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YR3 Gastro > Oesophageal conditions > Flashcards

Oesophageal conditions Flashcards

1
Q

Describe the anatomy of the oesophagus

A

Muscular tube composed of two layers:

  • an outer longitudinal layer
  • an inner circular muscle layer

Connects the pharynx to the stomach

Striated (voluntary) muscle in upper portion gradually changes to smooth muscle in lower part to become continuous with muscle layer of the stomach

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2
Q

Define achalasia

A

An oesophageal motor disorder of unknown aetiology, characterised by oesophageal aperistalsis and insufficient lower oesophageal sphincter relaxation in response to swallowing.

The normal muscular activity of the oesophagus is disturbed (absent or uncoordinated)

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3
Q

What is the cause of achalasia?

A

Inflammatory destruction of inhibitory nitrinergic neurons (ganglion cells) in the oesophageal myenteric (Auerbach) plexus

Results in loss of peristalsis and incomplete lower oesophageal sphincter relaxation.

The exact cause of this inflammatory process is unknown, but possible triggers include infection, autoimmunity, and genetic factors.

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4
Q

Summarise the epidemiology of achalasia

A
  • Achalasia may occur at any age; however, incidence increases with age.
  • The median age at diagnosis is 53 years.
  • Achalasia affects both sexes equally.
  • Annual incidence 1/100,000
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5
Q

Recognise the presenting symptoms of achalasia

A

Achalasia cannot be diagnosed on the basis of history alone.

Symptom onset is insidious, during which time many patients may adapt to significant symptoms by slowly altering their diet or eating habits.

  1. The key symptom is dysphagia to solids and liquids.
    • liquids is common only in oesophageal motor disorders (not obstructions)
    • May be intermittent
  2. Retrosternal pressure/pain- may be relieved by drinking cold water.
  3. Regurgitation- when in recumbant position. different to GORD- food retained in oesophagous tastes bland not sour
  4. gradual weight loss- different to malignancy rapid WL
  5. heartburn- secondary to fermentation of food retained in the oesophagus
  6. slow eating
  7. coughing/choking while recumbent- 2/2 regurgitation of retained food and liquids
  8. recurrent chest infections- aspiration of retained food
  9. sensation of a lump in the throat (globus)
  10. hiccups- 2/2 delayed transit of food in the oesophagus and diaphragmatic irritation.
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6
Q

Recognise the signs of achalasia on physical examination

A

Posturing to aid swallowing- to manage dysphagia, patients may adopt particular postures, such as:

  • arching the neck and shoulders
  • raising the arms, standing
  • sitting up straight during the meal
  • walking around after a meal.

May show signs of complications:

  • Aspiration pneumonia
  • Malnutrition
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7
Q

Identify appropriate investigations for achalasia

A
  1. Upper gastrointestinal endoscopy
    • low sensitivity for the diagnosis of early achalasia
    • essential 1st line to exclude malignancy- causes pseudoachalasia
  2. Barium swallow
    • loss of peristalsis and delayed oesophageal emptying
    • dilated oesophagus that tapers smoothly to a beak-like narrowing at the gastro-oesophageal junction
    • advanced disease the dilated oesophagus may be tortuous and sigmoid-shaped with diverticula.
  3. High-resolution oesophageal manometry- assesses pressure at LOS. May show:
    • Elevated resting LOS pressure (> 45 mm Hg)
    • Incomplete LOS relaxation
    • Absence of peristalsis in the smooth muscle portion of the oesophagus
  4. CXR
    • Appearance may suggest achalasia, but test has a low sensitivity and is not diagnostic.
  5. Bloods:
    • may do serology for antibodies against T. cruzi if CHAGAS DISEASE is a possibility (and blood film may detect parasites)
    • presence of myenteric plexus antibodies
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8
Q

Algrove syndrome

A

The triple-A (Allgrove) syndrome, characterised by:

  • achalasia
  • alacrima
  • adrenocorticotrophic hormone-resistant adrenal insufficiency

Autosomal recessive disorder that has been mapped to chromosome 12.

