(See also Overview of Esophageal and Swallowing Disorders.)
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) and the patient's age. Factors that may contribute 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, calcium channel blockers, progesterone, and nitrates.
GERD may lead to esophagitis, peptic esophageal ulcer, esophageal stricture, Barrett esophagus, and esophageal 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, may aspirate the reflux material.
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 strictures cause 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.
(See also the American College of Gastroenterology’s guidelines for the diagnosis and treatment of gastroesophageal reflux disease.)
A detailed history points to the diagnosis. Patients with typical symptoms of GERD may be given a trial of acid-suppressing therapy. Patients who do not improve, or have long-standing symptoms or symptoms of complications, should undergo further testing.
Endoscopy, with cytologic washings and/or 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-hour pH testing. 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. Endoscopic findings can be used to grade the severity of reflux esophagitis (1):
Grade A: One or more mucosal breaks ≤ 5 mm that do not cross the tops of 2 mucosal folds
Grade B: One or more mucosal breaks > 5 mm that do not cross the tops of 2 mucosal folds
Grade C: One or more mucosal breaks that cross ≥ 2 mucosal folds and involve < 75% of the esophageal circumference
Grade D: One or more mucosal breaks involving ≥ 75% of esophageal circumference
Esophageal manometry is used 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 the following:
Weight loss is recommended for overweight patients and those who have gained weight recently.
Drug therapy is often with a proton pump inhibitor; all appear equally effective. For example, adults can be given oral omeprazole 20 mg, lansoprazole 30 mg, pantoprazole 40 mg, or esomeprazole 40 mg 30 minutes before breakfast. In some cases (eg, only partial response to once-a-day dosing), proton pump inhibitors may be given twice daily. Infants and children may be given these drugs at an appropriate lower single daily dose (ie, omeprazole 20 mg in children > 3 years, 10 mg in children < 3 years; 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. H2 blockers are also an effective treatment option for mildly symptomatic GERD. Promotility agents (eg, metoclopramide 10 mg orally 30 minutes before meals and at bedtime) are less effective but may be added to a proton pump inhibitor regimen.
Antireflux surgery (usually fundoplication via laparoscopy) is done in patients with grades C and D esophagitis, large hiatal hernias, hemorrhage, stricture, ulcers, large amounts of symptomatic nonacid reflux, or who cannot tolerate drug therapy. Esophageal strictures are most often managed by repeated endoscopic dilation.
Barrett esophagus may or may not regress with medical or surgical therapy. (See also the American College of Gastroenterology’s 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 3 to 5 years in nondysplastic disease. The American College of Gastroenterology's 2015 guidelines recommend endoscopic ablative therapy for patients with confirmed low-grade dysplasia and without life-limiting comorbidity; however, endoscopic surveillance every 12 months is an acceptable alternative. Patients with Barrett esophagus and confirmed high-grade dysplasia should be managed with endoscopic ablative therapy unless they have life-limiting comorbidity. Endoscopic ablative techniques for Barrett esophagus include mucosal resection, photodynamic therapy, cryotherapy, and laser ablation.
Lower esophageal sphincter incompetence and transient relaxations allow gastric contents to reflux into the esophagus and sometimes into the larynx or lungs.
Complications include esophagitis, peptic esophageal ulcer, esophageal stricture, Barrett esophagus, and esophageal adenocarcinoma.
The main symptom in adults is heartburn, and infants present with vomiting, irritability, anorexia, and sometimes symptoms of chronic aspiration; at any age, chronic aspiration may cause cough, hoarseness, or wheezing.
Diagnose clinically; do endoscopy in patients not responding to empiric treatment and 24-hour pH monitoring if endoscopy is normal in patients with typical symptoms.
Treat with lifestyle changes (eg, head of bed elevation, weight loss, dietary trigger avoidance) and acid-suppressing therapy.
Antireflux surgery can help patients with severe esophagitis, complications of esophagitis, intolerance to drug therapy, or a large amount of symptomatic nonacid reflux.
The following are English-language resources that may be useful. Please note that THE MANUAL is not responsible for the content of these resources.