test strips and blood glucose test strips should be available
. Patients must know how to contact their physician
Medical Management :
1. Rehydration is important for maintaining tissue perfusion and enhancing the e
xcretion of excessive glucose by the kidneys
2. The major electrolyte of concern during treatment of DKA is potassium. Potass
ium replacement is vital to avoid dysrhythmias that may occur with
hypokalemia
3. Insulin is usually infused IV at a slow, continuous rate
4. Dextrose is added to IVF, such as normal saline solution when blood glucose l
evel reach 250 to 300 mg/dl to avoid too rapid drop in the blood
glucose level
Nursing Management :
1. Nursing care focuses on monitoring fluid and electrolyte status, blood glucos
e levels, administering fluids, insulin and other medications and
preventing complications such as fluid overload.
2. Urine output is monitored to ensure adequate renal function
3. ECG is monitored for dysrhythmias
4. VS, arterial blood gases and other clinical findings are recorded on a flow s
heet
HYPEROSMOLAR HYPERGLYCEMIC NONKETOTIC COMA
Background: Hyperosmolar hyperglycemic nonketotic coma (HHNC) is a metabolic der
angement that occurs principally in patients with adult-
onset diabetes. The condition is characterized by hyperglycemia, hyperosmolarity
, and an absence of significant ketosis.
Despite the name, coma is present in fewer than 10% of cases. Most patients pres
ent with severe dehydration and focal or global neurologic
deficits. In many cases, the clinical features of HHNC and diabetic ketoacidosis
(DKA) overlap and are observed simultaneously.
Pathophysiology: HHNC most commonly develops in patients with diabetes who have
some concomitant illness that leads to a reduced fluid
intake. Infection is the most common cause, but many other conditions can cause
altered mentation and/or dehydration. Frequently, this
concomitant illness is not identifiable.
Hyperglycemia and hyperosmolarity lead to osmotic diuresis and an osmotic shift
of fluid to the intravascular space, resulting in further intracellular
dehydration.
Unlike patients with DKA, patients with HHNC do not develop ketoacidosis, but th
e reason for this is not known. Contributing factors include the limitation on k
etogenesis by hyperosmolarity, the lower levels of free fatty acids available fo
r ketogenesis, the availability of insulin in amounts sufficient to inhibit keto
genesis but not sufficient to prevent hyperglycemia, and the hepatic resistance
to glucagon in these patients.
Management: refer to DKA
THYROTOXIC CRISIS (THYROID STORM)
A severe form of hyperthyroidism marked by sudden release of thyroid hormone in
to the blood stream
Precipitating Factors :
1. Stress such as injury, infection, thyroidal and non-thyroid surgery, tooth ex
traction, insulin reaction, diabetic acidosis, pregnancy, digitalis
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intoxication, abrupt withdrawal of anti-thyroid medications, extreme emotional s
tress, or vigorous palpation of the thyroid.
Clinical Manifestations :
1. High fever
2. Diaphoresis
3. Cardiopulmonary symptoms : extreme tachycardia, HPN, arrhythmias, CHF, pulmon
ary edema
4. CNS symptoms : increasing feeling of tremulousness to severe agitation, psych
osis with developing apathy, irritability, coma , heat intolerance
5. GI disturbance : weight loss, diarrhea, abdominal pain
6. Increased T3T4 and elevated BUN
Medical Management:
1. Immediate objectives are to reduced body temperature and heart rate and to pr
event vascular collapse
2. Humidified oxygen is administered to improve tissue oxygenation and meet meta
bolic demands
3. Monitor respiratory status by arterial blood gas or pulse oximetry
4. PTU or methimazole is administered to impede formation of thyroid hormone and
block conversion of T4 to T3, the more active form of thyroid
hormone
5. Hydrocortisone is prescribed to treat shock or adrenal insufficiency.
6. Iodine is administered to decrease output of T4 from the thyroid gland
7. For cardiac problems, Sympatholytic agents may be administered. Propranolol i
n combination with digitalis, has been effective in reducing
severe cardiac problems
ADRENAL CRISIS
Pheochromocytoma
A tumor that originates from the chromaffin cells of the adrenal medulla
Peak incidence is between ages 20 and 50 years old
The cause of high BP in 0.9% to 2.2% of patients with HPN
One form of HPN that is usually cured by surgery
Clinical Manifestations:
Typical triad of symptoms: Headache, Diaphoresis, Palpitations
HPN may be intermittent or persistent
Tremor, flushing and anxiety
Hyperglycemia may result from conversion of liver and muscle glycogen to glucos
e
Clinical picture is usually characterized by:
1. Acute, unpredictable attacks, lasting seconds or several hours
2. Patient is anxious, tremulous and weak
3. Headache, vertigo, blurring of vision, tinnitus, air hunger, and dyspnea
4. Polyuria, nausea, vomiting, diarrhea, abdominal pain
5. Feeling of impending doom
6. Palpitations and tachycardia
7. BP as high as 350/200 mm Hg
Assessment/Diagnostic Findings:
Signs of sympathetic nervous system over activity: 5 H’s (HPN, headache, hyperh
idorsis (excessive sweating), hypermetabolism, and
hyperglycemia)
Medical Management:
Pharmacologic Therapy
Close monitoring of ECG changes and careful administration of alpha-adrenergic
blocking agents, muscle relaxants – to lower BP quickly
Long-acting alpha blocker to prepare patient for surgery
Beta-adrenergic blocking agents for patients with cardiac dysrhythmias
Surgical Management:
Adrenalectomy- surgical removal of the tumor
HEPATIC FAILURE (Hepatic Coma)
An end stage of liver disease, usually arises as a complication of conditions t
hat cause liver dysfunction although it can be idiopathic
Also called Hepatic coma because the patient’s neurologic status gradually dete
riorates
Represents the most advanced stage of hepatic encephalopathy
A life threatening crisis may occur if the serum ammonia level rises, causing c
erebral ammonia intoxication
Causes:
1. Cirrhosis
2. Hepatitis
3. Drug or toxin-induced damage
4. Fatty liver
5. Portal HPN
6. Surgically-created portal systemic shunts that bypass the liver and allow tox
ins into the blood
Pathophysiology:
Liver disease alters liver structure and compromises essential functions. This l
eads to impaired protein, fat and carbohydrate metabolism, fluid and
electrolyte imbalance, poor lymphatic drainage, reduced coagulation and impaired
detoxification of ammonia and of the metabolites. Ammonia
accumulation and intoxication is the primary pathogenesis of hepatic failure and
the ensuing encephalopathy. Ammonia accumulates because liver
cells cannot detoxify and convert to urea the ammonia that is in constant supply
in GI tract blood. Remaining liver functions may become impaired
and may be difficult to treat or control. Hepatic failure may progress insidious
ly to a comatose state from which the patient rarely recovers.
Clinical Findings:
Stage 1
Slight personality and mood changes, disorientation, forgetfulness, slurred spe
ech, slight tremors, periods of lethargy and euphoria, mild
confusion, inability to concentrate, hyperactive reflexes, sleep-wake patterns,
handwriting starts to decline and mild asterixis (flapping tremors
of the hand) may appear
Stage 2
The patient grows more disoriented and drowsy. He may display inappropriate beh
avior, mood swings, agitation, apraxia. His hand writing
becomes illegible and asterixes may become pronounced
Stage 3
The patient becomes severely confused and may become combative, incoherent and
hard to arouse. Sleeps most of the time. You may detect
hyperactive deep tendon reflexes and rigid extremities
Stage 4
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The pupil is comatose and does not react to stimuli. Pupils are dilated and lac
k corneal and deep tendon reflexes. Extremities are flaccid and
may assume flexion or extension posturing, decebrate rigidity. The EEG is marked
ly abnormal.
Assessment and Diagnostic Findings:
1. Elevated arterial ammonia blood levels
2. The encephalogram shows generalized slowing and an increase in amplitude of b
rain waves and the appearance of characteristic triphasic
waves
3. Occasionally, fetor hepaticus, a characteristic breath odor like freshly mowe
d grass, acetone, or old wine, may be noticed.
4. In a more advanced stage, there are gross disturbances of consciousness and t
he patient is completely disoriented with respect to time and
place
5. With further progression of the disorder, the patient lapses into frank coma
and may have seizures.
Intervention:
1. Anti-infective agents – to decrease bacterial action in the colon.
2. Ammonia detoxicants – to reduce ammonia. Lactulose (Duphulac) is administered
3. Cleansing enemas with diluted acetic acid or neomycin
4. Discontinuation of any precipitating substance: Dietary proteins, sedatives,
diuretic therapy, analgesics
5. IV administration of glucose to minimize protein breakdown
6. Oxygen administration
7. Correction of any electrolyte imbalance
8. Promote rest, comfort and quiet environment
Nursing Diagnosis:
1. Altered thought process
2. Potential impaired skin integrity
3. Impaired skin integrity
RENAL DISORDER
RENAL FAILURE
Renal Failure is a systemic disease and is a final common pathway of many diffe
rent kidney and urinary tract diseases.
Results when the kidneys are unable to remove the body’s metabolic wastes or pe
rform their regulatory functions
The substances normally eliminated in the urine accumulate in the body fluids a
s a result of impaired renal excretion and lead to a disruption
in endocrine and metabolic functions and fluid and electrolyte, an acid-base dis
turbances.
ACUTE RENAL FAILURE
Acute renal failure is a sudden and almost complete loss of kidney function ove
r a period of hours to days.
