A number of dietary and lifestyle modifications have been applied to minimize exposure to acidic foods and reduce anatomic and physiologic causes of reflux (Table 3.1). Of these, only head of bed elevation for nighttime symptoms, weight loss [2], and smoking cessation [3], have been demonstrated to reduce objective pH measures of reflux severity, although mixed data exists when evaluating the impact of weight loss on subjective reflux symptoms [4, 5]. Head of bed elevation physiologically reduces acid reflux with the assistance of gravity. This generally requires raising the head of bed with the frame by 6–8 inches rather than using wedges and electric hospital-type beds that flex the patient at the hip and potentially increase intra-abdominal pressures. Weight loss, on the other hand, reduces intra-abdominal pressure, and may also have a hormonal influence on reflux that is incompletely understood. Tobacco may weaken the lower esophageal sphincter (LES) and increase transient lower esophageal sphincter relaxation (TLESR) episodes that characterize most episodes of pathologic GERD [6]. Because of the relatively low risk of pursuing such measures, general lifestyle modification is a reasonable initial management tool for all patients suspected of GERD. Routine elimination of all potential food triggers is not recommended [1], although avoidance of specific triggers may be reasonable on an individual basis. Additionally, medications with anticholinergic properties, such as calcium channel blockers, nitrates, and antidepressants, may promote GERD, so a careful medication review may be helpful.

Over-the-counter antacids are often used by patients or primary care practitioners to treat mild reflux symptoms occurring less than once per week. These medications often include calcium carbonate, aluminum hydroxide, and other chemicals that neutralize gastric pH temporarily for symptom relief. These effects are usually not durable. Additionally, surface agents such as sucralfate and sodium alginate (Gaviscon^®) can adhere to peptic mucosa and protect against further injury. The latter, generally compounded with varying particulate antacids, floats on top of the gastric pool and is touted to protect the cardia, which is susceptible to an “acid pocket” effect. However, the limited clinical efficacy of sucralfate in GERD symptom management has reduced its applicability in non-pregnant patients [1]. Additionally, there is poor agreement on the clinical role of these agents, as sodium alginate was not discussed as a treatment option in the most recent clinical guidelines, although it has demonstrated some efficacy as an adjunctive treatment for GERD in a recent clinical trial [7].

Acid suppression medications form the bulk of GERD management. Histamine-2 receptor antagonists (H2RA) decrease acid secretion through inhibition of the histamine-2 receptor on the gastric parietal cell. Proton-pump inhibitors (PPI) irreversibly bind and inhibit the hydrogen-potassium ATPase proton pump, creating more potent inhibition of gastric acid secretion. A recent Cochrane systematic review demonstrated that H2RA are less effective than PPI in the treatment of clinical symptoms of non-erosive reflux disease [8]. Another downside is the potential development of tachyphylaxis with H2RA use [9]. Due to common hepatic clearance pathways, H2RA, and cimetidine in particular, are more susceptible than PPI to interaction with frequently prescribed medications such as beta blockers, warfarin, anti-epileptic drugs, calcium channel blockers, and tricyclic antidepressants, among others. Finally, the superiority of PPI in erosive esophagitis treatment [10] relegates H2RA to acute treatment of mild GERD with non-erosive disease, or for maintenance therapy. H2RA also has been studied as an adjunctive medication to PPI in controlling nocturnal acid breakthroughs, and can be applied at bedtime for this purpose [11].

Given the above findings, empiric treatment of GERD should begin with an 8-week course of PPI [1], which addresses reflux symptoms as well as any possible contribution from erosive esophagitis. PPI should be administered 30-60 minutes before the first meal of the day. In patients with incomplete response, a second dose may be added 30-60 minutes before the last meal of the day, or a different PPI can be tried. In patients with minimal response, further evaluation by a gastroenterologist should be considered, which may include upper endoscopy or motility testing.

Notably, a significant number of patients with non-erosive reflux and almost all patients with erosive esophagitis will experience symptom relapse [1]. Patients that redevelop symptoms after completion of the initial 8-week course require additional clinical evaluation, and possibly longer term maintenance therapy. For maintenance, the lowest effective dose of PPI should be used or changed to H2RA in the absence of erosive disease. This will hopefully reduce the potential side effects of long-term PPI use, which have been documented with greater frequency over the past few years (Table 3.2). However, it should be noted that while patients with reflux esophagitis maintained on standard PPI dose have relapse rates well under 20% over the first year, patients changed to H2RA have increased relapse rates of 50–70% [12], so one must carefully weigh the risks and benefits of long term PPI therapy.