What is acid reflux?

Acid Reflux Causes

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Pathogenesis.
The extent and severity of esophageal injury due to GER depend on the frequency and the duration of esophageal exposure to the refluxed material, the volume and potency of gastric juice available for reflux, and the ability of the esophageal mucosa to withstand injury and to repair itself.
The pathogenesis of reflux esophagitis or GERD is a multifactorial process. The following factors all contribute to the development of GERD:
Antireflux mechanisms. A positive pressure gradient exists between the abdomen and the thorax. If there were no physiologic barrier at the area of the gastroesophageal junction, GER would occur continuously, especially with increases in intraabdominal pressure or changes in gravitational position and during events associated with abdominal muscle contraction, such as coughing, sneezing, straining, bending, turning in bed, and exercise. The antireflux barrier can be divided into two categories.
Anatomic factors extrinsic to the lower esophageal sphincter (LES) that augment the LES to prevent GER include a distal esophageal mucosal flap, the acute esophagogastric angle, compression of the esophagogastric junction by gastric sling fibers, the diaphragmatic crus acting as pinchcock, a hiatal tunnel, the sling action of the right diaphragmatic crus, and the intraabdominal junction of the esophagus. The longer the intraabdominal segment, the less likely reflux is to occur.
The presence of hiatal hernia with loss of the abdominal esophageal segment supported by the diaphragm and the normal acute esophagogastric angle may lead to GER. However, a direct causal relationship has not been found between hiatal hernia and GER. Nevertheless, a hiatal hernia generally (90%) accompanies reflux esophagitis. It is possible that hiatal hernia enhances the likelihood of LES dysfunction due to the loss of angulation at the esophagogastric junction and the direct transmission of intragastric pressure to the infrathoracic LES. Also, the hiatal hernia may act as a reservoir of refluxate and impair esophageal clearance in the recumbent position, thus promoting esophageal injury.
The closure strength and efficacy of LES
LES corresponds to the 2- to 4-cm zone of asymmetrically thickened smooth muscle at the esophagogastric junction.
LES maintains a high-pressure tone during resting conditions and relaxes with swallowing, esophageal distention, and vagal stimulation. These properties are independent of the diaphragm and persist even when the LES is in the thorax, as in patients with hiatal hernia.
LES is innervated by both excitatory and inhibitory autonomic nerves carried in the vagi to the esophageal plexuses. The major function of the LES inhibitory nerves is to mediate sphincter relaxation in response to swallowing.
LES pressure (LESP) is controlled by neural (most likely cholinergic), hormonal, and myogenic factors.
Resting LES pressure is not constant and varies from minute to minute in the awake state. During sleep, this variability is diminished.
The intrinsic tone (the resting LESP) is one of the major factors that prevent spontaneous GER.
In general, patients with GER have lower LESPs than controls. A minimum resting LESP in the range of 6 to 10 mm Hg prevents GER even during transient increases in intraabdominal pressure.
Changes in resting LES pressure occur throughout the day, especially during the postprandial period. In addition, transient episodes of LES relaxation occur not only in response to swallowing but also spontaneously, a process referred to as inappropriate LES relaxation or transient LES relaxation (TLESR). In physiologic refluxers, most reflux events occur during the relaxation events. In pathologic refluxers (i.e., patients with reflux disease), other mechanisms of reflux also occur, including gradual decreases in resting pressure and episodes of increased intragastric pressure. However, most reflux events continue to occur during TLESR.
TLESR appears to represent a physiologic response to increased gastric distention to relieve intragastric pressure.
Some GER occurs in all individuals with normal or lower-than-normal LESP throughout the day. The frequency of GER increases for 2 hours postprandially. However, patients with esophagitis have significantly more and longer episodes of GER than controls.
Low resting LESP seen in patients with esophagitis may be primary or secondary to injury from reflux and inflammation.
LESP is affected by various drugs and hormones. Avoidance of agents that decrease the LESP and use of agents that increase LESP can be helpful in diminishing GER symptoms and esophageal damage.

Gastric factors
Gastric volume
The occurrence of GER depends on an available reservoir of gastric fluid.
The probability and rate of GER are related to gastric volume.
The rate of reflux and the volume of the refluxate increase with incremental increases in gastric volume, intragastric pressure, and the pressure gradient between the stomach and the esophagus.
Gastric volume is determined by several factors.
Volume and composition of ingested materials.
Rate and volume of gastric secretion.
Rate and efficiency of gastric emptying.
Frequency and volume of duodenogastric reflux.
One or more of the factors in d that favor an increase in gastric volume also favor the occurrence of GER.
Pyloric channel or duodenal ulcers may result in delayed gastric emptying and predispose to increased GER and GERD.
Delayed gastric emptying due to neuromuscular abnormalities such as in collagen vascular diseases, diabetes mellitus, and hypothyroidism or mechanical gastric outlet obstruction may also predispose to GERD.

Irritant potency of the refluxed material
The composition of the material refluxed into the esophagus is important in determining the nature and extent of esophageal injury.
Gastric acid causes esophageal injury by protein denaturation and back diffusion of hydrogen ion into deeper layers of the esophageal wall to cause deeper injury.
Pepsin, a protease, digests esophageal epithelial intercellular substance, causing shedding of epithelial cells.
Duodenogastric reflux, especially postprandially, introduces bile salts and pancreatic enzymes into the stomach, which may then reflux into the esophagus. Bile salts may result in micellar dissolution of the lipids in the esophageal epithelial cell membranes and increase the permeability of the esophageal mucosa to hydrogen ion back diffusion. Pancreatic enzymes may cause proteolytic injury.
Pancreatic digestive enzymes and bile salts may be the significant agents of esophageal injury in patients with gastric hypochlorhydria and near-neutral pH.

Esophageal clearance
The severity of esophageal injury from GER depends on the irritant potency of the refluxed material and its contact time with the esophagus.
The rate of esophageal clearance determines the duration of the exposure of the esophageal mucosa to the refluxed material.
Esophageal clearance of the refluxed material involves three mechanisms:
Volume clearance involves the emptying out of the esophagus of the volume of the refluxed material. It is facilitated by gravity, esophageal motor activity, and salivation.
Normal esophageal motor activity (peristalsis) is required for esophageal clearance.
Primary peristalsis is initiated by swallowing, and the contraction wave progresses in a sequential fashion throughout the entire length of the esophagus, resulting in esophageal emptying into the stomach. Normally, primary peristalsis occurs about once a minute while an individual is awake. It is the main esophageal motor event that clears the esophagus of refluxed material. The absence of swallowing and esophageal peristalsis during sleep impedes esophageal clearance of refluxed material and predisposes to esophageal injury. Similarly in patients with abnormal esophageal motility, increased nonperistaltic contractions lead to increased reflux injury to the esophagus.
Secondary peristalsis is elicited with distention of the esophagus by a bolus of food or refluxed fluid. It has a limited effect on volume clearance, because it does not result in a complete stripping peristaltic wave.
Acid clearance involves the disappearance of the hydrogen ion from the esophageal mucosa after the reflux of acid fluid. It is accomplished by a neutralizing action of swallowed saliva.
Saliva is the third factor that contributes to esophageal clearance.
Normal awake individuals generate 0.5 mL of saliva per minute.
Salivation stops during sleep.
Salivation stimulates swallowing.
Stimuli that increase salivary secretion include sucking, eating, intubation, and cholinergic agents.
Under basal conditions, saliva has a pH of 6 to 7 due to the presence of bicarbonate ion as the major buffer.
During stimulation, both the salivary volume and the bicarbonate ion concentration increase.
Normal salivary flow effectively neutralizes small volumes (-1 mL) of refluxed acid.
Salivation, by promoting swallowing and primary stripping peristalsis, clears the esophagus of the main volume of the refluxed material. Subsequently saliva itself clears the acid from the esophageal mucosa by its neutralizing action.
Diminished salivation, primary (e.g., in Sjogren's syndrome) or secondary (e.g., due to anticholinergic drugs), causes delayed acid clearance and promotes esophageal injury.

Tissue resistance of the esophageal mucosa.
The esophageal mucosa itself has intrinsic protective mechanisms that resist and limit mucosal injury.
Preepithelial defenses
The luminal surface of esophageal epithelium is lined by a layer of mucus that serves as both a lubricant and a protective barrier against noxious and irritant luminal contents. This viscous gel layer prevents large protein molecules like pepsin from contacting the underlying epithelium directly and slows down hydrogen ion back diffusion.
Underneath the mucous layer, there is an area of low turbulence called the unstirred water layer, which is rich in bicarbonate. This layer establishes a protective alkaline microenvironment on the epithelial surface, neutralizing the hydrogen ion that penetrates the mucous layer.
Mucus and bicarbonate are secreted by salivary glands and submucosal glands located just below the upper esophageal sphincter and near the esophagogastric junction. The rate of secretion of these glands increases with vagal stimulation and with prostaglandins.
Postepithelial defenses. As in all tissues, adequate blood flow and normal tissue acid-base status are essential for the maintenance of a healthy epithelium. Blood flow provides the epithelium with oxygen, nutrients, and bicarbonate (HCO3-) as buffer and removes injurious waste products.

Epithelial regeneration.
Despite the intrinsic ability of the esophageal mucosa to resist injury, prolonged exposure to noxious substances results in epithelial cell necrosis. Cell death further increases epithelial permeability, setting up a vicious circle for further damage. The replicating cells of the stratum basale along the basement membrane need to be protected for epithelial regeneration. The destruction of this layer appears to be necessary for the development of esophageal ulcers, strictures, and Barrett's epithelium. There is evidence that epithelial cell turnover and replication is increased after hydrogen (H+) injury. Basal cell hyperplasia seen in mucosal biopsies of patients with reflux esophagitis lends further support to this finding. Normal turnover rate for esophageal epithelium is 5 to 8 days. This rate seems to be increased to 2 to 4 days with injury. This will allow for epithelial renewal and repair in a short time if further injury is prevented.

Acid Reflux Disease Diagnosis

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A history of recurrent heartburn along with a positive response to antacids or acid-suppressing medication is adequate to diagnose Acid Reflux Disease. Specific testing is reserved for patients who have (1) Acid Reflux Disease plus alarm symptoms of dysphagia, weight loss, or gastrointestinal bleeding; (2) Acid Reflux Disease of sufficient chronicity (e.g., 5 years) to raise concern for Barrett's esophagus; and (3) suspected Acid Reflux Disease with atypical symptoms, such as chest pain or oropharyngeal, laryngeal, or airway symptoms.

Establishing Acid Reflux Disease as a Cause of Nonheartburn Symptoms

Currently, the preferred method for establishing Acid Reflux Disease as the cause of symptoms (e.g., chest pain, wheezing) is an empirical trial of acid suppression with a PPI (e.g., omeprazole, 20 mg twice daily), which normalizes esophageal acidity in approximately 95% of subjects. In some instances, a bedtime dose of a histamine H2-receptor antagonist (e.g., ranitidine, 300 mg) is added to reduce the possibility of nocturnal acid breakthrough. The treatment period in which to expect a satisfactory response is 2 to 4 weeks for chest pain and 2 to 3 months for inflammatory disease of the airway. Resolution of the symptoms supports Acid Reflux Disease as possibly causal. Confirmation may be obtained by relapse when medication is withdrawn and by a subsequent positive response to re-treatment, as confirmed by documenting control of esophageal acidity on pH monitoring while undergoing PPI therapy. Failure of symptoms to improve with PPI therapy is not generally an indication for antireflux surgery (see later) but rather an indication to search for another disease. A rarely used alternative is the Bernstein test, in which acid (0.1 N HCl, pH 1.1) or saline (control) is perfused through a catheter positioned in the midesophagus. If symptoms typical of those that occur spontaneously develop with acid but not saline, the test is considered positive for Acid Reflux Disease.

Tests for Reflux

Documenting acid reflux is not necessary except when symptoms fail to respond to PPI therapy or when surgery is being considered. Esophageal pH monitoring, the “gold standard” for identifying acid reflux, is performed by fixing a small pH probe in the esophagus, 5 cm above the LES, and recording all episodes in which esophageal pH drops to less than 4 over a 24- to 48-hour period. The number and duration of each acidic event, when combined, yield a value for total esophageal acid contact time. Total acid contact times of greater than 5% are abnormal and consistent with a diagnosis of Acid Reflux Disease. An event marker activated by the patient also allows symptoms to be related to episodes of esophageal acidity. An upper gastrointestinal series can detect grossly abnormal reflux by observing movement of barium from the stomach to the esophagus with the patient in the head-down position. It has low sensitivity but, when positive, has high predictive value. The positive predictive value is much lower, however, if reflux is induced by having the subject sip water through a straw in the head-down position. This test is rarely useful for therapeutic decisions.

Tests for Esophageal Injury
Endoscopic signs.

Tests of Esophageal Motor Function

An upper gastrointestinal series or barium swallow is valuable for identifying gross reflux and marked abnormalities in esophageal anatomy (e.g., hiatal hernia, diverticulum) and peristaltic and sphincter function. More subtle abnormalities, however, require esophageal manometry. Low mean LES pressure (<10 mm Hg) is a specific but insensitive marker of Acid Reflux Disease, with 60% of patients having normal values. Currently, the major uses of esophageal manometry in Acid Reflux Disease are to (1) position the pH probe for reflux testing, (2) exclude motor disease (achalasia, scleroderma), and (3) quantify peristaltic amplitudes before surgical fundoplication. If contraction amplitudes average less than 30 mm Hg, a partial (Toupet) rather than complete (Nissen) wrap may be preferable to avoid postoperative dysphagia.

Acid Reflux Symptoms

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Recurrent heartburn, when properly defined, is the hallmark of Acid Reflux Disease and enables the diagnosis to be made by the history alone. The heartburn associated with Acid Reflux Disease typically occurs once or twice per day and lasts from a few minutes to an hour or more if untreated. This pattern recurs, but with considerable variation in frequency and severity. However, neither the frequency, severity, nor duration of heartburn predicts disease severity on endoscopy. Acid Reflux Disease can also be associated with dysphagia, an alarm symptom because it raises concern for the presence of a peptic stricture or adenocarcinoma arising in Barrett's esophagus. For this reason, dysphagia is an indication for early endoscopy.

The damage in Acid Reflux Disease is best assessed by upper endoscopy and esophageal biopsy. Endoscopy may reveal friability, erosions, ulcers, strictures, or Barrett's esophagus in a third of subjects. In the other two thirds, endoscopic findings are normal but esophageal biopsy may show basal cell hyperplasia, elongation of the rete pegs, inflammatory cell infiltrates, cell edema, dilated intercellular spaces in squamous epithelium, or any combination of these findings. “Dilated intercellular spaces” is the earliest detectable lesion in NERD and correlates with heartburn because it reflects “leakiness” of the paracellular pathway to refluxed gastric acid. A barium swallow or upper gastrointestinal series may also detect ulcers, strictures, and hiatal hernias, but it does not reliably detect inflammation, erosions, or Barrett's esophagus.

Although Acid Reflux Disease is often used synonymously with reflux damage to the esophagus, Acid Reflux Disease includes reflux damage to the oropharynx, larynx, and respiratory tract. Consequently, symptoms and signs of Acid Reflux Disease can include sore throat/pharyngitis, earache/otitis, eroded tooth enamel, hoarseness/laryngitis, bronchitis/chronic cough, asthma/wheezing, and aspiration pneumonia. With the exception of pneumonia, which occurs as a result of gross regurgitation and aspiration of mixed gastric content, damage to the oropharynx, larynx, and airways is mediated by refluxed gastric acid. Asthma (wheezing) and bronchitis (chronic cough) can be triggered either directly by contact of acid with airway epithelium (microaspiration) or indirectly through an esophagopulmonary vagal reflex initiated by contact of acid with esophageal epithelium. The frequency with which Acid Reflux Disease causes, as opposed to being caused by, wheezing/asthma, chronic cough/bronchitis, and hoarseness/laryngitis is unknown.

Associated Conditions
Acid Reflux Disease can develop as a consequence of other conditions, such as Zollinger-Ellison syndrome, scleroderma, diabetes mellitus, nasogastric intubation, and pregnancy.

What is Acid Reflux ?

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Gastroesophageal reflux is a physiologic process that refers to the effortless movement of stomach contents from the stomach to the esophagus. It occurs in everyone, multiple times every day, usually without producing symptoms or signs of damage. Reflux can also be pathologic and produce symptoms and signs of injury to the esophagus, oropharynx, larynx, and respiratory tract. Reflux damage to the esophagus (reflux esophagitis) is the most common form of Acid Reflux Disease and is most often recognized by recurrent heartburn. In almost all patients with heartburn, esophageal mucosal pathology is identifiable, although only about 40% have endoscopically detectable erosions. The remaining 60% of patients with heartburn have endoscopically undetectable (microscopic) pathology—termed nonerosive reflux disease (NERD).

Acid Reflux Disease is one of the most common diseases in the Western world based on the prevalence of heartburn. In the United States, about 45% of adults have heartburn at least once a month, about 20% once a week, and about 10% daily. Heartburn affects men two- to threefold more often than it affects women and is more common in whites than blacks. Although Acid Reflux Disease rarely causes death, it reduces quality of life and has a morbidity rate of 10 to 15% secondary to ulceration, bleeding, stricture, Barrett's esophagus, and adenocarcinoma. The overall risk for esophageal adenocarcinoma in patients with heartburn is very low, with estimates of 1 in 2500 cases per year for those with daily heartburn to 1 in 10,000 cases per year for those with monthly heartburn.

