Diseases of the esophaguslecture 2

DR. Arwa Mahmood Fuzi Alsaraf

Motility disordersBenign oesophageal strictureTumours of the oesophagus

Perforation of the oesophagus

Motility disorders

Pharyngeal pouch

* Herniation within the pharynx through the cricopharyngeus muscle and formation of a pouch, due to incoordination of swallowing.

*Common in elderly.

*Usually have no symptoms, may cause regurgitation, halitosis, dysphagia and gurgling

Investigation: -Barium swallow demonstrates the pouch and

reveals incoordination of swallowing, pulmonary aspiration.

-Endoscopy may be hazardous since the instrument may enter and perforate the pouch.

Treatment:

Surgical myotomy and resection of the pouch .

Achalasia of the oesophagus

*Affecting 1:100 000 people.

*Develops in middle life but can occur at any age.

Pathophysiology 1- A hypertonic lower oesophageal sphincter which

fails to relax in response to the swallowing wave 2- Failure of propagated oesophageal contraction,

leading to progressive dilatation of the gullet.

Causes: 1-Defective release of nitric oxide by inhibitory

neurons in the lower oesophageal sphincter

2- Degeneration of ganglion cells within the sphincter and the body of the oesophagus.

3- Loss of the dorsal vagal nuclei within the brain.

4- Infection with Trypanosoma cruzi in Chagas

disease.

Clinical features: 1- Dysphagia. is initially intermittent, and is worse for solids and eased by

drinking liquids, and by standing and moving around after eating. (Heartburn does not occur because the closed oesophageal sphincter prevents gastro-oesophageal reflux)

2- Chest pain due to oesophageal spasm.

3- Nocturnal pulmonary aspiration develops . 4-Achalasia predisposes to squamous carcinoma of the

oesophagus.

Investigation:

1- Endoscopy to exclode carcinoma of the cardia (can mimic the presentation and radiological and manometric features of achalasia 'pseudo-achalasia').

2- Barium swallow shows tapered narrowing of the lower oesophagus and in late disease the oesophageal body is dilated, aperistaltic and food-filled.

3-Manometry confirms the high-pressure, non-relaxing lower oesophageal sphincter with poor contractility of the oesophageal body.

Management

1-Forceful pneumatic dilatation using a 30-35 mm diameter fluoroscopically positioned balloon disrupts the oesophageal sphincter and improves symptoms in 80% of patients.

2- Injection of botulinum toxin into the

lower oesophageal sphincter induces clinical remission, but relapse is common.

3-Surgical myotomy ('Heller's operation'):

performed either laparoscopically or as an open operation,

accompanied by a partial fundoplication anti-reflux procedure.PPI therapy is necessary after surgery.

Complications of traetment: gastro-oesophageal reflux,

severe oesophagitis because oesophageal clearance is so poor.

Other oesophageal motility disorders

Diffuse oesophageal spasm *Presents in late middle age with *Episodic chest pain which may mimic angina, transient

dysphagia. *Some cases occur in response to gastro-oesophageal reflux.

Treatment - PPI drugs when gastro-oesophageal reflux is present. - Oral or sublingual nitrates or nifedipine. (Drug therapy is often

disappointing, as are the surgical alternatives)

'Nutcracker' oesophagus *extremely forceful peristaltic activity leads to episodic chest pain and

dysphagia. *Treatment is with nitrates or nifedipine.

oesophageal motility disorders not fit into a specific disease

*The patients are usually elderly *dysphagia and chest pain. *Manometric abnormalities ranging from poor peristalsis to spasm

occur. *Treatment is with dilatation and/or vasodilators for chest pain.

Secondary causes of oesophageal dysmotility

Systemic sclerosis The muscle of the oesophagus is replaced by fibrous tissue which

causes failure of peristalsis leading to heartburn and dysphagia. Oesophagitis is often severe, and benign fibrous strictures occur. These patients require long-term therapy with PPIs.

Dermatomyositis

Rheumatoid arthritis

Myasthenia gravis

Oesophageal stricture

Oesophageal stricture

Causes of oesophageal strictur Gastro-oesophageal reflux disease Webs and rings Carcinoma of the oesophagus or cardia Eosinophilic oesophagitis Extrinsic compression from bronchial carcinoma Corrosive ingestion Post-operative scarring following oesophageal resection Post-radiotherapy Following long-term nasogastric intubation

Benign oesophageal stricture

Benign oesophageal stricture *A consequence of gastro-oesophageal reflux disease *Most often in elderly patients

Rings, due to submucosal fibrosis, * At the oesophago-gastric junction ('schatzki ring') *cause intermittent dysphagia, starting in middle age.

