Clinical manifestations reflect the severity of thrombocytopenia. Infants may be born with severe, generalised petechiae, rash or purpura or may appear normal at birth and may develop symptoms and signs of thrombocytopenia any time during 2-3 day post-partum and are rarely associated with other disorders or factors that accounts for thrombocytopenia. Usually they are otherwise healthy infants born to healthy mother with normal platelet count and neonates often associated with thrombocytopenia < 50,000/u/L.

Most severe complication is intracranial hemorrhage which is seen in approximately 10-15% cases and half of these occurs in utero as early as 20 weeks of pregnancies (31) and majority of them have neuro-developmental sequele and hence USG skull should be performed to all neonates with Feto-Maternal Neonatal Allo-Immune Thrombocytopenia (FMNAIT) before discharge (31-33).

Confirmation of diagnosis ideally requires demonstration of maternal and fetal platelet incompatibility and absence of antigen in mother's serum, which is present in the child. When tested against panel of platelets of known antigenicity, specific antigen involved (usually PLA1) can be demonstrated to be lacking on the mother's platelet but is present in newborn's and father's platelets. However, laboratory facilities may not be available in the majority of centers (32,33).

Autoimmune thrombocytopenia

Autoimmune thrombocytopenic purpura in neonate is mediated by transplacental passage of maternal antiplatelet antibodies. However, antibodies responsible for these cases binds both maternal and fetal platelets leading to thrombocytopenia in both mother and neonate (1).

Studies done on neonatal thrombocytopenia caused by maternal factors are few (7,11,12, 24, 25, 42, 43, 44, 45).

The main causes of thrombocytopenia in mother have been reported to be due to :

• incidental or gestational thrombocytopenia of pregnancy (74%)
• hypertensive diseases of pregnancy (21%)
• immune thrombocytopenic disorders during pregnancy like idiopathic thrombocytopenic purpura and systemic lupus erythematosis (4%)
  
  

• Gestational or incidental thrombocytopenia seen in healthy women without ITP or any other autoimmune process. Usually this condition leads to mild decrease in platelet count, which is first detected in pregnancy and resolves after the delivery. This condition however is associated with very low risk of thrombocytopenia in newborn (12,24,36,40). However, differentiation between ITP during pregnancy and gestational thrombocytopenia is difficult.
  
  
• In most recent studies on ITP in pregnancy, severe fetal thrombocytopenia in utero is distinctly uncommon. These studies also indicated neonatal morbidity and mortality that can occur can be prevented by early recognition and therapeutic intervention. Incidence of neonatal thrombocytopenia (platelet count < 150,000/ml) with maternal ITP ranges from 13-64% and severe neonatal thrombocytopenia - platelet count < 50,000/cmm from 5-20% (39,40,41,42,43).
  
  
• Most studies have reported a very low rate of significant bleeding complication particularly intracranial hemorrhage (ICH) around 3% (25). In addition they found no significant association between the mode of delivery - caesarian Vs vaginal and the rate of intracranial hemorrhage (25,39,40,41, 45).
  
  
• Inspite of extensive study no factors predictive of the severity of neonatal or fetal thrombocytopenia are available. Maternal platelet count, history of splenectomy, titers of PAIgG or serum platelet-bindable IgG and platelet counts of older siblings have not been found to be useful. Absence of history of ITP and negative results on circulating antibody testing were associated with minimal risk of severe neonatal thrombocytopenia. Measurement of antiplatelet antibody titer unfortunately have not been useful in predicting likelihood of fetus being affected. Lack of uniform predictive factors have complicated obstetric management and pregnant women with ITP (42,43,45).