GASTRO-ESOPHAGEAL REFLUX DISEASE (GERD)
Western dietary habits have made GERD a common disease. Richter and associates reported that 25-40% of Americans experience symptomatic GERD at some point.(1)
Jafri et al. reported that the prevalence of GERD is 24% in Pakistan in 2005.(2)
Schematically, the esophagus, lower esophageal sphincter (LES), and stomach can be envisioned as a simple plumbing circuit as described by Stein and coworkers.(3) The esophagus functions as an antegrade pump, the LES as a valve, and the stomach as a reservoir. The abnormalities that contribute to GERD can stem from any component of the system. Poor esophageal motility decreases clearance of acidic material. A dysfunctional LES allows reflux of large amounts of gastric juice. Delayed gastric emptying can increase the volume and pressure in the reservoir until the valve mechanism is defeated, leading to GERD. From a medical or surgical standpoint, it is extremely important to identify which of these components is defective so that effective therapy can be applied.
Gastroesophageal reflux disease (GERD) is associated with a set of typical (esophageal) symptoms, including heartburn, regurgitation, and dysphagia. (However, a diagnosis of GERD based on the presence of typical symptoms is correct in only 70% of patients.) In addition to these typical symptoms, abnormal reflux can cause atypical (extraesophageal) symptoms, such as coughing, chest pain, and wheezing.
Gastroesophageal reflux (GER) is extremely common in healthy infants, in whom gastric fluids may reflux into the esophagus 30 or more times daily.(4) Many, but not all of these reflux episodes result in regurgitation into the oral cavity. The frequency of reflux, as well as the proportion of reflux episodes that result in regurgitation, declines with increasing age, such that physiologic regurgitation or vomiting decreases toward the end of the first year of life, and is unusual in children older than 18 months old.
The American College of Gastroenterology (ACG) published updated guidelines for the diagnosis and treatment of GERD in 2005. According to the guidelines, for patients with symptoms and history consistent with uncomplicated GERD, the diagnosis of GERD may be assumed and empirical therapy begun. Patients who show signs of GERD complications or other illness or who do not respond to therapy should be considered for further diagnostic testing.(5)
A history of nausea, vomiting, or regurgitation should alert the physician to evaluate for delayed gastric emptying.
Patients with GERD may also experience significant complications associated with the disease, such as esophagitis, stricture, and Barrett esophagus. Approximately 50% of patients with gastric reflux develop esophagitis.
SIGN AND SYMPTOMS:
The most common symptoms of gastroesophageal reflux disease (GERD) are heartburn (pyrosis), regurgitation, and dysphagia. A variety of potential extraesophageal manifestations have also been described including bronchospasm, laryngitis, and chronic cough. Complications from GERD can arise even in patients who lack typical esophageal symptoms:
- Heartburn is typically described as a burning sensation in the retrosternal area(6), most commonly experienced in the postprandial period.
- Regurgitation is defined as the perception of flow of refluxed gastric content into the mouth or hypopharynx(6). Patients typically regurgitate acidic material mixed with small amounts of undigested food.
- Dysphagia is common in the setting of longstanding heartburn commonly attributable to reflux esophagitis but potentially indicative of a stricture(7)
Other symptoms of GERD include chest pain, water brash, globus sensation, odynophagia, and nausea.
The diagnosis of gastroesophageal reflux disease (GERD) can be based upon clinical symptoms alone. In patients presenting with any of the clinical manifestations described above, a presumptive diagnosis of GERD can be made.
Response to antisecretory therapy is not a diagnostic criterion for GERD.(8) A meta-analysis of diagnostic test characteristics found that a response to proton pump inhibitors (PPIs) did not correlate well with objective measures of GERD such as ambulatory pH monitoring.(9)
UPPER GASTROINTESTINAL ENDOSCOPY FINDINGS — The findings on upper endoscopy are variable. Upper endoscopy may be normal in patients with GERD, or there may be evidence of esophagitis of varying degrees.
HISTOLOGY — A review of the literature suggested that about two-thirds of patients who have symptoms of GERD, but have no visible endoscopic findings (i.e. nonerosive reflux disease) have histologic evidence of esophageal injury that responds to acid suppression.
RADIOGRAPHIC FINDINGS — Double contrast barium swallow examination is of limited use because of its low sensitivity in patients with mild GERD. Radiologic evaluation is most useful in the detection of peptic stricture.
PATIENT SELECTION FOR TREATMENT:
Patients with gastroesophageal reflux disease (GERD) may be managed with a step-up or step-down approach to therapy. The step-up approach involves incrementally increasing the potency of therapy until symptom control is achieved. The step-down approach starts with potent antisecretory agents and then involves incrementally decreasing the potency of therapy until breakthrough symptoms define the treatment necessary for symptom control.
