What is acid reflux relief?

In medically oriented terms, antonyms of the word relief include pain, distress or damage. That links its meaning to both subjective and objective aspects. Subjective, denoting sensations experienced by the sufferer such as pain and objective, meaning physical findings detected by specialists which are either functional distress or organic damage. Actually relief is related to control measures and it quantitatively signifies removal of an unpleasant existence or reduction of its magnitude. The definition of relief, therefore encompasses alleviation of pain, relaxation of distress and healing of damage. Acid reflux on the other hand has two sides; the subjective side (symptoms) which reflects the symptom of heartburn and the objective side (signs) that reflects the functional and/or organic signs of esophageal changes. Acid reflux relief is therefore a broad term that covers all the measures used to control symptoms and signs of acid reflux disease. Normally, the lower esophageal sphincter remains closed except during swallowing. This prevents the passage of food and acid from the stomach into the esophagus. If the lower esophageal sphincter becomes weakened or relaxed, stomach acid may back up into the esophagus. Frequent acid reflux can irritate and inflame the lining of the esophagus, causing symptoms and signs of acid reflux. A better understanding of relief would thus entail knowledge of some aspects of normal structure and function, so that changes in the disease and its control could be easily considered. Actually acid reflux relief involves both preventive and curative measures, and in addition to treatment; orientation with the causes, symptoms and complications of acid reflux are essential for proper management. Acid reflux relief includes: dietary changes,lifestyle modifications, specific medications and surgical operations.Basic knowledge of the underlying causes and progression of acid reflux and answering frequently asked questions about its relief; add to the depth of understanding.

Saturday, December 22, 2007

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Mildly symptomatic esophageal strictures can be handled by careful attention to dietary intake, and use of medical therapy, primarily proton-pump inhibitors. Short, simple strictures can be dilated with weighted rubber or Teflon dilators (e.g., Hurst-Maloney). Tortuous or angulated strictures are more easily approached over a previously placed guidewire passed through an endoscope or under radiographic control (Savary dilators). Graded-steel olives (Eder-Puestow olive dilators), a dilator with graded increases of size (Celestin dilator), or a balloon with a fixed maximal diameter (Cooke balloon) can be passed over the previously placed wire. Alternatively, a balloon of fixed maximal diameter can be passed through the large channel of an endoscope during diagnostic endoscopy and dilated under direct vision (through-the-scope [TTS] dilation). Once the lumen is restored to a diameter of 13 to 15 mm, most patients swallow without difficulty. If the stricture is stable and requires dilation only every 4 to 6 months, no other therapy is necessary.
High-dose H2 -antagonists or, preferably, proton-pump inhibitors and dilation of the stricture can lead to healing of the mucosa and less need for repeated stricture dilation. Patients who do not tolerate dilation or require vigorous dilation every 3 to 4 weeks need a definitive antireflux operation, following which the stricture may regress. If strictures persist after antireflux surgery, esophageal replacement by colon, jejunum, or stomach is a surgical maneuver of last resort associated with a relatively high morbidity and mortality. Patients afflicted by strictures may have significant lung and cardiovascular disease that makes them unsuitable operative candidates.
Esophageal ulcers also represent a major therapeutic problem. They usually require treatment with a proton-pump inhibitor.
Barrett's Esophagus
Barrett's (columnar) epithelium may be premalignant and can be removed only by esophageal resection. Adequate antireflux therapy with high-dose H2 -antagonists or with a proton-pump inhibitor causes regression of columnar epithelium in some patients.
Patients with Barrett's epithelium should be followed up with periodic endoscopic biopsies every 1 to 3 years to look for dysplasia and early changes of adenocarcinoma. The persistence of confirmed high-grade dysplasia is an indication for esophagectomy, because high-grade dysplasia may progress to carcinoma and because coexistent carcinoma may be undetected on biopsy. If low-grade dysplasia is present, the patient is treated medically with proton-pump inhibitors and undergoes biopsy every 6 to 12 months. Experimental endoscopic ablation therapies using photodynamic therapy, laser, or multipolar electrocoagulation are being tried to remove the columnar epithelium with the hope of subsequent growth of the normal squamous epithelium, primarily in patients with low-grade dysplasia or in patients with high-grade dysplasia who are not surgical candidates. Following these new ablation techniques, either long-term gastric acid suppression or laparoscopic Nissen fundoplication is needed to control the reflux and prevent recurrence of Barrett's epithelium.
Pulmonary Complications
Treatment of the pulmonary complications of reflux in adults relies on improved night posture, gastric acid suppressants, and prokinetic agents. Caution is advised before recommending esophageal surgery in patients with reflux and predominant pulmonary problems, because the cause-and-effect relationship may be uncertain in individual patients.

Barrett's esophagus Treatment: Photodynamic therapy
Photodynamic therapy may effectively treat superficial esophageal cancer and Barrett's esophagus. The treatment begins with an injection of a light sensitive medication. Your normal body cells can get rid of this medication, but precancerous and cancerous cells in your esophagus cannot, so it accumulates in these tissues and makes them sensitive to light. Two days after the injection, your doctor inserts an endoscope — a long, flexible instrument — into the diseased area of your esophagus. The light from a laser on the endoscope activates the medication, killing the light sensitive cancerous cells.

This medication will make all the cells in your body light sensitive, so talk to your doctor about how you can avoid sunlight for up to 6 weeks after the treatment.

Heartburn Relief : Acid Reflux Treatment
The management of frequent heartburn entails certain measures to confirm the diagnosis of GERD. Following these diagnostic procedures, treatment of acid reflux disease should be considered.
Acid Reflux Treatment

The aim of treatment are to reduce refluxing, render the refluxate harmless, improve esophageal clearance, and protect the esophageal mucosa. The management of non-complicated cases generally includes weight reduction, sleeping with the head of the bed elevated by about 4 to 6 in. with blocks, and elimination of factors that increase abdominal pressure. Patients should not smoke and should avoid consuming fatty foods, coffee, chocolate, alcohol, mint, orange juice, and certain medications (such as anticholinergic drugs, calcium channel blockers, and other smooth-muscle relaxants). They should also avoid ingesting large quantities of fluids with meals. In mild cases, life-style changes and over-the-counter antisecretory agents may be adequate. In moderate cases, H2receptor blocking agents (cimetidine, 300 mg; ranitidine, 150 mg bid; famotidine, 20 mg bid; nizatidine 150 mg bid) for 6 to 12 weeks are effective in symptom relief. Higher doses are necessary for healing erosive esophagitis, but proton pump inhibitors (PPIs) are more effective in this setting.

In cases resistant to H2receptor blockers and severe cases, rigorous acid suppression with aPPI is recommended. The PPIs are comparably effective: omeprazole (40 mg/d), lansoprazole (30 mg/d), pantoprazole (40 mg/d), and rabeprazole (20 mg/d) for 8 weeks can heal erosive esophagitis in up to 90% of patients. Reflux esophagitis requires prolonged therapy, for 3 to 6 months or longer if the disease recurs quickly. After initial therapy, a lower maintenance dose of PPI is used. Side effects are minimal. Aggressive acid suppression causes hypergastrinemia but does not increase the risk for carcinoid tumors or gastrinomas. Vitamin B12 absorption is compromised by the treatment. Patients with reflux esophagitis who have complications, such as Barrett's esophagus with concomitant esophagitis, should be treated vigorously. Patients who have an associated peptic stricture are treated with dilators to relieve dysphagia as well as provided with vigorous treatment for reflux.

Antireflux surgery, in which the gastric fundus is wrapped around the esophagus (fundoplication), increases theLESpressure and should be considered for patients with resistant and complicated reflux esophagitis that does not respond fully to medical therapy or for patients for whom long-term medical therapy is not desirable. Laparoscopic fundoplication is the surgery of choice. Ideal candidates for fundoplication are those in whom motility studies show persistently inadequate LES pressure but normal peristaltic contractions in the esophageal body.

Patients with alkaline esophagitis are treated with general antireflux measures and neutralization of bile salts with cholestyramine, aluminum hydroxide, or sucralfate. Sucralfate is particularly useful in these cases, as it also serves as a mucosal protector.

Acid Reflux Relief : Combination Therapy
Most patients treated with PPIs in conventional dosages do not exhibit complete suppression of stomach acid secretion. Approximately 70% of individuals who take a PPI twice a day experience nocturnal stomach acid breakthrough (defined as a stomach pH lesser than 4 for more than 1 hour at night). Brief episodes of acid reflux occur frequently during these breakthrough periods in patients with GERD. For some patients taking a PPI twice daily, nocturnal acid breakthrough can be abolished by adding a histamine H2-receptor blocker at bedtime. It is not clear that this approach is desirable, however. Complete elimination of acid reflux usually is not necessary to effect the healing of reflux esophagitis. Indeed, most patients who are treated with a PPI in conventional dosage exhibit complete healing of their symptoms and signs of GERD. No clear clinical benefit yet has been demonstrated for the practice of adding a histamine H2-receptor blocker at bedtime to PPI therapy.

A few older investigations have explored the value of combination drug therapy for the healing of GERD. The great efficacy of the PPIs used as single agents in this condition has discouraged investigators from undertaking new studies on combination therapy. Drug combinations that have been studied have included an H2 blocker plus either sucralfate or a prokinetic agent. Cimetidine (1200 mg/d) combined with sucralfate (5 g/d) was found to be superior to cimetidine alone for relieving daytime heartburn and for improving the endoscopic signs of esophagitis. For patients unresponsive to treatment with cimetidine alone, the addition of metoclopramide resulted in symptomatic improvement significantly more often than the addition of placebo, but side effects of metoclopramide were frequent. A combination of ranitidine (300 mg/d) plus metoclopramide (40 mg/d) was not found to be as effective as omeprazole alone (20 mg/d) in healing the signs and symptoms of esophagitis. Some studies explored combination therapy with the prokinetic agent cisapride, but these studies are of historical interest only because cisapride has been withdrawn from general use due to serious side effects (lethal arryhythmias). For patients with moderately severe reflux esophagitis, the use of combination therapy may eliminate the need for treatment with a PPI. However, the addition of a second medication increases the cost of therapy and the potential for side effects. Furthermore, the long-term benefit of combination therapy has not been demonstrated. For patients who are refractory to single-agent therapy (with an H2 blocker, sucralfate, or a prokinetic), a change to a PPI generally is more likely to effect healing than the addition of a second drug.

Treatment of Barrett's esophagus
The relief of symptoms remains the primary force driving antireflux surgery in patients with Barrett's esophagus. Healing of esophageal mucosal injury and the prevention of disease progression are important secondary goals. In this regard, patients with Barrett's esophagus are no different than the broader population of patients with GE reflux. Antireflux surgery should be considered when patient factors suggest severe disease or predict the need for long-term medical management, both of which are almost always true in patients with Barrett's esophagus.
PPI therapy, both to relieve symptoms and to control any coexistent esophagitis or stricture, is an acceptable treatment option in patients with Barrett's esophagus. Once initiated, however, most patients with Barrett's will require lifelong treatment. Complete control of reflux with PPI therapy can be difficult, however, as has been highlighted by studies of acid breakthrough while on therapy. Ablation trials have shown that mean doses of 56 mg of omeprazole are necessary to normalize 24-hour esophageal pH studies. Antireflux surgery likely results in more reproducible and reliable elimination of reflux of both acid and duodenal content, although long-term outcome studies suggest that as many as 25% of patients postfundoplication have persistent pathologic esophageal acid exposure confirmed by 24-hour pH studies.58
An important consideration is that patients with Barrett's esophagus generally have severe GERD, with its attendant sequelae such as large hiatal hernia, stricture, shortened esophagus, and poor motility. These anatomic and physiologic features make successful antireflux surgery a particular challenge in this population. Indeed, recent data suggest that antireflux surgery in patients with Barrett's esophagus may not be as successful in the long term as in those without Barrett's.
Studies focusing on the symptomatic outcome following antireflux surgery in patients with Barrett's esophagus document excellent to good results in 72% to 95% of patients at 5 years following surgery The outcome of laparoscopic Nissen fundoplication in patients with Barrett's esophagus has been assessed at 1 to 3 years after surgery.Reflux symptoms were absent postoperatively in 79% of the patients. Postoperative 24-hour pH was normal in 17 of 21 (81%) patients. Ninety-nine percent of the patients considered themselves cured or improved, and 97% were satisfied with the surgery.

What is Barrett's esophagus?

Barrett's esophagus is the metaplastic complication of Acid Reflux Disease.
It is the condition whereby the tubular esophagus is lined with columnar epithelium rather than squamous epithelium was first described by Norman Barrett in 1950. He incorrectly believed it to be congenital in origin. It is now realized that it is an acquired abnormality, occurring in 7% to 10% of patients with GERD, and represents the end stage of the natural history of this disease. It is also understood to be distinctly different from the congenital condition in which islands of mature gastric columnar epithelium are found in the upper half of the esophagus.
The definition of Barrett's esophagus has evolved considerably over the past decade. Traditionally, Barrett's esophagus was identified by the presence of any columnar mucosa extending at least 3 cm into the esophagus. Recent data indicating that specialized intestinal-type epithelium is the only tissue predisposed to malignant degeneration, coupled with the finding of a similar risk of malignancy in segments of intestinal metaplasia less than 3 cm long, have resulted in the diagnosis of Barrett's esophagus, given any length of endoscopically visible tissue that is intestinal metaplasia on histology. Whether to call long segments of columnar mucosa without intestinal metaplasia Barrett's esophagus is unclear. The hallmark of intestinal metaplasia is the presence of goblet cells. Recent studies have identified a high prevalence of biopsy-proved intestinal metaplasia at the cardia, in the absence of endoscopic evidence of a columnar-lined esophagus. The significance and natural history of this finding remains unknown. The term Barrett's esophagus should currently be used in the setting of an endoscopically visible segment of intestinal metaplasia of any length or columnar replacement of the esophagus of 3 cm or more.
Factors predisposing to the development of Barrett's esophagus include early-onset GERD, abnormal LES and esophageal body physiology, and mixed reflux of gastric and duodenal contents into the esophagus. Direct measurement of esophageal bilirubin exposure as a marker for duodenal juice has shown that 58% of the patients with GERD have increased esophageal exposure to duodenal juice and that this exposure is most dramatically related to Barrett's esophagus.
Pathophysiology of Barrett's Metaplasia
Recent studies suggest that the metaplastic process at the GE junction may begin by conversion of distal esophageal squamous mucosa to cardiac-type epithelium, heretofore presumed to be a normal finding. This is likely due to exposure of the distal esophagus to excess acid and gastric contents via prolapse of esophageal squamous mucosa into the gastric environment. This results in inflammatory changes at the GE junction or a metaplastic process, both of which may result in the loss of muscle function and a mechanically defective sphincter allowing free reflux with progressively higher degrees of mucosal injury. Intestinal metaplasia within the sphincter may result, as in Barrett's metaplasia of the esophageal body. This mechanism is supported by the finding that as the severity of GERD progresses, the length of columnar lining above the anatomic GE junction is increased.

