A zone of high pressure can be identified at the junction of the esophagus and stomach. This lower esophageal sphincter provides the barrier between the esophagus and stomach that normally prevents gastric contents from entering the esophagus. It has no anatomic landmarks, but its presence can be identified by a rise in pressure over gastric baseline pressure as a pressure transducer is pulled from the stomach into the esophagus. This high-pressure zone is normally present except in two situations: (a) after a swallow, when it momentarily relaxes to allow passage of food into the stomach and (b) when the fundus is distended with gas, it is eliminated to allow venting of the gas (a belch). The common denominator for virtually all episodes of GE reflux, whether physiologic or pathologic, is the loss of the normal high-pressure zone and the resistance it imposes to the flow of gastric juice from an environment of higher pressure, the stomach, to an environment of lower pressure, the esophagus. In severe disease, this is usually due to the permanent nonexistent or a reduced high pressure zone. In early disease or normal subjects, loss of the high-pressure zone is transient.
Three characteristics of the LES maintain its resistance or barrier function to intragastric and intraabdominal pressure challenges. These are its pressure, its overall length, and the length exposed to the positive-pressure environment of the abdomen. The tonic resistance of the LES is a function of both its pressure and the length over which this pressure is exerted. The shorter the overall length of the high-pressure zone, the higher the pressure must be to maintain sufficient resistance to remain competent. Consequently, a normal sphincter pressure can be nullified by a short overall sphincter length. Further, as the stomach fills, the length of the sphincter decreases, rather like the neck of a balloon shortening as the balloon is inflated. If the overall length of the sphincter is abnormally short when the stomach is empty, then with minimal gastric distention there will be insufficient sphincter length for the existing pressure to maintain sphincter competency, and reflux will occur.
The third characteristic of the LES is its position, in that a portion of the overall length of the high-pressure zone should be exposed to positive intraabdominal pressure. During periods of increased intraabdominal pressure, the resistance of the LES would be overcome if the abdominal pressure were not applied equally to the high-pressure zone and stomach. Think of sucking on a soft soda straw immersed in a bottle of carbonated beverage; the hydrostatic pressure of the fluid and the negative pressure inside the straw due to sucking cause the straw to collapse instead of allowing the liquid to flow up the straw in the direction of the negative pressure. If the abdominal length is inadequate, the sphincter cannot respond to an increase in applied intraabdominal pressure by collapsing and reflux is more likely to result.
If the pressure in the high-pressure zone is abnormally low, the overall length is short, or the zone is minimally exposed to the abdominal pressure environment in the fasting state, then the LES resistance is permanently lost, and the reflux of gastric contents into the esophagus is unhampered throughout the circadian cycle. A permanently defective sphincter is thus identified by one or more of the following characteristics: a high-pressure zone with an average pressure of less than 6 mm Hg, an average overall length of 2 cm or less, and an average length exposed to the positive-pressure environment of the abdomen of 1 cm or less. In comparison with values in normal subjects, these values are below the percentile for each parameter. The most common cause of a permanently defective sphincter is an inadequate abdominal length, likely secondary to the near ubiquitous presence of a hiatal hernia in patients with GERD.
For the clinician, the finding of a permanently defective sphincter has several implications. Foremost, it is almost always associated with esophageal mucosal injury and predicts that the patient symptoms will be difficult to control with medical therapy. It is a signal that surgical therapy is likely to be needed for consistent and long-term control of the patient's symptoms. It is now accepted that when the sphincter is permanently defective, it is irreversible, even when the associated esophagitis is healed. The presence of a permanently defective sphincter is commonly associated with reduced esophageal body function, and if the disease is not brought under control, the progressive loss of effective esophageal clearance can lead to severe mucosal injury, repetitive regurgitation, aspiration, and pulmonary failure.
A transient loss of the high-pressure zone can also occur and usually results from a functional problem of the gastric reservoir. Excessive air swallowing or food can result in gastric dilatation, and if the active relaxation reflex has been lost, an increased intragastric pressure. When the stomach is distended, the vectors produced by gastric wall tension pull on the GE junction with a force that varies according to the geometry of the cardia; that is, the forces are applied more directly when a hiatal hernia exists than when a proper angle of His is present. The forces pull on the terminal esophagus, causing it to be taken up into the stretched fundus and thereby reducing the length of the high-pressure zone or sphincter. This process continues until a critical length is reached, usually about 1 to 2 cm, when the pressure drops precipitously and reflux occurs. The mechanism by which gastric distention contributes to shortening of the length of the high-pressure zone, so that its pressure drops and reflux occurs, provides a mechanical explanation for transient relaxations of the LES without invoking a neuromuscular reflex. Rather than a spontaneous muscular relaxation, there is a mechanical shortening of the high-pressure zone, secondary to progressive gastric distention, to the point where it becomes incompetent. These transient sphincter shortenings occur in the initial stages of GERD and are the mechanism for the early complaint of excessive postprandial reflux. After gastric venting, the length of the high-pressure zone is restored and competence returns until distention again shortens it and encourages further venting and reflux. This sequence results in the common complaints of repetitive belching and bloating in patients with GERD. The increased swallowing frequency seen in patients with GERD contributes to gastric distention and is due to their repetitive ingestion of saliva in an effort to neutralize the acid refluxed into their esophagus. Thus, GERD may begin in the stomach, secondary to gastric distention resulting from overeating and the increased ingestion of fried foods, which delay gastric emptying. Both characteristics are common in Western society and may explain the high prevalence of the disease in the Western world.
