The squamous epithelium of the esophagus is not designed to resist the digestive action of the acidic gastric juice and it frequently becomes inflamed and eroded in patients with GERD. The primary determinant of GERD appears to be transient relaxations of the lower esophageal sphincter not induced by swallowing.20,21 Episodes of transient relaxation are more common after meals. Slow gastric emptying and increases in intra-abdominal pressure may also induce reflux.
A hiatal hernia, i.e., a small hernial pouch, can serve as a reservoir for gastric contents. Transient relaxation of the lower esophageal sphincter is more likely to be followed by an episode of reflux when there is a hiatal pouch with retained gastric acid. GERD is further exacerbated by obesity and smoking (nicotine relaxes the lower esophageal sphincter). The extent of damage will depend on the intrinsic resistance of the esophageal epithelium to the digestive action of gastric acid.
Other modulating factors include the characteristics of the refluxed fluids: acid and pepsin together are more damaging to the esophageal epithelium than either one alone, the presence of bile, and the duration of contact between the refluxed gastric acid and the mucosa. The duration of contact depends on the number of reflux episodes per unit time, salivary neutralization of the refluxed acid, and the efficiency of esophageal peristalsis to remove the refluxed bolus of gastric acid.
Typical symptom associated with GERD is substernal burning pain radiating up to the neck (relieved immediately by antacids) brought on by positional changes of the body, e.g., lying flat in a supine position or stooping after a meal, which encourage gastroesophageal reflux.21 Esophageal pain may sometimes mimic cardiac pain. Bleeding is rare, presenting as hematemesis (vomiting of blood), which sometimes may cause severe, at first, obscure anemia.
Complications of GERD include peptic strictures due to scarring of inflamed tissue, asthma, hoarseness, and dental erosions. Additionally, prolonged acid injury may lead to metaplastic transformation of the esophageal squamous epithelium (Barrett’s esophagus) with a potential for malignant transformation.20 Medical treatment for GERD includes histaminergic H2‑receptor blocking agents such as ranitidine and/or proton pump inhibitors such as omeprazole.2,3,20,21
Other strategies include the administration of metoclopramide; a prokinetic drug that sensitizes tissues to the action of acetylcholine and thereby stimulates motility of the upper gastrointestinal tract that effectively decreases the contact time between gastric acid and the esophageal mucosa.2,3,20,21 Sucralfate, a cytoprotective agent, which electrostatically binds to positively charged proteins in ulcerative tissue retards acidic and proteolytic damage.2,3,20,21
When treating patients with a history of GERD recognize that these patients may experience episodes of reflux when in a supine position - they tend to do better in the perioperative period in a semi-reclining position. Patient may report substernal pain radiating up to the neck (relieved by antacids) mimicking pain of cardiac origin (relieved by nitroglycerin). When managing odontogenic pain keep in mind the well-established ulcerogenic effect of NSAIDs.