Acid Reflux Disease Complications
The complications of GE reflux result from the damage inflicted by gastric juice on the esophageal mucosa. Mucosal complications, include esophagitis and stricture. The prevalence and severity of complications is related to the degree of loss of the GE barrier, defects in esophageal clearance, and the content of refluxed gastric juice.
The potential injurious components that reflux into the esophagus include gastric secretions, such as acid and pepsin, biliary and pancreatic secretions that regurgitate from the duodenum into the stomach, and toxic compounds generated in the mouth, esophagus, and stomach by the action of bacteria on dietary substances.
Studies have shown that acid alone does minimal damage to the esophageal mucosa, but the combination of acid and pepsin is highly deleterious. Hydrogen ion injury to the esophageal squamous mucosa occurs only at a pH below 2. In acid refluxate, the enzyme pepsin appears to be the major injurious agent. Similarly, the reflux of duodenal juice alone does little damage to the mucosa, whereas the combination of duodenal juice and gastric acid is particularly noxious. Reflux of bile and pancreatic enzymes into the stomach can either protect against or augment esophageal mucosal injury. For instance, the reflux of duodenal contents into the stomach may prevent the development of peptic esophagitis in a patient whose gastric acid secretion maintains an acid environment, because the bile salts would attenuate the injurious effect of pepsin and the acid would inactivate the trypsin. Such a patient would have bile-containing acid gastric juice that, when refluxed, would irritate
the esophageal mucosa but cause less esophagitis than if it were acid gastric juice containing pepsin. In contrast, the reflux of duodenal contents into the stomach of a patient with limited gastric acid secretion can result in esophagitis, because the alkaline intragastric environment would support optimal trypsin activity, and the soluble bile salts with a high pKa would potentiate the enzyme's effect. Hence, duodenal-gastric reflux and the acid secretory capacity of the stomach interrelate by altering the pH and enzymatic activity of the refluxed gastric juice to modulate the injurious effects of enzymes on the esophageal mucosa.
This disparity in injury caused by acid and bile alone, as opposed to the gross esophagitis caused by pepsin and trypsin, provides an explanation for the poor correlation between the symptom of heartburn and endoscopic esophagitis. The reflux of acid gastric juice contaminated with duodenal contents could break the esophageal mucosal barrier, irritate nerve endings in the papillae close to the luminal surface, and cause severe heartburn. Despite the presence of intense heartburn, the bile salts present would inhibit pepsin, the acid pH would inactivate trypsin, and the patient would have little or no gross evidence of esophagitis. In contrast, the patient who refluxed alkaline gastric juice may have minimal heartburn because of the absence of hydrogen ions in the refluxate but have endoscopic esophagitis because of the bile salt potentiation of trypsin activity on the esophageal mucosa. This is supported by recent clinical studies which indicate that the presence of alkaline reflux is associated with the development of mucosal injury.
Although numerous studies have suggested the reflux of duodenal contents into the esophagus in patients with GERD, few have measured this directly. The components of duodenal juice thought to be most damaging are the bile acids and, as such, they have been the most commonly studied. Most studies shown that, patients with GERD have greater and more concentrated bile acid exposure to the esophageal mucosa than do normal subjects. This increased exposure occurs most commonly during the supine period while asleep and during the upright period following meals. Most studies have identified the glycine conjugates of cholic, deoxycholic, and chenodeoxycholic acids as the predominant bile acids aspirated from the esophagus of patients with GERD, although appreciable amounts of taurine conjugates of these bile acids were also found. Other bile salts were identified but in small concentrations. This is as one would expect because glycine conjugates are three times more prevalent than taurine conjugates in normal human bile.
The potentially injurious action of toxic compounds either ingested or newly formed on the mucosa of the GE junction and distal esophagus has long been postulated. Investigators have recently shown that dietary nitrate consumed in the form of green vegetables and food contaminated by nitrate-containing fertilizers results in the generation of nitric oxide at the GE junction in concentrations high enough to be potentially mutagenic. Previous studies have shown that nitrate ingested in food is reabsorbed in the small bowel with approximately 25% resecreted into the mouth via the salivary glands. Oral bacteria chemically transform the relatively innocuous nitrate to the more toxic nitrite, which is swallowed and subsequently converted to nitric oxide and other toxic nitroso-compounds by acid and ascorbic acid in the stomach. Whether this mechanism in fact contributes to injury and or neoplastic transformation in the upper stomach, GE junction, and distal esophagus is currently unknown.

Anti reflux Surgery Complications
Postoperative complications were found to occur in approximately 8% of patients, with the rate of conversion to an open procedure of about 4%. The most common perioperative complication was early wrap herniation (1.3%), defined as occurring within 48 hours of surgery. This is one complication that may be more common with the laparoscopic than open approach. The explanation for this is unclear but may be related to the opening of tissue planes by the pneumoperitoneum and the reduced tendency for adhesion formation after laparoscopic compared to open surgery. In an attempt to eliminate this complication, most surgeons routinely perform a crural repair.
Both pneumothorax and pneumomediastinum have been reported. The occurrence of pneumothorax is related to breach of either pleural membrane, usually the left, during the hiatal dissection. Chest drain insertion is usually not required because accumulated carbon dioxide rapidly dissipates following release of pneumoperitoneum by a combination of positive pressure ventilation and absorption.
As with any laparoscopic procedure, instrumental perforation of the hollow viscera may occur. Early esophageal perforation may arise during passage of the bougie, during the retroesophageal dissection, or during suture pull-through. Late esophageal perforation is related to diathermy injury at the time of mobilization. Gastric perforations usually resulted from excessive traction on the fundus for retraction purposes. Recognition of the problem at the time of surgery requires repair, which may be performed either laparoscopically or by an open technique.
Hemorrhage during the course of laparoscopic fundoplication usually arises from the short gastric vessels or spleen. Rarer causes include retractor trauma to the liver, injury to the left inferior phrenic vein, an aberrant left hepatic vein, or the inferior vena cava. Cardiac tamponade as a result of right ventricular trauma has also been reported. Major vascular injury mandates immediate conversion to an open procedure to achieve hemostasis.

Acid reflux disease facts
The diagnosis of GE reflux based on symptoms alone is correct in only approximately two thirds of patients because the symptoms are often nonspecific and can be caused by other conditions.

The three characteristics of the LES that maintains its resistance or barrier function to intragastric and intraabdominal pressure challenges are pressure, overall length, and length exposed to the positive pressure environment of the abdomen.

An important complication of GE reflux is the development of reflux-induced respiratory symptoms either with or without heartburn.

Antireflux surgery improves respiratory symptoms in nearly 90% of children and 70% of adults with asthma and reflux disease.

Factors predisposing to the development of Barrett's esophagus include early-onset GERD, abnormal lower esophageal and esophageal body physiology, and mixed reflux of gastric and duodenal contents into the esophagus.

PPI therapy, both to relieve symptoms and to control esophagitis, is an acceptable treatment, although most patients will require life-long treatment.

Progression of nondysplastic Barrett's epithelium occurs with 5% to 10% of patients per year progressing to dysplasia and 0.5% to 1% per year progressing to cancer

The standard of care of the treatment of confirmed Barrett's esophagus with high-grade dysplasia is esophagectomy because approximately 50% will harbor invasive cancer

Three factors predictive of a successful outcome following antireflux surgery are (a) an abnormal score on 24-hour esophageal pH monitoring; (b) the presence of typical symptoms of GERD, namely heartburn or regurgitation; and (c) symptomatic improvement in response to acid-suppression therapy prior to surgery.

Endoscopic investigation of gastro-esophageal reflux
The development of fibre-optic endoscopy revolutionized the ability to investigate the gastrointestinal tract. Flexible endoscopes often have a diameter of less than 1 cm, with a control head and a flexible shaft with a manoeuvrable tip. The head is connected to a light source and can transmit images to a video image screen.
All endoscopes have multiple small lumens allowing transmission of air and water and for suction. The suction channel can also be used for the passage of interventional devices, for example biopsy forceps. The ability to transmit air (insufflation) allows the endoscopist to inflate the lumen to obtain optimal views. The water channel provides a means of washing mucosal surfaces, and suction maybe used to remove pools of fluid within the gastrointestinal tract, thus ensuring that all mucosal surfaces are inspected.
Diagnostic indications include the investigation of gastro-esophageal reflux (diagnostic investigation or surveillance endoscopy of Barrett's esophagus).
Therapeutic procedures that can be undertaken include mucosal biopsy, stent insertion for strictures, and dilatation of strictures.
Patient preparation
Informed consent is required, and patients are fasted for 4-6 hours prior to the procedure. Although most patients do not require sedation, the choice is offered and discussed. Sedation involves the use of a short-acting benzodiazepine which provides a sedative and amnesic effect. Monitoringis required (pulse oximetry) with sedation due to the risk of respiratory depression. Antibiotic prophylaxis is administered to patients with heart valve disease to prevent bacterial endocarditis.
A mouthguard is used. The endoscope is introduced into the pharynx, then the oesophagus. Patients may retch during this procedure. The endoscope is progressively introduced to inspect the oesophagus, stomach and proximal small bowel (duodenum).
The overall complication rate is approximately 1 per 1000 with a mortality rate of approximately 1 per 25000. Complications include bleeding, perforation and respiratory arrest (a complication of sedation).
Post procedure care
Patients are monitored in a recovery area until safe for discharge.

Hiatal hernia and GERD
A hiatal hernia is the protrusion (or herniation) of the upper part of the stomach into the thorax through a tear or weakness in the diaphragm. The most common (95%) is the sliding hiatal hernia, where the gastroesophageal junction moves above the diaphragm together with some of the stomach.

Hiatal hernias affect anywhere from 1 to 20% of the population. Of these, 9% are symptomatic, depending on the competence of the lower esophageal sphincter (LES). 95% of these are "sliding" hiatal hernias, in which the LES protrudes above the diaphragm along with the stomach, and only 5% are the "rolling" type (paraesophageal), in which the LES remains stationary but the stomach protrudes above the diaphragm. People of all ages can get this condition, but it is more common in older people.

There are three anatomical factors that contribute to the prevention of reflux: (i) the acute angle at which the esophagus enters the stomach with its associated valve (called the angle of His); (ii) the phrenoesophageal ligament that seems to hold the gastroesophageal junction in place; and (iii) the diaphragmatic crura (which act to prevent reflux due to the position of the stomach below the diaphragm) and the intra-abdominal segment of lower esophageal sphincter. It has been reported that the angle of His is larger in the symptomatic group of endoscopically diagnosed acid reflux than in the asymptomatic group, indicating the importance of this angle with regard to gastroesophageal reflux.
Following any disturbance at any of these mechanisms, a sliding hernia would occur and cause gastroesophageal reflux. It is presumed that the tissues around the diaphragmatic hiatal that prevent GER maintain the form of cardia whenever abdominal pressure is increased.

The following are possible causes or contributing factors for having a hiatal hernia.
* Increased pressure within the abdomen caused by:
o Heavy lifting or frequent bending over
o Frequent or hard coughing
o Hard sneezing
o Violent vomiting
o Straining with constipation
o Obesity (extra weight pushes down on the abdomen increasing the pressure)
o Use of the sitting position for defecation.
* Heredity
* Smoking
* Drug use, such as cocaine.
* Stress

If mechanical forces set in play by stomach distention are important in pulling on the terminal esophagus and shortening the length of the high-pressure zone or sphincter, then the geometry of the cardia, that is, the presence of a normal acute angle of His or the abnormal dome architecture of a sliding hiatal hernia, should influence the ease with which the sphincter is pulled open. A close relationship exists between the degree of stomach distention necessary to overcome the high-pressure zone and the morphology of the cardia. Greater stomach dilatation, as reflected by a higher pressure inside stomach, is necessary to open the sphincter in patients with an intact angle of His compared to those with a hiatal hernia. This is what would be expected if the high-pressure zone were shortened by mechanical forces and accounts for why a hiatal hernia is often associated with the presence of GERD.

The symptoms include acid reflux, and pain, similar to heartburn, in the chest and upper stomach.
In most patients, hiatal hernias cause no symptoms. Sometimes patients experience heartburn and regurgitation, when stomach acid refluxes back into the esophagus.
A hiatal hernia per se may not cause any symptoms. The condition promotes reflux of stomach contents (via its direct and indirect actions on the anti-reflux mechanism) and thus is associated with gastroesophageal reflux disease (GERD). In this way a hiatal hernia is associated with all the potential consequences of GERD - heartburn, esophagitis, Barrett's esophagus and esophageal cancer. However the risk attributable to the hiatal hernia is difficult to quantify, and at most is low.

Besides discomfort from GERD and dysphagia, hiatal hernias can have severe consequences for patients if not treated. While sliding hernias are primarily associated with gastroesophageal acid reflux, rolling hernias can strangulate a portion of the stomach above the diaphragm. This strangulation can result in esophageal or GI tract obstruction and the tissue even become ischemic and necrose.
Another severe complication, although very rare, is a large herniation that can restrict the inflation of a lung, causing pain and breathing problems.

The diagnosis of a hiatal hernia is typically made through an upper GI series or endoscopy.
Gastroesophageal scintigraphy is a sensitive and non-invasive method for evaluation of GER. Most patients with typical GER symptoms exhibit scintigraphic evidence of reflux, and the severity of their reflux symptoms is correlated with the scintigraphic reflux index. The reflux index also increases as endoscopic esophagitis become more severe. The severity of reflux symptoms could be correlated with the reflux index, and the index increased significantly as endoscopic esophagitis became more severe. Therefore, the reflux index appeared to be a reliable measure of GER.
The severity of sliding hernia could be classified by esophagogastroscopy. Using the diameter of the fiberscope (9–10 mm) to estimate hernia size; also on the basis of severity. Evaluation of the relationship between the reflux index and the endoscopic grade of hiatal hernia demonstrated that the index was significantly higher in the mild hernia group compared with the severe group. Endoscopic esophagitis was found to be more prevalent in the severe group than in the mild group.
The relationship between reflux esophagitis and the size of the sliding hernia was also studied, concluding that hernia was significantly larger in patients with erosive esophagitis than in those without esophagitis and that hiatal hernia size was a reliable indicator of the severity of esophagitis.

