Incompetence of the lower esophageal sphincter allows reflux of gastric contents into the esophagus, causing burning pain. Prolonged reflux may lead to esophagitis, stricture, and rarely metaplasia or cancer. Diagnosis is clinical, sometimes with endoscopy, with or without acid testing. Treatment involves lifestyle modification, acid suppression using proton pump inhibitors, and sometimes surgical repair.
(See also the American College of Gastroenterology's updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease.)
Gastroesophageal reflux disease (GERD) is common, occurring in 10 to 20% of adults. It also occurs frequently in infants, typically beginning at birth (see Gastroesophageal Reflux in Infants).
The presence of reflux implies lower esophageal sphincter (LES) incompetence, which may result from a generalized loss of intrinsic sphincter tone or from recurrent inappropriate transient relaxations (ie, unrelated to swallowing). Transient LES relaxations are triggered by gastric distention or subthreshold pharyngeal stimulation.
Factors that contribute to the competence of the gastroesophageal junction include the angle of the cardioesophageal junction, the action of the diaphragm, and gravity (ie, an upright position). Factors contributing to reflux include weight gain, fatty foods, caffeinated or carbonated beverages, alcohol, tobacco smoking, and drugs. Drugs that lower LES pressure include anticholinergics, antihistamines, tricyclic antidepressants, Ca channel blockers, progesterone, and nitrates.
GERD may lead to esophagitis, peptic esophageal ulcer, esophageal stricture, Barrett esophagus, and esophageal adenocarcinoma (see Adenocarcinoma). Factors that contribute to the development of esophagitis include the caustic nature of the refluxate, the inability to clear the refluxate from the esophagus, the volume of gastric contents, and local mucosal protective functions. Some patients, particularly infants, aspirate the reflux material.
Symptoms and Signs
The most prominent symptom of GERD is heartburn, with or without regurgitation of gastric contents into the mouth. Infants present with vomiting, irritability, anorexia, and sometimes symptoms of chronic aspiration. Both adults and infants with chronic aspiration may have cough, hoarseness, or wheezing.
Esophagitis may cause odynophagia and even esophageal hemorrhage, which is usually occult but can be massive. Peptic stricture causes a gradually progressive dysphagia for solid foods. Peptic esophageal ulcers cause the same type of pain as gastric or duodenal ulcers, but the pain is usually localized to the xiphoid or high substernal region. Peptic esophageal ulcers heal slowly, tend to recur, and usually leave a stricture on healing.
A detailed history points to the diagnosis. Patients with typical symptoms of GERD may be given a trial of therapy. Patients who do not improve, or have long-standing symptoms or symptoms of complications, should be studied. Endoscopy, with cytologic washings and biopsy of abnormal areas, is the test of choice. Endoscopic biopsy is the only test that consistently detects the columnar mucosal changes of Barrett esophagus. Patients with unremarkable endoscopy findings who have typical symptoms despite treatment with proton pump inhibitors should undergo 24-h pH testing (see Ambulatory pH Monitoring). Although barium swallow readily shows esophageal ulcers and peptic strictures, it is less useful for mild to moderate reflux; in addition, most patients with abnormalities require subsequent endoscopy. Esophageal manometry may be used to guide pH probe placement and to evaluate esophageal peristalsis before surgical treatment.
Management of uncomplicated GERD consists of elevating the head of the bed about 15 cm (6 in) and avoiding eating within 2 to 3 h of bedtime, strong stimulants of acid secretion (eg, coffee, alcohol), certain drugs (eg, anticholinergics), specific foods (eg, fats, chocolate), and smoking. Weight loss is recommended for overweight patients and those who have gained weight recently.
Drug therapy is with a proton pump inhibitor; all appear equally effective. For example, adults can be given omeprazole 20 mg, lansoprazole 30 mg, or esomeprazole 40 mg 30 min before breakfast. In some cases (eg, only partial response to once/day dosing), proton pump inhibitors may be given bid. Infants and children may be given these drugs at an appropriate lower single daily dose (ie, omeprazole 20 mg in children > 3 yr, 10 mg in children < 3 yr; lansoprazole 15 mg in children ≤ 30 kg, 30 mg in children > 30 kg). These drugs may be continued long-term, but the dose should be adjusted to the minimum required to prevent symptoms, including intermittent or as-needed dosing. H2blockers (eg, ranitidine 150 mg at bedtime) or promotility agents (eg, metoclopramide 10 mg po 30 min before meals and at bedtime) are less effective.
Antireflux surgery (usually fundoplication via laparoscopy) is done on patients with serious esophagitis, large hiatal hernias, hemorrhage, stricture, or ulcers. Esophageal strictures are managed by repeated balloon dilation.
Barrett esophagus may or may not regress with medical or surgical therapy. (See also the American College of Gastroenterology's updated guidelines for the diagnosis, surveillance, and therapy of Barrett's esophagus.) Because Barrett esophagus is a precursor to adenocarcinoma, endoscopic surveillance for malignant transformation is recommended every 1 to 2 yr. Surveillance has uncertain cost-effectiveness in patients with low-grade dysplasia but is important in high-grade dysplasia in patients who are unable to undergo surgical resection. Alternatively, Barrett esophagus may be treated with endoscopic mucosal resection, photodynamic therapy, cryotherapy, or laser ablation.
Last full review/revision May 2014 by Michael C. DiMarino, MD
Content last modified May 2014