HEMATOLOGIC DISEASES IN PREGNANCY

Thrombocytopenia in pregnancy: is this immune

thrombocytopenia or?
Terry B. Gernsheimer1,2
1Puget

Sound Blood Center, Seattle, WA, and 2University of Washington, Seattle, WA

Thrombocytopenia is a common finding in pregnancy. Establishing the diagnosis of immune thrombocytopenia (ITP) in
a pregnant patient is similar to doing so in a nonpregnant patient, except that the evaluation must specifically rule out
other disorders of pregnancy associated with low platelet counts that present different risks to the mother and fetus
and may require alternate distinct therapy. Many of the same treatment modalities are used to manage the pregnant
patient with ITP, but others have not been determined to be safe for the fetus, are limited to a particular gestational
period, or side effects may be more problematic during pregnancy. The therapeutic objective differs from that in
chronic ITP in the adult because many pregnant patients recover or improve spontaneously after delivery and therefore
maintenance of a safe platelet count, rather than prolonged remission, is the goal. Thrombocytopenia may the limit
choices of anesthesia, but does not guide mode of delivery, and the fetus is rarely severely affected at birth. Patients
should be advised that a history of ITP or ITP in a previous pregnancy is not a contraindication to future pregnancies
and that, with proper management and monitoring, positive outcomes can be expected in the majority of patients.

Scope of the problem

Table 1. Causes of thrombocytopenia in pregnancy

Thrombocytopenia is a very common finding in pregnancy, occurring in approximately 10% of women.1,2 Although most women
maintain a normal platelet count throughout gestation, the normal
range of platelet counts decreases, and it is not uncommon for the
platelet count to decrease as pregnancy progresses. Most low
platelet counts observed in the pregnant patient are due to normal
physiologic changes,3 whereas some disorders associated with
thrombocytopenia occur with higher frequency and some causes are
exclusive to pregnancy.4 When considering the diagnosis of immune thrombocytopenia (ITP) in pregnancy, all potential causes of
thrombocytopenia must be considered and ruled out in turn.

Gestational (incidental) thrombocytopenia

Preeclampsia
HELLP syndrome
Acute fatty liver of pregnancy
Thrombotic thrombocytopenic purpura
Hemolytic uremic syndrome
Systemic lupus erythematosus
Antiphospholipid Ab syndrome
Disseminated intravascular coagulation
Viral infection
Nutritional deficiency
Drug use
Primary BM disorder

Differential diagnosis of thrombocytopenia during

pregnancy

Gestational thrombocytopenia
Incidental or gestational thrombocytopenia is the most common
cause of pregnancy-associated thrombocytopenia, accounting for
65%-80% of cases.1,4 Increased blood volume, an increase in
platelet activation, and increased platelet clearance contribute to a
physiologic decrease in the platelet count.3 Platelet counts are
slightly lower in women with twin compared with singleton
pregnancies, possibly due to increased coagulation system activation in the placenta. These changes generally bring about only a
mild decrease in the platelet count, typically approximately 10%.5
The mean platelet count in pregnant women at term was found to be
213 000/L compared with 248 000/L in age-matched controls.1,6
Gestational thrombocytopenia tends to occur late, usually during the
third trimester,7 but it should be noted that thrombocytopenia that
appears during the last weeks of pregnancy can be the harbinger of
HELLP syndrome (hemolysis, elevated liver function tests, low
platelets) or acute fatty liver.8 Platelet counts 70 000-80 000/L
or occurring during the first or early in the second trimester suggest
an etiology other than gestational thrombocytopenia and require
further evaluation.9

198

Gestational thrombocytopenia is not associated with adverse outcomes to the mother or fetus, and if the infant is thrombocytopenic,
other etiologies such as infection and neonatal alloimmune thrombocytopenia should be investigated.4 Thrombocytopenia in the mother
generally resolves quickly after delivery, usually within days and
always within weeks.