What is acid reflux relief?
Wednesday, February 27, 2008
What is ًthe Antireflux Barrier?
Posted by SSS at 6:21 AM
Monday, February 25, 2008
The lower Esophageal Sphincter: LES
The LES provides a pressure barrier between the esophagus and stomach. Although an anatomically distinct LES has been difficult to identify, microdissection studies show that, in humans, the sphincterlike function is related to the architecture of the muscle fibers at the junction of the esophageal tube with the gastric pouch. The sphincter actively remains closed to prevent reflux of gastric contents into the esophagus and opens by a relaxation that coincides with a pharyngeal swallow . The LES pressure returns to its resting level after the peristaltic wave has passed through the esophagus. Consequently, reflux of gastric juice that may occur through the open valve during a swallow is cleared back into the stomach.
If the pharyngeal swallow does not initiate a peristaltic contraction, then the coincident relaxation of the LES is unguarded and reflux of gastric juice can occur. This may be an explanation for the observation of spontaneous LES relaxation, thought by some to be a causative factor in gastroesophageal reflux disease (GERD). The power of the esophageal body is insufficient to force open a valve that does not relax. The relaxation of the LES that occurs with pharyngeal swallowing or distention of the esophagus is mediated by parasympathetic activity. Consequently, vagal function appears to be important in coordinating the relaxation of the LES with esophageal contraction.
The LES has intrinsic myogenic tone, which is modulated by neural and hormonal mechanisms. Alpha-adrenergic neurotransmitters or beta-blockers stimulate the LES, and alpha blockers and beta stimulants decrease its pressure. It is not clear to what extent cholinergic nerve activity controls LES pressure. The vagus nerve carries both excitatory and inhibitory fibers to the esophagus and sphincter. The hormones gastrin and motilin have been shown to increase LES pressure; and cholecystokinin, estrogen, glucagon, progesterone, somatostatin, and secretin decrease LES pressure. The peptides bombesin, B-enkephalin, and substance P increase LES pressure; and calcitonin gene-related peptide, gastric inhibitory peptide, neuropeptide Y, and vasoactive intestinal polypeptide decrease LES pressure. Some pharmacologic agents such as antacids, cholinergics, domperidone, metoclopramide, and prostaglandin F2 are known to increase LES pressure; and anticholinergics, barbiturates, calcium channel blockers, caffeine, diazepam, dopamine, meperidine, prostaglandin E1 and E2, and theophylline decrease LES pressure. Peppermint, chocolate, coffee, ethanol, and fat are all associated with decreased LES pressure and may be responsible for esophageal symptoms after a sumptuous meal.
During 24-hour esophageal pH monitoring, healthy individuals have occasional episodes of GE reflux. This physiologic reflux is more common when a person is awake and in the upright position than during sleep in the supine position. When reflux of gastric juice occurs, normal subjects rapidly clear the acid gastric juice from the esophagus regardless of their position.
Posted by SSS at 11:26 AM
Friday, February 22, 2008
Thursday, February 21, 2008
Pathophysiology of Gastroesophageal Reflux Disease
Recent data support the likelihood that GERD begins in the stomach. Fundic distention occurs because of overeating and delayed gastric emptying secondary to the high-fat Western diet. The distention causes the sphincter to be taken up by the expanding fundus, exposing the squamous epithelium with the high-pressure zone, which is the distal 3 cm of the esophagus, to gastric juice. Repeated exposure causes inflammation of the squamous epithelium, columnarization, and carditis. This is the initial step and explains why in early disease the esophagitis is mild and commonly limited to the very distal esophagus. The patient compensates by increased swallowing, allowing saliva to bathe the injured mucosa and alleviate the discomfort induced by exposure to gastric acid. Increased swallowing results in aerophagia, bloating, and repetitive belching. The distention induced by aerophagia leads to further exposure and repetitive injury to the terminal squamous epithelium and the development of cardiac-type mucosa. This is an inflammatory process, commonly referred to as carditis and explains the complaint of epigastric pain so often registered by patients with early disease. The process can lead to a fibrotic mucosal ring at the squamocolumnar junction and explains the origin of a Schatzki ring. Extension of the inflammatory process into the muscularis propria causes a progressive loss in the length and pressure of the distal esophageal high-pressure zone associated with an increased esophageal exposure to gastric juice and the symptoms of heartburn and regurgitation. The loss of the barrier occurs in a distal to proximal direction and eventually results in the permanent loss of LES resistance and the explosion of the disease into the esophagus with all the clinical manifestations of severe esophagitis. This accounts for the observation that severe esophageal mucosal injury is almost always associated with a permanently defective sphincter. At any time during this process and under specific luminal conditions or stimuli, such as exposure time to a specific pH range, intestinalization of the cardiac-type mucosa can occur and set the stage for malignant degeneration.
