Pyloric stenosis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]
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Overview
Pathophysiology
The pathogenesis of infantile hypertrophic pyloric stenosis is not fully understood but it could be due abnormal innervation of the pyloric smooth muscle.
The gastric outlet obstruction due to the hypertrophic pylorus impairs emptying of gastric contents into the duodenum. As a consequence, all ingested food and gastric secretions can only exit via vomiting, which can be of a projectile nature. The vomited material does not contain bile because the pyloric obstruction prevents entry of duodenal contents (containing bile) into the stomach.
This results in loss of gastric acid (hydrochloric acid). The chloride loss results in hypochloremia which impairs the kidney's ability to excrete bicarbonate. This is the significant factor that prevents correction of the alkalosis.[1]
A secondary hyperaldosteronism develops due to the hypovolaemia. The high aldosterone levels causes the kidneys to:
- Avidly retain Na+ (to correct the intravascular volume depletion)
- Excrete increased amounts of K+ into the urine (resulting in hypokalaemia).
The body's compensatory response to the metabolic alkalosis is hypoventilation resulting in an elevated arterial pCO2.
Associated Conditions
About 7% of babies will have other conditions such as intestinal malrotation, urinary tract obstruction, and esophageal atresia.
References
- ↑ Kerry Brandis, Acid-Base Physiology. Retrieved December 31, 2006.