Disorders associated with thrombocytopenia in

pregnancy
Many disorders are exacerbated by pregnancy or may be quiescent
until the immunologic stimulation that occurs with pregnancy
provokes their recrudescence (Table 1). Autoimmune disorders
such as systemic lupus erythematosus may first appear or increase in
severity during pregnancy, and hypothyroidism may first manifest
during gestation. The antiphospholipid Ab syndrome, which is
accompanied by thrombocytopenia in approximately 10%-30% of
cases,10 must be considered because of its association with fetal loss
and the need for anticoagulation.11
Thrombocytopenia first noted in the second or third trimester
requires evaluation. Disorders that may first manifest at that time

American Society of Hematology

include preeclampsia, HELLP syndrome, acute fatty liver, disseminated intravascular coagulation, thrombotic thrombocytopenic purpura, and hemolytic uremic syndrome. The abnormal clinical and
laboratory findings that accompany these nutritional and BM
disorders are the basis for distinguishing them from ITP. Careful
review of the blood smear will help to exclude the thrombotic
microangiopathies associated with pregnancy (ie, HELLP syndrome, thrombotic thrombocytopenic purpura, and hemolytic uremic syndrome) by the absence of schistocytes. Normal coagulation
studies will be helpful in excluding acute fatty liver and disseminated intravascular coagulation.
Thrombocytopenia may be the primary manifestation of viral
infections such as HIV, viral hepatitis, EBV, and CMV. Thrombocytopenia is also a common adverse reaction from many drugs and
supplements. Women who receive low-molecular-weight or unfractionated heparin are at risk of heparin-induced thrombocytopenia
and should undergo testing, particularly in the presence of new or
worsening thrombosis.

Evaluation of the pregnant patient with thrombocytopenia

The history and physical examination are important in providing
clues to the diagnosis of thrombocytopenia in pregnancy, either by
disclosure of preexisting thrombocytopenia or bleeding symptoms
or by clinical findings of hypertension, edema, neurologic abnormalities, or signs of autoimmune disease. ITP diagnosed during pregnancy is usually relatively asymptomatic, and manifests in only
mild symptoms and physical signs.12,13 Changes associated with a
procoagulant state in pregnancyincreased levels of fibrinogen,
factor VIII, and VWF; suppressed fibrinolysis; and decreased
protein S activitymay explain in part why severe bleeding is only
rarely seen in the pregnant patient with ITP.14 Although fatigue is a
common symptom during pregnancy, other constitutional symptoms such a weight loss or drenching night sweats may signal
etiologies of greater concern.
Medical history may be helpful in elucidating associated disorders
such as thyroid disease or other autoimmune disorders. Frequent
childhood infections may suggest an immune deficiency syndrome
that can be associated with ITP.15 It is important to ascertain all drug
and toxin exposures, including over-the-counter remedies and
supplements. The nutritional history or a history suggestive of
malabsorption may be helpful in the discovery of deficiencies that
can manifest with thrombocytopenia. A family history of thrombocytopenia must also be investigated so that congenital thrombocytopenia is not mistaken for an acquired disorder.

Laboratory investigation of thrombocytopenia in

pregnancy
A complete blood count and review of the peripheral blood smear
is mandatory in the evaluation of the thrombocytopenic patient
(Table 2). Occasional large platelets may be seen in ITP, but they
should otherwise appear normal. The presence of large and/or
hypogranular platelets may suggest a congenital thrombocytopenia.
Morphologic RBC abnormalities such as schistocytes, target cells,
macrocytosis, or spherocytes may be clues to thrombotic microangiopathy, liver disease, nutritional deficiency, or autoimmune
hemolysis. By definition, thrombocytopenia is an isolated hematologic abnormality in ITP, but anemia of pregnancy or anemia
associated with chronic bleeding and iron deficiency may also be
present. A direct antiglobulin test or Coombs test is necessary to rule
out complicating autoimmune hemolysis (Evans syndrome). Screen-

Hematology 2012

Table 2. Recommended testing in the differential diagnosis of

thrombocytopenia in pregnancy
Peripheral blood smear review
Reticulocyte count
Direct antiglobulin test
Coagulation screening
Liver function tests
Lupus anticoagulant, cardiolipin, and -2-glycoprotein IgG and
IgM Abs
Systemic lupus erythematosus serology
Thyroid function tests
Viral screening (HIV, HBV, HCV, and CMV)
Consider testing
Quantitative Igs
Not routinely recommended:
Antiplatelet Ab testing
BM examination
HBV indicates hepatitis B virus; and HCV, hepatitis C virus.

