A neonate given prophylactic chloramphenicol becomes gray, hypothermic, hypotensive and refuses feeds within 48 hours. The pathogenesis of this gray baby syndrome is:

• A Hemolysis from maternal anti-D antibodies compounded by the drug
• B Immature renal tubular secretion causing accumulation of the inactive metabolite
• C Immature hepatic glucuronidation leading to accumulation of unconjugated chloramphenicol ✓
• D Direct toxic effect of chloramphenicol on the neonatal myocardium

Explanation

Neonates, especially preterm infants, have deficient UDP-glucuronosyltransferase activity and reduced glomerular filtration, so unconjugated chloramphenicol accumulates. Free chloramphenicol inhibits mitochondrial electron transport in myocardial and vascular smooth muscle cells, producing the gray color, shock and collapse of gray baby syndrome. Renal immaturity contributes secondarily but the key defect is conjugation, not secretion of metabolite. The syndrome is dose related and preventable by keeping levels below 25 microgram/mL.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.