COMPLICATIONS AGGRAVATED BY PREGNANCY, LABOUR AND THE PUERPARIUM

A. BLEEDING DISORDERS: ECTOPIC PREGNANCY Descriptio

Implantation of products of conception in a site other than the uterine cavity (e.g., fallopian tube, ovary, cervix, or peritoneal cavity.)

Sites o! ectopic pre" # c$. N%&'ers i (ic#te t)e or(er o! pre*#+e ce.

Etio+o"$

Ectopic pregnancy can result from conditions that hinder ovum passage through the fallopian tube and into the uterine cavity, such as:

1. Salpingitis . !iverticula ". #umors

$. %dhesions from previous surgery &. #ransmission of the ovum from one ovary to the opposite fallopian tube. P#t)op)$sio+o"$

#he uterus is the only organ capable of containing and sustaining a pregnancy. 'hen the fertili(ed ovum implants in other locations the body is unable to maintain the pregnancy.

Assess&e t ,i (i "s 1. Associ#te( !i (i "s

Suspect ectopic pregnancy in a client )hose history includes a missed menstrual period, spotting, or bleeding pelvic or shoulder pain, use of intrauterine device, pelvic infections, tubal surgery, or previous ectopic pregnancy.

*e a)are of grief and lost manifestations in the client and family.

. +ommon c+i ic#+ &# i!est#tio s. (#he client )ith ectopic pregnancy may report signs and symptoms of a normal pregnancy or may have no symptoms at all.)

!i((iness and syncope (faintness) Sharp abdominal pain and referred shoulder pain ,aginal bleeding %dnexal mass and tenderness A r%pt%re( !#++opi# t%'e c# pro(%ce +i!e -t)re#te i " co&p+ic#tio s, s%c) #s )e&orr)#"e, s)oc., # ( perito itis.

". L#'or#tor$ # ( (i#" ostic st%($ !i (i "s

*lood samples for hemoglobin value, blood type, and group, and crossmatch. % pregnancy test reveals elevated serum -uantitative beta h+.. /ltrasound )ill confirm extrauterine pregnancy.

N%rsi " M# #"e&e t 1. E s%re t)#t #ppropri#te p)$sic#+ ee(s #re #((resse( # ( &o itor for complications. %ssess vital signs, bleeding, and pain.

. Pro*i(e c+ie t # ( !#&i+$ te#c)i " to re+ie*e # /iet$.

Explain the condition and expected outcome.

o

0aternal prognosis is good )ith early diagnosis and prompt treatment, such as laparotomy, to ligate bleeding vessels and repair or remove the damaged fallopian tube.

1harmacologic agents, such as methotrexate follo)ed by leucovorin, may be given orally )hen ectopic pregnancy is diagnosed by routine sonogram before the tube has ruptured. % hysterosalpingogram usually follo)s this therapy to confirm tubal patency.

2h3negative )omen must receive 2ho.%0 to provide protection from isoimmuni(ation for future pregnancies

b. !escribe self3care measures, )hich depend on the treatment.

". A((ress e&otio #+ # ( ps$c)osoci#+ ee(s.

SPONTANEOUS ABORTION Descriptio Spontaneous abortion is the expulsion of the fetus and other products of conception from the uterus before the fetus is capable of living outside of the uterus. 1. #ypes of spontaneous abortions
o

T)re#te e( #'ortio 3 is characteri(ed by cramping and vaginal bleeding in early pregnancy )ith no cervical dilation. It may subside or an incomplete abortion may follo).

I&&i e t or i e*it#'+e #'ortio 4 is characteri(ed by bleeding, cramping and cervical dilation. #ermination cannot be prevented.

I co&p+ete #'ortio 4 is characteri(ed by expulsion of only part of the products of conception (usually the fetus). *leeding occurs )ith cervical dilation.

Co&p+ete #'ortio 4 is characteri(ed by complete expulsion of all products of conception.

Misse( #'ortio 4 is characteri(ed by early fetal intrauterine death )ithout expulsion of the products of conception. #he cervix is closed, and the client may report dar5 bro)n vaginal discharge. 1regnancy test findings are negative.

Rec%rre t 0)#'it%#+1 #'ortio 4 is spontaneous abortion of three or more consecutive pregnancies.

,i"%re 2 T)ree T$pes o! Spo t# eo%s A'ortio Etio+o"$

Spontaneous abortion may result from unidentified natural causes or from fetal, placental or maternal factors.

1. Fetal Factors a. !efective embryologic development b. 6aulty ovum implantation c. 2e7ection of the ovum by the endometrium d. +hromosomal abnormalities . Placental Factors

a. 1remature separation of the normally implanted placenta b. %bnormal placental implantation c. %bnormal placental function ". Maternal Factors a. Infection b. Severe malnutrition c. 2eproductive system abnormalities (eg, incompetent cervix) d. Endocrine problems (eg, thyroid dysfunction) e. #rauma f. !rug ingestion

P#t)op)$sio+o"$

#he fetal or placental defect or the maternal condition results in the disruption of blood flo), containing oxygen and nutrients, to the developing fetus. #he fetus is compromised and subse-uently expelled from the uterus.

Assess&e t ,i (i "s 1. Associ#te( !i (i "s 4 #he client and family may exhibit a grief reaction at the loss of pregnancy, including: a. +rying b. !epression c. Sustained or prolonged social isolation d. 'ithdra)al

. C+i ic#+ M# i!est#tio s 4 include common signs and symptoms of spontaneous abortion. a. ,aginal bleeding in the first 8 )ee5s of pregnancy b. +omplaints of cramping in the lo)er abdomen c. 6ever, malaise or other symptoms of infection ". L#'or#tor$ # ( (i#" ostic st%($ !i (i "s a. Serum beta h+. levels are -uantitatively lo) b. /ltrasound reveals the absence of a viable fetus. I&p+e&e t#tio 1. Pro*i(e #ppropri#te &# #"e&e t # ( pre*e t co&p+ic#tio s

%ssess and record vital signs, bleeding and cramping of pain. 0easure and record intravenous fluids and laboratory test results. In instances of heavy vaginal bleeding9 prepare for surgical intevention (! : +) if indicated.