ing for coagulation abnormalities (ie, with prothrombin time,

activated partial thromboplastin time, and fibrinogen time), liver
function (ie, tests for bilirubin, albumin, total protein, transferases,
and alkaline phosphatase), antiphospholipid Abs, and lupus anticoagulant and serology may all be helpful in differentiating ITP
from other disorders with associated low platelet counts. Viral
screening (ie, for HIV, hepatitis C virus, and hepatitis B virus), as in
the evaluation of nonpregnant patients with ITP,16 is recommended.
A careful assessment of thyroid function is indicated because
abnormalities are common in both ITP and pregnancy. Thyroid
disorders are associated with significant pregnancy-related complications and with significant fetal risk, and the associated thrombocytopenia frequently responds to therapy. If the medical history
suggests frequent infections, quantitative Ig testing may be appropriate. A review of preexisting laboratory data may reveal abnormalities that preceded the pregnancy or were present only during a
prior pregnancy.
Only rarely is BM examination necessary for the finding of
thrombocytopenia in a pregnant patient, and it is not required to
make the diagnosis of ITP. As in the nonpregnant patient, the
measurement of antiplatelet Abs has no value in the routine
diagnosis of ITP in pregnancy, is not predictive of neonatal
thrombocytopenia, nor is it specific.17 Women with gestational
thrombocytopenia cannot be distinguished from women with ITP
based on detection of antiplatelet Abs, suggesting either that some
cases thought to be physiologic gestational thrombocytopenia are
actually due to immune destruction playing a role or may be an
unmasking of previously compensated ITP.

Presentation of ITP during pregnancy

ITP occurs in approximately 2 of 1000 pregnant women.18 ITP may
develop at any time during pregnancy, but is often initially
recognized in the first trimester and is the most common cause of
isolated thrombocytopenia in this time period. In some cases, ITP
presents for the first time during pregnancy, whereas preexisting
cases of ITP may either worsen or remain quiescent.19,20 A review of
the clinical courses of 92 women with ITP during 119 pregnancies
over an 11-year period found that women with previously diagnosed
ITP were less likely to require therapy for ITP than those with newly
diagnosed ITP,11 but the course varies widely.

199

Okay, I think its ITP: now what?

Management of ITP during gestation

ITP in the first and second trimesters is generally treated when the
patient is symptomatic with bleeding, platelet counts are in the
20-30 000/L range, or a planned procedure requires a higher
platelet count. In a retrospective analysis of 119 pregnancies in ITP
patients, Webert et al found that only 89% of patients had platelet
counts 150 000/L.11 Most patients had only mild to moderate
thrombocytopenia and the pregnancies were uneventful, but 31%
required intervention to increase the platelet count. Despite remaining relatively stable through most of the pregnancy, platelet counts
may decrease during the third trimester and monitoring should be
more frequent.15 Therapy late in gestation is generally based on the
risk of maternal hemorrhage at delivery.
First-line therapy for ITP in pregnancy is similar to the management
of acute ITP: corticosteroids21 and IV Igs.22 A combination of the
216 may be effective when a patient does not respond to a single
agent alone. There are no comparative trials of the 2 agents, but
responses appear to be similar to that in nonpregnant patients. Oral
prednisone or prednisolone may be started at a low dose (10-20 mg/d)
and adjusted to maintain a safe platelet count. Prednisone is
generally safe in pregnancy, but it can increase weight gain and
exacerbate hypertension and hyperglycemia, resulting in adverse
effects on pregnancy outcome.23 Very high doses of corticosteroids
are not harmful to the fetus and may have an effect of accelerating
lung maturation, but antenatal corticosteroids have not been found
to have an effect on the neonatal platelet count24 and should not be
administered to the near-term mother with this objective. The
emotional effect of corticosteroids or their rapid withdrawal in the
postpartum period should be carefully monitored and dosage should
be tapered to avoid a rapid decrease in the platelet count after
delivery. IV Igs can be used for a rapid increase in platelet count or
to maintain safe platelet counts when patients are not responsive to
steroids or there are poorly tolerated side effects. Anti-RhD Ig is
generally not used as a first-line agent because of concerns for acute
hemolysis and anemia, but has been used in refractory cases
throughout pregnancy with successful outcomes.25 If anti-RhD
(50-75 g/kg) is administered, the neonate should be carefully
monitored for a positive direct antiglobulin test, anemia, and
jaundice because the Ab may cross the placenta.
When a patient is only partially responsive or refractory to first-line
therapy, azathioprine may be effective and has been safely administered during pregnancy.26,27 High-dose methylprednisolone may
also be used in combination with IV Igs or azathioprine for the
patient who is refractory to oral corticosteroids or IV Igs alone or
has a less than adequate response.
Many agents that are frequently used in nonpregnant ITP patients,
such as vinca alkaloids and cyclophosphamide, cannot be used in
pregnant patients because of known or concern for teratogenicity.
Cyclosporine A has not been associated with significant toxicity to
the mother or fetus during pregnancy when used for inflammatory
bowel disease,28 but there is no published experience on its use in
ITP in pregnancy.
Although there are case reports of treatment of lymphoproliferative
disorders with rituximab early in pregnancy,29,30 experience is
limited and its use for pregnancy-associated ITP cannot be recommended because of its potential for crossing the placenta. Shortterm therapy with danazol in combination with high-dose IV Igs and

