• Extremely common: found in approximately 10–20% of the general population undergoing upper GI endoscopy or barium swallow, though many are asymptomatic
• Type I (sliding) accounts for ~90–95% of all hiatus hernias
• Prevalence increases markedly with age:
  • Rare in children (unless congenital)
  • ~10% in those < 40 years
  • ~60–70% in those > 60 years — this is a disease of ageing
• Western populations have higher prevalence than Asian populations, likely due to differences in obesity rates, diet, and intra-abdominal pressure
• HK context: incidence of GERD (closely linked to hiatus hernia) is rising in Hong Kong (2.5% in 2002 → 3.7% in 2011) ^[4], and with the rising obesity epidemic in Asia, hiatus hernia prevalence is expected to continue increasing

• Slight female predominance overall (possibly related to pregnancy as a risk factor and hormonal effects on connective tissue)
• However, GERD complications (Barrett's, adenocarcinoma) are more common in males

• Incidence increases with age due to progressive weakening of the diaphragmatic crura and loss of elasticity of the phrenoesophageal membrane

• The oesophageal hiatus is an opening in the right crus of the diaphragm at the level of T10 (the aortic hiatus is at T12, the IVC hiatus at T8 — remember "I 8 10 Eggs At 12" for IVC-T8, Oesophagus-T10, Aorta-T12)
• The hiatus is formed by the two limbs (pillars) of the right crus of the diaphragm, which cross over each other and form a muscular sling around the oesophagus
• Structures passing through the oesophageal hiatus:
  • Oesophagus
  • Anterior and posterior vagal trunks
  • Oesophageal branches of left gastric artery and vein

Multiple mechanisms normally prevent reflux and herniation — the anti-reflux barrier is a multi-component system:

In hiatus hernia, the anti-reflux mechanism is eliminated ^[1]:

1. Loss of intra-abdominal oesophageal segment: When the GOJ slides above the diaphragm, there is no longer a segment of oesophagus exposed to positive intra-abdominal pressure → loss of the flutter-valve effect
2. Disappearance of the oblique angle between oesophagus and cardia (angle of His) ^[5] → loss of the flap-valve mechanism
3. Loss of crural pinchcock: The diaphragmatic crura no longer compress the oesophagus effectively because the GOJ has migrated above them
4. Decreased pressure gradient between abdominal and thoracic cavity ^[5] → the hiatus no longer "pinches" the oesophagus
5. Mucosal fold mechanism lost ^[1] — the mucosal rosette is disrupted
6. Phrenoesophageal membrane stretched/attenuated: No longer tethers the GOJ in position
7. Hernia sac acts as an acid reservoir: Gastric acid trapped in the hernia sac above the diaphragm can reflux back into the oesophagus during swallowing when the LES relaxes ("re-reflux" phenomenon)

(See Classification section below for detailed type descriptions)

• Herniation of the OGJ (oesophagogastric junction) above the diaphragm ^[1]
• The GOJ and the gastric cardia slide upward through the oesophageal hiatus into the posterior mediastinum
• The phrenoesophageal membrane is diffusely weakened rather than having a focal defect
• Clinically: Strongly associated with GERD ^[4] because ALL anti-reflux mechanisms are disrupted
• The hernia moves up and down — it may reduce spontaneously when the patient is upright and herniate when supine or with increased abdominal pressure
• 97% of Schatzki rings are associated with sliding hiatus hernia ^[6]

• Herniation of the gastric fundus alongside the oesophagus, but the OGJ remains fixed in its normal position below the diaphragm ^[1]
• There is a focal defect in the phrenoesophageal membrane, usually anterolateral to the oesophagus
• The fundus rolls up through this defect into the thorax alongside the oesophagus
• Clinically: Because the GOJ stays in place, the anti-reflux mechanism is relatively preserved → less GERD
• However, there is increased risk of mechanical complications: gastric volvulus, strangulation, gastric perforation, gangrene ^[1] — this is the dangerous type
• The fundus can progressively herniate more and more, eventually resulting in an "upside-down stomach"

