Hiatal hernia

Herniation of elements of the abdominal cavity through the oesophageal hiatus

Anatomy

• Phreno-oesophageal membrane is responsible for maintaining the oesophagus in its position below the diaphragm - a continuation of the endoabdominal peritoneum that reflects onto the oesophagus at the hiatus
  • Subject to wear and tear with aging
  • Plus repetitive stress of swallowing, abdominal straining, vomiting
  • Potentially also due to tonic contraction of oesophageal longitudinal muscles in response to GORD

Pathophysiology (para-oesophageal)

• Para-oesophageal hernias form after two key events:
  • Widening of the diaphragmatic crura at the oesophageal hiatus
  • Stretching of the para-oesophageal membrane, as it balloons into the posterior mediastinum
• Viscera enter hernial sac repeatedly, and eventually adhesions form
• Most commonly gastric fundus

Types:

• The key differentiating factor is the location of GOJ and fundus
• Type I - sliding (95%)
  • Displacement of GOJ above diaphragm into the posterior mediastinum
  • Fundus below diaphragm (no paraoesophageal hernia)
  • Occurs because of laxity of the phreno-oesophageal membrane
  • Associated with trauma, congenital, iatrogenic
  • Often leads to GORD, with larger hernias conveying a higher risk for pathological GORD
• Paraoesophageal - true hernia with a sac and part of the fundus above the diaphragm
  • Recognised complication of surgical dissection of the hiatus
  • II - defect in phreno-oesophageal membrane - fundus is above but GOJ remains anchored in the abdomen
  • III - mixed - elements of I and II - both GOJ and fundus herniate through hiatus
  • IV - large defect in phreno-oesophageal membrane - includes other organs in hernial sac, e.g. colon, spleen, pancreas, or small bowel

Natural history

• Increases in size over time
• 25% of sliding hiatus hernias become a paraoesophageal hernia

Clinical features

Type I

• Generally asymptomatic
• May have symptoms of GORD (heartburn, regurgitation, dysphagia)

Type II, III, IV

• Mostly asymptomatic or vague, intermittent symptoms
• More likely to see obstructive symptoms - dysphagia, early satiety, post-prandial epigastric pain
• Can also be associated with typical GORD symptoms
• Complications
  • Gastric volvulus
    • Risk is approximately 1% per year
    • See separate topic
  • Respiratory complications
    • Mass effect of hernia in chest
    • Shortness of breath is common
  • Bleeding
    • Results from mucosal ischaemia or mechanical ulceration of the gastric mucosa
    • Cameron's ulcer

Diagnosis

• Barium swallow - sliding = >2cm gap between B-ring and diaphragm
• Upper endoscopy - >2cm between B ring and diaphragmatic impression

Investigation pre-op: (these guidelines are American - unsure if applicable here)

• Acid exposure test to document GORD
• Manometry (ensure dysmotility isn't contributing to reflux)
• Barium swallow (look out for short oesophagus)
• Gastroscopy (exclude malignancy) - can be done at time of repair

Cameron's says pH testing and manometry aren't necessary in most patients

Management

• Type I
  • Asymptomatic - no intervention
  • Symptomatic - treat as for GORD - ie medical management, then reflux control surgery, especially if they had a good response to treatment.
• Paraoesophageal
  • Asymptomatic - somewhat controversial, but no intervention probably best
    • Large hernias should probably be repaired in patients with low anaesthetic/operative risk, to prevent volvulus/strangulation
  • Symptomatic - repair indicated electively
  • Emergent repair indicated if gastric volvulus, bleeding, perforation, obstruction, resp compromise present

Paraoesophageal hernia repair

• Can be done open, lap, or transthoracic
• First, endoscopy
• Lap probably best first option although never been compared directly

Indications:

• Patients with volume reflux
• Symptoms respond to PPI
• GORD with negative test for oesophageal dysmotility
  • Lithotomy, both arms at 90deg. Surgeon between legs.
  • Nathanson retractor to pull up left lobe of liver
  • Divide lesser omentum to expose the right hiatal liver
    • Be aware of hepatic branch of vagus nerve and aberrant left hepatic artery
  • Dissect hernial sac and completely remove from mediastinum - circumferential dissection
  • Mobilise oesophagus
  • Tension-free repair of hiatal defect, generally without mesh. Mostly interrupted sutures - maybe
  • Perform complete Nissen fundoplication
  • Anterior gastropexy to reduce risk of reherniation

Complications

• • Intra-operative
    • Hepatic/splenic injury
    • Bleeding from short gastrics
    • Perforation of oesophagus
    • Inability to reduce oesophagus - happens with long-term GORD - scarred
    • Pneumothorax - common - won't be any consequences, will disappear after laparoscopy
  • Long-term
    • Dysphagia, gas bloat, difficulty to belch
    • Vagotomy
  • Dysphagia
    • Too tight wrap
    • Disruption of wrap
    • Sliding HH - stomach slides up under wrap
    • Slipped fundoplication - wrap falls down
    • Intra-thoracic migration

Post-op

• • Antiemetics - don't want vomiting
  • Barium swallow D1 post op - look for leak/recurrence, evaluate gastric emptying
  • If swallow ok, start of clear fluids
  • Discharge after a couple of days generally
  • Start soft/puree diet D4, then normal diet in four weeks. Avoid large meals early.
  • Expect some degree of dysphagia for 4 weeks or so.

Outcomes

• • 90% have long-term symptoms relief
  • 40% have some degree of radiographic recurrence

Controversies

• • Open vs laparoscopic
    • Lap should now be standard of care, even for massive and/or recurrent
    • If lap fails, left thoracotomy would be best approach
  • Also do antireflux?
    • Almost certainly yes
  • Mesh?
    • Long-term risk of erosion is unknown
    • Onlay biologic prosthetic mesh if needed in preference to synthetic
  • Ligation of short gastrics - no evidence it improves wrap, but it does make it easier to flip fundus over