Modern Approach to Benign Esophageal Disease: Diagnosis and Surgical Therapy
The recently introduced technique of ambulatory hour monitoring of esophageal motor activity multiplies the number of esophageal contractions available for analysis and provides an opportunity to assess esophageal motor function under a variety of physiologic situations. This increases the accuracy and dependability of the measurement. The degree of reclassification of esophageal motor disorders resulting from analysis of ambulatory manometry studies indicates that the classification of esophageal motor disorders based on standard manometry is inappropriate.
The intermittency of esophageal motor abnormalities can be missed easily or overdiagnosed in the unphysiologic setting of standard manometry, but are detected with a higher degree of reliability when motor activity is monitored over 24 hours in a variety of physiologic conditions. Based on these observations, esophageal motility disorders should be viewed as a spectrum of abnormalities that reflect various stages of destruction of esophageal motor function rather than separate entities. Using simultaneous manometry and fluoroscopy, Kahrilas et al.
This correlates with the observation that patients with nonobstructive dysphagia show an inability of the esophageal body to organize the motor activity into peristaltic contractions during meals. In normal asymptomatic volunteers the prevalence of "effective contractions," peristaltic contractions with sufficient amplitude to propel a bolus, increases with increasing states of consciousness, that is, from sleep, to upright, and to meal periods.
This is probably due to a modulatory effect of the central nervous system on esophageal motor activity. Patients with nonobstructive dysphagia lack this ability to increase the prevalence of "effective contractions" with increasing states of consciousness.
Ambulatory hour esophageal manometry in the evaluation of esophageal motor disorders and noncardiac chest pain. Surgery , The use of this parameter for the evaluation of esophageal body function obviates the need for the current categories of esophageal motor disorders and permits an objective assessment of the effect of medical or surgical therapy.
Ambulatory hour motility monitoring in these patients has, however, shown that chest pain is rarely related to abnormal esophageal motor activity. Rather, episodes of gastroesophageal reflux appear to be the most common esophageal cause of noncardiac chest pain. Occasionally a markedly increased frequency of simultaneous and repetitive contractions appears to precede chest pain. The ischemia may become critical in situations where the resting blood flow to the esophagus is already compromised, as demonstrated in the hypertrophic esophageal muscle of patients with esophageal motor disorders.
A burst of disorganized motor activity in this situation may give rise to ischemic pain.
Consequently, we have termed chest pain caused by a burst of incoordinated esophageal motor activity under ischemic conditions "esophageal claudication. Esophageal clearance of refluxed gastric juice is determined by the esophageal motor activity, salivation, gravity, and the presence of an anatomic alteration such as a hiatal hernia. The competency of the lower esophageal sphincter depends on its pressure, overall length, and length exposed to abdominal pressure. Gastric function abnormalities causing gastroesophageal reflux include increased intragastric pressure, gastric dilation, decreased emptying rate, and increased gastric acid secretion.
What is the proportion of normal lower esophageal sphincter in gastroesophageal reflux patients?
Outpatient physiologic testing and surgical management of foregut motility disorders. Curr Probl Surg , Increased esophageal exposure to gastric juice may result from three known causes. The identification of a defective sphincter as the cause of increased esophageal acid exposure is important because it is the one causative factor that antireflux surgery is designed to correct.
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The other two causes are inefficient esophageal clearance of refluxed gastric juice and abnormalities of the gastric reservoir that augment physiologic reflux. These factors cannot be corrected by an antireflux procedure. Conceptually, the three main causes of gastroesophageal reflux can be thought of as the failure of a pump, a valve, or a reservoir Fig. The relative contributions of each of these components of the antireflux mechanism to increased esophageal exposure to gastric juice should be determined prior to considering specific therapy for the disease.
Modern Approach to Benign Esophageal Disease
The distribution of these causes of gastroesophageal reflux in a consecutive series of patients with increased esophageal exposure to gastric juice is shown in Fig. Failure of the lower esophageal sphincter can be caused by inadequate pressure, overall length, or intra-abdominal length, the portion of the sphincter exposed to the positive pressure environment of the abdomen.
Failure of one or two of the components of the sphincter may be compensated for by the clearance of the esophageal body. Failure of all three sphincter components inevitably leads to increased esophageal exposure to gastric juice. The most common cause of a mechanically defective lower esophageal sphincter is inadequate sphincter pressure most likely caused by an abnormality of myogenic function Fig.