Posted by SSS at 5:47 AM
Sunday, February 17, 2008
Privacy Policy for acid-reflux-relief.blogspot.com
Posted by SSS at 6:50 PM
Thursday, February 7, 2008
Acid reflux relief: Outcomes following surgery
Studies of long-term outcome following both open and laparoscopic fundoplication document the ability of laparoscopic fundoplication to relieve typical reflux symptoms (heartburn, regurgitation, and dysphagia). Laparoscopic fundoplication results in a significant increase in LES pressure and length, generally restoring these values to normal. Postoperative pH studies indicate that the pH tracings of more than 90% of patients will normalize. The results of laparoscopic fundoplication compare favorably with those of open fundoplication. They also indicate the less predictable outcome of atypical reflux symptoms (cough, asthma, laryngitis) after surgery being relieved in only two thirds of patients. Some patients have symptoms after Nissen fundoplication severe enough to warrant evaluation with 24-hour ambulatory esophageal pH monitoring. Heartburn and regurgitation were the only symptoms that were significantly associated with an abnormal pH study. Most patients using acid-suppression medications after surgery for acid reflux relief do not have abnormal esophageal acid exposure. Objective evidence of reflux should be obtained in patients who complain of postoperative symptoms.
The goal of surgical treatment for GERD is to relieve the symptoms of reflux by reestablishing the GE barrier. The challenge is to accomplish this without inducing dysphagia or other untoward side effects. Dysphagia or difficulty in swallowing that existed prior to surgery usually improves following laparoscopic fundoplication. Temporary dysphagia is common after surgery and generally resolves within 3 months. Dysphagia persisting beyond 3 months has been reported in up to 10% of patients. There is some improvement in postoperative dysphagia with time. Induced dysphagia is usually mild, does not require dilatation, and is temporary. It can be induced by technical misjudgments, but this explanation does not hold in all instances. In experienced hands, its prevalence should be less than 3% at 1 year. Other side effects common to surgery for acid reflux relief include the inability to vomit and increased flatulence. Most patients cannot vomit through an intact wrap, though this is rarely clinically relevant. Hyperflatulence is a common and noticeable problem, likely related to increased air swallowing that is present in most patients with reflux disease.
Quality-of-life analyses have become an important part of surgical outcome assessment, with both generic and disease-specific questionnaires in use, in an attempt to quantitate quality of life before and after surgical intervention. In general, these measures relate the effect of disease management to the overall well-being of the patient. Most studies have utilized the Short Form 36 (SF-36) instrument, because it is rapidly administered and well validated. This questionnaire measures 12 different health-related quality-of-life parameters encompassing mental and physical well-being. Data from Los Angeles indicate significant improvements in scores for the area of bodily pain and in a portion of the general health index. Some investigators have also reported improvement in quality of life following surgery for acid reflux relief. Utilizing the Psychological General Well Being Index and the Gastrointestinal Symptom Rating Scale to evaluate quality of life in patients following laparoscopic surgery for acid reflux relief. Scores with both instruments were improved following surgery for acid reflux relief and better than in untreated patients. Of particular note was that scores were as good as or better than those of patients receiving optimal medical therapy. Others using a 10-item health-related quality-of-life questionnaire specific for GERD, have also shown an improvement in quality of life following surgery for acid reflux relief. The quality of life after antireflux surgery has been compared with nonoperative management for severe GERD. Follow-up quality of life was measured using the SF-36, and heartburn severity was measured using the Health Related Quality of Life (QOL) scale. Detailed outcomes were reviewed for both surgical and medical patients. Mean QOL scores were better in the surgical group. More of the medical patients were dissatisfied with therapy. SF-36 scores were better in six of eight domains for surgical patients. These data support the notion that surgery for acid reflux relief, performed on properly selected patients, can significantly improve quality of life and may outperform medical therapy in this regard.
Posted by SSS at 8:40 PM