Pyloric stenosis

Epidemiology

Pyloric stenosis occurs in 1 in 500-1000 live births, affecting 4 males for every 1 female¹.

Pathophysiology

Pyloric stenosis is characterised by progressive hypertrophy of the pyloric muscle, causing gastric outlet obstruction². The aetiology remains unknown².

Risk Factors

The primary risk factors are male gender and a family history of pyloric stenosis³.

Clinical Features

Pyloric stenosis presents at around 4-6 weeks of age with non-bilious vomiting after every feed³. Vomiting is very forceful, and is typically described as projectile². Despite this, babies will continue to feed hungrily. Haematemesis has also been reported. Weight loss and dehydration are very common at presentation³, ranging from mild dehydration to hypovolaemic shock.

On examination, there may be visible peristalsis and a palpable olive-sized pyloric mass, best felt during a feed³ (see below).

Differential Diagnosis

• Gastroenteritis
• Gastro-oesophageal reflux, including Sandifer syndrome
• Over-feeding
• Sepsis
• UTI
• Food allergy

If bilious vomiting is reported, don’t forget to think malrotation!

Investigations

A test feed should be performed with a NG tube in situ and the stomach aspirated. Whilst the child is feeding, the examiner should palpate for a pyloric mass and observe for visible peristalsis.

Ultrasound is the imaging modality of choice⁴. An ultrasound of the abdomen will demonstrate hypertrophy of the pyloric muscle, with wall thickness >3mm, length >15mm and diameter >11mm⁵. See https://radiopaedia.org/cases/pyloric-stenosis for useful images.

Blood gases will typically show a hypokalaemia, hypochloraemic metabolic alkalosis² (Figure 1). This is due to the loss of hydrochloric acid with the repeated vomiting of stomach acid causing a hypochloraemia and metabolic alkalosis². The kidneys will then exchange potassium to retain protons to attempt to compensate, leading to a hypokalaemia². Metabolic derangement is less commonly seen now, due to earlier presentation and diagnosis³.

By TeachMeSeries Ltd (2026)

Figure 1: Blood gas demonstrating hypochloraemic, hypokalaemic metabolic alkalosis

Management

Peri-operatively it is important to correct any underlying metabolic abnormalities. Patients may require 10-20ml/kg fluid boluses for acute hypovolaemia. Oral feeding should be stopped and a NG tube passed and aspirated at 4 hourly intervals. Rehydration should then be commenced at 150ml/kg/day, using crystalloid as per trust policy. Blood gases and U+E’s should be checked regularly, and acted upon accordingly. Once dehydration and electrolyte abnormalities have been corrected, fluid can be reduced to usual maintenance rates.

Pyloric stenosis is surgically managed, with a Ramstedt’s pyloromyotomy⁷ and should not be undertaken until any fluid or electrolyte abnormalities have been correction. Surgery can be performed laprascopically or through a supra-umbilical incision and the muscle is divided along down to the mucosa⁷ (Figure 2).This is successful in the majority of patients, with only 1-2% experiencing restenosis². Babies can resume feeding after 6 hours, although there may be some residual vomiting⁸. Post–operative vomiting is common after surgery, due to gastric distension and dysmotility⁹, and is not necessarily a sign of incomplete myotomy.

https://commons.wikimedia.org/wiki/File:Pyloric_Stenosis.png

Figure 2: Diagrammatic representation of pyloric muscle before and after surgical correction

Complications

Pre-operative:

•  Hypovolaemia
•  Apnoea – secondary to hypoventilation associated with metabolic acidosis

Post-operative:

• Wound dehiscence
• Infection
• Bleeding
• Perforation
• Incomplete myotomy

References