Acid Reflux Disease develops when acidic stomach contents reflux into the esophagus and remain there long enough to overcome the resistance of the esophageal epithelium. Based on 24-hour esophageal pH monitoring, Acid Reflux Disease develops in at least two fundamentally different ways: (1) under conditions in which there is prolonged contact of the esophageal epithelium with refluxed stomach acid and (2) under conditions in which the esophageal epithelium is damaged despite a normal duration of contact with refluxed stomach acid. Prolonged acid contact results from defects in the antireflux barriers or luminal clearance mechanisms (or both), with transient LES relaxations accounting for more than 50% of acid reflux events in NERD. These relaxations are non–swallow-induced, reflex relaxations of the LES caused by stomach fundic distention. They are associated with acid reflux because they are twice as long as relaxations with swallowing and, unlike swallow-induced LES relaxations, are accompanied by inhibition of diaphragmatic contraction and unaccompanied by lumen-obliterating esophageal peristalsis. The cause of the increase in the frequency of acid reflux episodes associated with transient relaxations in patients with Acid Reflux Disease is unclear but is unrelated to delayed stomach emptying or infection with Helicobacter pylori. A diet rich in nonabsorbable carbohydrates may be one possible provocateur. In erosive esophagitis, transient LES relaxations account for less than 50% of acid reflux events, with most occurring across a mechanically weak LES. Whether LES weakness causes erosive esophagitis or is a consequence of it remains unclear because products released during inflammation can impair LES contractility. Similarly, hiatal hernias and impaired peristalsis are common in erosive esophagitis, but whether they are cause or consequence is also unclear because esophagitis can result in both esophageal shortening (by sustained contraction of the longitudinal muscle) and peristaltic dysfunction (by weakening circular muscle contractility). Patients with heartburn despite normal acid contact time presumably have primary defects in tissue resistance, with these defects probably being acquired by dietary indiscretions such as excess exposure to alcoholic, hypertonic, or hot-temperature products.

What is Gastroesophageal Reflux Disease?

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Gastroesophageal reflux disease (GERD) is defined as symptoms or tissue damage resulting from reflux of gastric acid into the esophagus and more proximal structures.
The predominant symptoms of GERD are heartburn and regurgitation.
Atypical symptoms include cough, asthma, hoarseness, chest pain, hiccups, and dental erosions.
Symptom response to a therapeutic trial of PPIs can be diagnostic.
Endoscopic evaluation is recommended for patients with warning symptoms of dysphagia, odynophagia, early satiety, weight loss, or bleeding, and atypical symptoms (cough, asthma, hoarseness, chest pain, aphthous ulcers, hiccups, dental erosions).
Patients with symptoms refractory to empiric acid suppression or requiring continuous medication for prolonged periods should also undergo endoscopy.
Ambulatory pH monitoring is used to establish elevated esophageal acid exposure and symptom-reflux correlation in patients with ongoing symptoms despite acid suppression (especially if endoscopy is negative) or those with atypical symptoms. It is also used to determine adequacy of acid suppression in patients with established GERD and ongoing symptoms.
Lifestyle Modification
The basics of lifestyle modification include eating small meals; refraining from eating for 2-3 hours before lying down; elevating the head of the bed 4-6 in.; decreasing intake of fatty foods, chocolate, coffee, cola, and alcohol; and smoking cessation.
Lifestyle modification also includes avoiding medications such as calcium channel blockers, theophylline, sedatives/tranquilizers, and anticholinergics, as they may potentiate reflux.
Lifestyle modifications alone are unlikely to resolve symptoms in the majority of GERD patients, but should be recommended in conjunction with medications.
Medications
In patients with mild or intermittent symptoms, over-the-counter antacids and H2RAs can be used intermittently or prophylactically if necessary.
PPIs have been demonstrated to be more effective than placebo or standard-dose H2RA in symptomatic relief as well as endoscopic healing of GERD. Higher doses (omeprazole, 20â€“40 mg PO bid or equivalent) may be required in severe esophagitis or persistent symptoms. Continuous long-term PPI therapy is safe and effective in maintaining remission of GERD symptoms, and is recommended for patients with erosive esophagitis, Barrett's esophagus, and severe symptoms.
Standard doses of H2RAs can result in symptomatic benefit in up to 60% of patients and endoscopic healing in 50%. Higher doses of H2RAs (equivalent to ranitidine, 600 mg daily) improve the healing rate to 75% at a higher cost. Dosage adjustments are required in renal insufficiency.
Surgery
Indications for fundoplication include the need for continuous or increasing doses of medication in patients who are good surgical candidates. Patients who require aggressive long-term medical therapy should be offered the surgical option. Other indications include patient preference for surgery and noncompliance with medical therapy.
The success rate of laparoscopic fundoplication in controlling GERD symptoms exceeds 90%, with fewer complications compared to the open technique. Elevated esophageal acid exposure and correlation of symptoms to reflux events on ambulatory pH monitoring predict a higher likelihood of a successful outcome.
Patients with medical treatment failures need careful evaluation to determine whether symptoms are indeed related to acid reflux before surgical options are considered; these patients often have other diagnoses including visceral hypersensitivity and functional heartburn.
Complications
Esophageal ulceration and stricture formation can occur in patients with GERD. Iron-deficiency anemia is less common.
GERD can contribute to laryngitis, laryngeal ulcers, asthma, and dental caries.
Barrett's esophagus is a change in the esophageal mucosa from normal squamous epithelium to specialized intestinal metaplastic epithelium due to longstanding acid related injury. It carries a small risk of progression to esophageal adenocarcinoma. Endoscopic surveillance for Barrett's esophagus should be considered in patients with a symptom history that exceeds 5 years.

GERD diagnosis

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The history and clinical manifestations of Acid Reflux Disease are the most important diagnostic aids; objective testing can quantify the extent and severity of the process. In the vast majority of sufferers, typical symptoms of Acid Reflux Disease and the response to initial gastric acid suppressive therapy make the diagnosis relatively easy. Diagnostic evaluation becomes important when symptoms are atypical and/or do not respond to therapy.
DOCUMENTING REFLUX.
Reflux during a barium swallow in adults is uncommon unless vigorous provocative maneuvers are employed. When spontaneous reflux of barium is seen, it usually denotes free reflux. The absence of reflux seen radiographically does not, however, imply that the sufferer does not have Acid Reflux Disease.
The 24-hour monitoring of esophageal pH can be performed with a portable unit, which allows the sufferer to follow an almost normal lifestyle. During the prolonged monitoring period, the relationship between symptoms (heartburn, chest pain, wheezing) and episodes of acid reflux can be ascertained, and calculations can be made of the number of episodes of reflux and the amount of time the esophagus is acidified (pH - 4). A small amount of reflux, especially in the postprandial period, can be seen normally. Repeated and prolonged bursts of acid exposure suggest that abnormal gastroesophageal reflux is present.
In children and infants, reflux can be measured noninvasively by scanning the esophageal area with a gamma-camera after placing a solution of 99m Tc sulfur colloid in the stomach. An abdominal binder is used to increase intra-abdominal pressure and to stress the gastroesophageal junction if free reflux is not seen.
LINKING REFLUX TO SYMPTOMS.
If pain is the predominant symptom, rather than heartburn, a Bernstein test may be performed using the same catheter as is used for esophageal manometry. After a 5-minute period of dripping normal saline in the mid-esophagus, the infusion is changed to 0.1 N hydrochloric acid. Reproduction of the symptoms during acid infusion (usually 4 to 5 minutes into the infusion), followed by rapid symptom disappearance after returning to a saline infusion, suggests an esophageal cause of the discomfort.
As another approach, the sufferer is asked to signal the time of discomfort during prolonged pH monitoring of the esophagus. If the sufferer signals discomfort at the same time that acid reflux is demonstrated by the pH probe, then a causal relationship is more likely.
ASSESSING THE EFFECT OF REFLUX ON THE ESOPHAGEAL MUCOSA.
A barium swallow detects gross changes, such as stricture formation or a deep esophageal ulcer, but misses the much more common shallow ulcerations and erosions, which are detected by endoscopy. Only discrete lesions such as erosions and ulcerations should be taken as proof of esophageal damage, because endoscopic findings, such as erythema, edema, or friability, are subject to wide interobserver variation. In approximately one-half of sufferers with moderate to severe symptoms of Acid Reflux Disease, the mucosa appears absolutely normal, but a biopsy may demonstrate the histologic changes of reflux.
APPROACH
Endoscopy is generally indicated if symptoms are prolonged and do not respond to empiric treatment, or if systemic manifestations, such as weight loss, anemia, and occult blood-positive stool are present. If the appearance of the esophageal mucosa is normal during endoscopy, biopsies can also be obtained to search for objective evidence of microscopic esophagitis. If dysphagia is present, a barium swallow is appropriate. Uncommonly, reflux is demonstrated, a stricture found, or a deep ulcer seen, which leads to immediate endoscopy for more complete evaluation. After first evaluation, it may be appropriate to begin empiric therapy (see Treatment, below). If the response to therapy is poor, esophageal pH monitoring can confirm the diagnosis. At the same time, esophageal manometry may be performed to estimate LES pressure and to determine the presence or absence of peristaltic waves.

Acid Reflux Causes: (LES)

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Prevention of retrograde flow of gastrointestinal contents is a major function of the lower esophageal sphincter (LES) . Retrograde flow is prevented by the lower esophageal sphincters, which remain closed between swallows.
The lower esophageal sphincter is composed of smooth muscle and is innervated by parallel sets of parasympathetic excitatory and inhibitory pathways. It remains closed because of its intrinsic myogenic tone, which is modulated by the excitatory and inhibitory nerves. It opens in response to the activity of the inhibitory nerves. The neurotransmitters of the excitatory nerves are acetylcholine and substance P, and those of the inhibitory nerves are vasoactive intestinal peptide (VIP) and nitric oxide. The function of the LES is supplemented by the striated muscle of the diaphragmatic crura, which surrounds the LES and acts as an external LES. Relaxation of the LES without esophageal contraction occurs during belching and gastric distention. Gastric distention-evoked transient lower esophageal sphincter relaxation (tLESR) is a vasovagal reflex. Fatty meals, smoking, and beverages with a high xanthine content (tea, coffee, cola) also cause a reduction in sphincter pressure. Many hormones and neurotransmitters can modify LES pressure. Muscarinic M2 and M3receptor agonists, a-adrenergic agonists, gastrin, substance P, and prostaglandin F2acause contraction. Nicotine, b-adrenergic agonists, dopamine, cholecystokinin, secretin, VIP, calcitonin gene-related peptide (CGRP), adenosine, prostaglandin E, and nitric oxide donors such as nitrates reduce sphincter pressure.

Acid Reflux Symptoms

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Antegrade esophageal flow is achieved by the act of swallowing with the initiation of primary peristalsis. Gastroesophageal reflux is prevented by the physiologic lower esophageal sphincter (LES).
When the LES fails to function as an effective barrier to reflux, gastroesophageal reflux develops, with the associated complications of mucosal inflammation (reflux esophagitis).
Gastroesophageal reflux disease (GERD) refers to the varied clinical manifestations of reflux of stomach and duodenal contents into the esophagus and is preferable to the term "reflux esophagitis." Although GERD may be associated with a sliding hiatal hernia, the term "symptomatic hiatal hernia" tends to emphasize an anatomic entity and not the underlying pathophysiology. GERD can be characterized by any combination of symptoms and radiologic, endoscopic, or pathologic changes. In its milder manifestations, it is a common disease; its most florid state is uncommon but may be life-threatening.
HEARTBURN
Heartburn is the most common manifestation of esophageal disease and may occur in up to 20% of the population. The term "burning" rather than "pain" is usually used, although heartburn can increase in intensity until it is perceived as chest pain. Patients often illustrate heartburn with a movement of the open hand up and down the sternum, as compared with the stationary, tightly clenched fist of angina pectoris. Heartburn is usually relieved, even if only temporarily, by taking antacids. A constant burning unrelieved by antacids may well be of esophageal origin, but it does not represent heartburn. Heartburn is often worse after recumbency or lifting and may follow overeating or alcoholic indiscretion.
REGURGITATION
Regurgitation of fluid contents into the mouth often accompanies heartburn. Sometimes regurgitation is associated with eructation; often it accompanies bending over, lifting, or lying down at night. The bitter regurgitated fluid is often described as yellow-brown or green. Regurgitation at night may lead to stridor or to wheezing, a hoarse voice, and other respiratory symptoms from unrecognized reflux.
SPONTANEOUS ESOPHAGEAL CHEST PAIN
In addition to the discomfort from severe reflux, which can advance from heartburn into pain, abnormal contractile activity of the esophageal muscle can cause severe chest pain that is clinically indistinguishable from angina pectoris in terms of intensity, radiation, relationship to exercise, and even response to nitroglycerin. pain of esophageal origin can radiate directly through to the back and is often found in patients who also have dysphagia. Esophageal chest pain can last from several seconds to many hours.

Acid Reflux Disease: Reflux Esophagitis

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REFLUX ESOPHAGITIS
Reflux of stomach contents into the lower esophagus is the first and foremost cause of esophagitis. Many causative factors are involved, less well characterized than the name implies:

Decreased efficacy of esophageal antireflux mechanisms, particularly LES tone. Central nervous system depressants, hypothyroidism, pregnancy, systemic sclerosing disorders, alcohol or tobacco exposure, or the presence of a nasogastric tube may be contributing causes. In most instances, no antecedent cause is identified.

Presence of a sliding hiatal hernia.

Inadequate or slowed esophageal clearance of refluxed material.

Delayed stomach emptying and increased stomach volume, contributing to the volume of refluxed material.

Reduction in the reparative capacity of the esophageal mucosa by protracted exposure to stomach juices.
Any one of the aforementioned influences may assume primacy in an individual case, but more than one is likely to be involved in most instances. The acid-peptic action of stomach juices is critical to the development of esophageal mucosal injury; in severe cases, refluxed bile from the duodenum also may contribute to the mucosal disruption.

MORPHOLOGY.
The anatomic changes depend on the causative agent and on the duration and severity of the exposure. Simple hyperemia ( redness) may be the only alteration. In uncomplicated reflux esophagitis, three histologic features are characteristic
1. The presence of inflammatory cells, including eosinophils, neutrophils, and excessive numbers of lymphocytes, in the epithelial layer

2. Basal zone hyperplasia exceeding 20% of the epithelial thickness

3. Elongation of lamina propria papillae with congestion, extending into the top third of the epithelial layer
Infiltrates of intraepithelial eosinophils are believed to be an early histologic abnormality, since they occur even in the absence of basal zone hyperplasia. Intraepithelial neutrophils are markers of more severe injury, such as ulceration, rather than reflux esophagitis per se.

Clinical Features.
Although largely limited to adults over age 40, reflux esophagitis is occasionally seen in infants and children. The clinical manifestations consist principally of dysphagia; heartburn; and sometimes regurgitation of a sour brash, hematemesis, or melena. The severity of symptoms is not related closely to the presence or degree of histologic esophagitis; most people experience reflux symptoms without damage to the distal esophageal mucosa, owing to the short duration of the reflux. Anatomic damage appears best correlated with prolonged exposure of the lower esophagus to refluxed material. Rarely, chronic symptoms are punctuated by attacks of severe chest pain that may be mistaken for a heart attack. The potential consequences of severe reflux esophagitis are bleeding, development of stricture, and a tendency to develop Barrett esophagus, with its attendant risks.

Upper GI Endoscopy

2008-06-08T14:35:00.000-07:00

Narrated slide presentation of the UPPER GI ENDOSCOPY

Gastroesophageal Reflux Disease (GERD)

2008-06-08T14:27:00.000-07:00

Narrated slide presentation about GERD

Acid Reflux Causes and mechanisms

2008-06-07T13:06:00.000-07:00

Several factors must work in concert to produce clinical effects of esophageal reflux. Normal subjects may have a few short-duration reflux episodes postprandially and in the upright position. Those in whom reflux has produced symptoms or pathologic changes will demonstrate more frequent and prolonged episodes of reflux, which also tend to occur at night. The factor or factors that cause this difference are not entirely known. However, important differences between persons with and without reflux might help explain these findings.

The LES is a specialized bundle of circular muscle at the lower end of the esophagus with different physical and pharmacologic characteristics when compared with the circular muscle above and below it. Although mean LES pressure is significantly lower in subjects with GERD than in normal persons, much overlap occurs between the groups; LES pressure is not very useful in predicting whether reflux is present in an individual patient unless the pressure is very low. The most common event associated with reflux appears to be a transient relaxation of the LES unassociated with either swallowing or the distention of the esophageal body by refluxed fluid. Thus, two abnormalities of LES may be associated with reflux: a sphincter with very low tone, as measured by LES pressure, or inappropriate relaxation of a normally competent sphincter.

Several factors are important in removing refluxed material from the esophagus. The upright position facilitates esophageal emptying by gravity. Peristaltic waves initiated by swallowing or by esophageal distention help remove the refluxed material. Acid placed within the esophagus is cleared less well by patients with GERD than by normal subjects, although the manometric tracings seen in both groups seem identical. Clearing of acid regurgitation occurs in two phases: the bulk of the fluid is returned to the stomach by a peristaltic contraction, and the remaining acid film clinging to the esophageal wall is neutralized by swallowed saliva.

