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Y4 final checklist_ SURGERY > Oesophageal Disease > Flashcards

Oesophageal Disease Flashcards

1
Q

Pathophysiology of GORD

A

GORD

Physiology: reflux of gastric content into the oesophagus → a normal event

Pathology: clinical symptoms occur if the contact of gastric content and oesophagus is prolonged

Due to: lower oesophageal sphincter tone being reduced or/and delayed gastric emptying

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2
Q

Factors predisposing to GORD

A
  • rich, spicy food
  • alcohol
  • hiatus hernia
  • obesity
  • pregnancy
  • systemic sclerosis
  • anything that could increase intra-abdominal pressure e.g. swimming
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3
Q

Symptoms of GORD

A
  • heartburn
  • regurge
  • cough
  • dysphagia
  • aspiration of gastric content into the lungs → breathing affected
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4
Q

Investigations for GORD

A
  • clinical diagnosis → most patients treated without investigations
  • oesophagogastroduodenoscopy (OGD) in ALARM symptoms*

*explained further on different card

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5
Q

ALARM symptoms that indicate the need for OGD

A

A - anorexia

L - loss of weight

A - anaemia due to iron deficiency

R - recent or persistent vomiting

M - melaena or haematemesis

In addition: dysphagia (progressive), epigastric mass, suspicious barium meal

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6
Q

Management (in order of treatment) (5)

A
  1. Lifestyle changes (less alcohol, diet change, quit smoking, weight loss)
  2. OTC antacids (containing Alginate)
  3. PPIs (e.g. Omeprazole)
  4. H2 receptor antagonist
  5. Surgery
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7
Q

How do PPIs work?

A

irreversibly inhibit ATPase and block the luminal secretion of Gastric Acid.

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8
Q

Complications of GORD

A
  • oesophagitis
  • ulcers
  • anaemia
  • benign strictures
  • Barrett’s oesophagus
  • oesophageal carcinoma
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9
Q

Epithelium change in Barett’s Oesophagus

A

From squamous to columnar

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10
Q

Treatment for endoscopically proven oesophagitis

A

Endoscopically proven oesophagitis

  • full dose proton pump inhibitor (PPI) for 1-2 months
  • if response then low dose treatment as required
  • if no response then double-dose PPI for 1 month
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11
Q

Treatment for endoscopically negative reflux disease

A

Endoscopically negative reflux disease

  • full dose PPI for 1 month
  • if response then offer low dose treatment, possibly on an as-required basis, with a limited number of repeat prescriptions
  • if no response then H2RA or prokinetic for one month
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12
Q

What’s Barrett’s Oesophagus?

A
  • metaplasia of the lower oesophageal mucosa → usual squamous epithelium being replaced by columnar epithelium
  • increased risk of oesophageal adenocarcinoma
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13
Q

Is there a screening programme for Barrett’s?

A

No screening → identified when patients have an endoscopy for evaluation of upper gastrointestinal symptoms such as dyspepsia

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14
Q

Histological features of Barrett’s

A

The columnar epithelium may resemble that of either the cardiac region of the stomach or that of the small intestine (e.g. with goblet cells, brush border)

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15
Q

How often do we do endoscopy in Barrett’s

A

Endoscopic surveillance

  • for patients with metaplasia (but not dysplasia) endoscopy is recommended every 3-5 years
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16
Q

RIsk factors for Barrett’s

A
  • gastro-oesophageal reflux disease (GORD) is the single strongest risk factor
  • male gender (7:1 ratio)
  • smoking
  • central obesity
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17
Q

Management of Barrett’s

A
  • endoscopic surveillance with biopsies
  • high-dose proton pump inhibitor
  • If dysplasia of any grade is identified endoscopic intervention is offered. Options include:
  • endoscopic mucosal resection
  • radiofrequency ablation
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18
Q

Pathophysiology of achalasia

A
  • Pathophysiology: Decrease in ganglionic cells in the nerve plexus of the oesophageal wall and degeneration of vagus nerve
  • Result: Oesophageal aperistalsis and failure of relaxation of LOS → impaired oesophageal emptying (swallowing)
    cause: unknown
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19
Q

Typical presentation of achalasia

A
  • long history of difficulty in swallowing of BOTH liquids and solids
  • possible regurgitation
  • chest pain →although an unusual symptom
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20
Q

Investigations of achalasia

A
  • OGD → dilated oesophagus + tapering /zwezajacy/ lower end
  • barium swallow
  • oesophageal manometry → gold standard
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21
Q

Management of achalasia

A
  • no very effective treatment
  • endoscopic dilatation with balloon → maybe helpful
22
Q

What happens in hiatus hernia?

