Distinguish progressive non-bilious gastric-outlet vomiting from bilious intestinal obstruction in early infancy, correct physiological derangement and secure time-critical imaging and paediatric surgical care.
Ask when vomiting began, relation to feeds, force, colour, volume, blood, hunger afterwards, stool, urine and weight. Parents may call yellow fluid bile, so use a visual reference and inspect a sample when possible; clinically important bile is dark green. Examine hydration and perfusion, observe a feed when safe and inspect the abdomen for distension, visible peristalsis, tenderness, mass and hernia. Pyloric palpation should not delay ultrasound.
Hypertrophic pyloric stenosis evolves rather than presenting at birth. Repeated vomiting loses hydrogen and chloride and contracts extracellular volume. The kidney retains sodium in exchange for hydrogen and potassium, producing paradoxical aciduria in advanced disease. Ultrasound measures pyloric muscle and channel dynamically. Biochemistry assesses resuscitation needs. Surgery is delayed until circulation and electrolytes are corrected because alkalosis increases anaesthetic and apnoea risk.
Bilious vomiting follows reflux of bile from obstruction distal to the duodenal ampulla. Malrotation with volvulus is the time-critical diagnosis, particularly in neonates, but normal stool or a soft abdomen early does not exclude it. Stabilise, decompress and call surgery immediately. Plain radiography may show obstruction or perforation but can be normal. A stable infant usually needs urgent specialist upper-GI contrast imaging; an unstable child with peritonism may proceed directly according to surgical judgement.
Progressive thickening and elongation of pyloric circular muscle narrows gastric outflow, usually becoming symptomatic in the first two months.
Abnormal fetal intestinal rotation creates a narrow mesenteric base and obstructing Ladd bands, allowing the midgut to twist around its vascular pedicle.
Atresia, meconium disease, Hirschsprung disease, incarcerated hernia and adhesions can also generate bilious vomiting at different ages.
Sepsis, UTI, metabolic disease, milk-protein allergy and raised intracranial pressure may cause non-bilious vomiting without mechanical gastric outlet obstruction.
Pyloric narrowing retains milk in stomach, causing increasingly forceful non-bilious emesis because obstruction lies proximal to bile entry.
Repeated gastric vomiting produces hypochloraemic metabolic alkalosis, potassium depletion and secondary renal sodium conservation with paradoxical aciduria.
Volvulus obstructs bowel and mesenteric veins before arterial inflow, causing oedema, ischaemia, necrosis and eventual perforation.
Obstruction distal to the ampulla permits bile to enter vomit, although colour description should be clarified directly with a green chart or sample.
Increasingly forceful non-green vomiting after feeds with renewed hunger and weight loss over the first weeks is characteristic.
Low chloride and potassium with raised bicarbonate reflects prolonged gastric acid loss and volume-conserving renal physiology.
Dark-green fluid indicates bile and demands urgent assessment for obstruction distal to its duodenal entry.
Pain, distension, bloody stool, acidosis, shock and peritonism suggests compromised mesenteric blood supply.
A soft abdomen and preserved stool do not exclude malrotation before vascular compromise or complete blockage develops.
Effortless small milk regurgitation in a thriving comfortable infant lacks progressive force, bile, dehydration and abdominal disease.
Diarrhoea, fever, sick contacts or systemic instability may indicate infection, but bilious colour still demands obstruction assessment.
Eczema, blood or mucus in stool and chronic feeding symptoms may accompany vomiting but do not cause the classic pyloric biochemical pattern.
Bulging fontanelle, abnormal consciousness, seizures or focal neurology directs urgent neurological investigation alongside stabilisation and glucose measurement.
Continued pyloric vomiting reduces circulating volume and chloride, causing renal impairment, hypokalaemia and paradoxical aciduria before treatment.
Repeated vomiting and starvation increase aspiration risk and deplete glucose stores rapidly in a young infant.
Untreated midgut volvulus can destroy extensive small bowel, causing sepsis, short-bowel syndrome, multiorgan failure or death.
Persistent gastric obstruction reduces retained milk and produces weight loss despite continued hunger and eager feeding after vomiting.
Direct colour clarification prevents dangerous obstruction being mislabeled as ordinary reflux.
The operation is urgent but not performed through correctable alkalosis and dehydration that increase anaesthetic risk.
Bowel gas may appear nonspecific before volvulus progresses, so definitive anatomy still requires specialist assessment.
Volume-depleted kidneys exchange sodium for hydrogen despite systemic alkalosis when potassium is scarce.
Calling dark-green bilious vomiting physiological reflux.
Using projectile force to assume pyloric stenosis without checking colour.
Sending an alkalotic dehydrated infant directly to anaesthesia before correction.
Using a normal abdominal radiograph to exclude malrotation.
Waiting for a palpable olive before ordering ultrasound.
Ignoring recurrent bile after surgery.
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A five-week-old has progressive projectile non-bilious vomiting, hunger after feeds and weight loss. Which investigation is first line to confirm the likely diagnosis?
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Pyloromyotomy divides hypertrophied muscle after correction of physiology. Small postoperative vomits can occur initially, but persistent bile, worsening distension or systemic decline needs reassessment. Malrotation is treated by urgent Ladd procedure with untwisting, division of bands and assessment of bowel viability; necrotic bowel may need staged resection to preserve length.
Explain the different logic clearly to families: projectile describes force, while bilious describes location relative to bile entry. Either can coexist with dehydration, but only bile makes distal obstruction the immediate concern. Give feeding and wound plans after surgery and monitor weight. Reassess siblings or future symptoms clinically; neither diagnosis should be inferred from ordinary posseting.