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9
Q

Define GORD

A

Symptoms or complications resulting from the reflux of gastric contents into the oesophagus or beyond, into the oral cavity (including larynx) or lung

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10
Q

Explain the risk factors of GORD

A
  • family history of heartburn or GORD
  • older age
  • hiatus hernia- reducing competence of the gastro-oesophageal junction and inhibiting clearance of oesophageal acid post-reflux
  • obesity/pregnancy- intr-abdominal portion of oesophagus uses diaphragm as a sphincter
  • diet: LOS pressure reduced by smoking, alcohol and coffee and some drugs (calcium-channel blockers, nitrates, beta-blockers, progesterone).
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11
Q

State some mechanisms that usually prevent reflux

A
  • Lower oesophageal sphincter
  • Acute angle of junction (angle of His)
  • Mucosal rosette
  • Sling fibres around the cardia
  • Crural fibres of the diaphragm
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12
Q

Explain the aetiology of disease of GORD

A
  • LOS regulates food passage from the oesophagus to the stomach
  • Contains both intrinsic smooth muscle and skeletal muscle.
  • Episodes of transient LOS relaxation are a normal phenomenon, but they occur more frequently in GORD, causing reflux of gastric contents into the oesophagus.
  • Transient LOS relaxation is more common after meals and is stimulated by fat in the duodenum.
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13
Q

Summarise the epidemiology of GORD

A

common- affects between 10% and 30% of people in developed countries.

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14
Q

Recognise the presenting symptoms of GORD

A
  1. Retrosternal burning pain, radiating to epigastrium, jaw and arms.(Oesophageal pain is often confused with cardiac pain.)
  2. Aggravated by:
    • Lying supine
    • Bending
    • Large meals
    • Drinking alcohol
    • Pain is relieved by antacids
  3. Waterbrash (regurgitation of an excessive accumulation of saliva from the lower part of the oesophagus often with some acid material from the stomach)
  4. Aspiration - may result in hoarseness, laryngitis, nocturnal cough and wheeze +/- pneumonia (rare)
  5. Dysphagia - caused by formation of peptic stricture after long-standing reflux
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15
Q

Recognise the signs of GORD on physical examination

A

Usually NORMAL- can have halitosis, enamel erosion

Occasionally -

  • epigastric tenderness
  • wheeze on chest auscultation
  • dysphonia
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16
Q

Identify appropriate investigations for GORD and interpret the results

A

Diagnosis is clinical, supported by testing when required. Heartburn and regurgitation are the most reliable symptoms

  1. If suspected: PPI Trial
    • Further tests are indicated if symptoms do not improve with therapeutic 8-week trial of a PPI
    • or if patient has alarm symptoms

If GORD persists:

  1. Oesophagogastroduodenoscopy (OGD) and biopsy
    • may show oesophagitis (erosion, ulcerations, strictures) or Barrett’s oesophagus
    • can exclude malignancy – must exclude for all >55 years
  2. Barium swallow and meal: sliding hiatus hernia, oesophageal ulcer,stricture.
  3. Ambulatory 24-hour pH monitoring: assess the degree of reflux.
  4. Oesophageal manometry
    • evaluates oesophageal contractions and lower oesophageal sphincter function.
    • It may detect subtle presentations of oesophageal motility disorders such as achalasia or diffuse oesophageal spasm.
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17
Q

State a general management plan for GORD

A

Lose weight, avoid smoking, coffee, alcohol, chocolate, tomatoes and citrus juices.

Avoid tight garments, stooping and large meals.

Elevate head of bed. Avoid of late-night eating if nocturnal symptoms are present.

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18
Q

State a medical management plan for GORD

A

Control acid secretion

  • H2 receptor antagonists (e.g. ranitidine)
  • PPIs (e.g. omeprazole, esomeprazole).
  • Antacids (sodium bicarbonate) may be effective in controlling symptoms in mild disease.
  • Provides rapid symptom relief and healing in oesophagitis (>80% of patients).

Minimize effects of reflux

  • Alginates to protect oesophagus

Improve LOS tone and promote gastric emptying.