A

Part of the stomach herniates through oesophagal hiatus of the diaphragm

23
Q

What’s A and what’s B?

A

A - sliding hiatal hernia

B - rolling hiatal hernia

24
Q

Sliding hiatal hernia

- what happens

  • how common is it
  • symptoms
A

Sliding Hernia

  • gastro-oesophageal junction slides through the hiatus and lies above the diaphragm
  • accounts for 95% causes of hiatal hernia
  • it does not cause any symptoms unless there is also a reflux
25
Q

Rolling para-oesophageal hernia

  • what happens
  • is it common?
  • does it need to be treated
A

Rolling hernia

  • Gastric fundus rolls up through the hiatus alongside the oesophagus & the gastro-oesophageal junction reminds below the diaphragm
  • it is uncommon
  • it needs to be treated due to serious complications → surgery
26
Q

Conservative management of hiatus hernia

A
  • ### PPIs → to reduce gastric acid secretion and aiding in symptom control
  • lifestyle modification → weight loss, alteration of diet (low fat, earlier meals, smaller portions), and potentially sleeping with increased numbers of pillows
  • Smoking cessation and reduction in alcohol intake → both nicotine and alcohol are thought to inhibit lower oesophageal sphincter function, thereby worsening symptoms.
27
Q

When surgical management of hiatus hernia is indicated?

A

Surgical management is indicated when:

  • Remaining symptomatic, despite maximal medical therapy
  • Increased risk of strangulation/volvulus* (rolling type or mixed type hernia, or containing other abdominal viscera)
  • Nutritional failure (due to gastric outlet obstruction)
28
Q

When do we need to decompress the stomach before hiatal hernia surgery?

A

Any patients presenting with suspected cases of:

  • obstruction
  • strangulation
  • stomach volvulus

Stomach should be decompressed via a NG tube prior to surgical intervention.

29
Q

How does surgery for hiatal hernia look like? Two types

A
  • Cruroplasty – hernia is reduced from the thorax into the abdomen and the hiatus reapproximated to the appropriate size. Any large defects usually require mesh to strengthen the repair.
  • Fundoplication – The gastric fundus is wrapped around the lower oesophagus and stitched in place
    • Aims to strengthen the LOS thus helping to prevent reflux and keep the GOJ in place below the diaphragm – the wrap may be full or partial
30
Q

What type of hiatal hernia is more prone to complications?

A

Hiatus hernias, especially the rolling type, are prone to incarceration and strangulation, like any other type of hernia.

31
Q

What complication of hiatal hernia requires an immediate surgery?

A

A gastric volvulus can also occur whereby the stomach twists on itself by 180 degrees, leading to obstruction of the gastric passage and tissue necrosis

32
Q

How does gastric volvulus due to hiatal hernia may present?

A

Clinically, this can present with Borchardt’s triad:

  • Severe epigastric pain
  • Retching without vomiting
  • Inability to pass an NG tube
33
Q

What’s Borchardt’s triad?

A

Borchardt’s triad → gastric volvulus due to hiatal hernia:

  • Severe epigastric pain
  • Retching without vomiting
  • Inability to pass an NG tube
34
Q

Two main types of oesophageal teras

A
  • superficial mucosal tears (Mallory-Weiss tears)
  • full thickness ruptures
35
Q

What’s Boerhaave’s syndrome?

A

Oesophageal perforation is a full-thickness rupture of the oesophageal wall; if it is spontaneous (often due to vomiting)

36
Q

Complications of Boerhaave’s syndrome

A

Boerhaave’s syndrome = full-thickness rupture of oesophageal wall

Perforation → leakage of stomach contents into the mediastinum and pleural cavity → severe inflammatory response → physiological collapse, multi-organ failure, and death

Rapid identification and management is therefore essential.

