Pyloric stenosis

Surgical approach

Operation: Ramstedt pyloromyotomy (splitting hypertrophied pyloric muscle down to mucosa to relieve gastric outlet obstruction).
- Approach: open (RUQ transverse incision) or laparoscopic (ports; insufflation).
- Key steps: identify pylorus (“olive”), longitudinal seromuscular incision, spread muscle fibres until mucosa bulges; ensure complete myotomy; check for mucosal perforation/bleeding.
- Post-op feeding: usually early graded feeds; vomiting can persist briefly despite adequate myotomy.

Anaesthetic management

Type of anaesthesia: General anaesthesia (no role for regional as sole technique).
Airway: cuffed ETT preferred; RSI with cricoid (modified for neonate/infant) due to full stomach/aspiration risk. Avoid SGA.
- Pre-induction: gastric decompression with wide-bore NG/OG; aspirate in multiple positions (supine, left, right, prone if safe) to minimise residual milk/secretions.
Duration: typically 30–60 min (longer if laparoscopic/complications).
Pain: usually mild–moderate; manage with paracetamol ± small-dose opioid; consider local infiltration/TAP block (operator dependent).
Key principle: resuscitation before anaesthesia (this is a medical emergency, not a surgical emergency).
Ventilation: avoid hyperventilation; aim normocapnia to reduce risk of post-op apnoea (alkalosis blunts ventilatory drive).

Definition & epidemiology

IHPS = hypertrophy/hyperplasia of pyloric circular muscle causing gastric outlet obstruction in early infancy.
Typical age: 2–8 weeks; more common in males (classically first-born).
Associations: macrolide exposure (e.g. erythromycin/azithromycin) in early life; family history.

Clinical features

History: progressive non-bilious projectile vomiting after feeds; hungry after vomiting; poor weight gain; dehydration.
Examination: dehydration; visible gastric peristalsis; palpable pyloric “olive” (may be difficult).
Differential: sepsis, gastro-oesophageal reflux, milk protein allergy, intestinal obstruction (bilious vomiting suggests distal obstruction), raised ICP.

Investigations

Ultrasound: thickened pyloric muscle and elongated pyloric canal (diagnostic).
Blood gas/U&Es: hypochloraemic, hypokalaemic metabolic alkalosis; may have paradoxical aciduria; assess glucose.
Assess hydration: weight trend, urine output, capillary refill; consider FBC/CRP if infection suspected.

Pathophysiology & anaesthetic implications

Vomiting of gastric HCl → loss of H+ and Cl− → metabolic alkalosis + hypochloraemia.
Volume depletion → RAAS activation → renal Na+ retention with K+ and H+ loss → worsens hypokalaemia/alkalosis; can cause paradoxical aciduria.
Alkalosis reduces ionised calcium and can depress ventilation; in infants, alkalosis may increase risk of post-op apnoea (central drive blunted).
Stomach is full despite fasting → high aspiration risk; NG/OG decompression reduces but does not eliminate risk.

Pre-operative optimisation (core FRCA content)

Priorities: correct hypovolaemia, electrolytes, and alkalosis before theatre; treat hypoglycaemia.
IV access + monitoring; measure weight; strict fluid balance; consider warming measures early.
Fluid resuscitation: 0.9% saline boluses (e.g. 10–20 mL/kg) if shocked/dehydrated; then maintenance + deficit replacement with chloride-rich fluid.
- Add potassium only once urine output established and K+ known (typical 10–20 mmol/L in maintenance fluid, per local policy).
Targets often used before anaesthesia (institutional variation): Cl− ≥ 100 mmol/L, HCO3− < 30 mmol/L (or base excess near normal), K+ corrected, clinically euvolaemic.
NG/OG tube: aspirate regularly; keep on free drainage until induction; remove/leave in situ per local practice (often left for decompression until after induction).
Fasting: treat as full stomach regardless; follow milk/clear fluid rules but do not rely on them to reduce aspiration risk.