1repare for 2ho.%0 administration to an 2h3negative mother, as prescribed. 'henever the placenta is dislodged (birth, ! : +, abruptio) some of the fetal blood may enter maternal circulation. If the )oman is 2h negative, enough 2h3positive blood cells may enter her circulation to cause isoimmini(ation, the production of antibodies against 2h3positive blood, thus endangering the )ell3being of future pregnancies. *ecause the blood type of the conceptus is not 5no)n, all )omen )ith 2h3negative blood should receive 2ho.%0 after an abortion.

2ecommended iron supplements and increased dietary iron as indicated to help prevent anemia.

. Pro*i(e c+ie t # ( !#&i+$ te#c)i "

;ffer anticipatory guidance relative to expected recovery, the need for rest and delay of another pregnancy until the client fully recovers.

Suggest avoiding intercourse until after the next menses or using condoms )hen engaging in intercourse.

Explain that in many cases, no cause for the spontaneous abortion is ever identified.

". A((ress e&otio #+ # ( ps$c)osoci#+ ee(s. PLACENTA PREVIA

Descriptio

1. #he placenta implants in the lo)er uterine segment, near the cervical os. #he degree to )hich it covers the os leads to three different classifications.
o

Tot#+ p+#ce t# pre*i# occurs )hen the placenta completely covers the internal os.

P#rti#+ p+#ce t# pre*i# occurs )hen the placenta partially covers the internal os.

Lo34+$i " or +o34i&p+# t#tio p+#ce t# pre*i# occurs )hen the placental border reaches the border of the internal os.

. #he incidence of placenta previa is three to six per 1,888 deliveries. Etio+o"$ Pre(isposi " !#ctors include:

1. 0ultiparity (<8= of affected clients are multiparous) . %dvanced maternal age (older than "& years in ""= of cases) ". 0ultiple gestation $. 1revious cesarean birth &. /terine incision >. 1rior placenta previa (incidence is 1 times greater in )omen )ith previous placenta previa)

P#t)op)$sio+o"$

1. 1athologic process seems to be related to the conditions that alter the normal function of the uterine deciduas and its vasculari(ation. . *leeding, )hich results from tearing of the placental villi from the uterine )all as the lo)er uterine segment contracts and dilates, can be slight or profuse.

Assess&e t ,i (i "s

1. Associ#te( !i (i "s. In cases of suspected placenta previa, a vaginal examination is delayed until ultrasound results are available and the client is moved to the operating room for )hat is termed a double3set3up procedure. #he operating room is needed because the examination can cause further tearing of the villi and hemorrhage, )hich can be fatal to the client and fetus. 5. Co&&o c+i ic#+ &# i!est#tio s i c+%(e:
o o o

*right red, painless vaginal bleeding Soft, nontender abdomen9 relaxes bet)een contractions, if present. 6?2 stable and )ithin normal limits.

". L#'or#tor$ # ( (i#" ostic st%($ !i (i "s. #ransabdominal ultrasonography confirms suspicion of placenta previa.

N%rsi " M# #"e&e t 1. E s%re t)e p)$sio+o"ic 3e++4'ei " o! t)e c+ie t # ( !et%s.

#a5e and record vital signs, assess bleeding, and maintain a perineal pad count. 'eigh perineal pads before and after use to estimate blood loss.

;bserve for shoc5, )hich is characteri(ed by a rapid pulse, pallor, cold moist s5in, and a drop in blood pressure.

0onitor the 6?2. Enforce strict bed rest to minimi(e ris5 to the fetus. ;bserve for additional bleeding episodes.

. Pro*i(e c+ie t # ( !#&i+$ te#c)i "

Explain the condition and management options. #o ensure an ade-uate blood supply to the mother and fetus, place the )oman at bed rest in a side3lying position. %nticipate the order for a sonogram to locali(e the placenta. If the condition of mother or fetus deteriorates, a cesarean birth )ill be re-uired.

1repare the client for ambulation and discharge (may be )ithin $< hours of last bleeding episode).

!iscuss the need to have transportation to the hospital available at times. Instruct the client to return to the hospital if bleeding recurs and to avoid intercourse until after the birth.

Instruct the client on proper hand)ashing and toileting to prevent infection.

". A((ress e&otio #+ # ( ps$c)osoci#+ ee(s.

;ffer emotional support to facilitate the grieving process, if needed. %fter birth of the ne)born, provide fre-uent visits )ith the ne)born that mother can be certain of the infant@s condition.

ABRUPTIO PLACENTA Descriptio

%bruptio placenta is premature separation of a normally implanted placenta after the 8th )ee5 of pregnancy, typically )ith severe hemorrhage.

Etio+o"$ 1. #he cause of abruptio placenta is un5no)n.

. 2is5 factors include:

/terine anomalies 0ultiparity 1reeclampsia 1revious cesarean delivery 2enal or vascular disease #rauma to the abdomen 1revious third trimester bleeding %bnormally large placenta Short umbilical cord

P#t)op)$sio+o"$

#he placenta detaches in )hole or in part from the implantation site. #his occurs in the area of the deciduas basalis.

Assess&e t ,i (i "s 1. Associ#te( !i (i "s. Severe abruption placentae may produce such complications as: a. 2enal failure b. !isseminated intravascular coagulation c. 0aternal and fetal death

. +ommon c+i ic#+ &# i!est#tio include: a. Intense, locali(ed uterine pain, )ith or )ithout vaginal bleeding. b. +oncealed or external dar5 red bleeding c. /terus firm to boardli5e, )ith severe continuous pain d. /terine contractions e. /terine outline possibly enlarged or changing shape f. 6?2 present or absent. g. 6etal presenting part may be engaged. ". L#'or#tor$ # ( (i#" ostic st%($ !i (i "s.

/ltrasound may be able to identify the extent of abruption. ?o)ever, the absence of an ultrasound finding does not rule out the presence of abruption.

N%rsi " M# #"e&e t 1. Co ti %o%s+$ e*#+%#te &#ter #+ # ( !et#+ p)$sio+o"ic st#t%s, p#rtic%+#r+$:

,ital signs *leeding Electronic fetal and maternal monitoring tracings Signs of shoc53rapid pulse, pallor, cold and most s5in, decrease in blood pressure !ecreasing urine output Aever perform a vaginal or rectal examination or ta5e any action that )ould stimulate uterine activity.

