Introduction

Fetal thrombocytopenia is a rare but potentially devastating condition, which puts the fetus at risk of bleeding. Thrombocytopenia is commonly defined as a platelet count <150 × 109/l. However, clinically significant bleeding problems are only likely to occur with platelet counts below 50 × 109/l (although some experts set this level at ≤30 × 109/l). The most feared and indeed morbid complication is intracranial hemorrhage (ICH), often associated with perinatal death or major neurological damage as a consequence.

Many fetomaternal and neonatal conditions are associated with thrombocytopenia (Table 7.1) [1].Thrombocytopenia with an immunological origin is encountered in 0.3% of the newborns [1–3]. Fetal and neonatal alloimmune thrombocytopenia (FNAIT) and idiopathic thrombocytopenic purpura (ITP) are the most important immune-mediated thrombocytopenias.

The focus in this chapter will be on FNAIT, which is one of the major causes of both severe thrombocytopenia and ICH in fetuses and term neonates.

FNAIT is caused by maternal immunization against human platelet antigens (HPAs) on fetal platelets, inherited from the father and different from those present in the mother. The IgG alloantibodies are transported through the placenta to the fetus, and cause destruction of fetal platelets. h is disease is the platelet equivalent of red cell alloimmunization. The resulting fetal thrombocytopenia is associated with risk of bleeding complications. The most feared complication is ICH and subsequent neurological morbidity or death.