![]() Mutations of glucuronyl transferase (i.e., Crigler-Najjar syndrome, Gilbert syndrome)Ĭonjugated bilirubinemia implies a hepatic or post hepatic cause.Red blood cell membrane disorders: spherocytosis, ovalocytosis.Red blood cell enzyme defects: G6PD Deficiency, pyruvate kinase.Blood group incompatibility: ABO, Rh factor, minor antigens.Best diagnosed by looking for signs of dehydration and comparing weight to birth weight. Patient does not receive adequate oral intake which then causes reduced bowel movement/bilirubin excretion.It may start as early as 3rd day and reaches peak by 3rd week of life. Due to substances in milk that inhibits glucuronyl transferase.More common causes are listed first, followed by less common causes Recognize the clinical manifestations of acute bilirubin encephalopathy and. breast milk jaundice, breast feeding jaundice)ĭifferential Diagnosis Indirect (Unconjugated) Hyperbilirubinemia Distinguish between physiologic jaundice and pathologic jaundice of the newborn. This can occur in any newborn who has an exaggerated form of physiologic (normal) jaundice. Paragraph(s) Pathologic jaundice, however, involves a higher level of bilirubin and requires treatment to hasten the removal of bilirubin. Unlikely when caused by a benign process (e.g. Physiologic jaundice poses no danger to the newborn.Lethargy, if progression to severe elevation.Jaundice within the first 4-7 days of life.The most important piece of the evaluation is distinguishing between unconjugated and conjugated hyperbilirubinemia since a conjugated (direct) hyperbilirubinemia is always pathologic and often more severeĬlinical Features General neonatal jaundice features.It is also the most common cause for hospital readmission for neonates post birth. Neonatal jaundice can affect up to 84% of term newborns and is often a benign process that is quickly corrected once identified. ![]()
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