• Herniation of both the OGJ AND the gastric fundus through the hiatus ^[1]
• This combines features of both Type I and Type II
• Most large paraesophageal hernias are actually Type III
• Both GERD and mechanical complication risks are present

• Herniation of organs other than the stomach through the oesophageal hiatus ^[1]
• In addition to the stomach, other abdominal viscera herniate: omentum, colon, spleen, small bowel, pancreas
• Represents a very large defect in the hiatus
• Highest risk of complications (volvulus, strangulation, respiratory compromise from mass effect)

• The most common presentation is asymptomatic ^[1] — many hiatus hernias are discovered incidentally on imaging or endoscopy
• When symptomatic, the clinical features depend on:
  1. Type of hernia (sliding → GERD symptoms; rolling → mechanical symptoms)
  2. Size of hernia (larger hernias → more symptoms)
  3. Presence of complications (strangulation, volvulus, bleeding)

• Almost all patients who develop oesophagitis, Barrett's oesophagus, and peptic strictures have hiatus hernia ^[5]
• Hiatus hernia is an exacerbating factor — it increases both the frequency and duration of reflux episodes
• Mechanism: the hernia sac acts as a reservoir that traps acid above the diaphragm, allowing prolonged exposure during oesophageal peristalsis and LES relaxation

• The metaplasia-dysplasia-carcinoma sequence: obesity → GERD → Barrett's oesophagus → low-grade dysplasia → high-grade dysplasia → adenocarcinoma ^[4]
• 80% of Barrett's oesophagus patients have hiatus hernia ^[4]
• Hiatus hernia is a risk factor for Barrett's oesophagus ^[7]
• Barrett's involves replacement of stratified squamous epithelium by columnar glandular epithelium with goblet cells (intestinal metaplasia) — an adaptive response because intestinal-type epithelium withstands acid exposure better than squamous epithelium ^[7]

This is the most common presentation of a sliding (Type I) hiatus hernia. The differential here is essentially the differential of GERD and dyspepsia ^[9][10]:

Dysphagia is a key symptom of both sliding hiatus hernia (from strictures or Schatzki ring) and paraesophageal hernia (from mechanical compression or incarceration). The differential of oesophageal dysphagia is broad ^[15][16]:

Step 1: Determine if mechanical or functional

Step 2: Identify the cause

Chest pain is common in both hiatus hernia (from GERD-related oesophageal pain, or mechanical irritation in paraesophageal types) and many other conditions. The critical first step is always to rule out life-threatening cardiac causes ^[14][17]:

Life-threatening causes to exclude first:

Non-cardiac causes (once cardiac excluded):

A hiatus hernia, especially Types II–IV, may be discovered incidentally on CXR as a retrocardiac gas shadow (gastric bubble) ^[1]. The differential of a retrocardiac opacity or posterior mediastinal mass includes:

When a paraesophageal hernia presents acutely (volvulus, strangulation), the differential includes other acute abdominal and thoracic emergencies:

Unlike conditions such as rheumatoid arthritis or systemic lupus erythematosus, hiatus hernia does not have published consensus diagnostic criteria from a professional body. This is because it is an anatomical diagnosis — you either see a herniation of gastric/abdominal contents through the oesophageal hiatus or you don't. The diagnosis is therefore made by direct visualisation (endoscopy or imaging) rather than by fulfilling a checklist.

That said, there are well-defined endoscopic and radiological criteria used in clinical practice:

On OGD, a hiatus hernia is diagnosed when:

• The gastro-oesophageal junction (GOJ / Z-line / squamocolumnar junction) is seen to be displaced ≥ 2 cm above the diaphragmatic impression (the hiatal pinch)
• In retroflexion, gastric folds are seen to extend above the level of the diaphragmatic hiatus

The severity of the endoscopic flap valve is graded using the Hill classification ^[1]:

Exam pearl: The Hill classification grades the competence of the gastro-oesophageal flap valve on endoscopy, not the size of the hernia. Grades III–IV are strongly associated with pathological acid reflux.

