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This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
The Bottom Line
- Hypertrophy of pyloric muscle causing gastric outlet obstruction — presents at 2–8 weeks (peak 3–5 weeks)
- Projectile, non-bilious vomiting immediately after feeds — baby hungry and wants to feed again (hungry vomiter)
- Classic examination finding: palpable olive-shaped mass in the right upper quadrant during a test feed
- Diagnosis confirmed by abdominal ultrasound: pyloric muscle thickness >3 mm, pyloric channel length >15 mm
- Biochemistry: hypochloraemic, hypokalaemic metabolic alkalosis with paradoxical aciduria — classic exam finding
- Treatment: correct electrolytes and dehydration FIRST, then Ramstedt pyloromyotomy (curative)
Overview
Infantile hypertrophic pyloric stenosis (IHPS) is caused by progressive hypertrophy of the circular muscle of the pylorus, leading to gastric outlet obstruction. The aetiology is multifactorial with genetic and environmental components. It typically presents at 2–8 weeks of age with progressively worsening, forceful, projectile vomiting that is always non-bilious (obstruction is proximal to the ampulla of Vater). The infant is characteristically hungry and eager to feed again immediately after vomiting.
Epidemiology
Incidence is approximately 2–4 per 1,000 live births in the UK. Male:female ratio is 4:1 (much more common in boys). Firstborn males are most commonly affected. Risk factors include family history (especially maternal), erythromycin or azithromycin use in the first 2 weeks of life, and maternal smoking. There is an association with blood group B and O.
Clinical Features
Symptoms
Projectile, non-bilious vomiting — progressively worsening over days to weeks
Vomiting occurs immediately after feeds
Baby is hungry and wants to feed again after vomiting ("hungry vomiter")
Weight loss or poor weight gain
Constipation and reduced wet nappies (dehydration)
Bilious (green) vomiting (suggests a different diagnosis — malrotation/volvulus)
Signs
Palpable olive-shaped mass in right upper quadrant — best felt during a test feed when the stomach contracts
Visible gastric peristalsis — waves passing from left to right across the upper abdomen
Signs of dehydration: sunken fontanelle, dry mucous membranes, reduced skin turgor
Jaundice (unconjugated) — occurs in ~5% due to reduced hepatic glucuronyl transferase activity from starvation
Investigations
First-line
Abdominal ultrasoundGold standard diagnostic test. Pyloric muscle thickness >3 mm and channel length >15 mm are diagnostic. Also shows failure of gastric emptying through the pylorus
Blood gas and electrolytesClassic finding: hypochloraemic, hypokalaemic metabolic alkalosis (from loss of HCl in vomitus). Paradoxical aciduria (kidneys excrete H+ to retain K+)
Second-line
Test feedFeed the baby while examining abdomen — may feel the olive mass and see gastric peristalsis. Less used now that USS is readily available
Specialist
Upper GI contrast studyRarely needed — shows string sign (elongated pyloric channel) and shoulder sign. Only if USS equivocal
Management
Paediatric surgical guidelines1
Resuscitation — correct before surgery
- IV fluid resuscitation: 0.9% saline with added KCl once urine output established
- Correct dehydration and electrolyte abnormalities — surgery should NOT proceed until metabolic alkalosis corrected
- Typically takes 24–48 hours to correct biochemistry
- Keep nil by mouth, insert NG tube if vomiting profuse
2
Ramstedt pyloromyotomy
- Definitive treatment — curative
- Longitudinal incision through the hypertrophied pyloric muscle down to but not through the mucosa
- Can be performed open (RUQ incision or periumbilical) or laparoscopically
- Post-operatively: graded feeds starting 4–6 hours post-op, usually tolerating full feeds within 24 h
- Prognosis is excellent — cure rate approaching 100%
Complications
- Pre-operative: Dehydration, electrolyte disturbance, aspiration, failure to thrive
- Surgical: Mucosal perforation (duodenal — requires repair), wound infection, incomplete myotomy (rare, requires revision)
- Post-operative vomiting: Common in first 24–48 h but resolves spontaneously — does not indicate incomplete myotomy
UKMLA Exam Tips
- 1Projectile NON-BILIOUS vomiting at 2–8 weeks in a firstborn male = pyloric stenosis until proven otherwise
- 2Bilious vomiting = NOT pyloric stenosis — think malrotation with volvulus (surgical emergency)
- 3The biochemical finding is HYPOCHLORAEMIC, HYPOKALAEMIC METABOLIC ALKALOSIS — most commonly examined biochemistry question in paediatrics
- 4Paradoxical aciduria: despite systemic alkalosis, kidneys excrete H+ to retain K+ and Na+
- 5USS is the diagnostic test: muscle >3 mm thick, channel >15 mm long
- 6Correct electrolytes BEFORE surgery — operating on a baby in metabolic alkalosis is dangerous
- 7Olive mass is felt in the RUQ during a test feed — classic clinical finding
practicetest your knowledge on pyloric stenosisApply what you've learnt with UKMLA-style questions from the iatroX Q-Bank — paediatrics and beyond.
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