  • prokinetic agents
  • (e.g. bethanechol, metoclopramide, domperidone)
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19
Q

State a surgical/interventional management plan for GORD

A

Endoscopy:

  • Annual endoscopic surveillance - looking for Barrett’s Oesophagus
  • May be necessary for stricture dilation or stenting

Surgery:

  • Antireflux surgery if refractory to medical treatment
  • eg Nissen Fundoplication: fundus of the stomach is wrapped around the lower oesophagus - helps reduce the risk of hiatus hernia and reduce reflux
  • gives excellent results.
  • Indicated in approximately 20% of patients with GORD:
    • failed optimum medical treatment
    • complications of reflux (benign stricture, Barrrett’s oesophagus)
    • severe oesophagitis on endoscopy
    • ‘large volume’ reflux.
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20
Q

Identify the possible complications of GORD

A
  • Oesophageal ulceration
  • Peptic stricture
  • Anaemia
  • Barrett’s oesophagus
  • Oesophageal adenocarcinoma
  • Associated with asthma and chronic laryngitis
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21
Q

Summarise the prognosis of patients with GORD

A
  • 50% respond to lifestyle measures alone
  • In patients that require drug therapy, withdrawal is often associated with relapse- however, there are risks associated with long-term use of these drugs
  • 20% of patients undergoing endoscopy for GORD have Barrett’s oesophagus
  • Oesophageal adenocarcinoma may be a serious though rare complication of GORD.
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22
Q

Define Barrets oesophagus

A

A metaplastic change in the normal squamous epithelium of the oesophagus to specialised intestinal metaplasia (columnar epithelium)

SQUAMOUS → COLUMNAR

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23
Q

Explain the aetiology of Barrett’s oesophagus

A

The primary aetiological factor involved in Barrett’s oesophagus is gastro-oesophageal reflux.

However, there is evidence that combined acid and bile reflux are the primary causative agents.

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24
Q

Explain the pathophysiology of Barrett’s oesophagus

A

Prolonged exposure of the normal squamous epithelium to refluxate of GORD leads to mucosal inflammation and erosion

This leads to replacement of the mucosa with metaplastic columnar stem cell

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25
Q

State the risk factors for Barrets oesophagus

A

Mix of environmental and genetic factors

  • acid/bile reflux or GORD
  • increased age
  • white ethnicity
  • male sex
  • family history of Barrett’s oesophagus or oesophageal adenocarcinoma
  • obesity
  • smoking
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26
Q

Why is Barrets oesophagus potentially life-threatening?

A

Intestinal cell metaplasia caused by Barrets could develop to low-grade dysplasia

This is a PREMALIGNANT condition - high grade displasia can then develop to adenocarcinoma

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27
Q

Summarise the epidemiology of Barrett’s oesophagus

A
  • twice as common in males
  • Prevalence 0.5-2%
  • The frequency of oesophageal adenocarcinoma in men has quadrupled in the past few years.
  • This may be linked to an increase in incidence of GORD
  • 3-5% of people with GORD will develop Barrett’s oesophagus
28
Q

Recognise the presenting symptoms of Barrett’s oesophagus

A

Common symptoms:

  • Heartburn
  • Regurgitation

Patients are likely to experience symptoms of GORD:

  • Nausea
  • Water-brash (sour taste in the mouth)
  • Bloating
  • Belching
  • Burning pain when swallowing (dysphagia)

Atypical symptoms:

  • chest pain
  • laryngitis
  • cough
  • dyspnoea or wheezing- reflux-induced asthma or reactive airway disease
  • history of aspiration pneumonia
29
Q

Identify appropriate investigations for Barrett’s oesophagus

A
  1. Gastroscopy (OGD - Oesophago-gastro-duodenoscopy)
    • ​​See abnormal epithelium proximal to the gastro-oesophageal junction.
    • Areas of ulceration, narrowing (stricture), and nodularity should be targeted for biopsy because they are more likely to contain areas of dysplasia and adenocarcinoma
  2. Barium oesophagogram
    • May be considered as the initial test in patients with dysphagia in order to evaluate for a mass lesion or stricture before endoscopy.
    • Cannot diagnose Barrett’s oesophagus.
    • Can document other signs of GORD or a hiatal hernia, which are risk factors for Barrett’s oesophagus.
30
Q

Generate a management plan for Barrett’s oesophagus

A

PPI → radiofrequency ablation → endoscopic mucosal resection → oesophagectomy

non-dysplastic Barrett’s oesophagus

  • 1st line – PPI + surveillance
  • Adjunct – radiofrequency ablation
  • 2nd line – anti-reflux surgery plus surveillance

low-grade (non-nodular) dysplasia

  • 1st line – radiofrequency ablation
  • +/- endoscopic mucosal resection (nodular regions)

high-grade dysplasia

  • 1st line – radiofrequency ablation +/- endoscopic mucosal resection
  • Plus – PPI
  • 2nd line – oesophagectomy- definitive treatment option (20-40% will have early adenocarcinoma)
31
Q

Summarise the prognosis for patients with Barrett’s oesophagus

A

Barrett’s oesophagus carries a 30-60x higher risk of oesophageal adenocarcinoma than the general population

5-10% of those with Barrett’s oesophagus will develop adenocarcinoma over 10-20 years

Generally, adenocarcinomas discovered while screening for Barrett’s oesophagus are early-stage lesions and have good prognosis (5-year survival >85%).