Categories of Acute Renal Failure:
1. Prerenal Condition (hypoperfusion of kidney). Occurs as a result of impaired
blood flow that leads to hypoperfusion of the kidney and a drop
in the GFR. Common clinical situations are volume-depletion states (hemorrhage o
r gastrointestinal losses), impaired cardiac performance and
vasodilation (sepsis or anaphylaxis)
2. Intrarenal. Intrarenal causes of acute renal failure are the result of actual
parenchymal damage to the glomeruli or kidney tubules. Conditions
such as burns crush injuries, and infections, as well as nephrotoxic agents, may
lead to acute tubular necrosis and cessation of renal function. Severe transfus
ion reaction may also cause intrarenal failure. Medications may also predispose
a patient to intrarenal damage, esp. nonsteroidal anti-inflammatory drugs and AC
E inhibitors
3. Post renal conditions. Postrenal causes of acute renal failure are usually th
e result of an obstruction somewhere distal to the kidney.
PHASES OF ACUTE RENAL FAILURE:
1. Initiation period – begins with the initial insult and ends when oliguria dev
elops.
2. Period of Oliguria – accompanied by a rise in the serum concentration of subs
tances usually excreted by the kidney (urea, creatinine, uric acid,
organic acids and the intracellular cations – potassium and magnesium
3. Period of diuresis – The patient experiences a gradual increase in urinary ou
tput, which signals that glomerular filtration has started to recover.
Laboratory values start rising and eventually begin a downward trend.Uremic symp
toms may still be present. The patient must be closely monitored
for dehydration during this phase; if dehydration occurs, the uremic symptoms ar
e likely to increase.
4. Period of Recovery – signals the improvement of renal function. Laboratory va
lues return to the patient’s normal level.
Clinical Manifestations:
1. May appear critically ill and lethargic
2. Persistent nausea, vomiting and diarrhea
3. The skin and mucous membranes are dry due to dehydration
4. Uremic fetor – breath have the odor of urine
5. CNS manifestations: drowsiness, headache, muscle twitching, and seizures
Assessment and Diagnostic Findings:
1. Changes in urine. The urinary output varies (from scanty to normal volume). H
ematuria may be present and urine has low-specific gravity.
Patients with prerenal azotemia have a decreased amount of sodium. Those patient
s with intrarenal azotemia usually have urinary sodium levels
greater than 40 mEq/L.
2. Increased blood urea nitrogen and creatinine levels (Azotemia)
3. Hyperkalemia
4. Metabolic acidosis
5. Calcium and Phosphorus Abnormalities
6. Anemia – due to reduced erythropoietin production, uremic gastrointestinal le
sions, reduced Rbc lifespan, and blood loss
Prevention:
1. Renal function must be monitored closely if patient has been taking nephrotox
ic antibiotic agents or has been exposed to environmental toxins.
Blood should be drawn for determining baseline and monitoring serum BUN and crea
tinine levels by 24 hours after initiation of medication therapy
Medical Management:
1. Prerenal azotemia is treated by optimizing renal perfusion.
2. Postrenal failure is treated by relieving the obstruction
3. Overall, medical management includes maintaining fluid balance, avoiding flui
d excesses, or performing dialysis
4. The elevated potassium levels may be reduced by administering ion-exchange re
sins (sodium polystyrene sulfonate “kayexalate”)
5. Diuretics are used for management of volume status
6. Low-dose dopamine is often used to dilate the renal arteries
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7. Atrial natriuretic peptide – inhibits sodium and water absorption and dilates
the afferent arteriole, thus improving blood flow to the glomerulus
8. Correction of acidosis and elevated phosphate levels. When severe acidosis is
present, the arterial blood gases or serum bicarbonate levels
must be monitored because patient may require sodium bicarbonate therapy or dial
ysis. Patient’s elevated phosphate level may be controlled with
phophate-binding agents (aluminum hydroxide).
9. Nutritional Therapy. Dietary proteins are limited to about 1 g/kg during the
oliguric phase. High-carbohydrate meals to meet caloric requirements.
Foods and fluids containing potassium and phosphorus are restricted.
Nursing Management:
1. Monitoring fluid and electrolyte balance. Hyperkalemia is the most immediate
life-threatening imbalance seen in acute renal failure.
2. Reducing metabolic rate. To reduce catabolism and the subsequent release of p
otassium and accumulation of endogenous waste products. Bed
rest is indicated and fever and infection are prevented or treated promptly.
3. Promoting pulmonary function. Patient is assisted to turn, cough and take dee
p breaths frequently to prevent atelectasis and respiratory
infection.
4. Preventing Infection. Asepsis is essential with invasive lines and catheters
5. Providing skin care. Meticulous skin care is important. Massaging bony promin
ences, turning the patient frequently, and bathing the patient with
cool water are comforting and prevent skin breakdown
6. Providing support. The patient and family will need assistance, explanation a
nd support during this time.
