Gastro-esophageal Reflux Disease (GERD) and Barrett's Esophagus

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Onto today's topic:

Who hasn’t had the experience of heartburn or reflux? It is an extremely common condition, and TV ads promoting various brands of antacids can be seen all the time. I myself always pack some antacids with me on holiday—feasting and lounging occasionally give way to reflux. But what is reflux? What causes it, and how is it treated?

The definition of gastroesophageal reflux disease is: a condition in which the stomach contents (solid or liquid) moves backwards from the stomach into the esophagus. This is due to inappropriate relaxations of lower esophageal sphincter; most common contributing factors include: delayed esophageal clearance, delayed gastric emptying, obesity, pregnancy, acid hypersecretion from Zollinger-Ellison syndrome (very rare). A hiatus hernia can worsen reflux but does not cause it.

The most common clinical feature of GERD is “heartburn” and acid regurgitation (together are 80% sensitive and specific for reflux). Sour regurgitation—also known as water brash—can also be present, as well as the sensation of a lump in the throat (bolus sensation) and frequent belching. Non-esophageal symptoms such as cough, chest pain, and hoarseness are increasingly recognized of being poor prognosis indicator of reflux.

Usually a clinical diagnosis is made based on the history, and a trial of pharmacotherapy using PPI (symptom relief 80% sensitive for reflux) usually takes place. When the patient has a history of reflux accompanied by red flags (e.g. anorexia, dysphagia, bleeding, weight loss etc.), persistent reflux symptoms or previous severe erosive esophagitis after therapeutic trial of PPI for 4~8 weeks, history of esophageal stricture with persistent dysphagia, or is at high risk for Barrett’s esophagus (male, age > 50, obese, white, tobacco use, and long history of symptoms), then endoscopy is indicated. Endoscopy usually will reveal two kinds of findings: Non-erosive reflux disease (NERD) where the esophagus is normal—the treatment will consist of symptom relief with PPI PRN—and esophagitis, where treatment will aim to heal the inflammation—either through indefinite PPI therapy or surgical fundoplication. Repeat endoscopy after 6~8 weeks of PPI therapy is indicated if the patient has severe esophagitis (because it may mask underlying Barrett’s esophagus), if the patient has known Barrett’s esophagus, or if there is recurrence of symptoms. Esophageal manometry is a study of esophageal motility and can be done to diagnose abnormal peristalsis and/or decreased LES tone—but it cannot detect the presence of reflux. Esophageal manometry is usually done before surgical fundoplication (wrapping the gastric fundus around the lower end of esophagus; procedure of choice for GERD when all medical management has failed) to ensure that the esophagus is functional. 24-hour pH monitory is a very accurate test but rarely required or performed.

So to recap, the most effective therapy for GERD is PPI; it usually needs to be continued as maintenance therapy, with adjuvant antacids or H2-blocks as needed. Dietary changes such as avoidance of alcohol, coffee, spices etc. will help the symptoms but will not alter disease progression. The only true beneficial lifestyle changes are weight loss (from obesity) and elevating the head of bed for improvement of nocturnal symptoms.

Possible complications of GERD include:

·      Esophageal stricture disease—scarring can lead to dysphagia (mostly solids)

·      Ulceration

·      Bleeding

·      Barrett’s esophagus and esophageal adenocarcinoma

What is Barrett’s esophagus? It is defined as a metaplasia of normal squamous esophageal epithelium to abnormal columnar epithelium containing intestinal metaplasia. The etiology of Barrett’s esophagus is thought to be acquired via long-standing GERD and subsequent damage to the squamous epithelium; however, it has been found that increased gastric acid secretion is also associated with Barrett’s esophagus as opposed to reflux alone. Risk factors include being male, age > 50, Caucasian, smoking, obesity, hiatus hernia, and long history of reflux. In North America and Western Europe, 0.5~2% of adults are thought to have Barrett’s esophagus; up to 10% of GERD patients will have already developed Barrett’s esophagus by the time they seek medical attention. The diagnosis of Barrett’s esophagus relies on biopsy through endoscopy, and often endoscopy will show erythematous epithelium in the distal esophagus. Barrett’s esophagus is a predisposition to pre-malignant changes (i.e. the change before the change before actual cancer). The abnormal columnar epithelium will undergo dysplasia (low or high-grade) before progressing to adenocarcinoma; the rate of malignant transformation starts off at approximately 0.12% per year for patients with Barrett’s esophagus and rises with the degree of dysplasia.

Management includes acid suppressive therapy with high-dose PPI indefinitely or surgical fundoplication. Patients should have an endoscopy every 3 years if there is no dysplasia. For patients with low-grade dysplasia, regular surveillance is warranted, and endoscopic ablation/resection can be considered. For patients with high-grade dysplasia, regular and frequent surveillance must be done. In these patients, intensive biopsy, endoscopic ablation/resection, or esophagectomy produce similar outcomes; however, evidence increasingly favor endoscopic ablation with mucosal resection.

Bonus: Eosinophilic Esophagitis

Eosinophilic esophagitis is an inflammatory condition with prominence of eosinophils on esophageal biopsy. It is most commonly found in children but is increasingly recognized in adults. The etiology is unknown and may be an “allergic” disorder in children. Clinical features include odynophagia or dysphagia (mostly of solids), with the history often dating back to childhood. The first presentation may be to the ER with food bolus impaction.

The main investigation is endoscopy, which may reveal multiple rings or “crepe-paper” appearance. Biopsy showing increased eosinophils is necessary to confirm the diagnosis.

Management includes corticosteroid spray (e.g. fluticasone), which is swallowed, not inhaled (as in asthma) and leukotriene B4 inhibitors (e.g. Montelukast). Elimination diets that cut out food allergies have been an effective therapy in children.

The main complication of Eosinophilic esophagitis is increased risk of perforation with endoscopic dilatation procedures.