James W. Maher, M.D.
University of Iowa Hospitals and Clinics
First Published: Fall 2001
Last Revised: February 2003
Peer Review Status: Internally Peer Reviewed
Highlights:
History: For most of the 20th century, gastroesophageal reflux (GER) symptoms were attributed to the presence of a sliding hiatal hernia. In the 1950s, Allison postulated that they were actually caused by reflux of the stomach content into the distal esophagus. This view was slowly accepted in the following decades. Recent data show that, while it is true that GER is accompanied by a sliding hiatal hernia in 80% of patients, hiatal hernia is not necessarily accompanied by GER and can be demonstrated in about 50% of the population.
Twenty-four-hour pH monitoring of normal subjects has shown that postprandial reflux occurs in everyone. However, the reflux becomes pathologic only when the refluxed material is in contact with the esophageal mucosa for a prolonged period of time. A pathologic GER is characterized by a normal histologic appearance, typical reflux symptoms, and abnormal 24-hour pH findings.
The condition, in which GER causes inflammation of the esophageal lining, is defined as reflux esophagitis. Usually, there is a poor correlation between symptoms and the severity of macro- and microscopic findings of reflux esophagitis.
New facts: The major barrier to GER is the lower esophageal sphincter (LES). Although the very anatomical existence of LES was long denied, it has now been clearly identified, and its involvement in reflux protection has been extensively studied. Patients who have severe reflux esophagitis tend to have LES pressure lower than individuals without reflux. Moreover, in patients who have reflux with normal resting LES pressure, the reflux mechanism appears to be defective, with inappropriate relaxation of the LES. It is not clear whether the low sphincter pressure produces the esophagitis or the esophagitis damages the sphincter, causing its low pressure.
The consequence of a low LES pressure is that stomach content rich in acid and pepsinæand sometimes duodenal contentæcomes into contact with the esophageal squamous mucosa. This results in esophageal injuries even during short exposure, since this mucosa is not as resistant to the digestive effect of acid and pepsin as the columnar epithelium lining the stomach.
Since postprandial reflux is normal in everyone, a mechanism exists that clears acid from the esophagus. This mechanism includes the primary peristaltic wave and the neutralizing effect of swallowed saliva. Approximately 30-40% of patients with severe reflux esophagitis are found to display a high rate of failure of their primary peristalsis.
The symptoms of reflux are secondary to the irritating effects of stomach and gastroduodenal contents. The classic manifestation of GER disease (GERD) is heartburn (pyrosis). It is a burning retrosternal or epigastric pain that commonly occurs after heavy meals, between meals, or at night. Some patients may also have a squeezing type of substernal pain that can be difficult to distinguish from angina. There may be excessive belching and regurgitation of small amounts of sour or bitter gastric contents into the throat. This symptom is dissimilar from vomiting because it is effortless and is not accompanied by nausea.
A disquieting symptom is dysphagia. Dysphagia may indicate the development of an esophageal stricture and mandates esophagoscopy to rule out the possibility of cancer.
Practice: Clinical symptoms are not adequate for confirming a diagnosis of GERD. Regurgitation in the supine position is a relatively reliable symptom, but the pain of pyrosis may be very similar to the pain of biliary tract disease, peptic ulcer, or gastritis. At UI Hospitals and Clinics, we advocate a trial of acid suppression to make the diagnosis, but if this does not result in prompt relief, or if symptoms recur when therapy is stopped, a diagnostic evaluation is carried out. It includes radiology, endoscopy, 24-hour pH studies, and esophageal manometry.
Barium examination can be used to demonstrate hiatal hernia and to document reflux. It is also very useful in detecting esophageal shortening secondary to esophagitis or stricture.
Endoscopy is less sensitive than pH assessment in detecting reflux but is extremely useful in eliminating other possible diagnoses. To confirm a diagnosis of esophagitis for surgical therapy, the patient must have a biopsy-proven esophagitis or obvious ulcerations.
24-hour pH studies are the gold standard for determining whether a patient has pathologic GER. They should be used to document reflux in patients who have symptoms of reflux and normal mucosal biopsies before any consideration of surgical therapy.
First-line medical therapy for GERD boils down to changes in diet and lifestyle as well as aiding in clearing refluxed acid from the esophagus. These include abstaining from fatty food, chocolate, peppermint, alcohol, and coffee, stopping smoking, avoiding meals close to bedtime, and elevating the head of the bed.
Second-line therapy aims at decreasing the damaging nature of the refluxed material using antacids. The next line of therapy includes H2-receptor antagonists, such as cimetidine, ranitidine, or famotidine. H2-receptor blockade decreases the heartburn and improves the endoscopic appearance of the mucosa.
The gold standard for medical therapy is the use of proton-pump inhibitors. Oral proton-pump inhibitors result in endoscopic healing of esophagitis in over 90% of patients. However, acid-reducing drugs only neutralize the caustic nature of the refluxed material. They do not combat reflux. A worrying consideration is that proton-pump inhibitors seem to hasten the onset of atrophic gastritis in patients who are infected with Helicobacter pylori. Atrophic gastritis is a precancerous condition. It remains to be determined whether eradication of H. pylori in these patients will prevent atrophic gastritis.
Although medical therapy achieves excellent results in most patients who have GERD, a small minority fail to get satisfactory relief or develop complications that do not respond to medical treatment. Surgical treatment is a viable option for such patients. The indications for operation for reflux include stricture and bleeding, asthma, laryngeal irritation, and cough due to reflux esophagitis and not amenable to medical therapy. Surgery is also considered in the presence of intractable symptoms secondary to esophagitis documented by biopsy or pathologic GER documented by 24-hour pH monitoring.
At UI Hospitals and Clinics we pursue three goals in any operation to treat GERD. First, the barrier to GER must be re-established by either increasing LES pressure or restoring the distal esophagus to its normal intra-abdominal position or both. Second, the surgically created barrier to reflux must relax in response to deglutition like a normal LES does. The fundus of the stomach, which is generally used to construct the wrap, participates in the receptive relaxation of the normal sphincter. However, relaxation is not always complete. Finally, while restoring the barrier to reflux, surgical procedures should not create a potential antegrade barrier to deglutition, which may cause dysphagia.
A condition secondary to GER is Barrett's esophagus in which the squamous lining of the esophagus is replaced by columnar gastric mucosa. This ectopic mucosa may be complicated with strictures and punched-out ulcers. Barrett's mucosa is associated with the development of adenocarcinoma in a small percentage of patients. Therefore, patients with Barrett's esophagus need periodic endoscopic surveillance to detect severe dysplasia.
See related Provider Textbooks about Surgery.
See related Provider Topics Digestive System, Gastroesophageal Reflux/Hiatal Hernia, Gastrointestinal, Procedures and Therapies or Surgery.
See related Patient Textbooks about Surgery.
See related Patient Topics Digestive System, Gastroesophageal Reflux/Hiatal Hernia, Gastrointestinal, Procedures and Therapies or Surgery.
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