Hiatus hernia

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

The diaphragmatic crura, phreno-oesophageal attachments and lower oesophageal sphincter normally align to form the antireflux barrier. In a sliding hernia the gastro-oesophageal junction and proximal stomach move cranially, weakening this alignment and increasing reflux propensity. Sliding hernias are common with age, central adiposity and raised intra-abdominal pressure, but an image alone does not prove the cause of every chest or upper abdominal symptom. Treat the clinical reflux phenotype and investigate alarm features rather than chasing small changes in measured hernia size.

Paraoesophageal hernias preserve or displace the junction in differing ways while part of the stomach lies alongside the oesophagus; type IV can contain colon, small bowel, spleen or other viscera. A large intrathoracic stomach may reduce meal capacity, compress lung or heart, kink the outlet, bleed at the diaphragmatic impression or rotate around its axes. Chronic intermittent symptoms can abruptly become an emergency. Pain, retching and obstruction may precede ischaemia, and lactate can remain normal early, so the clinical and imaging pattern drives urgent surgical discussion.

Elective management should be proportionate. Acid suppression and weight or meal measures help reflux but not mechanical obstruction. Persistent dysphagia, anaemia attributable to Cameron lesions, recurrent aspiration, postprandial pain, organoaxial rotation or declining respiratory function may justify specialist repair. Preoperative endoscopy, contrast imaging and oesophageal physiology are selected according to symptoms and planned fundoplication. The procedure may include reduction, sac dissection, crural repair and a tailored antireflux component; mesh, gastropexy and fundoplication choices vary by anatomy, frailty, surgeon and local protocol.

Key points

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.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Hiatal tissue laxity

Age-related or connective-tissue weakening enlarges the diaphragmatic hiatus and loosens attachments around the oesophagogastric junction under pressure.

Raised intra-abdominal pressure

Obesity, pregnancy, chronic cough and straining can promote upward stomach displacement when the hiatus and phrenoesophageal ligament are susceptible.

Para-oesophageal anatomy

Congenital or acquired abnormal fixation permits fundus and occasionally other viscera to herniate beside the oesophagus while the junction may remain below.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Transhiatal migration
The junction slides above the diaphragm or the gastric fundus rolls through beside the oesophagus, creating distinct anatomical hernia patterns.
2
Antireflux barrier disruption
Separation of sphincter and diaphragmatic crura weakens the pressure barrier and delays clearance, increasing reflux exposure in sliding hernia.
3
Mechanical rotation or compression
A large para-oesophageal stomach can obstruct, twist and compromise venous then arterial supply, causing volvulus and ischaemia.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Incidental sliding hernia

A small axial hernia is reported during endoscopy or imaging without dysphagia, bleeding or troublesome reflux and may require explanation only.

Reflux-associated presentation

Heartburn, sour regurgitation and meal-related retrosternal burning accompany a sliding hernia, but cardiac symptoms and oesophageal alarm features still require separate triage.

Large paraoesophageal syndrome

Early satiety, postprandial pressure, progressive meal intolerance, dysphagia, regurgitation, breathlessness or recurrent aspiration suggests clinically important intrathoracic stomach.

Chronic blood-loss complicationRed flag

Fatigue and iron-deficiency anaemia can result from Cameron lesions, but another gastrointestinal source or malignancy must not be presumed absent.

Acute gastric volvulusRed flag

Sudden severe epigastric or chest pain, repeated dry retching, distension and inability to swallow may represent rotation with closed-loop obstruction.

