Gastroesophageal Reflux Disease Patient Information
Gastroesophageal reflux disease (GERD) is defined as a condition which develops when reflux of stomach contents into the esophagus causes troublesome symptoms and/or complications. The classic symptoms of GERD are heartburn and acid regurgitation and atypical symptoms include chest pain, trouble swallowing [dysphagia] and painful swallowing [odynophagia]. A variety of extraesophageal manifestations of reflux disease have also been described including cough, laryngitis, asthma and dental erosions, although good evidence for causation only exists if these manifestations are accompanied by classic signs and symptoms of reflux disease. Other proposed associations that are not clearly established include pharyngitis, sinusitis, otitis media and idiopathic pulmonary fibrosis.
GERD, defined as at least weekly heartburn and/or acid regurgitation, is a very common problem and has a prevalence ranging from 10% to 20% in the Western world. A number of risk factors have been identified for GERD including obesity and possibly increasing age, but not sex. A genetic component may also play a role as GERD is more common in identical twin pairs.
Reflux of gastric contents from the stomach into the esophagus occurs normally in all healthy individuals. The esophagus is protected by three lines of defense: the antireflux barrier at the gastroesophageal junction, esophageal clearance mechanisms and epithelial defensive factors. Disruption of these defense mechanisms leads to pathologic amounts of reflux.
Hiatal hernias play an important role in the pathophysiology of reflux disease. It is well known that hiatal hernia size is a predictor of severity of reflux. A hiatal hernia predisposes to reflux events by widening the opening of the gastroesophageal junction and decreasing the pressure of the lower esophageal sphincter. This then results in increased acid exposure and increased reflux episodes. The hernia acts as a reservoir for gastric contents whereby normal esophageal clearance results in trapping of fluids in the hernia sac which subsequently reflux into the esophagus.
Obesity is a key contributor to compromise of the barrier function. Obesity results in an increase in intragastric pressure, which increases the gastroesophageal pressure gradient and thereby predisposing gastric contents to migrate into the esophagus. In addition, obesity predisposes individuals to a hiatal hernia.
Symptoms, both typical and atypical of GERD, are described above. However, there is no clear relationship between severity of symptoms and esophageal damage. Typically, approximately two thirds of individuals with reflux symptoms have no evidence of esophageal damage at the time of endoscopy. When excessive gastric contents overwhelm the esophageal protective factors, esophagitis may ensue. This may manifest itself as erosions or ulceration of the esophagus and may also lead to scarring and Barrett’s esophagus. Finally, a very small subset of individuals with GERD may go on to develop esophageal adenocarcinoma, a well recognized complication of this disease.
When signs and symptoms of GERD are typical i.e. heartburn and/or acid regurgitation and are responsive to antisecretory therapy, no diagnostic evaluation is warranted. Diagnostic testing is warranted in individuals failing to respond to therapy or in the setting of alarm signs such as dysphagia, weight loss, anemia, gastrointestinal bleeding or chest pain. Endoscopy permits the detection of erosive esophagitis and complications such as strictures and Barrett’s esophagus. However, endoscopy fails to reveal mucosal damage in the majority of these patients whether on or off of antisecretory therapy.
Esophageal manometryis useful to exclude mimics of GERD, most notably achalasia. Reflux testing may be done with 24 hour transnasal pH monitoring, 48 hour prolonged devices attached to the esophageal lumen (Bravo) or 24 hour combined impedance- pH monitoring. Barium radiography has no role in the diagnostic evaluation of patients with reflux disease.
A variety of lifestyle measures such as avoiding foods that precipitate reflux, avoidance of acidic foods that cause heartburn and adherence to behaviors that may reduce acid exposure have traditionally been recommended for the initial treatment of GERD. However, data to support these maneuvers are lacking. Avoidance of foods or beverages that provoke symptoms such as alcohol coffee, spicy foods and late meals makes physiologic sense. Similarly, elevation of the head of the bed for patients with nocturnal regurgitation or heartburn also is logical. Given the association of obesity and GERD symptoms, weight loss should be part of any treatment program for obese subjects, especially for patients who only developed symptoms after weight gain.
Inhibition of gastric acid production is the cornerstone of treatment of GERD. Proton pump inhibitors (PPIs) are superior to histamine H2 receptor antagonists for both healing of esophagitis and symptom control. However, the response of heartburn symptoms is less predictable than healing of esophagitis even with PPIs. There appears to be no major differences in treatment efficacy between the various PPIs, and it is not usually necessary to use twice daily dosing of these agents.
The goal of treatment is to find the lowest drug dose to control symptoms.
While the safety profile of PPIs is excellent, short term adverse events such as headaches and diarrhea may occur. Recent epidemiologic studies suggest that long term PPI use may be associated with an increased risk of Clostridium difficile infection, community acquired pneumonia, hip fracture and vitamin B-12 deficiency, but the magnitude of this effect if any is small.
There are no high quality data to support the common practice of metoclopramide as a treatment for reflux disease. Furthermore, the significant adverse effect profile of this compound strongly argues against the use of this drug in any GERD patients. Sucralfate is likely of little value as well.
Antireflux surgery is another treatment option for patients with GERD. Criteria for surgery have evolved over time. Currently, the best indications for surgery are for patients with documented esophagitis who are intolerant of PPIs and GERD unresponsive to PPIs in the setting of predominant volume regurgitation. It is now clear from randomized controlled trials that treatment with laparoscopic fundoplication yields results comparable to continued PPI therapy. However, surgery has a number of potential serious complications which may impact quality of life including dysphagia, vagal nerve injury, gas bloat syndrome and diarrhea. Furthermore, efficacy or surgery declines with redo operations making initial patient selection and operative technique critically important. There are inadequate data to support any of the many proposed endoscopic approaches to GERD at present.
Patient Resources for GERD
American Cancer Society
250 Williams Street NW
Atlanta, GA 30303
Internet site: http://www.cancer.org
American College of Gastroenterology
6400 Goldsboro Road, Suite 200
Bethesda, MD 20817
Internet site: http://www.gi.org
American Gastroenterological Association
4930 Del Ray Avenue
Bethesda, MD 20814
Internet site: http://www.gastro.org
International Foundation for Functional Gastrointestinal Disorders
P.O. Box 17864
Milwaukee, WI 53217
Telephone: 414-1799 | 1-888-964-2001
Internet site: http://www.aboutgerd.org/
International Society for Diseases of the Esophagus
1177 West Hastings Street, Suite 2101
Vancouver, Britsh Columbia
Canada V6E 2K3
Internet site: http://www.isde.net/
National Digestive Disease Information Clearinghouse
Two Information Way
Bethesda, MD 20892
Internet site: http://digestive.niddk.nih.gov/resources/organizations.aspx
National Institute of Diabetes and Digestive Disorders
9000 Rockville Pike
Building 31, Room 904A
Bethesda, MD 20892
Internet site: http://www2.niddk.nih.gov/