Oesophageal rupture is a surgical emergency and patients deteriorate rapidly, rapid identification and management is therefore essential.

37
Q

Causes of a full-thickness oesophageal rupture (2)

A
  • iatrogenic (e.g. endoscopy)
  • forceful vomiting
38
Q

Clinical presentation of oesophageal rupture

A
  • severe sudden-onset retrosternal chest pain
  • respiratory distress
  • subcutaneous emphysema

* symptoms often following severe vomiting or retching

*subcutaneous emphysema is frequently absent and the full combination of vomiting, chest pain and subcutaneous emphysema (Mackler’s triad) is only seen in around 15% of patients.

39
Q

What’s Mackler’s triad?

A

combination of :

  • vomiting
  • chest pain
  • subcutaneous emphysema

*indicative of oesophageal rupture

*seen only in 15% of cases

40
Q

Investigations of oesophageal rupture

A
  • Routine bloods, group and save → take urgently for all those with suspected perforation
  • CXR →pneumomediastinum; intra-thoracic air-fluid levels
  • urgent CT chest abdomen pelvis with IV and oral contrast* → gold standard; air or fluid in the mediastinum and pleural cavity; leakage of oral contrast from the oesophagus into the mediastinum or chest is pathognomonic
  • if there is a high level of clinical suspicion (based on the history and examination) → urgent endoscopy in theatre
41
Q

What’s that?

A
42
Q

Initial management of oesophageal rupture

A
  • urgent and aggressive resuscitation
  • high flow oxygen
  • IV access
  • fluid resuscitation
  • broad spectrum antibiotics
43
Q

Aim of definitive management (after initial resuscitation) of Boerhaave’s syndrome

A
  1. Control of the oesophageal leak
  2. Eradication of mediastinal and pleural contamination
  3. Decompress the oesophagus (typically via a trans-gastric drain or endoscopically-placed NG tube)
  4. Nutritional support
44
Q

Surgical management of Boerhaave’s syndrome

A
  • immediate surgery to control the leak and wash out of the chest →via a thoracotomy
  • on-table OGD to determine the site of perforation
  • feeding jejunostomy insertion → due to leakage being common and the patients should have a CT scan with contrast at 10-14 days before starting oral intake
45
Q

Pathophysiology of diffuse oesophageal spasm (DOS)

A
  • multi-focal high amplitude contractions of the oesophagus
  • caused by the dysfunction of oesophageal inhibitory nerves

* In some individuals, DOS can progress to achalasia.

46
Q

Pathophysiology of Diffuse Oesophageal Spasm (DOS)

A
  • severe dysphagia to both solids and liquids
  • central chest pain → exacerbated by food
  • Examination is often normal

###

47
Q

What’s that?

A
48
Q

Investigations for Diffuse Oesophageal Spasm (DOS)

A
  • Endoscopy is usually normal
  • Manometry shows a pattern of repetitive, simultaneous, and ineffective contractions of the oesophagus. There may also be dysfunction of the lower oesophageal sphincter.

*A barium swallow is rarely performed, but can show a ‘corkscrew’ appearance

49
Q

Management of Diffuse Oesophageal Spasm (DOS)

(3)

A
  • nitrates or calcium channel blockers (CCBs) → first line; they relax oesophageal smooth muscle
  • pneumatic dilatation* → if diffuse oesophageal spasm and documented hypertension of the lower oesophageal sphincter
  • myotomy → reserved for the most severe cases and must be used with caution due to the invasive nature, with the incision involving the entire spasmodic segment and the lower oesophageal sphincter

*Pneumatic dilatation → air-filled cylinder-shaped balloon disrupts the muscle fibers of the lower esophageal sphincter

50
Q

Autoimmune and connective tissue disorders that may cause oesophageal dysmotility (3)

A
  • systemic sclerosis (most common)
  • polymyositis
  • dermatomyositis

In these cases treatment is directed at the underlying cause (e.g. immunosupression in autoimmune-mediated disease), with nutritional modification and proton pump inhibitors as required.

Y4 final checklist_ SURGERY (25 decks)

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