OBJECTIVE: The optimal management of pregnancies at risk for neonatal alloimmune thrombocytopenia is debated. Proposed management includes the administration of intravenous immunoglobulin and serial determination of the fetal platelet count. The aims of our study were to determine the effectiveness and likely mechanism of action of intravenous immunoglobulin and to evaluate the safety of cordocentesis in cases of neonatal alloimmune thrombocytopenia. STUDY DESIGN: Eighteen mother-infant pairs were studied. All were at risk for neonatal alloimmune thrombocytopenia on the basis of delivery of a previously affected infant and confirmation of specific maternal antiplatelet antibodies. The pertinent antigen was HPA-1a in 13 cases, HPA-3a in 2 cases, and undetermined in 3 cases. Serial cordocenteses were used to determine fetal platelet counts. If the platelet count was <50,000/microL before 37 weeks' gestation, treatment was initiated with intravenous immunoglobulin administered to either the fetus (n = 2) or the mother (n = 8). In 3 cases fetal and maternal immunoglobulin G levels were determined before and after treatment. RESULTS: Seven (39%) fetuses had adequate platelet counts, were not treated, and were delivered of infants with normal platelet counts. Eleven (61%) fetuses were thrombocytopenic. Eight thrombocytopenic infants were treated with maternally administered intravenous immunoglobulin. In 6 (75%) of 8 cases the fetal platelet count increased after administration of intravenous immunoglobulin, but 2 fetuses remained severely thrombocytopenic. Two thrombocytopenic fetuses were treated with intravenous immunoglobulin infusion directly into the umbilical vein; both remained thrombocytopenic. Moreover, fetal immunoglobulin G levels did not correlate well with the response to intravenous immunoglobulin. Two (5.3%) of 38 cordocenteses were complicated by hemorrhagic complications, necessitating immediate cesarean delivery despite the use of prophylactic platelet transfusion in one case. CONCLUSION: Severe fetal alloimmune thrombocytopenia does not always occur in subsequent fetuses. Thus either fetal antigen status or platelet counts or both of these are necessary to determine whether treatment is needed. The effect of intravenous immunoglobulin on raising the fetal platelet count is inconsistent and appears to be caused by maternal or placental factors rather than a direct inhibition of fetal platelet destruction by immunoglobulin. The risk of hemorrhagic complications from cordocentesis in pregnancies complicated by neonatal alloimmune thrombocytopenia is higher than generally appreciated and is not always avoided by platelet transfusion at the time of the procedure.
OBJECTIVE: The optimal management of pregnancies at risk for neonatal alloimmune thrombocytopenia is debated. Proposed management includes the administration of intravenous immunoglobulin and serial determination of the fetal platelet count. The aims of our study were to determine the effectiveness and likely mechanism of action of intravenous immunoglobulin and to evaluate the safety of cordocentesis in cases of neonatal alloimmune thrombocytopenia. STUDY DESIGN: Eighteen mother-infant pairs were studied. All were at risk for neonatal alloimmune thrombocytopenia on the basis of delivery of a previously affected infant and confirmation of specific maternal antiplatelet antibodies. The pertinent antigen was HPA-1a in 13 cases, HPA-3a in 2 cases, and undetermined in 3 cases. Serial cordocenteses were used to determine fetal platelet counts. If the platelet count was <50,000/microL before 37 weeks' gestation, treatment was initiated with intravenous immunoglobulin administered to either the fetus (n = 2) or the mother (n = 8). In 3 cases fetal and maternal immunoglobulin G levels were determined before and after treatment. RESULTS: Seven (39%) fetuses had adequate platelet counts, were not treated, and were delivered of infants with normal platelet counts. Eleven (61%) fetuses were thrombocytopenic. Eight thrombocytopenicinfants were treated with maternally administered intravenous immunoglobulin. In 6 (75%) of 8 cases the fetal platelet count increased after administration of intravenous immunoglobulin, but 2 fetuses remained severely thrombocytopenic. Two thrombocytopenic fetuses were treated with intravenous immunoglobulin infusion directly into the umbilical vein; both remained thrombocytopenic. Moreover, fetal immunoglobulin G levels did not correlate well with the response to intravenous immunoglobulin. Two (5.3%) of 38 cordocenteses were complicated by hemorrhagic complications, necessitating immediate cesarean delivery despite the use of prophylactic platelet transfusion in one case. CONCLUSION: Severe fetal alloimmune thrombocytopenia does not always occur in subsequent fetuses. Thus either fetal antigen status or platelet counts or both of these are necessary to determine whether treatment is needed. The effect of intravenous immunoglobulin on raising the fetal platelet count is inconsistent and appears to be caused by maternal or placental factors rather than a direct inhibition of fetal platelet destruction by immunoglobulin. The risk of hemorrhagic complications from cordocentesis in pregnancies complicated by neonatal alloimmune thrombocytopenia is higher than generally appreciated and is not always avoided by platelet transfusion at the time of the procedure.