Newborn thrombocytopenic purpura
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)
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.
For more information, see OMIM.
D69.42 – Congenital and hereditary thrombocytopenia purpura
302873008 – Thrombocytopenic purpura
- Subcutaneous fat necrosis
- Wiskott-Aldrich syndrome
- Congenital leukemia
- Kasabach-Merritt syndrome
- Cytomegalovirus infection
- Candidal sepsis
- Congenital rubella
- Congenital syphilis
- Hypergammaglobulinemic purpura of Waldenstrom
- Disseminated intravascular coagulation
- Platelet function defects
- Vitamin C or K deficiency
- Deficiency or dysfunction of protein S or protein C
- Hepatic insufficiency