Strangulation or perforationRed flag

Peritonism, shock, fever, rising oxygen requirement, haematemesis, mediastinal gas or pleural contamination indicates threatened or established tissue necrosis and sepsis.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Upper gastrointestinal endoscopyFirst step
Why
Assess reflux injury, narrowing, mucosal bleeding and possible malignancy.
Interpretation and limitations
Describe the diaphragmatic pinch and junction, inspect for oesophagitis, Barrett change and Cameron lesions, and biopsy abnormalities. Endoscopy may underestimate complex organ rotation and must be cautious if perforation is suspected.
02
Contrast-enhanced CT chest and abdomen
Why
Define acute hernia contents, transition points, volvulus and complications.
Interpretation and limitations
Look for intrathoracic stomach, abnormal axis, closed-loop obstruction, poor wall enhancement, pneumatosis, free gas, fluid or pleural contamination. Concerning anatomy warrants immediate specialist discussion even before biochemical deterioration.
03
Barium swallow or upper-GI contrast study
Why
Map elective anatomy and dynamic bolus passage.
Interpretation and limitations
It can show junction position, organoaxial or mesenteroaxial rotation, obstruction and oesophageal shortening. It is not the first study for an unstable patient with suspected ischaemia or perforation.
04
Full blood count and iron studies
Why
Identify blood loss associated with mucosal trauma or another lesion.
Interpretation and limitations
Microcytic anaemia and low ferritin support iron deficiency but do not establish Cameron lesions as the only source; use age, symptoms and endoscopic findings to investigate appropriately.
05
High-resolution manometry
Why
Characterise peristalsis and junction function before selected elective repair.
Interpretation and limitations
Results help plan an antireflux component and exclude achalasia, but large hernia anatomy can cause catheter angulation and artefact requiring expert interpretation.
06
Ambulatory reflux monitoring
Why
Provide objective reflux evidence when symptoms and endoscopy are inconclusive before invasive care.
Interpretation and limitations
The physiology service chooses on- or off-treatment testing. A hernia on imaging does not by itself establish pathological acid exposure or symptom association.
07
Serum lactate and organ profile
Why
Assess physiological consequence during suspected strangulation or sepsis.
Interpretation and limitations
Raised lactate, kidney injury or acidosis increases urgency, but normal early values cannot rule out compromised gastric perfusion and must not delay CT or surgery.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

GORD without hernia

Typical reflux can occur with normal junction anatomy; endoscopy or imaging showing a hernia does not prove that every symptom arises from it.

Cardiac chest pain

Exertional pressure, dyspnoea or autonomic symptoms require cardiac evaluation before attributing retrosternal discomfort to reflux or hernia.

Gastric outlet or oesophageal motor disease

Persistent vomiting, retained food or mixed-consistency dysphagia directs endoscopy, contrast imaging and manometry towards obstruction, achalasia or gastroparesis.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Sliding herniaTreat symptoms rather than the imageFirst stepA type I hiatus hernia accompanies uncomplicated reflux without a mechanical alarm feature.

1Confirm that chest symptoms are not cardiac and screen for dysphagia, bleeding, vomiting, anaemia and unintentional weight loss.
2Offer individual weight, meal-timing and positional measures and an evidence-based GORD medicine course rather than promising anatomical correction.
3Review response and step to the lowest effective treatment; arrange endoscopy or physiology when symptoms persist, alarms develop or surgery is being considered.
4Refer for specialist antireflux assessment only when objectively supported disease, preference and operative fitness justify the risk of dysphagia, gas-bloat and recurrence.

02Elective paraoesophageal careSelect patients for planned repairA large or non-sliding hernia causes dysphagia, postprandial distress, anaemia, aspiration or cardiopulmonary compromise.

1Document meal tolerance, weight, respiratory effect and bleeding, then define anatomy with endoscopy and contrast imaging while excluding cancer and unrelated sources of symptoms.
2Correct iron deficiency and malnutrition, optimise respiratory and cardiac disease and review frailty, anticoagulation and anaesthetic risk.
3Discuss observation versus repair in a specialist upper-GI service using symptom burden, volvulus features, anatomy, patient goals and local outcome data.
4If operating, tailor reduction, crural closure, gastropexy and antireflux steps to physiology and anatomy, then establish nutrition, reflux and recurrence follow-up.

03Acute obstructionResuscitate and secure urgent source controlSevere pain, retching or systemic compromise suggests volvulus, strangulation or perforation.

1Keep nil by mouth, assess airway and circulation, provide oxygen when indicated, obtain large-bore IV access, send urgent bloods and begin balanced resuscitation and analgesia.
2Contact upper-GI surgery and radiology early, arrange urgent contrast-enhanced CT and begin local sepsis antimicrobials when ischaemia or perforation is suspected.
3Attempt nasogastric decompression only with experienced guidance; inability to pass the tube supports obstruction, and forceful blind attempts risk injury.
4Proceed to urgent endoscopic reduction, laparoscopy or open surgery according to stability, viability, perforation and local expertise, with resection or drainage when required.