A normal sphincter pressure can be nullified by an inadequate abdominal length or by an abnormally short overall length of the sphincter. An adequate abdominal length of sphincter is important in preventing reflux caused by increases in intra-abdominal pressure. An adequate overall length is important to increase the resistance to reflux caused by increases in intragastric pressure independent of intra-abdominal pressure.
This can be done by calculating the volume of the three-dimensional sphincter pressure profile, the sphincter pressure vector volume. A second cause of increased esophageal exposure to gastric juice is inefficient esophageal clearance of refluxed material. This situation is relatively uncommon, and ineffective clearance is more likely to be seen in association with a mechanically defective sphincter, where it augments the esophageal exposure to gastric juice by prolonging the duration of each reflux episode Fig.
The three-dimensional lower esophageal sphincter pressure profile in gastroesophageal reflux disease. Ann Surg , The four factors important in esophageal clearance are gravity, esophageal motor activity, salivation, and anchorage of the distal esophagus in the abdomen. The bulk of refluxed gastric juice is cleared from the esophagus by a primary peristaltic wave initiated by a pharyngeal swallow.
Salivation contributes to esophageal clearance by neutralizing the minute amount of acid that is left following a peristaltic wave. The presence of a hiatal hernia can also cause a reduction in the efficiency of acid clearance. Gastric abnormalities that increase esophageal exposure to gastric juice include gastric dilation, increased intragastric pressure, a persistent gastric reservoir, and increased gastric acid secretion. The effect of gastric dilation is to shorten the overall length of the lower esophageal sphincter resulting in a decrease in the sphincter resistance to reflux.
Increased intragastric pressures occur in patients with outlet obstruction due to a scarred pylorus or duodenum, or after vagotomy. The persistence of the gastric reservoir results from delayed gastric emptying secondary to myogenic abnormalities such as is seen in patients with advanced diabetes, diffuse neuromuscular disorders, and post-viral infections. Gastric hypersecretion can increase esophageal exposure to gastric juice by the physiologic reflux of large amounts of concentrated acid.
Complications of gastroesophageal reflux result from the damage inflicted by gastric juice on the esophageal mucosa or the respiratory epithelium and the changes caused by their subsequent repair and fibrosis. The presence of the complications of GERD is directly related to the prevalence of a mechanically defective sphincter17 Fig. This indicates that a mechanically defective sphincter is the major factor in the development of complications of the disease. The observation that a mechanically defective sphincter also occurs in a significant number of patients who do not have a complication of increased esophageal exposure to gastric juice suggests that the defect in the sphincter is primary and not the result of inflammation or tissue damage.
Complications of GERD can also occur in patients with a normal lower esophageal sphincter, while some patients with a defective sphincter do not develop complications. This suggests that the composition of refluxed gastric juice may also be an important factor in the pathogenesis of esophageal mucosal injury. Experimental studies have shown that gastric acid and alkaline duodenogastric reflux interrelate and modulate the content and injurious effects of refluxed gastric juice in the distal esophagus.
Complications of GERD are particularly frequent and severe in patients with a mechanically defective sphincter and an alkaline component to the refluxate. These studies suggest that the lower esophageal sphincter is the primary barrier against reflux of any gastric contents and that reflux of gastric juice contaminated with duodenal contents is more detrimental to the esophageal mucosa than reflux of only acid gastric juice. Secondary Esophageal Motor Disorders Esophageal motility disorders may also result from more generalized neural, muscular, or metabolic systemic abnormality disturbances or inflammation and neoplasia of the esophagus.
The esophagus is particularly affected by almost any of the collagen vascular disorders. The most common are progressive systemic sclerosis, mixed connective tissue disease, polymyositis, and dermatomyositis. In most cases the disease follows a prolonged course and usually only affects the smooth muscle in the distal two thirds of the esophagus.
Typical findings on esophageal manometry are normal peristalsis in the proximal striated esophagus, with weak or absent peristalsis in the distal smooth muscle portion. The lower esophageal sphincter pressure is progressively weakened as the disease advances, resulting in increased esophageal exposure to gastric juice due to a mechanically defective lower esophageal sphincter and poor clearance function of the esophageal body.
In patients with polymyositis or dermatomyositis the upper striated muscle portion is the major site of esophageal involvement causing aspiration, nasopharyngeal regurgitation, and cervical dysphagia. Mixed connective tissue disease shows a mixture of the manometric findings of progressive systemic sclerosis and polymyositis.
Modern Approach to Benign Esophageal Disease : Diagnosis and Surgical Therapy
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Esophageal Motility Testing. New York: Elsevier, Indications, technique, and clinical use of ambulatory hour esophageal motility monitoring in a surgical practice.