Chronic Idiopathic Thrombocytopenic Purpura Causing Neonatal Thrombocytopenia

Author Information

Goel A*, Jain P**, Shende D***, Chauhan AR****.
(* Third Year Resident, ** Second Year Resident, *** Assistant Professor, **** Additional Professor. Department of Obstetrics and Gynecology, Seth GS Medical College & KEM Hospital, Mumbai, India.)


Idiopathic thrombocytopenic purpura (ITP) in pregnancy is uncommon. It usually presents in first trimester of pregnancy but may present at any point of gestation. A case of chronic ITP in pregnancy leading to neonatal thrombocytopenia is presented here.


Thrombocytopenia complicates 10% of all pregnancies.[1] The most common cause of isolated thrombocytopenia in first and second trimesters of pregnancy is ITP, which accounts for 5% of all pregnancy associated thrombocytopenia. Incidence of ITP is 1-2/1000 pregnancies.[2] Making a diagnosis is complex and challenging as time of onset of thrombocytopenia and its clinical manifestations usually overlap. ITP may lead to maternal and neonatal complications. Its management requires collaboration between obstetrician and hematologist.

Case Report

A 35 year old female, diagnosed case of chronic ITP, Gravida 2 Para 1 with previous neonatal death, registered antenatally at 6 weeks of gestation with severe thrombocytopenia (platelet count of 10000/μL). She was diagnosed as a case of chronic ITP 4 years ago, when she was started on corticosteroids, azathioprine and dapsone. As she did not respond to medical treatment, she underwent splenectomy. She was then started on penicillin prophylaxis (tablet penicillin G 400 mg twice daily) and corticosteroids (tablet dexamethasone 40 mg for four days every month). She conceived 2 years later, and received 18 platelet transfusions and intravenous immunoglobulins during peripartum period. She delivered a male child of 2.5 kg by outlet forceps application. However, the baby died on day 1 of life due to unknown cause.
She was antenatally registered with us in this pregnancy and had regular follow-up. She was admitted at 34 weeks of gestation as she developed steroid induced diabetes mellitus. On examination, her vital parameters were normal. On abdominal examination the uterus was 34 weeks of gestation and relaxed, the presentation was cephalic, fetal heart sounds were regular (140 bpm). Vaginal examination was unremarkable.
Hematological investigations showed normal hemoglobin of 11.7 g/dL, normal total and differential white blood cell counts, but abnormality in the form of isolated thrombocytopenia (platelet count of 10,000/μL) and  anisocytosis, poikilocytosis, crenated red blood cells on peripheral smear. Her fasting and postprandial blood sugars were elevated FBS- 103 mg/dl, PLBS- 124 mg/dl, oral glucose tolerance test (100 g - Carpenter and Coustan) 99/121/102/93, Serum LDH was elevated (777 U/L). Renal, thyroid and liver function tests were within normal limits.
She was treated with tablet metformin and injection human insulin after endocrinologist’s opinion. Blood sugar levels and blood pressure monitoring was done. The treatment plan was to increase the platelet count prior to anticipated delivery. In view of her persistently low platelet counts, she was started on injection methyl prednisolone 500 mg IV for 3 days, which raised her platelet count to only 40000/μL. Injection dexamethasone 40 mg in 100 ml normal saline once daily for 4 days was given intravenously, which raised her platelet count to 86,000/μL. Intravenous immune globulin (IVIg) 1 g/kg body weight was transfused and her platelet count rose to 1,20,000/μL; hence induction was planned. However, she went into spontaneous labor a day prior to planned induction and delivered a male child of 2.6 kg vaginally. On day 2 of delivery, her platelet counts started to decline again (platelet count- 95,000 /μL).
In view of maternal history and previous neonatal loss, serial platelet counts of the neonate were done, and the baby developed neonatal thrombocytopenia (platelet count- 20,000/μL). The neonate was given 2 doses of injection methyl prednisolone intravenously on day 2 of life. Neonatal thrombocytopenia resolved spontaneously after a few days and both mother and child were discharged on day 7 after delivery.