The composition and perhaps the quantity of the refluxed material also play a role in the production of GERD. Gastric acid and pepsin seem clearly important in the pathogenesis of GERD. Bile salts, and possibly pancreatic enzymes, may be responsible in patients in whom acid is absent. The combination of bile salts plus acid is more injurious to the esophagus than either agent alone. Other less well-studied factors, such as altered or abnormal esophageal mucus, swallowed saliva of high bicarbonate content, and diminished resistance of the esophageal mucosa to digestion, may be important in determining the amount of mucosal damage in GERD.

Esophageal squamous epithelium reacts to reflux by an increase in the basal cell or germinative layer. The dermal pegs are increased in height and may become more vascular. If the process becomes more severe, the epithelial layer is destroyed, with the appearance of micro-ulcers and classic signs of inflammation in the lamina propria, such as infiltration with polymorphonuclear leukocytes and edema. Even deeper lesions cause first submucosal and then muscular inflammation and fibrosis, resulting in an esophageal stricture. Why reflux is so common, yet inflammation and stricture formation are relatively uncommon, is not known.

Reflux during pregnancy, once thought to be due to the increased abdominal pressure from the fetus, may be due mainly to diminished LES strength caused by increased estrogen and progesterone. Weight gain also tends to aggravate reflux through an unknown mechanism. Resection of the lower esophageal area for cancer or myotomy for achalasia can lead to severe postoperative reflux. Gastroesophageal reflux with stricture formation is especially severe in patients with progressive systemic sclerosis.

The crural diaphragm usually wraps around the gastroesophageal junction to augment the intrinsic LES. In a hiatal hernia, an anatomic displacement of the LES and crural diaphragm is seen. Although hiatal hernias may be associated with reflux, the presence of a hiatal hernia is now considered to be much less of a factor in GERD than previously thought, because it is present in a large percentage of normal subjects. It is not appropriate to spend time trying to define whether a hiatal hernia is present or absent in dealing with most patients with GERD; rather, the focus should be on the symptoms of reflux.

What is acid reflux disease?

2008-06-06T10:47:00.000-07:00

GASTROESOPHAGEAL REFLUX DISEASE
GERD is one of the most prevalent gastrointestinal disorders. Population-based studies show that up to 15% of individuals have heartburn at least once a week and about 7% have heartburn daily. Symptoms are caused by back flow of gastric acid and other gastric contents into the esophagus due to incompetent barriers at the gastroesophageal junction.

Pathophysiology: The normal antireflux mechanisms consist of the LES, the crural diaphragm, and the anatomic location of the gastroesophageal junction below the diaphragmatic hiatus. Reflux occurs only when the gradient of pressure between the LES and the stomach is lost. It can be caused by a sustained or transient decrease in LES tone. A sustained hypotension of the LES may be due to muscle weakness that is often without apparent cause. Secondary causes of LES incompetence include scleroderma-like diseases, myopathy associated with chronic intestinal pseudo-obstruction, pregnancy, smoking, anticholinergic drugs, smooth-muscle relaxants [b-adrenergic agents, aminophylline, nitrates, calcium channel blockers, phosphodiesterase inhibitors that increase cyclic AMP or cyclic GMP (including sildenofil)], surgical destruction of the LES, and esophagitis.tLESRwithout associated esophageal contraction is due to a vagal reflex in which LES relaxation is elicited by gastric distention. Increased tLESR is associated with GERD. A similar reflex operates during belching. Apart from incompetent barriers, gastric contents are most likely to reflux (1) when gastric volume is increased (after meals, in pyloric obstruction, in gastric stasis, during acid hypersecretion states), (2) when gastric contents are near the gastroesophageal junction (in recumbency, bending down, hiatus hernia), and (3) when gastric pressure is increased (obesity, pregnancy, ascites, tight clothes). Incompetence of the diaphragmatic crural muscle, which surrounds the esophageal hiatus in the diaphragm and functions as an external LES, also predisposes to GERD.
The total exposure of the esophagus to refluxed acid correlates with potential for mucosal damage. Exposure depends on the amount of refluxed material per episode, frequency of episodes, and rate of clearing the esophagus by gravity and peristaltic contractions. When peristaltic contractions are impaired, esophageal clearance is impaired. Acid refluxed into the esophagus is neutralized by saliva. Thus, impaired salivary secretion also increases esophageal exposure time. If the refluxed material extends to the cervical esophagus and breaches the upper sphincter, it can enter the pharynx, larynx, and trachea, causing chronic cough, bronchoconstriction, pharyngitis, laryngitis, or bronchitis.

Reflux esophagitis is a complication of reflux and develops when mucosal defenses are unable to counteract the damage done by acid, pepsin, and bile. Mild esophagitis involves microscopic changes of mucosal infiltration with granulocytes or eosinophils, hyperplasia of basal cells, and elongation of dermal pegs. Endoscopic appearance may be normal. Erosive esophagitis involves endoscopically apparent mucosal damage, redness, friability, bleeding, superficial, linear ulcers, and exudates. Peptic stricture results from fibrosis that causes lumenal constriction. These strictures occur in ~10% of patients with untreated GERD. Short strictures caused by spontaneous reflux are usually 1 to 3 cm long and are present in the distal esophagus near the squamocolumnar junction. Long, tubular peptic strictures can result from persistent vomiting or prolonged nasogastric intubation. Erosive esophagitis may cause bleeding and heal by intestinal metaplasia (Barrett's esophagus) that is a risk factor for adenocarcinoma.

Clinical Features: Regurgitation of sour material in the mouth and heartburn are the characteristic symptoms of GERD. Heartburn is produced by the contact of refluxed material with the inflamed or sensitized esophageal mucosa. Angina-like or atypical chest pain occurs in some patients, while others experience no heartburn or chest pain. Persistent dysphagia suggests development of a peptic stricture. Most patients with peptic stricture have a history of several years of heartburn preceding dysphagia. However, in one-third of patients, dysphagia is the presenting symptom. Rapidly progressive dysphagia and weight loss may indicate the development of adenocarcinoma in Barrett's esophagus. Bleeding occurs due to mucosal erosions or Barrett's ulcer. Severe reflux may reach the pharynx and mouth and result in laryngitis, morning hoarseness, and pulmonary aspiration. Recurrent pulmonary aspiration can cause aspiration pneumonia, pulmonary fibrosis, or chronic asthma. By contrast, many patients with GERD remain asymptomatic or self-treated and do not seek attention until severe complications occur.

Acid Reflux Disease (GERD) Treatment

2008-06-06T00:52:00.000-07:00

TREATMENT OF GASTROESOPHAGEAL REFLUX DISEASE (GERD)

Most mildly symptomatic patients with reflux and some moderately afflicted individuals can be helped by simple measures designed to alter the frequency or type of esophageal reflux. Elevating the head of the bed by 6 to 8 inches is a simple and effective form of therapy. Esophageal pH monitoring has shown that this simple measure decreases the frequency and length of reflux episodes. Pillows to elevate the thorax do not work well, as patients tend to roll off the pillows during the night. A foam rubber wedge can be used if the bed frame cannot be moved. Avoiding food and fluid for at least 3 hours before retiring decreases the amount of material available for reflux at night. Avoiding food that the patient finds distressing and that may decrease LES pressure, such as fatty foods, chocolate, and onions, makes sense but has never been subjected to clinical trial. Acid can be neutralized by taking 30 mL of aluminum hydroxide-magnesium hydroxide antacid 1 and 3 hours after meals and at bedtime, but most patients do not tolerate frequent antacid administration. An attempt should be made to have the patient stop smoking, drinking alcohol, and overeating.

If these simple measures are not effective, systemic medical treatment is indicated. The H2 -receptor antagonists in the usual dosage range for duodenal ulcer and titrated to the individual patient improve heartburn better than placebo. An increased frequency of administration and/or higher dosage regimens--cimetidine, 800 mg; ranitidine, 300 mg; or famotidine, 40 mg (each twice per day)--are more effective for controlling symptoms and healing peptic esophagitis, which usually requires 12 weeks.

The proton-pump inhibitors omeprazole (20 mg/day) or lansoprazole (30 mg/day) can give dramatic symptom relief and heal esophagitis in 4 to 8 weeks. Proton-pump inhibitors are usually the treatment of choice for mucosal disease, especially moderate to severe esophagitis seen endoscopically.

Prokinetic agents may also be useful in the treatment of GERD symptoms with no to mild esophagitis, occasionally in addition to gastric acid suppressants. Metoclopramide, 10 mg given three times a day, can be helpful, but CNS side effects can occur in 25% of cases and may limit its usefulness.

Summary:

Step 1. Simple measures (lifestyle changes , dietary modifications and OTC antacids)
A. Elevate head of bed
B. Avoid food and fluid intake before bedtime
C. Avoid cigarettes, coffee, alcohol
D. Avoid chocolate, peppermint
E. Avoid tight clothing around the waist
F. Take antacids 1 hour after meals, at bedtime, and as needed
G. Reduce fat in diet
H. Lose weight

Step 2. Measures for resistant cases (systemic treatment)
Step 2a.H2 -receptor antagonists
A. Cimetidine, 300 mg q.i.d.
B. Ranitidine, 150 mg b.i.d.
C. Famotidine, 20 mg b.i.d.
D. Nizatidine, 150 mg b.i.d.
Step 2b. Prokinetic agents
Metoclopramide, 10 mg q.i.d.

Step 3. Measures for patients with GERD resistant to H2 -receptor antagonists
Proton pump inhibitor: omeprazole, 20 mg/day, or lansoprazole, 30 mg/day

Step 4. Measures for patients with GERD resistant to steps 1, 2, and 3 or patients who need long-term maintenance treatment
Surgical fundoplication

Once healing of esophagitis has been achieved with either an H2 -antagonist or a proton-pump inhibitor, recurrence rates exceed 80% if no maintenance therapy is used. Maintenance therapy for esophagitis generally requires full dosage of an H2 -receptor antagonist or a proton-pump inhibitor.

GERD diagnosis : Esophagitis Severity Grading

2008-06-05T12:23:00.000-07:00

The most thoroughly evaluated classification scheme for esophagitis is the Los Angeles system, which categorizes mucosal injury as grade A, B, C, or D. However, it is important to note that the Los Angeles system does not consider strictures, hiatal hernia, or Barretts metaplasia; the endoscopist is required to describe these separately.

Los Angeles Endoscopic Grading Scheme for Esophagitis Severity
Grade A
One (or more) mucosal breaks no longer than 5 mm that do not extend between the tops of two mucosal folds.
Grade B
One (or more) mucosal breaks more than 5 mm long that do not extend between the tops of two mucosal folds.
Grade C
One (or more) mucosal breaks that are continuous between the tops of two or more mucosal folds but involve lesser than 75% of the circumference.
Grade D
One (or more) mucosal breaks that involve at least 75% of the esophageal circumference.

What is acid reflux?

2008-06-03T09:39:00.000-07:00

What is acid reflux disease? An acid reflux flash animation that simply answers frequently asked questions about GERD and Acid Reflux Surgery.

Acid Reflux Disease Complications

2008-06-02T14:24:00.000-07:00

Acid Reflux Disease Complications

Hemorrhage and Perforation
Hemorrhage and esophageal perforation are rare complications of reflux esophagitis and are usually associated with deep esophageal ulcers or severe diffuse esophagitis. Clinically important hemorrhage has been reported in 7% to 18% of patients with GERD. Esophageal perforations are very rare in the PPI era, but they can result in mediastinitis and can be fatal if they are not rapidly recognized and treated.

Peptic Esophageal Strictures
Strictures occur in 7% to 23% of patients with untreated reflux esophagitis, especially in older men. They usually evolve over many years and may be linked to the long-term use of nonsteroidal antiinflammatory drugs. The mechanism of stricture formation is complex, starting as a reversible inflammatory process with edema, cellular infiltration, and vascular congestion, progressing to deposition of connective tissue and collagen, and ending in irreversible fibrosis. With the onset of dysphagia, there is often less heartburn, reflecting the stricture’s acting as a barrier to reflux. Dysphagia is usually limit to solids, but it may progress to liquids. Unlike malignant strictures, patients with peptic strictures have a good appetite, alter their diet, and lose little weight.
Radiographically, peptic strictures are smooth-walled, tapered, circumferential narrowings in the lower esophagus, which are usually less than 1 cm long, but occasionally they extend to 8 cm in length. In these unusual cases, the clinician should suspect a predisposing condition, such as the Zollinger-Ellison syndrome, superimposed pill esophagitis, or prolonged nasogastric intubation. A stricture in the middle to upper esophagus should raise the suspicion of Barrett esophagus or malignant disease. Although once controversial, most data today suggest that a Schatzki ring is a forme fruste of an early peptic stricture. In all cases, the nature of a peptic stricture needs to be confirmed by endoscopy with biopsies because some patients may have Barrett esophagus or unsuspected cancer.

Acid Reflux Disease

2008-06-01T13:56:00.000-07:00

The clinical course of reflux esophagitis depends to a great extent on whether the patient has erosive or nonerosive GERD on initial presentation. Furthermore, patients tend not to cross over from one group to another unless they are treated medically or surgically: in follow-up ranging from 6 months to more than 5 years, only 15% of patients with nonerosive disease evolved over time to having esophagitis or complications of GERD.

Nonerosive Acid Reflux Disease

Although early studies from tertiary referral centers suggested that nearly half of patients with GERD had esophagitis, studies carried out in community practices reveal that up to 70% of the patients with GERD had a normal endoscopic examination. Furthermore, another community-based study of antacid users found that 53% of patients with GERD had nonerosive disease, and two thirds of the remaining had only minimal erosive changes at endoscopy. Endoscopy-negative patients with GERD are more likely to be female, younger, thin, and without hiatal hernia. Despite their mild mucosal damage, these patients demonstrate a chronic pattern of symptoms with periods of exacerbation and remission.

Nonerosive GERD is suspected by the presence of typical reflux symptoms with a normal endoscopic examination and is confirmed by the patient’s response to antisecretory therapy. When performed, 24-hour esophageal pH monitoring identifies three distinct subset of patients with nonerosive disease. First, there are the patients with abnormal acid exposure time who are usually responsive to antisecretory therapy. Second are the patients with normal reflux parameters but a good relationship between acid reflux episodes and symptoms. This group represents 30% to 50% of patients with nonerosive GERD and has “functional heartburn.” These patients probably have heightened esophageal sensitivity to acid and are less likely to respond to antireflux therapy. The third group is characterized by normal acid exposure times and poor symptom correlation. Despite sometimes having classical reflux symptoms, other diseases such as achalasia, gastroparesis, bile reflux, or functional dyspepsia are the cause of their symptoms. Overall, patients with nonerosive GERD do not respond to antireflux treatments as well as do patients with erosive GERD, probably because these three subsets are not carefully defined before treatment.

Erosive Acid Reflux Disease

The clinical course of patients with erosive esophagitis is more predictable and is associated with complications of GERD. Controlled studies have shown that in the absence of ongoing maintenance therapy, up to 85% of patients with erosive GERD will have a relapse within 6 months, and the relapse rate is highest in those with the more severe grades of esophagitis. This observation, however, should not prevent at least one attempt to withdraw medication, because 20% of patients remain in remission for up to 1 year, especially those with milder esophagitis grades. Although the natural history of untreated erosive GERD is well studied, two European studies suggest that these patients are more prone to reflux complications. In a Finnish study, 20 patients with erosive GERD treated with lifestyle changes, antacids, and prokinetic drugs were followed up for a median of 19 years. Fourteen patients continued to have erosions, and 6 new cases of Barrett esophagus were detected. Likewise, a large retrospective European study with 6.5 years of follow-up found a high rate of complications (21%) including 13 esophageal ulcers, 15 with strictures, and 45 patients with Barrett epithelium. However, these data must be contrasted with other studies in which no patients with erosive esophagitis developed Barrett esophagus in a 2-year trial in the United States, and over a 12-year period, in 3800 French patients, development of stricture was reported in only 0.26%.

GERD diagnosis : Acid Suppression Test

2008-05-31T09:55:00.000-07:00

DIAGNOSTIC EVALUATION
Many tests are available for evaluating patients with suspected GERD. These tests are often unnecessary because the classical symptoms of heartburn and acid regurgitation are sufficiently specific to identify reflux disease and to begin medical treatment. However, this may not always be the case, and the clinician must decide which test to choose to arrive at a diagnosis in a reliable, timely, and cost-effective manner, depending on the information desired.

Empiric Trial of Acid Suppression
The simplest and most definitive method for diagnosing GERD and assessing its relation to symptoms (either classical or atypical) is the empiric trial of acid suppression. Unlike other tests that only suggest an association (e.g., esophagitis at endoscopy or positive symptom index on pH testing), the response to antireflux therapy ensures a cause-and-effect relationship between GERD and symptoms. Therefore, it has become the “first” test used in patients with classical or atypical reflux symptoms without “alarm” complaints. The popularity of this approach was aided by the introduction of the PPIs, which, unlike the histamine 2 receptor antagonists (H 2RAs), could drastically reduce the amount of acid reflux into the esophagus. Symptoms usually respond to a PPI trial in 7 to 14 days. If symptoms disappear with therapy and then return when the medication is stopped, GERD may be assumed.
In the reported empiric trials with heartburn, the initial dose of PPI was high (e.g., omeprazole 40 to 80 mg/d) and was given for not less than 14 days. A positive response is defined as at least 50% improvement in heartburn. Using this approach, the PPI empiric trial had a sensitivity of 68% to 83% for determining the presence of GERD. Empiric trials using a 2- to 4-month regimen of PPIs taken twice a day also are commonly used in patients with suspected GERD-associated asthma and GERD complaints related to the ear, nose and throat.

