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Gastroesophageal Reflux Disease

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Last Update: October 27, 2018.

Introduction

Gastroesophageal reflux disease (GERD) is a condition that develops when there is a retrograde flow of stomach contents causing symptoms or complications. GERD can present as Non-erosive reflux disease (NERD) when typical symptoms of GERD occur in the absence of visible mucosal injury during endoscopy, or as erosive esophagitis (EE) when patients have histopathological changes in esophageal mucosa. The latter is also called reflux esophagitis.

The typical symptom is heartburn. This most often occurs 30 min to 60 min after meals and upon reclining. Patients often report relief from antacids or baking soda. When patients present with this description of symptoms, the diagnosis can be established with a high degree of confidence.

Epidemiology

GERD is extremely common, with a prevalence of approximately 20% of adults in the western culture. Most adults with GERD have mild disease, but esophageal mucosa damage (reflux esophagitis) can develop in up to a third of the patients. Symptoms occur daily in approximately 7% of patients, weekly in 14% and monthly in 15% to 40% of all patients.

There is no significant difference in prevalence among males and females, but males seem to have a higher rate of complications. The rate of esophagitis is 2:1 and the rate of Barrett's is 0:1 in males compared to females.

GERD incidence increases with age, particularly after age 40.

Obesity also seems to increase the risk of GERD. A meta-analysis published in the Annals of Internal Medicine in 2005 concluded that obesity was associated with a statistically significant increase in the risk of GERD symptoms, erosive esophagitis, and esophageal carcinoma. The ProGERD study published in 2005 evaluated the predictive factors for erosive reflux disease in more than six thousand patients with reflux disease. They found the odds ratio for erosive disease increased with the body mass index (BMI), with patients with a BMI greater than 30 Kg/m2 to 40 Kg/m2 having an odds ratio of 1.97 (95% confidence level 1.32 to 2.92).

Pathophysiology

There are few components of the pathophysiology of GERD.

  1. Impaired Lower Esophageal Sphincter (LES) Function: the LES functions as an anti-reflux barrier at the gastroesophageal junction, preventing acid from the stomach from entering the esophagus. In healthy individuals, a certain amount of physiologic gastroesophageal reflux occurs by means of transient relaxation of the LES, which increases after a meal to permit gas to be vented from the stomach. In patients with GERD, there may be an increased transient relaxation of the LES associated with a reduction in the pressures of the sphincter. The mechanisms of increased transient relaxation are unknown. However, there are several known risk factors for decreased LES pressures: pregnancy, diabetes, scleroderma, obesity, and medications such as calcium channel blockers, cholinergic antagonists, glucagon, nicotine from cigarette smoking and oral contraceptives.
  2. A hiatal hernia: hiatal hernias are common and usually do not cause symptoms. In patients with GERD, however, they are associated with higher amounts of acid reflux and delayed esophageal acid clearance. Large hiatal hernias seem to contribute to decreasing LES tone. Hiatal hernias are found in a fourth of patients with non-erosive GERD, in three-fourths of patients with erosive GERD, and in over 90% of patients with Barrett Disease.
  3. Irritant effects of Refluxate: the gastric acid fluid (pH less than 4) is extremely caustic. Prolonged contact of gastric contents with esophageal mucosa leads to damage (esophagitis). In some patients, reflux of bile or alkaline pancreatic secretions can also lead to damage.
  4. Abnormal esophageal clearance: the acid that reaches the esophagus is normally cleared and neutralized by esophageal peristalsis and salivary bicarbonate. During sleep, peristalsis is infrequent, prolonging acid exposure to the esophageal mucosa. Alcohol and sedatives also seem to decrease peristalsis. Researchers estimate that 50% of patients with GERD have some degree of decrease peristalsis. Also, conditions such as Sjogrën disease that affect the quality or quantity of the saliva, anticholinergic medications, and oral radiation can further worsen the natural protective mechanisms and lead to higher exposure of the esophageal mucosa to damage.

History and Physical

The typical manifestation of GERD is heartburn, regurgitation, and dysphagia. Other symptoms include a globus (lump in the throat) sensation, odynophagia, and nausea. Heartburn is defined as a retrosternal burning discomfort, located in the epigastric area that may radiate up towards and neck and typically occurs in the postprandial period. Patients often report that postural changes, such as bending forward, can worsen the symptoms. Symptoms are usually also aggravated by ingestion of certain foods or beverages such as tomato sauce, chocolate, coffee, teas, and alcohol.

Atypical presentation refers to symptoms that are extraesophageal, including pulmonary, ear, nose and throat manifestations, as well as non-cardiac chest pain.

Evaluation

Initial diagnostic tests are not warranted for patients with typical GERD symptoms. Practitioners should further investigate patients with "alarm features" such as troublesome dysphagia, odynophagia, weight loss, iron deficiency anemia, and in patients with troublesome symptoms that persist despite appropriate empiric proton pump inhibitor therapy. It must be remembered that diabetic patients may present with dyspeptic symptoms during a myocardial infarction. Thus, a high index of suspicion should be maintained in these patients in the acute setting.

Radiographic studies are of limited use in the management of GERD due to poor sensitivity in milder forms of GERD, but they can detect moderate to severe esophagitis, strictures, hiatal hernia, and tumors. The studies most commonly used are the barium swallow, which only examines the esophagus, and the upper gastrointestinal series, which examines the esophagus, stomach, and small intestines.