On barium swallow or CT, a hiatus hernia is diagnosed when:

• The GOJ (identified as the B-ring or junction of tubular oesophagus with gastric saccular configuration) is located > 2 cm above the diaphragmatic hiatus
• For paraesophageal types: gastric fundus (or other organs) is seen above the diaphragm with or without GOJ displacement

The diagnosis of hiatus hernia is anatomical/imaging-based. Clinical symptoms alone are insufficient — many patients with hiatus hernia are asymptomatic, and GERD symptoms can occur without hiatus hernia.

Rationale: CXR is often the first investigation that raises suspicion for hiatus hernia, especially large paraesophageal types (Types II–IV). It is quick, cheap, widely available, and part of routine workup for chest pain, dyspnoea, or preoperative assessment.

Key Findings ^[1]:

Limitations: CXR has low sensitivity for small sliding hernias (they may appear normal). CXR is most useful for large paraesophageal/Type III–IV hernias. A normal CXR does NOT exclude hiatus hernia.

Rationale: CT is the diagnostic investigation of choice ^[1]. It provides excellent anatomical detail of the hiatus, the position of the GOJ, the relationship of abdominal organs to the diaphragm, and any complications.

Why oral contrast? — Oral contrast opacifies the stomach and bowel, making it easy to identify which viscera are above and below the diaphragm. Without contrast, a herniated stomach might be difficult to distinguish from a mediastinal mass.

Key Findings:

Advantages over other modalities:

• Non-invasive, fast, widely available
• Can identify complications (volvulus, strangulation, perforation)
• Excellent for surgical planning — determines hernia size, contents, relationship to surrounding structures
• Can assess for incidental findings (pulmonary, cardiac, other abdominal pathology)

When specifically indicated:

• Suspected paraesophageal hernia (Types II–IV) — these are surgical conditions and need anatomical characterisation
• Acute presentations (suspected volvulus, strangulation, perforation)
• Pre-operative planning for large or complex hernias
• When CXR shows a retrocardiac opacity of uncertain nature

Rationale: OGD is the key investigation for assessing the mucosal consequences of hiatus hernia (oesophagitis, Barrett's, strictures, malignancy, Cameron lesions). It also allows direct visualisation and classification of the hernia.

Technique relevant to hiatus hernia ^[21]:

• Position: left lateral, neck flexed forward
• At the GOJ: look for upward displacement of the Z-line ^[1] (the squamocolumnar junction — where pale pink squamous oesophageal mucosa meets salmon-coloured columnar gastric mucosa)
• Retroflexion (J-manoeuvre) is required to visualise the gastric cardia and proximal stomach — hiatus hernia is better visualised in this position ^[21]
• Assess the flap valve using the Hill classification ^[1]

Key Findings:

OGD Indications in the context of hiatus hernia:

• GERD symptoms with alarm features (dysphagia, odynophagia, GI bleeding, anaemia, weight loss, recurrent vomiting) ^[4]
• Symptoms refractory to PPI therapy
• Screening for Barrett's oesophagus in high-risk patients
• Pre-operative assessment before fundoplication
• Assess Cameron lesions in patients with iron deficiency anaemia and known large hernia

Limitations:

• Small sliding hernias may reduce during the procedure and be missed
• Majority of GERD patients have non-erosive reflux disease (NERD) → OGD has low negative predictive value for GERD ^[4]
• Cannot assess motility or quantify reflux

Rationale: A barium swallow is a dynamic fluoroscopic study that provides real-time visualisation of swallowing, oesophageal peristalsis, GOJ position, and gastric morphology. It is particularly useful for characterising the morphology of the hernia and identifying complications.

Technique: Patient swallows barium sulphate suspension while standing. Fluoroscopic images are taken in real-time and spot films captured. Provocative manoeuvres (Valsalva, Trendelenburg position, water siphon test) can elicit a sliding hernia that reduces at rest.

