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Old 06-21-2011
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Question jaundiced infant case

A 12-hour-old infant is noted by the neonatologist to have jaundiced skin and sclera. On physical exam, the infant appears well except for mild jaundice. Laboratory studies reveal unconjugated hyperbilirubinemia. What might be the source of this condition?

Answer Choices
A. α1 antitrypsin deficiency
B. Dubin–Johnson syndrome
C. Extra-hepatic biliary atresia
D. Galactosemia
E. Hemolytic anemia
F. Physiologic jaundice of the newborn
G. Rotor syndrome
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Old 06-21-2011
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I think the answer is E because it is a pathologic jaundice since it presents in the first day of life. It probably is also Coombs positive.
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Old 06-21-2011
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Hmm, hemolytic anemia seems the most probable answer..
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E. Hemolytic anemia
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Old 06-22-2011
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Option E (Hemolytic anemia ) is correct. Hemolytic anemia may appear within the first hours after birth. It results in unconjugated hyperbilirubinemia, as this patient has. It may be congenital, such as spherocytosis, glucose-6-phosphate dehydrogenase (G6PD), or pyruvate kinase (PK) deficiency. It can also be acquired due to ABO/Rhesus (Rh) isoimmunization, infection, twin–twin transfusion, chronic fetal hypoxia, maternal diabetes mellitus (DM), delayed cord clamping, or drugs.

Option A (α1 antitrypsin deficiency) is incorrect. α1 antitrypsin deficiency may be an abnormal cause of hyperbilirubinemia, but it will lead to conjugated, not unconjugated hyperbilirubinemia. Conjugated hyperbilirubinemia in infancy is generally infectious (TORCHeS, listeria), metabolic (galactosemia, α1 antitrypsin deficiency), or congenital (extrahepatic biliary atresia, Dubin–Johnson or Rotor syndrome). The condition may lead to cirrhosis and emphysema. Treatment for α1 antitrypsin is replacement of the enzyme.

Option B (Dubin–Johnson syndrome) is incorrect. Dubin–Johnson syndrome is a congenital abnormal cause of hyperbilirubinemia, but it will lead to conjugated, not unconjugated hyperbilirubinemia. Conjugated hyperbilirubinemia in infancy is generally infectious (TORCHeS, listeria), metabolic (galactosemia, α1 antitrypsin deficiency), or congenital (extrahepatic biliary atresia, Dubin–Johnson or Rotor syndrome). Dubin–Johnson syndrome is an autosomal recessive disease, which presents shortly after birth with an increase of conjugated bilirubin without elevation of liver enzymes alanine aminotransferase (ALT) and aspartate aminotransferase (AST). It is caused by a failure of hepatocytes to transfer conjugated bilirubin to bile canaliculi.

Option C (Extra-hepatic biliary atresia) is incorrect. Extra-hepatic biliary atresia is an abnormal cause of hyperbilirubinemia, but it will lead to conjugated, not unconjugated hyperbilirubinemia. Conjugated hyperbilirubinemia in infancy is generally infectious (TORCHeS, listeria), metabolic (galactosemia, α1 antitrypsin deficiency), or congenital (extrahepatic biliary atresia, Dubin–Johnson or Rotor syndrome). This condition is confirmed with ultrasound and treated with surgery.

Option D (Galactosemia) is incorrect. Galactosemia may be an abnormal cause of hyperbilirubinemia, but it will lead to conjugated, not unconjugated hyperbilirubinemia. Conjugated hyperbilirubinemia in infancy is generally infectious (TORCHeS – for toxoplasmosis, rubella, cytomegalovirus, Herpes simplex, syphilis, listeria), metabolic (galactosemia, α1-antitrypsin deficiency), or congenital (extrahepatic biliary atresia, Dubin–Johnson or Rotor syndrome).

Option F (Physiologic jaundice of the newborn) is incorrect. Physiologic jaundice of the newborn occurs at 24–48 hours after birth. It does have unconjugated hyperbilirubinemia, but not in the first day of delivery. A total of 50% of neonates have physiologic jaundice. It is caused by increased bilirubin production and relative deficiency in glucuronyl transferase in the liver.

Option F (Rotor syndrome) is incorrect. Rotor syndrome may be an abnormal cause of hyperbilirubinemia, but it will lead to conjugated, not unconjugated hyperbilirubinemia. Conjugated hyperbilirubinemia in infancy is generally infectious (TORCHeS, listeria), metabolic (galactosemia, α1 antitrypsin deficiency), or congenital (extrahepatic biliary atresia, Dubin–Johnson or Rotor syndrome). Rotor syndrome is a benign condition whose pathophysiology is similar to Dubin–Johnson, and there is no need to treat it.


High-yield Hit 1
Jaundice
Neonatal jaundice
Physiologic jaundice occurs in many newborn infants, especially if born preterm. A combination of increased red cell breakdown and immaturity of the hepatic enzymes causes unconjugated hyperbilirubinemia. It is exacerbated by dehydration, which can occur if establishment of feeding is delayed.
Onset of jaundice in the first 24 hours of life is always pathologic; the causes are listed in Fig. 9.3. Recognition and treatment of severe neonatal unconjugated hyperbilirubinemia are important to avoid kernicterus (brain damage due to deposition of bilirubin in the basal ganglia). Evaluation of persistent conjugated hyperbilirubinemia is important to allow early (<6 weeks) diagnosis and treatment of biliary atresia.
Onset of jaundice in the first 24 hours of life is always pathologic.
Consider biliary atresia in an infant with persistent neonatal jaundice due to conjugated hyperbilirubinemia and pale stools (rare but treatable).


Figure 9.3 Causes of neonatal jaundice.
http://usmlesteps123.examweb.com/ass...1-009-f003.jpg
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