. Assess t)e ee( !or i&&e(i#te (e+i*er$. If the client is in active labor and bleeding cannot be stopped )ith bed rest, emergency cesarean delivery may be indicated. ". Pro*i(e #ppropri#te &# #"e&e t.

;n admission, place the )oman on bed rest in a lateral position to prevent pressure on the vena cava.

Insert a large gauge intravenous catheter into a large vein for fluid replacement. ;btain a blood sample for fibrinogen level.

0onitor the 6?2 externally and measure maternal vital signs every & to 1& minutes. %dminister oxygen to the mother by mas5.

1repare for cesarean section, )hich is the method of choice for the birth.

$. Pro*i(e c+ie t # ( !#&i+$ te#c)i ". &. A((ress e&otio #+ # ( ps$c)osoci#+ ee(s. ;utcome for the mother and fetus depends on the extent of the separation, amount of fetal hypoxia, and amount of bleeding. POSTPARTUM HEMORRHAGE Descriptio

1ostpartum hemorrhage is blood loss of more than &88 mB follo)ing the birth of a ne)born.

Etio+o"$

1. Early postpartum hemorrhage, )hich is usually due to uterine atony, lacerations, or retained placental fragments, occurs in the first $ hours after delivery.

. Bate postpartum hemorrhage occurs after the first $ hours after delivery and is generally caused by retained placental fragments or bleeding disorders.

P#t)op)$sio+o"$

!elayed uterine atony or placental fragments prevent the uterus from contracting effectively. #he uterus is unable to form an effective clot structure and bleeding ensues or continues.

Assess&e t ,i (i "s : +ommon c+i ic#+ &# i!est#tio s include:

1. ,aginal bleeding is the obvious sign of postpartum hemorrhage9 amount and character vary )ith cause.

. Signs of impending shoc5 include changes in s5in temperature and color, and altered level of consciousness.

N%rsi " M# #"e&e t 1. Pre*e t e/cessi*e '+oo( +oss # ( res%+ti " co&p+ic#tio s. a. 0assage the uterus, facilitate voiding, and report blood loss. b. 0onitor blood pressure and pulse rate every & to 1& minutes. c. 1repare for intravenous infusion, oxytocin and blood transfusion, if needed. d. %dminister medications and oxygen as prescribed. ( !rug +hart ) e. 0easure and record fluid inta5e and output. f. *e prepared for possible dilation and curettage (!:+). . Assist t)e c+ie t # ( !#&i+$ to (e#+ 3it) p)$sic#+ # ( e&otio #+ stresses o! postp#rt%& co&p+ic#tio s. Dr%" C)#rt Me(ic#tio s Use( !or Postp#rt%& Co&p+ic#tio s C+#ssi!ic#tio s %nticoagulants ?eparin sodium in7ection (?epalean) Bovenox

Use( !or

Se+ecte( I ter*e tio s

*loc5s the conversion of prothrombin to thrombin and fibrinogen to fibrin thus decreasing clotting ability Inhibits thrombus and clot formation

?eparin I, should be administered as a Cpiggy bac5D infusion.

?eparin SE is given deep into the site (abdomen), sites are rotated, do not aspirate, apply pressure (do not massage).

/sed to prevent and treat

pulmonary embolism and thrombosis.

Interferes )ith hepatic synthesis of vitamin F 4dependent clotting factors (II,,II, IG, G)

'omen on anticoagulopathy therapy should no be given estrogen or aspirin.

'arfarin sodium (+oumadin, 'arfilone)

;btain baseline coagulation studies.

;btain serial coagulation studies )hile the client is on therapy.

Feep protamine sulfate readily available in case of heparin overdose.

%ssess client for bleeding from nose, gums, hematuria, and blood in stool.

;bserve color and amount of lochia. Institute pad count.

%void I0 in7ections to avoid formation of hematomas.

Inform the client that this drug does not pass into breast mil5.

0onitor for the follo)ing side effects9 hemorrhage, bruising urticaria, and thrombocytopenia.

'omen on anticoagulant therapy should not be given estrogen or aspirin.

;btain baseline coagulation studies )hile on therapy.

Feep %-ua0E1?H#;A (vitamin F) on hand in case of +oumadin overdose.

%ssess client for bleeding from nose, gums, hematuria, and blood in stool.

;bserve color and amount of lochia. Institute a pad count.

%void I0 in7ections to avoid formation of hematomas.

Inform the client that this drug passes into breast mil5 and its use is contraindicated during pregnancy. 0onitor the follo)ing side effects:

hemorrhage, fever, nausea, and cramps.

!irectly stimulates uterine and vascular smooth muscle

;btain a baseline calcium level.

;xytoxic methylergonovine maleate (methergine) (1;, I0, I,)

%dvise the client that this medication )ill cause menstrual3li5e cramps.

1romotes uterine contraction /sed for prevention and treatment of postpartum or postabortion hemorrhage caused by uterine atony or subinvolution.

%ssess for numb fingers and toes, cold, chest pain, nausea, vomiting, muscle pain, and )ea5ness. 0ay cause decreased serum prolactin. I, administration is used for emergency dosage only. %dminister at a rate of 8. mg over at least 1 minute.

!; A;# 0IG #?IS !2/. 'I#? %AH ;#?E2 !2/..

/se solution only if it is clear and colorless, )ith no precipitate. 0ay store at room temperature for >8 days. #he drug deteriorates )ith age.

0onitor for the follo)ing side effects: dyspnea, palpitations, diaphoresis, chest pain, hypotension, and headache.