Key Findings:

Barium vs Gastrografin (Water-Soluble Contrast):

• Barium: better mucosal coating, better image quality. But if aspirated → barium pneumonitis (rare, usually benign); if perforation → barium peritonitis/mediastinitis (severe — avoid barium if perforation suspected)
• Gastrografin: safe if perforation suspected (absorbed). But if aspirated → chemical pneumonitis (hyperosmolar → draws fluid into alveoli). Avoid if aspiration risk
• Rule of thumb: Suspect perforation → use gastrografin. Suspect aspiration → use barium ^[20]

When to use barium swallow:

• Dysphagia with OGD negative but still suspect mechanical obstruction ^[22]
• Dynamic assessment of hernia morphology (hernia may only appear during Valsalva)
• Pre-operative assessment — defines anatomy for the surgeon
• Contraindicated if suspecting oesophageal diverticulum or web (risk of perforation with blind passage of a rigid endoscope — but barium swallow is safe here) ^[22]

Rationale: Used specifically when perforation is suspected (post-operative, Boerhaave syndrome, acute complication of hiatus hernia).

Key Finding:

• Contrast extravasation into the mediastinum or peritoneal cavity confirms perforation
• Can demonstrate the position of the stomach/small bowel relative to the diaphragm (useful in diaphragmatic rupture) ^[18]

Rationale: Oesophageal manometry measures pressure within the oesophagus and across the LES. It does NOT diagnose hiatus hernia per se, but is essential for:

1. Pre-operative assessment before anti-reflux surgery (fundoplication) ^[9][22]
2. Excluding motility disorders (achalasia, diffuse oesophageal spasm) that might contraindicate fundoplication
3. Locating the LES for accurate placement of pH monitoring probe

Technique ^[9]:

• A pressure-sensitive catheter with 36 circumferential channels, each with 12 sensors ^[22], is inserted through the nose into the oesophagus
• The patient swallows on command → pressures generated by muscle contractions are recorded
• Reading a manometry contour plot ^[22]: vertical axis = distance down oesophagus; horizontal axis = time

Key Findings Relevant to Hiatus Hernia:

Indications in hiatus hernia ^[9]:

• Diagnosis of GERD is doubtful
• Planning for endoscopic or surgical therapy (must confirm adequate peristalsis before wrapping the oesophagus)
• NOT recommended in patients with uncomplicated GERD ^[9]

Rationale: This is the gold standard ^[9] for objectively documenting and quantifying acid reflux. It correlates symptoms with reflux episodes.

Technique ^[9]:

• A slim catheter with a pH-sensitive probe is positioned 5 cm above the GOJ (located by manometry)
• The patient wears the device for 24 hours while undergoing normal daily activities, keeping a diary of symptoms, meals, and body position
• Alternatively, the BRAVO™ system ^[9] is a wireless capsule pinned to the oesophageal mucosa during endoscopy — naturally falls off after 48 hours (up to 4 days). It is more comfortable and allows a PPI trial from day 3

Key Findings and Interpretation ^[9]:

Multichannel Intraluminal Impedance (MII) ^[4]:

• Newer technology, usually combined with pH monitoring (MII-pH)
• Principle: measures impedance between ring electrodes → detects bolus movement (both liquid and gas, both acid and non-acid reflux)
• Advantage: can detect non-acid reflux (important in patients on PPI who still have symptoms — their reflux may be non-acidic but still symptomatic)

Indications ^[9]:

• Diagnosis of GERD is doubtful
• Planning for endoscopic or surgical therapy
• Persistent symptoms despite PPIs (to determine if ongoing acid exposure is present)
• Persistent symptoms despite anti-reflux surgery (to determine surgical failure)
• Sensitivity: ~80–90% for GERD with oesophagitis; much lower for NERD ^[4]
• Seldom used as first-line due to being inconvenient, uncomfortable, and not widely available ^[9]

Blood tests do not diagnose hiatus hernia but assess its consequences:

Conservative management is indicated for sliding hernia (Type I) ^[1] — the vast majority of hiatus hernias. The rationale is that Type I hernias cause symptoms primarily through GERD, and GERD is a medical disease in the first instance.

