Part IV. Digestive Disease

Chapter 31. Esophageal Diseases

31.1. Gastroesophageal reflux disease

Gastroesophageal reflux disease (GERD) is a disorder related to inflammatory changes in the distal esophagus and/or presenting with typical symptoms caused by regularly repeated gastric and/or duodenal contents regurgitation into the esophagus.

GERD (as defined by the Russian Association of Gastroenterology) is a chronic recurrent condition caused by a violation of motor-evacuation function of the gastroesophageal area organs and presenting with regular regurgitation of gastric and duodenal contents into the esophagus that results in clinical symptoms affecting quality of life and disrupting distal esophageal mucosa, with further development of dystrophic changes in stratified non-squamous epithelium, catarrhal or erosive-ulcerative esophagitis (reflux esophagitis), and in some patients — columnar epithelial metaplasia.

Epidemiology

The true prevalence of GERD is unknown due to the great variability of clinical symptoms — from episodic heartburn to vivid signs of complicated reflux esophagitis. The true prevalence of GERD is significantly higher than published statistics, that is explained by difficulties in the application of diagnostic techniques. Moreover, less than 1/3 GERD patients seek doctor’s advice.

GERD is one of the most common gastrointestinal (GI) disorders. Symptoms of GERD are revealed in 20–50% of adults, and endoscopic signs are found in more than 7–10% of those studied among the population. Esophagitis develops in 45–80% of GERD patients. The prevalence of Barrett’s esophagus (BE) among those with esophagitis is close to 8% (ranging from 5 to 30%).

Classification

According to the International Classification of Diseases, 10th ed., GERD with esophagitis (reflux esophagitis) (K21.0) and GERD without esophagitis (K21.9) are differentiated.

In clinical practice, another terminology is commonly used:

• endoscopy-negative reflux disease, or non-erosive reflux disease;
• endoscopy-positive reflux disease, or reflux esophagitis.

To describe reflux esophagitis in detail, a classification following the 10th World Congress of Gastroenterology (Los Angeles, 1994 (Table 31.1; Fig. 31.1) is recommended.

Fig 31.1. Grades of reflux esophagitis

Table 31.1. Grades of reflux esophagitis

Complications of GERD include peptic strictures, esophageal bleeding, BE.

Approximately 60% of patients are diagnosed with non-erosive reflux disease, 30% are found to have reflux esophagitis, and 5% develop complications. Bleeding occurs in 2% of patients with erosive and ulcerative esophageal lesions, and peptic esophageal strictures develop in 2–20% of GERD patients. The most dangerous complications of GERD include BE, since it poses an increased risk of esophageal adenocarcinoma development; its incidence has increased by 3–3.5 times over the past 20 years. Some authors report that GERD also contributes to laryngeal cancer.

Etiology and Pathogenesis

The factors causing GERD development include the following:

• decreased anti-reflux barrier function (gastric cardiac closing mechanisms);
• decreased esophageal clearance;
• impaired resistance of esophageal mucosa to damaging factors;
• increased hydrochloric acid and pepsin production in stomach, bile regurgitation into the stomach.

Since gastric pressure is always higher than thoracic pressure, a specific mechanism exists that prevents the reflux of gastric contents — the so-called cardiac closing mechanisms. Normally, reflux is rare and short-term (< 5 min). This is a physiological process observed after eating and characterized by the absence of clinical symptoms and a short duration of episodes, it may occur during sleep. The normal pH in the lower third of the esophagus is 6.0.

Esophageal reflux is considered pathological if the time during that the esophagus pH reaches 4.0 or less is 1 hour per day or the total number of gastroesophageal refluxes during the day exceeds 50, they develop both during the day and night.

The mechanisms supporting viable gastroesophageal junction functioning (cardiac closing mechanisms) include the following:

• lower esophageal sphincter (LES);
• phrenoesophageal ligament;
• mucous rosette;
• acute angle of His that forms the Gubarev’s fold;
• intra-abdominal LES location;
• circular muscle fibers of gastric cardia.

Lower Esophageal Sphincter

The condition of LES plays a key role in functioning of the closing mechanism. At rest, it is closed in a healthy individual. Normally, transient relaxation lasts 5–30 seconds and contributes to removal of excess air swallowed while eating from the stomach. In GERD patients, these spontaneous episodes of LES relaxation are frequent and prolonged. The reasons for this are impaired esophageal motility, fast and plentiful eating accompanied by swallowing a large amount of air.