200

corticosteroids has been used for refractory thrombocytopenia in the

third trimester,31 but longer-term use is likely to be teratogenic and
should be avoided. There are no data on the use of thrombopoietin
receptor agonists in pregnancy, and their effects on the fetus are
unknown.
Splenectomy can be safely performed during the second trimester,32,33 when risks of anesthesia to the fetus are minimal and uterine
size will not complicate the procedure. This approach may be useful
for patients who remain refractory to therapy or who incur
significant toxicity, and may even induce a remission.

Management of delivery
ITP in the mother is not an indication for Caesarean section,34 and
the mode of delivery in a pregnant patient with ITP is based on
obstetric indications. Most neonatal hemorrhage occurs at
24-48 hours35,36 and is not related to trauma at the time of delivery.
Determination of the fetal platelet count by periumbilical blood
sampling37 or fetal scalp vein blood draws present a potential
hemorrhagic risk to the fetus and may inaccurately predict a low
platelet count.16 For this reason, fetal platelet count measurement is
not recommended. The best predictor of thrombocytopenia at birth
is its occurrence in an older sibling. In this case, Caesarean section
may be more prudent than vaginal delivery.
Maternal anesthesia must be based on safety of the mother. The risk
of spinal hematoma at lower platelet counts is unknown, but recent
recommendations are to withhold spinal anesthesia for women with
platelet counts below 75 000/L.38-40 Thromboelastograms have
been suggested to evaluate the entire hemostatic state of the
mother,41 but their usefulness is unclear. The bleeding time has also
been suggested as a mode of establishing the safety of the platelet
count,42 but most centers no longer offer this test and the experience
in using it to predict bleeding at delivery is limited. For patients who
have not required therapy during gestation but have platelet counts
below the threshold required for epidural anesthesia, short-term
corticosteroids (1-2 weeks) or IV Igs may help in preparing for the
procedure. Platelet transfusion is not appropriate to prepare the
mother for spinal anesthesia because posttransfusion increments
may be inadequate or short-lived and should be reserved to treat
bleeding only.

Monitoring and management of the neonate

Neonatal ITP accounts for only 3% of all cases of thrombocytopenia
at delivery.43 There are no accurate predictors of fetal platelet count
and the correlation between maternal and fetal platelet counts is
poor.1,44,45 A recent retrospective study of 127 pregnancies in
88 women with ITP in Japan showed a trend toward lower platelet
counts in the offspring of mothers with less than 100 000 platelets,
but this was not statistically significant.46 Splenectomized mothers
were also found to have a greater risk. Platelet count at birth appears
to be related to the presence of alloantibody (in neonatal alloimmune thrombocytopenia), but not autoantibody, so platelet Ab
testing is not recommended. A history of thrombocytopenia in a
previous affected sibling appears to be the best predictor of
thrombocytopenia in the neonate.45,47 Severe thrombocytopenia in
the neonate delivered to a mother with ITP is relatively uncommon,
with platelet counts 50 000/L occurring in 4.9%-25%.34,35,48,49
Mortality is rare ( 1%) and estimates of the incidence of intracranial hemorrhage in the neonate range from 0%-1.5%. At delivery, a
cord blood platelet count should be obtained to determine the need
for immediate therapy. Intramuscular injections such as vitamin K

