Oesophagus, Stomach and Duodenum 1

Question 1

Dysphagia - Causes

Answer 1

• Mechanical block – malignant stricture (oesophageal, gastric or pharyngeal), benign stricture (oesophageal web or peptic stricture), extrinsic pressure (lung malignancy, mediastinal lymph nodes, retrosternal goitre, aortic aneurysm or left atrial enlargement) or a pharyngeal pouch.
• Motility – achalasia, diffuse oesophageal spasm, systemic sclerosis, myasthenia gravis, bulbar palsy, pseudobulbar palsy, syringobulbia, bulbar poliomyelitis or Chagas’ disease.
• Other – oesophagitis (infection – candida or HSV of reflux oesophagitis) or globus hystericus.

Question 2

Dysphagia - Questions to Ask

Answer 2

• Was there difficulty swallowing solids and liquids from the start? – if yes then suspect a motility disorder or a pharyngeal cause. If no suspect a stricture either benign or malignant.
• Is it difficult to make the swallowing movement? – if yes then suspect a bulbar palsy.
• Is swallowing painful (odynophagia)? – if yes suspect malignancy, oesophageal ulcer or spasm.
• Is the dysphagia intermittent or constant and getting worse? – if it is intermittent suspect an oesophageal spasm but if constant and worsening suspect a malignant stricture.
• Does the neck bulge or gurgle on drinking? – if yes suspect a pharyngeal pouch.

Question 3

Dysphagia - Signs

Answer 3

• Is the patient cachectic or anaemic?
• Examine the mouth and feel the supra-clavicular nodes (Virchow’s node (left supraclavicular) enlargement suggests intra-abdominal malignancy).
• Look for signs of systemic disease e.g. systemic sclerosis or central nervous system disease e.g. weakness elsewhere.

Question 4

Dysphagia - Investigations

Answer 4

• FBC for anaemia, U+Es for dehydration and CXR for mediastinal fluid level, absent gastric bubble or aspiration.
• Upper GI endoscopy ± biopsy is usually first line investigation but a barium follow through ± video fluoroscopy is useful to diagnose high dysphagia or dysmotility e.g. achalasia.
• Manometry can be used to provide details about the lower oesophageal sphincter and peristalsis.

Question 5

Achalasia - Definition and Investigations

Answer 5

• The lower oesophageal sphincter fails to relax (due to degeneration of the myenteric plexus) and causes dysphagia, regurgitation, substernal cramps and weight loss.
• Investigations - the barium swallow will show a dilated, tapering oesophagus.

Question 6

Achalasia - Management and Prognosis

Answer 6

• Management – endoscopic balloon dilation or Heller’s procedure (cardiomyotomy) followed by proton pump inhibitors. Botulinum toxin injection can be used for patients unsuitable for an invasive procedure.
• Prognosis – long term achalasia is a risk factor for developing oesophageal malignancy.

Question 7

Benign Oesophageal Stricture

Answer 7

• Can be caused by gastro-oesophageal reflux disease, corrosives, surgery or radiotherapy.
• Treatment is also with endoscopic balloon dilation.

Question 8

Pharyngeal Pouch - Definition

Answer 8

Aka Zenker’s diverticulum – an outpouching of the pharynx usually between the upper border of the cricopharyngeous muscle and the lower border of the inferior constrictor muscle of the pharynx. This corresponds with a weak area called Killian’s dehisance.

Question 9

Pharyngeal Pouch - Clinical Features

Answer 9

Food debris may collect within the diverticulum which can in turn expand and press on the adjacent oesophagus causing dysphagia.

Patients may also complain of regurgitation of food, gurgling sounds or bad breath from decaying food.

Question 10

Pharyngeal Pouch - Complications and Management

Answer 10

• Complication – perforation can occur if an endoscope enters the pharyngeal pouch.
• Management – simple excision or endoscopic stapling of the bridge between the pouch and the oesophagus, opening up the pouch and allowing it to drain more freely.

Question 11

Oesophageal Ca - Incidence and Risk Factors

Answer 11

• Incidence – variable (per 100,000) - <5 in Oz, <9 in the UK but >100 in Iran. Male to female ratio is 3:1.
• Risk factors – poor diet – obesity and diet low in vitamins A and C, excess alcohol, smoking, achalasia, reflux oesophagitis ± Barrett’s oesophagus, Plummer-Vinson syndrome or nitrosamine exposure.

Question 12

Oesophageal Ca - Barrett’s Oesophagus

Answer 12

A condition in which the normal squamous epithelium in the distal oesophagus is replaced with columnar epithelium.

It is secondary to gastro-oesophageal reflux of gastric contents, in particular acid. It is associated with an increased risk of developing oesophageal adenocarcinoma.

Question 13

Oesophageal Ca - Site affected

Answer 13

20% in the upper section, 50% in the middle section and 30% in the lower section of the oesophagus.

The malignancy can be squamous cell or adenocarcinoma (65% and incidence is rising).

Question 14

Oesophageal Ca - Presentation

Answer 14

Dysphagia, weight loss, retrosternal chest pain and lymphadenopathy (but this is rare).

In addition there are signs from the upper third of the oesophagus – hoarseness and a cough.

As swallowing is impaired there’s an increased risk of aspiration pneumonia (especially when lying down).

