Synopsis
Distinguish common sliding hiatus hernia from paraoesophageal complications, manage associated reflux and escalate obstruction, volvulus or ischaemia without delay.
- A hiatus hernia occurs when abdominal viscera, usually the stomach, pass through the diaphragmatic oesophageal hiatus; many are incidental and require no hernia-specific treatment.
- Type I sliding hernia moves the gastro-oesophageal junction above the diaphragm and commonly accompanies reflux, but size and symptom severity correlate imperfectly.
- Types II to IV are paraoesophageal patterns in which the fundus or other organs herniate beside the oesophagus and can obstruct, rotate or compromise blood supply.
- Heartburn and acid regurgitation are managed as GORD; a PPI treats acid exposure but cannot reduce the anatomical hernia.
- Postprandial pressure, early satiety, dysphagia, regurgitation, dyspnoea or iron-deficiency anaemia can indicate a clinically important large hernia.
- Cameron erosions or ulcers occur at the diaphragmatic pinch in some large hernias and can cause occult or overt blood loss.
- Endoscopy assesses mucosa and malignancy, whereas contrast CT or barium imaging better defines organ position, volvulus and complex anatomy.
- Borchardt's classic triad of severe pain, unproductive retching and inability to pass a nasogastric tube is memorable but often incomplete and should not be awaited.
- Elective repair is individualised by symptoms, anatomy, operative fitness and specialist outcomes; an incidental asymptomatic hernia is not an automatic indication for surgery.
- Acute volvulus or strangulation needs early resuscitation and expert source control because delay risks necrosis, perforation, mediastinal contamination and shock.
Key red flags
Fatigue and iron-deficiency anaemia can result from Cameron lesions, but another gastrointestinal source or malignancy must not be presumed absent.
Sudden severe epigastric or chest pain, repeated dry retching, distension and inability to swallow may represent rotation with closed-loop obstruction.
Peritonism, shock, fever, rising oxygen requirement, haematemesis, mediastinal gas or pleural contamination indicates threatened or established tissue necrosis and sepsis.
Investigation priorities
Assess reflux injury, narrowing, mucosal bleeding and possible malignancy.
Management branches
A type I hiatus hernia accompanies uncomplicated reflux without a mechanical alarm feature.
- Confirm that chest symptoms are not cardiac and screen for dysphagia, bleeding, vomiting, anaemia and unintentional weight loss.
- Offer individual weight, meal-timing and positional measures and an evidence-based GORD medicine course rather than promising anatomical correction.
- Review response and step to the lowest effective treatment; arrange endoscopy or physiology when symptoms persist, alarms develop or surgery is being considered.
- Refer for specialist antireflux assessment only when objectively supported disease, preference and operative fitness justify the risk of dysphagia, gas-bloat and recurrence.
Key medicines
Proton pump inhibitorFor reflux symptoms use a licensed full-dose PPI for four or eight weeks according to NICE CG184 and the selected product, then reduce to the lowest dose that maintains control; bleeding lesions require an endoscopy-led plan.Check adherence and interactions and review long-term need. Persistent dysphagia, anaemia, vomiting or postprandial pain requires anatomical reassessment rather than indefinite dose escalation.
Oral or intravenous iron replacementUse the current BNF and local iron-deficiency pathway, selecting oral or intravenous replacement from severity, tolerance, ongoing loss and urgency, with a calculated course and response review.Iron treatment must not replace investigation for cancer or another bleeding lesion. Oral preparations can cause gastrointestinal adverse effects and dark stools; intravenous products require product-specific observation and reaction precautions.