Induction & airway (RSI details)

Preparation: full monitoring; suction ready; difficult airway plan; pre-oxygenate (gentle CPAP if needed, avoid gastric insufflation if possible).
Modified RSI: gentle mask ventilation may be required in infants to prevent desaturation; keep pressures low; apply cricoid carefully (avoid airway obstruction).
Induction agents: propofol or thiopentone (haemodynamics/experience); ketamine may be considered if unstable; opioid sparing.
Neuromuscular block: rocuronium (rapid onset) or suxamethonium (if no contraindication); ensure full paralysis before laryngoscopy.
Tube: appropriately sized cuffed ETT; confirm with capnography; secure well (shared airway not typical but infant movement risk).

Maintenance

Anaesthesia: volatile (sevoflurane) or TIVA; maintain normothermia (forced-air warmer, warmed fluids).
Fluids: isotonic balanced crystalloid or 0.9% saline per local policy; avoid hypotonic fluids; monitor glucose (risk of hypoglycaemia).
Analgesia: paracetamol; local infiltration; small-dose opioid (e.g. fentanyl) if needed; avoid excessive opioids due to apnoea risk.
Antiemetic: variable; vomiting may occur post-op regardless; consider ondansetron per local practice.
Laparoscopy considerations: insufflation → reduced venous return, ↑ airway pressures, hypercarbia; adjust ventilation; watch for vagal bradycardia.

Emergence & post-operative care

Extubation: fully awake with good tone/ventilation; ensure stomach decompressed; suction pharynx; consider lateral position.
Apnoea monitoring: consider HDU/appropriate monitoring, especially if premature, significant residual alkalosis, anaemia, sepsis, or opioid exposure.
Feeding: early feeds per surgical protocol; manage ongoing vomiting conservatively unless persistent/concerns for incomplete myotomy or mucosal perforation.
Complications: aspiration pneumonitis, mucosal perforation (peritonitis), bleeding, incomplete myotomy (persistent obstruction), wound infection.

A 5-week-old, 3.8 kg infant with suspected pyloric stenosis is listed for pyloromyotomy. What are your immediate priorities before anaesthesia?

Focus on optimisation and making theatre safe; surgery should wait until resuscitated.

Confirm diagnosis and severity: history of non-bilious projectile vomiting, dehydration, weight loss; review ultrasound.
Assess and correct dehydration/hypovolaemia: clinical signs + urine output; IV access; consider 10–20 mL/kg 0.9% saline bolus if needed.
Correct biochemical derangements: hypochloraemic metabolic alkalosis ± hypokalaemia; repeat gases/U&Es until acceptable.
Use chloride-rich fluids; add K+ only after urine output established and K+ known.
Treat/prevent hypoglycaemia: check glucose and give appropriate dextrose-containing maintenance if indicated (per neonatal policy).
Reduce aspiration risk: NG/OG decompression with repeated aspiration in different positions; treat as full stomach regardless of fasting time.

Explain the acid–base disturbance in pyloric stenosis and why it matters to the anaesthetist.

Link vomiting physiology to ventilation and peri-operative apnoea risk.

Vomiting gastric HCl → loss of H+ and Cl− → metabolic alkalosis + hypochloraemia.
Volume depletion → RAAS → renal Na+ retention with K+ and H+ excretion → worsens hypokalaemia/alkalosis; can cause paradoxical aciduria.
Alkalosis blunts ventilatory drive; infants are vulnerable → increased risk of post-operative apnoea, especially with opioids or residual alkalosis.
Hypokalaemia increases risk of arrhythmias and potentiates neuromuscular blockade; correct before GA where possible.

What biochemical targets would you like before proceeding to theatre?

State pragmatic targets commonly used; acknowledge local variation.

Clinically euvolaemic with adequate urine output.
Chloride corrected (commonly aim Cl− ≥ 100 mmol/L).
Alkalosis improved (commonly HCO3− < 30 mmol/L or base excess near normal).
Potassium normalised (or trending to normal with safe replacement and ECG stability).
Glucose in acceptable range for age; normothermic.

