Thrombocytopenia in Pregnancy J Am Board Fam Pract: First Published As on 1 July 2002

CLINICAL REVIEW Thrombocytopenia in Pregnancy J Am Board Fam Pract: first published as on 1 July 2002. Downloaded from

Jeffrey A. Levy, CPT, MC, FS, and Lance D. Murphy, MD

Background: Thrombocytopenia, deﬁned as a platelet count of less than 150,000/␮L, has been more commonly diagnosed in pregnant women in the last 20 years because platelet counts are included with the automated blood cell counters. Evaluation and treatment of this condition can be expensive and invasive and can result in an adverse outcome. Methods: MEDLINE was searched from 1980 to present using the key words. “thrombocytopenia,” “pregnancy,” and “platelet.” Case reports were excluded from literature review. Results and Conclusions: Thrombocytopenia is the second most common hematologic abnormality during pregnancy and is usually a benign condition. Some patients, however, will have chronic medical disorders or pregnancy-induced conditions that require further evaluation and therapy. Even with its wide differential diagnosis, the cause of thrombocytopenia during pregnancy can usually be determined with a thorough history, physical examination, and directed laboratory studies. The challenge to the clinician is to weigh the risks of maternal and fetal bleeding complications against the beneﬁts of diag- nostic tests and interventions. (J Am Board Fam Pract 2002;15:290–7.)

Thrombocytopenia is classically deﬁned as a plate- rather than vaginal delivery, has not improved let count of less than 150,000/␮L.1,2 Counts from outcome. Health care providers must weigh the 100,000 to 150,000/␮L are considered mildly de- beneﬁts of interventions in relation to cost and pressed, 50,000 to 100,000/␮L are moderately morbidity against the risk of maternal and fetal depressed, and less than 50,000/␮L are severely bleeding complications. http://www.jabfm.org/ 3 depressed. Use of automated blood counters in The overall incidence of thrombocytopenia in routine prenatal screening has resulted in an in- pregnancy is 8%, but when patients with obstetric creased diagnosis. Thrombocytopenia is second or medical conditions are excluded, the incidence only to anemia as the most common hematologic drops to 5.1%.4 The most common cause is ges- 4 abnormality during pregnancy. Some causes are tational thrombocytopenia (Table 1),1 which unique to pregnancy, whereas others can be serious accounts for almost three fourths of all cases. Hy- on 27 September 2021 by guest. Protected copyright. medical conditions that have been previously undi- pertensive disorders account for 21%.1 Thrombo- agnosed. cytopenia occurs more commonly in patients with The increased recognition of maternal and fetal eclampsia (30%) than in patients with both mild thrombocytopenia has resulted in controversies re- and severe forms of preeclampsia (15%–18%).4 Of garding management. In fact, screening at all for the patients who have severe preeclampsia, 4% to thrombocytopenia is an issue, because the reason 12% will manifest criteria for HELLP syndrome for this common condition usually is benign. Per- (hemolysis, elevated liver enzymes, and low platelet forming studies on both the mother and the fetus counts).4 Immune-mediated thrombocytopenia, in- can cause considerable morbidity and mortality, cluding idiopathic thrombocytopenia purpura and and the mode of delivery, eg, cesarean section neonatal alloimmune thrombocytopenia, is respon- sible for 4.1% of cases,1 which is a proportionally Submitted, revised, 7 November 2001. small number. These conditions, however, can From the United States Army Health Clinic (JAL), Fried- berg, Germany; the Department of Obstetrics and Gynecol- cause considerable morbidity and mortality and ogy (LDM), DeWitt Army Family Practice Residency, Fort must be managed closely. Other, less common Belvoir, VA, and the Division of Obstetrics and Gynecology (LDM), Uniformed Services University of Health Sciences, causes include rheumatologic disease (eg, systemic Bethesda, Md. Address reprint requests to Jeffrey A. Levy, lupus erythematosus), disseminated intravascular DO, CPT, MC, DeWitt Family Practice Residency, De- Witt Army Community Hospital, 9501 Farrell Rd, Fort coagulation, thrombotic thrombocytopenia pur- Belvoir, VA 22060. pura, fatty liver, antiphospholipid syndrome, hu-

