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GERD is the most common condition to affect the esophagus. The disease spectrum ranges from patients with heartburn and other reflux symptoms without morphologic evidence of esophagitis (the so-called acid-sensitive esophagus) to patients with deep ulcer, stricture or Barrett's epithelium. Everyone has some degree of gastroesophageal reflux; it becomes pathological only when associated with troublesome symptoms or complications. Fortunately, the vast majority of patients suffering from GERD have an easily controlled disorder. At the other end of the spectrum, there are patients who develop severe damage to the esophagus. Some will develop Barrett's metaplasia as a consequence of gastroesophageal reflux, which in turn predisposes them to adenocarcinoma.
GERD results from the reflux of gastric contents into the esophageal lumen. Early pathogenesis concepts focused on anatomic factors: reflux was considered a mechanical problem, related to the development of a hiatus hernia. We now know, however, that a hiatus hernia can occur without GERD, and conversely, GERD can occur without a hiatus hernia. Many factors are involved in the pathogenesis of GERD.
By far the most important barrier to gastroesophageal reflux is the LES. Factors such as the intra-abdominal location of the sphincter, extrinsic compression exerted by the diaphragmatic crura and the angle of His (which forms a "mucosal flap valve") may augment this barrier but play a minor role relative to the LES itself. Some patients developing reflux esophagitis have feeble LES tone, but in most, resting LES pressure is nearly normal. Gastro-esophageal reflux occurs by three major mechanisms, as outlined in Figure 5.
Once reflux occurs, the duration of insult to the esophageal mucosa depends on the rapidity with which the esophagus clears this material. Once the initial (primary) peristaltic wave has passed, the bolus (a portion of which frequently remains) is cleared by one or two secondary peristaltic waves. The remaining small adherent acidic residue is then neutralized by saliva, which is carried down by successive swallows. Disorders of salivation or esophageal motor function will impair this clearance mechanism and predispose to the development of GERD. Patients with severe GERD may have frequent prolonged nighttime reflux episodes because during sleep, peristalsis seldom occurs and salivary flow virtually ceases. Hence the contact time of refluxed material with the esophagus is markedly increased.
In some patients delayed gastric emptying further predisposes to the development of GERD. Bile salts and pancreatic enzymes, if refluxed back into the stomach, can in turn reflux into the esophagus and may inflict worse damage than when gastric juice is refluxed alone. Such reflux into the stomach and then the esophagus may occur after gastric surgery, when the pylorus is destroyed. Whenever there is increased gastric pressure or an increase in gastric contents, there is greater likelihood that reflux will occur when the sphincter barrier becomes deficient.
The degree of damage to esophageal mucosa depends not only on the composition of the refluxed material and the amount and duration of reflux, but also on defensive factors within the mucosa itself. Certain patients are more susceptible to the development of actual mucosal damage, for reasons that are not clear.
Most patients present with heartburn and acid regurgitation that onset after eating certain foods or following various postural maneuvers (e.g., bending over, lying flat). Frequency varies from once a week or less to daily episodes with disruption of sleep. Other presenting symptoms include waterbrash, angina-like chest pain, dysphagia and various respiratory symptoms (hoarseness, cough, wheezing). The dysphagia may be due to the development of a reflux-induced stricture or to abnormal motility induced by the refluxed acid. Odynophagia is rarely a symptom of GERD and should alert the physician to another diagnosis such as infectious esophagitis. Reflux symptoms are common during pregnancy because of increased intra-abdominal pressures and the LES-relaxant effect of progesterone. Physical examination in patients with GERD rarely reveals associated physical signs. In severe cases with stricture formation there may be weight loss secondary to decreased caloric intake, or findings of consolidation, bronchospasm or fibrosis on respiratory examination in patients who have GE reflux with aspiration.
In the vast majority of patients, GERD can be diagnosed from the history alone and treated without further investigation. Several tests are useful in the assessment of suspected GERD, depending on the information sought: Is there an abnormal degree of reflux? Are symptoms in fact due to reflux? Is there mucosal damage or other complications (Table 1)? Some specialists believe that all patients with symptomatic gastroesophageal reflux should undergo endoscopy. The argument in favor of this approach is that Barrett's esophagus will be found in about 10% of these patients. This identifies those at increased risk for the development of adenocarcinoma (Section 7.5.2). Most physicians, however, feel that in young patients with typical symptoms that are infrequent and relatively mild, empiric therapy should be instituted first without further investigation. In patients with frequent or more severe symptoms but without symptoms that suggest complications, endoscopy is necessary to rule out other diseases and to document the presence or absence of mucosal damage or Barrett's metaplasia. Endoscopic biopsy may also detect microscopic evidence of esophagitis (hyperplasia of the basal zone layer, elongation of the papillae and inflammatory cell infiltration) when the esophageal mucosa appears macroscopically normal. Many patients will have normal endoscopy and biopsy even though significant GERD is present. In these patients or in patients with atypical or multiple symptoms, it is worthwhile to do a Bernstein test and/or a 24-hour pH reflux study to establish that the symptom(s) are in fact due to acid reflux. It is important to first rule out ischemic heart disease if the presenting symptom is angina-like chest pain.
All patients who present with symptoms of complicated GERD (i.e., dysphagia, bleeding or respiratory symptoms) need to be fully investigated. If dysphagia is present, a barium x-ray study should be performed, followed by endoscopy. Further investigations will depend on the results of the initial tests. Esophageal manometry has little role to play in the routine assessment of patients with GERD. It is useful in the assessment of patients with atypical symptoms, and can be combined with an acid perfusion (Bernstein) test as well as with other provocative tests. It is important to perform manometry prior to surgical intervention, because patients with significant underlying primary motor disorders of the esophagus (e.g., scleroderma) often develop severe dysphagia following an antireflux procedure.
