A premature neonate receiving IV chloramphenicol for suspected sepsis becomes lethargic, hypotensive, ashen grey, and refuses feeds on day three of therapy. The underlying reason for this presentation is:

• A Immune-mediated hemolysis from maternal antibody transfer
• B Deficient hepatic glucuronidation leading to drug accumulation ✓
• C Dose-independent aplastic marrow suppression
• D Displacement of bilirubin from albumin causing kernicterus

Explanation

This is the classic gray baby syndrome. Neonates, especially preterm infants, have immature hepatic UDP-glucuronosyltransferase activity and reduced renal clearance, so unmetabolized chloramphenicol accumulates and blocks mitochondrial electron transport in myocardium, producing shock and collapse. Option C describes aplastic anemia, which is idiosyncratic and occurs weeks later, not acutely in neonates. Bilirubin displacement is a separate concern with sulfonamides.

Reference: Katzung Basic and Clinical Pharmacology, 15th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.