Prognosis
Most neonates with neonatal unconjugated hyperbilirubinemia do well after phototherapy and/or exchange transfusion. Kernicterus should be preventable if recommendations for hyperbilirubinemia management are carried out in a timely manner.[7]
For neonates with hemolytic anemia secondary to blood group incompatibility, hemolysis should not present as a problem once the maternal antibodies are gone.
Babies with polycythemia and extravasation of blood should not have any problem once the extra hemoglobin breakdown is taken care of.
Surgical causes of increased enterohepatic circulation should resolve once the specific condition is treated. Bilirubin levels of babies with partial specific enzymatic conjugation defects can usually be kept under control with night-time phototherapy.
For neonates with conjugated hyperbilirubinemia, the outlook depends on the etiology of the condition. The clinical course is variable in babies with alpha 1-antitrypsin deficiency and cystic fibrosis. In babies with Zellweger syndrome, the prognosis is poor, with most neonates dying during the first year or surviving with profound developmental delay and seizures. Patients with Dubin-Johnson and Rotor syndromes (inherited as autosomal recessive) have an excellent prognosis. The prognosis of babies with other metabolic/genetic defects depends on early recognition and management of the specific enzyme deficiencies and accumulation of metabolites. Parenteral-induced cholestasis should improve if enteral feeding can be established. Some of the infectious etiologies (such as congenital syphilis, bacterial) of hepatitis improve with specific treatments; others resolve over time. Supportive treatment is needed for survivors of kernicterus. Rehabilitative treatment is recommended for the specific neurologic deficits.
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