In an effort to prevent antepartum intracranial bleeding, Nicolini et al.  and Murphy et al.  have described the use of serial platelet transfusions throughout the third trimester. Both patients cited had previous infants with PlA1 antigen alloimmune thrombocytopenia leading to severe antepartum intracranial hemorrhage with neurologic sequelae. Fetal thrombocytopenia was documented, and weekly platelet transfusions were begun at 26 to 29 weeks. Platelets transfused in utero (even PlA1 -negative platelets) have a short lifespan, and counts dropped from post-transfusion levels of over 150,000 cells/mul to less than 50,000 cells/mul at the next weekly transfusion. The pregnancies were carried to 32 and 35 weeks, respectively, and delivered by cesarean section. Neonatal platelet counts were greater than 44,000 cells/mul, and neither infant suffered intracranial bleeding. Further experience and data are needed to confirm the efficacy of this approach because of the potentially high fetal morbidity and mortality associated with frequent cordocentesis in alloimmune thrombocytopenia  and the difficulty and risks of repeated maternal platelet pheresis. Also, fetal intracranial hemorrhage is rare before the third trimester, and it has been suggested that the weekly intrauterine platelet transfusion might be limited to the third trimester, with delivery as soon as pulmonary maturity is documented.  
The most widely used management for fetal thrombocytopenia involves the maternal administration of high-dose immunoglobulin (IgG).   This treatment is based on the well-established observation that most cases of neonatal alloimmune thrombocytopenia are effectively treated by giving the neonate intravenous IgG.    The mechanism of action is uncertain but may involve Fc-receptor blockade in the fetal reticuloendothelial system and inhibition of uptake of IgG-coated platelets by reticuloendothelial cells, or Fc-receptor binding in the placenta, inhibiting the transplacental transfer of antiplatelet antibody. Reports of umbilical cord infusion of IgG failing to improve fetal platelet count suggest that any beneficial effect of maternal immunoglobulin infusion is due to maternal or placental factors. 
Expanding on an earlier report,  Lynch and coworkers  administered intravenous (maternal) immunoglobulin and serially measured fetal platelet counts in 18 women who had previously delivered an infant with severe alloimmune thrombocytopenia. After confirming thrombocytopenia at 20 to 22 weeks' gestation or at referral, weekly infusions of intravenous immunoglobulin (1.0 g/kg body weight) were initiated. Umbilical blood sampling was repeated in 4 to 6 weeks to assess the effect of the therapy and then again at term to determine the mode of delivery. Nine of the 18 patients also received corticosteriods. The median platelet count rose from 32,000 cells/mul before treatment to 60,000 cells/mul at birth. Only three infants had a fetal platelet count less than 30,000 cells/mul at term, and there were no cases of intracranial hemorrhage (compared with seven of the previous, untreated siblings). Steroid treatment did not appear to have a beneficial effect on fetal platelet count.
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