A child with infantile hypertrophic pyloric stenosis has multiple episodes of non-bilious vomiting. Which of the following metabolic abnormality is likely to be seen in this condition?

Correct Answer: C. Hypochloremic, hypokalemic alkalosis

Infantile hypertrophic pyloric stenosis (IHPS) causes persistent non-bilious vomiting because the pyloric outlet is obstructed. The vomitus contains gastric juice rich in hydrochloric acid (HCl) and electrolytes. Repeated loss of HCl leads to three sequential metabolic derangements: (1) Hypochloremia — direct loss of chloride in gastric secretions; (2) Hypokalemia — loss of potassium in vomitus AND secondary renal potassium wasting (explained below); (3) Metabolic alkalosis — loss of H+ ions shifts the acid-base balance toward alkalinity. The alkalosis is perpetuated by volume depletion activating the renin-angiotensin-aldosterone system (RAAS), which increases renal sodium reabsorption and potassium/H+ excretion, worsening both hypokalemia and alkalosis. This creates a "contraction alkalosis" — the kidney paradoxically excretes H+ despite systemic alkalosis because it prioritizes sodium conservation. The classic triad is hypochloremic, hypokalemic metabolic alkalosis. This is the hallmark electrolyte pattern in IHPS and is seen in Indian pediatric practice as a common presentation in infants aged 3–5 weeks, particularly in males.

Why the other options are wrong

A. Hypokalemic hyperchloremic alkalosis — This is wrong because IHPS causes loss of chloride in gastric secretions, not retention. Hyperchloremia would occur in conditions with chloride retention (e.g., renal tubular acidosis type 1, diarrhea with bicarbonate loss). The presence of alkalosis with hyperchloremia is also metabolically incongruent in the context of gastric outlet obstruction. B. Hyperchloremic hypokalemic acidosis — This is wrong because IHPS causes metabolic alkalosis, not acidosis. Loss of HCl shifts pH upward. Hyperchloremic acidosis is seen in diarrhea (bicarbonate loss) or renal tubular acidosis, not in pyloric stenosis. This option confuses the acid-base consequence of gastric versus intestinal fluid loss. D. Hypochloremic, hypokalemic acidosis — While hypochloremia and hypokalemia are correct, the acid-base disturbance is alkalosis, not acidosis. Acidosis would occur if the child had diarrhea (bicarbonate loss) or renal failure. In IHPS, the loss of gastric acid (HCl) directly causes alkalosis. This option reverses the pH direction and is a common NBE trap.

High-Yield Facts

Mnemonics

IHPS Electrolyte Pattern: 'HCl Loss = Opposite' Gastric HCl loss → lose H+ (alkalosis), lose Cl– (hypochloremia), lose K+ (hypokalemia). Remember: opposite of what you'd expect in diarrhea (which causes acidosis + hyperchloremia). Contraction Alkalosis: 'RAAS Worsens It' Volume depletion → RAAS activation → Na+ reabsorption + H+/K+ excretion → alkalosis persists despite low Cl–. Fix: give saline, not just fluids.

NBE Trap

NBE pairs IHPS with "hypokalemic acidosis" (option D) to trap students who confuse gastric outlet obstruction with diarrhea or who incorrectly assume that electrolyte loss always causes acidosis. The key discriminator is recognizing that loss of gastric acid causes alkalosis, not acidosis.

Clinical Pearl

In Indian pediatric practice, an infant presenting with projectile vomiting, visible peristaltic waves, and a palpable "olive" in the epigastrium should immediately raise suspicion for IHPS. Pre-operative fluid resuscitation with normal saline (not dextrose) is critical — it corrects hypochloremia and suppresses aldosterone, allowing the kidney to excrete the excess bicarbonate and normalize pH before surgery.

_Reference: OP Ghai (Pediatrics) Ch. 8 (Fluid & Electrolyte Disorders); Harrison Ch. 46 (Acid-Base Disorders); KD Tripathi Ch. 15 (Fluid & Electrolyte Balance)_