A 6-week-old male infant presents with progressively worsening non-bilious projectile vomiting after every feed. He is visibly hungry post-vomiting. Palpation reveals an olive-shaped mass in the right hypochondrium. Electrolytes show hypochloremic hypokalemic metabolic alkalosis. What is the mechanism of the metabolic derangement?

• A Loss of alkaline pancreatic secretions through the obstructed duodenum
• B Increased adrenal aldosterone secretion from stress leads to Na+ retention and K+ loss
• C Loss of HCl from projectile vomiting leads to chloride depletion; the kidney compensates by excreting K+ and H+ in exchange for Na+ (paradoxical aciduria), causing hypokalemia and alkalosis ✓
• D Starvation ketoacidosis with compensatory chloride retention

Explanation

In hypertrophic pyloric stenosis, loss of HCl-rich gastric acid via vomiting depletes plasma chloride. To maintain electroneutrality and Na+, the kidney reabsorbs Na+ in exchange for H+ (as NH4+) and K+ via aldosterone-stimulated channels, leading to hypokalemia. Chloride depletion prevents normal bicarbonate excretion (HCO3- cannot be secreted without Cl-), perpetuating alkalosis — the classic 'paradoxical aciduria' where urine is acidic despite systemic alkalosis. Resuscitation with 0.9% NaCl + KCl correction must precede surgery (Ramstedt pyloromyotomy); operating on unresuscitated alkalosis carries anesthesia risks.

Reference: Bailey & Love's Short Practice of Surgery, 27th ed.

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Written and medically reviewed by the StethoPrep medical team.