Q3
What is the pathophysiology behind the development of this condition?
✅ Model Answer:
• Pathophysiology: Idiopathic hypertrophy of the pyloric muscle (circular and longitudinal layers) → progressive narrowing of the pyloric canal → gastric outlet obstruction → forceful projectile vomiting.
• Loss of gastric contents (H⁺, Cl⁻, K⁺) leads to hypochloremic metabolic alkalosis.
• The exact cause is unknown but associated with genetic factors (linkage to chromosome 11q14-22) and environmental factors.
Q4
What are the ultrasound criteria for diagnosing hypertrophic pyloric stenosis?
✅ Model Answer:
• Ultrasound criteria for HPS:
- Pyloric muscle thickness ≥4 mm (normal 1.5-2.5 mm)
- Pyloric channel length ≥15-20 mm (normal 10-12 mm)
- Pyloric diameter ≥14 mm
- "Target sign" or "doughnut sign" on transverse view
- "Cervix sign" on longitudinal view
- Lack of passage of gastric contents through the pylorus
Q5
What is the initial management of this infant before surgery?
✅ Model Answer:
• Initial management (pre-operative):
- IV fluid resuscitation with 0.9% saline + KCl to correct dehydration and electrolyte imbalance
- Monitor urine output and electrolytes
- Correct hypochloremia and hypokalemia before surgery
- Keep NPO (nil per os)
- NG tube decompression if severe distension
- Surgical consult for pyloromyotomy (Ramstedt procedure)
Q6
What is the definitive surgical treatment for this condition? Describe the procedure.
✅ Model Answer:
• Ramstedt pyloromyotomy is the definitive surgical treatment.
• Procedure: Longitudinal incision of the hypertrophied pyloric muscle down to the submucosa, allowing the mucosa to bulge through, relieving the obstruction.
• Can be performed open (small right upper quadrant incision) or laparoscopic.
• Post-operative feeding: Start with small frequent feeds (usually 4-6 hours after surgery) and advance gradually.
Q7
What are the potential complications of untreated hypertrophic pyloric stenosis?
✅ Model Answer:
• Complications of untreated HPS:
- Severe dehydration and electrolyte imbalance
- Hypochloremic metabolic alkalosis → cardiac arrhythmias
- Failure to thrive and poor weight gain
- Malnutrition
- Aspiration pneumonia
- Jaundice (indirect hyperbilirubinemia)
- Gastric perforation (rare)
- Death (if severe dehydration and electrolyte imbalance are not corrected)
Q8
What is the post-operative follow-up and prognosis for this condition?
✅ Model Answer:
• Post-operative follow-up:
- Feeding advancement: Start with small frequent feeds (4-6 hours post-op), advance as tolerated
- Monitor weight gain and hydration status
- Monitor for surgical complications (bleeding, perforation, infection)
- Follow-up with paediatric surgeon
• Prognosis: Excellent with prompt diagnosis and surgical treatment. Most infants recover completely with normal growth and development. No long-term gastrointestinal sequelae.
⚠️ Key Concept: Approach to Projectile Vomiting
• Projectile non-bilious in 2–8 week old → pyloric stenosis until proven otherwise.
• Classic triad: projectile vomiting, palpable olive, hypochloremic metabolic alkalosis.
• Ultrasound: muscle thickness ≥4 mm, channel length ≥15 mm.
• Management: IV fluid resuscitation, electrolyte correction, surgical pyloromyotomy.
📌 High-yield takeaway:
• Pyloric stenosis is the most common cause of projectile non-bilious vomiting in young infants.
• Hypochloremic metabolic alkalosis is the hallmark electrolyte disturbance.
• Ultrasound is the diagnostic test of choice (thickened pyloric muscle).
• Pyloromyotomy (Ramstedt) is the definitive surgical treatment.
📋 Mock Test Feedback
💡 Examiner's note: Compare your answers with the model answers. In real TOACS, you would discuss these with the examiner.