In most cases, sufferers experience no discomfort and no treatment is required. However, when the hiatal hernia is large, or is of the paraesophageal type, it is likely to cause esophageal stricture and discomfort. Symptomatic patients should elevate the head of their beds and avoid lying down directly after meals until treatment is rendered. If the condition has been brought on by stress, stress reduction techniques may be prescribed, or if overweight, weight loss may be indicated. Medications that lower the lower esophageal sphincter (or LES) pressure should be avoided. Antisecretory drugs like proton pump inhibitors and H2 receptor blockers can be used to reduce acid secretion.
Where hernia symptoms are severe and chronic acid reflux is involved, surgery is sometimes recommended, as chronic reflux can severely injure the esophagus and even lead to esophageal cancer.
The surgical procedure used is called Nissen fundoplication. In fundoplication, the stomach fundus (upper part) of the stomach is wrapped, or plicated, around the inferior part of the esophagus, preventing herniation of the stomach through the hiatus of the diaphragm and the reflux of stomach acid. The procedure is now commonly performed laparoscopically. With proper patient selection, laparoscopic fundoplication has low complication rates and a quick recovery.
Complications include gas bloat syndrome, dysphagia (difficult swallowing), dumping syndrome, excessive scarring, and rarely, achalasia. The procedure sometimes fails over time, requiring a second surgery to make repairs.

GERD Asthma Relief

Once GERD is suspected or thought to be responsible for asthma symptoms, treatment may be with either prolonged PPI (proton pump inhibitor) therapy or anti reflux surgery. A 3- to 6-month trial of high-dose PPI therapy [twice a day (b.i.d.) or three times a day (t.i.d.) dosing] may help confirm (by virtue of symptom resolution) that GERD is partly or completely responsible for the asthma symptoms. The persistence of symptoms despite PPI treatment, however, does not necessarily rule out GERD as a potential contributor.
Based on reported observations, relief of asthma symptoms can be anticipated for 25% to 50% of patients with GERD asthma treated with anti reflux medications.
Fewer than 15%, however, can be expected to have objective improvements in their pulmonary function. The reason for this apparent paradox may be that most studies employed relatively short courses of anti reflux therapy (less than 3 months). This time period may have been sufficient for symptomatic improvement but insufficient for recovery of pulmonary function. The chances of success with medical treatment are likely directly related to the extent of GERD elimination. The conflicting findings of reports of anti reflux therapy may well be to the result of inadequate control of GERD in some studies. The literature indicates that anti reflux surgery improves asthma symptoms in nearly 90% of children and 70% of adults with asthma and GERD. Improvements in pulmonary function were demonstrated in around one third of patients. Comparison of the results of uncontrolled studies of each form of therapy and the evidence from the two randomized controlled trials of medical versus surgical therapy indicate that fundoplication is the most effective therapy for GERD asthma. The superiority of the surgical anti reflux barrier over medical therapy is probably most noticeable in the supine posture, which corresponds with the period of acid breakthrough with PPI therapy and is the time in the circadian cycle when asthma symptoms and peak expiratory flow rates are at their worst.
It is also important to realize that, in asthmatic patients with a non reflux induced motility abnormality of the esophageal body, performing an anti reflux operation may not prevent the aspiration of orally regurgitated, swallowed liquid or food. This can result in asthma symptoms and airway irritation that may elicit an asthmatic reaction. This factor may explain why surgical results appear to be better in children than adults, because disturbance of esophageal body motility is more likely in adult patients.

GERD Asthma
Two mechanisms have been proposed as the pathogenesis of GERD asthma. The first, the so-called reflux theory, maintains that asthma is the result of the aspiration of gastric contents. The second or reflex theory maintains that vagally mediated bronchoconstriction follows acidification of the lower esophagus. The evidence supporting a reflux mechanism is fivefold. First, clinical studies have documented a strong correlation between idiopathic pulmonary fibrosis and hiatal hernia. The presence of GERD was shown to be highly associated with several pulmonary diseases, not only asthma, in recent studies. Second, pathologic acid exposure in the proximal esophagus is often identified in patients with asthma and reflux disease. Third, scintigraphic studies have shown aspiration of ingested radioisotope in some patients with reflux and respiratory symptoms. Fourth, simultaneous tracheal and esophageal pH monitoring in patients with reflux disease has documented tracheal acidification in concert with esophageal acidification. Finally, animal studies have shown that tracheal instillation of hydrochloric acid profoundly increases airways resistance.
A reflex mechanism is primarily supported by the fact that bronchoconstriction occurs following the infusion of acid into the lower esophagus. This can be explained by the common embryologic origin of the tracheoesophageal tract and its shared vagal innervation. Second, patients with asthma and pathologic distal esophageal acid exposure but normal proximal esophageal acid exposure may experience an improvement in their asthma after antireflux therapy.
The primary challenge in implementing treatment for reflux-associated asthma lies in establishing the diagnosis. In patients with predominantly typical reflux symptoms and secondary respiratory complaints, the diagnosis may be straightforward. However, in a substantial number of patients with GERD asthma, the respiratory symptoms dominate the clinical scenario. GE reflux in these patients is often silent and is uncovered only when investigation is initiated. A high index of suspicion is required, notably in patients with poorly controlled asthma despite appropriate bronchodilator therapy. Supportive evidence for the diagnosis can be gleaned from endoscopy and stationary esophageal manometry. Endoscopy may show erosive esophagitis or Barrett's esophagus. Manometry may indicate a hypotensive LES or ineffective body motility, defined by 30% or more contractions in the distal esophagus of less than 30 mm Hg in amplitude.
The gold standard for the diagnosis of GERD asthma is ambulatory dual-probe pH monitoring. One probe is positioned in the distal esophagus and the other at a more proximal location. Sites for proximal probe placement have included the trachea, pharynx, and proximal esophagus. Most authorities would agree that the proximal esophagus is the preferred site for proximal probe placement. Although ambulatory esophageal pH monitoring allows a direct correlation between esophageal acidification and respiratory symptoms, the chronologic relationship between reflux events and bronchoconstriction is complex.

What is (GERD)?
(GERD) Gastro-esophageal reflux disease
Spontaneous gastro-esophageal reflux may occur as a normal event, but gastro-esophageal reflux disease (GERD) is defined as symptoms (heartburn) and/or tissue damage caused by retrograde flow of gastric contents into the esophagus.
Symptoms of GERD have been reported in approximately 44% of a surveyed population, but the precise prevalence varies according to the definition of the disease. The incidence increases with age and peaks at the age of 55-64 years, with an approximately equal gender distribution.
The normal anti-reflux mechanism involves both anatomical and physiological factors: the lower esophageal sphincter, angle of His, crura of the diaphragm, mucosal rosette, swallowed saliva (lubrication and neutralization of acid), antegrade esophageal peristalsis and normal gastric motility/emptying.
A mild degree of reflux is experienced in most normal individuals, but a major cause of significant GERD is inappropriate transient lower esophageal sphincter relaxations (not preceded by a primary propagated esophageal contraction initiated by swallowing). Other causes include hiatus hernia and delayed gastric emptying.
Although a greater proportion of patients with symptoms of GERD smoke and consume alcohol, clinical studies confirm that traditional risk factors of increasing age, male sex, smoking and alcohol consumption are not strongly associated with symptoms of GERD.
Scope of disease
The majority have mild disease without esophagitis (non-erosive reflux disease). Symptoms can arise with minimal gastric reflux due to increased sensitivity of the esophagus to acid. Moderate disease is associated with esophagitis, and severe chronic disease results in the development of Barrett's esophagus (defined as metaplastic columnar degeneration above the gastro-esophageal junction). This is a premalignant condition, with a 0.5% per patient-year risk of malignant change to adenocarcinoma.
Severe or prolonged reflux can lead to ulceration, bleeding or perforation. Healing occurs by fibrosis and may lead to stricture formation. Severe reflux may also produce a hoarse voice from laryngitis. If the refluxate is aspirated, pneumonia may develop.
Clinical features
Most patients complain of heartburn, characterized by retrosternal burning pain, precipitated by meals. It may be aggravated by posture (lying flat, stooping, bending forwards) and conditions that raise intra-abdominal pressure (sneezing and coughing). It is often relieved by antacids and may be associated with water brash, the excessive secretion of saliva preceding reflux.
Atypical symptoms include back pain, cardiac-type chest pain, chronic wheeze, nocturnal 'asthma' or recurrent chest infections (due to aspiration), sore throat, hoarse voice, halitosis or dental decay. Dysphagia may occur with esophageal strictures from chronic disease.
Initial investigations
In general, the history can lead to a confident diagnosis of GERD and initial treatment can commence for uncomplicated cases. Older patients, or those who experience weight loss, dysphagia or hematemesis will require further investigations.
Further investigations
Upper gastrointestinal endoscopy
esophagoscopy is appropriate for patients with symptoms suggestive of complications (weight loss, dysphagia, hematemesis), when the diagnosis is unclear, when symptoms cannot be adequately controlled on medical therapy, or for screening for Barrett's epithelium (in patients over50 with chronic symptoms).
esophageal abnormalities that can be diagnosed at endoscopy include hiatus hernia, esophagitis, Barrett's esophagus, strictures and tumours. The severity of reflux esophagitis can also be assessed at endoscopy, and biopsies can be taken. GERD cannot be excluded by a normal endoscopy.
24-hour pH measurement
Intra-esophageal pH measurement may be required to diagnose GERD if the initial endoscopy is normal or if symptoms do not respond to medical therapy. It is usually performed as an ambulatory test over a 24-hour period, facilitating the diagnosis of GERD by assessment of the duration, frequency and severity of reflux attacks in relation to the pH of the esophagus. It does not provide any information as to the etiology of GERD and may be normal (false negative) in patients with significant bile or volume reflux.
esophageal manometry
Esophageal manometry is a useful investigation to assess esophageal function when planning surgical intervention, especially if achalasia and other esophageal motility disorders are suspected. It is possible to determine the length and position of the lower esophageal sphincter and to measure the sphincter pressure. A short or weak lower esophageal sphincter is often a major contributing cause of reflux esophagitis.
Initial management
Lifestyle modification
Suggestions that may improve symptoms include weight loss for obese patients, stopping smoking, frequent small meals, avoiding foods that are known to precipitate symptoms, avoiding eating for several hours before bedtime, and raising the head of the bed. However, evidence for improvement associated with these measuresis scarce.
Medical management
There are three pharmacological approaches to controlling symptoms of GERD: neutralization of acid (antacids and alginates), reduction in acid production (H2-receptor blockers, proton pump inhibitors) and increasing gastrointestinal motility (metoclopramide).
Step-up therapy
Most agents for initial therapy are available without prescription, and pharmacists offer the first-line management of GERD in a step-up regimen (starting from the simplest, most cost-effective agent).
Antacids and alginates
Antacids, such as bicarbonate, act by reducing the acidity within the stomach and lower esophagus. Alginate preparations (such as Gaviscon) act by coating the top of the gastric contents to reduce the effect of acid on the esophageal mucosa. Both these agents are effective, but the effects are often short-lived and suitable only for patients with mild symptoms.
H2-receptor antagonists
H2-receptor antagonists (e.g. cimetidine, ranitidine) block the H2-receptors in gastric mucosa, leading to a marked reduction in gastric acid production. Initial symptomatic relief is experienced in approximately 60%.
Step-down therapy
Patients who seek medical attention may already be on a combination of antacids, alginates and H2-receptor antagonists. Current consensus favours step-down therapy (starting with the most effective agent), as it is associated with greater symptomatic relief and fewer treatment failures and physician consultations.
Proton pump inhibitors
The proton pump inhibitors (e.g. omeprazole, lansoprazole) act by blocking the proton pump within the gastric mucosa, almost completely abolishing gastric acid production. Initial symptomatic relief is experienced in approximately 83%.6 An initial 2-4-week course is recommended followed by maintenance therapy. Failure to respond to initial therapy is an indication for further investigations (endoscopy, pH studies) to confirm and assess the severity of the disease.
Prokinetic agents
Due to the superiority of proton pump inhibitors, the role of prokinetic agents (metoclopramide) is ill defined. Prokinetic agents are usually reserved for use in combination with proton pump inhibitor for step-up therapy, or in combination with an H2-receptor blocker for long-term maintenance step-down therapy.
Maintenance therapy
After 6 months of initial therapy 75% of patients experience symptom relapse. A trial of withdrawal of drug therapy may be initiated but the majority will require maintenance therapy either by step-down treatment (long-term H2-receptor blocker) or intermittent on-demand proton pump inhibitor therapy, a 2-4-week course each time symptoms recur.
Surgical management
Before considering anti-reflux surgery, upper gastrointestinal endoscopy, 24-hour pH studies and esophageal manometry are required for confirmatory diagnosis and documentation of the presence and severity of reflux.
Anti-reflux surgery provides effective long-term treatment of GERD with symptomatic control equivalent to medical therapy but lower rates of esophagitis.10 The indications for surgery are failure of medical treatmentor development of complications (ulceration, strictures, Barrett's esophagus or respiratory complications). Relative indications include volume reflux (i.e. excessive volume rather than acid content) and patient preference.
Anti-reflux surgery has a 90% initial success rate. Complications of surgery include dysphagia (usually short-lived)in about 10%, inability to belch, the so-called 'gas bloat syndrome' (20%) and excessive flatus.
Nissen fundoplication
The most common operation is the Nissen (360 degree) fundoplication, which can be performed via an abdominal incision (midline laparotomy) or laparoscopically. The hiatus of the diaphragm is repaired, the lower esophagus is mobilized, then the greater curvature of the stomach via division of the short gastric arteries. The fundus of the stomach is wrapped completely around the lower esophagus.
To reduce the risk of dysphagia, various partial fundoplications have been described, including the anterior partial (Watson), posterior partial (Toupet) and Lind (270 degree) subtotal fundoplications.
Collis-Nissen procedure
This uncommon procedure is reserved for situations where the gastro-esophageal junction cannot be reduced below the diaphragm. An abdominal approach is used and a linear stapler is used to 'lengthen' the esophagus by incorporating the cardia of the stomach prior to creating the wrap.
Management of benign strictures
A barium swallow is often performed to delineate the site and extent of the stricture, followed by endoscopy and biopsies to determine the etiology. The treatment of benign strictures consists of bougie dilatation, and several sessions may be required for resistant strictures. Further treatment options include resection or bypass of the stricture and long-term intubation of the esophagus.
Following esophageal dilatation, the patient is keptnil by mouth if symptoms such as chest or back pain or surgical emphysema develop. A chest film is performed to exclude a pneumomediastinum, which will suggest esophageal perforation.
GERD is a chronic relapsing condition. Long-term studies report 10-year recurrence rates (based on use of anti-reflux medications) in 62% of surgically treated and 92% of medically treated patients. If Barrett's esophagus develops, regular endoscopic surveillance for dysplasia is required.