Disse&i #te( I tr#*#sc%+#r Co#"%+#tio 0DIC1

What is disseminated intravascular coagulation (DIC)? Disseminated intravascular coagulation (DIC) is a rare, life-threatening condition that prevents a person's blood from clotting normally. It may cause excessive clotting (thrombosis) or bleeding (hemorrhage) throughout the body and lead to shoc , organ failure, and death. In DIC, the body's natural ability to regulate blood clotting does not function properly. !his causes the blood's clotting cells (platelets) to clump together and clog small blood vessels throughout the body. !his excessive clotting damages organs, destroys blood cells, and depletes the supply of platelets and other clotting factors so that the blood is no longer able to clot normally. !his often causes "idespread bleeding, both internally and externally. What causes DIC? DIC can be triggered by a health problem that sets the clotting cascade in motion. #uch health problems include$

#ome types of bacterial, viral, or fungalinfection. #evere trauma, especially from brainin%uries, crushing in%uries, burns, and extremely lo" body temperature (hypothermia). #ome cancers. Complications during pregnancy. #ome types of sna ebite. In most cases, the condition causing the DIC "ill be no"n (such as severe trauma). In rare cases, extensive bleeding caused by DIC "ill be the first symptom of the disease or condition causing it (such as cancer). What are the symptoms? &hen DIC causes the blood's platelets and clotting factors to become depleted, excessive bleeding (hemorrhage) occurs throughout the body. !he severity of bleeding can range from small red dots and bruises under the s in to heavy bleeding from surgical "ounds or body openings, such as the mouth, nose, rectum, or vagina. #ymptoms of organ damage caused by excessive blood clotting may include shortness of breath from lung damage, lo" urine output from idney damage, orstro e from damage to the brain. In severe cases, shoc , "ith lo" blood pressureand "idespread organ failure, may occur.

In a less severe type of DIC called chronic DIC, the body is able to compensate for the abnormal clotting. Chronic DIC may produce no symptoms or only mild blood clotting or minimal bleeding from the s in or mouth. How is DIC diagnosed? DIC is a very complex condition that can be hard to diagnose. !here is no single test that is used to diagnose DIC. In some cases, several different tests given over a period of time may be needed for an accurate diagnosis. ' doctor may suspect DIC in a person "ho has symptoms of excessive bleeding or clotting. (lood tests to measure the amount of platelets and other substances (such as prothrombin and fibrinogen) that affect clotting can help confirm the diagnosis. !ests that may be used to diagnose DIC include$

D-dimer test. !his blood test helps determine "hether a person's blood is clotting normally by measuring a substance (fibrin) that is released as a blood clotbrea s up. D-dimer levels are often higher than normal in people "ho have abnormal blood clotting. )rothrombin time ()!*I+,). !his blood test measures ho" long it ta es blood to clot. 't least a do-en blood proteins, or clotting factors, are needed to clot blood and stop bleeding (coagulation). )rothrombin, or factor II, is one of several clotting factors produced by the liver. ' long prothrombin time can be a sign of DIC. .ibrinogen. !his blood test measures ho" much fibrinogen is in the blood. .ibrinogen is a protein that plays a part in blood clotting. ' lo" fibrinogen level can be a sign of DIC. It happens "hen the body is using fibrinogen faster than the body can ma e it. Complete blood count (C(C). ' complete blood count (C(C) involves ta ing a blood sample and counting the number of red blood cells and "hite blood cells. C(C results cannot diagnose DIC, but they provide information to help the doctor ma e a diagnosis. (DIC often causes the platelet count to drop.) (lood smear. In this test, a drop of blood is smeared on a slide and stained "ith a special dye. !he slide is then examined under a microscope. !he number, si-e, and shape of red blood cells, "hite blood cells, and platelets are recorded. (lood cells often loo damaged and abnormal in people "ho have DIC. How is it treated? !reatment for DIC depends on the medical condition that is causing it. If that condition can be treated, the DIC may get better. )eople "ith acute DIC re/uire hospitali-ation, often in an intensive care unit (IC0), "here treatment "ill attempt to correct the problem causing the DIC "hile maintaining the function of the organs.

!ransfusions of blood cells and other blood products may be needed to replace blood that has been lost through bleeding and to replace clotting factors used up by the body. In some cases a blood thinner, such as heparin, is used. !his shuts do"n the cascade of events that ma e the body overuse its blood clotting factors.

Thromboembolism

!hromboembolism encompasses 1 interrelated conditions that are part of the same spectrum, deep venous thrombosis (D2!) and pulmonary embolism ()3). !he spectrum of disease ranges from clinically unsuspected to clinically unimportant to massive embolism causing death.

Signs and symptoms

#igns and symptoms of thromboembolism include the follo"ing$

'cute onset of shortness of breath4 dyspnea is the most fre/uent symptom of )3 )leuritic chest pain, cough, or hemoptysis ("ith a smaller )3 near the pleura) #yncope ("ith a massive )3) #ense of impending doom, "ith apprehension and anxiety Complaints related to signs of D2!, lo"er-extremity s"elling, and "armth to touch or tenderness !achypnea (respiratory rate 567 breaths*min) !achycardia 'ccentuated second heart sound .ever +ormal findings from lung examination Cyanosis

Diagnosis
&or up for thromboembolism includes the follo"ing$

)ulmonary angiography$ Diagnostic standard for )3 2entilation-perfusion scanning$ 8ost common screening techni/ue 2enography$ #tandard test for validating ne" diagnostic procedures 'rterial blood gas values on room air$ 9ypoxemia, elevated alveolar-arterial oxygen gradient 'cid-base status$ ,espiratory al alosis 3n-yme-lin ed immunoassay (3:I#') for D-dimer 3lectrocardiography, especially for ruling out myocardial infarction Chest radiography$ 8ost often normal but occasionally suggestive 9elical (spiral) computed tomography of pulmonary vessels Doppler ultrasonography of venous system 3chocardiography Impedance plethysmography$ ;f limited value "hen D2! is asymptomatic or distal or "hen findings are nonocclusive

anagement
'nticoagulant medications include the follo"ing$

9eparin or a lo"-molecular-"eight heparin (:8&9) #ubse/uent administration of an oral coumarin derivative (typically, "arfarin sodium) ;ral factor <a inhibitors (eg, rivaroxaban) !hrombolytic options (for initial treatment of patients "ith acute, massive )3 causing hemodynamic instability) include the follo"ing$

!issue plasminogen activator (t-)'4 first-choice thrombolytic agent), including the recombinant agents alteplase, reteplase, and tenecteplase #trepto inase (ris of antibody development) 0ro inase (of limited availability) #urgical interventions include the follo"ing$

!hrombectomy 3mbolectomy (limited to massive )3 "hen thrombolysis is contraindicated or other treatments have failed) 2enous interruption (currently rare)

Prevention !hromboprophylaxis reduces the incidence of D2! and fatal )3 and may be achieved by pharmacologic or mechanical means. 8edications used for prevention of thromboembolism include the follo"ing$

0nfractionated heparin :8&9 Danaparoid &arfarin 'spirin 8echanical approaches to thromboprophylaxis include the follo"ing$ 3xternal compression 3arly ambulation

Hemolytic Disease of the Fetus and Newborn

Description
1. Hemolytic disease of the fetus and newborn is an immune reaction of the mothers blood against the blood group factor on the fetus RBCs. . !hen Rho"#$ %Rh immune globulin& became a'ailable in the 1()*s to treat isoimmuni+ation in Rh,negati'e women- the incidence of hemolytic disease in the fetus and newborn dropped significantly.

