A neonate treated with chloramphenicol for a resistant infection becomes lethargic, feeds poorly, turns ashen grey, and develops hypotension and abdominal distension. The underlying mechanism of this presentation is:
- A Immune-mediated hemolysis from maternal antibodies
- B Displacement of bilirubin from albumin causing kernicterus
- C Direct mitochondrial toxicity causing lactic acidosis
- D Deficient hepatic glucuronidation leading to accumulation of unconjugated drug ✓
Explanation
Gray baby syndrome results from immature hepatic UDP-glucuronosyltransferase activity in neonates, especially preterm infants. Unconjugated chloramphenicol accumulates because it is normally inactivated mainly by glucuronide conjugation, producing cardiovascular collapse, vomiting, hypotonia and the characteristic grey coloration. Displacement of bilirubin contributes to jaundice but is not the primary cause of collapse. The syndrome is prevented by limiting doses to below 25 mg/kg/day in neonates.
Reference: Katzung Basic and Clinical Pharmacology, 16th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.