Barrett's esophagus overview

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Overview

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Amresh Kumar MD [2], Hamid Qazi, MD, BSc [3]

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Overview

Barrett's esophagus refers to an abnormal change (metaplasia) in the cells of the lower end of the esophagus thought to be caused by damage from chronic acid exposure, or reflux esophagitis. It is a condition in which any extent of metaplastic columnar epithelium replaces the normal stratified squamous epithelium in the distal esophagus. Intestinal metaplasia is required for the diagnosis of Barrett's esophagus.

Historical Perspective

Barrett's esophagus was first discovered by Dr. Norman Barrett, a Australian-born British surgeon at St Thomas' Hospital, in 1957.

Classification

Barrett's esophagus may be classified according to the distance between Z line and GEJ (Gastroesophgeal Junction) into two subtypes which are long segment barrett's esophagus and short segment barrett's esophagus.

Pathophysiology

Barrett's esophagus is marked by the presence of columnar epithelium in the lower esophagus, replacing the normal squamous cell epithelium; an example of metaplasia. The columnar epithelium is better able to withstand the erosive action of the gastric secretions; however, this metaplasia confers an increased cancer risk of the adenocarcinoma type.

Causes

Barrett's esophagus is commonly caused by Gastroesophageal reflux disease.

Differentiating Barrett's Esophagus from Other Diseases

Barrett's esophagus must be differentiated from esophagitis, peptic ulcer disease, esophageal carcinoma and esophageal motor disorders.

Epidemiology and Demographics

Barrett's esophagus can be seen in younger patients, but is most commonly diagnosed in patients around 55 years of age. The prevalence of Barrett's esophagus is approximately 2000 per 100,000 individuals worldwide.

Risk Factors

The most potent risk factor in the development of Barrett's esophagus is chronic GERD. Other risk factors include age (>older than 50 years), sex (male), race (caucasian), hiatal hernia, elevated body mass index and intra-abdominal distribution of body fat.

Screening

Barrett's esophagus is a major risk factor for development of esophageal adenocarcinoma. After diagnosis, regular surveillance is needed based on the grade of dysplasia. Weak recommendation, moderate-quality evidence: screening in patients with multiple risk factors for esophageal adenocarcinoma: age > 50 years old, male, white, chronic GERD, hiatal hernia, elevated BMI (body mass index), and intra-abdominal distribution of body fat. Strong recommendation, low-quality evidence against screening general population with GERD and no risk factors.

Natural History, Complications, and Prognosis

Common complications of Barrett's esophagus include esophageal carcinoma, esophageal stricture and esophageal ulcers.

Diagnosis

Diagnostic Criteria

The diagnosis of Barrett's esophagus is made on endoscopy, when at least 2 of the following diagnostic criteria are met which include presence of columnar epithelium in the distal esophagus and the presence of intestinal metaplasia in the columnar epithelium lining the distal esophagus.

History and Symptoms

Common symptoms of Barrett's esophagus include heartburnregurgitation, and dysphagia. A positive history of nauseavomiting, and regurgitation is suggestive of Barrett's esophagus. Other symptoms of Barrett's esophagus include chest paincough, and odynophagia.

Physical Examination

Patients with Barrett's esophagus usually appear ill due to the pain. Common physical examination include hoarseness of voicelaryngitisotitis media, and lung wheezes.

Laboratory Findings

Laboratory findings consistent with diagnosis of Barrett's esophagus is the presence of acidic reflux in the esophagus through the ambulatory reflux monitoring.

Electrocardiogram

There are no EKG findings associated with Barrett's esophagus. However, EKG can be performed to exclude the cardiac causes of chest pain that can be presented in cases of atypical GERD.

X-ray

There are no x-ray findings associated with Barrett's esophagus.

Ultrasound

There are no echocardiography or ultrasound findings associated with Barrett's esophagus.

CT scan

There are no CT scan findings associated with Barrett's esophagus.

MRI

There are no MRI findings associated with Barrett's esophagus.

Other Imaging Findings

Unsedated esophagoscopy and capsule esophagoscopy may be helpful in the diagnosis of Barrett's esophagus.

Other Diagnostic Studies

There are no other diagnostic studies associated with Barrett's esophagus.

Treatment

Medical Therapy

According to the American College of Gastroenterology, the patients with Barrett's esophagus are treated with both lifestyle changes and medications. The lifestyle changes includes avoiding dietary fat, chocolate, caffeine, peppermint, alcohol, tobacco, avoiding lying down after meals, losing weight, sleeping with the head of the bed elevated and taking all medications with plenty of water. The medications used to treat Barrett's esophagus are H2-receptor antagonists, Proton pump inhibitor and Photosensitizers.

Surgery

According to the American College of Gastroenterology, there are various surgical methods used for the treatment of Barrett's esophagus which includes (1) antireflux surgery considered in those with incomplete control of reflux on optimized medical therapy, (2)esophagectomy in cases of Endoscopic adenocarcinoma (EAC) with invasion into the submucosa and (3) Nissen fundoplication used in the patient with GERD symptoms.

Primary Prevention

Effective measures for the primary prevention of Barrett's esophagus include lifestyle modifications and medical therapy for GERD. Lifestyle modification include weight loss, head of bed elevation, avoidance of nighttime meals, and elimination of trigger foods such as chocolate, caffeine and alcohol. Medical therapy include the use of proton pump inhibitors.

Secondary Prevention

Effective measures for the secondary prevention of Barrett's esophagus include primary prevention along with endoscopic surveillance every 3-5 years for no dysplasia, 6-12 months for low-grade dysplasia, and every 3 months for high-grade dysplasia in the absence of eradication therapy.

References


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