These are first-line for ALL patients with hiatus hernia ± GERD. Each intervention targets a specific pathophysiological mechanism:

Surgical management (hernia repair + fundoplication) is indicated in ^[1][11]:

Before any anti-reflux surgery, a comprehensive workup is mandatory:

These are newer, less-invasive options that are still considered emerging (not yet standard of care):

Paraesophageal hiatus hernia is a contraindication to ERCP ^[21] — the altered anatomy (stomach displaced into the thorax, gastric volvulus, or gastric outlet obstruction) makes safe passage of the side-viewing duodenoscope extremely difficult and increases the risk of perforation.

Similarly, large hiatal hernia is a contraindication to Sengstaken-Blakemore tube placement ^[23] — the balloon may inflate in the hernia sac rather than the stomach, causing oesophageal rupture.

Patients with hiatus hernia are at high risk of aspiration during anaesthesia because the anti-reflux barrier is compromised. This is why rapid sequence induction (RSI) with cricoid pressure is used ^[8] — reducing the duration of unprotected airway and occluding the oesophagus to prevent passive regurgitation.

Pathophysiology: Chronic reflux of gastric acid (HCl, pH ~1–2), pepsin, and bile salts onto the oesophageal squamous mucosa → chemical injury → inflammation → mucosal erosion.

Why does the oesophagus get damaged but the stomach doesn't? The stomach has a thick mucous-bicarbonate barrier and rapid epithelial turnover specifically adapted to resist acid. The oesophageal squamous epithelium has none of these protections — it was never designed to be exposed to acid.

Grading — LA (Los Angeles) Classification ^[5]:

Clinical features: Odynophagia due to oesophagitis and ulcers ^[4]; heartburn that is persistent and severe.

Management: PPI therapy — standard dose for Grades A–B; double dose for Grades C–D followed by step-down. OGD follow-up for Grade C–D to confirm healing.

Pathophysiology: Severe, deep erosion through the oesophageal mucosa into the submucosa or muscularis → ulcer formation. Occurs when the balance tips further towards mucosal injury (more acid, less clearance, longer exposure).

Clinical features:

• Odynophagia (painful swallowing — food passing over an open ulcer)
• Bleeding (oesophageal ulceration) ^[1] — can cause haematemesis or melaena; chronic occult bleeding → iron deficiency anaemia
• Chest pain

Complications of ulceration: Haemorrhage, perforation (rare), stricture formation (healing with fibrosis).

Pathophysiology: Chronic cycles of oesophageal inflammation → ulceration → healing → fibrosis → deposition of collagen in the submucosa and muscularis → progressive concentric narrowing of the oesophageal lumen. This is the body's attempt to heal chronic injury, but the fibrotic scar contracts and narrows the tube.

Can occur as a consequence of long-standing oesophagitis ^[4].

Clinical features:

• Dysphagia due to strictures ^[4] — progressive dysphagia for solids worse than liquids (because the lumen is narrowed but not completely obstructed; liquids can still pass through a narrow opening, solids cannot) ^[4]
• May or may not have a history of heartburn (some patients "lose" their heartburn when a tight stricture prevents reflux from reaching the upper oesophagus — a paradoxical improvement that is actually a worrying sign)

Diagnosis: Endoscopy with biopsy to rule out malignant stricture ^[4] — any stricture must be biopsied because oesophageal carcinoma can present as a stricture.

Management: Endoscopic balloon dilation + long-term full-dose PPI to ↓ risk of recurrent oesophagitis and strictures ^[4]. Serial dilations may be needed.

Pathophysiology: Chronic acid exposure → the oesophageal squamous epithelium undergoes intestinal metaplasia — it is replaced by columnar glandular epithelium with goblet cells ^[4]. This is an adaptive response: intestinal-type epithelium withstands acid exposure better than squamous epithelium ^[7]. However, this metaplastic tissue is intrinsically unstable and predisposed to dysplasia and malignancy.

