Yenidoğan Bebeklerde İndirekt Hi̇perbi̇li̇rubi̇nemi̇ye Yaklaşim
Synopsis
Jaundice, which develops when serum bilirubin levels exceed 5 mg/dL in newborns, occurs in 60-70% of term infants and 80% of preterm infants during their first week of life. Indirect bilirubin, a hydrophobic and lipophilic molecule formed by hemoglobin catabolism, binds to albumin to be transported to the liver, where it is converted into a water-soluble conjugated form via the UDPGT enzyme. Elevated unbound free indirect bilirubin levels can cross the blood-brain barrier, leading to acute bilirubin encephalopathy and kernicterus, a condition characterized by yellow staining of the basal ganglia and permanent neurological damage. Unlike physiological jaundice, which usually resolves spontaneously, pathological jaundice—manifesting within the first 24 hours, displaying a rapid bilirubin rise, or persisting beyond two weeks—stems from conditions such as ABO/Rh isoimmunization, G6PD and pyruvate kinase enzyme deficiencies, membrane defects like spherocytosis, erythrocyte sequestrations such as cephalhematoma, infections, and conjugation disorders including Crigler-Najjar and Gilbert syndromes. In cases of prolonged jaundice lasting more than two weeks, breast milk jaundice is the most frequent cause. Diagnosis and risk assessment combine transcutaneous or total serum bilirubin (TSB) measurements with hour-specific risk nomograms. Phototherapy serves as the primary treatment option, supplemented with IVIG in isoimmune hemolytic diseases, while emergency exchange transfusion is performed in severe hyperbilirubinemia or when acute encephalopathy signs are present.
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