PHYSIOLOGICAL JAUNDICE

Physiological jaundice is a sign of developmental immaturity in bilirubin metabolism, seen in gt;50% of Term newborns and gt;80% of preterms.

Cardinal features of physiological jaundice are:

• Onset beyond 24 hours of birth (N: 48-72 hours)

• Maximum intensity on 4^th day (5/6^th day in preterms)

• Maximum.

• Disappears by 10^th day (14^th day in preterms)

• Active newborn without other problems

Etiophysiology: Physiological jaundice indicates various developmental immaturities in newborns, as follows:

• Increased bilirubin production, ~3 times higher than in adults, due to higher hemoglobin content and shorter lifespan of fetal RBCs (90 days).

• Developmental hepatic immaturity with relative defi­ciency of Ligandin for bilirubin transport within hepatocytes and UDPGT for conjugation.

• Underdeveloped gut flora, with inadequate conversion of conjugated bilirubin into excretable pigments- Stercobilinogen and urobilinogen. Consequent delay in bilirubin excretion facilitates entero-hepatic circulation.

• Increased enterohepatic circulation due to high #946;-gluco- ronidase activity in gut, especially when feeding is delayed. Early feeding promotes development of normal flora, which destroys this enzyme and limits enterohepatic circulation.

These physiological handicaps are more pronounced in preterm, LBW and sick newborns, e.g. hypoglycemia, asphyxia, etc., leading to exaggerated physiological jaundice. Diagnosis of physiological jaundice rests on cardinal features (as above) and exclusion of pathological causes. Management: No specific treatment is needed in physiological jaundice, except—(a) proper feeding, (b) prevention of hypothermia, and (c) clinical monitoring and follow-up after 10-14 days to confirm disappearance of jaundice. However, cases with exaggerated physiological jaundice need to be treated as pathological jaundice.

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