Paraesophageal Hernia
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Direct answer
The danger of a paraesophageal hernia is gastric volvulus: the stomach rolls or folds through a hiatal defect into the chest, and the combination of sudden severe epigastric or chest pain, unproductive retching and inability to pass a nasogastric tube (Borchardt triad) marks strangulating volvulus — an emergency requiring decompression (endoscopic or radiological, then urgent repair). Electively, the type classification drives decisions: type I sliding hernia (gastro-oesophageal junction above the diaphragm) is the commonest and usually managed as reflux disease; type II has the fundus herniated alongside a normally positioned junction; type III combines both; type IV contains additional organs (colon, omentum, spleen). Symptomatic type II–IV hernias are repaired laparoscopically by reduction, sac excision, crural repair (± mesh reinforcement) and — because dismantling the hiatus creates reflux — an accompanying fundoplication; small asymptomatic hernias in the frail elderly can reasonably be watched.
What you must remember
- Types: I — sliding, gastro-oesophageal junction migrates up (about 90–95 per cent of hiatal hernias); II — true paraesophageal, junction remains below the diaphragm while fundus rolls up (rare); III — mixed (junction plus fundus, the usual "paraesophageal" hernia in practice); IV — other viscera in the sac.
- Mechanism of volvulus: organoaxial (rotation along the long axis, prone to strangulation and ischaemia) versus mesenteroaxial (rotation along the short axis, more often intermittent and obstructive); the herniated stomach in type II–IV is the setup.
- Borchardt triad: sudden severe pain, retching without vomitus, and inability to pass a nasogastric tube — with progressive tenderness it signals ischaemia; contrast CT (whirl sign, herniated stomach) confirms.
- Chronic symptoms of large hernias: postprandial chest fullness and early satiety ("I fill up after two bites"), anaemia from Cameron ulcers (linear erosions on the diaphragmatic crease of the herniated stomach), dysphagia, dyspnoea and arrhythmias from cardiac compression.
- Elective repair steps (laparoscopic standard): complete sac excision and reduction, restoration of 2–3 cm intra-abdominal oesophagus (mediastinal mobilisation, rarely a Collis gastroplasty lengthens a short oesophagus), tension-free crural closure, and fundoplication (usually Nissen, partial if dysmotility) — leaving the hiatus wide invites recurrence, omitting the wrap invites reflux.
- Emergency management: resuscitation, attempted endoscopic or radiological decompression of volvulus as a bridge, then urgent repair; gangrenous stomach needs resection; a genuinely stable, chronically comorbid patient with an asymptomatic small hernia may be observed with counselling about alarm symptoms.
A typical exam case
A 72-year-old woman presents with recurrent postprandial chest discomfort, early satiety and haemoglobin of 8.6 g/dL with iron deficiency; colonoscopy is normal, and a chest radiograph shows a retrocardiac air-fluid level. Barium swallow demonstrates most of the stomach above the diaphragm with the gastro-oesophageal junction also herniated — a type III paraesophageal hernia. Reason it through: her symptoms plus chronic anaemia from Cameron ulcers make this a symptomatic hernia, and she is medically fit, so elective laparoscopic repair is planned rather than watchful waiting. In theatre: the sac is fully reduced and excised, the oesophagus mobilised to achieve an adequate intra-abdominal length (a short oesophagus would need a Collis gastroplasty), the crura are closed behind the oesophagus, and a floppy Nissen fundoplication is added because sac excision destroys the anti-reflux competence of the remodelled hiatus. Contrast the emergency version of the same disease: the same woman arriving with Borchardt triad and peritonitic tenderness — decompress endoscopically if possible, resuscitate, and take her urgently; if the stomach is dusky or gangrenous at laparoscopy/laparotomy, resect the non-viable portion rather than force a reduction-and-wrap.
Where students slip
The recurring error is classifying all hiatal hernias as one disease: the exam rewards the four-type split, with the note that type II is the "pure" paraesophageal hernia while type III (mixed) is what most surgeons actually see. The second slip is repairing the hernia without fundoplication — dismantling the hiatus produces postoperative reflux in a majority, which is why the wrap is routine. Third, students forget Cameron ulcers as the cause of unexplained iron-deficiency anaemia in the elderly, even though it is the finding that often triggers the whole diagnosis.
Frequently asked questions
What distinguishes type I from type II hiatal hernia?
Type I is a sliding hernia with the gastro-oesophageal junction above the diaphragm; type II is a true paraesophageal hernia where the fundus herniates alongside a normally positioned junction.
What is Borchardt triad?
Sudden severe epigastric or chest pain, retching without vomiting, and inability to pass a nasogastric tube — the classic warning of gastric volvulus with strangulation risk.
Why is fundoplication added during paraesophageal hernia repair?
Reducing the sac and repairing the crura removes the anatomical anti-reflux barrier, and postoperative reflux is otherwise common — so a wrap (total or partial per motility) is built at the same operation.
What are Cameron ulcers?
Linear mucosal erosions at the diaphragmatic impression of a herniated stomach, causing chronic occult blood loss and iron-deficiency anaemia — a classic paraesophageal hernia presentation.