290 JABFP July–August 2002 Vol. 15 No. 4 Table 1. Cause of Thrombocytopenia During Table 2. Medications Associated with Pregnancy. Thrombocytopenia. J Am Board Fam Pract: first published as on 1 July 2002. Downloaded from Gestational thrombocytopenia Class Medication Pregnancy-induced hypertension HELLP (hemolysis, elevated liver enzymes, and low platelets) Antibiotics Ampicillin syndrome Penicillin Rifampin Spurious thrombocytopenia Human immunodeficiency virus (HIV) infection Diuretics Thiazides Immune thrombocytopenic purpura Furosemide Systemic lupus erythematosus Analgesics Aspirin Antiphospholipid syndrome Acetaminophen Hypersplenism Indocin Disseminated intravascular coagulation Anticonvulsants Phenytoin Thrombotic thrombocytopenic purpura Valproic Acid Hemolytic uremic syndrome Carbamazepine Congenital thrombocytopenia Miscellaneous Methyldopa Medication Heparin Folate deficiency Digitalis Ranitidine Primary bone marrow dysfunction: Cimetidine Leukemia Procainamide Aplastic anemia Gold compounds Cis-platinum Cyclosporin man immunodeficiency virus (HIV) infection, and medications (Table 2).1 history of bleeding complications and have thrombocytopenia on a prepregnancy platelet count.

The cause of gestational thrombocytopenia is http://www.jabfm.org/ Methods unclear, although it might be secondary to an ac- MEDLINE was searched from 1980 to the present, celerated platelet consumption and the increased using the key words “thrombocytopenia,” “preg- plasma volume associated with pregnancy.5 Anti- nancy,” and “platelet.” Case reports were excluded platelet antibodies have been detected in the serum, from the literature review. but this finding does not differentiate it from idiopathic thrombocytopenia purpura, and the pres- on 27 September 2021 by guest. Protected copyright. ence of antiplatelet antibodies is not specific for Major Causes gestational thrombocytopenia. Gestational Thrombocytopenia Gestational thrombocytopenia essentially poses Gestational thrombocytopenia is a diagnosis of ex- no risk to either the mother or fetus-neonate. A clusion, and the following five characteristics make prospective cohort study by Burrows and Kelton6 it more likely: (1) the degree of thrombocytopenia of 756 women with a diagnosis of gestational is usually mild to moderate, usually remaining thrombocytopenia showed that none of the moth- greater than 70,000 ␮L (however, the lower level ers and only 1 infant, which had congenital bone has never been established); (2) patients are asymp- marrow dysfunction diagnosed later, had any tomatic with no history of bleeding; (3) there is no bleeding complication. In another study by Nagey preconception history of thrombocytopenia; (4) an et al7 of 730 pregnancies with platelet counts of less early gestation or preconception platelet count is than 150,000/␮L, no neonate had a platelet count normal; and (5) the platelet count returns to normal of less than 100,000 ␮L, and no bleeding compli- within 2 to 12 weeks postpartum.5 The early ges- cations were observed. Thus, it appears that mildly tation or preconception platelet count becomes ex- to moderately depressed platelet counts from ges- tremely important when differentiating this disor- tational thrombocytopenia are not associated with der from idiopathic thrombocytopenia purpura, any adverse effects to either the fetus, neonate, or with which it is commonly confused. Women with mother, and no management is necessary other idiopathic thrombocytopenia purpura often have a than periodic monitoring.

