A 3-week-old male infant presents with projectile non-bilious vomiting immediately after feeds, with visible peristalsis from left to right in the epigastrium. The infant appears hungry after vomiting. Electrolytes show Na 130 mEq/L, K 2.8 mEq/L, Cl 82 mEq/L, bicarbonate 32 mEq/L, pH 7.52. The PATHOLOGICAL metabolic abnormality and its MECHANISM are BEST described as:
- A Hypochloremic hypokalemic metabolic alkalosis due to loss of HCl in vomitus and paradoxical aciduria ✓
- B Metabolic acidosis due to hydrogen ion production from pyloric hypertrophy
- C Hyperchloremic metabolic acidosis due to sodium-hydrogen exchange impairment
- D Respiratory alkalosis with compensatory metabolic acidosis
Explanation
Hypertrophic pyloric stenosis causes repeated loss of highly acidic, chloride-rich gastric contents in vomitus. The resultant depletion of HCl generates hypochloremic metabolic alkalosis. The kidneys initially conserve sodium by exchanging Na+ for H+/K+, worsening hypokalemia and producing paradoxical aciduria (acid urine despite systemic alkalosis). Correction requires IV 0.9% NaCl with KCl supplementation before undertaking Ramstedt pyloromyotomy — surgery on an uncorrected alkalotic, dehydrated infant carries anesthetic risk.
Reference: Ghai Essential Pediatrics, 10th ed.
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Written and medically reviewed by the StethoPrep medical team.