A 3-week-old male infant presents with non-bilious, projectile vomiting after every feed. On examination a palpable 'olive' is felt in the epigastrium. Ultrasound confirms pyloric muscle thickness >4 mm and channel length >16 mm. After correcting hypochloraemic hypokalaemic metabolic alkalosis, the definitive treatment is:
- A Laparotomy with Heineke-Mikulicz pyloroplasty
- B Intravenous atropine for 2 weeks to relax the pyloric smooth muscle
- C Ramstedt pyloromyotomy (open or laparoscopic) dividing the hypertrophied pyloric muscle down to mucosa longitudinally without entering the mucosa ✓
- D Balloon dilation of the pylorus via endoscopy
Explanation
Hypertrophic pyloric stenosis (HPS) is treated by Ramstedt pyloromyotomy — a longitudinal incision through the hypertrophied pyloric muscle down to the submucosa without violating the mucosa, allowing the mucosa to bulge. Metabolic correction is mandatory pre-operatively because the hypochloraemic metabolic alkalosis (from HCl loss in vomit with paradoxical aciduria) increases anaesthetic risk. Atropine (IV or oral) can be used non-operatively in mild cases but the surgical cure rate is near-100% vs. atropine's 85-90%. Pyloroplasty is used for pyloric stenosis in adults (peptic ulcer disease), not HPS.
Reference: Bailey & Love's Short Practice of Surgery, 27th ed.
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Written and medically reviewed by the StethoPrep medical team.