Thrombocytopenia in Pregnancy 291 Pregnancy-Induced Hypertension second to third decades of life, accounts for 3% of The thrombocytopenia in pregnancy-induced hy- all cases of thrombocytopenia during pregnancy.1,6 J Am Board Fam Pract: first published as on 1 July 2002. Downloaded from pertension is moderate, and the platelets rarely Immune thrombocytopenic purpura is an auto- drop below 20,000/␮L.5 Hemorrhage is an uncom- immune disorder in which patients produce IgG mon event unless the patient develops disseminated antiplatelet antibodies to their own platelet mem- intravascular coagulation, but thrombocytopenia brane glycoproteins. Increased platelet destruction can be a sign of worsening hypertensive disease. A occurs in the reticuloendothelial system, primarily slowly decreasing platelet count can be noted be- the spleen. The rate of platelet loss is greater than fore the clinical manifestations of pregnancy- production, and thrombocytopenia ensues. induced hypertension. When accompanied by Recent advances have produced antigen capture microangiopathic hemolytic anemia, hemolysis, el- assays for platelet glycoproteins that help provide a evated liver enzymes, and low platelets, HELLP definitive diagnosis of immune thrombocytopenic syndrome is diagnosed. purpura in approximately two thirds of cases.8 Im- The causes of thrombocytopenia from preg- mune thrombocytopenic purpura has traditionally nancy-induced hypertension and HELLP syn- been a diagnosis of exclusion, however, and these drome are unknown. One explanation is that it studies are usually not necessary if a complete his- might be related to abnormal vascular tone with tory, physical examination, and early platelet count resultant accelerated platelet destruction, platelet 5 are obtained. Many women already have a history activation, and coagulation defects. The increased of immune thrombocytopenic purpura before be- levels of platelet-associated immunoglobulin G coming pregnant, and the early gestation platelet (IgG) that have been detected in patients with count will help differentiate this disorder from ges- pregnancy-induced hypertension have been shown tational thrombocytopenia. If this count is less than to be nonspecific and do not necessarily imply an 100,000/␮L, immune thrombocytopenic purpura is immunologic basis for the thrombocytopenia.5 likely,5 whereas the platelets in a patient with ges- HELLP syndrome appears to be initiated by mi- tational thrombocytopenia are usually not affected crovascular damage that results in platelet activa- http://www.jabfm.org/ until the second or third trimester. Five character- tion. Degranulation of the platelets is followed by istics of immune thrombocytopenic purpura make vasospasm and further endothelial damage. The the diagnosis likely: (1) moderate thrombocytope- only known therapy for this cycle is delivery of the nia (50,000–100,000/␮L), (2) a preconception or fetus. Patients with disseminated intravascular co- early gestation platelet count that is less than agulation are at risk of catastrophic bleeding com- ␮ plications secondary to rapid consumption of plate- 100,000/ L, (3) normal to increased megakaryo- on 27 September 2021 by guest. Protected copyright. lets and coagulation factors. cyte levels as determined by bone marrow biopsy, Preterm neonates of mothers with pregnancy- (4) exclusion of other systemic disorder or use of induced hypertension are at risk for neonatal drugs that might be associated with decreasing thrombocytopenia and resulting bleeding compli- platelet counts (Table 2), and (5) an absence of 5,8 cations, such as excessive bleeding from blood splenomegaly. draws or circumcision, mucosal bleeds in the gas- Pregnancy does not seem to worsen the course trointestinal tract, cephalohematomas, subgaleal of immune thrombocytopenic purpura, but cases of bleeding, and intracranial hemorrhages. Full-term severe thrombocytopenia can cause serious mor- infants have no specific risk when considering bidity and mortality to the mother and fetus. The bleeding complications but are at an increased risk mother is at risk for spontaneous hemorrhage, par- for intrauterine growth retardation.5 ticularly if the platelet count drops to less than 20,000/␮L. The maternal IgG will cross the placenta and could cause fetal thrombocytopenia. This Immune Thrombocytopenic Purpura condition is manifested by purpura, ecchymosis, Immune thrombocytopenic purpura is an immune- melena, and even intracranial hemorrhage in the mediated process resulting in platelet destruction. neonatal period. A retrospective case series showed It has an acute form, usually affecting children with that 12% to 15% of infants born to women with viral infections, which is self-limited. The chronic immune thrombocytopenic purpura develop plate- form, which predominately affects women in their let counts of less than 50,000/␮L, with 3% having