How common is Acid Reflux?
Population-based studies have reported that one third of Western populations experience the symptoms of GERD at least once a month, with 4% to 7% of the population experiencing daily symptoms. Judging from the high prevalence of heartburn in the general population, GERD is a very common condition. Most patients with mild symptoms carry out self-medication, whereas those with more severe and persistent symptoms seek out medical attention. Further, the prevalence and severity of GERD is likely increasing. This is in contrast to duodenal ulcer disease where the prevalence has markedly decreased. These trends may be in part related to the effects of Helicobacter pylori. The diagnosis of a columnar-lined esophagus is also increasing at a rapid rate, and deaths from end-stage benign esophageal disease are on an upward trend. These epidemiologic changes have occurred despite dramatic improvements in the efficacy of treatment options.
Studies on the natural history of GERD are rare. The few that do exist usually involve patients who were receiving some form of therapy. One of the most detailed studies on the natural history of the disease comes from Lausanne, Switzerland, where an intensive endoscopic follow-up of a defined population of 959 patients was performed over a 30-year period. The study involved only patients who had endoscopic esophagitis and did not include those who had symptoms without mucosal injury. It showed that in about 45% of patients esophagitis developed as an isolated episode and does not return while on acid suppression therapy. In the remaining patients esophagitis intermittently recurs on acid suppression therapy, and in 42% it progressed on therapy to more severe mucosal injury. This latter group makes up about 23% of the initial population of patients with esophagitis. The study also showed that 18% of the initial population acquired, while on therapy and within as short a period of 6 weeks, a columnar-lined lower esophagus with intestinal metaplasia.

Medications for Acid Reflux Relief
Medical Treatment of Gastroesophageal Reflux Disease
GERD is such a common condition that most sufferers with mild symptoms carry out self-medication. Sufferers when first seen with symptoms of heartburn without obvious complications can reasonably be placed on 8 to 12 weeks of simple antacids before extensive investigations are carried out. In many situations, this successfully aborts the attacks. Sufferers should be advised to elevate the head of the bed; avoid tight clothing; eat small, frequent meals; avoid eating their nighttime meal shortly before retiring; lose weight; and avoid alcohol, coffee, chocolate, and peppermints, which may aggravate the symptoms. Alginic acid, used in combination with simple antacids, may augment symptomatic relief by creating a physical barrier to reflux as well as by acid reduction. Alginic acid reacts with sodium bicarbonate in the presence of saliva to form a highly viscous solution that floats like a raft on the surface of the gastric contents. When reflux occurs, this protective layer is refluxed into the esophagus and acts as a protective barrier against the noxious gastric contents. Medications to promote gastric emptying, such as metoclopramide, domperidone, or cisapride, are beneficial in early disease but of little value in more severe disease. The mainstay of medical therapy is acid suppression. Sufferers with persistent symptoms should be given hydrogen potassium PPIs, such as omeprazole. In doses as high as 40 mg per day, they can effect an 80% to 90% reduction in gastric acidity. This usually heals mild esophagitis, but healing may occur in only three fourths of sufferers with severe esophagitis. It is important to realize that in sufferers who reflux a combination of gastric and duodenal juice, inadequate acid suppression therapy may give symptomatic improvement while still allowing mixed reflux to occur. This can result in an environment that allows persistent mucosal damage in an asymptomatic sufferer. Unfortunately, within 6 months of discontinuation of any form of medical therapy for GERD, 80% of sufferers have a recurrence of symptoms. In sufferers with reflux disease, esophageal acid exposure is reduced by up to 80% with H2-receptor antagonists and up to 95% with PPIs. Despite the superiority of the latter class of drug over the former, emerging evidence suggests that periods of acid breakthrough still occur. This occurs most commonly at nighttime and is some justification for a split rather than a single dosing regimen. Sufferers with breakthrough reflux symptoms were studied while on omeprazole 20 mg b.i.d. and found that many of them were still refluxing. Intragastric pH monitoring in 28 healthy volunteers and 17 sufferers with reflux disease revealed that nocturnal recovery of acid secretion (more than1 hour) occurred in 75% of the individuals. Recovery of acid secretion occurred within 12 hours of the oral evening dose of PPI, the median recovery time being 7.5 hours. This is particularly pertinent because it is during the nighttime and early morning that asthma symptoms are most pronounced and that peak expiratory flow rate is at its lowest. There have been also shown that ranitidine 300 mg at bedtime is superior to omeprazole 20 mg at bedtime in preventing acid breakthrough. it was speculated to be due to the abolition of histamine-mediated acid secretion in the fasting state. Sufferers presenting for the first time with symptoms suggestive of GE reflux may be given initial therapy with H2 blockers. In view of the availability of these as over-the-counter medication, many sufferers will have already self-medicated their symptoms. Failure of H2 blockers to control the symptoms or immediate return of symptoms after stopping treatment suggests that either the diagnosis is incorrect or the sufferers had relatively severe disease. Endoscopic examination at this stage of the sufferer's evaluation provides the opportunity for assessing the severity of mucosal damage and the presence of Barrett's esophagus. Both of these findings on initial endoscopy predict a high risk for medical failure. A measurement of the degree and pattern of esophageal exposure to gastric and duodenal juice, with 24-hour pH and bilirubin monitoring, should be obtained at this point. The status of the LES and the function of the esophageal body should also be measured. These studies identify features that predict a poor response to medical therapy, frequent relapses, and the development of complications and include supine reflux, poor esophageal contractility, erosive esophagitis or a columnar-lined esophagus at initial presentation, bile in the refluxate, and a structurally defective sphincter. Sufferers who have these risk factors should be given the option of surgery as a primary therapy with the expectation of long-term control of symptoms and complications.

Assessment of esophageal body and gastric function
The presence of poor esophageal body function can impact the likelihood of relief of regurgitation, dysphagia, and respiratory symptoms following surgery and may influence the decision to undertake a partial rather than a complete fundoplication. When peristalsis is absent or severely disordered, many would opt for a partial fundoplication, although recent studies would suggest a complete fundoplication may be appropriate even in this setting. The less favorable response of atypical, compared with typical, reflux symptoms after fundoplication may be related to persistent poor esophageal propulsive function and the continued regurgitation of esophageal contents.
The function of the esophageal body is assessed with esophageal manometry. This is performed with five pressure transducers located in the esophagus. To standardize the procedure the most proximal pressure transducer is located 1 cm below the well-defined cricopharyngeal sphincter. With this method a pressure response along the entire esophagus can be obtained during one swallow. The study consists of recording ten standard wet swallows with 5 mL of water. Amplitude, duration, and morphology of contractions following each swallow are all calculated at the five discrete levels within the esophageal body. The delay between onset or peak of esophageal contractions at the various levels of the esophagus is used to calculate the speed of wave propagation and represents the degree of peristaltic activity.
Esophageal disorders are frequently associated with abnormalities of duodenogastric function. Symptoms suggestive of gastroduodenal pathology include nausea, epigastric pain, anorexia, and early satiety. Abnormalities of gastric motility or increased gastric acid secretion can be responsible for increased esophageal exposure to gastric juice. If not identified before surgery, unrecognized gastric motility abnormalities are occasionally unmasked by an antireflux procedure, resulting in disabling postoperative symptoms. Considerable experience and judgment are necessary to identify the patient with occult gastroduodenal dysfunction. The surgeon should maintain a keen awareness of this possibility and investigate the stomach given any suggestion of problems. Tests of duodenogastric function that are helpful when investigating the patient with GE reflux include gastric emptying studies, gastric acid analysis, 24-hour gastric pH monitoring, and ambulatory bilirubin monitoring of the esophagus and stomach.
Poor gastric emptying or transit can provide for reflux of gastric contents into the distal esophagus. Standard gastric emptying studies are performed with radionuclide-labeled meals. They are often poorly standardized and difficult to interpret. Emptying of solids and liquids can be assessed simultaneously when both phases are marked with different tracers. After ingestion of a labeled standard meal, gamma camera images of the stomach are obtained at 5- to 15-minute intervals for 1.5 to 2 hours.
After correction for decay, the counts in the gastric area are plotted as percentage of total counts at the start of the imaging. The resulting emptying curve can be compared with data obtained in normal volunteers. In general, normal subjects will empty 59% of a meal within 90 minutes.

Radiographic evaluation
Radiographic assessment of the anatomy and function of the esophagus and stomach is one of the most important parts of the preoperative evaluation. Critical issues are assessed, including the presence of esophageal shortening, the size and reducibility of a hiatal hernia, and the propulsive function of the esophagus for both liquids and solids.
The definition of radiographic GE reflux varies depending on whether reflux is spontaneous or induced by various maneuvers. In only about 40% of patients with classic symptoms of GERD is spontaneous reflux observed by the radiologist (i.e., reflux of barium from the stomach into the esophagus with the patient in the upright position). In most patients who show spontaneous reflux on radiography, the diagnosis of increased esophageal acid exposure is confirmed by 24-hour esophageal pH monitoring. Therefore, the radiographic demonstration of spontaneous regurgitation of barium into the esophagus in the upright position is a reliable indicator that reflux is present. Failure to see this does not indicate the absence of disease.
A carefully performed video esophagram can provide an enormous amount of information on the structure and function of the esophagus and stomach. The modern barium swallow emphasizes motion-recording (video), utilizes a tightly controlled examination protocol, and requires an understanding of esophageal physiology.
Videotaping the study greatly aids the evaluation, providing the surgeon with a real-time assessment of swallowing function, bolus transport, and the size and reducibility of hiatal hernias. Given routine review before antireflux surgery, its value becomes increasingly clear. The study provides structural information including the presence of obstructing lesions and anatomic abnormalities of the foregut. A hiatal hernia is present in more than 80% of patients with GE reflux and is best demonstrated with the patient in the prone position, which causes increased abdominal pressure and promotes distention of the hernia above the diaphragm. The presence of a hiatal hernia is an important component of the underlying pathophysiology of GE reflux. Other relevant findings include a large (greater than 5 cm) or irreducible hernia, suggesting the presence of a shortened esophagus; a tight crural collar that inhibits barium transit into the stomach, suggesting a possible cause of dysphagia; and the presence of a paraesophageal hernia.
Lower esophageal narrowing resulting from a ring, stricture, or obstructing lesion is optimally viewed with full distention of the esophagogastric region. A full-column technique with distention of the esophageal wall can be used to discern extrinsic compression of the esophagus. Mucosal relief or double-contrast films should be obtained to enhance the detection of small esophageal neoplasms, mild esophagitis, and esophageal varices. The pharynx and upper esophageal sphincter are evaluated in the upright position, and an assessment of the relative timing and coordination of pharyngeal transit is possible.
The assessment of peristalsis on video esophagram often adds to, or complements, the information obtained by esophageal motility studies. This is in part because the video barium study can be done both upright and supine and with liquid and solid bolus material, which is not true of a stationary motility examination. This is particularly true with subtle motility abnormalities. During normal swallowing, a stripping wave (primary peristalsis) is generated that completely clears the bolus. Residual material can stimulate a secondary peristaltic wave, but usually a second pharyngeal swallow is required. Motility disorders with disorganized or simultaneous esophageal contractions have tertiary waves and provide a segmented appearance to the barium column, often referred to as beading or corkscrewing. In dysphagic patients, a barium-impregnated marshmallow, bread, or hamburger is a useful adjunct, which can discern a functional esophageal transport disturbance not evident on the liquid barium study. Reflux is not easily seen on video esophagram, and motility disorders that cause retrograde barium transport may be mistaken for reflux.
Assessment of the stomach and duodenum during the barium study is a necessity for proper preoperative evaluation of the patient with GERD. Evidence of gastric or duodenal ulcer, neoplasm, or poor gastroduodenal transit has obvious importance in the proper preoperative evaluation.

Assessment of esophageal length
Esophageal shortening is a consequence of scarring and fibrosis associated with repetitive esophageal injury. Anatomic shortening of the esophagus can compromise the ability to perform an adequate tension-free fundoplication and may result in an increased incidence of breakdown or thoracic displacement of the repair. Esophageal length is best assessed preoperatively using video roentgenographic contrast studies and endoscopic findings. Endoscopically, hernia size is measured as the difference between the diaphragmatic crura, identified by having the patient sniff, and the GE junction, identified as the loss of gastric rugal folds. We consider the possibility of a short esophagus in patients with strictures or those with large hiatal hernias (greater than 5 cm), particularly when the latter fail to reduce in the upright position on a video barium esophagram.
The definitive determination of esophageal shortening is made intraoperatively when, after thorough mobilization of the esophagus, the GE junction cannot be reduced below the diaphragmatic hiatus without undue tension on the esophageal body. Surgeons performing fundoplication have reported varying incidences of esophageal shortening, attesting to the judgment inherent in defining and recognizing undue tension. An advantage of transthoracic fundoplication is the ability to mobilize the esophagus extensively from the diaphragmatic hiatus to the aortic arch. With the GE junction marked with a suture, esophageal shortening is defined by an inability to position the repair beneath the diaphragm without tension. In this situation, a Collis gastroplasty coupled with either a partial or complete fundoplication may be performed.
Potential pitfalls of laparoscopic fundoplication include the elevation of the diaphragm due to pneumoperitoneum, potentially contributing to a false impression that esophageal length is adequate, and the limited ability to mobilize the esophagus relative to the transthoracic approach. In our experience, the failure to appreciate esophageal shortening is a major cause of fundoplication failure and is often the explanation for the slipped Nissen fundoplication. In many such instances, the initial repair is incorrectly constructed around the proximal tubularized stomach rather than the terminal esophagus. Surgeons opting to perform fundoplication laparoscopically in the setting of potential esophageal shortening must be vigilant of esophageal tension, technically facile at extensive mediastinal mobilization of the esophagus while preserving vagal integrity, and able to perform a laparoscopic or open transabdominal Collis gastroplasty should esophageal lengthening be necessary.