32
Q

Define oesophageal cancer and state the 2 main types

A

Malignant tumour arising in the oesophagus. There are TWO major histological types:

  • Squamous cell carcinoma
  • Adenocarcinoma
33
Q

Explain the risk factors for oesophageal cancer (adenocarcinoma and SCC)

A

common risk factors

  • male sex (M:F 7:1)
  • low socioeconomic status
  • a diet low in fresh fruit and vegetables
  • achalasia (10-fold risk increase)

SCC

  • tobacco use
  • excessive alcohol intake
  • family history of oesophageal, stomach, oral, or pharyngeal cancer
  • non-white race (squamous cell carcinoma)
  • high-temperature beverages and foods (squamous cell carcinoma)
  • drinking maté (squamous cell carcinoma)

Adenocarcinoma

  • GORD and Barrett’s oesophagus
  • hiatus hernia- 2-6-fold increase due to GORD
  • obesity
34
Q

Summarise the epidemiology of oesophageal cancer

A

Incidence varies widely

M:F = 7:1

average rate for Western countries of 3 per 100,000

  • Squamous has decreased (decreased tabacco/alcohol consumption) in the west
  • adenocarinoma has increased (increased incidence of barretts oesophagus) in the west
  • Squamous more common in developing countries
  • Adenocarcinoma more common in western world
35
Q

Recognise the presenting symptoms of oesophageal cancer

A

Often asymptomatic until locally advanced disease- patients present late

Common symptoms:

  • dysphagia
    • progressive- initially worse for solids
    • most common PC- only occurs after there is an obstruction >2/3rds of the lumen
  • odynophagia (painful swallowing)
    • one of the signs of a locally advanced tumour with possible invasion of the airway or mediastinum.
  • weight loss
    • often overlooked as broad differentials when not paired with previous 2 PCs

Others:

  • Regurgitation
  • Cough- may indicate the presence of an oesophagotracheal/bronchial fistula resulting from local tumour invasion
  • Hiccups- phrenic nerve involvement
  • Choking after food
  • Voice hoarseness
  • Fatigue (due to iron deficiency anaemia)
36
Q

Recognise the signs of oesophageal cancer on physical examination

A

May be no signs

Metastatic disease may cause:

  • Supraclavicular lymphadenopathy
  • Hepatomegaly
  • Hoarseness
  • Signs of bronchopulmonary involvement
37
Q

Identify appropriate investigations for oesophageal cancer

A

1st investigations

  1. oesophagogastroduodenoscopy (OGD) with biopsy
  2. comprehensive metabolic profile-
    • ​​advanced cases with near or complete oesophageal obstruction
    • Patients may become severely volume-depleted → hypokalaemia, elevated creatinine and serum urea/nitrogen

2nd investigations- cancer staging

  • Staging - CT chest and abdomen
    • ​indicates size of primary tumour, local invasion, and presence or absence of metastases
  • FDG-PET scan
    • see hyperactivity (hot spot) at primary tumour site and locoregional disease; may also show activity in lungs, liver, or bones suggestive of metastases
    • done before EUS to avoid unnecessary testing in patients with metastatic disease.
  • Endoscopic ultrasound (EUS) ± FNA
    • standard pre-treatment test.
    • It can identify all the histological layers of the oesophagus and thereby confirm the T-stage with 90% accuracy.
    • ​indicates extent of local invasion and presence or absence of spread to lymph nodes
  • Other - bronchoscopy, lung function tests and ABG
38
Q

Define Mallory-Weiss tear

A

Tear/laceration often along the right border of, or near, the gastro-oesophageal junction, as a result of violent retching, vomiting, coughing, or straining.

