Gastroesophageal reflux disease (GERD) is a common disease that accounts for approximately 75% of esophageal pathology when tissues are examined under laboratory microscopes. Despite its high prevalence, it can be one of the most challenging diagnostic and therapeutic problems in benign esophageal disease. A contribut¬ing factor to this is the lack of a universally accepted definition of the disease.
Some degree of gastroesophageal reflux (back-flow of gastric or duodenal contents into the esophagus) is normal in both adults and children. Excessive reflux may occur because of an incompetent lower esophageal sphincter, pyloric stenosis, or a motility disorder. The incidence of reflux seems to increase with aging.
Diagnostic testing may include an endoscopy or barium swallow to evaluate damage to the esophageal mucosa. Ambulatory 12- to 36-hour esophageal monitoring is used to evaluate the degree of acid reflux. Exposure to bile can cause mucosal damage as seen under laboratory microscopes.
The simplest approach is to define the gastroesophageal reflux disease by its symptoms. However, symptoms thought to be indicative of GERD, such as heartburn or acid regurgitation, are very common in the general population, and many individuals consider them to be normal and do not seek medical attention. Even when excessive, these symptoms are not specific for GERD, and can be caused by other diseases such as achalasia, diffuse spasm, esophageal carcinoma, pyloric steno¬sis, cholelithiasis, gastritis, gastric or duodenal ulcer, and coronary artery disease. In addition, patients with GERD can present with atypical symptoms, such as nausea, vomiting, postprandial fullness, chest pain, choking, chronic cough, wheezing, and hoarseness. Fur¬thermore, bronchiolitis, recurrent pneumonia, idiopathic pulmonary fibrosis, and asthma can be primarily due to GERD. To confuse the issue more, GERD can coexist with cardiac and pulmonary disease. Thus using clinical symptoms to define GERD lacks sensitivity and specificity.
An alternative definition for GERD is the presence of endos¬copic esophagitis. Using this criterion for the disease diagnosis assumes that all patients who have esophagitis have excessive regurgitation of gastric juice into their esophagus. This is true in 90% of patients, but in 10% the esophagitis has other causes, the most common being unrecognized chemical injury from drug ingestion. In addition, the definition leaves undiagnosed those patients who have symptoms of gastroesophageal reflux but do not have endoscopic esophagitis.
A third approach to defining GERD is to measure the basic patho¬physiologic abnormality of the disease; that is, increased exposure of the esophagus to gastric juice when tissue samples are studied under laboratory microscopes. In the past, this was inferred by the presence of a hiatal hernia, later by endoscopic esophagitis, and more recently by a hypotensive LES pressure. The development of miniaturized pH electrodes and data recorders allowed measurement of esophageal exposure to gastric juice by calculating the percent¬age of time the pH was less than 4 over a 24 hour period. This provided an opportunity to objectively identify the presence of the disease, and stimulated a rational stepwise approach to determining the cause for the abnormal esophageal exposure to gastric juice.