Etiology
1. Hemolytic disease occurs most fre.uently when the mother does not ha'e the Rh factor present in her blood but the fetus has this factor. #nother common cause of hemolytic disease is #B/ incompatibility. 0n most cases of #B/ incompatibility- the mother has blood type / and the fetus has blood type #. 0t may also occur when the fetus has blood type B or #B.

. Hemolysis is occasionally caused by maternal anemias- such as thalassemia or from other blood group antigens %anti,D&.

Pathophysiology
1. 1his disorder occurs when the fetus has a blood group antigen that the mother does not posses. 1he mothers body forms an antibody against that particular blood group antigen- and hemolysis begins. 1he process of antibody formation is called maternal sensiti+ation. . 1he fetus has resulting anemia from the hemolysis of blood cells. 1he fetus compensates by producing large numbers of immature erythrocytes- a condition 2nown as erythroblastosis fetalis- hemolytic disease of the newborn- or hydrops fetalis. Hydrops refers to the edema and fetalis refers to the lethal state of the infant. 3. 0n Rh incompatibility- the hemolysis usually begins in utero. 0t may not affect the first pregnancy but all pregnancies that follow will e4perience this problem. 0n #B/ incompatibility- the hemolysis does not usually does not usually begin until the birth of the newborn.

Assessment Findings
1. Clinical manifestations

1he hemolytic response in #B/ incompatibility usually begins at birth with a resulting newborn 5aundice. Rh incompatibility may lead to6
o o o

Hydramnios in the mother 74cess bilirubin le'els in the amniotic fluid. 8arying degrees of hemolytic anemia %erythroblastosis& in the fetus. 0f the condition is left unmanaged- 9: of affected infants may die or suffer permanent brain damage.

. Laboratory and diagnostic study findings

1he indirect Coombs test can aid in the search for agglutination of Rh,positi'e RBCs to determine if antibodies are present. #mniocentesis is used to determine optical density and estimate fetal hemolysis. ;pectrophotometer readings are made of the amniotic fluid collected. 1he readings are obtained to determine fluid density. 1hey are plotted on a graph and correlated with gestational age. 1he amount of bilirubin resulting from the hemolysis of red blood cells can then be estimated. #n antibody titer should be drawn at the first prenatal 'isit on all Rh,negati'e women. 0t should also be drawn at < and 3) wee2s of pregnancy and again at deli'ery or abortion. 1he normal 'alue is *. 1he result is usually reported as a ratio= normal is 16<. 0f the titer is absent or minimal %16<&- no therapy is needed. # rising titer indicates the need for Rho"#$ and 'igilant monitoring of fetal well,being.

Nursing Management
1. Administer RhoGAm to the unsensiti ed Rh!negati"e client as appropriate

#dminister Rho"#$ at < wee2s gestation- e'en when titers are negati'e- or after any in'asi'e procedure- such as amniocentesis. Rho"#$ protects against the effects of early transplacental hemorrhage %as recommended by the #merican College of "ynecologists&. !hen the Rh,negati'e mother is in labor- crossmatch for Rho"#$- which must gi'en within > hours of deli'ery of the newborn.

. Pro"ide management for the sensiti ed Rh!negati"e mother and Rh!positi"e fetus#

Focus management of the sensiti+ed Rh,negati'e mother on close monitoring of fetal well,being- as reflected by Rh titers- amniocentesis results- and sonography. 0f there is e'idence of erythroblastosis- notify the perineal team of the possibility for deli'ery of a compromised newborn.

3. Pro"ide management for A$% incompatibility#

?hototherapy usually can resol'e the newborn 5aundice associated with #B/ incompatibility. 0n addition- initiation of early feeding and e4change blood transfusions may be immediate measures re.uired to reduce indirect bilirubin le'els. ?ro'ide client and family teaching.

Hyperemesis "ra'idarum
Description

Hyperemesis gra'idarum is se'ere and e4cessi'e nausea and 'omiting during pregnancy- which leads to electrolyte- metabolic- and nutritional imbalances in the absence of the medical problems.

Etiology

1he etiology of hyperemesis gra'idarum is obscure= suggested causati'e factors include6

1. . 3. @. 9.

High le'els of hC" in early pregnancy $etabolic or nutritional deficiencies $ore common in unmarried white women and first pregnancies #mbi'alence toward the pregnancy or family,related stress 1hyroid dysfunction

Pathophysiology
1. Continued 'omiting results in dehydration and ultimately deceases the amount of blood and nutrients circulated to the de'eloping fetus. . Hospitali+ation may be re.uired for se'ere symptoms when the client needs intra'enous hydration and correction of metabolic imbalance.

Assessment Findings

;igns and symptoms occur during the first 1) wee2s of pregnancy and are intractable. Anremitting nausea and 'omiting. 8omitus initially containing undigested food- bile- and mucus= later containing blood and material that resembles coffee grounds !eight loss ?ale- dry s2in Rapid pulse Fetid- fruity breath odor from acidosis Central ner'ous system effects- such as confusion- delirium- headache- and lethargy- stupor- or coma.

1. Clinical manifestations include6

. /ther common signs and symptoms include6

Nursing Management
1. Promote resolution of the complication#

$a2e sure that the client is N?/ until cessation of 'omiting. #dminister intra'enous fluids as prescribed= they may be gi'en on an ambulatory basis when dehydration is mild. $easure and record fluid inta2e and output. 7ncourage small fre.uent meals and snac2s once 'omiting has subsided. #dminister antiemetics as prescribed. client and family can e4press concerns and resol'e some of their fears.

