🍼🤮 Hypertrophic pyloric stenosis (HPS) – Infants typically develop hypochloraemic, hypokalaemic metabolic alkalosis. Diagnosis is confirmed with ultrasound (USS) 🖥️.
📖 About
- A common cause of projectile, non-bilious vomiting in infants 🚼.
- Caused by hypertrophy of the pyloric muscle → gastric outflow obstruction.
- Often presents as a surgical emergency but prognosis is excellent once treated.
🧬 Aetiology
- 👦 More common in first-born male infants.
- 📈 Incidence: ~2–4 per 1000 live births.
- 👩👦 Family history (especially maternal side) suggests genetic predisposition.
- Mechanism: pyloric muscle hypertrophy + hyperplasia → narrowing of pyloric channel.
🩺 Clinical Features
👉 To palpate the “olive”: stand on the baby’s left side, palpate with the left hand along the lateral border of the right rectus in the RUQ, ideally during a feed.
- ⏰ Usually presents between 2–7 weeks of age.
- 🤮 Non-bilious, projectile vomiting shortly after feeds.
- 🍽️ Infant remains hungry after vomiting ("hungry vomiter").
- 🚫 No diarrhoea – constipation is common; may pass “starvation stools”.
- ⚠️ Large-volume vomiting within minutes of feeding → weight loss, dehydration.
- 👶 Infant often alert, anxious, and malnourished if untreated.
- ✋ Palpable olive-shaped mass in RUQ = classic sign.
- 👀 Visible peristalsis may be seen across the abdomen after a feed.
🖼️ Image
🔎 Investigations
- Bloods: Classic finding = hypochloraemic, hypokalaemic metabolic alkalosis 🧪.
Hypokalaemia usually develops after 2–3 weeks of persistent vomiting.
- Ultrasound (USS): 📏 Diagnostic test of choice – pyloric thickness >3mm and length >15mm = HPS.
- Barium meal: Rarely used; may show “string sign” but generally unnecessary.
💊 Management
- Initial Stabilisation:
- 💧 IV fluid resuscitation + electrolyte correction (replace K⁺ and Cl⁻ until Cl⁻ >90 mmol/L).
- 🛑 Delay surgery until metabolic derangements are corrected (to avoid anaesthetic risk).
- 🧴 NG tube decompression if severe gastric distension.
- Definitive Treatment:
- ✂️ Ramstedt’s pyloromyotomy = standard surgical cure. Muscle split along pylorus, mucosa left intact.
- 🚼 Usually performed laparoscopically in modern practice.
- 📈 Excellent prognosis – most feed normally within 24–48h post-op.
⚠️ Complications if Untreated
- 💧 Severe dehydration & electrolyte imbalance
- 📉 Failure to thrive
- 🫀 Shock & metabolic alkalosis complications (e.g., hypoventilation, seizures)
🧑🏫 Exam Tip
The triad of hypertrophic pyloric stenosis =
1️⃣ Non-bilious projectile vomiting,
2️⃣ Palpable olive-shaped mass,
3️⃣ Visible gastric peristalsis.
Always link the metabolic alkalosis (low Cl⁻, low K⁺, raised HCO₃⁻) to the underlying repeated vomiting of gastric contents. This is a classic finals OSCE favourite 🎯.
Cases — Infantile Hypertrophic Pyloric Stenosis
- Case 1 — Classic presentation 🍼: A 6-week-old first-born boy presents with 2 weeks of progressively worsening non-bilious, projectile vomiting after feeds. Exam: visible gastric peristalsis and an olive-shaped mass in the right upper quadrant. Bloods: hypochloraemic, hypokalaemic metabolic alkalosis. Diagnosis: classic hypertrophic pyloric stenosis. Managed with IV fluid and electrolyte correction followed by Ramstedt pyloromyotomy.
- Case 2 — Failure to thrive 📉: A 7-week-old girl presents with poor weight gain, constipation, and frequent vomiting. She is dehydrated with sunken eyes and dry mucous membranes. Blood gas: metabolic alkalosis. Ultrasound: elongated, thickened pylorus. Diagnosis: pyloric stenosis with dehydration and failure to thrive. Managed with urgent fluid/electrolyte replacement and planned surgical pyloromyotomy.
- Case 3 — Atypical late presentation ⚠️: A 12-week-old boy presents with persistent vomiting and irritability. Exam: abdominal distension and metabolic alkalosis. History of delayed diagnosis due to atypical age. Ultrasound confirms pyloric stenosis. Diagnosis: delayed diagnosis of pyloric stenosis. Managed with fluid resuscitation, correction of electrolytes, and surgery.
Teaching Point 🩺: Infantile hypertrophic pyloric stenosis usually presents at 2–8 weeks of life, more common in first-born males.
Key features: projectile non-bilious vomiting, palpable olive-shaped mass, visible peristalsis.
Biochemical hallmark: hypochloraemic, hypokalaemic metabolic alkalosis.
Management = correct fluids/electrolytes first, then Ramstedt pyloromyotomy.