Describe your induction technique and justify it.

High aspiration risk + infant physiology drives a modified RSI with careful preparation.

Treat as full stomach: NG/OG decompression immediately pre-induction; suction and assistance available.
Pre-oxygenate; consider gentle CPAP if needed; avoid excessive mask pressures to reduce gastric insufflation.
Modified RSI: induction agent + rapid NMBD; gentle ventilation may be required to prevent desaturation; apply cricoid carefully.
Intubate with cuffed ETT; confirm with capnography; secure tube; avoid SGA due to aspiration risk.

How do you decompress the stomach effectively and why might a single aspiration be inadequate?

Milk curds/secretions can remain despite fasting; position changes help empty dependent areas.

Use wide-bore NG/OG; aspirate until minimal return.
Repeat aspiration in different positions (supine, left lateral, right lateral; some also use prone with appropriate support).
Single aspiration may miss pooled contents or thick milk curds; pyloric obstruction prevents emptying into duodenum.
Even after decompression, aspiration risk persists → RSI strategy still required.

What are the key intra-operative concerns specific to pyloric stenosis?

Think aspiration, temperature, glucose, ventilation, and drug sensitivity.

Aspiration risk at induction/emergence; ensure suction, awake extubation, and gastric decompression.
Maintain normothermia (small infant, short surgery but high heat loss).
Monitor and manage glucose (limited glycogen stores).
Avoid hyperventilation; aim normocapnia to reduce post-op apnoea risk.
Cautious opioids due to apnoea risk; use multimodal analgesia.

The surgeon plans a laparoscopic pyloromyotomy. What additional anaesthetic considerations are there?

Insufflation effects are more pronounced in small infants.

CO2 insufflation → ↑ intra-abdominal pressure → ↓ venous return and potential hypotension; manage with fluids/anaesthetic depth.
CO2 absorption → hypercarbia; increase minute ventilation and monitor ETCO2 closely.
↑ airway pressures and reduced compliance; adjust ventilator settings and consider recruitment if needed.
Vagal responses/bradycardia with peritoneal stretch; be ready to ask for desufflation and treat with atropine if required.

How would you plan extubation and post-operative monitoring?

Aim to minimise aspiration and apnoea risk.

Extubate fully awake with good respiratory effort and tone; suction oropharynx; consider lateral positioning.
Ensure adequate analgesia with minimal opioids; use paracetamol and local techniques.
Monitor for apnoea (especially ex-premature infants, residual alkalosis, opioid exposure, intercurrent illness).
Observe for ongoing vomiting; small amounts can be normal early; persistent vomiting may indicate incomplete myotomy or other pathology.

What complications should you discuss in a focused consent/parental explanation from an anaesthetic perspective?

Keep it relevant: aspiration, airway, apnoea, common GA risks in infants.

Aspiration risk despite precautions; potential respiratory complications (desaturation, pneumonitis).
Airway complications: difficult intubation is uncommon but possible; sore throat/hoarseness (less common in infants).
Post-op apnoea/need for monitoring or temporary respiratory support.
Nausea/vomiting may persist for a short period after surgery.
General risks: IV access issues, temperature instability, rare drug reactions.

An infant arrives in theatre still alkalotic (HCO3− 36) but the list is pressured. What do you do and how do you justify it?

This tests prioritisation and patient safety: pyloric stenosis is not a surgical emergency.

Do not proceed routinely; request delay for further resuscitation/correction (patient safety, reduced apnoea/arrhythmia risk).
Explain risks: persistent alkalosis → ventilatory depression/post-op apnoea; associated electrolyte abnormalities (hypochloraemia/hypokalaemia) and aspiration risk remain.
Escalate appropriately: discuss with surgeon, paediatric team, anaesthetic consultant; document decision-making.
If exceptional circumstances mandate proceeding (rare): optimise as much as possible, plan HDU/PICU monitoring, minimise opioids, strict normocapnia, and correct electrolytes aggressively with senior support.