292 JABFP July–August 2002 Vol. 15 No. 4 major bleeding complications and less than 1% examination (Figure 1) help to narrow the focus having intraventricular hemorrhage.9,10 when determining the cause of maternal thrombo- J Am Board Fam Pract: first published as on 1 July 2002. Downloaded from cytopenia. Questions focusing on the cardinal signs Neonatal Alloimmune Thrombocytopenia and symptoms of pregnancy-induced hypertension Neonatal alloimmune thrombocytopenia results are helpful. Patients with immune thrombocytope- from maternal alloimmunization to fetal platelet nic purpura have a history of easy bruising, gingival antigens. The exact process of sensitization is un- bleeding (often while brushing their teeth), and known, but it is theorized that the maternal im- menometrorrhagia. Patients should also be ques- mune system recognizes as foreign the fetal plate- tioned about possible systemic diseases associated lets that cross the placental barrier.11 The maternal with thrombocytopenia, such as a history consistent immune system produces IgG antiplatelet anti- with systemic lupus erythematosus, antiphospho- bodies to the fetal platelet antigens, particularly lipid syndrome, or possible HIV exposure. Also, PLA1.11 PLA1 is inherited from the father and is certain medications can cause a depressed platelet 4 recognized as foreign by the mother’s immune sys- count (Table 2). Signs of petechia, purpura, ane- tem.11 The IgG antiplatelet antibodies then cross mia, splenomegaly, and joint arthralgias found dur- the placental barrier and cause platelet destruc- ing the physical examination help aid the diagnosis. tion.11 It is the platelet equivalent of red cell he- The laboratory evaluation begins with a com- molytic (Rh) disease of the newborn. It affects ap- plete blood count and peripheral smear. The com- proximately 1 in 1,000 to 2,0004,5,11 live births and plete blood count is done to evaluate all the blood causes serious morbidity and mortality. cell lines. Visualizing the smear is essential to rule One difference between Rh disease and neonatal out spurious thrombocytopenia. Clumping of alloimmune thrombocytopenia is the occurrence in platelets is common and can artificially lower the the first pregnancy. Fifty percent of neonatal allo- total platelet count. Antiplatelet antibodies can be immune thrombocytopenia cases are discovered in measured, but this test does not differentiate ges- the first live-born infant,11 and subsequent preg- tational thrombocytopenia from immune thrombo- http://www.jabfm.org/ nancies are affected in similar to increasing sever- cytopenic purpura, is expensive, and has poor stan- ity. Most cases are diagnosed after delivery. The dardization.12 It is therefore not recommended for maternal history and pregnancy are unremarkable, routine use. and the platelet count is often normal. The gestational age helps in differentiating be- Neonates manifest evidence of severe thrombo- tween diagnoses. A mother in the first or early cytopenia either at delivery or during the first few second trimester who has thrombocytopenia will hours of life. Petechia or ecchymosis appear over have either immune thrombocytopenic purpura or on 27 September 2021 by guest. Protected copyright. the fetal presenting part, their platelet count is gestational thrombocytopenia – although the latter severely depressed, and they have considerable is much more common in later gestation. In gen- bleeding when circumcised or when blood is eral, women with no history of thrombocytopenia, drawn. The most serious complication, intracranial a normal early-gestation platelet count, and mild hemorrhage, occurs in 10% to 20% of all infants thrombocytopenia are likely to have gestational 5 affected and occurs in utero 25% to 50% of the thrombocytopenia. If the platelet count is abnor- 12 time. Ultrasound findings of fetal bleeding com- mal early in gestation and drops to less than plications can be used to differentiate neonatal al- 70,000/mL, immune thrombocytopenic purpura is loimmune thrombocytopenia from immune throm- likely. At levels of less than 50,000/␮L, immune bocytopenic purpura, which occurs during the thrombocytopenic purpura is almost certain.5 If the neonatal period and is associated with maternal patient develops thrombocytopenia late in the thrombocytopenia. Findings on a sonogram can third trimester or during the postpartum period, include intracranial hemorrhage, porencephalic pregnancy-induced hypertension, thrombotic cysts, hydrocephalus, and fetal hydrops.5 thrombocytopenia purpura, hemolytic uremic syndrome, acute fatty liver, and disseminated intra- Workup for Maternal Thrombocytopenia vascular coagulation should be entered into the A detailed medical history (to include family his- differential diagnosis, and the patient should be tory, sexual history, and drug use) and physical appropriately evaluated.

