Anesthesiology APPLIED Exam › Pediatric and neonatal

Pyloric stenosis

T1Pediatric and neonatal·958 words · ~5 min read·v0.1DRAFT

Why examiners ask this

Pyloric stenosis is the cleanest test of one principle: this is a medical emergency and a surgical urgency, never a surgical emergency. The examiner wants to see whether I will resist the surgeon's schedule until the infant is resuscitated, whether I can explain hypochloremic hypokalemic metabolic alkalosis from first principles, and whether I can run a full-stomach induction in a 4-kg patient. It stresses judgment and organization more than knowledge.

The 60-second answer

A 4-week-old with projectile vomiting and a palpable olive has a full stomach, is volume-depleted and has a hypochloremic, hypokalemic metabolic alkalosis with paradoxical aciduria. My first move is to decline the operating room until resuscitation is complete: I rehydrate with 20 mL/kg boluses of isotonic saline, then run dextrose-containing saline with potassium once the infant is voiding, and I recheck electrolytes every 4–6 hours. My endpoints are a chloride above 100 mEq/L, bicarbonate below 30 mEq/L, potassium normal and urine output above 1 mL/kg/h. In the operating room I empty the stomach with a large orogastric tube in supine, left and right lateral positions, pre-oxygenate, and perform a rapid sequence induction with propofol and succinylcholine or rocuronium, intubating the trachea. I keep opioids minimal, use acetaminophen and local infiltration, extubate awake, and monitor for apnea for 12–24 hours afterward.

Decision points and the "why"

Delay for resuscitation — the alkalosis and hypovolemia are what harm the infant; the pylorus is not. A bicarbonate above 30 mEq/L means compensatory hypoventilation and a CSF alkalosis that persists after the serum corrects, which is why these babies have postoperative apnea. I change nothing about this plan when the surgeon pushes; I give the timeline of 12–48 hours and the endpoints.
Saline, not lactated Ringer's — the deficit is chloride, and chloride is what the kidney needs to stop exchanging hydrogen for sodium. Lactate is metabolized to bicarbonate and worsens the alkalosis. I add potassium 20 mEq/L only after urine output is documented.
Orogastric suction before induction — the stomach holds barium or formula regardless of the fasting interval; a 14-Fr tube aspirated in three positions removes most of it. I still treat the patient as a full stomach because emptying is never complete.
Rapid sequence with intubation — this is the standard of care; awake intubation in a vigorous infant causes hypoxemia, bradycardia and intracranial pressure surges, and I do not do it. I use propofol 2–3 mg/kg with succinylcholine 2 mg/kg or rocuronium 1.2 mg/kg, and I have atropine drawn up because succinylcholine causes bradycardia in infants.
Minimal opioids — pyloromyotomy is a short, low-pain operation, and opioids add to the central apnea risk from the CSF alkalosis. Acetaminophen 10–15 mg/kg IV and surgical infiltration of bupivacaine 0.25% within 2.5 mg/kg suffice.
Awake extubation — the stomach is still potentially full and the infant is at apnea risk; I extubate with eyes open, strong flexion of the hips and a regular breathing pattern.

The complication they will inject

The surgeon wants to proceed tonight; the labs show chloride 88 mEq/L, bicarbonate 36 mEq/L and potassium 2.9 mEq/L. I recognize an under-resuscitated infant and say so plainly: the risk of proceeding is postoperative apnea, arrhythmia from hypokalemia under volatile anesthesia, and hypotension on induction. I communicate a concrete plan, saline 20 mL/kg now, maintenance with potassium, repeat labs in 6 hours, and a target time for surgery. The alternative inject is intraoperative: the saturation drops after induction with a high airway pressure. I rule out esophageal or bronchial intubation and aspiration, suction the tube, and if the abdomen is distended I decompress the stomach, because the surgeon's laparoscopic insufflation adds to the diaphragm splinting in a 4-kg patient. I ask for insufflation pressure under 8 mmHg.

Pitfalls that cost points

Agreeing to an emergency operation because the stem calls it an emergency.
Quoting "metabolic alkalosis" without explaining paradoxical aciduria or why saline corrects it.
Describing an awake intubation as the safe option; examiners expect a rapid sequence induction.
Giving fentanyl 2 mcg/kg "for the surgery" and then being asked why the infant stopped breathing in recovery.
Forgetting the dextrose: a fasting neonate on saline alone becomes hypoglycemic.

Rapid-why

Q: Why paradoxical aciduria? A: Once the kidney has exhausted sodium and chloride, it reabsorbs sodium in exchange for hydrogen to defend volume, excreting acid urine despite alkalemia.

Q: Why is the CSF alkalosis the apnea mechanism? A: The blood-brain barrier equilibrates bicarbonate slowly; the central chemoreceptors remain alkalotic after the serum normalizes, so ventilatory drive stays depressed for a day.

Q: Why does potassium fall? A: Vomiting loses little potassium; the kidney wastes it in exchange for sodium under aldosterone, and alkalosis shifts it into cells.

Q: Would you use a caudal? A: No; the incision is supraumbilical and brief, and infiltration gives the same benefit without the dural risk in a dehydrated infant.

Numbers to know

Item	Value
Resuscitation endpoints	Cl⁻ >100 mEq/L, HCO₃⁻ <30 mEq/L, K⁺ normal, urine >1 mL/kg/h
Fluid bolus	20 mL/kg 0.9% saline, repeated to effect
Maintenance	D5 0.45% saline + KCl 20 mEq/L after voiding
Induction	Propofol 2–3 mg/kg; succinylcholine 2 mg/kg or rocuronium 1.2 mg/kg; atropine 20 mcg/kg available
Bupivacaine infiltration limit	2.5 mg/kg
Postoperative apnea monitoring	12–24 h

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