04Iron deficiencyTreat blood loss without anchoringA patient with a large hernia develops iron-deficiency anaemia or overt upper-GI bleeding.

1Assess haemodynamic stability and use the acute bleeding pathway for melaena, haematemesis or symptomatic circulatory compromise.
2Confirm iron deficiency and perform adequate endoscopic inspection for Cameron lesions, cancer and other upper-GI sources while completing lower-GI investigation when indicated.
3Replace iron and treat acid injury according to the current BNF, then document haemoglobin and ferritin response rather than assuming correction.
4AlternativeRefer persistent or recurrent hernia-attributable bleeding for surgical review after alternative sources and operative risk have been addressed.

Key medicines and prescribing safety2 treatments · regimens, roles and cautions

Reduces acid-mediated reflux symptoms and supports healing of oesophagitis or Cameron mucosal injury but does not reduce the hernia or correct volvulus.

Proton pump inhibitor

For 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.

Restores iron stores when chronic hernia-associated mucosal blood loss contributes to anaemia while definitive source assessment continues.

Oral or intravenous iron replacement

Use 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.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Reflux oesophagitis and stricture

Chronic acid exposure can cause erosions, bleeding, Barrett metaplasia and fibrotic narrowing with progressive solid-food dysphagia.

Volvulus and strangulation

A para-oesophageal stomach may rotate, obstruct and become ischaemic, producing severe pain, retching and inability to pass a tube.

Cameron lesions and anaemia

Mechanical trauma where a large hernia crosses the diaphragm can erode gastric folds and cause chronic occult blood loss.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

For conservatively managed hernia, record change in dysphagia, meal size, postprandial pain, regurgitation, vomiting, weight and exertional breathlessness rather than image size alone.
Repeat full blood count and ferritin after iron treatment and investigate an inadequate or transient response for ongoing or alternative blood loss.
During PPI therapy review symptom benefit, administration, adverse effects and continuing indication, while recognising that mechanical complaints will not respond reliably.
After repair monitor early swallowing, oral intake, respiratory function, wound or infective complications and warning symptoms of leak or recurrent obstruction.
Longer-term surgical review should cover recurrent hernia, reflux, gas-bloat and dysphagia, using imaging or physiology only when the result will guide care.
Give every patient with a paraoesophageal component clear same-day advice for sudden pain, repeated retching, inability to swallow, bleeding or collapse.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Hernia size is not a symptom score

A small sliding hernia can coexist with severe reflux, while a large hernia may be quiet until meal intolerance or an acute mechanical event develops.

Dry retching is a warning

Unproductive retching with severe epigastric pain suggests a closed-loop gastric problem and should accelerate surgical imaging even if the classic triad is incomplete.

Anaemia needs a wide lens

Cameron lesions are easy to miss at the diaphragmatic pinch, yet finding a large hernia should never prematurely end investigation for other blood-loss causes.

Acid treatment is not anatomy treatment

A good PPI response supports management of reflux symptoms but does not protect against volvulus or relieve mechanical compression.

Frailty changes the operation

A tailored gastropexy or non-operative plan may be appropriate in selected high-risk patients, but it requires explicit specialist reasoning and emergency safety-netting.

11Common pitfallsFrequent interpretation and management errors.

01
Attributing acute lower chest pain to a known hiatus hernia without cardiac and aortic risk assessment.
02
Reassuring after a normal lactate when the clinical and CT picture suggests early gastric ischaemia.
03
Using PPI escalation to manage persistent vomiting or meal obstruction caused by a paraoesophageal hernia.
04
Assuming iron-deficiency anaemia comes from Cameron lesions without completing appropriate malignancy and bleeding evaluation.
05
Forcing a nasogastric tube repeatedly through a suspected volvulus without surgical or endoscopic guidance.
06
Offering every incidentally imaged hernia surgery without balancing symptoms, fitness, anatomy and recurrence risk.