A number of conditions and lifestyle choices increase the risk for reflux esophagitis (Box 31.1). The primary pathophysiologic mechanism contributing to the development of GERD is an incompetent lower esophageal sphincter (LES). Inability of the LES to prevent reflux of stomach contents is influenced by esophageal anatomy, impaired gastrointestinal motility, acid hypersecretion, and increased abdominal pressure. Patients with a higher incidence of hiatal hernias, low LES pressure confirmed by manometry, and increased levels of reflux confirmed by esophageal pH monitoring have been shown to experience more severe GERD symptoms.⁵

The entire esophageal lumen is lined with stratified squamous epithelium, which is susceptible to injury by acidic gastric contents. Gastric acid, bile, or pepsin that passively regurgitates into the esophagus can irritate the mucosa and may cause erosions and ulcerations. In cases of persistent reflux, a metastatic columnar lining may replace the normal stratified squamous epithelium; this premalignant condition is called Barrett esophagus. Studies have demonstrated a clear relationship between Barrett esophagus and the development of esophageal adenocarcinoma.

Presenting Signs and Symptoms

The most common symptom of reflux esophagitis is “heartburn,” or the epigastric, retrosternal burning sensation that typifies GERD. Heartburn often radiates to the back and neck and may be described as burning, pressure, squeezing, or sharp pain. With severe GERD, patients may demonstrate diaphoresis, dyspnea, nausea, and vomiting. The entire symptom complex may be clinically indistinguishable from cardiac ischemia.

Heartburn is more severe when patients are supine, bend forward, wear tight clothing, or consume large meals. The pain may last from minutes to hours and may resolve spontaneously or with antacids. Patients with nocturnal symptoms often complain of “water brash,” which is the bitter, metallic taste of regurgitated gastric contents noted on arising from sleep. Approximately 80% of patients with GERD have primarily nocturnal symptoms that are exacerbated by being supine.⁶ Patients with daytime symptoms have postprandial heartburn and fullness even when upright. GERD can cause chronic cough, recurrent throat clearing, and wheezing as a result of aspiration of gastric contents from the esophagus into the trachea and larynx.⁷ A complaint of dysphagia in the setting of GERD is an ominous sign that should prompt endoscopic evaluation for underlying strictures or adenocarcinoma.

Differential Diagnosis and Medical Decision Making

GERD is a clinical diagnosis elicited by a detailed and directed history of the present illness. GERD should be diagnosed only after other life-threatening causes of chest pain have been convincingly excluded (Box 31.2). Providers must consider the potential life threats and serious medical conditions that can be manifested in a similar fashion to GERD. A thorough history is the most important consideration in the differentiation diagnosis of patients with GERD-like symptoms. The initial history should be obtained in concert with immediate electrocardiography. Physical examination, laboratory testing, and radiographic imaging aid only in the exclusion of alternative diagnoses. Cardiac stress testing may be required in certain patient populations. A reported clinical response to antacids should not be used to make the presumptive diagnosis of GERD in the emergency department (ED).

Treatment

Lifestyle modifications may reduce symptoms by decreasing the frequency and amount of gastric reflux. Examples of low-cost, low-risk recommendations are summarized in the Patient Teaching Tips box in this section of the chapter.⁸

Acid-suppressive medications are indicated in patients without adequate relief from lifestyle modifications. The two most commonly used drugs for the treatment of GERD are H₂ receptor antagonists (H2RAs) and proton pump inhibitors (PPIs). Acid-suppressive medications do not prevent reflux; they improve GERD symptoms by suppressing production of acid in the stomach and raising the pH of the refluxed material.

H2RAs have similar efficacy with equivalent dosing schedules (Table 31.1). These agents have previously been recommended as first-line therapy; however, a Cochrane review suggests that PPIs relieve heartburn better than H2RAs do in patients treated without specific diagnostic testing.⁹ These medications should be used for 2 to 4 weeks before any reassessment of symptoms. Recurrence is a common problem in patients with reflux, and therefore many patients require long-term maintenance therapy.

Table 31.1 Equivalent Dosages for Histamine H₂ Receptor Antagonists

DRUG	RECOMMENDED DOSE
Cimetidine	400 mg twice daily OR 800 mg at bedtime

Ranitidine

Famotidine

Nizatidine

Success rates with PPIs approach 90%, and all agents have equal efficacy at appropriate doses (Table 31.2). Once-daily dosing before breakfast is sufficient for the control of mild to moderate GERD; twice-daily dosing should be considered for those with severe or refractory symptoms. Gastroprokinetic agents (cisapride) and coating agents (sucralfate) are less effective than PPIs but may be useful in selected patients as second-line agents.

Table 31.2 Equivalent Dosages for Proton Pump Inhibitors

DRUG	RECOMMENDED DOSE
Omeprazole	20 mg before breakfast OR 20 mg twice daily ^*
Lansoprazole	30 mg before breakfast OR 30 mg twice daily ^*
Rabeprazole	20 mg before breakfast OR 20 mg twice daily ^*
Pantoprazole	40 mg before breakfast
Esomeprazole	20 mg or 40 mg before breakfast