39
Q

Explain the aetiology of Mallory-Weiss tear

A

Factors such as:

  • coughing, retching, vomiting, straining, hiccups
  • closed-chest pressure or cardiopulmonary resuscitation
  • acute abdominal blunt trauma
  • alcohol
  • medications (aspirin or other non-steroidal anti-inflammatory drugs [NSAIDs])
  • chemotherapeutic agents
  • oesophageal instrumentation have been associated with MWT..
40
Q

Explain the risk factors for Mallory-Weiss tear

A
  • condition predisposing to retching, vomiting, and/or straining
    • GI obstruction
    • gastroentiritis
    • hyperemesis gravidarium
    • bulimia nervosa
  • chronic cough
    • ​whooping cough, bronchitis, bronchiectasis, emphysema, COPD, or lung cancer
  • hiatal hernia
    • ​precipitating factor found to be present in 40-100% of patients with MWT
  • retching during endoscopy or other instrumentation
    • ​eg NG tube, ERCP
  • significant alcohol use
    • ​reported association in 40-80% of patients
  • previous instrumentation
41
Q

Summarise the epidemiology of Mallory-Weiss tears

A
  • Most common between the ages of 30-50 years
  • More common in men than in women in a ratio of 3:1
  • Represents 3-15% of cases of upper GI bleeding- quite rare
  • Recurrent bleeding is common
42
Q

Recognise the presenting symptoms of Mallory-Weiss tears

A

The classic presentation of MWT consists of a small and self-limited episode of haematemesis

This varies from flecks of blood mixed with gastric contents and/or mucus, and blackish or ‘coffee grounds’, to a bright-red bloody emesis

After a bout of retching, vomiting, coughing, or any other factors that increase pressure at the level of the GOJ

Other less common presentations:

  • dizziness, syncope
  • dysphagia
  • odynophagia
  • melaena
  • haematochezia
  • retrosternal pain with interscapular radiation
  • midepigastric abdominal pain.
43
Q

Recognise the signs of Mallory-Weiss tears on physical examination

A

There are no specific physical signs in patients with MWT

44
Q

Identify appropriate investigations for Mallory-Weiss tears

A

Initial laboratory investigation- bloods

  • Hb, Hct, platelets (plt), U+Es
    • evaluate severity of bleeding
    • check for anaemia
  • Cross matching/G+S
    • ​those with anaemia at presentation or ongoing bleeding.
  • PT and aPTT, INR
    • in all patients on anticoagulants or those suspected of coagulopathy.
  • LFTs
    • rule out liver disease which may predispose a patient to oesophageal varices

Other initial investigations

  • Oesophagogastroduodenoscopy
    • diagnostic test of choice
    • should be performed in all patients with upper GI bleed after stabilisation
  • CXR
    • Laceration or tear is not visible under conventional radiography
    • May be an initial test diagnosis in patients with suspected oesophageal perforation.
45
Q

Generate a management plan for Mallory-Weiss tears

A

80-90% of the time, the bleeding from a Mallory-Weiss tear will stop on its own

If bleeding is continuous:

  1. urgent evaluation + monitoring
    • phytomenadione (Vit K) IV
    • crystalloid fluid replacement
    • Blood transfusion (packed red blood cells) for ongoing bleeding/Hb <80 g/L
    • Prolonged PT/INR should be corrected with FFP
  2. Endoscopy
    • Haemoclip placement
    • thermocoagulation therapy
    • endoscopic band ligation (EBL)
  3. Surgery
    • should be reserved for situations where endoscopic haemostasis of bleeding has failed
    • laproscopic/angiotherapy
46
Q

Identify + describe a rare but serious complication of Mallory-Weiss tears

A

Boerhaave’s perforation

Oesophageal perforation carries a high mortality secondary to rapidly developing mediastinitis and sepsis.

Signs and symptoms:

  • Retrosternal or epigastric pain with interscapular radiation immediately following an episode of vomiting.
  • dyspnoea (due to pleural effusion)
  • cyanosis
  • fever + sweating
47
Q

Summarise the prognosis for patients with Mallory-Weiss tears

A

For most patients, bleeding is self-limited, and will have stopped by the time of endoscopy.

Prognosis is excellent in patients without associated disease or complications.

Re-bleeding occurs in about 8-15% of patients, usually within the first 24 hours

High-risk factors for re-bleeding:

  • old age (aged >65 years)
  • haematemesis and/or haematochezia at presentation
  • haemodynamic instability/shock
  • alcoholism
  • aspirin/NSAID use
  • comorbidities (anaemia, chronic liver disease, CAD, COPD, renal failure)
48
Q

Define hiatus hernia

A

Protrusion of intra-abdominal contents (usually stomach) through an enlarged oesophageal hiatus of the diaphragm.