While the optimal strategy is controversial, both have advantages. The step-up approach minimizes the use of proton pump inhibitors (PPIs) and their associated costs and side effects, whereas step-down therapy provides faster symptom relief.
In patients who are naïve to treatment, we initially recommend lifestyle and dietary modification and, as needed, low-dose histamine 2 receptor antagonists (H2RAs). We suggest concomitant antacids as needed if symptoms occur less than once a week. For patients with continued symptoms despite these measures, we increase the dose of H2RAs to standard dose, twice daily for a minimum of two weeks. Further increases in the dose of H2RA, prolonging the course of treatment, or switching to another H2RA is unlikely to control symptoms.(10, 11) Therefore, if symptoms of GERD persist, we discontinue H2RAs and initiate once-daily PPIs at a low dose and then increase to standard doses if required. Once symptoms are controlled, treatment should be continued for at least eight weeks.
LIFE STYLE MODIFICATIONS:
The following lifestyle and dietary measures are suggested:(12, 13)
- Weight loss for patients with GERD who are overweight or have had recent weight gain.
- Elevation of the head of the bed in individuals with nocturnal or laryngeal symptoms (e.g. cough, hoarseness, throat clearing). This can be achieved either by putting six- to eight-inch blocks under the legs at the head of the bed or a Styrofoam wedge under the mattress. We also suggest a corollary to this recommendation: refraining from assuming a supine position after meals and avoidance of meals two to three hours before bedtime.
- Dietary modification should not be routinely recommended in all patients with GERD. However, we suggest selective elimination of dietary triggers (fatty foods, caffeine, chocolate, spicy foods, food with high fat content, carbonated beverages, and peppermint) in patients who note correlation with GERD symptoms and an improvement in symptoms with elimination.
Other measures that have a physiologic basis but have not consistently been demonstrated to improve reflux symptoms include:(14, 15)
- Avoidance of tight-fitting garments to prevent increasing intragastric pressure and the gastroesophageal pressure gradient.
- Promotion of salivation through orallozenges / chewing gum to neutralize refluxed acid and increase the rate of esophageal acid clearance.
- Avoidance of tobacco and alcohol as both reduce lower esophageal sphincter pressure and smoking also diminishes salivation.
- Abdominal breathing exercise to strengthen the antireflux barrier of the lower esophageal sphincter.
Antacids — As antacids do not prevent GERD, their role is limited to intermittent (on-demand) use for relief of mild GERD symptoms that occur less than once a week.(16)
Surface agents and alginates — Sucralfate (aluminum sucrose sulfate), a surface agent, adheres to the mucosal surface, promotes healing, and protects from peptic injury by mechanisms that are incompletely understood.
Histamine 2 receptor antagonists — Histamine 2 receptor antagonists (H2RAs) decrease the secretion of acid by inhibiting the histamine 2 receptor on the gastric parietal cell. However, the development of tachyphylaxis within two to six weeks of initiation of H2RAs limits their use as maintenance therapy for GERD.(17)
Proton pump inhibitors — Proton pump inhibitors (PPIs) should be used in patients who fail twice-daily H2RA therapy and in patients with erosive esophagitis and / or frequent (two or more episodes per week) or severe symptoms of GERD that impair quality of life.
Transthoracic and transabdominal fundoplications are performed for gastroesophageal reflux disease, including partial (anterior or posterior) and circumferential wraps. Open and laparoscopic techniques may be used.
Placement of a device to augment the lower esophageal sphincter is another surgical option.
GOALS OF THERAPY:
The goals of treatment are:
- Provide complete (sufficient) relief from heartburn and other symptoms.
- Heal underlying esophagitis.
- Treat or, ideally, prevent complications.
Treatment for GERD is based on guidelines from the prestigious society such as The American College of Gastroenterology (ACG).
To review the guidelines of ACG in the management of GERD, click on the below link
LONG TERM MONITORING:
Approximately two-thirds of patients with nonerosive reflux disease (NERD), and nearly all patients with erosive esophagitis (EE), relapse when acid suppression is discontinued. However, a trial off of medications should be considered in all patients with gastroesophageal reflux disease (GERD) whose symptoms resolve with acid suppression, except those with severe EE (Los Angeles classification Grade C and D) and Barrett's esophagus.(18) Patients with severe esophagitis should remain on maintenance acid suppression with a proton pump inhibitor (PPI) as they are likely to have recurrent symptoms and complications if acid suppression is decreased or discontinued.(18-21)
Patient should be instructed on following precautions:
- Lose weight (if patient is overweight)
- Raise the head of bed by 6 to 8 inches
- Avoid foods that make GERD symptoms worse (examples include coffee, chocolate, alcohol, peppermint, and fatty foods)
- Cut down on the amount of alcohol
- Stop smoking, if patient smoke
- Eat a bunch of small meals each day, rather than 2 or 3 big meals
- Avoid lying down for 3 hours after a meal
- Herbella FA, Sweet MP, Tedesco P, Nipomnick I, Patti MG. Gastroesophageal reflux disease and obesity. Pathophysiology and implications for treatment.J Gastrointest Surg. 2007 Mar. 11(3):286-90
- Jafri N, Yakoob J, Islam M, Manzoor S, Jalil A, Hashmi F. Perception of gastroesophageal reflux disease in urban population in Pakistan.J Coll Physicians Surg Pak. 2005;15:532–4.
