Pyloric Stenosis
Pathophysiology & Risk Factors
Hypertrophy of the circular muscle at the pylorus creates a near-complete gastric outlet obstruction. Because the obstruction sits proximal to the ampulla of Vater, vomit is non-bilious. Repeated vomiting of gastric HCl drives hypochloremic, hypokalemic metabolic alkalosis. Classically presents at 2-6 weeks of age.
Pyloric stenosis pathophysiology cascade
- Hypertrophied pylorusCircular muscle thickens
- Gastric outlet obstructionProximal to ampulla of Vater
- Projectile non-bilious vomitingForceful, after feeds
- Loss of HCl + dehydrationH+, Cl-, K+ depleted
- Hypochloremic hypokalemic metabolic alkalosisClassic lab triad
Signs & Symptoms
Diagnostics & Labs
Pyloric stenosis vs. mimics
Pyloric stenosis
- Vomit character
- Projectile, non-bilious
- Feeding behavior
- Hungry, eager after
- Classic finding
- Olive-shaped RUQ mass
- Acid-base
- Metabolic alkalosis
Intussusception / distal obstruction
- Vomit character
- Bilious (green)
- Feeding behavior
- Disinterested / pain
- Classic finding
- Currant-jelly stools / distension
- Acid-base
- Acidosis if lower-GI loss
GERD
- Vomit character
- Effortless spit-up
- Feeding behavior
- Content
- Classic finding
- Back-arching when supine
- Acid-base
- Usually normal
Interventions & Priorities
Treatments & Medications
Patient Teaching
Clinical Pearl
Non-bilious + projectile + hungry after = pyloric stenosis. Fix the fluids and alkalosis FIRST, then the surgeon fixes the pylorus.