American Society of Hematology

should be avoided unless it has been determined that the neonate has
a safe platelet count. The nadir platelet count frequently occurs 2-5
days after birth, so the mother needs to be made aware of signs of
bleeding and the baby should be checked early on by a pediatrician
if he/she has been discharged to home. The thrombocytopenia can
last weeks to months.50 A platelet count 50 000/L may be
treated with IV Ig (1 g/kg), which can be repeated every few weeks
as necessary to maintain a safe platelet count until the count
spontaneously recovers.

9.

10.

Conclusion
ITP occurs fairly commonly in otherwise uncomplicated, normal
pregnancies, but must be distinguished from more commonly
occurring incidental gestational thrombocytopenia. Other disorders
that may be associated with thrombocytopenia must be considered
and ruled out so that appropriate therapy can be instituted. The
diagnosis and management of ITP in pregnancy is similar to that in
the nonpregnant adult patient, but the risks to the developing fetus
must be taken into account when choosing treatment and the
maintenance of a safe platelet count, rather than prolonged remission, is the goal. Mode of delivery must be guided by obstetrical
indications. A history of ITP or ITP in a previous pregnancy is not a
contraindication to pregnancy, and the majority of patients deliver
nonthrombocytopenic or only mildly thrombocytopenic infants.

Disclosures
Conflict-of-interest disclosure: The author has received research
funding from Shionogi; has consulted for Glaxo-SmithKline, Clinical Options, Symphogen, Amgen, and Cangene; and has received
honoraria from Hemedicus, Laboratorios Raffo, and Amgen. Offlabel drug use: rituximab and azathioprine for ITP in pregnancy.

11.
12.

13.

14.
15.

16.

17.

18.

Correspondence
Terry B. Gernsheimer, MD, Box 357710, University of Washington, Seattle, WA 98195; Phone: 206-292-6521; Fax: 206-233-3331;
e-mail: bldbuddy@u.washington.edu.

19.

References

20.

1. Sainio S, Kekomaki R, Riikonen S, Teramo K. Maternal

thrombocytopenia at term: a population-based study. Acta
Obstet Gynecol Scand. 2000;79(9):744-749.
2. Burrows RF, Kelton JG. Incidentally detected thrombocytopenia in healthy mothers and their infants. N Engl J Med.
1988;319(3):142-145.
3. Matthews JH, Benjamin S, Gill DS, Smith NA. Pregnancyassociated thrombocytopenia: definition, incidence and natural
history. Acta Haematol. 1990;84(1):24-29.
4. Burrows RF, Kelton JG. Thrombocytopenia at delivery: a
prospective survey of 6715 deliveries. Am J Obstet Gynecol.
1990;162(3):73134.
5. Verdy E, Bessous V, Dreyfus M, et al. Longitudinal analysis of
platelet count and volume in normal pregnancy. Thromb
Haemost. 1997;77(4):806-807.
6. Boehlen F, Hohlfeld P, Extermann P, et al. Platelet count at
term pregnancy: A reappraisal of the threshold. Obstet Gynecol.
2000;95(1):29-33
7. Gernsheimer T, McCrae KR. Immune thrombocytopenic purpura in pregnancy. Curr Opin Hematol. 2007;14(5):574-580.
8. Minakami H, Yamada H, Suzuki S. Gestational thrombocytopenia and pregnancy-induced antithrombin deficiency: progeni-

Hematology 2012

21.
22.

23.

24.

25.