The treatment of GERD is directed toward the abnormal pathophysiology (Table 2). In patients with mild or infrequent symptoms, lifestyle modifications, dietary advice, elevation of the head of the bed and p.r.n. antacids are usually all that is required. If possible, the patient should avoid ingestion of various agents that are known to inhibit LES tone and promote reflux (Table 3). In patients with more severe symptoms or who do not respond to these simple measures, addition of an H2-receptor antagonist is indicated. Prokinetic agents such as cisapride may also be used alone or in combination with other agents in the treatment of GERD, but are probably best suited to the subgroup of patients who have gastroparesis or coexistent functional, nonulcer dyspepsia (gas-bloat syndrome). Proton pump inhibitors such as omeprazole and lansoprazole represent the most efficacious therapy currently available for GERD. They should be used in patients with complicated GERD (e.g., frank erosive esophagitis, peptic stricture or Barrett's ulcer) or in patients who have not responded to H2-receptor antagonists. GERD is a chronic relapsing condition that usually requires long-term treatment. As a general rule the physician should use the simplest, least expensive and least potent therapeutic regime that will keep the patient's symptoms in check.
Antireflux surgery should be considered in patients with reflux esophagitis whose symptoms are not controlled with the aforementioned medical regimen and in younger patients who would prefer to avoid long-term pharmacological therapy. Some patients who develop the complications of GERD (Section 7.5) are also best managed surgically. Several different operative techniques are used for this condition. The most popular are the Nissen fundoplication, the Belsey Mark IV repair and the Hill posterior gastropexy. Currently, many surgeons are doing antireflux surgery via a laparoscopic approach. All procedures adhere to the same basic principles: restoration of the LES to an intra-abdominal position, extrinsic bolstering of the LES pressure and repair of the patulous hiatus. The results of antireflux surgery depend more on the expertise and experience of the surgeon than on the specific operative procedure. In expert hands, surgery will produce a good-to-excellent result in 85-95% of patients; however, in up to 50% of these patients, objective evidence of recurrent pathological reflux will be present five years after surgery, even though symptomatic benefit is maintained. Overall operative mortality for first-time operations is in the order of 0.5%. Between 10 and 20% of patients develop significant problems with dysphagia and/or gas-bloat symptoms after surgery. In most cases these problems resolve with time.
7.5.1 PEPTIC STRICTURE Chronic GERD may lead to peptic stricture formation. This is a fibrous stricture related to collagen deposition that occurs in the course of repair of esophagitis. Patients are usually asymptomatic until the luminal narrowing has reached 12-14 mm. At this point dysphagia to solids occurs. As the stricture progresses, the dysphagia gradually progresses to semisolids and then liquids. Treatment of peptic strictures involves peroral dilation, using either mercury-filled rubber bougies, rigid dilators passed over guidewires, or balloons passed through endoscopes. In close to 50% of patients one or two dilation sessions prove adequate, and no further dilations are required because ongoing medical treatment of the reflux is successful. In others, the stricture recurs and periodic dilations are required to maintain luminal patency. In patients who are otherwise healthy, consideration should be given to antireflux surgery if frequent dilations are required to maintain luminal patency. The success rate of antireflux surgery is lower in such patients with peptic stricture. Strictures are less likely to recur following dilation if the patient is treated with omeprazole. For this reason, long-term treatment with this agent seems appropriate for patients with peptic stricture.
In this condition the squamous epithelium of the distal esophagus is replaced by metaplastic columnar epithelium. Deep ulcers as well as strictures at the new squamocolumnar junction may also develop. Severe hemorrhage may complicate the deep ulcers. This condition occurs in approximately 10% of patients with chronic GERD, although recent prospective studies in which careful biopsies were performed from the region of the gastroesophageal junction suggest that the incidence is actually higher. Barrett's epithelium is a premalignant condition. At the time of initial presentation, up to 10% of patients found to have Barrett's esophagus will have coexistent adenocarcinoma arising in the Barrett's epithelium. This number gives an exaggerated impression of the magnitude of risk, because Barrett's esophagus patients with cancer are more likely to seek medical attention. The true incidence of adenocarcinoma developing in Barrett's epithelium is only about 1 case for every 200 patient-years of follow-up. This nevertheless represents about a 30- to 40-fold increase over the risk faced by the general population. For this reason patients with Barrett's esophagus should be followed periodically with endoscopy and mucosal biopsy in order to detect early cancer. Most patients will develop severe dysplasia before frank invasive carcinoma occurs. Thus, if patients are found to have severe dysplasia or early mucosal carcinoma, esophageal resection should be considered in order to prevent the development of invasive carcinoma. Although there have been case reports of Barrett's esophagus regressing after successful anti-reflux surgery, it is unlikely that such surgery decreases the risk of cancer in the majority of patients. For this reason, Barrett's esophagus per se should not be an indication for antireflux surgery. Surgery should be performed if the patient has symptoms or complications not readily managed by medical therapy.
In some patients the refluxed gastric contents may get past the UES and into the larynx and lungs. This produces recurrent chest infections, chronic cough and laryngitis. In addition, gastroesophageal reflux may trigger broncho-spasm or cough via a neural reflex. GERD with aspiration is more commonly seen in the pediatric age group; when present, antireflux surgery should be performed unless there is a well-documented response to medical therapy. |
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