- Stein HJ, DeMeester TR. Outpatient physiologic testing and surgical management of foregut motility disorders.Curr Probl Surg. 1992 Jul. 29(7):413-555
- Vandenplas Y, Goyvaerts H, Helven R, Sacre L. Gastroesophageal reflux, as measured by 24-hour pH monitoring, in 509 healthy infants screened for risk of sudden infant death syndrome. Pediatrics 1991; 88:834
- DeVault KR, Castell DO. Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease.Am J Gastroenterol. 2005 Jan. 100(1):190-200.
- Vakil N, van Zanten SV, Kahrilas P, et al. The Montreal definition and classification of gastroesophageal reflux disease: a global evidence-based consensus. Am J Gastroenterol 2006; 101:1900.
- Vakil NB, Traxler B, Levine D. Dysphagia in patients with erosive esophagitis: prevalence, severity, and response to proton pump inhibitor treatment. Clin Gastroenterol Hepatol 2004; 2:665.
- Bytzer P, Jones R, Vakil N, et al. Limited ability of the proton-pump inhibitor test to identify patients with gastroesophageal reflux disease. Clin Gastroenterol Hepatol 2012; 10:1360.
- Numans ME, Lau J, de Wit NJ, Bonis PA. Short-term treatment with proton-pump inhibitors as a test for gastroesophageal reflux disease: a meta-analysis of diagnostic test characteristics. Ann Intern Med 2004; 140:518
- Kahrilas PJ, Fennerty MB, Joelsson B. High- versus standard-dose ranitidine for control of heartburn in poorly responsive acid reflux disease: a prospective, controlled trial. Am J Gastroenterol 1999; 94:92.
- Sontag SJ. The medical management of reflux esophagitis. Role of antacids and acid inhibition. Gastroenterol Clin North Am 1990; 19:683.
- DeVault KR, Castell DO, American College of Gastroenterology. Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease. Am J Gastroenterol 2005; 100:190.
- Ness-Jensen E, Hveem K, El-Serag H, Lagergren J. Lifestyle Intervention in Gastroesophageal Reflux Disease. Clin Gastroenterol Hepatol 2016; 14:175.
- Ness-Jensen E, Lindam A, Lagergren J, Hveem K. Tobacco smoking cessation and improved gastroesophageal reflux: a prospective population-based cohort study: the HUNT study. Am J Gastroenterol 2014; 109:171.
- Kaltenbach T, Crockett S, Gerson LB. Are lifestyle measures effective in patients with gastroesophageal reflux disease? An evidence-based approach. Arch Intern Med 2006; 166:965.
- Sontag SJ. The medical management of reflux esophagitis. Role of antacids and acid inhibition. Gastroenterol Clin North Am 1990; 19:683.
- Komazawa Y, Adachi K, Mihara T, et al. Tolerance to famotidine and ranitidine treatment after 14 days of administration in healthy subjects without Helicobacter pylori infection. J Gastroenterol Hepatol 2003; 18:678.
- Peura DA, Freston JW, Haber MM, et al. Lansoprazole for long-term maintenance therapy of erosive esophagitis: double-blind comparison with ranitidine. Dig Dis Sci 2009; 54:955.
- Vigneri S, Termini R, Leandro G, et al. A comparison of five maintenance therapies for reflux esophagitis. N Engl J Med 1995; 333:1106.
- Schindlbeck NE, Klauser AG, Berghammer G, et al. Three year follow up of patients with gastrooesophageal reflux disease. Gut 1992; 33:1016.
- Ip S, Bonis P, Tatsioni A, et al. Comparative Effectiveness of Management Strategies for Gastroesophageal Reflux Disease. Evidence Report/Technology Assessment No. 1. (Prepared by Tufts-New England Medical Center. Evidence-based Practice Center under Contract No. 290-02-0022.) Rockville, MD: Agency for Healthcare Research and Quality. December 2005 www.effectivehealthcare.ahrq.gov/reports/final.cfm (Accessed on March 28, 2012).