Ans. b (Phenytoin sodium). (Ref. Nelson Textbook of Pediatrics 17th ed., 593, 597) # Jaundice during the 1st 24 hrs of life warrants diagnostic evaluation and should be considered to be due to hemolysis until proved otherwise. Septicemia and intrauterine infections such as syphilis, cytomegalovirus, and toxoplasmosis should also be considered, especially in infants with an increase in plasma direct-reacting bilirubin. # Jaundice after the 1st 24 hrs may be "physiologic" or may be due to septicemia, hemolytic anemia, galactosemia, hepatitis, congenital atresia of the bile ducts, inspissated bile syndrome after erythroblastosis fetalis, syphilis, herpes simplex, or other congenital infections. Physiologic jaundice (icterus neonatorum) # Under normal circumstances, the level of indirect-reacting bilirubin in umbilical cord serum is l-3mg/dL and rises at a rate of less than 5mg/dL/24hr; thus, jaundice becomes visible on the 2nd-3rd day, usually peaking between the 2nd and 4th days at 5-6 mg/dL and decreasing to below 2mg/dL between the 5th - 7th days of life. # Jaundice associated with these changes is designated "physiologic" and is believed to be the result of increased bilirubin production after the breakdown of fetal red blood cells combined with transient limitation in the conjugation of bilirubin by the liver. # Risk factors for indirect hyperbilirubinemia include maternal diabetes, race (Chinese, Japanese, Korean, and Native American), prematurity, drugs (vitamin K3, novobiocin), altitude, polycythemia, male sex, trisomy 21, cutaneous bruising, cephalohematoma, oxytocin induction, breastfeeding, weight loss (dehydration or caloric deprivation), delayed bowel movement, and a sibling who had physiologic jaundice. # A family history of neonatal jaundice, exclusive breastfeeding, bruising, cephalohematoma, Asian race, and maternal age older than 25 yr identify approximately 60% of cases of extreme hyperbilirubinemia. # Indirect bilirubin levels in full-term infants decline to adult levels (mg/dL) by 10-14 days of life. # Persistent indirect hyperbilirubinemia beyond 2 wk suggests hemolysis, hereditary glucuronosyl transferase deficiency, breast milk jaundice, hypothyroidism, or intestinal obstruction. Jaundice associated with pyloric stenosis may be due to caloric deprivation, deficiency of hepatic UDP-glucuronyl transferase or ileus-induced increased enterohepatic circulation of bilirubin. Treatment of hyperbilirubinemia Phototherapy # Clinical jaundice and indirect hyperbilirubinemia are reduced on exposure to a high intensity of light in the visible spectrum. # Bilirubin absorbs light maximally in the blue range (420-470 nm). Nonetheless, broad-spectrum white, blue, special narrow-spectrum (super) blue, less often, green lights are effective in reducing bilirubin levels. # Bilirubin in the skin absorbs light energy, which by photo-isomerization converts the toxic native unconjugated 4Z, 15Z-bilirubin into the unconjugated configurational isomer 4Z,15E-bilirubin. # Phototherapy also converts native bilirubin, by an irreversible reaction, to the structural isomer lumirubin, which is excreted by the kidneys in the unconjugated state. # When indications for exchange transfusion are present, phototherapy should not be used as a substitute. # However, phototherapy may reduce the need for repeated exchange transfusions in infants with hemolysis. # Phototherapy is indicated only after the presence of pathologic hyperbilirubinemia has been established. # The basic cause or causes of jaundice should be treated concomitantly. # Prophylactic phototherapy in VLBW infants may prevent hyperbilirubinemia and may reduce the incidence of exchange transfusions. # Dark skin does not reduce the efficacy of phototherapy. # Maximal intensive phototherapy should be used when indirect bilirubin levels approach. Such therapy includes "special blue" fluorescent tubes, placing the lamps within 15-20 cm of the infant, and placing a fiberoptic phototherapy blanket under the infant's back to increase the exposed surface area. # Complications of phototherapy include loose stools, erythematous macular rash, a purpuric rash associated with transient porphyrinemia, overheating and dehydration (increased insensible water loss, diarrhea), chilling from exposure of the infant, and bronze baby syndrome. # Phototherapy is contraindicated in the presence of porphyria. # The term bronze baby syndrome refers to a dark grayish brown discoloration of the skin sometimes noted in infants undergoing phototherapy. Almost all infants observed with this syndrome have had a mixed type of hyperbilirubinemia with significant elevation of direct-reacting bilirubin and often with other evidence of obstructive liver disease. # Those using phototherapy should remain alert to these possibilities and avoid any unnecessary use because untoward effects on DNA have been demonstrated in vitro. Exchange transfusion. # Exchange transfusion is performed if intensive phototherapy has failed to reduce bilirubin levels to a safe range and if the risk of kernicterus exceeds the risk of the procedure or the infant has signs of kernicterus. # Potential complications from exchange transfusion are not trivial and include acidosis, electrolyte abnormalities, hypoglycemia, thrombocytopenia, volume overload, arrhythmias, NEC, infection, graft vs host disease, and death. # The appearance of clinical signs suggesting kernicterus is an indication for exchange transfusion at any level of serum bilirubin. Other therapies # Tin (Sn)-protoporphyrin (or tin-mesoporphyrin) administration has been proposed for reduction of bilirubin. It may inhibit the conversion of biliverdin to bilirubin by heme oxygenase. A single intramuscular dose on the 1st day of life may reduce the need for phototherapy. Such therapy may be beneficial when jaundice is anticipated (G6PD deficiency) or when blood products are discouraged (Jehovah's Witness). Complications include transient erythema if the infant is receiving phototherapy. # IV immunoglobulin (500 mg/kg/dose over a 4hr period), given ql2hr for 3 doses, is effective in reducing bilirubin levels in patients with Coombs-positive hemolytic anemia, presumably by reducing hemolysis.