Twenty-four hour ambulatory pH monitoring
The most direct method of assessing the relationship between symptoms and GERD is to measure the esophageal exposure to gastric juice with an indwelling pH electrode. Miller first reported prolonged esophageal pH monitoring in 1964, although it was not until 1973 that its clinical applicability and advantages were demonstrated by Johnson and DeMeester. Ambulatory pH testing is considered by many to be the gold standard for the diagnosis of GERD, because it has the highest sensitivity and specificity of all tests currently available. Some experts have suggested that 24-hour pH monitoring be used selectively, limited to patients with atypical symptoms or no endoscopic evidence of GE reflux. Given present-day referral patterns, more than half of the patients referred for antireflux surgery will have no endoscopic evidence of mucosal injury. For these patients, 24-hour pH monitoring provides the only objective measure of the presence of pathologic esophageal acid exposure. Although it is true that most patients with typical symptoms and erosive esophagitis have a positive 24-hour pH result, the study provides other useful information. It quantifies the actual time that the esophageal mucosa is exposed to gastric juice, measures the ability of the esophagus to clear refluxed acid and correlates esophageal acid exposure with the patient's symptoms. It is the only way to quantitatively express the overall degree and pattern of esophageal acid exposure, both of which may impact the decision toward surgery. Patients with nocturnal or bipositional reflux have a higher prevalence of complications and failure of long-term medical control. For these reasons, we continue to advocate its routine use in clinical practice.
The units used to express esophageal exposure to gastric juice are (a) cumulative time the esophageal pH is below a chosen threshold, expressed as the percent of the total, upright, and supine monitored time; (b) frequency of reflux episodes below a chosen threshold, expressed as number of episodes per 24 hours; and (c) duration of the episodes, expressed as the number of episodes greater than 5 minutes per 24 hours and the time in minutes of the longest episode recorded. The upper limits of normal were established at the 95th percentile. Most centers use pH 4 as the threshold. Combining the result of the six components into one expression that reflects the overall esophageal acid exposure below a pH threshold, a pH score was calculated by using the standard deviation of the mean of each of the six components measured.

Endoscopic evaluation
Endoscopic visualization of the esophagus equates to the physical examination of the foregut and is a critical part of the preoperative evaluation of patients with GERD. Its main aim is to detect complications of GE reflux, the presence of which may influence therapeutic decisions.
In every patient, the locations of the diaphragmatic crura, the GE junction, and the squamocolumnar junction are determined. These anatomic landmarks are commonly at three different sites in patients with GERD. The crura are usually evident and can be confirmed by having the patient sniff during the examination. The anatomic GE junction is identified as the point where the gastric rugal folds meet the tubular esophagus and is often below the squamocolumnar junction, even in patients without otherwise obvious Barrett's esophagus.
Endoscopic esophagitis is defined by the presence of mucosal erosions . When present, the grade and length of esophageal mucosal injury are recorded. The presence and length of columnar epithelium extending above the anatomic GE junction is also noted. It is suspected at endoscopy when there is difficulty in visualizing the squamocolumnar junction at its normal location and by the appearance of a velvety red luxuriant mucosa. The presence of Barrett's esophagus is confirmed by biopsy evidence of specialized intestinal metaplasia and is considered histologic evidence of GERD. Endoscopic visualization of columnar lining without histologic confirmation of specialized intestinal metaplasia is not considered Barrett's esophagus and likely has no premalignant potential. Multiple biopsies should be taken in a cephalad direction to determine the level at which the junction of Barrett's epithelium and normal squamous mucosa occurs. Barrett's esophagus is susceptible to ulceration, bleeding, stricture formation, and malignant degeneration. Dysplasia is the earliest sign of malignant change. Because dysplastic changes typically occur in a random distribution within the distal esophagus, a minimum of four biopsies (each quadrant) every 2 cm should be obtained from the metaplastic epithelium. Particular attention must be paid to the squamocolumnar junction in these patients, where a mass, ulcer, nodularity, or inflammatory tissue is always considered suspicious for malignancy and requires thorough biopsy. The GE junction is defined endoscopically where the tubular esophagus meets gastric rugal folds, and the squamocolumnar junction is where there is an obvious change from the velvety and darker columnar epithelium to the lighter squamous epithelium.
After completion of the esophageal examination, the first and second portions of the duodenum and the stomach are systematically inspected. This is commonly done on withdrawal of the endoscope. When the antrum is visualized, the incisura angularis appears as a constant ridge on the lesser curve. Turning the lens of the scope 180 degrees allows inspection of the fundus and cardia. Attention is paid to the frenulum (angle of His) of the esophagogastric junction and to the closeness with which the cardia grips the scope. The appearance of this valve have been graded on a scale from I to IV according to the degree of unfolding or deterioration of the normal valve architecture. This grading system has been correlated with the presence of increased esophageal acid exposure, occurring predominantly in patients with a grade III or IV valve.
A hiatal hernia is endoscopically confirmed by finding a pouch lined with gastric rugal folds lying 2 cm or more above the margins of the diaphragmatic crura. A prominent sliding hernia is frequently associated with increased esophageal exposure to gastric juice. When a paraesophageal hernia exists, particular attention is given to exclude a gastric ulcer or gastritis within the pouch. The intragastric retroflex or J maneuver is important in evaluating the full circumference of the mucosal lining of the herniated stomach. As the endoscope is removed, the esophagus is again examined and biopsies taken. The location of the cricopharyngeus is identified and the larynx and vocal cords are visualized. Acid reflux may result in inflammation of the larynx. Vocal cord movement is recorded both as a reference for subsequent surgery and an assessment of the patient's ability to protect the airway.

Surgery for Acid Reflux Relief
Indications of Antireflux Surgery
Antireflux surgery is indicated for the treatment of objectively documented, relatively severe GERD. Candidates for surgery include not only patients with erosive esophagitis, stricture, and Barrett's esophagus but also those without severe mucosal injury who are dependent on PPIs for symptom relief. Patients with atypical or respiratory symptoms who have a good response to intensive medical treatment are also candidates. The option of antireflux surgery should be given to all patients who have demonstrated the need for long-term medical therapy, particularly if escalating doses of PPIs are needed to control symptoms. Antireflux surgery may be the preferred option in patients younger than 50 years, those who are noncompliant with their drug regimen, those for whom medications are a financial burden, and those who favor a single intervention over long-term drug treatment. It may be the treatment of choice in patients who are at high risk of progression despite medical therapy. Although this population is not well defined, risk factors that predict progressive disease and a poor response to medical therapy include (a) nocturnal reflux on 24-hour esophageal pH study, (b) a structurally deficient LES, (c) mixed reflux of gastric and duodenal juice, and (d) mucosal injury at presentation.
Preoperative Evaluation
Successful antireflux surgery is largely defined by two objectives: the achievement of long-term relief of reflux symptoms and the absence of complications or complaints after the operation. In practice, achieving these two deceptively simple goals is difficult. Both are critically dependent on establishing that the symptoms for which the operation is performed are the result of excess esophageal exposure to gastric juice, as well as the proper performance of the appropriate antireflux procedure. Success can be expected in the vast majority of patients if these two criteria are met. The status of the LES is not as important a factor as in the days of open surgery. Patients with normal resting sphincters are often selected for antireflux surgery in the era of laparoscopic fundoplication. The outcome is not dependent on sphincter function.
There are four important goals of the diagnostic approach to patients suspected of having GERD and being considered for antireflux surgery.
Objective Documentation
The introduction of laparoscopic access, coupled with the growing recognition that surgery is a safe and durable treatment for GERD, has dramatically increased the number of patients being referred for laparoscopic fundoplication. The threshold for surgical referral is such that increasing numbers of patients without endoscopic esophagitis or other objective evidence of the presence of reflux are now considered candidates for laparoscopic antireflux surgery. These facts combine to underscore the importance of selecting patients for surgery who are likely to have a successful outcome. Although a Nissen fundoplication will reliably and reproducibly halt the return of gastroduodenal juice into the esophagus, little benefit is likely if the patient's symptoms are not caused by this specific pathophysiologic derangement. Thus, in large part, the anticipated success rate of laparoscopic fundoplication is directly proportional to the degree of certainty that GERD is the underlying cause of the patient's complaints.
Three factors predictive of a successful outcome following antireflux surgery have emerged . These are (a) an abnormal score on 24-hour esophageal pH monitoring; (b) the presence of typical symptoms of GERD, namely heartburn or regurgitation; and (c) symptomatic improvement in response to acid suppression therapy prior to surgery. It is immediately evident that each of these factors helps to establish that GERD is indeed the cause of the patient's symptoms and that they have little to do with the severity of the disease.

Acid Reflux Symptoms
The most common complaints in patients with GERD are heartburn; regurgitation; and, occasionally, dysphagia or difficult swallowing. These represent the so-called typical symptoms of GERD. Although none of these are specific to GERD, the latter is more commonly a sign of serious underlying pathology, including esophageal carcinoma. Dysphagia should always be investigated promptly and thoroughly.
Heartburn is characterized as a substernal burning discomfort often radiating from epigastrium to sternal notch. Occasionally patients will refer to it as chest pain rather than heartburn, and the two can be difficult to distinguish. Even the location can be variable with patients occasionally experiencing discomfort in the epigastrium, base of the neck, back, or other areas. Heartburn is typically made worse by spicy foods such as tomato sauce, citrus juices, chocolate, coffee, and alcohol. It occurs 1 to 2 hours after eating, often at night and is relieved by antacids and antisecretory agents such as the over-the-counter histamine-2 blockers. It is well recognized that the severity of symptoms is not necessarily related to the severity of the underlying disease.
Regurgitation is the spontaneous return of gastric contents proximal to the GE junction. Its spontaneous nature distinguishes it from vomiting. The patient often gets a sensation that fluid or food is returning into the esophagus, even if it does not reach as high as the pharynx or mouth. It is typically worse at night in the recumbent position or when lying down after a meal. Patients commonly compensate by not eating late at night or by sleeping partially upright with several pillows or in a chair. This symptom is often less well relieved with antacids and antisecretory agents, although it may change in character from acid to a more bland nature.
Dysphagia is present in up to 40% of patients with GERD. It is generally manifested by a sensation of food hanging up in the lower esophagus (esophageal dysphagia) rather than difficulty transferring the bolus from the mouth to the esophageal inlet (oropharyngeal dysphagia). Classically dysphagia limited to only solid food, with normal passage of liquids, suggests a mechanical disorder such as a large hernia, stricture, or tumor, whereas difficulty with both solids and liquids suggest a functional or motor disorder. It often develops slowly enough that the patient may adjust his or her eating habits and not necessarily notice that it is happening. Thus, a thorough esophageal history includes an assessment of the patient's dietary history. Questions should be asked regarding the consistency of food that is typically eaten; whether the patient requires liquids with the meal; is the last to finish; has interrupted a social meal; chokes or vomits with eating; or whether he or she has been admitted on an emergency basis for food impaction. These assessments, in addition to the ability to maintain nutrition, help to quantify the dysphagia and are important in determining the indications for surgical therapy.
Many patients with GE reflux often manifest atypical symptoms, such as cough, asthma, hoarseness, and noncardiac chest pain. Atypical symptoms are the primary complaint in 20% to 25% of patients with GERD and are secondarily present in association with heartburn and regurgitation in many more. It is considerably more difficult to prove a cause-and-effect relationship between atypical symptoms and GE reflux than it is to do so for the typical symptoms. Consequently, the results of surgical therapy have been correspondingly less good. That is not to say that patients with atypical symptoms are not good candidates for antireflux surgery, because many will benefit greatly, but that in these patients it should be applied cautiously. Often a trial of high-dose proton pump inhibitors (PPIs) is helpful. Given atypical symptoms, the outcome of antireflux surgery is optimal in patients with a good response to medical treatment rather than in those who fail to respond.
The diagnosis of GERD based on symptoms alone is correct in only approximately two thirds of patients.20 This is because these symptoms are not specific for GE reflux and can be caused by other diseases such as achalasia, diffuse spasm, esophageal carcinoma, pyloric stenosis, cholelithiasis, gastritis, gastric or duodenal ulcer, and coronary artery disease. This fact underscores the need for objective diagnosis before the decision is made for surgical treatment.

What is ًthe Antireflux Barrier?
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.

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.

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.

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.

Prevacid for acid reflux relief
Prevacid is a Proton Pump Inhibitor, Proton Pump Inhibitors work directly on active acid pumps to significantly inhibit acid production. PPIs allow just enough acid to be produced for normal digestion of food. They can provide 24-hour treatment with each pill. Prevacid is commonly used for acid reflux relief.
The indications for Prevacid include: the treatment of heartburn and other symptoms of gastroesophageal reflux disease (GERD) and to assist the healing, symptom relief and maintenance of healed erosive esophagitis, a condition in which the lining of the esophagus has been damaged. Controlled studies for maintenance indications did not extend beyond 12 months. The most frequently reported adverse events include:
* Infrequent: dry mouth, insomnia, drowsiness, blurred vision, rash, pruritus
* Rare: taste disturbance, liver dysfunction, peripheral oedema, hypersensitivity reactions (including bronchospasm, urinary, angioedema, anaphylaxis), photosensitivity, fever, sweating, depression, interstitial nephritis, blood disorders (including leukopenia, leukocytosis, pancytopenia, thrombocytopenia), arthralgia, myalgia, skin reactions (including Stevens-Johnson syndrome, toxic epidermal necrolysis, bullous eruption)
* Severe: Gastro-intestinal disturbances (such as nausea, abdominal pain, and diarrhea.
Preparations: Capsules: 15 and 30 mg. Oral suspension: in 15 and 30 mg unit dose cartons of 30. Prevacid also is available in 15 and 30 mg tablets that disintegrate when placed under the tongue (Prevacid SoluTab). Prevacid is available for intravenous injection in vials containing 30 mg of powdered lansoprazole (30 mg/5 ml when mixed with sterile water).
Prevacid, like other proton-pump inhibitors, blocks the enzyme in the wall of the stomach that produces acid. By blocking the enzyme, the production of acid is decreased, and this allows the esophagus to heal resulting in acid reflux relief.
Dosing: For the treatment of GERD, the recommended initial treatment is 15 mg for up to 8 weeks. For maintaining healing (long-term) in GERD the recommended treatment is 15 mg daily. For initial treatment of severe(erosive) esophagitis, the recommended dose for adults is 30 mg daily for 4-8 weeks. It is recommended that capsules be taken before meals for maximum effect. Capsules should be swallowed whole and should not be crushed, split or chewed.

Prevacid for acid reflux relief in children:
Recurrent vomiting, stomach pain, coughing, wheezing and difficulty swallowing are all symptoms of pediatric GERD or gastroesophageal reflux disease.
If a child has GERD, Prevacid is the treatment that can help relieve the painful symptoms and heal the damage (sores, also called erosions) to the child's esophagus.
Treating kids GERD with Prevacid
Prevacid is the only medicine in its class approved for use in children with GERD (acid reflux disease) as young as 12 months of age. The same Prevacid has been used to treat millions of adults with GERD.
Prevacid is easy to take. Prevacid is taken once a day before a meal. If Prevacid is right for your child, your healthcare provider will tell you how much Prevacid your child should take each day and for how long it needs to be taken. Treatment with Prevacid usually lasts 8 or 12 weeks, depending on your child's age. If Prevacid is not taken every day as prescribed, it may not heal the damage to your child's esophagus.
There are lots of ways to give your child Prevacid. Children have different needs when it comes to taking medicine. That's why there are more ways for your child to take Prevacid than any other medicine like it. Prevacid® SoluTab™ (lansoprazole) is a strawberry-flavored tablet that melts in your child's mouth. No water, no messy spills—easy for them and easy for you!

