The Preterm Infant

• Autores: Michael Kaplan, Cathy Hammerman, Vinod K. Bhutani
• Localización: Clinics in Perinatology, ISSN 0095-5108, Vol. 43, Nº. 2, 2016, págs. 325-340
• Idioma: inglés
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• Resumen

  • Prematurity and glucose-6-phosphate dehydrogenase (G6PD) deficiency are risk factors for neonatal hyperbilirubinemia. The 2 conditions may interact additively or synergistically, contributing to extreme hyperbilirubinemia, with the potential for bilirubin neurotoxicity. This hyperbilirubinemia is the result of sudden, unpredictable, and acute episodes of hemolysis in combination with immaturity of bilirubin elimination, primarily of conjugation. Avoidance of contact with known triggers of hemolysis in G6PD-deficient individuals will prevent some, but not all, episodes of hemolysis. All preterm infants with G6PD deficiency should be vigilantly observed for the development of jaundice both in hospital and after discharge home.