An empiric trial of PPIs for diagnosing GERD has many advantages. The test is office based, is easily performed, is relatively inexpensive, is available to all physicians, and avoids many needless procedures. Disadvantages are few, including a placebo response and uncertain symptomatic end point if symptoms do not resolve totally with extended treatment.

Acid Reflux Symptoms : Atypical, Extraesophageal

2008-05-30T09:28:00.000-07:00

Extraesophageal Manifestations
It has been suggested that GER may be the cause of a wide spectrum of conditions including noncardiac chest pain, asthma, posterior laryngitis, chronic cough, recurrent pneumonitis, and even dental erosion. Some of these patients have classical reflux symptoms, but many are “silent refluxers,” contributing to problems in making the diagnosis. Furthermore, it may be difficult to establish a causal relationship even if GER can be documented by testing (e.g., pH studies), because patients may simply have two common diseases without a cause-and-effect relationship.

Chest Pain

GER-related chest pain may mimic angina pectoris. The chest pain is usually described as squeezing or burning, substernal in location, and radiating to the back, neck, jaw, or arm. It often is worse after meals, awakens the patient from sleep, and may worsen during periods of emotional stress. Heavy exercise, even treadmill testing, may provoke GER. Reflux-related chest pain may last minutes to hours, often resolves spontaneously, and may be eased with antacids. Most patients with GERD-induced chest pain have heartburn symptoms. Early studies suggested that spastic motility disorders were the most common esophageal cause of chest pain. However, more recent studies using ambulatory esophageal pH and pressure monitoring suggest that about 25% to 50% of patients with noncardiac chest pain have GERD. Overall, these series of reports found that 41% of patients had abnormal 24-hour pH test results, whereas 32% had chest pain that was clearly associated with acid reflux. Patients with coronary artery disease commonly have coexisting esophageal diseases, but the evidence that GER causes ischemic pain is controversial. The mechanism for GERD-related chest pain is not clearly understood and probably is multifactorial, related to H + ion concentration, volume and duration of acid reflux, and secondary esophageal spasm.

Asthma and Other Pulmonary Diseases

The association of GERD and pulmonary diseases was recognized by Sir William Osler, who recommended that asthmatic patients should “learn to take their large daily meal at noon to avoid nighttime asthma which occurred if they ate a full supper.” More recent studies suggest the coexistence of the two diseases in up to 80% of asthmatic patients, irrespective of the use of bronchodilators. GERD should be considered in asthmatic patients who present in adulthood, those without an intrinsic component, and those not responding to bronchodilators or steroids. Up to 30% of patients with GERD-related asthma have no other esophageal complaints. Other pulmonary diseases associated with GERD include aspiration pneumonia, interstitial pulmonary fibrosis, chronic bronchitis, bronchiectasis, and possibly cystic fibrosis, neonatal bronchopulmonary dysplasia, and sudden infant death syndrome. Proposed mechanisms of reflux-induced asthma are either aspiration of gastric contents into the lungs with secondary bronchospasm or activation of a vagal reflex from the esophagus to the lungs causing bronchoconstriction. Animal and human studies report bronchoconstriction after esophageal acidification, but the response tends to be mild and unpredictable. In contrast, intratracheal infusion of even small amounts of acid induces profound and reproducible bronchospasm in cats. The reflux of acid into the trachea as compared with the esophagus alone predictably caused marked changes in peak expiratory flow rates in asthmatic patients. Although either mechanism may be responsible for reflux-induced asthma, most patients probably suffer from intermittent microaspiration.

Ear, Nose, and Throat Diseases

GERD may be associated with a variety of laryngeal conditions and symptoms, of which reflux laryngitis is perhaps the most common. These patients present with hoarseness, globus sensation, frequent throat clearing, recurrent sore throat, and prolonged voice warmup. Ear, nose, and throat signs attributed to GERD include posterior laryngitis with edema and redness, vocal cord ulcers and granulomas, leukoplakia, and even carcinoma. These changes usually are limited to the posterior third of the vocal cords and interarytenoid areas, both in close proximity to the upper esophageal sphincter. GERD is the third leading cause of chronic cough (after sinus problems and asthma), accounting for 20% of cases. Dental erosion, defined as the loss of tooth structure by chemical processes not involving bacteria, can be caused by GER in healthy persons and in patients with bulimia. Despite the association between ear, nose, and throat diseases and GERD, overt esophagitis usually is absent, and most patients have only mild reflux symptoms, if any. Microaspiration of gastric contents is the most likely cause of these complaints. Animal studies find that the combination of acid and pepsin is very injurious to the larynx. Human studies report that proximal esophageal acid exposure, especially at night while sleeping, is significantly increased in patients with laryngeal symptoms and signs.

Acid Reflux Symptoms : Typical, Esophageal

2008-05-29T09:14:00.000-07:00

Classical Reflux Symptoms
Heartburn is the classical symptom of GERD, with patients generally reporting a burning feeling, rising from the stomach or lower chest and radiating toward the neck, throat, and occasionally the back. Usually, it occurs postprandially, particularly after large meals or the consumption of spicy foods, citrus products, fats, chocolates, and alcohol. Recumbency and bending over may exacerbate heartburn. When heartburn dominates the patients’ complaints, it has very high specificity (89%), but low sensitivity (38%) for GERD as diagnosed by abnormal 24-hour esophageal pH testing. The diagnosis of GERD usually is based on the occurrence of heartburn on 2 or more days a week, although less frequent symptoms do not preclude the disease. Although this symptom is an aid to diagnosis, the frequency and severity of heartburn do not predict the degree of esophageal damage. Heartburn is caused by acid stimulation of sensory nerve endings in the deeper layers of the esophageal epithelium. These nerve endings are normally protected by a relatively impermeable epithelium, but with epithelial changes caused by reflux, they may be stimulated by H + or spicy foods.

Other common symptoms of GERD are acid regurgitation and dysphagia. The effortless regurgitation of acidic fluid, especially after meals and exacerbated by stooping or recumbency, is highly suggestive of GERD. Among patients with daily regurgitation, the LES pressure usually is low, many have associated gastroparesis, and esophagitis is common. For these reasons, acid regurgitation may be more difficult to control medically then classical heartburn complaints. Dysphagia is reported by more than 30% of patients with GERD. It usually occurs in the setting of long-standing heartburn, with slowly progressive dysphagia primarily for solids. Weight loss is uncommon because patients have good appetites. The most common causes are a peptic stricture or Schatzki ring, but other causes include severe esophageal inflammation alone, peristaltic dysfunction, and esophageal cancer arising from Barrett esophagus.

Less common reflux-associated symptoms include water brash, odynophagia, burping, hiccups, nausea, and vomiting. Water brash is the sudden appearance in the mouth of a slightly sour or salty fluid. It is not regurgitated fluid, but rather secretions from the salivary glands in response to acid reflux. Odynophagia, pain on swallowing, can occasionally be seen with severe ulcerative esophagitis. However, its presence should raise the suspicion of an alternative cause of esophagitis, especially infections (candidiasis, herpes) or pills (tetracycline, potassium chloride, quinine, vitamin C, alendronate).

In contrast to the previously described symptomatic presentations, some patients with GERD are asymptomatic. This is particularly true in elderly patients because of decreased acidity of the reflux material or decreased pain perception. Many elderly patients present first with complications of GERD because of long-standing disease with minimal symptoms. For example, up to one third of patients with Barrett esophagus are insensitive to acid at the time of presentation.

Acid Reflux Causes : Role of the Stomach

2008-05-28T05:12:00.000-07:00

Factors related to the Stomach:
Stomach factors (particularly stomach content's volume and certain aggressive factors found in the refluxate) are potentially important in the production of reflux esophagitis. Stomach volume is determined by the basal acid secretion rate, concomitant H pylori infection, duodenogastric reflux, and the rate of stomach emptying. Increased stomach volume not only provides more stomach contents available for reflux, but also increases the rate of transient LESRs.

Stomach Acid Secretion

The primary importance of stomach acid is indisputable in the production of reflux esophagitis, but its mechanism may involve activation of pepsin rather than direct damage from acid alone. In animal studies, acid causes minimal injury at a pH of less than 3.0, primarily by protein denaturation. However, the combination of acid and even small amounts of pepsin disrupts the mucosal barrier resulting in increased H + permeability, histological changes, and gross hemorrhage. Complementing the animal studies, a series of clinical reports showed that patients with various grades of esophagitis, including Barrett esophagus, have increased frequency and duration of esophageal exposure to Stomach refluxate of pH lower than 4. Conversely, perfusing the esophagus of animals with a pepsin solution of pH 7.5 produces minimal mucosal disruption or changes in permeability. These observations are the cornerstone of acid suppressive therapy in the treatment of GERD.

Some studies have suggested that patients with reflux, especially those responding poorly to conventional antisecretory therapy, may have higher rates of acid secretion than controls. However, most evidence finds no abnormality of Stomach acid secretion in patients with GERD. Factors that reduce Stomach acid secretion naturally, for example, concomitant infection with H pylori, especially if it is the cagA + virulent strain, may protect from the development of severe esophagitis and Barrett esophagus. H pylori infection, particularly infection with this virulent strain, is a biologic antisecretory agent that lowers Stomach acidity. It produces severe corpus gastritis and accelerates the progression to multifocal atrophic gastritis and intestinal metaplasia, with concomitant lower acid output. In addition, the bacteria produce ammonia that acts as a powerful neutralizing agent at elevated pH conditions. The corpus mucosa returns to normal when the H pylori infection is cured, increasing acid secretion and possibly contributing to the reports of esophagitis after successful treatment of H pylori infection. The consequences of long-term normalization of parietal cell function and return to higher intragastric acidity is unknown, but they could promote the development of more severe GERD, Barrett esophagus, and adenocarcinoma in Western populations.

Duodenogastric Reflux

Bile acids have been implicated in the development of esophagitis, especially in the presence of increased duodenogastric reflux. Studies in animals demonstrate that conjugated bile acids produce their greatest injury in the presence of acid and pepsin, whereas trypsin, deconjugated bile salts, are more damaging in the absence of acid. Several surgical reports have suggested that duodenogastric reflux into the esophagus is frequent and may predispose to complications of GERD. However, accurate measurement of duodenogastric reflux is difficult. Duodenogastric reflux may be indirectly estimated by ambulatory pH studies using an esophageal pH of less than 7 to indicate alkaline reflux. However, the reliability of this indirect marker is now questioned by newer techniques, which either spectrophotometrically measure bilirubin, the most common pigment in bile, or measure esophageal impedance of the flow of liquids and gases independent of pH. These studies show that acid reflux and bile reflux increase together across the spectrum of GERD, making it nearly impossible to incriminate one agent over the other in the development of esophagitis. In addition, aggressive acid suppression with proton pump inhibitors (PPIs) decreases both acid and duodenogastric reflux probably by decreasing the volume of Stomach contents available to reflux into the esophagus. Finally, the absence of membrane microvesiculation and intracellular bile deposits in human esophageal biopsies, two distinctive morphologic features of experimental acid-bile salt injury, also argue against an important role for bile salts in GERD.

Delayed Stomach Emptying

The importance of delayed Stomach emptying in the pathogenesis of GERD is controversial. Early studies observed a delay in the Stomach emptying of solids in up to 50% of patients with reflux. More recent studies found only a 6% to 38% rate of delayed Stomach emptying, regardless of the severity of the esophagitis. Nevertheless, delayed Stomach emptying may be a major factor contributing to GERD in some groups, such as diabetic patients with autonomic peripheral neuropathy.

Associated Conditions

Certain medical and surgical conditions can predispose a person to GERD. The most common is pregnancy; 30% to 50% of pregnant women complain of heartburn, especially in the first trimester. Pregnancy increases the risk for reflux by the relaxing effects of circulating estrogens and progesterones on LES pressure. Although symptoms may be severe, esophagitis is uncommon, and this type of “situational” GERD is cured with childbirth.

Up to 90% of patients with scleroderma have GERD as the result of smooth muscle fibrosis causing low LES pressure and weak or absent peristalsis. Severe disease is common; up to 70% of patients have esophagitis, many have peptic strictures, and Barrett esophagus and carcinoma of the esophagus have been reported.

Unlike the previous two conditions that are characterized by LES dysfunction, hypersecretion of acid and increased Stomach volume are the major factors causing GERD in patients with the Zollinger-Ellison syndrome. In these patients, the esophagitis and complications may be more difficult to treat than the ulcer disease. After Heller myotomy, 10% to 20% of patients may develop GERD. Finally, prolonged nasogastric intubation may contribute to the development of reflux esophagitis, in part because acid tracks orad along the tube and because the tube mechanically interferes with LES barrier function.

Acid Reflux Causes (3)

2008-05-27T20:41:00.000-07:00

Esophageal Acid Clearance
The second tier against reflux damage is esophageal acid clearance. Reflux events determine the frequency and extent that gastric contents enter the esophagus, but esophageal acid clearance time determines the duration the mucosa is exposed to acid and probably the severity of acid damage. Esophageal acid clearance involves two related but separate processes: volume clearance, which is the actual removal of the reflux material from the esophagus, and acid clearance, which is the restoration of normal pH in the esophagus after acid exposure through titration with base, rather than true removal of the refluxed material.
Volume Clearance
Esophageal peristalsis operates to clear the acid volume in both the upright and supine positions, but it is inoperative during deep rapid eye movement sleep. Primary peristalsis is elicited by swallowing, which occurs with a frequency of once per minute in awake subjects, regardless of whether reflux occurs. Secondary peristalsis, initiated by esophageal distention from acid reflux, is much less effective in promoting clearance of refluxate, thus offering only an ancillary protective role. Peristaltic dysfunction, that is, failed peristaltic contractions and hypotensive (<30 style="font-style: italic;">Salivary and Esophageal Gland Secretions
Saliva is the second essential factor required for normal esophageal clearance of acid. Saliva has a pH of 6.4 to 7.8 and therefore is a weak base compared with the acidic gastric contents. The high rate of spontaneous swallowing results in saliva production of approximately 0.5 mL per minute. Although saliva is ineffective in neutralizing large volumes of acid (5 to 10 mL), it can neutralize small residual amounts of acid remaining in the esophagus after the volume of refluxed material has been cleared by several peristaltic contractions The importance of swallowed saliva is supported by findings that increased salivation induced by oral lozenges or bethanechol is associated with a significant decrease in acid clearance time. In contrast, suction aspiration of saliva is accompanied by a marked prolongation of esophageal clearance, despite the presence of normal peristaltic contractions. Physiological or pathological compromises of salivation may contribute to GERD. Diminished salivation during sleep explains why nocturnal reflux episodes are associated with markedly prolonged acid clearance times. Similarly, chronic xerostomia is associated with prolonged esophageal acid exposure and esophagitis. Cigarette smoking may promote GER. This was originally attributed to the effects of nicotine on lowering LES pressure, but more recent studies suggest that cigarette smokers have hyposalivation, which may also prolong esophageal acid clearance. Finally, the esophagosalivary reflex may be impaired in patients with reflux esophagitis. This is a vasovagal reflex demonstrated by perfusing acid into the esophagus, thereby stimulating increased salivation. This reflex may explain the symptoms of water brash (copious salivation) observed in some patients with reflux disease. The esophagosalivary reflex is very active in healthy persons, with a doubling or tripling of the salivary flow rate on exposure to acid. However, this reflex is diminished in patients with esophagitis and in those with strictures. In addition to the role of saliva, dilution and neutralization of residual acid are achieved by the aqueous bicarbonate (HCO 3 -)-rich secretions of the esophageal submucosal glands. These glands have been identified in the opossum as well as in the human esophagus. Reflux of acid into the esophageal lumen stimulates these glands and helps to neutralize the acid, even if swallowing does not occur.

Tissue Resistance
Although clearance mechanisms minimize acid contact time with the epithelium, even healthy persons may have their esophagus exposed to acid 1 to 2 hours during the day and sometimes at night. Nevertheless, only a few persons experience symptomatic GER, and even fewer suffer GERD. This is the result of a third tier for esophageal defense, known as tissue resistance. Tissue resistance is not a single factor, but a group of dynamic mucosal structures and functions that interact to minimize mucosal damage from the noxious gastric refluxate. Conceptually, tissue resistance can be subdivided into preepithelial, epithelial, and postepithelial factors.
The preepithelial defense in the esophagus, in contrast to the stomach and duodenum, is poorly developed. There is neither a well-defined mucous layer nor a buffering capacity by the surface cells to secrete HCO 3 - into the unstirred water layer. This results in a lumen-to-surface pH gradient in the esophagus of 1:10, in contrast to the stomach and duodenum, where the gradient can range from 1:1000 to 1:10,000.
The epithelial defenses in the esophagus consist of both structural and functional components. Structural components include the cell membranes and intercellular junctional complexes of the esophageal mucosa. This structure is a 25- to 30-cell-thick, nonkeratinized squamous epithelium functionally divided into a proliferating basal cell layer (stratum basalis), a midzone layer of metabolically active squamous cells (stratum spinosum), and a 5- to 10-cell-thick layer of dead cells (stratum corneum). The esophageal mucosa is a relatively “tight” epithelium with resistance to ionic movement at the intercellular as well as the cellular level as the result of both tight junctions and the matrix of lipid-rich glucoconjugates in the intercellular space. The functional components of tissue resistance include the ability of the esophageal epithelium to buffer and extrude hydrogen ions (H +). Intracellular buffering is accomplished by negatively charged phosphates and proteins, as well as HCO 3 -. When the buffering capacity is exceeded and intracellular pH falls, it has the capacity actively to remove H + from the cells. This is possibly by the action of two transmembrane proteins, one a sodium (Na +)/H + exchanger and the other a Na +-dependent chloride (Cl -)/HCO 3 - exchanger. After reflux-induced cell acidification, these transporters restore the intracellular pH to neutrality by exchanging H + for extracellular Na + or by exchanging Cl - for extracellular HCO 3 -, respectively. Additionally, esophageal cells contain within their membrane a Na +-independent Cl -/HCO 3 - exchanger that extrudes HCO 3 - from the cytoplasm when the intracellular pH is too high. When the epithelial cells are no longer able to maintain intracellular pH, they lose their ability to regulate volume, edema occurs, and balloon cells develop.
The postepithelial defense is provided by the esophageal blood supply. Blood flow delivers oxygen, nutrients, and HCO 3 - and removes H + and carbon dioxide, thereby maintaining normal tissue acid-base balance. Blood flow to the esophageal mucosa increases in response to the stress of lumenal acid. Cellular injury also stimulates cell proliferation, which results in thickening of the basal cell layer of the epithelium. Unlike the stomach, in which superficial mucosal injury is repaired in hours, the esophagus repairs itself more slowly over days to weeks.