Adrenergic drugs and acid reflux
The lower esophageal sphincter is a physiological sphincter acting like a valve. It is a ring of smooth muscle fibers at the junction of the esophagus and stomach.
As the stomach generates strong acids and enzymes to aid in food digestion; it is protected at the same time by virtue of its inner lining which has several mechanisms to resist the effect of gastric juice on itself. On the other hand the mucosa of the esophagus does not have these protective mechanisms. Fortunately the esophagus is normally protected from these acids by this one-way valve mechanism at its junction with the stomach i.e. lower esophageal sphincter (LES), which prevents gastric juice from flowing back into the esophagus.
During peristalsis, the LES allows the food bolus to pass into the stomach. It prevents chyme (a mixture of bolus, stomach acid, and digestive enzymes) from returning up the esophagus. The LES is aided in the task of keeping the flow of materials in one direction by external supportive muscle fibers derived from the diaphragm.
Contraction of smooth muscle fibers of the lower esophageal sphincter is controlled by many factors, of which the adrenergic receptors are of utmost importance.
A receptor is a molecule on the surface of the smooth muscle cell that recognizes and binds with specific molecules, producing some effect in the cell. The cell is called the effector as it performs the action dictated by a signal released following stimulation of the specified receptor.
The term adrenergic means having physiological effects similar to those of epinephrine, a hormone and neurotransmitter released at the nerve endings in contact with smooth muscle fibers.
Receptors are named after the action of epinephrine, the alternative name for adrenaline. Alpha receptors, which are stimulated by norepinephrine and blocked by agents such as phenoxybenzamine, produce contraction of the smooth muscles of the sphincter. Beta receptors, which are stimulated by epinephrine and blocked by agents such as propranolol, produce smooth muscle relaxation.
The term adrenergic is also used for drugs, which have effects similar to, or the same as, epinephrine (adrenaline). Adrenergic drugs that stimulate a response are called (agonists) and those that inhibit a response called (antagonists).
Accordingly, Alpha Adrenergic Agonists produce contraction of the lower esophageal sphincter and Beta Adrenergic Agonists are associated with relaxation of the sphincter and trigger reflux.
On the contrary, Alpha Adrenergic Antagonists produce sphincter relaxation and Beta Adrenergic Antagonists increase lower esophageal sphincter pressure.
Alpha blockers and beta-agonists are directly related to relaxation of the LES and acid reflux.
Alpha blockers ( alpha-adrenergic blocking agents) constitute a variety of drugs which block alpha-adrenergic receptors in arteries and smooth muscles.
These drugs may be used to treat:
benign prostatic hyperplasia (BPH)
high blood pressure (hypertension).
symptoms of non inflammatory chronic pelvic pain syndrome.
Examples include:
Doxazosin (Cardura)
Prazosin (Minipress)
Phentolamine (Regitine)
Tamsulosin (Flomaxtra/Flomax)
Alfuzosin (Uroxatral)
Terazosin (Hytrin)
Beta adrenergic receptor agonists are a class of drugs used to treat asthma and other pulmonary disease states.
They act on the beta-adrenergic receptor, thereby causing smooth muscle relaxation resulting in dilation of bronchial passages, vasodilation in muscle and liver, relaxation of uterine muscle and release of insulin. All beta agonists are available in inhaler form (either metered-dose inhalers, which aerosolize the drug, or dry powder which can be breathed in).
In addition, several of these medications are available in intravenous forms including both salbutamol and terbutaline. It can be used in this form in severe cases of asthma, but more commonly it is used to suppress premature labor because it also relaxes uterine muscle, thereby inhibiting contractions.
Examples include:
salbutamol (albuterol)
bitolterol mesylate
In patients with acid reflux disease, drug history should be reviewed to detect any of these drugs associated with sphincter relaxation. The physician, would evaluate the medical background and reconsider all medications given.

The role of saliva in acid reflux relief
What about chewing gums for acid reflux relief?
The importance of saliva in acid reflux relief can be predicted by considering a scenario where an individual is about to vomit. Vomit contains gastric substances which are extremely acidic and injurious. A protective reflex occurs before the individual prepares to vomit. Signals are sent from the brain to the salivary glands via the involuntary nervous system to cause increased saliva secretion, even before vomiting occurs. Thus, when vomiting does occur, there is already saliva available for acting to minimize the acidity and thus prevent tissue destruction.
Saliva is formed mainly in the major glands of the parotid, submandibular, and sublingual, as well as minor glands. The constituents of saliva are mediators of its various functions and effects in relation to acid reflux relief. As saliva is a viscous liquid mainly composed of water and containing mucin; one of its important functions is acting as a lubricant for the passage of food into the esophagus, moistening food and helping to create a food bolus, so it can be swallowed easily. Diminished salivary production deprives the swallowed food bolus of its water content and the lubricant effect of mucin, it would thus be irritating to the esophageal lining.
Saliva contains all the ions usually present in body fluids, and of these, bicarbonate ions which play a major role in determining the pH and buffering capacity of saliva. The primary salivary buffer is composed of bicarbonate (HCO3-). Bicarbonate is excreted through the duct system by means of an active transport mechanism. Salivary bicarbonate can help protect the esophgus against attack from refluxed acid produced by the stomach. This buffer system forms the first line of defense against acidic challenges, a salivary function of utmost importance in esophageal clearance and acid reflux relief.
Salivary responses to chewing and taste stimuli are innate. Salivary flow increases during eating. The physical action of chewing stimulates nerve endings in the tissues around the teeth. Flavorful substances stimulate taste buds. Both of these stimuli are potent initiators of salivary flow. Signals from nerve endings in the mouth evoke salivation by exciting the salivary centers in the brain stem. Salivary secretion is controlled by the autonomic nervous system. The importance of chewing and avoiding medications that affect the involuntary nervous system is thus quite clear for acid reflux relief. Smoking is also a known factor in the causation of dry mouth and should be stopped.
Secretion of the salivary glands is 1-1.5 liters daily. When salivary flow is too low, dry mouth (xerostomia) may result. Here, normal oral functions such as chewing and swallowing can be uncomfortable and difficult to perform and acid reflux is aggravated.
Emotional disturbances affect the rate of salivary secretion leading to xerostomia. A lowered rate of flow has been noted in patients suffering from depression. However, most xerostomia is due to medications used in the management of these problems. Again, these factors should be considered for proper management of acid reflux.

The role of Antacids in acid reflux relief
What about Tums for acid reflux relief?
Acid produced in the stomach is the main injurious factor inducing inflammation of the esophagus in acid reflux disease. Since Antacids are medicines that neutralize stomach acid, the refluxed contents would thus be free of the heartburn initiating component. Antacids have a rapid onset and short duration of action, and are most appropriate for rapid acid reflux relief for a short period of time. In contrast to H-2 receptor blockers and proton pump inhibitors which reduce acid production by the stomach, Antacids have no direct effect upon acid producing mechanisms. There are two types of Antacids: the first is sodium bicarbonate which chemically neutralizes the acid and is absorbable, accordingly its use is limited because of the associated systemic side effects. The second type is non-absorbable and acts by attracting acid molecules to its surface, consequently preventing their action, a process called adsorption. Calcium and magnesium salts are examples of the second group and are commonly used.
Acid rebound is a phenomenon encountered during the usage of antacids in which acid returns in greater concentration after the drug effect has stopped.
Another disadvantage of Antacids is that they interact with certain drugs and limit their simultaneous usage. They may also be associted with diarrhea and constipation.
Additional components of some formulations include dimethicone which reduces pain resulting from gaseous distention and alginic acid which, in combination with antacids, may help manage acid reflux.
Additional uses of non-absorbable Antacids include prevention of osteoporosis as the calcium salts would act as dietary supplement. Aluminum carbonate is also useful for binding phosphate, preventing the formation of urinary phosphate stones.
Antacids should be taken when gastric acidity is most likely to be increasing — namely, between one and three hours after each meal and at bedtime.
Examples of Antacids include:
* Aluminum hydroxide (Amphojel®, AlternaGEL®)
* Magnesium hydroxide (Phillips’® Milk of Magnesia)
* Aluminum hydroxide and magnesium hydroxide (Maalox®, Mylanta®)
* Aluminum carbonate gel (Basaljel®)
* Calcium carbonate (Alcalak®, Calcium Rich Rolaids®, Quick-Eze®, Rennie®, Titralac®, Tums®)
* Sodium bicarbonate (Bicarbonate of soda, Alka-Seltzer®)
* Hydrotalcite (Mg6Al2(CO3)(OH)16 · 4(H2O); Talcid®)
* Bismuth subsalicylate (Pepto-Bismol)
* Magaldrate + Simethicone (Pepsil)
Reduced stomach acidity may result in an impaired ability to digest and absorb certain nutrients, such as iron and the B vitamins. Since the normal acidity of the stomach normally kills ingested bacteria, Antacids increase the vulnerability to infection.

The role of H2 receptor blockers in acid reflux relief
Reflux of stomach contents into the esophagus is known to produce inflammatory changes in the esophageal lining. There are two components in that content responsible for such a damage. These are the hydrochloric acid and a biologically active substance called pepsin, an enzyme which digests protein. Both of acid and pepsin contribute to esophagitis. Inside the stomach acid is mainly produced to activate pepsin from a precursor known as pepsinogen. That reveals the dual effect of the stomach acid in relation to esophageal damage. The first effect being direct and the second indirect through the activation of pepsin which in turn irritates the esophagus.
It is well evident from the previous facts that reduction of acid production prevents damage of the esophageal lining. Acid is produced by cells lining the stomach known as parietal cells. These cells have chemical pumps called proton pumps which moves hydrogen ion from the inside of the parietal cell into the stomach lumen against a concentration gradient. Before this pumping activity the cell responds to signals initiating the process. These signals are: 1- Acetylcholine, a chemical substance released at the nerve endings supplying stomach glands, 2- Gastrin: a local hormone released from capillaries adjacent to stomach glands, and 3- Histamine: a biologically active chemical produced by specialized local cells in the stomach wall. These signals act upon specific sites in the membrane enclosing each parietal cell called receptors and each receptor is named after the name of stimulus which acts upon. Accordingly there are Aceylcholine, Gastrin and histamine receptors.
Acetylcholine is released through the various neurological mechanisms which follow food intake and its digestion. Gastrin is a local hormone produced by G cells located in the wall of the distal part of the stomach called the antrum in response to the chemical effect of digested proteins. Histamine is released mechanically by distention of the stomach and chemically by products of protein breakdown.
Theoretically speaking, we can block acid production by preventing the stimulatory effect of Acetylcholine, Gastrin and Histamine upon the parietal cells. Acetylcholine has well known antagonists but they have generalized effects as Acetylcholine is a universal neuro-transmitter. So far no Gastrin blocker is yet available. In 1964 the role of histamine as a parietal cell stimulant was discovered, however the use of traditional antihhistamine did not reduce acid secretion. That led scientists to postulate the existence of two histamine receptors, the one acted upon by traditional antihistamines (H1) and the other residing in parietal cell wall (H2).
H2-receptor antagonists have some similarity in structure to histamine, consequently they compete with its molecules and combine with receptors instead, of course they don't have the functional activity of histamine. Fortunately, this binding effect is simultaneously accompanied by a reduced stimulating effect of both Acetylcholine and Gastrin upon the parietal cell.
Examples of H2 receptor blockers include: Cimitedine (Tagamet),Ranitidine (Zantac), Nizatidine (Axid) and Famotidine (Pepcid).
They are equally effective, and the standard dose for mild to moderate acid reflux is: 400mg, 150mg, 150mg and 20mg respectively. This dosage is given twice daily for 6-12 weeks. Approximately 50% of patients with esophagitis heal on this regimen. However a high relapse rate of 50% has been reported within two months. Maintenance treatment is indicated in severe esophagitis associated with complications and if symptoms are relapsing immediately after treatment stops. The dosage may be given three times daily in some cases for proper relief of symptoms and healing of complications.
Generally speaking they are more effective than antacids but less effective than proton pump inhibitors.
Together with other measures for acid reflux relieve such as dietary control and lifestyle modifications, they have proven efficacy in mild to moderate symptoms. They are available as over the counter and prescription forms and have relatively lower cost.

Rule out heart disease even if acid reflux is diagnosed
There are two types of pain related to acid reflux:
1- The classical heartburn characteristic of acid reflux resulting from irritation of the esophageal surface lining.
2- The chest pain which is similar to that associated with coronary artery disease (coronary arteries are blood vessels supplying the heart with its essential requirements of oxygen and nutrients). This pain is due to spasm of the esophageal wall muscles.
It is evident that acid as a pain stimulus acts on surface receptors in case of heartburn. On the other hand it stimulates deeper receptors when causing chest pain and that suggests the pre-existence of breaks in the esophageal surface lining in the form of erosions or ulcers or an increase in the distance of spaces between cells lining the esophageal surface. Both of these mechanisms favor further acid diffusion deeper into the wall of the esophagus.
At times differentiation between esophageal and cardiac causes is very difficult.
In this situation the priority is for considering causes related to the heart first, simply because heart disease is serious and the chest pain may be a symptom of myocardial infarction which is an emergency condition following obstruction of coronary blood supply to the heart and resulting in impending death of a localized area of the musculture of the heart. That is why exclusion of heart disease is important to save life.
Needless to say that this rule applies especially to older patients with hypertension or diabetes or known heart disease.
Actually, both acid reflux and ischemic heart disease may co-exist as they are common health problems and that complicates the decision making process.
Out of all cases, having chest pain similar to typical heart attack, though their coronary arteries are normal, acid reflux contributes to 40-60% of the causes. This finding is documented by ambulatory esophageal acid monitoring.
To recall chest pain associated with heart disease (called angina) is a sense of fullness or tightness, dull aching or crushing in nature, in the middle of the chest. That pain may spread into the neck, shoulder or arm and is associated with difficulty in breathing and a cold sweat. On the other hand, chest pain of esophageal origin spreads more frequently to the back, is initiated by the same factors that trigger heartburn like fatty foods, lying down immediately after meals and is lasting for minutes or hours. Esophageal pain may also be associated with other symptoms of acid reflux such as heartburn, regurgitation and difficult swallowing. It is characteristically relieved with antacids. Diagnosis is confirmed with esophageal manometry which detects abnormalities in esophageal motility.
Chest pain of cardiac origin usually follows exertion and is relieved by rest. Nitrates and calcium channel blockers which are known to alleviate angina, aggravates pain of esophageal origin at the same time as they relaxes the lower esophageal sphincter.

