Oesophageal Disease Flashcards
Pathophysiology of GORD
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
Factors predisposing to GORD
- rich, spicy food
- alcohol
- hiatus hernia
- obesity
- pregnancy
- systemic sclerosis
- anything that could increase intra-abdominal pressure e.g. swimming
Symptoms of GORD
- heartburn
- regurge
- cough
- dysphagia
- aspiration of gastric content into the lungs → breathing affected
Investigations for GORD
- clinical diagnosis → most patients treated without investigations
- oesophagogastroduodenoscopy (OGD) in ALARM symptoms*
*explained further on different card
ALARM symptoms that indicate the need for OGD
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
Management (in order of treatment) (5)
- Lifestyle changes (less alcohol, diet change, quit smoking, weight loss)
- OTC antacids (containing Alginate)
- PPIs (e.g. Omeprazole)
- H2 receptor antagonist
- Surgery
How do PPIs work?
irreversibly inhibit ATPase and block the luminal secretion of Gastric Acid.
Complications of GORD
- oesophagitis
- ulcers
- anaemia
- benign strictures
- Barrett’s oesophagus
- oesophageal carcinoma
Epithelium change in Barett’s Oesophagus
From squamous to columnar
Treatment for endoscopically proven oesophagitis
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
Treatment for endoscopically negative reflux disease
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
What’s Barrett’s Oesophagus?
- metaplasia of the lower oesophageal mucosa → usual squamous epithelium being replaced by columnar epithelium
- increased risk of oesophageal adenocarcinoma
Is there a screening programme for Barrett’s?
No screening → identified when patients have an endoscopy for evaluation of upper gastrointestinal symptoms such as dyspepsia
Histological features of Barrett’s
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)
How often do we do endoscopy in Barrett’s
Endoscopic surveillance
- for patients with metaplasia (but not dysplasia) endoscopy is recommended every 3-5 years
RIsk factors for Barrett’s
- gastro-oesophageal reflux disease (GORD) is the single strongest risk factor
- male gender (7:1 ratio)
- smoking
- central obesity
Management of Barrett’s
- 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
Pathophysiology of achalasia
- 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
Typical presentation of achalasia
- long history of difficulty in swallowing of BOTH liquids and solids
- possible regurgitation
- chest pain →although an unusual symptom
Investigations of achalasia
- OGD → dilated oesophagus + tapering /zwezajacy/ lower end
- barium swallow
- oesophageal manometry → gold standard
Management of achalasia
- no very effective treatment
- endoscopic dilatation with balloon → maybe helpful
What happens in hiatus hernia?
Part of the stomach herniates through oesophagal hiatus of the diaphragm
What’s A and what’s B?
A - sliding hiatal hernia
B - rolling hiatal hernia
Sliding hiatal hernia
- what happens
- how common is it
- symptoms
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
Rolling para-oesophageal hernia
- what happens
- is it common?
- does it need to be treated
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
Conservative management of hiatus hernia
- ### 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.
When surgical management of hiatus hernia is indicated?
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)
When do we need to decompress the stomach before hiatal hernia surgery?
Any patients presenting with suspected cases of:
- obstruction
- strangulation
- stomach volvulus
Stomach should be decompressed via a NG tube prior to surgical intervention.
How does surgery for hiatal hernia look like? Two types
- 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
What type of hiatal hernia is more prone to complications?
Hiatus hernias, especially the rolling type, are prone to incarceration and strangulation, like any other type of hernia.
What complication of hiatal hernia requires an immediate surgery?
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
How does gastric volvulus due to hiatal hernia may present?
Clinically, this can present with Borchardt’s triad:
- Severe epigastric pain
- Retching without vomiting
- Inability to pass an NG tube
What’s Borchardt’s triad?
Borchardt’s triad → gastric volvulus due to hiatal hernia:
- Severe epigastric pain
- Retching without vomiting
- Inability to pass an NG tube
Two main types of oesophageal teras
- superficial mucosal tears (Mallory-Weiss tears)
- full thickness ruptures
What’s Boerhaave’s syndrome?
Oesophageal perforation is a full-thickness rupture of the oesophageal wall; if it is spontaneous (often due to vomiting)
Complications of Boerhaave’s syndrome
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.
Causes of a full-thickness oesophageal rupture (2)
- iatrogenic (e.g. endoscopy)
- forceful vomiting
Clinical presentation of oesophageal rupture
- 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.
What’s Mackler’s triad?
combination of :
- vomiting
- chest pain
- subcutaneous emphysema
*indicative of oesophageal rupture
*seen only in 15% of cases
Investigations of oesophageal rupture
- 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
What’s that?
Initial management of oesophageal rupture
- urgent and aggressive resuscitation
- high flow oxygen
- IV access
- fluid resuscitation
- broad spectrum antibiotics
Aim of definitive management (after initial resuscitation) of Boerhaave’s syndrome
- Control of the oesophageal leak
- Eradication of mediastinal and pleural contamination
- Decompress the oesophagus (typically via a trans-gastric drain or endoscopically-placed NG tube)
- Nutritional support
Surgical management of Boerhaave’s syndrome
- 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
Pathophysiology of diffuse oesophageal spasm (DOS)
- multi-focal high amplitude contractions of the oesophagus
- caused by the dysfunction of oesophageal inhibitory nerves
* In some individuals, DOS can progress to achalasia.
Pathophysiology of Diffuse Oesophageal Spasm (DOS)
- severe dysphagia to both solids and liquids
- central chest pain → exacerbated by food
- Examination is often normal
###
What’s that?
Investigations for Diffuse Oesophageal Spasm (DOS)
- 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
Management of Diffuse Oesophageal Spasm (DOS)
(3)
- 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
Autoimmune and connective tissue disorders that may cause oesophageal dysmotility (3)
- 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.