CHRONIC RENAL FAILURE
CRF is a progressive, irreversible deterioration in renal function in which the
body’s ability to maintain metabolic and fluid and electrolyte
balance fails, resulting in uremia or azotemia (retention of urea and other nitr
ogenous wastes in the blood)
Pathophysiology:
As renal function declines, the end products of protein metabolism (which are no
rmally excreted in urine) accumulate in the blood. Uremia develops
and adversely affects every system in the body.
4 Stages of Chronic Renal Disease:
Stage 1
Reduced renal reserve. Characterized by a 40 to 75% loss of nephron function. Th
e patient usually does not have symptoms because the
remaining nephrons are able to carry out the normal functions of the kidney.
Stage 2
Renal Insufficiency. Occurs when 75 to 90% of nephron function is lost. At this
point, the serum creatinine and blood urea nitrogen rise, the kidney
loses its ability to concentrate urine and anemia develops. The patient may repo
rt polyuria and nocturia.
Stage 3
Renal Disease. Edema, metabolic acidosis, and hypocalcemia occur. Patient may ex
hibit overt uremia with cardiovascular, gastrointestinal, and
neurologic complications.
Stage 4
End-stage renal Disease (ESRD). The final stage of CRF occurs when there is less
than 10% nephron function remaining. All of the normal
regulatory, excretory, and hormonal functions of the kidney are severely impaire
d. ESRD is evidenced by elevated creatinine and blood urea
nitrogen levels as well as electrolyte imbalances. Once the patient reaches this
point, dialysis is usually indicated.
Signs And Symptoms Of CRF:
1. Neurologic
Weakness and fatigue; confusion; inability to concentrate; disorientation; trem
ors; seizures; asterixis; restlessness of legs; burning of soles of
feet; behavior changes.
2. Integumentary
Gray-bronze skin color; dry, flaky skin; pruritus; ecchymosis; purpura; thin, b
rittle nails; coarse, thinning hair
3. Cardiovascular
HPN; pitting edema (feet , hands, sacrum), periorbital edema; pericardial frict
ion rub; engorged neck veins; pericarditis; pericardial effusion;
pericardial tamponade; hyperkalemia; hyperlipidemia
4. Pulmonary
Crackles; thick, tenacious sputum; depressed cough reflex; pleuritic pain; shor
tness of breath; tachypnea; kussmaul-type respirations; uremic
pneumonitis; “ uremic lung
5. Gastrointestinal
Ammonia odor to breath (uremic fetor); metallic taste; mouth ulcerations and bl
eeding; anorexia; nausea and vomiting; hiccups; constipation
or diarrhea; bleeding from GIT
6. Hematologic
Anemia; thrombocytopenia
7. Reproductive
Amenorrhea; testicular atrophy; infertility; decreased libido
8. Musculoskeletal
Muscle cramps; loss of muscle strength; renal osteodystrophy; bone pain; bone f
ractures; foot drop
Assessment And Diagnostic Findings:
•
Glomerular Filtration Rate. Decreased GFR can be detected by obtaining a 24-hour
urine analysis for creatinine clearance. As GFR
decreases, the creatinine clearance value decreases, whereas the serum creatinin
e and BUN levels increase.
•
Sodium and Water Retention. The kidney is unable to concentrate or dilute the ur
ine normally in ESRD. Some patients retain sodium and
water, increasing the risk for edema, CHF, and HPN.
•
Acidosis. With advanced renal disease, metabolic acidosis occurs because the kid
ney is unable to excrete increased loads of acid.
•
Anemia. Anemia develops as a result of inadequate erythoropoietin production, th
e shortened life span of RBC’s, nutritional deficiencies, and
the patient’s tendency to bleed, particularly from GIT
•
Calcium and Phosphorus Imbalance. The body’s serum calcium and phosphate levels
have a reciprocal relationship in the body; as one rises,
the other decreases.
Complications:
1. Hyperkalemia. Due to decreased excretion, metabolic acidosis, catabolism, and
excessive intake (diet, medications, fluids)
2. Pericarditis. Due to retention of uremic waste products and inadequate analys
is
3. Hypertension. Due to sodium and water retention and malfunction of the rennin
-angiotensin-aldosterone system
4. Anemia. Due to decrease erythropoietin, decreased RBC life span, GIT bleeding
and blood loss during dialysis.
5. Bone disease and metastatic calcifications. Due to retention of phosphorus, l
ow serum calcium levels, abnormal vitamin D metabolism, and
elevated aluminum levels
Medical Management:
1. Pharmacologic Therapy
Antacids. Hyperphosphatemia and hypocalcemia are treated with aluminum based ant
acids that bind dietary phophorus in the GIT
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