How serious is Barrett's esophagus?
What do you mean by Barrett's esophagus?
Norman Barrett (1903–1979), a British surgeon at St Thomas' Hospital, first described specified changes in the appearance of the esophageal lining of patients with acid reflux disease in 1950. These changes are in the form of abnormal pink projections extending upwards into the esophagus from the stomach. They represent replacement of the normal cells lining the esophagus with another type of cells peculiar to the stomach or the intestine.
When the stomach contents reflux into the esophagus, its cellular lining is eroded. This damage mainly affects the superficial cells and the deep or basal germinative cells (stem cells) usually survive. In these cells a genetic switch causes them to generate new cells of specialized characteristics that differ from native esophageal cells. The new cells produce mucus and are more resistant to acid. They also differ in shape, being columnar instead of the spindle shaped esophageal cells. They also have some cells which are goblet shaped and are stuffed with mucus. This cellular pattern is similar to intestinal cells and is diagnostic of Barrett's esophagus.
About 10% of patients with acid reflux disease have Barrett's esophagus. It's usually diagnosed during endoscopy and has specific features.
The pink projections characteristic of Barrett's esophagus vary in length, some are short (less than 3cm) and others long (more than 3cm) having higher risk of developing intestinal metaplasia . Proper diagnosis is confirmed by taking a specimen of this abnormal tissue and examining it under the microscope.
The process of replacement of esophageal cells with intestinal tissue (transformation of native cellular pattern with normal tissue of another organ) is called Metaplasia.
Metaplasia usually progresses into Dysplasia, a change in individual cellular features. Abnormalities involve cellular architecture, intracellular infrastructure and nuclei. Cells usually vary in size and shape and their nuclei reveal profound changes. Dysplasia may be low-grade or high-grade and this variety is pre-cancerous, usually complicated with a type of cancer called Adenocarcinoma of the esophagus. About 10% of patients with Metaplasia change into Dysplasia, and 1% of patients with Barrett's esophagus will have the risk of developing cancer.
As Barrett-type intestinal metaplastic cells are under-developed, they don't have normal sensory nerve supply and patients used to suffer from heartburn may not experience it any more. Accordingly, sufferers reporting spontaneous relief of symptoms after a long standing heartburn should be managed with a high index of suspicion.
In Barrett's esophagus It's mandatory to monitor cellular changes frequently. If no Dysplasia is associated endoscopy should be performed every year. When Dysplasia is detected, the opinion of an experienced pathologist is essential to confirm the diagnosis and differentiate between low-grade and high-grade types. In low-grade Dysplasia endoscopy should be repeated every six months to detect any progression. In high-grade Dysplasia, if the patient is at high risk for surgery, endoscopic ablative procedures should be considered. In fit patients surgical excision of the esophagus is the preferred approach, the operation is called esophagectomy.
Photo-dynamic therapy is an endoscopic ablative procedure which involves injecting a photo-sensitizing material followed by delivering red laser light to sensitized cells. Consequently, cells containing the drug are destroyed.
Endoscopic mucosal resection is safer than surgery and involves excision of dysplastic tissue, it also has a diagnostic role as it submits an adequate specimen for proper diagnosis and determining the depth of invasion.

Extra-esophageal symptoms of acid reflux
There are two types of symptoms in acid reflux disease: esophageal and extra-esophageal (also called typical and atypical). We all know about heartburn the typical symptom of acid reflux, which is initiated by the direct injurious effect of acid upon the esophageal lining. Heartburn has been linked to the esophageal entity because it represents a characteristic subjective sensation resulting specifically from esophageal irritation.
So, what about extra-esophageal symptoms?
The term extra-esophageal sounds anatomically; meaning sites other than the esophagus.
Extra-esophageal sites include the larynx, the trachea, the bronchi and both lungs.
The pharynx is a common compartment, at which portals of entry into the esophageal tube and the respiratory tract are located.
At the junction between the esophagus and the pharynx there is a sphincter, the upper esophageal sphincter which opens only during swallowing to allow ingested food pass from the mouth into esophagus. That means it's contracted most of the time and by this function it serves two important actions, first it prevents swallowing of air in one direction and second prevents the incidentally refluxed acid from entering the pharynx in the other direction.
Whenever a disturbance in this activity is encountered due to a motility disorder for example; acid being refluxed into the pharynx, would be aspirated into the larynx.
The effects of pharyngeal irritation are usually experienced as sore throat. The situation is quite different in case of laryngeal irritation because the surface lining of the larynx is very sensitive. Such a characteristic feature of the larynx is meant to protect the respiratory tract from the inhalation of any foreign material. The immediate response is severe cough to expel any aspirated substance. This cough mechanism as a line of defense is endorsed by the contraction of the upper esophageal sphincter on one hand and the esophageal acid clearance mechanisms on the other hand. Repeated exposure of the larynx to chemical irritation associated with acid reflux results in inflammation of the larynx (laryngitis) with symptoms as hoarseness of voice, vocal fatigue and voice breaks. These direct effects would also be encountered when the trachea and bronchi are affected with similar inflammatory changes as they are in continuity with the larynx and are usually complained of as chronic cough. Sometimes the reflux is aspirated in small amounts into the lung (micro-aspirations) and is complicated with inflammation (pneumonia) which may progress to lung fibrosis. These serious complications usually cause difficulty in breathing (dyspnea).
That is all about how acid reflux causes extra-esophageal symptoms by a direct effect upon the respiratory tract, and as we have noticed is associated with evidence of direct chemical irritation in the form of inflammation. That does not conclude the effects as some well known extra-esophageal presentations such as bronchial spasm is not associated with any organic changes; neither irritation nor inflammation?.
Well, that is the other side of the story; acid reflux causes extra-esophageal symptoms by reflex actions. A reflex action is an automatic (involuntary) neuromuscular action elicited by a defined stimulus. To simplify, a reflex action includes: a receptor; a specialized sense organ located in a surface and an effector; muscle fibers located in a wall which automatically respond to an electric impulse generated by stimulation of the receptor and transmitted through nerve fibers to the effector's site. For example, a person stepping on a sharp object would initiate the reflex action through the creation of a stimulus, within receptors located in the skin tissue of the foot. The resulting stimulus would be transmitted through sensory neurons to the spinal cord. This stimulus is usually processed to create an immediate response by initiating a muscular response which is acted upon by muscles of the leg, retracting the foot away from the object. In our case the acid replaces the sharp object (stimulus), the esophageal surface lining replaces the skin tissue of the foot (receptor) and muscle fibers in the wall of the bronchi instead of muscles of the leg (effector). Accordingly asthma like symptoms in the form of wheezing and difficulty in breathing are scenarios of broncho-constriction, a reflex action induced by acid reflux.
Anatomically related sites which show other manifestations of reflux include: para-nasal sinuses and the middle ear, both of them are communicating with the pharynx either directly or indirectly. The effects are mostly related to direct irritation followed by inflammation in the form of sinusitis and otitis media respectively.
Dental changes are due to enamel erosion and a bad breath is a reflection of infection on top of upper respiratory tract inflammation.
Inflammatory changes just enumerated may also be complicated by ulcers, polyps or even cancer and these implicate frequent endoscopies.
Another fact is that acid reflux may present only with these extra-esophageal symptoms without the classical heartburn.
A therapeutic trial of proton pump inhibitors should be attempted twice daily and if no relief within 4-6 weeks acid monitoring should be considered along with the treatment.
Frequent aspirations and recurrent lung inflammations are indications for surgery.

How to achieve acid reflux relief without any medication?
Symptoms of acid reflux usually respond to dietary and lifestyle modifications. These changes in diet and lifestyle are meant to accomplish specific goals. The main guide to apply these measures is understanding the normal aspects of esophageal and stomach functioning in addition to the common causative mechanisms underlying acid reflux disease.
The following points will cover, in a process oriented action model, the reasons for most of the practices that should be adopted in the treatment of heartburn.
1- Assisting natural processes which promote acid clearance and stomach emptying
Increasing the production of saliva: saliva is produced by the salivary glands located around the mouth and have a high bicarbonate content and therefore an alkaline reaction. One of the functions of saliva is to neutralize the acid accidentally refluxed into the esophagus. Smoking and salty snacks reduce saliva and contribute to heartburn, they should therefore be avoided. At the same time, chewing gum should be encouraged as a good habit for heartburn sufferers who complain of dryness of the mouth.
Chewing thoroughly: mechanical degradation of food is an important preparatory step prior to digestion as it prepares food for further digestion in the stomach. Eating quickly is a bad habit that results in large food particles which imposes more work activity upon the stomach in the form of increased motility and increased acid production. It thus stays for a longer time in the stomach and delays its emptying. all these factors predispose to acid reflux and the habit of eating quickly should therefore be discouraged.
Small meals: a small meal would be digested easily with small amounts of acid and enzymes produced by the stomach. It is also cleared rapidly and does not increase pressure inside the stomach, consequently favorable circumstances for reflux are minimized. On the other hand a large meal is associated with increased production of acid, increased pressure and distension and delayed emptying of the stomach. all these factors initiate reflux and large meals should be avoided.
Drinking water: water dilutes and washes acid refluxed into the esophagus and promotes its clearance. At the same time it accelerates stomach emptying and prevents reflux. Drinking water should thus be encouraged before and after meals.
Pro-gravity postures: the erect posture favors movement of refluxed acid back into the stomach by the effect of gravity. On the contrary lying down is an anti-gravity posture, this fact should be considered together with our knowledge of the location of the esophagus, mainly within the chest (with negative pressure) and the location of the stomach, inside the abdomen (with positive pressure) these factors favor flow towards the esophagus and hinders esophageal clearance. Another factor related to posture is the increased tone of muscles supporting the lower esophageal sphincter in the upright position, this support is abolished when lying down as these muscles relax. Practically speaking recumbency should be avoided for at least 3 hours after eating, one should not go to bed immediately after meals and in heartburn sufferers the head of the bed should be elevated about 6 inches to prevent reflux.
Increasing lower esophageal sphincter pressure: from the functional point of view, high protein diet stimulates gastrin production, a local hormone that increases the sphincteric pressure and prevents reflux. Anatomically, a healthy physical built maintains an optimum tone in the muscles supporting the lower esophageal sphincter. It's well known that obesity weakens body musculature and reduces its contractility. Accordingly, we should maintain a desirable body weight and a low-calorie diet can be used to promote weight loss if needed. a high protein diet is also recommended.
Promoting stomach emptying: an important function regulating pressure inside the stomach and the amount of acid produced. Whenever emptying is delayed significantly food, acid and enzymes accumulate inside the stomach resulting in increased pressure and distention in addition to increased acid volume. The rate of stomach emptying is proportional to the rate of completion of digestion of a certain amount of food. Accordingly, when the digestive load is increased as following a heavy meal or swallowing large food particles or particularly when the meal is mostly composed of fat, a longer time is needed for digestion and consequently emptying is delayed. Drinking water also promotes stomach emptying. The role of having small meals, chewing thoroughly, low fat diet and drinking water before and after meals should be overstressed.
2- Eliminating factors that initiate reflux into esophagus
Direct irritation of the surface lining the esophageal lumen: avoid citrus,onions, spices and acids from tomatoes
Increased relaxation of the lower esophageal sphincter: avoid eating foods and drinking beverages that reduce sphincter pressure such as:
Caffeinated, carbonated or alcoholic beverages
Citrus-based juices
Food ingredients:
Vinegar, spices, garlic, onion, tomato-based products and peppermint
Vegetables: raw onion and tomatoes
Citrus fruits: orange, lemon, grapefruit
Fatty meals: salad dressing and fried food
Dairy products: sour cream, milk shake, ice cream and cottage cheese
Sweets and desserts: chocolate and potato chips
Medications: avoid medications that lower sphincteric pressure such as: Theophylline, Anticholinergics, Progesterone, Calcium channel blockers, Alpha adrenergic antagonists, Diazepam and Meperidine.
Increased acid production: avoid heavy meals, spices and alcohol.
Increased pressure inside the stomach: avoid practices associated with increasing pressure. These originate either from within the stomach (internal) or from the outside (external). Internal pressures are generated following delayed gastric emptying associated with heavy meals with high fat content or secondary to obstruction of the stomach outlet.
External pressures are mostly due to compressive forces associated with practicing exercise following meals especially vigorous exercise with bending movements. Tight clothing also exerts external compression upon the stomach and heartburn sufferers should wear loose-fitting clothing. Obesity is also considered a compressive factor as it increases the bulk of viscera inside the abdomen and weight loss should be encouraged.
To summarize, the best measures for acid reflux relief are:
Understanding normal functions of the esophagus and stomach.
Enhancing normal functional mechanisms.
Avoiding foods, medications, and lifestyle practices which disturb normal functions and cause acid reflux.

A special advice on fatty meals for acid reflux relief
Why fatty meals out of all foods that cause acid reflux?
Fatty meals are considered the most aggravating foods that can cause or worsen heartburn. They are widely used as an additive ingredient or a frying medium in the cooking process of most meals. They also make food more palatable, having a special flavor. Fats in addition are a common constituent of delicious milk products as ice cream and favorable sweets like dough-nut which we all like.
Their contribution to acid reflux is multi-factorial. They are known to lower resting pressures of the lower esophageal sphincter and cause its relaxation resulting in acid reflux. Fatty foods release enterogastrone, a local hormone that inhibits motility of the stomach, consequently food stays longer and pressure builds up inside the stomach with the increased possibility of reflux. As they keep food longer, it stimulates the production of more acid and digestive enzymes.
People, used to consume large amounts of fat are also obese and that adds more to the risk.
So how to reduce fat in our meals?
1- Choosing the source of protein: fish and poultry should be the preferred proteins of animal source and dry beans or peas the source of plant proteins. Don't forget to remove poultry's skin before cooking.
2- Choosing the way of cooking: boiling and broiling instead of frying.
3- Choosing low fat versions: skimmed milk instead of whole milk
Avoid ground beef, chicken nuggets, buffalo wings, smashed potato, french fries, cottage cheese and corn chips.
Make up your mind and relieve your heartburn.