Thrombocytopenia in Pregnancy 293 J Am Board Fam Pract: first published as on 1 July 2002. Downloaded from http://www.jabfm.org/ on 27 September 2021 by guest. Protected copyright.

Figure 1. Evaluation of thrombocytopenia in pregnancy.

Screening for PLA1 antibodies on maternal the disorder recurring, however.11 Strategies for platelets is not recommended as a routine test to screening include determination of maternal rule out neonatal alloimmune thrombocytopenia.12 antiplatelet antibodies, zygosity of the paternal an- Subsequent pregnancies have almost 100% risk of tigens, and determination of the fetal platelet anti-

294 JABFP July–August 2002 Vol. 15 No. 4 gens.5,12 Fetal platelet antigens are fully expressed will usually increase platelet counts within 1 week. by 18 weeks’ gestation, and a percutaneous umbil- After 2 to 3weeks of therapy, the dosage can be ical artery sample can be performed at approxi- tapered by 10% to 20% per week to maintain J Am Board Fam Pract: first published as on 1 July 2002. Downloaded from mately 20 weeks’ gestational age.12 Fetal platelets adequate platelet levels.4,5 Two thirds of patients are counted and antigen assays performed looking respond to this therapy, and one quarter will go for PLA1. Chorionic villous sampling can increase into remission.4,5 fetal platelet sensitization and should not be per- When steroids are not successful, treatment may formed.10 include intravenous immunoglobulin. This therapy is also indicated for patients with platelet counts of less than 10,000/␮L in the third trimester, for pa- Management tients with platelet counts of less than 30,000/␮L Pregnancies with gestational thrombocytopenia are with bleeding complications, or for preoperative not at risk for fetal thrombocytopenia or maternal therapy.5,8 A response usually occurs within 6 to 72 bleeding complications. No intervention, such as a hours, but the platelet count will usually decrease to fetal platelet count or cesarean section, is neces- pretreatment levels within 30 days.8 sary.9 Periodic platelet counts, either once a trimes- Platelet transfusions are only temporizing mea- ter or every month, are recommended5 depending sures in life-threatening hemorrhages or preoper- on the level of thrombocytopenia. atively. The platelets transfused will also be af- Thrombocytopenia secondary to pregnancy- fected by the antiplatelet antibodies and will be induced hypertension or HELLP syndrome is destroyed. If this therapy is undertaken, 6 to 10 treated by delivery of the fetus.13 The underlying units of platelets should be transfused, because the pathophysiologic cause of the disorder is alleviated normal increase expected of 10,000/␮L per unit only after birth. In cases of severe thrombocytope- will not be achieved.5 nia, patients should be stabilized medically, and Splenectomy produces complete remission in preterm infants should be given steroids to treat approximately two thirds of patients, but this pro- fetal lung maturity. Platelet transfusions are less cedure is often difficult to perform during preg- http://www.jabfm.org/ effective in women with severe thrombocytopenia nancy and has serious fetal risks, particularly in the because of the ongoing process of platelet destruc- third trimester.5 Ideally, it should be performed tion.5 Two situations in which additional platelets during the first or second trimesters. It is ap- should be given are (1) to treat severe thrombocy- propriate therapy in patients who have failed topenia with ongoing bleeding, and (2) to increase both steroid and intravenous immunoglobulin the platelet count to more than 50,000/␮L for an therapy.5,8 on 27 September 2021 by guest. Protected copyright. operative delivery.5 The platelet count usually be- Therapy for immune thrombocytopenic pur- gins returning to normal within 72 hours of deliv- pura is often successful in improving the maternal ery.13,14 Therapies of uncertain benefit include platelet count but has been shown to be an unreli- plasmapheresis, steroids, and uterine curettage.5 able indicator of the fetal platelet count.8 To date, Management of patients with immune thrombo- there is insufficient evidence supporting maternal cytopenic purpura should be aimed at minimizing therapy to improve fetal outcome.8 bleeding complications associated with severe Patients with immune thrombocytopenic pur- thrombocytopenia. Because the platelets function pura require special considerations during their normally, however, it is not necessary to maintain prenatal care. Patients should avoid nonsteroidal a normal count. Most authorities agree that anti-inflammatory agents, aspirin, and trauma.5 If a 50,000/␮L is the cutoff point for therapy in asymp- splenectomy is performed, they should be immu- tomatic patients.5,8 Of course, patients with counts nized against Haemophilus influenzae, pneumococ- greater than 50,000/␮L and bleeding complications cus, and meningococcus.8 require treatment. Operative deliveries, regional The risk to the fetus, as previously discussed, anesthesia, or other invasive procedures increase results from maternal antiplatelet antibodies cross- the risk of hemorrhage, and platelet counts of ing the placenta and affecting the fetal platelets. greater than 50,000/␮L are usually recommended.5,8 Bleeding complications in a full-term fetus, partic- Initial therapy for immune thrombocytopenic ularly intracranial hemorrhage, are an uncommon purpura is prednisone, 1–2 mg/kg/d.4,5 This dosage but serious risk. Evaluation of the fetal platelet

