Gastroesophageal reflux disease is an exceptionally common ailment, and heartburn is an extremely common manifestation.  GERD results when gastric acid moves past a weak or compromised lower esophageal sphincter and there is an impaired ability to clear this excess acid from the esophagus.  Aside from heartburn, other symptoms include acid regurgitation, water brash, sour brash, chronic cough, asthma, aspiration pneumonia, interstitial pulmonary fibrosis, chronic bronchitis, bronchiectasis, ear pain, hoarseness, neck pain, throat pain, a globus sensation, a sensitive tongue, a burning sensation in the mouth, hiccups, dental erosions, nausea, chest pain, or epigastric pain.  Potential complications include Barrett’s esophagus and esophageal strictures.

     The diagnosis should be considered in patients with chest pain who have a negative work up for ischemic heart disease, and in patients with persistent chest pains despite adequate antianginal therapy.  Even patients with ischemic heart disease may sometimes manifest chest pain or other symptoms of GERD.  Many patients may be asymptomatic, but display changes consistent with marked reflux on endoscopic examination.  Dysphagia, odynophagia, vomiting, weight loss, guiac positive stools, pulmonary symptoms, and/or anemia are symptoms which are indicative of possibly more severe disease and warrant endoscopic investigation.  Persistent symptoms despite aggressive medical therapy (refractory GERD) are another indication for endoscopy.

     In most patients, the diagnosis may be established by the history and response to empiric therapy.  Esophagogastricduodenoscopy (EGD), the Bernstein test, esophageal manometry and 24 hour pH monitoring are the various methods to establish the diagnosis.  EGD offers the luxury of direct visualization and biopsy to evaluate for associated Barret”s esophagus, a premalignant condition; however, this test is very insensitive early in the course of GERD.  Barium studies are not sensitive for the evaluation of GERD; however, the presence of a hiatal hernia with appropriate symptoms is highly suggestive.  Aggravating factors include medications (oral contraceptives, narcotics, anticholinergics, and calcium channel blockers), dietary factors (fatty foods, chocolate, peppermint, and citrus), alcohol ingestion, smoking, hiatal hernia, obesity, and pregnancy.

     The main complication of GERD is its association with Barrett’s esophagus.  Barrett’s esophagus is seen in 10 to 15% of GERD patients.  This potentially premalignant condition refers to a change in the cell type of the distal esophageal epithelium from squamous cells to columnar cells, and there is an increased incidence of adenocarcinoma development.  Diagnosis is established by histologic examination of biopsy specimens obtained during endoscopic evaluation.  Endoscopy should only be performed while the patient is symptom free on therapy for optimum evaluation.  There is debate regarding the need to evaluate all patients with GERD for Barret’s esophagus.

     Subtypes of Barrett’s esophagus include fundic type (characterized by parietal and chief cells), cardiac type (absence of parietal or chief cells), and intestinal type (characterized by goblet cells).  It is the latter type (also known as intestinal metaplasia) which is believed to carry the risk for malignant transformation.  Dysplasia is an intermediate histologic finding in the progression (normal epithelium-metaplasia-dysplasia-carcinoma) of metaplasia towards carcinoma.  There are three types of dysplasia to include low-grade, high-grade, and indeterminate.  Surveillance endoscopy for low-grade dysplasia should be every six months for the first year and then annually thereafter.  Patients with high-grade dysplasia should be referred for surgery or ablation and the undergo surveillance endoscopy at least every three months initially.  Certain risk factors place patients at a greater propensity for having Barrett’s, and certainly patients with a long history of GERD symptoms, Caucasian male patients, and patients greater than 45 years of age should strongly be considered for an endoscopic evaluation.  Patients with the above mentioned symptoms of odynophagia, dysphagia, weight loss, anemia, guiac positive stools, vomiting, or pulmonary symptoms should definitely proceed to endoscopic evaluation with biopsy. Aggressive medical or surgical therapy does not seem to cause regression of established esophageal metaplasia; however, mucosal ablative techniques in conjunction with acid suppression therapy may induce squamous re-epithelialization.

     Another controversial issue in GERD is concomitant Helicobacter pylori infection.  The debate is whether physicians should test for infection in patients with GERD, and then if infection is discovered, whether treatment is beneficial or may actually worsen the symptoms of GERD.  Some advocates stress the association of malignancy (gastric cancer and MALT lymphoma) with H. pylori infection and thus the need for treatment.  At this time the issue of treating H. pylori in GERD patients is unresolved and requires further research.  Worsening of GERD symptoms may be anticipated after therapy for H. pylori eradication.

     Lifestyle changes are the first step in therapy and include: eliminating spicy, acidic, and fatty foods; decreasing the consumption of tea, coffee, and alcohol; weight loss; tobacco cessation; eating small amounts at meal time; and elevation of the head of the patient’s bed by at least 6 inches.  By the time most patients seek medical treatment, they have already tried many over the counter remedies to include antacids or low dose H2 receptor blocker therapy.  Proton pump inhibitors (PPIs) are effective therapies for heartburn.  Prescription strength H2 receptor blockers and prokinetic agents such as metoclopramide are other available therapies.  Surgical intervention may be offered in the form of laparoscopic fundoplication (wrapping the upper part of the stomach around the distal esophagus).

     When symptoms persist despite compliance to an adequate aggressive therapeutic regimen, the patient has either refractory GERD or an alternate etiology (achalasia, biliary disease, malignancy, gastroparesis, infectious esophagitis, nonulcer dyspepsia, or peptic ulcer disease) causing their symptoms.  If refractory GERD is suspected and an EGD has not been performed (the patient was started on empiric therapy based on symptoms) then this should be arranged.  If the EGD is negative or equivocal (this exam has a sensitivity of less than 60%), then esophageal pH monitoring should be performed.  Therapy consists of ensuring compliance with medication and lifestyle changes.  PPI's should be dosed 30 minutes before meals.  Twice daily dosing may be needed for some patients.  In appropriate cases (those who complain of nighttime symptoms), consider adding a bedtime dose of an H2 receptor antagonist, and aggressively titrate the dose upwards as needed.