. Address emotional and psychosocial needs. $aintain a non 5udgmental atmosphere in which the

?regnancy, 0nduced Hypertension %?0H= preeclampsia and eclampsia&

Description
1. ?reeclampsia is a hypertensi'e disorder of pregnancy de'eloping after * wee2s gestation and characteri+ed by edema- hypertension- and proteinuria. . 7clampsia is an e4tension of preeclampsia and is characteri+ed by the client e4periencing sei+ures.

Etiology
1. 1he cause of preeclampsia is un2nown. . ?ossible contributing factors include6

"enetic or immunologic ?rimigra'id status Conditions that create e4cess trophoblastic tissue- such as multiple gestationdiabetes- or hydatidiform mole. #ge younger than 1< or older than 39 years.

Pathophysiology

?reeclampsia is a multisystem- 'asospatic disease process characteri+ed by hemoconcentration- hypertension- and proteinuria.

Assessment Findings
&# Clinical manifestations of mild preeclampsia
o

Blood pressure e4ceeding 1@*B(* mmHg= or increase abo'e baseline of 3* mm Hg in systolic pressure or 19 mmHg in diastolic pressure on two readings ta2en ) hours apart. "enerali+ed edema in the face- hands- and an2les %a classic sign& !eight gain of about 1.9 2g %3.3 lb& per month in the second trimester or more than 1.3 to .3 2g %3 to 9 lb& per wee2 in the third trimester ?roteinuria 1C to C- or 3** mgBdD- in a @ hour sample

o o

'# (arning signs of )orsening preeclampsia

o o o o o

Rapid rise in blood pressure Rapid weight gain "enerali+ed edema 0ncreased proteinuria 7pigastric pain- mar2ed hyperrefle4ia- and se'ere headache- which usually precede con'ulsions in eclampsia 8isual disturbances /liguria %E1 * mD in @ hours& 0rritability ;e'ere nausea and 'omiting

o o o o

*# Clinical manifestations of se"ere preeclampsia

o

Blood pressure e4ceeding 1)*B11* mm Hg noted on two readings ta2en ) hours apart with the client on bed rest. ?roteinuria e4ceeding 9 gB @ hours /liguria %less than @** mDB @ hours& Headache Blurred 'ision- spots before eyes- and retinal edema ?itting edema of the sacrum- face- and upper e4tremities Dyspnea 7pigastric pain Nausea and 'omiting

o o o o o o o o

Hyperrefle4ia

@. Eclampsia e4ists once the patient has e4perienced a grand mal sei+ure. 1he patient may progress o more serious complications such as cerebral hemorrhage- li'er rupture- and coma. 9. Laboratory and diagnostic study findings# #bdominal test results are pro'ided in 1able.

TEST *lood ?ematocrit 2enal 6unction Serum uric acid

,INDINGS I$8= I&.& mgJdB >>.8 mgJdB (severe pregnancy3induced hypertension (1I?) I1.8 mgJdB .83".8 mgJdB (severe 1I?) K1&8 mBJmin <318 mgJdB 1831> mgJdB (severe 1I?) K188,888 mB (severe 1I?) I1> mgJmB (severe 1I?)

+reatinine +reatinine clearance */A +oagulation 1latelets 6ibrin degradation products

Nursing Management
1. Monitor for+ and promote the resolution of+ complications#

$onitor 'ital signs and FHR. $inimi+e e4ternal stimuli= promote rest and rela4ation. $easure and record urine output- protein le'el- and specific gra'ity. #ssess for edema of face- arms- hands- legs- an2les- and feet. #lso assess for pulmonary edema. !eigh the client daily. #ssess deep tendon refle4es e'ery @ hours. #ssess for placental separation- headache and 'isual disturbance- epigastric painand altered le'el of consciousness.

. Pro"ide treatment as prescribed#

$ild preeclampsia treatment consists of bed rest in left lateral recumbent positionbalanced diet with moderate to high protein and low to moderate sodium- and administration of magnesium sulfate.

;e'ere preeclampsia treatment consist of complete bed rest- balanced diet with high protein and low to moderate sodium- administration of sulfate- fluid and electrolyte replacements- and sedati'e antihypertensi'es- such as dia+epam or ?henobarbitalor an anticon'ulsant such as phenytoin. 7clampsia treatment consists of administration of magnesium sulfate intra'enously.

3. ,nstitute sei ure precautions. ;ei+ures may occur up to > hours after deli'ery. @. Address emotional and psychosocial needs#

"estational Diabetes

Description
1. "estational diabetes is abnormal carbohydrate- fat- and protein metabolism that is first diagnosed during pregnancy- regardless of the se'erity. . "estational diabetes is further classified as6
o

"estational diabetes characteri+ed by an abnormal glucose tolerance test %"11& without other symptoms. Fasting glucose is normal and the diabetes is controlled by diet %#1&. "estational diabetes characteri+ed by abnormal glucose tolerance test and ele'ated fasting glucose. 1his type of gestational diabetes must be controlled by insulin %# &.

3. #bout 19-*** infants are born to mothers with diabetes each year. ;ince 1(<*- the 0nternational !or2shop,Conference on gestational Diabetes and the #merican Diabetic #ssociation has recommended uni'ersal screening for gestational diabetes between @ and < wee2s of gestation.

Etiology

"estational diabetes is a disorder of late pregnancy %typically&- caused by the increased pancreatic stimulation associated with pregnancy.

