الفهرس 
Surgical anatomy of the lower esophageal sphincterOnly 14 pages are availabe for public view
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Abstract
Gastroesophageal reflux disease (GERD) is a common, chronic, and morbid disease that adversely affects quality of life and results in an enormous utilization of healthcare resources (Csendes et al., 2006).
Gastroesophageal reflux is one of the most prevalent conditions of the gastro-intestinal tract that may be effectively managed medically or surgically (Holzman et al., 2001). Despite the common prevalence of gastro-oesophageal reflux disease, it can be one of the most challenging diagnostic and therapeutic problems in benign esophageal disease. A contributing factor to this is the lack of a universally accepted definition of the disease (Peters and DeMeester, 1997).
The complex antireflux mechanism can be simplified by representing it as a mechanical model in which the oesophageal body acts as a pump, the lower oesophageal sphincter as a valve and the stomach as a reservoir. GERD results from a defect in any of these mechanisms. The most common abnormality is in the lower oesophageal sphincter, which is mechanically defective in about two-thirds of patients with GERD. It is important to identify such situations, because a defective lower oesophageal sphincter is related to poor response to medical therapy and leads to drug dependence. It is also irreversible, persisting even after endoscopic healing of oesophagitis. Finally such patients respond better to surgical treatment, since surgery restores the mechanical characteristics of the lower oesophageal sphincter to normal (Costantini et al., 1996).
On the other hand, in some patients with a normal valve the other two components (the pump and reservoir) may be affected. Isolated defects of the pump are rare, since they are usually associated with lower oesophageal sphincter deficiency, but they can cause important excessive oesophageal acid exposure due to abnormal wave progression, defective contractility or inadequate salivation. Alterations of the gastric reservoir are more common: they consist in hypersecretion, delayed gastric emptying and gastric dilatation, especially in response to large or fatty meals. These gastric abnormalities can probably cause reflux episodes by inducing TLESRs. The identification of these patients, who represent about one-third of all patients with GERD, is also important, because they respond well to medical treatment, which can eventually be discontinued in about half of them without recurrence of symptoms (Scarpognato, 1998).
A unifying theme of G.E.R.D. is increased acid exposure on vulnerable epithelia. In most cases, the vulnerable epithelium is the oesophagus, but alternatively it may be that of the supra oesophageal terrain which includes the larynx and the pharynx (Fernando et al., 2006)
Endoscopy is the primary technique for evaluating mucosal integrity, esophageal stricture formation, and Barrett’s esophagus with a sensitivity of 50% and specificity of 95% (Watson, 1998).
Endoscopic evidence of esophagitis occurs in less than 50% of people who have experienced heartburn greater than twice a week over a six-month time period. Esophagitis is best defined by the Los Angelos (LA) classification system and identifies the degree to which the mucosal breaks occur, graded in severity from A to D, with D being the most severe (Dent et al., 1999).
Many patients do not have evidence of esophagitis on endoscope and yet they respond to acid suppression and have behaviors and concerns that parallel those who have evidence of mucosal damage. Patients with endoscopic-negative GERD and who do not respond to medications are best evaluated by ambulatory PH monitoring (Devault, 1999).
Diagnostic modalities cannot reliably exclude GERD even if they are negative. Therefore an empiric trial may be the most expeditious way in which to diagnose GERD in those with classic symptoms and who do not have symptoms suggestive of complications (e.g., carcinoma, stricture) (Kim et al., 1999).
The management of GERD can be divided into five stages. Stages I through IV consist of medical management, and stage V entails surgical intervention. The ultimate goal of treatment is to minimize exposure of the esophagus to refluxate, thereby alleviating symptoms, healing the esophagus, preventing complications and maintaining remission (Richter, 1997).
Clinical data indicate that esophageal healing is influenced by both the degree and duration of gastric acid suppression. Healing rates increase in relation to the length of time that the intragastric pH remains above 4. The agents used in stage III treatment of GERD include scheduled H2-receptor blockers, prokinetic agents and proton pump inhibitors. The choice of agent depends primarily on the severity of symptoms and the presence or absence of oesophagitis (Bell and Hunt, 1992 and Howden, 1997).
The primary goal of anti-reflux surgery is to safely restore a good intra-abdominal segment of oesophagus and creation of a valve or flap at the lower end of the oesophagus, aiming to preserve the patient ability to swallow normally, to belch to relief gaseous distention, and to vomit when necessary (Shimi, 2002).
According to patient symptomatology (i.e. severity of symptoms), treatment can be planned as following:
• Mild symptomatic GERD can usually be managed empirically; lifestyle and dietary modifications along with antacids and nonprescription histamine-2 (H2) receptor antagonists are usually sufficient.
• Patients with debilitating symptoms usually require more intensive pharmacologic therapy (acid-suppressive and/or prokinetic) or antireflux surgery.
• Between these extremes, matching the potency of therapy with disease severity can be achieved either by a ”step up” approach (beginning with lifestyle and dietary measures and incrementally increasing the therapeutic intervention over time until symptom control is achieved) or a ”step down” approach (beginning with potent antisecretory agents to achieve rapid symptom control and then incrementally decreasing the intervention until break-through symptoms define the therapy necessary for continued symptom control (Sontag, 1995).
• There is no evidence to advocate medical or surgical therapy as the best therapy for GERD. The decision to have antireflux surgery must be individualized. All patients taking long-term medications for GERD should receive advice on the safety and wisdom of staying on that therapy and information on antireflux surgery. Fundoplication should be considered in three circumstances: 1. Patients who are intolerant of PPI therapy because of side effects should be considered for surgery. This situation will be less common now with five PPIs, however. 2. Patients who are poorly responsive to PPI therapy should be considered for surgery. This situation is probably not common, given the effectiveness of the currently available PPIs. It is more common in patients with atypical GERD. 3. Surgery should be considered when patients desire a permanent solution to free them of the need to take medications. These patients must be warned about the potential suboptimal results, including the frequent need for medication within a few years of having the procedure and the small but real possibility of becoming worse after the operation. Even in experienced hands, 1% to 2% of patients are worse after the procedure. A careful preoperative evaluation to ensure that the patient’s symptoms are reflux related and that the right operative procedure is performed offers the patient the best opportunity for success (Waring, 2002).