Thrombocytopenia in Pregnancy 295 count is controversial. The maternal course corre- been shown to be effective, but no additional ben- lates poorly with fetal well-being. Maternal sero- efit is noted if given to the fetus. The platelets for logic findings, history of splenectomy, platelet fetal transfusion are maternal, which could worsen J Am Board Fam Pract: first published as on 1 July 2002. Downloaded from count, and presence of antiplatelet antibodies do the alloimmunization, and a transfusion will need not provide an accurate assessment for the fetal to be repeated every week as a result of their short risks of bleeding.5,8 Scalp sampling is often inaccu- half-life. If the count is greater than 50,000/␮L, a rate and can produce a serious bleeding complica- trial of labor may be undertaken.5,10,16,17 For severe tion by itself.5 Cordocentesis carries a 1% to 2% thrombocytopenia, a cesarean section is usually risk of emergency cesarean delivery.5 With the low performed, although this has never been shown to risk of intracranial hemorrhage in a full-term fetus decrease the rate of intracranial hemorrhage.5 and lack of evidence supporting an operative delivery, fetal evaluation of platelet counts is unwar- Summary ranted in cases of maternal immune thrombocyto- 5 Pregnancy complicated with thrombocytopenia is a penic purpura. challenge to the clinician. The myriad of disease In the past, it has been common practice to processes, either pregnancy-induced disorders or perform cesarean sections on mothers with this preconception medical conditions, can cloud the disorder to lessen the risk of intracranial hemor- correct diagnosis. It is important to remember rhage possibly caused by vaginal deliveries. It has the great majority of patients will have a benign also been postulated that fetal platelet counts of less condition, but a minority of patients who have a ␮ than 50,000/ L place the fetus at greater risk of more serious disease are at risk for serious morbid- intracranial hemorrhage, and cesarean delivery 4 ity and mortality. With a thorough history, physical should be considered. Cesarean delivery, however, examination, focused laboratory evaluation, and ap- has not proved to decrease the incidence of intra- propriate consultation with obstetricians and he- ventricular hemorrhage in either situation, and the matologists, these patients uniformly have favor- mode of delivery should not be influenced based on able outcomes and can be safely managed by family