Question 15

Oesophageal Ca - Investigations

Answer 15

Barium swallow, chest x-ray, upper GI endoscopy with biopsy or brushings and CT or MRI.

A staging laparoscopy may be necessary if there is a significant infra-diaphragmatic component.

Question 16

Oesophageal Ca - TNM Staging

Answer 16

Spread is direct by submucosal infiltration and local spread to nodes or later via blood.

• Tumour – Tis – carcinoma in situ, T1 – invading the lamina propria or submucosa, T2 – invading the muscularis propria, T3 – invading the adventitia and T4 – invading adjacent structures.
• Nodes – Nx – nodes cannot be assessed, N0 – no node spread and N1 – regional node spread.
• Metastases – M0 – there is no distant spread and M1 – there are distant metastases present.

Question 17

Oesophageal Ca - Management

Answer 17

Survival rates are poor both with and without treatment.

If localised T1/T2 disease a radical curative oesophagectomy with pre-operative chemotherapy to improve survival may be tried. The tumour is excised and the stomach mobilised to form an anastomosis.

If surgery is not indicated then chemo-radiotherapy may be better than radiotherapy alone.

Palliation in advanced disease aims to restore swallowing with chemo-radiotherapy, stenting and use of lasers.

Overall 5 year survival is 10-15%.

Question 18

Gastric Ca - Incidence

Answer 18

Incidence of adenocarcinoma at the gastro-oesophageal junction is increasing in the West although incidence of distal and body gastric carcinoma has fallen sharply.

UK incidence is 23/100,000 per year.

Question 19

Gastric Ca - Pathology

Answer 19

Borrmann classification is used:

• 1 – polypoid (resembles a polyp) or fungating.
• 2 – excavating.
• 3 – ulcerating and raised.
• 4 – linitis plastica (uniform thickening of the stomach wall).
• Spread throughout the peritoneal cavity can occur, especially to the ovaries = Krukenburg tumour.

Question 20

Gastric Ca - Associations

Answer 20

Lower socioeconomic class, poor diet – high salt and low vitamin C, smoking, H pylori, atrophic gastritis, adenomatous polyps, pernicious anaemia, blood group A and nitrosamine exposure.

Question 21

Gastric Ca - Presentation

Answer 21

Symptoms – often non-specific e.g. dyspepsia, weight loss, vomiting, dysphagia or anaemia.

Signs suggesting an incurable disease – epigastric mass, hepatomegaly, jaundice, ascites, large left supra-clavicular lymph node = Trosier’s sign or acanthosis nigracans (darkened skin creases).

Question 22

Gastric Ca - Investigations

Answer 22

Gastroscopy and multiple ulcer edge biopsies – aim to biopsy all gastric ulcers as even malignant ulcers may appear to heal on drug treatment.

Endoscopic ultrasound and CT/MRI for staging and a staging laparoscopy is recommended if metastases are not detected on other investigations.

Question 23

Gastric Ca - Management

Answer 23

For tumours in the distal 2 thirds a partial gastrectomy may suffice but if more proximal a total gastrectomy may be required.

Combination chemotherapy appears to increase survival in advanced disease. Palliation is often needed for obstruction, pain or haemorrhage.

Question 24

Gastric Ca - Prognosis

Answer 24

5 years survival is <10% overall but nearly 20% for patients who have had radical surgery.

Question 25

GI Stromal Tumours

Answer 25

Mesenchymal tumours of the GI tract originate within the bowel wall. They are divided into 3 groups:

• Leiomyomas and leiomyosarcomas – tumours of smooth muscle found in the oesophagus.
• Neurofibromas – these tumours are positive for S100 indicating that they have a neural origin.
• Gastrointestinal stromal tumours (GISTs) – originate from the interstitial cells of Cajal – the pacemaker cells of the gastrointestinal tract. 60-70% of these tumours occur in the stomach.

Question 26

GI Stromal Tumours - Indicators of Malignancy

Answer 26

Three quarters are benign with indicators of malignancy being tumour size >10cm, extragastric position, mitotic index >5/10 and evidence of cystic degeneration on endoscopic ultrasound.

Question 27

GI Stromal Tumours - Presentation and Management

Answer 27

• Presentation – most are asymptomatic but can cause abdo pain, bleeding or obstructive symptoms.
• Management – surgical resection based on clinical indications e.g. size and level of obstruction.

Question 28

Oesophageal Rupture - Causes

Answer 28

Iatrogenic (85-90% - endoscopy, biopsy or dilatation), trauma (penetrating injury or ingestion of a foreign body), carcinoma, Boerhaave syndrome (due to violent emesis) or corrosive ingestion.

Question 29

Oesophageal Rupture - Presentation and Investigation

Answer 29

Presentation - odynophagia, tachypnoea, dyspnoea, fever, shock, surgical emphysema – a crackling sensation felt on palpating the skin over the chest or neck caused by air tracking from the lungs.

Investigations - plain chest x-ray, contrast swallow, endoscopy or CT scan to evaluate the perforation.

Question 30

Oesophageal Rupture - Management

Answer 30

Iatrogenic perforations are less prone to mediastinitis and sepsis so can be managed conservatively – with NG tube, PPIs and antibiotics. Others will require resuscitation, PPI, antibiotics, and surgery – debridement of the mediastinum, insertion of a T tube within the oesophagus and formation of an oesophago-cutaneous fistula.