Post-cricoid web * Rare complication of iron deficiency anaemia (paterson-kelly or plummer-vinson

syndrome), * complicated by the development of squamous carcinoma.

Benign strictures are treated by endoscopic dilatation,( wire-guided bougies or balloons are used to disrupt the fibrous tissue of the stricture).

Tumours of the oesophagus

Benign tumours

The most common is a gastrointestinal stromal tumour (GIST).

This is usually asymptomatic but may cause bleeding or dysphagia.

Carcinoma of the oesophagus(Squamous cell, adenocarinoma, small cell)

Squamous oesophageal cancer * Is relatively rare in Caucasians (4/100 000), whilst

common in Iran, parts of Africa and china (200 per 100 000).

* Arise in any part of the oesophagus. *Almost all tumors in the upper oesophagus are

squamous cancers.

Aetiological factors

Smoking

Alcohol excess Chewing betel nuts or tobacco Coeliac disease Achalasia of the oesophagus

Post-cricoid web

Post-caustic stricture Tylosis (familial hyperkeratosis of palms and soles)

Adenocarcinomas

*Arise in the lower third of the oesophagus from Barrett's oesophagus or from the cardia of the stomach.

*The incidence is 5:100 000 in the UK.

* Despite modern treatment, the overall 5-year survival of patients presenting with oesophageal cancer is only 9-13%.

Clinical features

* Progressive, painless dysphagia for solid foods in most patients.

*Others present acutely because of food bolus obstruction.

*Chest pain or hoarseness suggests mediastinal invasion.

* Coughing after swallowing, (due to Fistulation between the oesophagus and the trachea or bronchial tree).

*Pneumonia and pleural effusion.

* cachexia, cervical lymphadenopathy or other evidence of metastatic spread is common.

Investigation

*Upper gastrointestinal endoscopy with cytology and biopsy.

*Barium swallow demonstrates the site and length of the stricture. *Staging the tumour and define operability. -Thoracic and abdominal CT(identify metastatic spread and local

invasion. Invasion of the aorta and other local structures may preclude surgery.

- EUS the most sensitive method for determining depth of penetration of the tumour into the oesophageal wall and for detecting involved locoregional lymph nodes.

These investigations will define the TNM stage of the disease .

Management

Surgical treatment If the patient presents at a point at which resection is possible. Tumours which

have extended beyond the wall of the oesophagus and have lymph node involvement (T3,N1) are associated with a 5-year survival of around 10%. However, this figure improves significantly if the tumour is confined to the oesophageal wall and there is no spread to lymph nodes. Overall survival following 'potentially curative' surgery (all macroscopic tumour removed) is about 30% at 5 years,

Neoadjuvant (pre-operative) -Chemotherapy with cisplatin and 5-fluorouracil will improve prognosis (Although

squamous carcinomas are radiosensitive, radiotherapy alone is associated with a 5-year survival of only 5%,)

-combined chemoradiotherapy for these tumours can achieve 5-year survival rates of 25-30%.

Palliative treatment ( 70% of patients have extensive disease at presentation will benefit from

this treatment)

* Relief of dysphagia and pain.

1- Endoscopic laser therapy or self-expanding metallic stents are used

2- Radiotherapy may induce shrinkage of both squamous cancers and

adenocarcinomas but symptomatic response may be slow. * Nutritional support and appropriate analgesia

Perforation of the oesophagus

Causes

1- Endoscopic perforation complicating dilatation or intubation.

*Malignant, corrosive or post-radiotherapy strictures are more likely to be perforated

* peptic strictures.

Management *Perforated peptic stricture is usually managed conservatively using

broad-spectrum antibiotics and parenteral nutrition; most heal within days.

*Malignant, caustic and radiotherapy stricture perforations require surgical resection or intubation.

2-Spontaneous oesophageal perforation ('Boerhaave's syndrome')

*Results from forceful vomiting and retching. *Severe chest pain and shock occur as oesophago-gastric contents

enter the mediastinum and thoracic cavity. *Subcutaneous emphysema, pleural effusions and pneumothorax

develop. *The diagnosis by - water-soluble contrast swallow, - both CT and careful endoscopy (in an intubated pt) *Treatment is surgical. Delay in diagnosis is a key factor in the high mortality