Purpura from thrombocytopenia is usually seen with platelet counts below 20-50 000 per cubic mm. Thrombocytopenia may occur from decreased production, increased destruction, or platelet sequestration.

There are multiple possible causes:

• Immune mediated (neonatal alloimmune thrombocytopenia [NAIT], gestational thrombocytopenia, autoimmune thrombocytopenic purpura)
• Infection related (bacterial, fungal, and viral)
• Drug related
• Peripheral consumption of platelets (disseminated intravascular coagulation, necrotizing enterocolitis, hypersplenism)
• Genetic causes (thrombocytopenia with absent radii [TAR], Fanconi anemia, congenital amegakaryocytic thrombocytopenic purpura, congenital hypoplastic thrombocytopenia with microcephaly, familial thrombocytopenias, chromosomal abnormalities, and inherited metabolic disorders)
• Miscellaneous (intrauterine growth retardation, pregnancy-induced hypertension, perinatal asphyxia)

Two percent of term infants are thrombocytopenic at birth, but severe thrombocytopenia (< 50 000) is seen in less than 3/1000 term infants, with the usual cause being NAIT, occurring in 1/1000 births. Other common causes in term infants include bacterial sepsis and perinatal asphyxia.

Preterm and neonatal intensive care unit (NICU) infants are more often affected by severe thrombocytopenia, seen in over a quarter of NICU admitted patients.

Thrombocytopenia is further characterized by being early onset (within 72 hours of birth) or late onset (after 72 hours). Early-onset thrombocytopenia is usually associated with placental insufficiency or fetal hypoxia. It is usually mild, self-limited, and requires no therapy. Late-onset thrombocytopenia is more often severe, associated usually with bacterial sepsis or necrotizing enterocolitis, and requires platelet transfusions.

Intracranial hemorrhage complicates NAIT in 10%-15% of cases, half in utero; it may be a complication of any severe thrombocytopenia.