Step 1: Understanding the Question:
The question asks about the metabolic complication that follows from the persistent vomiting seen in pyloric stenosis, whether congenital or acquired.
Step 2: Key Concept or Approach:
Pyloric stenosis obstructs gastric outflow, so the patient repeatedly vomits gastric contents that are rich in hydrogen and chloride ions. Losing this acidic, chloride-rich fluid, combined with the kidney's response to volume depletion, decides the acid-base disturbance that develops.
Step 3: Working Through the Options:
The direct loss of hydrogen and chloride ions in vomitus raises the blood pH, producing an alkalosis rather than an acidosis, which rules out both metabolic acidosis and hypochloremic acidosis. As the patient becomes dehydrated, the kidneys try to conserve sodium and water; the distal tubule reabsorbs sodium in exchange for potassium and hydrogen ions, which are excreted in the urine even though the blood is already alkalotic — this is the classic paradoxical aciduria. The chloride lost in vomitus is not replaced, so the alkalosis is specifically hypochloremic, not hyperchloremic, which rules out hyperchloremic alkalosis.
Step 4: Conclusion:
The important complication of pyloric stenosis is hypochloremic alkalosis, usually with accompanying hypokalemia and paradoxical aciduria.