Acid Reflux Causes : Hiatal Hernia

2008-05-26T08:48:00.000-07:00

The relationship between hiatal hernia and GERD remains controversial. Mainstream opinion has shifted widely from one that virtually equated hiatal hernia with GERD to one that denied it a causal role. Currently, both epidemiologic and physiological data confirm the importance of the hiatal hernia in patients with more severe esophagitis, peptic stricture, or Barrett esophagus. Hiatal hernias, identified endoscopically or radiologically, are reported in 54% to 94% of patients with reflux esophagitis; a rate strikingly higher than in the healthy population.
The functional impact of the hiatal hernia has been clarified by elegant combined manometry and videofluoroscopic studies that show that hiatal hernia impairs LES function through several mechanisms as well as impairing esophageal clearance. Reflux is worse in patients who have a nonreducible as opposed to a reducible hiatal hernia. Nonreducing hernias are those in which the gastric rugal folds remain above the diaphragm between swallows. Furthermore, statistical modeling has revealed a significant interaction between hiatal hernia and LES pressure, such that the likelihood of GER is increased as basal LES pressure decreases, an effect that is substantially amplified by the presence of a hiatal hernia and as hernia size increases.
Displacement of the LES from the crural diaphragm into the chest reduces basal LES pressure and shortens the length of the high-pressure zone primarily because of the loss of the intra-abdominal LES segment. Both these effects are caused by the loss of the extrinsic support of the diaphragmatic crura resulting in increased GER. Hiatal hernia virtually eliminates the increase of LES pressure that occurs during straining and may increase the triggering of transient LESRs during gastric insufflation with gas. , Large, nonreducible hernias also impair esophageal acid clearance because of increased tendency for reflux to occur from the hernia sac during swallow-induced LESRs.
The origin of hiatal hernia remains unclear. Familial clustering of GERD suggests the possibilities of inherited muscle weakness in this area. Animal studies propose that reflux itself causes esophageal shortening promoting the development of a hiatal hernia. Other studies find an association with obesity and lifting of heavy weights, raising the possibilities that over time, chronic intra-abdominal stressors may weaken the esophageal hiatus and may cause the development of a hiatal hernia. This theory is attractive because it helps to reconcile the increased prevalence of hiatal hernias as the population ages.

Acid Reflux Causes (2)

2008-05-25T08:04:00.000-07:00

Mechanisms of Reflux
Transient Lower Esophageal Sphincter Relaxations
This is the most common mechanism underlying GER and also accounts for the reflux of gases during belching. Transient LESRs are not associated with antecedent pharyngeal contractions, are unaccompanied by esophageal peristalsis, persist for longer periods (>10 seconds) than swallow-induced LESRs, and are always accompanied by inhibition of the crural diaphragm. Transient LESRs account for nearly all reflux episodes in healthy persons and for 50% to 80% in patients with GERD, depending on the severity of associated esophagitis. However, one study suggested that low basal LES pressure, rather than transient LESRs, may be the primary mechanism of GER in patients with nonreducible hernias. Transient LESRs are not always associated with GER. In healthy persons, about 40% to 60% of transient LESRs are accompanied by reflux episodes, compared with 60% to 70% in patients with GERD. The rate of transient LESR is increased by gastric distention, whether by gas or a meal, by stress, and, to a lesser extent, by subthreshold (for swallowing) stimulation of the pharynx. Under normal circumstances, meals are the major stimuli for transient LESRs, but the importance of specific foods is unknown. Transient LESRs are inhibited by the supine position, sleep, general anesthesia, and vagal cooling. Various drugs also impair transient LESRs including cholecystokinin A antagonists, anticholinergic drugs, morphine, somatostatin, nitric oxide inhibitors, 5-hydroxytryptamine 3 (5-HT 3) antagonists, and d-aminobutyric acid B (GABA B) agonists. Current evidence indicates that transient LESRs are mediated through vagal pathways. Gastric distention activates mechanoreceptors in the proximal stomach adjacent to the gastric cardia that send signals to the brainstem center through vagal afferent pathways. The structured sequence of motor events including LESR, inhibition of the crural diaphragm, and contractions of the esophageal body suggest that this process occurs in a programmed manner, probably controlled by a pattern generator within the vagal nuclei. The motor arm is in the vagus nerve and shares common elements with swallow-induced LESR.
Swallow-Induced Lower Esophageal Sphincter Relaxations
About 5% to 10% of reflux episodes occur during swallow-induced LESRs. Most of these episodes are associated with defective or incomplete peristalsis. During a normal swallow-induced LESR associated with normal peristalsis, reflux is uncommon because of the absence of concomitant crural diaphragm relaxation, the relatively short duration of LES relaxation (5 to 10 seconds), and the prevention of reflux by the oncoming peristaltic wave (see Reflux during swallow-induced LESR is more common in the presence of a hiatus hernia because of pooling of gastric liquids in the hernia sac and the absence of any residual diaphragmatic support during the LESR.
Hypotensive Lower Esophageal Sphincter Pressure
Stress reflux and free reflux are two mechanisms by which GER can be associated with diminished LES. Stress reflux results when a relatively hypotensive LES is overcome and is “blown open” by an abrupt increase in intra-abdominal pressure from coughing, straining, or bending. Stress reflux is unlikely when the LES pressure is greater than 10 mm Hg. Free reflux is characterized by a fall in intraesophageal pH without an identifiable change in intragastric pressure, and it usually occurs when the LES pressure is 0 to 4 mm Hg. Reflux as the result of low or absent LES pressure is uncommon. It is found mostly in patients with severe esophagitis, in whom it may account for up to 23% of reflux episodes, and rarely in patients without endoscopic evidence of esophagitis. The mechanisms of a low LES pressure are poorly understood. The presence of a hiatus hernia reduces LES pressure because the intrinsic support of the crural diaphragm is lost. Some LES weakness may be secondary to impairment of the excitatory cholinergic pathways to the LES as a result of esophagitis. Induction of experimental esophagitis in cats affects the release of acetylcholine and lowers LES pressures; changes that are reversible on healing of the esophagitis. However, healing of esophagitis in humans is rarely accompanied by an increase in LES pressure.

Acid Reflux Causes (1)

2008-05-24T07:34:00.000-07:00

PATHOPHYSIOLOGY
The pathophysiology of GERD is complex and results from an imbalance between defensive factors protecting the esophagus (antireflux barriers, esophageal acid clearance, tissue resistance) and aggressive factors from the stomach contents (gastric acidity and volume and duodenal contents). The intermittent nature of symptoms and esophagitis in many patients suggests that the aggressive and defensive forces are part of a delicately balanced system.
Antireflux Barriers
The first tier of the three-tiered esophageal defense against acid damage consists of the antireflux barriers. This is an anatomically complex region that includes the intrinsic lower esophageal sphincter (LES), the diaphragmatic crura, the intra-abdominal location of the LES, the phrenoesophageal ligaments, and the acute angle of His.
The LES is a tonically contracted segment of distal esophagus about 3 to 4 cm in length. It is the major component of the antireflux barrier and is capable of preventing reflux even when it is completely displaced from the diaphragmatic crura because of a hiatus hernia. The proximal margin of the LES is normally about 1.5 to 2.0 cm above the squamocolumnar junction, whereas the distal segment, about 2 cm in length, lies within the abdominal cavity. This location of the distal LES contributes to the maintenance of gastroesophageal competence during intra-abdominal pressure events. Resting LES pressure ranges between 10 to 30 mm Hg and includes a generous reserve capacity, because a minimal basal LES pressure in the range of 5 to 10 mm Hg usually prevents GER. The LES maintains a high-pressure zone by the intrinsic tone of its muscle and by cholinergic excitatory neurons. There is considerable diurnal variation in basal LES pressure; it is lowest after meals and highest at night. It is also influenced by certain circulating peptides and hormones, foods (particularly fat), and numerous drugs. During swallowing, LES relaxation (LESR) occurs for 5 to 10 seconds, thus permitting esophageal peristalsis to sweep the swallowed bolus into the stomach.
Anatomically, the LES lies within the hiatus created by the right crus of the diaphragm, and it is anchored by the phrenoesophageal ligaments, which inserts at about the level of the squamocolumnar junction . Developmentally, the crural diaphragm arises from the dorsal mesentery of the esophagus and is innervated separately from the costal part of the diaphragm. It is inhibited by esophageal distention, during vomiting, and in association with transient LESRs, but not during swallowing. The crural diaphragm provides extrinsic squeeze to the intrinsic LES, contributing to resting pressure during inspiration and also augmenting LES pressure during periods of increased abdominal pressure such as coughing, sneezing, or bending. Crural contractions impose rhythmic pressure increases of about 5 to 10 mm Hg on the LES pressure recording. During deep inspirations and some periods of increased abdominal straining, these changes may reach 50 to 150 mm Hg.
The oblique entrance of the esophagus into the stomach creates a sharp angle on the greater curve aspect of the gastroesophageal junction, the angle of His. This angle has been shown in cadavers to create a flap valve effect that contributes to gastroesophageal junction competency.

What is acid reflux?

2008-05-23T06:46:00.000-07:00

The term acid reflux disease or (GERD) describes any symptomatic condition or histopathologic alteration resulting from episodes of acid reflux. Reflux esophagitis is a condition experienced by a subset of GERD patients with endoscopically evident lesions in the esophageal mucosa. However, acid reflux often causes symptoms in the absence of esophagitis, and 24-hour esophageal pH monitoring can be helpful in identifying this subset of GERD patients. Nonerosive, or endoscopy-negative, GERD patients have reflux symptoms and abnormal esophageal acid exposure during ambulatory 24-hour pH monitoring, but no endoscopic evidence of esophagitis. The acid sensitive esophagus patient is in a subset of the endoscopy-negative GERD population characterized by normal esophageal acid exposure but nonetheless a strong correlation between reflux symptoms and acid reflux events.
Acid reflux disease (GERD) results from the failure of the normal antireflux mechanism to protect against frequent and abnormal amounts of acid reflux (GER), that is, the effortless movement of gastric contents from the stomach to the esophagus. GER is not itself a disease, but a normal physiological process. It occurs in virtually everyone, multiple times everyday, especially after large meals, without producing either symptoms or signs of mucosal damage. In contrast, GERD is a spectrum of disease usually producing symptoms of heartburn and acid regurgitation. Most patients have no visible mucosal injury at the time of endoscopic examination (nonerosive GERD), whereas others have esophagitis, peptic strictures, Barrett esophagus, or evidence of extraesophageal diseases such as chest pain, pulmonary symptoms, or ear, nose, and throat symptoms. GERD is a multifactorial process, one of the most common human diseases, and of economic importance, contributing to the expenditure in the United States of 4 to 5 billion dollars per year for antacid medications.

Acid Reflux Disease

2008-05-22T03:21:00.000-07:00

In this videoclip, you get an idea of what the doctor sees at esophagoscopy in a case of severe acid reflux. This patient has a hiatal hernia and his LES "valve" is wide open allowing acid to splash upward. Over time, this acid reflux has damaged the lower esophagus creating inflammation and ulcers.

Acid Reflux Surgery

2008-05-21T02:55:00.000-07:00

Watch the laparoscopic Nissen procedure for hiatal hernia.

What is acid reflux?

2008-05-19T02:10:00.000-07:00

Provided by the GERD Health Channel on eMedTV.com

What is Acid Reflux

2008-05-18T00:56:00.000-07:00

What is hiatal hernia?

2008-05-17T00:47:00.000-07:00

Normally, the lower esophageal sphincter remains closed except when you swallow. This prevents the passage of food and acid from your stomach into your esophagus. If the lower esophageal sphincter becomes weakened or relaxed, stomach acid may back up into your esophagus. Frequent acid reflux can irritate and inflame the lining of your esophagus, causing symptoms of heartburn. Some cases of heartburn occur when a portion of the stomach extends through the diaphragm. This is called hiatal hernia.

Gastroesophageal reflux disease (4)

2008-05-16T08:13:00.000-07:00

GERD

Gastroesophageal reflux disease (3)

2008-05-15T08:12:00.000-07:00

GERD

Heartburn and Acid Reflux Testing - Endoscopy

2008-05-14T21:30:00.000-07:00

Gastroesophageal reflux disease (2)

2008-05-12T21:15:00.000-07:00

GERD

Gastroesophageal reflux disease (1)

2008-05-11T21:09:00.000-07:00

GERD

What is GERD?

2008-05-09T12:47:00.000-07:00

What is GERD

2008-05-08T12:08:00.000-07:00

What is acid reflux?

2008-05-07T12:02:00.000-07:00

Acid Reflux Images

2008-05-05T12:26:00.000-07:00

Acid Reflux Causes

Acid Reflux natural course

Acid Reflux Complications

Acid Reflux Progress

Parietal cell receptors for acid secretiom

Proton Pump Inhibitors Mechanism of Action

Proton Pump Inhibitors Mechanism of Action

Parietal cell receptors for acid secretiom

H2 Receptor Antagonists Mechanism of Action

Acid Reflux Surgery

Barrett's Esophagus

Barrett's Esophagus

Acid Reflux in Children (1)

2008-05-05T11:32:00.000-07:00

GERD diagnosis : Diagnostic Tests

2008-05-04T11:56:00.000-07:00

Esophageal Manometry
Esophageal manometry allows accurate assessment of LES pressure and relaxation, as well as peristaltic activity including contraction amplitude, duration, and velocity. However, esophageal manometry is generally not indicated in the evaluation of the patient with uncomplicated GERD because most of these patients have a normal resting LES pressure. It is an integral component of pH testing to define the LES location accurately, a task poorly performed by endoscopy, fluoroscopy, or the pH pull-through technique. Esophageal manometry is an essential test in the preoperative evaluation of patients for antireflux surgery. A normal LES pressure does not preclude surgery for the reasons discussed, yet occasionally an alternative diagnosis such as achalasia or scleroderma is made, which may change the clinical approach. Most importantly, the presence of ineffective peristalsis characterized by either low-amplitude (<30>

Radiolabeled technetium-99m sulfur colloid scintiscanning is useful as a semiquantitative test for detecting GER. After instilling 300 mL of radioisotope in saline through a nasogastric tube into the stomach, gamma counts over the esophagus are obtained in the supine position before and after provocation with abdominal compression. Although test specificity approaches 90%, the sensitivity is quite variable, from 14% to 90%.

The acid perfusion (Bernstein) test is useful for detecting the relationship of symptoms to esophageal acidification. The study is done with the patient upright with a nasogastric tube positioned in the midesophagus. Initially, normal saline is infused at 120 drops/min for 5 to 15 minutes, followed by an infusion of 0.1 N hydrochloric acid. If symptoms develop with acid infusion, saline is reinfused to assess symptom relief. Symptoms during acid infusion, but not saline infusion, constitute a positive test. The sensitivity of the Bernstein test for GERD ranges from 32% to 100%, and its specificity ranges from 40% to 100%. In clinical practice, 24-hour esophageal pH testing has generally replaced both these tests.

Ambulatory esophageal bilirubin monitoring
Bile reflux can be measured using ambulatory esophageal bilirubin monitoring (Bilitec: Medtronics, Minneapolis, MN), which uses the spectrophotometric property of bilirubin, the most common pigment in bile. As in pH testing, a fiberoptic light source is introduced into the esophagus with a data collection system worn on a waist belt. A spectrophotometer measures the wavelength absorption at 450 nm (bilirubin) and at 565 nm (reference) every 8 seconds. An integrated microcomputer calculates the difference of the absorbances, which is directly proportional to the bilirubin concentration in the sample. This allows a pH-independent assessment of duodenogastroesophageal reflux, which is preferable to the older method employing an esophageal pH of more than 7. 70 In the future, ambulatory measurements of esophageal impedance, which measures the electrical activity of liquid and gas moving up and down the esophagus, combined with pH monitoring may be the preferred technique for measuring nonacidic reflux.

