A premature neonate receiving high-dose chloramphenicol develops vomiting, refusal to feed, hypothermia, abdominal distension, and progressive cyanosis followed by cardiovascular collapse. The underlying mechanism of this presentation is:

• A Direct mitochondrial toxicity of chloramphenicol on cardiac myocytes
• B Immature renal tubular secretion causing accumulation of the inactive metabolite
• C Displacement of bilirubin from albumin causing kernicterus
• D Immature hepatic glucuronidation leading to accumulation of unconjugated chloramphenicol ✓

Explanation

The gray baby syndrome results from neonatal inability to conjugate chloramphenicol with glucuronic acid in the liver, combined with immature glomerular filtration. Unconjugated, active drug accumulates and suppresses mitochondrial respiration, producing the classic picture of vomiting, gray cyanosis, hypotension, and collapse within days of high-dose therapy. Bilirubin displacement causes kernicterus, a separate concern, but does not produce this syndrome. The idiosyncratic aplastic anemia of chloramphenicol is a later, unrelated phenomenon.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.