Pathophysiology
1. 0n gestational diabetes mellitus %type 000- "D$&- insulin antagonism by placental hormones- human placental lactogen- progesterone- cortisol- and prolactin leads to increased blood glucose le'els. 1he effect of these hormones pea2s at about ) wee2s gestation. 1his is called the diabetogenic effect of pregnancy. . 1he pancreatic beta cell functions are impaired in response to the increased pancreatic stimulation and induced insulin resistance. 3. ?regnancy complicated by diabetes puts the mother at increased ris2 for the de'elopment of complications- such as spontaneous abortion- hypertensi'e disorders- and preterm labor- infection- and birth complications. @. 1he effects of diabetes on the fetus include hypoglycemia- hyperglycemia- and 2etoacidosis. Hyperglycemic effects can include6 a. Congenital defects b. $acrosomia c. 0ntrauterine growth restriction d. 0ntrauterine fetal death e. Delayed lung maturity f. Neonatal hypoglycemia g. Neonatal hyperbilirubinemia

Assessment Findings
1. Associated findings include a poor obstetric history- including spontaneous abortions- une4plained stillbirth- une4plained hydramnios- premature birth- low birth weight or birth weight e4ceeding @-*** g %<lb- 13 o+&- and birth of a newborn with congenital anomalies. . Common clinical manifestations include6
o o o o

"lycosuria on two successi'e office 'isits Recurrent monilial 'aginitis $acrosomia of the fetus on ultrasound ?olyhydramnios

*# Laboratory and diagnostic study findings#

o o

Fasting blood sugar test will re'eal ele'ated blood glucose le'els. # 9*,g glucose screen %blood glucose le'el is measured 1 hour after client ingests a 9*,g glucose drin2& re'eals ele'ated blood glucose le'els. 1he normal plasma threshold is 139 to 1@* mgBdD.

# 3, hour oral glucose tolerance test %performed if 9*,g glucose screen results are abnormal& re'eals ele'ated blood glucose le'els. %1able 1& 1he glycosylated hemoglobin %Hb# 1c& test %measures glycemic control in the @ to < wee2s before the test is performed= performed on women with pre, e4isting diabetes& results reflect en+ymatic bonding of glucose to hemoglobin # amino acids. 1his is a useful indicator of o'erall blood glucose control. 1he upper normal le'el of Hb#1c is ): of total hemoglobin. ;creens for fetal %and later- neonatal& complications- including6

$aternal serum alpha,fetoprotein le'el to assess ris2 for neural tube defects in newborn. Altrasonography to detect fetal structural anomalies- macrosomia- and hydramnios. Nonstress test %as early as 3* wee2s&- contraction stress test- and biophysical profile because of ris2 of une4plained intrauterine fetal demise in the antepartum period. Dung maturity studies %by amniocentesis& to determine lecithinsphingomyelin %DB;& ratio and to detect phosphatidylglycerol %?"&= the ade.uacy of DB; and ?"- predictor of the newborns ability to a'oid respiratory distress

Nursing Management
&# Establish an initial database+ and maintain serial documentation of test results throughout the pregnancy# '# Pro"ide client and family teaching#

#ssess the clients understanding of "D$ and its implications for daily life. #s needed- e4plain the effects of gestational diabetes on the mother and fetus. ?oint out the need for fre.uent laboratory testing and follow,up for mother and fetus- for e4ample- to pre'ent infection and assess other potential complications. Discuss and demonstrate insulin self,in5ection

-able & Normal Glucose -olerance -est .alues

TEST TIMING 6asting 1 hr hr " hr

VENOUS PLASMA K18& mgJdB K1L8 mgJdB K1>& mgJdB K1$& mgJdB

6HOLE BLOOD KL8 mgJdB K1M8 mgJdB K1$& mgJdB K1 & mgJdB

PREGNANT 18& mgJdB 1L8 mgJdB 1>& mgJdB 1$& mgJdB

Demonstrate how to self,monitor blood glucose le'el. 74plain that blood is generally tested daily before meals and at bedtime. 74plain the need to test urine for 2etones- which are harmful to the fetus.

?oint out the importance of 2eeping daily records of blood glucose 'alues- insulin dose- dietary inta2e- periods of e4ercise- periods of hypoglycemia- 2ind and amount of treatment- and daily urine test results. Discuss potential complications and their management.
o

Diabetic 2etoacidosis is a multisystem disorder resulting from hyperglycemia in which plasma glucose le'els e4ceed 39* mgBdD. %1able 3& Hypoglycemia is a disorder caused by too much insulin- insufficient foode4cess e4ercise- diarrhea- or 'omiting. Client and Family 1eaching 1able @ list signs and symptoms of hypoglycemia and hyperglycemia.

%a& Discuss the management of hypoglycemia by administering 1 fluid o+ of orange 5uice %or * g of carbohydrates& and waiting * minutes before repeating the procedure. %b& Report the episode to the health care pro'ider as soon as possible.

74plain the need for continued e'aluation during the postpartum period until blood glucose le'els are within normal limits.

3. Arrange for the client to consult )ith a dietitian to discuss the prescribed diabetic diet and to ensure ade/uate caloric inta0e %1able & -able ' Generally recommended Caloric ,nta0e for Pregnant Diabetic (omen

CATEGORY %dult %dolescent /nder)eight ;bese

7CAL8LB PER DAY 1>.$ 8.& .M 1".>

TOTAL GAIN $3"8 lb "8 lb "8 lb 8 lb

@. Address emotional and psychosocial needs# 0nter'ene appropriately to allay an4iety regarding diabetes and childbirth. 9. Prepare the client for intensi"e fre/uent intrapartum assessment+ )hich may include1

Fetal monitoring 0ntra'enous infusion of glucose- insulin- and o4ytocin 7'aluation for diabetic 2etoacidosis %signs and symptoms include altered le'el of consciousness- labored breath sounds- fruity breath odor- and 2etonuria& 0ntra'enous fluid and electrolyte replacement therapy 0n'asi'e maternal cardiac monitoring

). ,dentify and ma0e referral to support groups and resources a"ailable to the client and family#

-able * Laboratory .alues in Diabetic 2etoacidosis 3D2A4

DEGREE O, D7A 0ild 0oderate Severe

TOTAL CO 13 <mE-JB 113 8 mE-JB K18 mE-JB

pH IM."8 M.183M."8 KM.18

-able 5 Client and Family -eaching

HYPOGLYCEMIA

HYPERGLYCEMIA

Sha5iness, di((iness S)eating 1allor, cold, clammy s5in !isorientation, irritability ?eadache ?unger *lurred vision Aervousness 'ea5ness, fatigue Shallo) respirations, but normal pulse rate /rine negative for glucose and acetone *lood glucose level belo) >8 mgJdB

6atigue 6lushed, hot s5in !ry mouth, excessive thirst 6re-uent urination 2apid, deep respirations, fruity odor !epressed reflexes !ro)siness, headache