DIFFERENTIAL DIAGNOSIS
Symptoms associated with GERD may be mimicked by other esophageal and extraesophageal diseases including achalasia, Zenker diverticulum, gastroparesis, gallstones, peptic ulcer disease, functional dyspepsia, and angina pectoris. These disorders usually can be identified by failure to respond to aggressive antisecretory therapy and by diagnostic tests such as endoscopy, barium esophagram, esophageal manometry, ultrasound, nuclear emptying studies, and various cardiac tests. Although GERD is the most common cause of esophagitis, other causes (esophagitis, infections, or radiation esophagitis) need to be considered in cases that are difficult to manage cases and in older or immunocompromised patients.

Acid Reflux in Children

2008-05-04T11:16:00.000-07:00

GERD diagnosis : Barium Esophagram

2008-05-03T11:28:00.000-07:00

Barium Esophagram
The barium esophagram is an inexpensive, readily available, and noninvasive esophageal test. It is most useful in demonstrating structural narrowing of the esophagus and in assessing the presence and reducibility of a hiatal hernia. Subtle findings such as Schatzki rings, webs, or minimally narrowed peptic strictures are often seen only with an esophagram; they are missed by endoscopy, which may not adequately distend the esophagus. This test, which involves consuming a 13-mm radiopaque pill or marshmallow along with the barium liquid, is the most sensitive for detecting esophageal narrowing, with values reported between 95% and 100%. By giving the patient in the prone oblique position swallows of barium, the barium esophagram also allows good assessment of peristalsis and is helpful preoperatively in identifying a weak esophageal pump.

The ability of the barium esophagram to detect esophagitis varies considerably. Although sensitivities of 79% to 100% have been reported with moderate to severe esophagitis, mild esophagitis is usually missed. Barium testing also falls short when addressing the presence of Barrett esophagus. Barium studies can identify GER when contrast moves in a retrograde fashion from the stomach into the esophagus. If this occurs spontaneously, repeatedly, or to a significant degree into the middle or proximal esophagus, the test is positive, but it has a sensitivity of only about 40% for defining GERD. Provocative maneuvers such as leg lifting, coughing, the Valsalva maneuver, or the water-siphon test can be used to elicit stress reflux. Although these tests can improve the sensitivity of the barium esophagram, some argue that they also decrease its specificity.

The barium esophagram is primarily used in evaluating the patient with GERD with new-onset dysphagia because it can define subtle strictures and rings as well as assess motility. Conversely, endoscopy is preferred in the patient with recurrent dysphagia known to have a stricture or for the assessment of esophagitis or Barrett esophagus.

GERD diagnosis : Esophageal pH Monitoring

2008-05-02T10:25:00.000-07:00

Esophageal pH Monitoring

Ambulatory intraesophageal pH monitoring is now the standard for establishing pathological reflux. The test is performed with a pH probe passed nasally and positioned 5 cm above the manometrically determined LES. The probe is connected to a battery-powered data logger capable of collecting pH values every 4 to 6 seconds. An event marker is activated by the subject in response to symptoms, meals, and body position changes. Patients are encouraged to eat normally and to pursue regular daily activities. Monitoring is carried out usually for 18 to 24 hours. Reflux episodes are detected by a drop in pH to less than 4. Commonly measured parameters include the percentage of total time that the pH is less than 4, the percentage of time upright and supine that the pH is less than 4, the total number of reflux episodes, the duration of longest reflux episode, and the number of episodes longer than 5 minutes. The total percentage of time that the pH is less than 4 is the most reproducible measurement for GERD, with reported upper limits of normal values ranging from 4% to 5.5%. Ambulatory pH testing can discern positional variations in GER, meals, and sleep-related episodes and helps to relate symptoms to reflux events. As the result of its reliability for measuring GER across normal activities, ambulatory pH testing has replaced other older studies, such as the standard acid reflux (Tuttle) test and radionuclide scintigraphy.

One important problem with esophageal pH monitoring is that there exists no absolute threshold value that reliably identifies pathological GER. Validation studies comparing the presence of esophagitis with abnormal pH test report sensitivities ranging from 77% to 100% with specificities from 85% to 100%. However, these patients rarely need pH testing; rather, the patients with normal endoscopic findings and suspected reflux symptoms should benefit most from ambulatory pH monitoring. Unfortunately, the data are much less conclusive in this group, with considerable overlap between controls and patients with nonerosive reflux. Other drawbacks of pH testing include possible equipment failure, the pH probe’s missing a reflux event because it is buried in a mucosal fold, and false-negative studies resulting from dietary or activity limitations from poor tolerability of the nasal probe.

An important advantage of ambulatory esophageal pH monitoring is its ability to record and correlate symptoms with reflux episodes over extended periods. For this indication, it has essentially replaced the shorter acid perfusion (Bernstein) test. Because only about 10% to 20% of reflux episodes are associated with reported symptoms, different statistical analyses have evolved attempting to define a significant association between these two variables including the symptom index, symptom sensitivity index, and symptom association probability. Unfortunately, no studies to date have defined the accuracy of any of these symptom scores in predicting response to therapy. Therefore, pH testing and symptom correlation can define an association between complaints and GER, but only treatment trials address the true definition of a causal relationship.

Definite clinical indications for ambulatory pH monitoring have been established. Before fundoplication, pH testing should be performed in patients with normal endoscopic findings to identify the presence of pathological reflux. If esophagitis is present, pH testing is not necessary because the disease has been established. After antireflux surgery, persistent or recurrent symptoms warrant repeat pH testing. In these situations, pH monitoring is performed with the patient discontinuing all antireflux medications (PPIs for 1 week, H 2RAs for 2 days). Esophageal pH testing is particularly helpful in the evaluation of patients with reflux symptoms resistant to treatment with normal or equivocal endoscopic findings. For this indication, pH testing is usually done in patients receiving therapy to define two populations: those with and those without continued abnormal esophageal acid exposure times. The group with persistent GER needs intensification of the medical regimen, whereas those patients with symptoms and adequate acid control have another cause of their complaints. Finally, ambulatory pH testing may help in defining patients with extraesophageal manifestations of GERD. In this situation, pH testing is usually done with additional pH probes placed in the proximal esophagus or pharynx. Initially, most of these studies were done when patients were not taking antireflux medications, to confirm the coexistence of GERD; however, this does not guarantee symptom causality. Therefore, the current approach is to treat the patients aggressively with PPIs first and to reserve pH testing only for those patients not responding after 4 to 12 weeks of therapy.

What is acid reflux?

2008-05-02T10:17:00.000-07:00

GERD diagnosis : Endoscopy

2008-05-01T10:14:00.000-07:00

Endoscopy

Upper endoscopy is the current standard for documenting the type and extent of mucosal injury to the esophagus. It identifies the presence of esophagitis and excludes other causes of the patient’s complaints. However, only 40% to 60% of patients with abnormal esophageal reflux by pH testing have endoscopic evidence of esophagitis. Thus, the sensitivity of endoscopy for GERD is 60% at best, but it has excellent specificity, at 90% to 95%.

The earliest endoscopic signs of acid reflux include edema and erythema. Neither finding is specific for GERD, and both are very dependent on the quality of endoscopic visual images. More reliable are the findings of friability, granularity, and red streaks. Friability (easy bleeding), occurring with gentle pressure on the mucosa, results from the development of enlarged capillaries near the mucosal surface in response to acid. Red streaks may extend upward from the esophagogastric junction along the ridges of the esophageal folds. In studies evaluating these stigmata, nearly all patients had GERD. With progressive acid injury, erosions develop. These are characterized by shallow thinning of the mucosa associated with a white or yellow exudate surrounded by erythema. Commonly located just above the esophagogastric junction, erosions may be either single lesions or coalesced regions. Typically, they occur along the tops of mucosal folds, areas most prone to acid exposure. Erosions may also be caused by nonsteroidal antiinflammatory drug use, heavy smoking, and infectious esophagitis. Ulcers reflect more severe esophageal damage. They penetrate the mucosa, tend to have either a white or yellow discolored base, and may be seen either isolated along a fold or surrounding the esophagogastric junction.

Endoscopic grading of GERD depends on the endoscopist’s interpretation of these visual images. Unfortunately, there exists no standard classification scheme for endoscopic findings. Instead, several grading systems are available, but none are completely satisfactory. In Europe, the most popular scheme is the Savary-Miller classification, which is based on degree of mucosal erosions. In the United States, the Hetzel and Los Angeles systems are most popular. The Hetzel system grades severity not by the number of erosions but by the area of mucosal injury. In the Los Angeles system, the number, length, and location of mucosal breaks determine the degree of esophagitis. These different classification systems diverge the most when defining the subtlest degree of injury. When erythema, edema, and an indistinct Z-line are included, the sensitivity of diagnosing GERD rises at the expense of specificity.

Most patients with GERD are treated initially without endoscopy. The important exception is the patient experiencing alarm symptoms: dysphagia, odynophagia, weight loss, and gastrointestinal bleeding. With such symptoms, endoscopy should be performed early to rule out other entities such as infections, ulcers, cancer, or varices.

The role of endoscopy in GERD in the absence of alarm symptoms is more controversial and is evolving in the era of PPI therapy. Initially, endoscopy was used to place patients into two groups—those with nonerosive or mild disease and those with severe erosive disease—and to direct their treatment more precisely. However, this practice is now less popular with the use of PPIs as the first line of therapy for GERD. Because these drugs treat both groups equally well, early endoscopy has less impact on the choice of therapy. Currently, the most important reason for performing endoscopy in patients with GERD is to identify peptic strictures or Barrett esophagus. Using this rationale, most patients with chronic GERD need only one endoscopic examination while they are receiving therapy.

Esophageal Biopsy

The ability to obtain tissue during endoscopy is very important. Biopsies of the esophagus help to identify reflux injury, exclude other esophageal diseases, and confirm the presence of complications, especially Barrett esophagus. Microscopic changes indicative of reflux may occur even when the mucosa appears normal endoscopically. In patients with classical esophagitis, biopsies are usually not taken unless they are needed to exclude other diagnoses such as neoplasm, infection, pill injury, or bullous disease. When Barrett esophagus is suspected, biopsies are mandatory and are best done when esophagitis is healed.

The most sensitive histological markers of GERD are reactive epithelial changes characterized by an increase in the basal cell layer greater than 15% of the epithelium thickness or papilla elongation into the upper third of the epithelium. These changes represent increased epithelial turnover of the squamous mucosa. Papilla, or rete peg, height increases as a result of loss of surface cells from acid injury, whereas basal cell hyperplasia is indicative of mucosal repair. Unfortunately, these changes are also noted in up to 50% of healthy persons when biopsies are taken from the distal 2 to 3 cm of the esophagus. Hence, the changes are sensitive markers for GERD but have poor specificity.

Acute inflammation characterized by the presence of neutrophils and eosinophils is very specific for esophagitis. Acid reflux injury to the vascular bed of the esophagus releases vasoactive substances that promote edema and migration of neutrophils and eosinophils into the area. Neutrophils are specific for acute esophagitis but are an insensitive marker, being present in only 15% to 40% of patients with GERD. Eosinophils are found more often on biopsy (19% to 63% of subjects) but are less specific, present in up to 33% of healthy adults. Interestingly, the sensitivity and specificity of eosinophils in children are much stronger, reflecting the lack of eosinophils in the juvenile inflammatory response.

Acid Reflux Treatment

2008-05-01T09:51:00.000-07:00

What is Hiatal Hernia?

2008-04-22T07:41:00.000-07:00

Hiatal Hernia

Definition and classification
hiatal hernia is an extension of the peritoneal cavity into the chest through the esophageal hiatal of the diaphragm. The hernia consists of a peritoneal sac which usually contains part or all of the stomach but can rarely contain other abdominal viscera such as the colon or spleen. hiatal hernias are classified according to the position of the gastroesophageal junction in relation to the diaphragm. The type I or sliding hiatal hernia is characterized by proximal herniation of the gastroesophageal junction though the esophageal diaphragmatic hiatus into the posterior mediastinum. In a type II hernia, also known as a rolling or pure paraesophageal hernia, the gastroesophageal junction is anchored in its normal subdiaphragmatic position, and the gastric fundus herniates alongside the esophagus into the chest. A type III hernia, also known as a combined sliding/rolling, or mixed hernia, is usually a large hernia and is characterized by proximal herniation of both the gastroesophageal junction and the gastric fundus through a widely open diaphragmatic hiatus. Type III hernias are commonly but inappropriately classified as type II paraesophageal hernias, but a pure type II hernia is a rare finding. The endstage of a type I or II hernia is a large type III hernia, which occurs when the entire stomach migrates up into the chest by rotating 180° around its longitudinal axis, with the gastroesophageal junction and pylorus as fixed points. The greater curvature is thus uppermost in the chest. In this situation, the abnormality is usually referred to as an intrathoracic stomach with organoaxial volvulus. In a type IV hernia, the hiatal defect is very large and has allowed other organs such as the colon, spleen, small intestine, and pancreas to enter the chest. Type IV hernias develop from type III hernias, and are exceedingly uncommon.

Prevalence of hiatal hernia
The majority of hernias, probably more than 95 per cent, are type I sliding hernias. The exact prevalence of hiatal hernia, both in the general population and in patients with foregut symptoms, remains unclear. Reasons for this uncertainty are that most hernias are small sliding hernias which reduce in the upright position, most are asymptomatic, and the detection rate varies with the method used for diagnosis and with the age of the population studied. The reported prevalence of hiatal hernia detected by barium contrast studies in the general population ranges from 10 per cent to more than 70 per cent. It is likely that some of these studies, especially if they are based on static rather than videotaped imaging, classified some physiologic hernias as pathologic hernias. A reasonable estimate of the prevalence of pathologic herniation in the general adult population is 20 per cent, with the prevalence of hernias in patients with gastroesophageal reflux disease being 80 per cent. The mean age of patients with a type I hernia is approximately 50 years and for those with a type III hernia is approximately 60 years. Type III hernias are more common in females, with a female:male ratio of 4:1.

Pathophysiology
A pathologic hiatal hernia is an acquired condition. Anatomic alterations found in patients with hiatal hernia are widening of the hiatus and thinning and lengthening of the phrenoesophageal membrane. The phrenoesophageal membrane consists of an upper fascial layer of loose connective tissue and a lower fascial layer of thicker, stronger, elastic tissue. The upper layer is formed by a supradiaphragmatic continuation of the endothoracic fascia. The more important lower layer is formed by a subdiaphragmatic continuation of the transversalis fascia. The phrenoesophageal membrane functions as an elastic barrier. In comparison with the other diaphragmatic openings, the esophageal hiatal is relatively incompletely filled by the esophagus, and the barrier function of the phrenoesophageal membrane is needed to close the gap between esophagus and diaphragm. The elastic function of the phrenoesophageal membrane allows it to stretch and contract with swallowing and respiration. There are normally more than 1000 swallows per day, and the diaphragm moves up and down between 16 000 and 35 000 times per day. The lengthening and loss of elasticity of the phrenoesophageal membrane that is found in a hiatal hernia is thought to be a gradual age-related wear and tear effect, but obesity, pregnancy, and sudden traumatic elevations in the intra-abdominal pressure may all place additional pressure on the phrenoesophageal membrane.
Mixed or type III hernias are thought to be complications of type I hernias, and are more likely in patients who have an abnormally wide esophageal hiatus. Pure paraesophageal or type II hernias are thought to arise by the same mechanism as sliding hernias, with the difference that the gastroesophageal junction is fixed below the hiatus by firm posterior fixation to the preaortic fascia and the median arcuate ligament. Another difference is that the herniation may occur either through a widened esophageal hiatus or through a defect adjacent to the esophageal hiatus. The fundus of the stomach rolls up alongside the esophagus through the widened hiatus or the adjacent defect, but the gastroesophageal junction remains in its normal intra-abdominal position.
A hiatal hernia predisposes to the development of gastroesophageal reflux by four mechanisms. First, contraction of the crural components of the diaphragm augments the antireflux mechanism by buttressing the lower esophageal sphincter, adding the pressure produced by crural contraction to the underlying pressure in the lower esophageal sphincter. The presence of a hiatal hernia interferes with this buttressing because the normal alignment between the crura and the lower esophageal sphincter is lost. This encourages reflux during periods of increased intra-abdominal pressure. Second, the formation of a hiatal hernia results in loss of the acute angle of His. Third, the clearance of refluxed acid from the esophagus is also impaired in patients with hiatal hernias, especially non-reducing hernias, due to loss of anchoring of the distal esophagus. Fourth, the presence of a hiatal hernia interferes with transhiatal flow of gastric juice. This occurs in particular in patients with a non-reducing hernia, in whom the hernia remains above the diaphragm during inspiration. Fluid trapped within the supradiaphragmatic stomach is prevented from flowing into the subdiaphragmatic stomach by closure of the crura during inspiration, and thus refluxes freely into the negative-pressure thoracic esophagus.

Symptoms
Symptoms in patients with a sliding hernia are mostly those of the associated gastroesophageal reflux. The likelihood of reflux increases with increasing hernia size. Dysphagia and intermittent vomiting can occur in patients with a large sliding hernia, due to diaphragmatic contraction obstructing the passage of a bolus through the herniated stomach. Dysphagia is common in patients with type II hernias, due to compression and angulation of the esophagus by the herniated gastric fundus. In large type III hernias with gastric volvulus, dysphagia can be caused by twisting of the gastroesophageal junction. Recurrent bleeding or anemia may be caused by ulceration or erosive gastritis secondary to ischemia of the herniated gastric mucosa. Crural contractions may also cause ‘riding ulcers' at the level of the diaphragmatic indentations. Respiratory symptoms such as dyspnea may occur from compression of the lungs by a very large hernia, and cough, choking, and pneumonia may result from aspiration of regurgitated gastric juice into the airways.
Type II or III hernias can cause acute life-threatening events in up to 20 per cent of patients due to acute obstruction from gastric torsion or volvulus. Swallowed air causes gastric distention, which compresses the blood supply passing to the intrathoracic stomach along the margins of the diaphragmatic hiatus. This can result in gastric ischemia, perforation, and sepsis. The triad of epigastric pain, inability to vomit, and difficulty in the ability to pass a nasogastric tube is an indication for immediate endoscopic decompression or operative intervention.