8 http://www.jabfm.org/ either ﬁnding. In a study of 474 neonates of moth- physicians. ers with immune thrombocytopenic purpura, 29% of vaginal and 30% of cesarean section births had a References bleeding complication.15 Additionally, 4% and 3% 1. Shehata N, Burrows R, Kelton JG. Gestational of vaginal and cesarean births, respectively, had 14 thrombocytopenia. Clin Obstet Gynecol 1999;42: immune thrombocytopenic purpura. It is also 327–34. well documented that platelet counts in neonates 2. Burrows RF, Kelton JG. Thrombocytopenia at de- on 27 September 2021 by guest. Protected copyright. decrease during the ﬁrst few days postpartum. This livery: a prospective survey of 6,715 deliveries. Am J decrease could precipitate serious bleeding compli- Obstet Gynecol 1990;162:731–4. cations unrelated to the mode of delivery. It is 3. Magann EF, Martin JN Jr. Twelve steps to optimal therefore recommended that the mode of delivery management of HELLP syndrome. Clin Obstet Gy- be determined by obstetric indications.11 Neonates necol 1999;42:532–50. from mothers with immune thrombocytopenic 4. Sullivan CA, Martin JN Jr. Management of the obstetric patient with thrombocytopenia. Clin Obstet purpura do require postpartum serial monitoring of Gynecol 1995;38:521–34. their platelet count. 5. Silver R, Berkowitz R, Bussel J. Thrombocytopenia Treatment of neonatal alloimmune thrombocy- in pregnancy. Practice bulletin, No 6. Chicago: topenia during pregnancy focuses on preventing American College of Obstetrics and Gynecology, intracranial hemorrhage and its complications. Be- 1999. cause of the high risk of complications during ges- 6. Burrows RF, Kelton GJ. Fetal thrombocytopenia tation, it is imperative to initiate treatment as soon and its relation to maternal thrombocytopenia. as the diagnosis is made. Treatment is aimed at N Engl J Med 1993;329:1463–6. fetuses who test positive for PLA1 antigen or 7. Nagey DS, Alger LS, Edelmann BB, Heyman MR, 5 Pupkin MU, Crenshaw C Jr. Reacting appropriately whose father is homozygous for the antigen. In- to thrombocytopenia in pregnancy. South Med J travenous immunoglobulin with steroids and fetal 1986;79:1385–8. platelet transfusions are the standard therapy. In- 8. Johnson JR, Samuels P. Review of autoimmune travenous immunoglobulin given to the mother has thrombocytopenia: pathogenesis, diagnosis, and

296 JABFP July–August 2002 Vol. 15 No. 4 management in pregnancy. Clin Obstet Gynecol 12. Skupski DW, Bussel JB. Alloimmune thrombocyto- 1999;42:317–26. penia. Clin Obstet Gynecol 1999;42:335–48.

9. Silver RM, Branch DW, Scott JR. Maternal throm- 13. Padden MO. HELLP syndrome: recognition and J Am Board Fam Pract: first published as on 1 July 2002. Downloaded from bocytopenia in pregnancy: time for a reassessment. perinatal management. Am Fam Physician 1999;60: Am J Obstet Gynecol 1995;173:479–82. 829–36, 839. 10. Payne SD, Resnik R, Moore TR, Hedriana HL, 14. Egerman RS, Sibai BM. HELLP syndrome. Clin Kelly TF. Maternal characteristics and risk of severe Obstet Gynecol 1999;42:381–9. neonatal thrombocytopenia and intracranial hemor- 15. Cook RL, Miller RC, Katz VL, Cefalo RC. Immune rhage in pregnancies complicated by autoimmune thrombocytopenic purpura in pregnancy: a reap- thrombocytopenia. Am J Obstet Gynecol 1997;177: praisal of management. Obstet Gynecol 1991;78: 149–55. 578–83. 11. Letsky EA, Greaves M. Guidelines on the investiga- 16. Carloss HW, McMillan R, Crosby WH. Manage- tion and management of thrombocytopenia in preg- ment of pregnancy in women with immune throm- nancy and neonatal alloimmune thrombocytopenia. bocytopenic purpura. JAMA 1980;244:2756–8. Maternal and Neonatal Haemostasis Working Party 17. Burrows RF, Kelton JG. Pregnancy in patients with of the Haemostasis and Thrombosis Task Force of idiopathic thrombocytopenic purpura: assessing the the British Society for Haematology. Br J Haematol risk for the infant at delivery. Obstetric Gynecol 1996;95:21–6. Surv 1993;48:781–8. http://www.jabfm.org/ on 27 September 2021 by guest. Protected copyright.

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