Information of Gastroesophageal reflux disease (GERD)

Gastroesophageal Reflux Disease: ( GERD)


GERD is one of the most prevalent gastrointestinal disorders. Population-based studies show that up to 15% of individuals have heartburn and/or regurgitation at least once a week, and 7% have symptoms daily. Symptoms are caused by backflow of gastric acid and other gastric contents into the esophagus due to incompetent barriers at the gastroesophageal junction.



The normal antireflux mechanisms consist of the LES, the crural diaphragm, and the anatomical location of the gastroesophageal junction below the diaphragmatic hiatus. Reflux occurs only when the gradient of pressure between the LES and the stomach is lost. It can be caused by a sustained or transient decrease in LES tone. A sustained hypotension of the LES may be due to muscle weakness that is often without apparent cause. Secondary causes of sustained LES incompetence include scleroderma-like diseases, myopathy associated with chronic intestinal pseudo-obstruction, pregnancy, smoking, anticholinergic drugs, smooth-muscle relaxants (-adrenergic agents, aminophylline, nitrates, calcium channel blockers, and phosphodiesterase inhibitors), surgical damage to the LES, and esophagitis. tLESR without associated esophageal contraction is due to a vagovagal reflex in which LES relaxation is elicited by gastric distention. Increased episodes of tLESR are associated with GERD. A similar reflex operates during belching. Apart from incompetent barriers, gastric contents are most likely to reflux (1) when gastric volume is increased (after meals, in pyloric obstruction, in gastric stasis, during acid hypersecretion states), (2) when gastric contents are near the gastroesophageal junction (in recumbency, bending down, hiatal hernia), and (3) when gastric pressure is increased (obesity, pregnancy, ascites, tight clothes). Incompetence of the diaphragmatic crural muscle, which surrounds the esophageal hiatus in the diaphragm and functions as an external LES, also predisposes to GERD. Obesity is a risk factor for GERD.

Esophageal exposure to refluxed gastric contents depends on the amount of refluxed material per episode, the frequency of reflux episodes, and the rate of clearing of the esophagus by gravity and peristaltic contractions. When peristaltic contractions are impaired, esophageal clearance is impaired. Acid refluxed into the esophagus is neutralized by saliva. Thus, impaired salivary secretion also increases esophageal exposure time. If the refluxed material extends to the cervical esophagus and crosses the upper sphincter, it can enter the pharynx, larynx, and trachea.

Reflux esophagitis is a complication of reflux. It develops when mucosal defenses are unable to counteract the damage caused by acid, pepsin, and bile. Mild esophagitis involves microscopic changes of mucosal infiltration with granulocytes or small numbers of eosinophils, hyperplasia of basal cells, and elongation of dermal pegs. In nonerosive reflux disease (NERD), the mucosa may be normal or mildly erythematous. Erosive esophagitis reveals clear mucosal damage with redness, friability, superficial linear ulcers, and exudates. Histology shows polymorphonuclear or mild eosinophilic infiltrates and granulation tissue. Peptic stricture results from fibrosis that causes luminal constriction. These strictures occur in ~10% of patients with untreated GERD. Short strictures caused by spontaneous reflux are usually 1–3 cm long and are present in the distal esophagus near the squamocolumnar junction (Fig. 286-2, panel 6). Long, tubular peptic strictures can result from persistent vomiting or prolonged nasogastric intubation. Erosive esophagitis may heal by intestinal metaplasia (Barrett's esophagus), a risk factor for adenocarcinoma.



Clinical Features

Heartburn and regurgitation of sour material into the mouth are the characteristic symptoms of GERD. Heartburn is induced by the contact of refluxed material with the sensitized or ulcerated esophageal mucosa. Angina-like or atypical chest pain occurs in some patients. Persistent dysphagia suggests development of a peptic stricture. Most patients with peptic stricture have a history of several years of heartburn preceding dysphagia. However, in one-third of patients, dysphagia is the presenting symptom. Rapidly progressive dysphagia and weight loss may indicate the development of adenocarcinoma in Barrett's esophagus. Bleeding occurs due to mucosal erosions or Barrett's ulcer. Many patients with GERD remain asymptomatic, while many symptomatic patients treat themselves and do not seek medical help until severe symptoms or complications occur.

Extraesophageal manifestations of GERD are due to reflux of gastric contents into the pharynx, larynx, tracheobronchial tree, nose, and mouth. It may cause chronic cough, laryngitis, and pharyngitis. Morning hoarseness may be noted. Recurrent pulmonary aspiration may cause or aggravate chronic bronchitis, asthma, pulmonary fibrosis, chronic obstructive pulmonary disease, or pneumonia. Chronic sinusitis and dental decay have also been ascribed to GERD.



The diagnosis can be made by history alone in many cases. A therapeutic trial with a PPI such as omeprazole, 40 mg bid for 1 week, provides support for the diagnosis of GERD.

Diagnostic studies are indicated in patients with persistent symptoms or symptoms while on therapy, or in those with complications. The diagnostic approach to GERD can be divided into three categories: (1) documentation of mucosal injury, (2) documentation and quantitation of reflux, and (3) definition of the pathophysiology.

Mucosal damage is documented by the use of barium swallow, esophagoscopy, and mucosal biopsy. Barium swallow is usually normal but may reveal an ulcer or a stricture. A high esophageal peptic stricture, a deep ulcer, or adenocarcinoma suggests Barrett's esophagus. Esophagoscopy may reveal the presence of erosions, ulcers, peptic strictures, or Barrett's metaplasia with or without ulcer, peptic stricture, or adenocarcinoma. A variety of in vivo imaging techniques that facilitate the identification of Barrett's mucosa, dysplasia, or carcinoma during the endoscopy are being developed. Esophagoscopy is not diagnostic of GERD; it is normal in NERD, which constitutes one-third to one-half of all cases of GERD. Mucosal biopsies and the Bernstein test may be helpful in the diagnosis of NERD. Mucosal biopsies may show early changes of esophagitis, including dilation of intracellular spaces. The mucosal biopsies should be performed at least 5 cm above the LES, as the esophageal mucosal changes of chronic esophagitis are quite frequent in the most distal esophagus in otherwise normal individuals. The Bernstein test involves the infusion of solutions of 0.1 N HCl or normal saline into the esophagus. In patients with symptomatic esophagitis, infusion of acid, but not of saline, reproduces the symptoms of heartburn. Infusion of acid in normal individuals usually produces no symptoms. Supraesophageal manifestations are documented by careful otolaryngologic and pulmonary examination.

Documentation and quantitation of reflux, when necessary, can be done by ambulatory long-term (24–48 h) esophageal pH recording. Long-term pH recording may be performed using a pH-sensitive capsule (BRAVO) that is anchored into the esophageal mucosa via an endoscope, rather than the traditional nasally placed pH probe. For evaluation of pharyngeal reflux, a system of recording simultaneously from pharyngeal and esophageal sites may be useful. The pH recordings are helpful only in the evaluation of acid reflux. Endoscopic esophagitis does not correlate with gastroesophageal reflux. Documentation of reflux is necessary only when the role of reflux in the symptom complex is unclear, particularly in evaluation of supraesophageal symptoms, in cases with NERD, and in cases with noncardiac chest pain. Reflux of nonacid contents may be responsible for symptoms of regurgitation and extraesophageal manifestations of GERD. Reflux of nonacid contents can be documented by the use of an impedance test.