Diagnosis
Radiology
Large hernias may be detected on an upright or lateral plain chest radiograph by the presence of a gas-filled viscus behind the heart. Smaller hernias require a barium swallow study for diagnosis. Barium studies are diagnostic in more than 90 per cent of patients. The barium swallow study should include examination in both upright and supine positions, to detect sliding hernias that reduce when upright. Video-esophagram studies demonstrate that most sliding hernias empty during expiration.
Endoscopy
A hiatal hernia is present endoscopically when the anatomic gastroesophageal junction, identified as the proximal extent of the gastric rugal folds, is more than 2 cm above the crura, identified by having the patient sniff. Small hernias are best detected endoscopically if the endoscope is retroflexed within the stomach, allowing inspection of the gastroesophageal junction from below. The geometry of the gastroesophageal junction seen on retroflexed view can be classified using the Hill grading system. This classification system emphasizes that development of a sliding hernia is accompanied by loss of the angle of His, signified by the loss of the normal frenulum over the endoscope on retroflexed viewing. A true paraesophageal hernia is identified on retroflexed view by noting a hernia orifice adjacent to the gastroesophageal junction. A type III hernia appears on retroflexed view as a sliding hernia with the gastroesophageal junction entering on the side of the sac, rather than at the apex of the sac as in a type I hernia.
Manometry
Stationary manometry studies are not used for the diagnosis of hiatal hernia, but an awareness of manometric features of hiatal hernia is helpful since many patients undergoing manometry for the investigation of reflux disease have a hiatal hernia. A ‘double hump' motility pattern is characteristic of a sliding hernia. As the manometry catheter is withdrawn from the stomach into the esophagus, pressurized areas or ‘humps' are recorded, with the distal hump corresponding to the crural compression of the stomach and the proximal hump corresponding to the lower esophageal sphincter. Between the two humps is a plateau region in which the pressure is slightly above the gastric baseline pressure. The plateau region corresponds to the hernia sac. The pressure fluctuations that occur with respiration indicate that the hernia sac may be exposed to both intra-abdominal and intrathoracic pressure conditions, depending upon whether the crura compartmentalize the herniated proximal stomach from the distal stomach and peritoneal cavity.

Treatment
Sliding hernias do not require treatment unless they produce symptoms specific to the presence of the hernia. In patients with gastroesophageal reflux disease, reduction of the hernia and closure of the hiatus is an essential part of operative treatment, and as a consequence the hernia is repaired. Patients with large hernias undergoing antireflux surgery are likely to have a shortened esophagus requiring special operative techniques. The high rate of serious or life-threatening complications in patients with type II or III hernias indicates that operative repair should be performed in all patients with these hernias, regardless of the presence or severity of symptoms or the size of the hernia. Type II or III hernias progressively worsen unless repaired by operation. There is an approximately 20 per cent mortality for emergency repair of an incarcerated paraesophageal hernia, compared with less than 1 per cent mortality for elective repair of a non-incarcerated hernia.
Repair of type II or III hernias by laparoscopic methods can be difficult and is associated with a higher rate of recurrence. We prefer an open approach to these large hernias. An open transthoracic approach allows full esophageal mobilization, resection of the sac, and proper closure of the wide hiatus. An open approach also facilitates performance of a Collis gastroplasty if this is needed to gain adequate esophageal length to reduce tension on the repair. The transabdominal open approach facilitates reduction of a volvulus, but it may be difficult to obtain an adequate view for dissection in the posterior mediastinum, the risk of vagus nerve injury is high, and stout closure of the widened hiatus may be compromised.

Acid Reflux Treatment : Lifestyle Modifications

2008-04-12T18:20:00.000-07:00

Lifestyle Modifications
Sensible changes in lifestyle, especially if their rationale is explained to the patient, should be part of the initial management of all subjects. These include head of the bed elevation, avoidance of tight-fitting clothes, weight loss, restriction of alcohol, elimination of smoking, dietary therapy, refraining from lying down after meals, and avoidance of evening snacks before bedtime. Physiological studies show that these maneuvers enhance esophageal acid clearance, minimize acid-reflux related events, or ease heartburn symptoms, but their therapeutic efficacy in controlled trials usually has not been evaluated. The head of the bed can be elevated either by putting 6- to 8-inch blocks under the legs of the bed or by using a Styrofoam wedge under the mattress to elevate the upper torso. Eating several hours before retiring and avoiding evening snacks keep the stomach empty at bedtime, thereby decreasing the number of nocturnal reflux episodes. These three lifestyle changes are recommended for patients with nocturnal GERD symptoms or laryngeal complaints. One study found that head of the bed elevation was nearly as effective as ranitidine therapy in healing esophagitis. Avoidance of tight-fitting clothes and weight loss are interventions aimed at reducing the incidence of reflux by the abdominal stress mechanism. The efficacy of weight reduction is especially controversial, but it may be helpful when discrete periods of weight gain can be associated with exacerbation of reflux symptoms. Cessation of smoking and elimination of alcohol are valuable because both agents lower LES pressure, reduce acid clearance, and impair intrinsic squamous epithelial protective functions. Dietary changes include reducing the size of the meal and intake of fats, carminatives, and chocolate, to reduce the frequency of reflux by decreasing gastric distention and by reducing the episodes of transient LESRs, and avoiding foods that lower basal LES pressure. Additionally, some patients complain of heartburn after consuming citrus drinks, spicy foods, tomato-based products, coffee, tea, or cola drinks. Stimulation of gastric acid or esophageal sensitivity to low pH or hyperosmolar liquid solutions may account for these symptoms. However, the indiscriminate prohibition of food products should be avoided, but rather tailored to those foods that bring on individual symptoms, to promote dietary compliance. Finally, patients should avoid, if possible, drugs that lower LES pressure or can promote localized esophagitis.

Acid Reflux Treatment

2008-04-11T18:14:00.000-07:00

The rationale for GERD therapy depends on a careful definition of specific aims. In patients without esophagitis, the therapeutic goals are simply to relieve the acid-related symptoms and to prevent frequent symptomatic relapses. In patients with esophagitis, the goals are to relieve symptoms and to heal the esophagitis while attempting to prevent further relapses and the development of complications. These goals are set against a complex background: GERD is a chronic disease that may wax and wane in intensity, and relapses are common.

Nonprescription Therapy
Although GERD is common in the United States, very few persons seek medical care for their complaints, instead choosing to change their lifestyles and self-medicate with over-the-counter (OTC) antacids and low doses of H 2RAs. These observations have led to the “iceberg” model of the GERD population. Most heartburn suffers are invisible because they self-medicate and do not seek professional help; only those at the tip of the iceberg, typically patients with severe symptoms or reflux complications, are seen by physicians.

Over-the-Counter Medications Over-the-counter antacids, Gaviscon, and H 2RAs are useful in treating mild and infrequent heartburn symptoms, especially when symptoms are brought on by lifestyle indiscretions. Antacids increase LES pressure but work primarily by buffering gastric acid in the esophagus and stomach, albeit for relative short periods. Heartburn symptoms are rapidly relieved, but patients need to take antacids frequently, usually 1 to 3 hours after meals and at bedtime, depending on symptom severity. Gaviscon, containing alginic acid and antacids, mixes with saliva to form a highly viscous solution that floats on the surface of the gastric pool and acts as a mechanical barrier. Both antacids and Gaviscon are more effective than placebo in relieving symptoms induced by a heartburn-promoting meal. However, these agents do not heal esophagitis, and long-term trials suggest effective symptom relief in only 20% of patients using antacids. Side effects of antacids and Gaviscon are minimal but include diarrhea from magnesium-containing antacids, constipation from aluminium-containing antacids, salt overload, magnesium or aluminium toxicity in patients with renal disease, and the milk-alkali syndrome (hypercalcemia, alkalosis, renal failure) from long-term and excessive use of calcium-containing antacids. H 2RAs are available in an OTC form at doses that are usually one half of the standard prescription dose. Although there are some differences in potency, duration, and rapidity of action, these drugs may be used interchangeably. Although their onset of relief is not as rapid as that of antacids, the OTC H 2RAs have a longer duration of action, up to 6 to 10 hours. Therefore, they are particularly useful when taken before a potentially refluxogenic activity, such as a heavy meal or exercise. Like antacids, the OTC H 2RAs are ineffective in healing esophagitis and should not be used regularly for more than 2 weeks.

Prescription Medication Therapy
Patients with frequent heartburn, esophagitis, or complications of GERD usually see a physician and receive prescription medications for their disease. Although prokinetic drugs attempt to correct the motility disorder associated with GERD, the most clinically effective medications for short- and long-term reflux treatment are the acid suppressive drugs.

GERD Treatment :Prokinetic Drugs

2008-04-10T18:00:00.000-07:00

Prokinetic Drugs
Until recently, three prokinetic drugs were available for the treatment of GERD: bethanechol, a cholinergic agonist; metoclopramide, a dopamine antagonist; and cisapride, a serotonin (5-HT 4) receptor agonist, which increases acetylcholine release in the myenteric plexus. These drugs improve reflux symptoms by increasing LES pressure, acid clearance, or gastric emptying. However, none alter the frequency of transient LESRs, and their physiological activity decreases as the disease severity worsens. Therefore, all the current prokinetics provide modest benefit in controlling heartburn, but they have little efficacy in healing esophagitis unless they are combined with an acid inhibiting drug. The use of prokinetic drugs is limited by their side effect profiles. Bethanechol commonly causes flushing, blurred vision, headaches, abdominal cramps, and urinary frequency. Metoclopramide, which crosses the blood-brain barrier, has a 20% to 50% incidence of fatigue, lethargy, anxiety, and restlessness and rarely causes tremor, parkinsonism, or tardive dyskinesia. It is possible to decrease the frequency of these side effects by dose reduction, by increasing the dosing regimen to twice a day, by taking a larger single dose before dinner or at bedtime, or by using a sustained-release tablet. Domperidone, another dopamine antagonist and one that does not cross the blood-brain barrier, has fewer side effects, but it is not available in the United States. Although the best prokinetic drug for treating GERD with an excellent safety profile, cisapride was withdrawn from the United States market because of increased reports of serious cardiac arrhythmias (ventricular tachycardia, ventricular fibrillation, torsades de pointes, and QT prolongation) with associated cardiac arrest and deaths related to possible drug interactions. These drugs included common antibiotics (clarithromycin, erythromycin), antifungals (fluconazole, itraconazole, ketoconazole), and some antiviral agents. When taken with cisapride, these drugs inhibited the cytochrome P450 3A4 enzyme that metabolizes cisapride, thereby increasing cisapride blood levels to potentially dangerous values.

GERD Treatment :Histamine 2 Receptor Antagonists

2008-04-08T17:50:00.000-07:00

Histamine 2 Receptor Antagonists
Cimetidine, ranitidine, famotidine, and nizatidine reduce acid secretion by competing with histamine receptors on the parietal cell. They are most effective in controlling nocturnal, as compared with meal-related acid, secretion because the parietal cell may also be stimulated postprandially by acetylcholine and gastrin. All the H 2RAs are equally effective when used in proper doses, usually twice a day before meals. Clinical GERD trials show that heartburn, both day and night, can be significantly decreased by H 2RAs, when compared with placebo, although symptoms are rarely abolished. Trials and a metaanalysis found that the overall esophagitis healing rates with H 2RAs rarely exceeded 60% after up to 12 weeks of treatment, even when higher than standard doses were used. Healing rates differ in individual trials, depending primarily on the degree of esophagitis being treated: grade I and II esophagitis heals in 60% to 90% of patients, whereas grade III and IV heals in 30% to 50% of patients despite high-dose regimens.

Reflux symptoms associated with nocturnal gastric acid breakthrough during PPI therapy have been recognized. At bedtime, H 2RAs successfully eliminated this problem, suggesting a new indication for H 2RAs in the PPI era. However, this study used only a single evening dose and did not account for the tolerance that frequently develops to H 2RAs over weeks to months. This may impair the ability of chronic long-term nocturnal dosing of H 2RAs to eliminate acid breakthrough symptoms, but it suggests an important clinical role as medications used on an as-needed basis when lifestyle indiscretions may promote nocturnal symptoms. As a class of drugs, the H 2RAs are very safe, with a side effect rate (most of which are minor and reversible) of about 4%. There have been some concerns about drug interactions with these agents. Serum concentrations of phenytoin, procainamide, theophylline, and warfarin are altered after the administration of cimetidine and, to a lesser degree, ranitidine, whereas this interaction is not reported with the other two H 2RAs. The former concern that these agents could alter blood ethanol levels has been discounted.

GERD Treatment :Proton Pump Inhibitors

2008-04-07T17:37:00.000-07:00

Proton Pump Inhibitors
This class of drugs markedly diminishes gastric acid secretion by inhibiting the final common pathway of acid secretion, the H +, K +-ATPase pump. PPIs inhibit daytime, nocturnal, and meal-stimulated acid secretion to a significantly greater degree than H 2RAs, but they rarely make patients achlorhydric. Unlike H 2RAs, the degree of acid inhibition with PPIs does not correlate with plasma concentration, but it is related to the concentration and duration. After oral ingestion, acid inhibition is delayed because PPIs need to accumulate in the secretory canaliculus of the parietal cell to bind irreversibly to actively secreting proton pumps. Therefore, the slower a PPI is cleared from the plasma, the more of it is available for delivery to the proton pumps. PPIs are best taken before the first meal of the day, when most proton pumps are active. Because not all pumps are active at any given time, a single PPI dose does not inhibit all pumps. A second dose, if needed, can be taken before the evening meal. The five available PPIs are omeprazole, lansoprazole, rabeprazole, pantoprazole, and esomeprazole, the S-isomer of the racemic omeprazole. Their superior efficacy compared with H 2RAs is based on their ability to maintain an intragastric pH high than 4 between 15 to 21 hours daily compared with approximately 8 hours daily with the H 2RAs. Multiple studies show that the PPIs are superior to H 2RAs in completely relieving heartburn symptoms in most patients with severe GERD, usually within 1 to 2 weeks. Symptom relief is slightly better in patients with erosive as compared with nonerosive disease. Controlled studies and a large metaanalysis report complete healing of even severe ulcerative esophagitis after 8 weeks in more than 80% of patients taking PPIs compared with 51% of patients taking H 2RAs and 28% receiving placebo. In those patients not healing initially, prolonged therapy with the same dose or an increased dose usually resulted in 100% healing. Studies with PPIs consistently show that they are superior to both regular and high-dose H 2RA therapy, but therapeutic efficacy among PPIs is similar. However, a large study found that the newest PPI, esomeprazole, at a dose of 40 mg, was superior to the parent compound (omeprazole, 20 mg) for complete healing of esophagitis at 4 and 8 weeks. This superiority over omeprazole is related to higher systemic bioavailability and less interpatient variability with esomeprazole. One PPI, pantoprazole, is available in the United States for intravenous use. All the PPIs, are well tolerated with headaches and diarrhea described as the most common side effects in clinical trials. Although increased gastrin levels are reported with all the PPIs, the elevations generally do not exceed the normal range for gastrin and return to normal values within 1 week of stopping the drug. Omeprazole may decrease the clearance of diazepam and warfarin because of competition for the cytochrome P450 isoenzyme P2C19. The four newer PPIs have minimal or no important drug-drug interactions.

Acid Reflux Surgery

2008-04-06T17:13:00.000-07:00

Surgical Treatment of Acid Reflux Disease

Antireflux surgery reduces GER by increasing basal LES pressure, decreasing episodes of transient LESRs, and inhibiting complete LESR. This is accomplished by reducing the hiatal hernia back into the abdomen and thereby restoring an adequate length of intra-abdominal sphincter, reconstructing the diaphragmatic hiatus, and reinforcing the LES. Before the explosion of laparoscopic surgery, the three most common operations were the Nissen fundoplication, the Belsey Mark IV repair, and the Hill posterior gastropexy repair. Since the advent of minimally invasive surgery, the two most popular procedures are the Nissen fundoplication and the Toupet partial fundoplication. The former is a superior operation with more long-term durability, but it has a higher frequency of postoperative dysphagia and gas bloat symptoms. Both are now routinely performed laparoscopically through the abdomen. The hospital stay is 1 to 2 days, and many patients return to normal activity in 7 to 10 days. Patients with more severe disease and a short esophagus manifested by a large nonreducible hernia, a tight stricture, or a long-segment Barrett esophagus require a Collis lengthening procedure creating a 3- to 5-cm neoesophagus, so the fundoplication can be placed in the abdomen under minimal tension.

The common indications for antireflux surgery have evolved with the availability of more powerful medications for treating GERD. In the PPI era, the resolution of symptoms on treatment helps to predicate the success of antireflux surgery for both classical and atypical symptoms. Antireflux surgery is a reasonable option in the following situations:

1. Healthy patients with GERD well controlled on PPIs who want alternative therapy because of drug expense, poor medication compliance, or a fear of unknown long-term side effects

2. Patients with atypical GERD symptoms responding to PPIs

3. Patients with volume regurgitation and aspiration symptoms not controlled on PPIs.

Patients recalcitrant to PPI therapy need to be approached cautiously with surgery because they may have another cause of their disorder (i.e., pill esophagitis, gastroparesis, functional heartburn).