0nfections during ?regnancy

Description
1. $aternal infections during pregnancy may contribute significantly to fetal morbidity and mortality. . 1wo of the most common groups of infections present during pregnancy are se4ually transmitted infections and 1/RCH infections. ;e4ually transmitted infections include6 1. Chlamydia

. "onorrhea 3. "roup B streptococcus @. Hepatitis B 9. Human papilloma'irus ). ;yphilis >. 1richomonas <. Candidiasis (. Bacterial 'aginosis 1*. Human immunodeficiency 'irus %H08& 1/RCH infections include6 1. 1o4oplasmosis . /ther infections, hepatitis #- infectious hepatitis- hepatitis C- or syphilis 3. Rubella @. Cytomegalo'irus 9. Herpes simple4 'irus

Etiology
1. 0nfections in this category may be caused by 'arious 'iruses. /ther organisms such as bacteria- spirochetes- proto+oa- or yeast also may cause maternal infectionswhich are harmful to the de'eloping fetus. 7'en though the infection in the mother may be 'ery mild- the effects on the fetus can be catastrophic. . 1he infections organism may be ac.uired during se4ual intercourse- through the use of contaminated articles- such as needles= from human body fluids %semen- sali'ablood- urine- cer'ical mucus- breast mil2- and stool&= by eating undercoo2ed meat= or by contact with infected cat feces in the litter bo4- sand bo4- or garden soil. 3. $ost organisms cross the placenta and infect the fetus- causing birth anomalies. 1he fetus may also ac.uire the organism as it tra'els the birth canal during laborcausing illness after birth.

Pathophysiology
1. 1hese infections organisms are capable of crossing the placenta and ad'ersely affecting the de'elopment of the fetus. ;pontaneous abortion or fetal newborn abnormalities may occur. . 0n some instances- the infection can also cause infertility or sterility in the mother.

Assessment Findings For 6e7ually -ransmitted Diseases

1. Associated findings a. ?re'ious history of se4ually transmitted disease or pel'ic inflammatory disease. b. Numerous se4ual partners c. Ase of intra'enous drugs or partners who use intra'enous drugs . Common clinical manifestations a. ?R/$ b. ?reterm birth c. ;ystemic fetal infection 3. Laboratory and diagnostic study findings. ;erologic and culture testing will re'eal infection.

Assessment Findings For -orch ,nfections

1. Common clinical manifestations a. 0nfluen+a,type symptoms b. Rash c. Dymphedema and lymphadenopathy . Laboratory and diagnostic study findings. ;erologic and culture testing will re'eal infection.

,mplementation
1. Carefully screen for infections during pregnancy and treat possible infections as ordered#

#t the first prenatal 'isit- the pregnant woman should ha'e a rubella titer drawn. # titer of 16< pro'ides e'idence of immunity. 0f the titer is below 16<- rubella 'accine is offered to the woman before discharge postpartum. 1hose women who re.uire the 'accine should be cautioned not to become pregnant for at least 3 months afterward. Cytomegalo'irus currently has no effecti'e therapy. 1his is important to remember because the highest rate of maternal infections occurs between the ages of 19 and 39. Asually- the infection is symptomatic. !omen who are presumed to be susceptible to 'aricella,+oster %chic2en,po4& should ha'e immune testing. 8aricella,+oster immune globulin should be administered to those who are susceptible or who ha'e been e4posed. 8aricella,+oster immune globulin should be administered to the e4posed newborn within > hours of their birth. #ll pregnant women should be screened for Hbs#g- the hepatitis B surface antigen. 1he hepatitis B immune globulin can pre'ent infection in both mother and newborn. #n initial in5ection can be gi'en to the newborn- followed by doses gi'en at 1 month

and ) months of age. #dults recei'e three in5ections that are gi'en o'er a ), to 1 , month period. . Pro"ide client and family teaching regarding the diagnosis of infection to promote compliance with the treatment plan.

74plain how maternal infections are ac.uired and transmitted to the de'eloping fetus during pregnancy. Demonstrate proper handwashing techni.ue- stressing that it is the single most successful means of pre'enting infection. Discuss hygienic and dietary measures that reduce the ris2 of infection. 74plain the organism- test- treatment- and fetal effects of the specific infection to the client and family. 0nclude the client in planning solutions for possible fetal effects. Discuss Fsafe se4G with the client and partner. ;ee2 the couples input for de'elopment of a plan for follow,up care.

Arinary 1ract 0nfection in ?ostpartum !omen

Description
1. # A10 is indicated by more than 1*9 bacterial coloniesBmD of urine in two consecuti'e clan- 'oided- mistream specimens. . 1wo common types of A10s are cystitis- inflammation of the urinary bladder- and pyelonephritis- inflammation of the renal pel'is. 3. A10s occur in about 9: of postpartum women= they occur in 19: of women who ha'e undergone postpartum catheteri+ation.

Etiology
1. #scending bacterial infections account for most A10s. . #nother cause of A10s is retention and residual urine due to o'erdistention and incomplete emptying of the bladder.

1emporary urine retention may be due to decreased perception of the urge to 'oidresulting from perineal trauma and the effects of analgesia- or anesthesia. Arinary stasis and residual urine pro'ide a medium for bacterial growthpredisposing the client to cystitis and pyelonephritis.

Pathophysiology
1. Causati'e organisms in cystitis and pyelonephritis include 7. coli %most common&?roteus- ?seudomonas- ;. aureus- and ;treptococcocus faecalis. . Conse.uences of not recogni+ing early symptoms of A10 include the e4tension of the infection upward with subse.uent permanent loss of 2idney function.

Assessment Findings
Clinical manifestations depend on the type of infection. 1. Clinical manifestations include fre.uency- urgency- dysuria- hematuria- nocturiatemperature ele'ation- and suprapubic pain. . ?yelonephritis manifestations include high fe'er- chills- flan2 pain- nausea- and 'omiting.

Nursing Management
Recogni+e signs of infection and pre'ent the de'elopment of further complications. 1. Determine if symptoms are present and if the woman had difficulty urinating after deli'ery. . /btain specimens- report findings- and administer antibiotics and medications as prescribed.

3. Describe self,care related to regular emptying of bladder- proper perineal cleansingand the need for increased fluids. @. 0nsert intermittent or indwelling catheter as needed. 9. /bser'e and record the response to treatment.