26.

tors to the development of the HELLP syndrome and acute fatty

liver of pregnancy. Semin Thromb Hemost. 2002;28(6):515518.
British Committee for Standards in Haematology General
Haematology Task Force. Guidelines for the investigation and
management of idiopathic thrombocytopenic purpura in adults,
children and in pregnancy. Br J Haematol. 2003;120(4):574596.
Godeau B, Piette JC, Fromont P, et al. Specific antiplatelet
glycoprotein autoantibodies are associated with the thrombocytopenia of primary antiphospholipid syndrome. Br J Haematol.
1997;98(4):873-879.
Oshiro BT, Silver RM, Scott JR, et al. Antiphospholipid antibodies
and fetal death. Obstet Gynecol. 1996;87(4):489-493.
Webert KE, Mittal R, Sigouin C, et al. A retrospective 11-year
analysis of obstetric patients with idiopathic thrombocytopenic
purpura. Blood. 2003;102(13):4306-4311.
Fujimura K, Harada Y, Fujimoto T, et al. Nationwide study of
idiopathic thrombocytopenic purpura in pregnant women and
the clinical influence on neonates. Int J Hematol. 2002;75(4):
426-433.
Calderwood CJ. Thromboembolism and thrombophilia in pregnancy. Curr Obstet Gynaecol. 2006;16:321-326.
Cines DB, Liebman HA. The immune thrombocytopenia syndrome: a disorder of diverse pathogenesis and clinical presentation. Hematol Oncol Clin North Am. 2009;23(6):1155-1161.
Provan D, Stasi R, Newland AC, et al. International consensus
report on the investigation and management of primary immune
thrombocytopenia. Blood. 2010;115(2):168-186.
Boehlen F, Hohlfeld P, Extermann P, de Moerloose P. Maternal
antiplatelet antibodies in predicting risk of neonatal thrombocytopenia. Obstet Gynecol. 1999;93(2):169-173.
Gill KK, Kelton JG. Management of idiopathic thrombocytopenic purpura in pregnancy. Semin Hematol. 2000;37(3):275-289.
Won YW, Moon W, Yun YS, et al. Clinical aspects of
pregnancy and delivery in patients with chronic idiopathic
thrombocytopenic purpura (ITP). Korean J Intern Med. 2005;
20(2):129-134.
Fujimura K, Harada Y, Fujimoto T, et al. Nationwide study of
idiopathic thrombocytopenic purpura in pregnant women and
the clinical influence on neonates. Int J Hematol. 2002;75(4):
426-433.
Karpatkin S. Autoimmune thrombocytopenic purpura. Semin
Hematol. 1985;22(4):260-288.
Besa EC, MacNab MW, Solan AJ, et al. High-dose intravenous
IgG in the management of pregnancy in women with idiopathic
thrombocytopenic purpura. Am J Hematol. 1985;18(4):373-379.
Metzger BE, Lowe LP, Dyer AR, et al; HAPO Study Cooperative Research Group. Hyperglycemia and adverse pregnancy
outcomes. N Engl J Med. 2008;358(19):1991-2002.
Christiaens GCML, Nieuwenhuis HK, von dem Borne AEGKr,
et al. Idiopathic thrombocytopenic purpura in pregnancy: A
randomized trial on the effect of antenatal low dose corticosteroids on neonatal platelet count. Br J Obstet Gynaecol.
1990;97(10):893-898.
Michel M, Novoa MV, Bussel JB. Intravenous anti-D as a
treatment for immune thrombocytopenic purpura (ITP) during
pregnancy. Br J Haematol. 2003;123(1):142-146.
Alstead EM, Ritchie JK, Lennard-Jones JE, et al. Safety of
azathioprine in pregnancy in inflammatory bowel disease.
Gastroenterology. 1990;99(2):443-446.

