Paeds SAQs · gastroenterology-hepatology-and-nutrition
Acute vomiting in infants and children: SAQ
Short-answer questions on acute vomiting in children covering the bilious-vomiting surgical emergency, the age-based differential, the metabolic derangement of pyloric stenosis, clinical dehydration assessment, oral rehydration and the selective role of ondansetron, and the dangerous non-gastrointestinal mimics.
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This infant has hypertrophic pyloric stenosis. The age of three weeks, the progressive projectile non-bilious vomiting in a hungry infant, the weight loss, the visible peristaltic wave, and the hypochloraemic hypokalaemic metabolic alkalosis on the gas together make the diagnosis, which is confirmed by an ultrasound showing a thickened, elongated pyloric muscle. [1]
Question 1 (10 marks)
Explain the diagnosis, the characteristic biochemical derangement, and how you would confirm it. (5 marks for the diagnosis and its clinical features; 5 marks for the biochemistry and confirmation.) [1]
The diagnosis is hypertrophic pyloric stenosis, which classically presents between two and eight weeks of age with progressively projectile, non-bilious vomiting in an infant who remains hungry, together with weight loss or poor weight gain. Supportive examination findings are a visible left-to-right peristaltic wave during a test feed and a palpable, olive-shaped pyloric mass in the right upper quadrant. The vomiting is never bilious, because the obstruction is proximal to the ampulla of Vater. [1]
The characteristic biochemical derangement is a hypochloraemic, hypokalaemic metabolic alkalosis. Persistent vomiting of gastric contents loses hydrogen and chloride, generating the alkalosis and the low chloride; potassium is lost in the vomit and further into the urine, and in the later dehydrated state the kidney conserves sodium and water at the expense of secreting hydrogen ions, producing the classic paradoxical aciduria. This infant's gas, with a pH of 7.52, a chloride of 88 mmol/L and a potassium of 3.0 mmol/L, fits this pattern exactly. [1]
Confirmation is by abdominal ultrasound, which demonstrates the thickened and elongated pyloric muscle and is the diagnostic investigation of choice. The essential accompanying blood tests are the venous gas and electrolytes, which both support the diagnosis and quantify the derangement that must be corrected before any operation. [2]
Question 2 (10 marks)
Outline your management, including the correct sequence of resuscitation and surgery, and state why bilious vomiting in an infant would change your approach entirely. (6 marks for the management sequence; 4 marks for the bilious-vomiting contrast.) [2]
The first principle is that pyloric stenosis is a medical emergency of fluid and electrolytes and a surgical condition only second. The infant is made nil by mouth, a nasogastric tube may be placed to decompress the stomach, and intravenous fluid resuscitation is started with an isotonic solution, followed by fluids that correct the chloride and potassium deficit. Surgery is deferred until the alkalosis and electrolytes are corrected, because operating and anaesthetising an alkalotic infant risks postoperative apnoea. [2]
The definitive treatment is a pyloromyotomy once the child is biochemically stable. Both open and laparoscopic pyloromyotomy are safe and effective, and a Cochrane review found comparable outcomes, with the laparoscopic approach offering a faster recovery in trained hands. Feeding is reintroduced after the procedure and the prognosis is excellent. [2]
Bilious vomiting would change the approach entirely. Green vomit signals an obstruction distal to the ampulla of Vater and, in an infant, means malrotation with midgut volvulus until proven otherwise. This is a time-critical surgical emergency, not the elective correction pathway of pyloric stenosis, because a volvulus can infarct the entire midgut within hours. The response is nil by mouth, nasogastric decompression, immediate fluid resuscitation, an urgent surgical opinion and an urgent upper gastrointestinal contrast study, or straight to theatre if the child has a surgical abdomen, and any delay costs bowel. [3]
References
- [1]Vinycomb TI, Laslett K, Gwini SM, et al. Presentation and outcomes in hypertrophic pyloric stenosis: An 11-year review. J Paediatr Child Health, 2019.PMID 30677197
- [2]Staerkle RF, Lunger F, Fink L, et al. Open versus laparoscopic pyloromyotomy for pyloric stenosis. Cochrane Database Syst Rev, 2021.PMID 33686649
- [3]Filion L, Beaunoyer M, Miron MC, et al. Infant malrotation with midgut volvulus: A retrospective review of clinical presentation and delays in care at a Canadian tertiary paediatric centre. Paediatr Child Health, 2025.PMID 41049711