• Characterised by intestinal metaplasia ^[4]
• An adaptive response against ↑ acid exposure ^[4]
• Premalignant condition ^[4] — associated with 30–125× ↑ risk of CA oesophagus ^[4], though the absolute risk is still low (0.1–0.5%/year, ~1/100–180 patients/year) ^[4]

Epidemiology ^[4]:

• 10–15% among patients with oesophagitis and persistent symptomatic GERD
• Prevalence: 1.3% in Asians, 5.6% in US
• Risk factors: white male, > 50 years, obese, 80% has hiatus hernia ^[4]

Classification:

• Long-segment Barrett's: Z-line to GOJ distance ≥ 3 cm ^[7]
• Short-segment Barrett's: Z-line to GOJ distance < 3 cm ^[7]
• Graded using Prague classification (C = circumferential extent, M = maximal extent in cm from GOJ) ^[4]

Management ^[4][7]:

• Standard PPI for ALL patients → prevents ongoing acid injury and allows partial re-epithelialisation by squamous epithelium
• Non-dysplastic: surveillance OGD every 3–5 years with 4-quadrant biopsies
• Low-grade dysplasia: surveillance OGD every 6 months × 1 year then annually if negative; OR endoscopic treatment (EMR + RFA)
• High-grade dysplasia: endoscopic mucosal resection (EMR) + radiofrequency ablation (RFA) to ablate remaining metaplastic epithelium. Oesophagectomy reserved for cases where endoscopic treatment fails or invasive carcinoma found ^[7]

Complications of Barrett's ^[7]: Oesophageal stricture, oesophageal ulceration, oesophageal haemorrhage, adenocarcinoma of oesophagus

Pathophysiology: The metaplasia → dysplasia → carcinoma sequence. Barrett's intestinal metaplasia → accumulation of genetic mutations (p53 loss, CDX2 upregulation, aneuploidy) → low-grade dysplasia → high-grade dysplasia → invasive adenocarcinoma.

The evolution: obesity → GERD → Barrett's oesophagus → low-grade dysplasia → high-grade → adenoCA ^[4].

• Oesophagitis can develop into ulcer → stricture → Barrett's oesophagus (10%) → metaplasia → adenoCA (7% of Barrett's) ^[11]

Key point: This entire cascade is driven by chronic acid reflux, which is enabled and worsened by hiatus hernia. Preventing reflux (with PPI or fundoplication) and surveilling for Barrett's are the main strategies to interrupt this cascade.

Epidemiology: Incidence rising rapidly in the West (paralleling rising obesity/GERD). Still uncommon in Asia but increasing.

• A concentric mucosal fold at the squamocolumnar junction, typically in the lower oesophagus
• Typically associated with hiatus hernia (97%) ^[6] and eosinophilic oesophagitis
• Pathophysiology: likely formed from chronic inflammation at the GOJ leading to submucosal fibrosis and mucosal folding
• Clinical features: intermittent dysphagia for solids (the "steakhouse syndrome" — a bolus of poorly chewed meat gets stuck at the ring). Between episodes, the patient is asymptomatic
• Management: endoscopic balloon dilation; PPI to reduce inflammation; fundoplication if symptomatic hiatus hernia

• Linear gastric erosions/ulcers at the level of the diaphragmatic hiatus
• Pathophysiology: the gastric mucosal folds riding over the edge of the diaphragmatic hiatus experience repetitive mechanical trauma (friction) as the stomach slides up and down → erosion of the mucosa → chronic occult bleeding
• Found almost exclusively in patients with large hiatus hernias
• Clinical features: iron deficiency anaemia from chronic occult blood loss; rarely overt GI bleeding
• Management: PPI + iron supplementation; surgical hernia repair if refractory (eliminates the mechanical cause)

Gastric volvulus occurs only in the rolling type ^[1].