49
Q

Explain the 3 causes of hiatus hernia

A
  1. Congenital
  2. Traumatic
  3. Non-traumatic
    • Sliding (80%)
    • Paraoesophageal (rolling, 20%)
    • Mixed
50
Q

Explain the classification of non-traumatic hiatus hernia

A

Type I

  • Sliding hiatus hernia
  • Protrusion of the gastro-oesophageal junction followed by the body of the stomach

Type II

  • Pure para-oesophageal hernia or rolling hiatus hernia
  • Herniation of the fundus or body of the stomach or both into the chest
  • maintenance of the gastro-oesophageal junction below the diaphragm.

Type III

  • Mixed or combined para-oesophageal hernia
  • Combination of types I and II.

Type IV

  • Giant hiatus hernia
  • herniation of one or more other organs, such as colon, small bowel, omentum, and spleen.
51
Q

What symptom can discerne between sliding and rolling hiatus hernias?

A

Acid reflux

Sliding (80%) -

  • the hernia moves in and out of the chest.
  • Acid reflux often happens as the lower oesophageal sphincter becomes less competent.

Paraoesophageal (rolling, 20%) -

  • Gastro-oesophageal junction remains intact so acid reflux uncommon
52
Q

state some risk factors for hiatus hernia

A

key risk factor = obesity

Other risk factors:

things that increase intra-abdominal pressure:

  • ascites
  • pregancy
  • chronic cough
  • pulmonary disease

things that weaken oesophageal hiatus:

  • chronic oesophagitis
  • structural abnormalities of the oesophageal hiatus or the phreno-oesophageal ligaments
  • previous gastro-oesophageal surgery
53
Q

Summarise the epidemiology of hiatus hernia

A
  • Common in WESTERN countries
  • Clinical estimates of the prevalence of hiatus hernia in western populations range up to 50%
  • 70% = > 70 yrs
  • Particularly common in older obese women
  • 50% have symptomatic GORD
54
Q

Recognise the presenting symptoms of hiatus hernia

A

Most are ASYMPTOMATIC

GORD symptoms + painless regurgitation = hiatus hernia

  • regurgitation esp when lying down

Patients may present with symptoms of GORD

  • Heartburn
  • Waterbrash

NO correlation between the size of the hernia and severity of the symptoms

55
Q

Identify appropriate investigations for hiatus hernia

A

Bloods

  • FBC - check for iron deficiency anaemia

Radiology

  • CXR (first line) - gastric air bubble may be seen above the diaphragm
  • Barium swallow – aka upper gastrointestinal series- best diagnostic test

Endoscopy

  • Upper GI endoscopy visualises the mucosa to detect oesophagitis but cannot reliably exclude a hiatus hernia
56
Q

Generate a MEDICAL management plan for hiatus hernia

A

Medical:

  • PPIs
  • Lifestyle changes-
    • losing weight
    • elevating the head of the bed
    • avoiding:
      • large meals
      • meals just before bedtime
      • alcohol
      • acidic foods.
57
Q

Explain the SURGICAL management of hiatus hernia- in whih patients is surgery indicated?

A

Nissen Fundoplication

Indicated in the minority, including patients with:

  • complications of GORD despite aggressive medical treatment
  • pulmonary complications (e.g. aspiration pneumonia)
  • Rolling hiatus hernia - prophylactically, even if asymptomatic, because of the long-term risk of strangulation and mediastinitis.

Gastric resection is reserved for patients with irreversible ischaemia or necrosis.

58
Q

Briefly explain a loose Nissen fundoplication

A

The stomach is pulled down through the oesophageal hiatus

Part of the stomach is wrapped (360 degrees) around the oesophagus

Makes a new sphincter and reduces the likelihood of herniation

59
Q

Identify possible complication of hiatus hernia

A

Oesophageal

  • Intermittent bleeding
  • Oesophagitis
  • Erosions
  • Barrett’s oesophagus
  • Oesophageal strictures

Non-Oesophageal

  • Incarceration of hiatus hernia (only with paraoesophageal hernias)
  • This can lead to strangulation and perforation
60
Q

Summarise the prognosis for patients with hiatus hernia

A
  • Generally GOOD
  • Sliding hernias have a better prognosis than rolling hernias
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YR3 Gastro (12 decks)

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