GASTROESOPHAGEAL REFLUX DISEASE
Definition. Gastroesophageal reflux disease (GERD) refers to a spectrum of clinical manifestations due to reflux of stomach and duodenal contents into the esophagus. (See Chapter 39 for a general discussion of acid-peptic disease.)
Etiology and Pathogenesis. The esophagus is normally protected from prolonged exposure to acid, pepsin, bile acids, and pancreatic enzymes by three mechanisms: (1) the antireflux barrier provided by tonic contraction of the lower esophageal sphincter, (2) rapid clearance of refluxed material via secondary peristalsis, and (3) alka-linization of acidic material by swallowed saliva. Patients with symptomatic GERD usually exhibit one or more of the following: decreased or absent tone in the lower esophageal sphincter, inappropriate relaxation of the lower esophageal sphincter unassociated with swallowing, and decreased acid clearance due to impaired secondary peristalsis. Other factors such as abnormal saliva and reflux of bile salts and pancreatic enzymes may be implicated in some patients.
Clinical Manifestations. Heartburn, ranging in degree from mild to severe, is the most common symptom of GERD and is often associated with regurgitation of acidic material. Aspiration pneumonia, nocturnal wheezing, and hoarseness may be seen in patients with frequent regurgitation, occasionally in the absence of heartburn. Dysphagia, bleeding from esophageal erosions, and stricture formation also occur. Smoking, alcohol or caffeine intake, and pregnancy, all of which decrease lower esophageal sphincter tone, may precipitate or exacerbate GERD.
Diagnosis. The diagnosis of GERD is best made based on the history and clinical manifestations. Objective tests are useful to quantify the extent and severity of disease and to address three questions: (1) Does reflux exist? (2) Is acid reflux responsible for the patient’s symptoms? (3J Has reflux led to esophageal damage? Reflux may be demonstrated during a barium swallow or by a radionuclide scintiscan after placement of “Tc-sulfur colloid in the stomach. Esophageal manometry is useful to demonstrate abnormal peristalsis and lower esophageal sphincter tone but will not show reflux per se. More sensitive tests for the presence of acid reflux include monitoring esophageal pH with a luminal pH probe for periods of 30 minutes to 24 hours either after instillation of HC1 in the stomach (Tuttle test) or under near-physiological conditions. The presence of reflux per se does not necessarily mean that reflux is responsible for the patient’s symptoms. If chest pain is not typical of heartburn, the Bernstein test may be performed to determine whether acid, but not saline, dripped into the esophagus via a nasogastric tube reproduces the patient’s symptoms. Finally, symptoms due to acid reflux do not always correlate with the extent of damage to the esophageal mucosa. Severe esophageal damage, such as a stricture or deep ulcer, can be assessed by barium’ swallow. However, endoscopy with suction biopsy is the most sensitive test for reflux-induced mucosal damage, which ranges from increased epithelial turnover and mild polymorphonuclear infiltration to frank ulceration. A few patients will exhibit Barrett’s esophagus, the presence of gastric columnar epithelium in the esophagus, which indicates severe chronic reflux and a greater risk of malignant transformation.
Treatment and Prognosis. Medical management of GERD is successful in all but the most severe cases, and, as outlined in Table 38-2, consists of maneuvers designed to decrease reflux and administration of antacids or H2-receptor blockers to decrease acid secretion. Chronic therapy may be necessary in patients with severe reflux. Surgical management, which is reserved for those few patients with objective evidence of reflux who fail to respond to an adequate trial of medical management, attempts to restore lower esophageal sphincter function by wrapping the lower esophagus with a cuff of gastric fundal muscle. These procedures are often successful but cannot be performed in patients with aperistalsis (e.g., scleroderma), who may have severe GERD.
Complications. GERD complications include esophageal (peptic) stricture, esophageal ulcer, Barrett’s esophagus, pulmonary aspiration, and upper gastrointestinal hemorrhage.
- Management
- TREATMENT
- Clinical Assessment of Anemia
- Tocainide
- THE COMMON CLINICAL MANIFESTATIONS OF GASTROINTESTINAL DISEASE
- RESPIRATORY SENSORS
- Bleeding Diatheses
- Familial Polyposis of the Colon
- PEPTIC ULCER DISEASE OF THE STOMACH AND DUODENUM
- Treatment and Prognosis
- Indications for Dialysis and Adequacy of Dialysis
- Pulmonary Infiltrates with Eosinophilia PIE
- Gastrointestinal Tract
- Cardiovascular
- PHYSICAL EXAMINATION
- Treatment
- Pneumonia in the Immunocompromised Host
- PHYSICAL THERAPY AND REHABILITATION
- Renal Tubular Acidosis
- LABORATORY TESTS TOR BILIRUBIN
- NONATHEROSCLEROTIC CAUSES OF CORONARY ARTERY OBSTRUCTION
- DISEASES OF THE ESOPHAGUS
- TREATMENT OF MALABSORPTION
- MYOCARDIAL METABOLISM
- SPECIFIC ENTITIES - DISEASES WITH KFiOWIi ETIOLOGIES -
- FACTORS AFFECTING THE RATE OF LOSS OF NEPHRONS
- Alberto N. v. Hawkins
- Texas MedicareRX
- Renal Biopsy and Other Diagnostic Tests
- DIFFUSE INFILTRATIVE DISEASES OF THE LUNG
- BILIRUBIN METABOLISM
- RHEUMATIC FEVER
- SYNCOPE
- Pyuria
- RENAL PARENCHYMAL