201

27. Price HV, Salaman JR, Laurence KM, Langmaid H. Immunosuppressive drugs and the foetus. Transplantation. 1976;21(4):
294-298.
28. Reddy D, Murphy SJ, Kane SV, Present DH, Kornbluth AA.
Relapses of inflammatory bowel disease during pregnancy:
in-hospital management and birth outcomes. Am J Gastroenterol. 2008;103(5):1203-1209.
29. Kimby E, Sverrisdottir A, Elinder G. Safety of rituximab
therapy during the first trimester of pregnancy: a case history.
Eur J Haematol. 2004;72(4):292-295.
30. Herold M, Schnohr S, Bittrich H. Efficacy and safety of a
combined rituximab chemotherapy during pregnancy. J Clin
Oncol. 2001;19(14):3439.
31. Orisaka M, Shukunami K, Orisaka S, et al. Combination
therapy for a pregnant woman with severe refractory ITP. Eur J
Obstet Gynecol Reprod Biol. 2005;121(1):119-120.
32. Anglin BV, Rutherford C, Ramus R, et al. Immune thrombocytopenic purpura during pregnancy: laparoscopic treatment.
JSLS. 2001;5(1):63-67.
33. Griffiths J, Sia W, Shapiro AM, et al. Laparoscopic splenectomy for the treatment of refractory immune thrombocytopenia
in pregnancy. J Obstet Gynaecol Can. 2005;27(8):771-774.
34. Laros RK, Kagan R. Route of delivery for patients with
immune thrombocytopenic purpura. Am J Obstet Gynecol.
1984;148(7):901.
35. Kaplan C, Daffos F, Forestier F, et al. Fetal platelet counts in
thrombocytopenic pregnancy. Lancet. 1990;336(8727):979982.
36. Bussel JB, Druzin ML, Cines DB, Samuels P. Thrombocytopenia in pregnancy. Lancet. 1991;337(8735):251.
37. Scioscia AL, Grannum PA, Copel JA, Hobbins JC. The use of
percutaneous umbilical blood sampling in immune thrombocytopenic purpura. Am J Obstet Gynecol. 1988;159(5):10661068.
38. Beilin Y, Zahn J, Comerford M. Safe epidural analgesia in
thirty parturients with platelet counts between 69,000 and
98,000 mm3. Anesth Analg. 1997;85(2):385-388.
39. Choi S, Brull R. Neuraxial techniques in obstetric and non-

202

40.

41.
42.

43.

44.

45.

46.

47.

48.

49.

50.

obstetric patients with common bleeding diatheses. Anesth

Analg. 2009;109(2):648-660.
van Veen JJ, Nokes TJ, Makris M. The risk of spinal
haematoma following neuraxial anaesthesia or lumbar puncture
in thrombocytopenic individuals. Br J Haematol. 2010;148(1):
15-25.
Hunt BJ, Lyons G. Thromboelastography should be available in
every labour ward. Int J Obstet Anesth. 2005;14(4):324-325.
Ballem PJ, Buskard N, Wittmann BK, et al. ITP in pregnancy:
Use of the bleeding time as an indicator for treatment. Blut.
1989;59(1):132-135.
Gill KK, Kelton JG. Management of idiopathic thrombocytopenic purpura in pregnancy. Semin Hematol. 2000;37(3):275289.
Kelton JG. Management of the pregnant patient with idiopathic
thrombocytopenic purpura. Ann Intern Med. 1983;99(6):796800.
Burrows RF, Kelton JG. Fetal thrombocytopenia and its
relation to maternal thrombocytopenia. N Engl J Med. 1993;
329(20):1463-1466.
Koyama S, Tomimatusu T, Kanagawa T, et al. Reliable
predictors of neonatal immune thrombocytopenia in pregnant
women with idiopathic thrombocytopenic purpura. Am J Hematol. 2012;87(1):15-21.
Christiaens GC, Nieuwenhuis HK, Bussel JB. Comparison of
platelet counts in first and second newborns of mothers with
immune thrombocytopenic purpura. Obstet Gynecol. 1997;90
(4 Pt 1):546-552.
Samuels P, Bussel JB, Braitman LE, et al. Estimation of the risk
of thrombocytopenia in the offspring of pregnant women with
presumed immune thrombocytopenic purpura. N Engl J Med.
1990;323(4):229-235.
Kadir RA, McLintock C. Thrombocytopenia and disorders of
platelet function in pregnancy. Semin Thromb Hemost. 2011;
37(6):640-652.
Burrows RF, Kelton JG. Low fetal risks in pregnancies
associated with idiopathic thrombocytopenic purpura. Am J
Obstet Gynecol. 1990;163(4 Pt 1):1147-1150.

American Society of Hematology