⚕️ FCPS MCPS IMM MD Paediatrics TOACS

Observed Station · Vomiting · Data Interpretation

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📋 Data Interpretation Station

Vomiting – Clinical Scenario with Lab & Imaging

3-week-old male with progressive projectile non-bilious vomiting after feeds. Hungry and irritable. Palpable mass in RUQ.

Q1 Identify the most likely diagnosis based on the clinical presentation and lab findings.
Serum Sodium132 mEq/L (low)
Serum Potassium2.9 mEq/L (low)
Serum Chloride82 mEq/L (low)
ABG pH7.52 (alkalosis)
Model Answer:
Diagnosis: Hypertrophic pyloric stenosis — projectile vomiting, palpable olive, hypochloremic metabolic alkalosis, ultrasound shows thickened pylorus (muscle ≥4mm, channel ≥15mm).
Any other test: Ultrasound abdomen for Pyloric muscle thickness 5 mm, channel length 20 mm, Renal function tests (BUN, creatinine), pre-operative labs (CBC, coagulation profile), ECG if severe hypokalemia.
What to do next: Correct dehydration and electrolytes (IV 0.9% saline + KCl). Surgical consult for pyloromyotomy (Ramstedt procedure).
Follow-up plan: Post-op feeding advancement (start 4-6 hours after surgery), monitor weight gain, wound care, ensure adequate hydration.
Q2 What is the characteristic electrolyte disturbance seen in this condition? Describe the pattern.
Model Answer:
Hypochloremic metabolic alkalosis — classic electrolyte pattern:
- Low serum chloride (↓Cl⁻)
- Low serum potassium (↓K⁺)
- Elevated pH (>7.45)
- Elevated bicarbonate (↑HCO₃⁻)
- Paradoxical aciduria (kidneys excrete H⁺ to conserve K⁺)
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.

🎯 Examiner Scoring Checklist

  • • Identifies pyloric stenosis (projectile, olive, alkalosis, US)
  • • Recognizes electrolyte derangements (hypochloremia, hypokalemia, alkalosis)
  • • Describes ultrasound criteria for diagnosis
  • • Plans fluid resuscitation (0.9% saline + KCl) before surgery
  • • Knows definitive treatment: Ramstedt pyloromyotomy
  • • Discusses complications of untreated HPS
  • • Understands post-operative care and prognosis
📌 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.