For term newborns, the American Academy of Pediatrics and the American College of Obstetricians and Gynecologists (2017) stress early detection and prompt phototherapy to prevent bilirubin encephalopathy. Despite these measures, bilirubin encephalopathy persists, and this is somewhat related to early hospital discharges (Gazzin, 2011; Kaplan, 2011; Sgro, 2011). According to Burke and coworkers (2009), hospitalizations for kernicterus in term newborns were 5.1 per 100,000 in 1988. Since then, however, this rate has dropped to 0.4 to 2.7 cases per 100,000 births (Watchko, 2013). This may be due in part to legislation, discussed in Chapter 36 (p. 662), to minimize brief postpartum hospital stays.
• Hemorrhagic Disease of the Newborn his disorder is characterized by spontaneous internal or external bleeding beginning any time after birth. Most hemorrhagic disease results from abnormally low levels of the vitamin K-dependent clotting factors-V, VII, IX, X, prothrombin, and proteins C and S (Zipursky, 1999). Newborns whose mothers took anticonvulsant drugs are at higher risk because these suppress maternal hepatic synthesis of some of these factors. Classic hemorrhagic disease is usually apparent 2 to 5 days after birth in neonates not given vitamin K prophylaxis at delivery (Busield, 2013). Delayed hemorrhage may occur at 2 to 12 weeks in exclusively breastfed infants because breast milk contains little vitamin K. Other causes of neonatal hemorrhage not related to vitamin K include hemophilia, congenital syphilis, sepsis, thrombocytopenia purpura, erythroblastosis, and intracranial hemorrhage.
The American Academy of Pediatrics and the American College of Obstetricians and Gynecologists (2017) recommend routine prophylaxis for hemorrhagic disease with a 0.5-to 1-mg dose of vitamin K\ (phytonadione) given intramuscularly. Oral administration is not efective, and maternal vitamin K administration results in very little transport to the fetus (Sankar, 2016).
Abnormally low platelet concentrations in term newborns may be due to various etiologies such as immune disorders, infections, drugs, or inherited platelet defects, or they may be part of a congenital syndrome (American College of Obstetricians and Gynecologists, 20 16b). In many, thrombocytopenia is an extension of a fetal disorder such as infection with B 19 parvovirus, cytomegalovirus, toxoplasmosis, and others discussed in Chapters 64 and 65. Neonatal thrombocytopenia has been reported with maternal antiretroviral therapy for human immunodeiciency virus (HIV) infection (Smith, 2016) . Term newborns admitted to NICUs, especially those with sepsis, have accelerated platelet consumption (Eissa, 2013).
In women with an autoimmune disorder such as systemic lupus erythematosus or immunological thrombocytopenia, maternal antiplatelet IgG is transferred to the fetus and can cause accelerated platelet destruction. Most cases are mild, and platelet levels usually reach a nadir at 48 to 72 hours. Maternal corticosteroid therapy generally has no efect on fetal platelets. Fetal blood sampling for platelet determination is seldom necessary, and platelets are usually adequate to prevent fetal hemorrhage during delivery (Chap. 56, p. 1086).