A 5-week-old with projectile vomiting and a hypochloraemic alkalosis

Vomiting causes loss of gastric hydrochloric acid, so hydrogen and chloride ions are lost from the body. This generates a metabolic alkalosis with a compensatory respiratory acidosis, which is why PaCO2 is 6.2 kPa. The alkalosis is maintained by chloride depletion and by reduced glomerular filtration from volume depletion. Volume depletion activates the renin–angiotensin–aldosterone system; aldosterone promotes sodium reabsorption in the distal nephron in exchange for potassium and hydrogen secretion. Because potassium is also depleted by vomiting, the kidney cannot exchange sodium for potassium, so it secretes hydrogen instead. This produces an acidic urine (pH 5.0) despite a systemic alkalosis - the so-called paradoxical aciduria. The low urine chloride of 4 mmol/L confirms chloride avidity and volume depletion, and the low urine sodium reflects sodium conservation. The correct treatment is therefore chloride-rich, potassium-containing isotonic saline, not bicarbonate or a potassium-sparing diuretic. Understanding this physiology explains why the alkalosis will not correct until chloride and potassium are replaced and the volume deficit is repaired.

I would give an initial 20 mL/kg bolus of 0.9% sodium chloride for the signs of hypovolaemia, then start 0.9% sodium chloride with 20 mmol/L potassium chloride at about 1.5 times maintenance. Maintenance for 3.6 kg by the 4-2-1 rule is roughly 14 mL/h, so the infusion would run at about 21 mL/h. I would avoid Ringer's lactate because its lactate is metabolised to bicarbonate and it is relatively hypotonic in chloride, and I would not give sodium bicarbonate. Electrolytes and venous gases should be rechecked every 6–12 hours, with continuous cardiac and oxygen saturation monitoring. The targets are a chloride above 100 mmol/L, bicarbonate below 26 mmol/L, potassium above 3.5 mmol/L and urine output above 1 mL/kg/h. Surgery should be deferred until these targets are met, usually after 24–48 hours of resuscitation. Operating on an alkalotic, hypokalaemic, volume-depleted infant risks postoperative apnoea, prolonged neuromuscular blockade and arrhythmias. I would also correct the haemoglobin if severely anaemic and ensure glucose is monitored.

I would place a nasogastric tube on free drainage and suction it immediately before induction to reduce the risk of aspiration. After pre-oxygenation I would perform a rapid-sequence induction with cricoid pressure, avoiding mask ventilation, using propofol or thiopentone and rocuronium 1.2 mg/kg; suxamethonium is an alternative but can cause bradycardia in infants and is best avoided when potassium is low. I would intubate, confirm placement with capnography, and ventilate with sevoflurane in air and oxygen, targeting normocapnia. Maintenance fluids should be isotonic with potassium, and glucose should be checked because hepatic glycogen stores are small. I would monitor temperature actively, use a forced-air warmer and warm fluids, and place a caudal or local anaesthetic infiltration for postoperative analgesia. Extubation should be planned when the infant is awake and ventilating adequately, with a high-dependency bed available afterwards. Postoperative apnoea is a real risk after general anaesthesia in this age group, particularly if alkalosis or hypokalaemia persists, so I would continue monitoring for at least 24 hours.