In addition to excluding the presence of other diseases such as tumors and peptic ulcers, an upper endoscopy can detect and grade the severity of GERD-induced esophagitis. Upper endoscopy is highly specific for GERD (90% to 95%) but has a limited sensitivity (approximately 50%). The Los Angeles (LA) Classification grades reflux esophagitis on a scale of A (one or more isolated mucosal breaks less than 5 mm that do not extend between the tops of two mucosal folds) to D (one or more mucosal breaks that involve at least 75% of the esophageal circumference).

Esophageal pH or combined esophageal impedance testing is usually unnecessary in most patients but may be indicated in patients who have atypical or extraesophageal symptoms or who are being considered for antireflux surgery. Impedance testing detects changes in the resistance of electrical current on a catheter placed within the esophagus. In addition to recording the esophageal pH, it can differentiate both antegrade and retrograde transit of liquid and gas. The test is helpful in patients who have suspected GERD but negative pH tests. Doctors only recommend this test after standard testing has failed to demonstrate significant GERD in patients with typical or atypical symptoms and patients with refractory GERD. 

Treatment / Management

The goals of treating GERD are to resolve symptoms, heal esophagitis, and prevent complications. Treatment options include lifestyle modifications, medical management with antacids and antisecretory agents, and mechanical therapies.

  • Lifestyle modifications are a cornerstone in the treatment of GERD. Medical practitioners should provide counseling about weight loss, head elevation, tobacco and alcohol cessation, avoidance of late meals, and cessation of foods that can potentially aggravate symptoms.
  • Medical treatments include antacid and antisecretory agents. Antacids are inexpensive, readily available, and effective. Histamine-2 (H2)-receptor antagonists, inhibit the secretion of gastric acid by competitively blocking the H2-receptors located in the gastric parietal cells. H2-blockers have an excellent safety profile and are available over the counter. These drugs are approximately 75% effective in patients with mild to moderate degrees of esophagitis. Proton pump inhibitors (PPIs) act by blocking the hydrogen-potassium ATPase on the apical surface of the parietal cells. PPIs are more effective than H2-blockers because they act on the common pathway of acid secretion. Practitioners use these as initial therapy in patients with moderate to severe GERD and patients with complications of GERD. These complications include bleeding and strictures. Studies comparing H2-blockers and PPIs have demonstrated that the latter has superior healing rates and decreased relapse rates.
  • Antireflux procedures include laparoscopic fundoplication and bariatric surgery in obese patients. Fundoplication offers excellent relief of symptoms and healing of esophagitis in over 85% of properly selected patients. Outcomes in patients who have extraesophageal symptoms and have had fundoplication surgery have been less encouraging.

Pearls and Other Issues

Barrett's esophagus is the only complication of GERD with malignant potential. Patients are typically middle-aged white males. In patient's with Barrett's esophagus, surveillance for dysplasia is warranted.

Questions

To access free multiple choice questions on this topic, click here.

References

1.
Katz PO, Gerson LB, Vela MF. Guidelines for the diagnosis and management of gastroesophageal reflux disease. Am. J. Gastroenterol. 2013 Mar;108(3):308-28; quiz 329. [PubMed: 23419381]
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Labenz J, Jaspersen D, Kulig M, Leodolter A, Lind T, Meyer-Sabellek W, Stolte M, Vieth M, Willich S, Malfertheiner P. Risk factors for erosive esophagitis: a multivariate analysis based on the ProGERD study initiative. Am. J. Gastroenterol. 2004 Sep;99(9):1652-6. [PubMed: 15330897]
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Hampel H, Abraham NS, El-Serag HB. Meta-analysis: obesity and the risk for gastroesophageal reflux disease and its complications. Ann. Intern. Med. 2005 Aug 02;143(3):199-211. [PubMed: 16061918]
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Ruigómez A, García Rodríguez LA, Wallander MA, Johansson S, Eklund S. Esophageal stricture: incidence, treatment patterns, and recurrence rate. Am. J. Gastroenterol. 2006 Dec;101(12):2685-92. [PubMed: 17227515]
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Fan X, Snyder N. Prevalence of Barrett's esophagus in patients with or without GERD symptoms: role of race, age, and gender. Dig. Dis. Sci. 2009 Mar;54(3):572-7. [PubMed: 18654849]
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Shaheen NJ, Falk GW, Iyer PG, Gerson LB., American College of Gastroenterology. ACG Clinical Guideline: Diagnosis and Management of Barrett's Esophagus. Am. J. Gastroenterol. 2016 Jan;111(1):30-50; quiz 51. [PubMed: 26526079]
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Vaishnav B, Bamanikar A, Maske P, Reddy A, Dasgupta S. Gastroesophageal Reflux Disease and its Association with Body Mass Index: Clinical and Endoscopic Study. J Clin Diagn Res. 2017 Apr;11(4):OC01-OC04. [PMC free article: PMC5449826] [PubMed: 28571180]
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Kellerman R, Kintanar T. Gastroesophageal Reflux Disease. Prim. Care. 2017 Dec;44(4):561-573. [PubMed: 29132520]
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Bookshelf ID: NBK441938PMID: 28722967

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