20. Diseases of the esophagus: diverticulosis, strictures; Barrett's esophagus

Diseases of the oesophagus: diverticula, strictures and Barrett oesophagus

The oesophagus extends from the pharynx to the stomach and has cervical, thoracic and abdominal segments. Physiological constrictions occur at the cricopharyngeus, aortic arch/left main bronchus and diaphragmatic hiatus.
Diverticula are outpouchings of the oesophageal wall. Zenker diverticulum is a pharyngoesophageal pulsion diverticulum above the cricopharyngeus; mid-oesophageal diverticula are often traction-related; epiphrenic diverticula are usually associated with motility disorders.
Symptoms include dysphagia, regurgitation of undigested food, halitosis, cough, aspiration and weight loss. Zenker diverticulum may cause gurgling in the neck and nocturnal aspiration.

Benign oesophageal strictures result from chronic reflux, caustic ingestion, radiation, surgery, anastomosis or medication injury. Malignancy must be excluded in new or progressive dysphagia.
Fibrosis narrows the lumen, initially impairing solid-food passage and later liquids. Alarm features include rapid progression, weight loss, odynophagia, anaemia and older age.
Endoscopy with biopsy is essential when malignancy is possible. Contrast swallow defines length, location and complexity; CT is used for suspected extrinsic disease or complications.
Treatment includes addressing the cause, acid suppression for peptic strictures, endoscopic dilation, and selected stenting or surgery for refractory disease. Dilation carries perforation and bleeding risks.

Barrett oesophagus is replacement of distal oesophageal squamous epithelium by specialised intestinal-type columnar metaplasia due to chronic gastro-oesophageal reflux.
It increases risk of oesophageal adenocarcinoma, especially when dysplasia is present. Risk factors include chronic reflux, central obesity, male sex, older age and smoking.
Diagnosis requires endoscopic visualisation and histological confirmation. Biopsies are taken using a systematic protocol; dysplasia should be confirmed by an expert gastrointestinal pathologist.
Management includes reflux control, surveillance endoscopy based on segment length and dysplasia status, endoscopic eradication therapy for confirmed dysplasia or selected early neoplasia, and surgery for invasive disease.
Barrett oesophagus is not synonymous with cancer. Patients should receive clear counselling about surveillance, symptom control and risk reduction.

Assess dysphagia carefully and protect against aspiration and malnutrition. Endoscopy is central but should be preceded by contrast imaging when a large Zenker diverticulum or complex anatomy is suspected.
Complications include aspiration pneumonia, bleeding, perforation, recurrent stricture, malnutrition and malignant transformation in Barrett-associated dysplasia.