Extensive physiological testing should be done before antireflux surgery is performed. All patients need endoscopy to exclude stricture, Barrett esophagus, and dysplasia. A barium esophagram can help define a nonreducible hernia, shortened esophagus, and poor esophageal motility. Esophageal manometry will identify ineffective esophageal peristalsis and previously misdiagnosed achalasia or scleroderma. Twenty-four hour pH testing is needed in all patients with nonerosive GERD or in those with esophagitis not responding to PPI therapy. Gastric analysis and gastric emptying studies may be indicated in selected patients. Careful testing will result in modification of the original operation or an alternative diagnosis in approximately 25% of patients.

Antireflux surgery relieves reflux symptoms and reduces the need for stricture dilation in more than 90% of patients, but Barrett esophagus rarely regresses, and the influence of surgery on the development of esophageal adenocarcinoma is controversial. Comparison studies have found antireflux surgery superior to lifestyle changes, antacids, and H 2RA and prokinetic therapy, but not PPI therapy, especially when dose titration is permitted. Mortality is rare (lesser than 1%) after antireflux surgery, but new postoperative complaints can occur in up to 25% of patients including dysphagia, gas bloat, diarrhea, and increased flatus. Most symptoms improve over 1 year, but persistent complaints suggest too tight a wrap, a displaced fundoplication, or inadvertent damage to the vagus nerve. Successful antireflux surgery, however, does not guarantee a permanent cure. The best surgical results are obtained by experienced surgeons in high-volume centers who report long-term symptom recurrence in only 10% to 15% of patients. However, most operations are performed by community or Veterans Affairs hospital surgeons. Here the results are not as good with studies finding relapse of esophagitis in 30% of patients and return to regular use of antireflux medications in 62% of patients 10 to 15 years after fundoplication. Potential factors contributing to these high relapse rates include inexperienced surgeons, low numbers of operations yearly per surgeon, and persistence of abdominal stressors (i.e., obesity, heavy isometric exercise or work) that gradually weaken the fundoplication. A suboptimal operation or severe symptom relapse may necessitate a second operation, which has less likelihood of a successful outcome. Because optimal medical therapy is available to all patients with GERD, the risk and benefits of both long-term medical treatment and antireflux surgery must be carefully discussed with patients, so they can take part in this important decision.

GERD Treatment (Elderly and Pregnant )

2008-04-05T16:59:00.000-07:00

Acid Reflux Treatment in Elderly Patients
Older patients often complain of less severe reflux symptoms than their younger cohorts, but because of prolonged acid exposure over years, the elderly may have more complicated disease. Treatment of the older patient with GERD follows the same principles as in other adults, although they may require more aggressive acid suppression therapy. Pill-induced esophagitis may complicate their treatment. Metoclopramide must be used with caution because of frequent side effects in the elderly. H 2RAs can be associated with mental changes in older patients, and doses need to be decreased in patients with renal insufficiency. Fewer drug interactions are seen with famotidine and nizatidine. Alternative methods of administering PPIs may be necessary in debilitated older patients who cannot swallow intact omeprazole or lansoprazole capsules. Both capsules can be opened and the granules taken with water, an HCO 3 --based suspension, or apple or orange juice, or the granules can be sprinkled on applesauce or yogurt.

Acid Reflux Treatment during Pregnancy
Teratogenicity or fetal harm from absorption of medications across the placenta is the foremost consideration in the treatment of GERD during pregnancy. Lifestyle modifications and antacids or Gaviscon remain the cornerstones of treatment, providing adequate relief to the majority of women with mild symptoms. Although rarely used in adults, sucralfate is a nonabsorbable mucosal binder that has been found superior to lifestyle changes in a controlled study in pregnant women. Metoclopramide, H 2RAs, and most PPIs (except omeprazole) have a Category B FDA safety profile for use during pregnancy, based on animal studies showing no risk, as well as on small case series and anecdotal human reports. Ranitidine is the only one of these drugs shown to be effective during pregnancy. PPIs may be safe for aspiration prophylaxis before anesthesia for elective cesarean sections. Antacids, sucralfate, and most H 2RAs (except nizatidine) are safe to use during lactation, even though the latter group of drugs is excreted in breast milk. PPIs are not recommended during breast-feeding, based on safety concerns in animal studies.

Treatment of Acid Reflux Complications

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Extraesophageal Presentations
Acid reflux–related chest pain is easily treated by H 2RAs or PPIs, with efficacy substantiated by placebo-controlled studies. The efficacy of acid suppression therapy in asthma, cough, and other pulmonary complications of GERD is more mixed. Medical antireflux therapy improves asthma symptoms and reduces the need for asthma medications in more than 60% of patients, but objective improvement of peak expiratory flow rates is observed in only 25% of patients. Best results are found with higher doses of PPIs (usually twice-daily administration) given for 2 to 3 months. Potential positive predictors of PPI response include asthma that is difficult to control, associated acid regurgitation, proximal reflux on pH testing, and healing of esophagitis with antireflux therapy. Case studies report that 60% to 96% of patients with suspected acid-related ear, nose, and throat symptoms and signs improve with acid suppression. Here again, PPIs are more effective than H 2RAs, and extended therapy for up to 3 months may be required. Predictors of response have not been identified, although patients with milder laryngeal signs show better symptom improvement. In all these possible extraesophageal presentations of GERD, failure to respond to aggressive PPI therapy, confirmed by adequate acid control by pH testing, suggests a cause of these complaints other than acid.

Esophageal Strictures
Dysphagia in patients with esophageal strictures is related to stricture diameter and severity of esophagitis. When the esophageal lumen diameter is less than 13 mm, dysphagia is a major complaint and esophageal dilation is required. Simple short strictures can be dilated by blind peroral passage of rubber Hurst (round ends) or Maloney (taper ends) mercury-filled dilators of increasing sizes (16 to 60 French, 3 French = 1 mm) to disrupt the fibrous bands producing the obstruction. Complicated longer, tighter, or more irregular strictures will require bougienage over a guidewire using hollow-centered Savary plastic-covered polyvinyl dilators or balloon (Gruentzig) dilators. Before and after dilation, medical therapy with PPI is indicated; it has been shown to be superior to H 2RAs in relieving symptoms and in reducing the frequency for repeat dilations. Maintenance PPI therapy for patients with strictures has dramatically reduced the incidence of repeat esophageal dilations and the cost of treating these patients. Recalcitrant strictures, requiring surgery, are now very uncommon and suggest another aggravating factor such as chronic pill injury.

Barrett’s Esophagus Treatment

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Barrett Esophagus In general, esophagitis in the presence of Barrett esophagus can be easily healed with PPI therapy, but meaningful regression of Barrett epithelium, except for small squamous islands, is rarely reported even with high-dose PPI therapy. Recent ex vivo studies have suggested that intermittent “pulses” of acid result in enhanced Barrett epithelial cell proliferation, possibly increasing the risk of dysplasia and cancer. Some have suggested the need to eliminate all acid reflux in patients with Barrett esophagus, but this would require high and frequent doses of expensive medications and serial pH monitoring to document efficacy of therapy. Pending further clinical studies, patients with Barrett esophagus should be treated like others with chronic GERD. Esophageal resection of Barrett esophagus can prevent the progression to cancer, but this requires a total esophagectomy with high mortality, except in selected surgical centers. Therefore, ablation of Barrett epithelium in the setting of strict PPI anacidity has been proposed. Photodynamic therapy, laser, multipolar electrocoagulation, argon plasma coagulation, and endoscopic mucosal resection have been used for this purpose. In these studies, Barrett mucosa can be reversed completely in 70% to 80% of patients, but intestinal metaplasia underlying the new squamous mucosa is reported in almost all series, with the occasional residual foci of metaplasia developing adenocarcinoma. Adverse effects of ablation therapy have ranged from mild chest pain, sore throat, or odynophagia to esophageal perforation and death. The incidence of adenocarcinoma in patients with Barrett esophagus without dysplasia is probably so low that endoscopic ablation cannot be advocated outside of study protocols. Endoscopic therapy for patients with high-grade dysplasia or early cancer holds more promise, especially in the older patients with comorbid illnesses. Because there is currently no way of eliminating the malignant risk of Barrett esophagus, regular endoscopic surveillance is recommended. Biopsies should be taken from each quadrant every 2 cm axially within the metaplastic tissue. The rationale is that dysplasia within Barrett epithelium is often multifocal, and obtaining fewer tissue samples increases the risk of missing dysplastic areas. Brush cytology can compliment endoscopic biopsies. Biomarkers, such as p53, and flow cytometry may augment the yield of histological examination of biopsy specimens. Although prospective studies are not available, case series confirm that esophageal adenocarcinomas detected by endoscopic surveillance are at an earlier stage with a more favorable survival than cancers detected at the time of diagnosis of Barrett, typically when patients present with dysphagia. The appropriate surveillance interval for patients with Barrett esophagus has not been studied prospectively. However, current programs, such as proposed by the American College of Gastroenterology, are based on the grade of dysplasia. In these recommendations, the management of high-grade dysplasia remains most controversial. Some groups suggest that high-grade dysplasia may regress to lesser grades, and an intensive biopsy protocol every 3 months will differentiate high-grade dysplasia from cancer. The surgical literature contrasts with this experience. Of 126 cases with high-grade dysplasia alone by endoscopic biopsies, 41% had cancer, although usually an early stage, at the time of esophagectomy. Nevertheless, most patients with Barrett esophagus never progress to important degrees of dysplasia. Predictors of cancer progression at the initial diagnosis of Barrett esophagus are needed to define individual surveillance programs more appropriately. One study suggested that patients whose baseline biopsies are negative or show only low-grade dysplasia without increased 4N or aneuploidy on flow cytometry may have surveillance deferred for up to 5 years. Another prospective multivariate analysis revealed that progression to high-grade dysplasia or cancer was significantly and independently associated with dysplasia at diagnosis or anytime during follow-up, hiatal hernia size greater than 2 cm, and Barrett esophagus length greater than 2 cm. These patients may warrant more frequent surveillance programs.

Barrett’s Esophagus (3)

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Patients with long-segment Barrett esophagus have an estimated 30 to 125 times increased risk of developing esophageal cancer compared with the general population. Early studies suggested that the median cancer incidence was 1 per 100 patient-years of follow-up, but more recent studies with longer follow-up suggest a lower cancer rate of 1 per 200 to 250 patient-years. This is an annual incidence of approximately 0.5%, with about 500 cases of adenocarcinoma diagnosed annually. However, since the early 1980s, the incidence of squamous cell carcinoma has stayed constant, whereas the incidence of adenocarcinoma of the esophagus and esophagogastric junction has risen fivefold—a growth rate exceeding that of any other cancer. Currently, adenocarcinoma accounts for more than half of all esophageal cancers in the United States. Despite this cancer risk, most patients with Barrett esophagus die of unrelated causes. More than 90% of patients who develop cancer present with symptoms caused by the tumor itself and are unaware of their antecedent Barrett esophagus. Epidemiologic data suggest that the mean interval from developing Barrett esophagus to evolution to cancer may be 20 to 30 years.

Management of patients with Barretts metaplasia has two aspects: treating the underlying GERD and managing the risk of adenocarcinoma of the esophagus. The principles for treating peptic esophagitis and controlling symptoms in Barretts metaplasia are the same as for uncomplicated GERD with the proviso that because it is associated with extreme esophageal acid exposure, it will likely require more intensive treatment. In general, mucosal damage and symptoms can be controlled with proton pump inhibitor therapy, but surgery may be needed, or even desirable, in refractory cases.
On the basis of in vitro and in vivo cell proliferation studies reporting increased cell proliferation and decreased differentiation in tissue exposed to acid, some authorities believe that complete acid suppression is desirable in therapy for Barretts metaplasia. However, there is no clinical evidence that aggressive antisecretory therapy or antireflux surgery prevents the occurrence of adenocarcinoma or causes regression of intestinal metaplasia. Proton pump inhibitor therapy has proved to be of no avail in reversing metaplasia or preventing adenocarcinoma. Thus, the available data support titrating therapy to control symptoms and treat esophagitis, irrespective of the presence of Barretts metaplasia.

Barrett’s Esophagus (2)

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Barrett esophagus is suspected at endoscopy and is confirmed by biopsy and histological examination. The columnar epithelium of the stomach is reddish pink, and the junction between the glossy white squamous mucosa and the columnar mucosa (Z-line) is normally found at the lower end of the tubular esophagus, just above the proximal folds of a hiatal hernia, if present. In Barrett esophagus, the distal esophagus is lined with columnar epithelium, extending upward for a variable distance, often 3 to 10 cm, but occasionally involving most of the esophagus.The proximal margin may be horizontal, or there may be irregular, often tongue-shaped upward extensions of columnar mucosa. Some patients have pale islands of regenerative or residual squamous epithelium, whereas others have punched-out benign ulcers in the columnar area. Strictures and esophagitis may be seen at the new squamocolumnar junction. The endoscopist should especially look for evidence of adenocarcinoma, such as nodularity or masses.

The characteristic histological finding in Barrett esophagus is a distinctive specialized intestinal epithelium. This is a glandular epithelium with mucin-type cells and the distinguishing presence of goblet cells. These are easily seen on hematoxylin and eosin–stained sections and can be demonstrated more prominently in sections stained with Alcian blue. It occupies most or all of the columnar-lined area and is the type of epithelium in which adenocarcinoma arises. Other types of epithelia seen with Barrett esophagus include gastric fundic and cardia-type epithelia, but these alone do not make the diagnosis of Barrett esophagus, nor are they associated with adenocarcinoma.

Currently, there is some controversy over the classification of Barrett esophagus. The classical or long-segment Barrett esophagus requires at least 3 cm of esophagus to be lined with columnar epithelium. This is the best-studied subset of Barrett esophagus, with traditional demographic features and a definite increased risk of becoming adenocarcinoma. Short-segment Barrett esophagus refers to shorter lengths or tongues of columnar epithelium, less than 3 cm, in the distal esophagus, with intestinal metaplasia on biopsy. This entity is three to five times more common than the long-segment variant, but, based on anecdotal reports, the risk of cancer appears to be lower. Intestinal metaplasia at the esophagogastric junction refers to microscopic findings on biopsy but no visible columnar epithelium in the esophagus at endoscopy. This finding has been reported in 10% to 32% of biopsies from unselected patients, many of whom have no reflux symptoms. The percentage of woman and African Americans is also higher with this lesion than with either long- or short-segment Barrett esophagus. The cause is controversial; some investigators suggest that this is the earliest form of GERD, whereas others believe these changes are secondary to H pylori infection. Cancer risk is minimal, if it exists at all.

Barrett’s Esophagus (1)

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In some patients with GERD, the squamous epithelium of the distal esophagus is replaced by specialized columnar epithelium, resembling that of the intestine and containing goblet cells. Although Dr. Norman Barrett thought this lesion was a congenitally shortened esophagus, studies consistently show that these patients have severe GERD with low LES pressures, poor esophageal motility, large hiatal hernias, and extensive acid and bile reflux. Furthermore, most patients have had chronic reflux symptoms for at least 10 years. Animal experiment show that, if the mucosal lining of the distal esophagus is excised in the setting of free acid reflux, columnar epithelium will regenerate in the area previously occupied by squamous epithelium. If reflux is controlled, the mucosal lining will regenerate with squamous epithelium. Pluripotential stem cells derived from the stratified squamous epithelium are the origin of the specialized columnar epithelium.

Barrett esophagus was once considered an uncommon condition, but estimates of its frequency at autopsy (1 in 57 to 1 in 105 cases), on general endoscopy survey (1 in 100 cases) and on endoscopic surveys of patients with GERD (10 in 100 to 15 in 100 cases), indicate that it is not uncommon, and it affects nearly 700,000 adults in the United States. An autopsy series from Olmsted County, Minnesota found that most cases of Barrett esophagus go undetected during life and thus are not accessible for cancer surveillance programs. Barrett esophagus is principally a disorder of white men; it is three times more frequent in men than in women and is rare in African Americans and Asians. It is found predominantly in middle-aged and older adults; the mean age at diagnosis is approximately 55 years, but it has been reported in children older than 5 years of age. The prevalence of Barrett esophagus increases with age, paralleling that of reflux esophagitis, but the length of the columnar-lined segment remains remarkably stable, even over years of endoscopic follow-up. This finding suggests that it arises rapidly in the susceptible reflux damaged esophagus and early in the course of disease. Families have been reported with multiple members having Barrett esophagus, some with cancer affecting more than one generation. Although the columnar-lined esophagus in itself does not cause symptoms, most patients complain of heartburn and regurgitations. Approximately 25% of patients with Barrett esophagus discovered at endoscopy have no esophageal symptoms.

What is acid reflux?

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Acid reflux is the back flow of stomach contents into the esophagus. These contents irritate the esophagus and cause heartburn. The esophagus is a tube that transports food into the stomach, it has a sphincter at its lower end which prevents reflux. Relaxation of this sphincter is the main factor responsible for this disease. Many foods and drugs relax the lower esophageal sphincter.
Fatty meals and nitrates are common causes. Other factors include smoking, coffee, chocolate, orange juice, obesity and tight clothes.
Acid reflux is also called GERD (G: gastro, E: esophageal, R: reflux and D: disease).

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