Achieving acid reflux relief with surgery
The frequency of heartburn is the main factor that should be considered in determining the best treatment. Heartburn may be infrequent, frequent or persistent. Infrequent bouts usually respond to lifestyle modifications and traditional OTC medications. Frequent heartburn is mostly relieved with proton pump inhibitors. On the other hand when heartburn is persistent the situation is different as it is considered a warning sign of acid reflux disease.
In view of the fact that the natural history of esophageal damage caused by acid reflux can involve rare and serious consequences, other treatment options should be seriously considered. Actually, surgery is being reserved for those who can develop serious complications.
But how can we select those who are more susceptible to complications?
1- By documenting the presence of visible changes in the appearance of the surface lining the esophagus.
2- By documenting that the cause of these changes is mostly attributable to acid reflux.
3- By documenting the association of lower esophageal sphincter motility functional disturbance.
These would be translated into Endoscopy, 24-hour esophageal acid monitoring and esophageal manometry respectively.
The aim of these procedures is to confirm the cause- effect relationship in the heartburn sufferer, and together with failure of medications to relieve symptoms (as revealed by the need for continuous drug treatment or of increasing doses of medication) would be an indication for surgery. Other factors related to failure of medical treatment include: non compliance with drug therapy, the financial burden of medications and the preference for surgery especially in young patients.
The purpose of surgery is to ensure the intra-abdominal location of the lower esophageal segment which has the lower esophageal sphincter at its lower end. That would keep it positioned where a positive (intra-abdominal) pressure is maintained.
The diaphragmatic opening through which the lower esophagus passes is also narrowed and the top part of the stomach (called fundus) is wrapped around the lower esophagus and sutured to itself to tighten lower esophageal end.
This operation is called Nissen Fundoplication and is considered the most effective and proven procedure.
Recently, innovative techniques have allowed surgeons to perform this operation laparoscopically. It takes about 90 minutes and improves symptoms in 90% of patients. The operation may reverse damage caused by acid reflux disease and patients may be able to stop medications completely. However, it has been reported that after 5 years some patients would require proton pump inhibitors to control symptoms.
The operation may also be associated with some complications as difficulty in swallowing, inability to vomit and failure to completely relieve reflux symptoms.
Patient selection is the key to effectiveness of this operation and should mainly be indicated on the basis of patient preference.
If Hiatal Hernia or frequent pulmonary aspiration is associated with acid reflux disease they add more indications for the operation and results are much improved.
Always consult your physician to determine if surgery is an appropriate option for you.

Mechanisms of acid reflux
The central mechanism in acid reflux disease is disturbed acid clearance. Acid is produced in the stomach, and as long as its rate of clearance from the stomach into the small intestine is normal, it will not accumulate in the stomach and reflux into the esophagus. An example of a disorder that hinders clearance of acid from the stomach is obstruction of its outlet resulting in an increased pressure inside the stomach.At certain circumstances during daily activities some acid may normally regurgitate from the stomach into the esophagus. Again acid clearance back into the stomach is accomplished by gravity and the esophageal propulsive movement towards the stomach. Accordingly any disturbance of esophageal motility would affect its acid clearance mechanism.Role of the lower esophageal sphincter:The sphincter is anatomically configured and functionally organized to act like a valve allowing one way movement of swallowed substances from the esophagus into the stomach. anatomical disturbances such as Hiatal Hernia and functional disorders as incompetence or transient relaxation would favor acid reflux.These are the main primary factors involved in causation and are mostly electromechanical.Secondary factors actually operate after reflux and are meant to prevent esophagitis. They are mainly chemical and include saliva and the bicarbonate content of the glandular secretions on the inner surface of the esophagus.All these factors should be well investigated when acid reflux relief is considered.

Acid reflux relief prevents complications
Why should you treat heartburn?The goal of treatment is not only to relieve the symptom of heartburn. Of course symptomatic treatment would be all that is needed when heartburn is not associated with acid reflux disease. That means in the functional stage or when there is acid reflux alone.When the disease develops (the organic stage) with changes of esophagitis diagnosed by the physician, the aim is to heal or cure these changes simply because all the complications of acid reflux disease are a sequel of untreated esophagitis. To avoid such complications as ulcers, strictures, Barrett's esophagus or even cancer you should start treatment. The use of proton pump inhibitors for example reduces acid production and promote healing of esophagitis since acid is its main causative factor.

The role of Proton Pump Inhibitors in acid reflux relief
What are proton pump inhibitors?A pump is a utility that moves a substance against a gradient.A well known example is the water pump which lifts water up against gravity.In our case, there are cells in the membrane lining the stomach lumen, these cells produce acid and pump it against the concentration gradient set by the previously formed acid into the stomach lumen.That means the concentration of acid in the stomach lumen is higher than that inside the cell and this gradient would favor movement of acid into the cell; however the cellular wall prevents this and at the same time pumps more acid into the lumen.Just like the water pump needs electric enrgy to lift water upwards; the cellular wall utilizes chemical energy to pump acid outwards.Acid is produced in the form of a positively charged subatomic particle called proton. The proton is the nucleus of the lightest chemical element, hydrogen. Actually the hydrogen atom consists of a proton as the nucleus, to which a negatively charged single electron is bound as opposite charges attract. Because the proton is 1836 times heavier than the electron, the proton is considered to constitute almost the entire mass of the hydrogen atom.So how proton pump inhibitors affect this mechanism?They accumulate on the luminal surface of the acid producing cells and inhibit the enzymes involved in the process of synthesis of chemical energy , essential for the pumping action.Consequently; no energy, no pump activity and no acid production (no proton flow into the lumen of the stomach).The above figure illustrates this cellular mechanism and also shows the receptor sites at which signals triggering acid secretion interact. These triggers are Histamine, Gastrin and Acetylcholine. They are chemical substances delivered around acid producing cells and are released from local cells, intestinal cells or nerve endings.The above figure also demonstrates how the acid pump is blocked and acid production consequently inhibited.Examples of Proton Pump Inhibitors:Omeprazole (Prilosec)Lansoprazole (Prevacid)Rabeprazole (Aciphex)Pantaprazole (Protonix)Esomeprazole (Nexium)Proton Pump Inhibitors are used for both diagnosis and treatment. In the Omeprazole test: a dose of 40mg is given in the morning and another 20mg in the evening for 7days to a heartburn sufferer. If symptoms are relieved following this regimen, the diagnosis of acid reflux is confirmed. It is considered a noninvasive and easily available test with reasonable cost.For acid reflux relief, they are considered the most effective agents and the standard medical therapy. All of them are effective but response may vary from patient to patient.Proper timing of intake is critical for efficacy, it should be 30minutes before breakfast or other large meal. For some patients with partial response or severe symptoms, the physician may advice a second additional dose before the evening meal. Being long acting (duration of action of a single dose is 24hours), they allow time for damaged tissues to heal. They have a healing rate of 80% in moderate to severe cases and relief of symptoms in up to 90% of patients. In comparison to Histamine type2 receptor antagonists, they are more effective and faster in promoting healing.

What relieves symptoms of acid reflux?
Short term relief of acid reflux symptoms is easy. The problem is that the disease relapses, and many sufferers will require long term management.There are general considerations that should be applied. These include: reducing acid, enhancing esophageal clearance and correcting anatomical or physiological defects.Antacids are used for short term relieve only. H2 blockers are also effective. Proton pump inhibitors have become the mainstay in acid reflux treatment. They could be used effectively for continuous therapy in complicated cases.Enhancing clearance and promoting mucosal defense could be attempted by such drugs as: Prokinetics, Alginates, Antacids and Mucosal protectants. These trials are practically not convincing.Correcting anatomical or physiological defects as Hiatal Henia and lower esophageal sphincter incompetence should be considered following diagnosis of these problems. The commonly used operation is Fundoplication. The hernia is reduced, the normal position of the sphincter is restored and consequently lower esophageal sphincter competence is reinforced. However, some complications may follow this operation such as difficulty in swallowing and inability to belch or vomit. The results would be much better with good selection of patients.

Acid reflux and bronchial asthma
Is there any relationship between heartburn and asthma?Bronchial asthma may cause acid reflux disease and heartburn:Mechanically by air trapping associated with bronchial asthma which results in flattening of the diaphragm. As the lower esophageal sphincter is surrounded by diaphragmatic muscle fibers, their weakened support increases relaxation of the sphincter and promotes reflux.Chemically by drugs commonly used for treatment of asthma:Theophylline increases gastric secretion and relaxes sphincterAlbuterol also relaxes lower esophageal sphincter.On the other hand, Acid reflux may cause bronchial asthma:Reflux may induce reflex bronchial spasmAcid may be aspirated in minimal amounts and initiate broncho-constrictionInflammation of the upper respiratory tract associated with reflux releases chemical substances which mediate bronchospasm.About 75% of patients with asthma have acid reflux disease. Reflux symptoms usually precede attacks of wheezy chest. Asthma is also initiated by the same dietary and lifestyle factors which trigger acid reflux symptoms. There is a good response to proton pump inhibitors given twice daily and treatment should continue for at least two months.

Progress of acid reflux disease
Untreated acid reflux is a progressive disease. Early stages characterized by episodes of heartburn are not associated with any signs of damage. later on signs of inflammation of the esophagus (esophagitis) are evident.Barrett's esophagus is a warning sign because it is considered a precancrous stage. To understand Barrett we should recall the normal cellular lining of the esophageal lumen which is a specialized type with characteristic number, shape and cell arrangement. This particular type is partly replaced by a cellular pattern characteristic of intestinal lining membrane. Such a cellular modification is a sort of adaptation to damage induced by acid reflux.Later on acid reflux disease may be complicated by malignant transformation or cancer on top of Barrett's esophagus called Adenocarcinoma.To summarize:Acid reflux: only symptoms(e.g heart burn).Acid reflux disease: evidence of esophageal damage.Complicated reflux disease: Barret's esophagus which may result in cancer.

Lifestyle changes can prevent reflux
It is well known that modifying lifestyle would reduce symptoms of acid reflux disease. The main effect is accomplished by minimizing exposure to factors that interfere with the normal function of the lower esophageal sphincter. Meals should be taken at least two hours before bed time to prevent regurgitation of stomach acids into the esophagus. Avoiding exercise immediately after meals would prevent generating forces that increases stomach pressure, also exercise would be associated with kinking of the full stomach. Obesity is another important factor and the heartburn sufferer should be encouraged to maintain a healthy body weight. Tight clothing, by squeezing the stomach would induce reflux of its contents into the esophagus and should be avoided. Reflux is usually experienced during sleep, and elevating the head of the bed will allow gravity to do its job. Stress has long been linked to aggravating reflux symptoms through many mechanisms. In an effort to cope with disruption in routine, caused by stress, unhealthy lifestyles become evident. Stress also depresses immunity state and predisposes to complications in acid reflux disease. It should therefore be alleviated by all means.

Esophageal defenses against reflux
With all these normal daily activities that would trigger regurgitation, the esophagus seems to be highly exposed to reflux?Actually the esophagus has many defenses against acid reflux and its consequences. Anatomical barriers in the form of muscles inside and outside(diaphragmatic) the wall of the esophagus enforce its lower sphincter to prevent reflux. Acid clearance from the lumen of the esophagus is mechanically assisted by gravity and its propulsive movement towards the stomach. Acid is chemically antagonized by saliva and the esophageal gland secretion.The third mechanism against reflux is tissue resistance. It includes the bicarbonate content of the glandular secretions on the surface of the esophagus; the tight junctions between cells lining its lumen and the normal blood flow in the wall of the esophagus.These defenses would be efficient only in cases of mild infrequent reflux.

About heartburn
What is heartburn?When acidic stomach juices flow backward into the esophagus a burning discomfort is felt in the mid-chest, behind the breastbone. This is the mechanism of causation of heartburn.But why acid flows backward?The esophagus is a tube-like structure that connects the pharynx to the stomach and acts as a passage way for food. This flow is normally uni-directional towards the stomach and the esophagus by virtue of its lower sphincter prevents backflow.The lower esophageal sphincter acts like a valve that keeps acid in the stomach and out of the esophagus. If the normally contracted muscle relaxes the stomach acid flows backward into the esophagus.So what are the causes of relaxation of the lower esophageal sphincter?Some medications and food are responsible, these include: chocolate, caffeine, fatty or spicy food, onions, mint and alcohol. Acidic foods and vegetables are also considered.Acid reflux relief could thus be prevented by avoiding such medications and food that relax the lower esophageal sphincter.

Preventive measures for acid reflux relief: avoid smoking
Why does smoking aggravates acid reflux symptoms?Smoking reduces the production of saliva which neutralizes acid, at the same time it increases acid secretion, in addition to these factors related to acid; smoking would increase relaxation of the lower esophageal sphincter.

Causes of acid reflux
What are the causes of acid reflux?
There are individual variations but common mechanisms include:
The relaxation of the lower esophageal sphincter
Increasing the amount of acid produced by the stomach
Increasing the stomach pressure
Making the esophagus more sensitive to the irritating effect of stomach acid.
Acid reflux relief deals with all these causes attempting to correct them.

Heartburn vs GERD
What is the difference between heartburn and GERD?
Heartburn is a symptom (an unpleasant sensation experienced by a patient)
GERD on the other hand is a disease with changes in function and/or appearance of the esophagus.
G: Gastro (related to the stomach); E: Esophageal; R: Reflux and D: Disease.

Acid reflux disease in pregnancy
Why acid reflux is common in pregnancy?
During pregnancy there is an increased level of progesterone (a hormone produced by the ovaries); this hormone increases relaxation of the lower esophageal sphincter. Also the growth of a baby inside the womb increases pressure upon the stomach. This pressure in turn induces regurgitation of acid into the esophagus. Such a mechanical effect is of course commonest during the third trimester.

Preventive measures for acid reflux relief: avoid alcohol
Why does alcohol increase acid reflux?
Alcohol would augment acid production and increase sensitivity of the esophagus to acid.
In addition it increases relaxation of the lower esophageal sphincter and disturbs motility of the esophagus.

Acid production in the stomach
But acid is normally produced in the stomach without heartburn?
Yes; the stomach is full of acid; but is built to handle it and is protected by a specialized barrier of mucus and cell wall. The esophagus on the other hand is not well protected from the injurious effect of acid and results in a burning sensation when acid regurgitates into the esophagus.

Constituents of the reflux
With all these normal daily activities that would trigger regurgitation, the esophagus seems to be highly exposed to reflux?
Actually the esophagus has many defenses against acid reflux and its consequences. Anatomical barriers in the form of muscles inside and outside(diaphragmatic) the wall of the esophagus enforce its lower sphincter to prevent reflux. Acid clearance from the lumen of the esophagus is mechanically assisted by gravity and its propulsive movement towards the stomach. Acid is chemically antagonized by saliva and the esophageal gland secretion.
The third mechanism against reflux is tissue resistance. It includes the bicarbonate content of the glandular secretions on the surface of the esophagus; the tight junctions between cells lining its lumen and the normal blood flow in the wall of the esophagus.
These defenses would be efficient only in cases of mild infrequent reflux.