Pathophysiology: In a paraesophageal hernia, the gastric fundus herniates through the hiatus alongside the oesophagus. Because the stomach is now partially in the thorax and partially in the abdomen, it can rotate along its axis:

• Organoaxial volvulus (more common, ~60%): rotation along the longitudinal axis connecting the GOJ and pylorus → the greater curvature flips upward
• Mesentericoaxial volvulus (~30%): rotation along the axis perpendicular to the long axis, connecting the greater and lesser curvatures → creates a "twist" in the middle of the stomach

The rotation causes:

1. Complete gastric outlet obstruction → patient cannot vomit (retching without emesis)
2. Closed-loop obstruction → rapidly increasing intraluminal pressure → ischaemia
3. Compression of blood supply → venous congestion → arterial compromise → ischaemia → gangrene

Clinical features — Borchardt's triad:

1. Severe epigastric/chest pain
2. Retching without ability to vomit (unproductive emesis)
3. Inability to pass an NG tube

Management: NG tube decompression + EOT ^[1]. Emergency surgery: detorsion, assess viability, hernia repair, fundoplication, gastropexy. Gastrectomy if gangrene.

Strangulation ^[1]: the herniated stomach (or other organ) becomes trapped in the hiatus such that its blood supply is compromised.

Pathophysiology: The narrow hiatal ring acts as a constricting band around the herniated viscera. If the hernia cannot reduce, the veins (low-pressure system) are compressed first → venous congestion → oedema → further swelling → arterial compromise → ischaemia → infarction.

This is the same mechanism as strangulation in any hernia — the neck of the sac compresses the contents. However, the consequences are particularly severe because the stomach is a highly vascular organ and progresses to gangrene rapidly.

Clinical features: Acute onset severe pain, tachycardia, fever, peritonism. CT shows gastric wall thickening, pneumatosis, or free fluid.

Management: Emergency surgery — same principles as volvulus.

Gastric perforation ^[1]: ischaemic or necrotic gastric wall perforates → gastric contents leak into the mediastinum or peritoneal/pleural cavity.

Pathophysiology: End-stage of strangulation. Ischaemic tissue loses structural integrity → perforation → peritonitis (if below diaphragm) or mediastinitis (if above diaphragm). Both are life-threatening.

Clinical features: Sudden deterioration, peritonism, sepsis, subcutaneous emphysema (if mediastinal perforation), pneumoperitoneum on CXR.

Management: Emergency surgery — repair or resection + washout. Broad-spectrum IV antibiotics. May require ICU support.

Gangrene ^[1]: complete necrosis of the gastric wall due to prolonged ischaemia.

Pathophysiology: The final stage of strangulation → tissue death → bacterial translocation → sepsis → multi-organ failure if untreated.

Management: Emergency gastrectomy (partial or total depending on extent) + hernia repair. Mortality is high (~15–40% depending on patient fitness and delay in treatment).

Pathophysiology: Large paraesophageal/Type III–IV hernias occupy significant thoracic volume → compressive atelectasis of the lower lobes → reduced functional residual capacity → dyspnoea, recurrent lower respiratory tract infections.

Additionally, chronic micro-aspiration of gastric contents (in sliding hernias with severe GERD) → chemical pneumonitis, recurrent aspiration pneumonia, pulmonary fibrosis (rare, chronic).

Pathophysiology: A large hernia in the posterior mediastinum can directly compress or irritate the left atrium and pericardial sac → palpitations, atrial fibrillation ^[1]. The mechanical compression distorts atrial geometry and triggers ectopic foci.

This can be mistaken for primary cardiac disease. Resolution of arrhythmia after hernia repair confirms the mechanical aetiology.

Patients with hiatus hernia have an incompetent anti-reflux barrier → high risk of passive regurgitation and aspiration during induction of anaesthesia. This is why hiatus hernia is an indication for rapid sequence induction (RSI) ^[8] with cricoid pressure.

Already discussed above — mechanical trauma to gastric folds at the hiatal level → chronic occult blood loss → iron deficiency anaemia. Often the presenting complaint of an otherwise asymptomatic large hiatus hernia.