NAIT is caused by antibodies specific for platelet antigens inherited from the father but which are absent in the mother.

[5] The diagnosis of NAIT is usually made after an incidental finding of a low platelet count on a blood test or because of bleeding complications ranging from bruising or petechiae to intracranial hemorrhage in the fetus or newborn.

[6] Frequently, the reduction in platelet count is mild and the affected neonates remain largely asymptomatic.

The most serious complication is intracranial hemorrhage, leading to death in approximately 10% of symptomatic babies[6] or neurologic sequelae in 20% of cases.

Approximately 10% of newborns affected by ITP will have platelet counts <50,000 μL−1 and 1% to 2% will have a risk of intracerebral hemorrhage comparable to infants with NAIT.

A woman with symptomatic thrombocytopenia and an identifiable anti-platelet antibody should be started on therapy for their ITP which may include steroids or IVIG.

[10][11] HPA-1a is present in 98% of the population of the United States, suggesting that approximately 2% of women who are HPA-1a negative may be at risk for NAIT during pregnancy.

[14][15][16][17] The offending antibodies are IgG subtype and therefore capable of crossing the placenta and entering the fetal circulation.

[citation needed] Unlike hemolytic disease of the fetus and newborn, NAIT occurs during the first pregnancy in up to 50% of cases,[1] and the affected fetuses may develop severe thrombocytopenia (<50,000 μL−1) very early during pregnancy (as early as 20 weeks gestation, consistent with the development of platelet antigens,[1] and the majority of the time in utero[18]).

During the first pregnancy, NAIT is often not detected until birth when the newborn presents with classic symptoms of thrombocytopenia including petechiae, bruising or intracranial hemorrhage.

[1] The recurrence of NAIT has been estimated to be more than 80% in subsequent pregnancies in which the fetus also carries the target platelet antigen.

[1] Doctors may consider a diagnosis of NAIT if they notice bleeding or bruising in a baby, or low platelet counts on a blood test after birth, or neurologic symptoms.

[12] Additionally, platelet antigen genotyping can be performed on the maternal and paternal blood to determine the exact nature of the incompatibility.

[citation needed] A review of the evidence has shown that invasive management resulted in a relatively high complication rate (mainly preterm emergency cesarean section) of 11% per treated pregnancy.

[9] They concluded that first-line antenatal management in NAIT should be non-invasive with weekly intravenous immunoglobulin administration, with or without the addition of corticosteroids.

[9] Fetal blood sampling from the umbilical cord and intrauterine platelet transfusion was the first antenatal treatment for NAIT to prevent intracerebral hemorrhage.

However, she must meet general criteria for donation and platelets received from the mother must be washed to remove the offending alloantibody and irradiated to reduce the risk of graft-versus-host disease.

[1] Any administered cellular blood products must be irradiated to reduce the risk of graft-versus-host disease in the fetus.

[19] If the platelet count is not known then assisted forms of delivery, for example forceps or ventouse, should be avoided to reduce the risk of harm.

[19][20] Any infant with suspected NAIT should have an ultrasound of the head within the first 24 hours after birth to make sure that there is no evidence of an intracranial hemorrhage.

[19] In the past, infusions of IVIG (1 g/kg/day for two days) have been given to the infant and have been shown to rapidly increase the platelet count.