ITP may be subdivided into primary and secondary types. Secondary ITP may be due to autoimmune disorder, HCV, HIV, H. pylori infection. It is most commonly due to clearance of platelet coated by IgG antiplatelet antibodies in spleen and less commonly due to direct activation of complement system, diminished production, and alteration in regulatory T cells.[3,4,5] ITP is likely to occur if there is a history of thrombocytopenia in prior pregnancy, underlying autoimmune disease or severe thrombocytopenia especially in first trimester of pregnancy.[6]
According to American Society of Hematology (ASH) [7] and British Committee for Standards in Hematology[8] guidelines, treatment is required for women with platelet count <10,000/μL at any time during pregnancy or <30,000/μL in second or third trimester or when thrombocytopenia is associated with bleeding.
Corticosteroids are the first line of management during pregnancy. Prednisone and prednisolone are preferred in pregnancy. Therapeutic dose of prednisolone is 1 mg/kg (based on pre pregnancy weight) which needs to be titrated to lowest effective dose after achieving a response. However steroids may cause gestational diabetes, weight gain, hypertension, acceleration of bone loss, placental abruption and preterm labor, orofacial clefts in the first trimester. Our patient developed steroid-induced diabetes mellitus. High dose IVIg (2 mg/kg over 2-5 days) is required to increase the platelet count rapidly. Multiple courses of IVIg are required as the response is usually transient; as this is expensive its use should be just prior to anticipated delivery. Combination of steroids and IVIg is used for refractory cases. Laparoscopic splenectomy may be considered in second trimester in cases who do not respond to steroids or IVIg. Anti-D immunoglobulin is relatively contraindicated but may be given in third trimester to refractory cases.[9] Cytotoxic drugs and immunosuppressive drugs are avoided in pregnancy. 
Mode of delivery should be determined by obstetric indications. Cesarean section should be done for obstetric indication only. According to ASH guidelines, platelet count should be > 50,000/μL for vaginal delivery and cesarean section. But according to BCSH guidelines, platelet count should be >50,000/μL for vaginal delivery and > 80,000/μL for cesarean section and epidural anesthesia, which is currently followed in our institute. Corticosteroids can be started 10 days prior to anticipated delivery for a patient whose platelet count is <80,000/μL and has not required therapy during pregnancy, as we did in our case. When the delivery is imminent, IVIg should be considered. Platelet transfusion is generally not useful in ITP. In emergency cases, platelet transfusion along with IVIg can be considered.
5% of the offspring develop fetal thrombocytopenia. Nadir in the infant platelet count occurs 2 to 5 days after delivery which spontaneously rises by day 7 of delivery. Most reliable predictor of neonatal thrombocytopenia is history of thrombocytopenia in prior sibling at delivery.[10] Risk of intracranial hemorrhage in neonate is below 1%. [11]


ITP can complicate pregnancy and its management. More aggressive treatment is required for preparing the patient for labor and delivery. The outcome of pregnancy is generally good. Other causes of thrombocytopenia need to be ruled out.

  1. Provan D, Newland A. Idiopathic thrombocytopenic purpura in adults. J Pediatr Hematol Oncol 2003;25(Suppl 1):S34.
  2. McCrae, K. Thrombocytopenia in Pregnancy. In: Michelson, A., editor. Platelets. New York, NY: Elsevier; 2006.
  3. Chang M, Nakagawa PA, Williams SA, et al. Immune thrombocytopenic purpura (ITP) plasma and purified ITP monoclonal autoantibodies inhibit megakaryocytopoiesis in vitro. Blood 2003;102(3):887.
  4. McMillan R, Wang L, Tomer A, et al. Suppression of in vitro megakaryocyte production by antiplatelet autoantibodies from adult patients with chronic ITP. Blood 2004;103(4):1364.
  5. McMillan R. The pathogenesis of chronic immune thrombocytopenic purpura. Semin Hematol 2007;44(4 Suppl 5):S3.
  6. Gill KK, Kelton JG. Management of idiopathic thrombocytopenic purpura in pregnancy. Semin Hematol 2000;37(3):275.
  7. Gernsheimer T, James AH, Stasi R, How I treat thrombocytopenia in pregnancy. Blood. 2013;121(1):38-47; and Neunert C, Lim W, Crowther M, Cohen A, Solberg L, Jr., Crowther MA. The American Society of Hematology 2011 evidence based practice guideline for immune thrombocytopenia. Blood. 2011;117(16):4190- 4207; and 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.
  8. Guidelines for the investigation and management of idiopathic thrombocytopenic purpura in adults, children and in pregnancy. British Committee for Standards in Haematology General Haematology Task Force. Br J Haematol. 2003 Feb;120(4):574-96.
  9. 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.
  10. Christiaens GC1, Nieuwenhuis HK, Bussel JB. Comparison of platelet counts in first and second newborns of mothers with immune thrombocytopenic purpura. Obstet Gynecol. 1997 Oct;90(4 Pt 1):546-52.
  11. Nationwide study of idiopathic thrombocytopenic purpura in pregnant women and the clinical influence on neonates.Fujimura K1, Harada Y, Fujimoto T, Kuramoto A, Ikeda Y, Akatsuka J, Dan K, Omine M, Mizoguchi H. Int J Hematol. 2002 May;75(4):426-33.

Goel A, Jain P, Shende D, Chauhan AR. Chronic Idiopathic Thrombocytopenic Purpura Causing Neonatal Thrombocytopenia. JPGO 2015. Volume 2 No. 11. Available from: