Esophagogastric region and its rings.
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Biomedical subjects
Publications and source records attributed to D O Castell.
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With the renewed interest in esophageal motility disorders, diffuse esophageal spasm is being diagnosed more frequently. In many clinical settings, however, the term is used as a synonym for noncardiac chest pain. Our review of the literature and broad clinical experience in studying the motility patterns of healthy subjects have helped us better define diffuse esophageal spasm. The diagnosis of diffuse esophageal spasm should be considered only in symptomatic patients showing simultaneous contractions after wet swallows during esophageal motility testing. Simultaneous contractions should occur after at least 10% of swallows and be intermixed with normal peristaltic contractions. Repetitive waves, contractions of prolonged duration, spontaneous activity, high-amplitude contractions, and lower esophageal sphincter abnormalities may be seen in diffuse esophageal spasm. None of these findings alone or in combination justifies a diagnosis of diffuse esophageal spasm unless associated with simultaneous esophageal contractions.
Various complications have been reported recently for the Angelchik antireflux prosthesis, a silicone-gel prosthesis used in the treatment of gastroesophageal reflux and associated hiatal hernia. We have studied the cases of 11 patients with complications of this prosthesis and have reviewed the literature for others. Complications included 8 erosions of the device into the gastrointestinal tract, 1 migration, 1 improper placement, and 1 case believed to be surgical trauma. These complications represent those typical to reflux surgery and some unique to the Angelchik prosthesis (migration and erosion). The exact frequency is unknown, with the manufacturer estimating migration at 0.81% and erosion at 0.15%. Available data indicate that complications may occur up to several years after implantation, and physicians may not recognize the problems with the prosthesis if they are unaware of the complications.
Previous studies of lower esophageal sphincter pressures during the menstrual cycle and pregnancy have suggested that the smooth muscle relaxing effect of progesterone depresses sphincter tone. Results, however, have been contradictory and limited to a small number of patients. We studied lower esophageal sphincter and distal peristaltic pressures during the follicular (days 2-8) and luteal (days 20-28) phases of the menstrual cycle. Twenty normal menstruating women (mean age 31 yr) not using oral contraceptives were evaluated. A low compliance pneumohydraulic infusion system was used for all studies. Lower esophageal sphincter pressure was determined by both rapid and station pull-through techniques. Distal peristaltic pressures were recorded 2 and 7 cm above the sphincter in response to 10 wet swallows (5 cc of H2O). Mean amplitude and duration in the distal esophagus were evaluated. Plasma progesterone and estrogen concentrations were obtained and correlated with changes in esophageal pressures. The results were as follows: (a) unlike prior investigations, we found the menstrual cycle had no effect on lower esophageal sphincter pressure and (b) likewise, no change in esophageal contractions in the distal esophagus was found during the cycle. We concluded that changes in female sex hormone concentrations that characterize the menstrual cycle are not associated with changes in parameters of esophageal motor function.
Technological advances in the investigation of oesophageal motility have resulted in progressive awareness of gastro-oesophageal reflux disease and motor disorders of the oesophagus as causes of obscure "noncardiac" chest pain, as well as for unexplained swallowing difficulties. Oesophageal motility studies should also be undertaken before surgery for reflux oesophagitis.
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Symptomatic patients with abnormal esophageal manometry characterized by esophageal peristaltic waves of increased amplitude ("the nutcracker esophagus," NE) have been recognized with increasing frequency. Whether or not this represents a true functional abnormality is unresolved at this time. We have utilized radionuclide transit (RT), a true esophageal function test, to evaluate patients with NE. Eighteen consecutive symptomatic patients with the NE and ten clinically and manometrically normal subjects constituted this study group. RT in normals were 6.8 +/- 0.2 sec (means +/- SE) and 27.6 +/- 3.8 in patients with NE. RT was abnormal in 17/18 patients with NE. Chaotic bolus transit was seen in 11/18 patients with NE but not in normals. The defect was localized to the distal esophagus since transit through the proximal esophagus was not significantly different between the two groups. This defect in RT may be related to spontaneous simultaneous contractions seen in 50% of these patients. Further work will be necessary to determine if NE is a true functional abnormality or a marker for other motility abnormalities such as diffuse esophageal spasm.
To determine the efficacy of atropine as an endoscopic premedication, we prospectively evaluated in double-blind fashion 196 elective endoscopies performed on 189 consecutive consenting patients. Group 1 (95 endoscopies) received meperidine, 1.5 mg/kg, intramuscularly 30 min prior to endoscopy. Group 2 (101 endoscopies) additionally received atropine, 0.6 mg, in the same injection. Endoscopy was performed by one of two investigators using a 13-mm fiberoptic instrument. Endoscopists and patients filled out postendoscopy questionnaires. Both endoscopists (p less than 0.01) and patients (p less than 0.05) noted less oral secretions after atropine. Endoscopists noted less gastric motility after atropine (p less than 0.05) and guessed correctly whether or not atropine had been given in two thirds of cases. They noted no overall difference, however, in the ease of the endoscopy (p greater than 0.05). Moreover, there were no differences in the patients' assessments of the acceptability of the procedure between the two groups (p greater than 0.05). We concluded that although atropine does not improve patients' tolerance for the examination or the endoscopists' ability to do an adequate examination, it does objectively decrease the amount of gastric motility and oral secretions. This latter effect could potentially decrease the hazard of aspiration, but such a benefit could not be demonstrated in our series.
The esophagus is thought to be the cause of a large proportion of noncardiac chest pain syndromes. Often this is established solely by exclusion of more serious cardiopulmonary and esophageal-structural diseases. Using currently available manometric technology, a standardized esophageal manometric study and carefully defined values for normal, esophageal motility disorders (EMD) can be clearly defined. The subsequent development of an appropriate and generally agreed on nosology of EMD should serve as a basis for the prospective evaluation of these disorders, hopefully leading to a clear understanding of their exact importance and natural history. If the scientific method is used, order can be brought to this confusing area of clinical medicine.
Thirty-four consecutive patients referred to a gastroenterology clinic with suspected esophageal motility abnormality as a cause of their chest pain or dysphagia, or both, were prospectively studied in an 18-mo period. Peristaltic response to 10 wet (5 ml H2O) swallows was recorded in all studies with a low-compliance infusion system. To provoke symptoms and motility abnormalities after baseline evaluation, all patients had acid infusions (0.1 N HCl) and administration of edrophonium (80 micrograms/kg i.v.), pentagastrin (6 micrograms/kg s.c.), and bethanechol (40 micrograms/kg s.c.). Tracings were coded, read, and interpreted blindly. Baseline tracings were abnormal in 23 of 34 patients (68%), including increased amplitude peristaltic contractions ("nutcracker esophagus") in 10 and nonspecific esophageal motor disorders in 13. Acid infusion produced substernal burning in 3 of 33 patients, in motility change in 1 patient. Edrophonium produced chest pain with manometric changes in 6 of 34 (18%) patients. Pentagastrin produced chest pain with manometric change in 1 patient. Bethanechol produced chest pain with manometric change in 2 patients. One patient with low amplitude had elevation of esophageal baseline and multiple simultaneous contractions but no chest pain (subsequently developed achalasia). It was concluded that (a) abnormal motility is a common finding in a symptomatic group of patients with presumed esophageal motility disorder, (b) the "nutcracker" esophagus is the most frequent defect, and (c) attempted provocation of symptoms with acid or drugs is not generally effective; however, edrophonium is the best tolerated and most effective of currently available drugs.
It has been shown that the ACAP causes significant increases in the LES pressure of supine primates which are maximal when properly placed at the EGJ. This effect appears to be due to posterior padding of the EGJ in supine animals and can be reproduced by dowel rods or Maloney dilators. Further studies to evaluate the contribution of this effect to the prevention of acid reflux are underway.
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Twenty-one patients referred for evaluation with a diagnosis of questionable ascites were examined independently by three investigators who performed five different physical examination maneuvers. With ultrasonography as the reference standard, six patients had ascites. The sensitivity and specificity of the physical examination maneuvers ranged from 50% to 94% and 29% to 82%, respectively. The overall accuracy of the maneuvers was only 58%. The results of this study indicate that routine physical examination has definite limitations in the precise diagnosis of equivocal ascites. The only conclusion that can be made by a physical maneuver with over 90% accuracy is that ascites is absent if no flank dullness is elicited. Ultrasonography is recommended in questionable cases.
Two patients are presented having lymphomatous involvement of the central nervous system in whom dysphagia was the predominant symptom. All indicated studies failed to reveal evidence of direct esophageal involvement, and the dysphagia improved during treatment of the neural component. Esophageal manometric studies revealed abnormalities of the striated muscle portion of the esophagus. These two case histories suggest that invasion of the central nervous system with lymphoma may produce abnormalities of the neuromuscular control of esophageal function resulting in dysphagia.
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Prostaglandins have been shown to produce significant decreases in lower esophageal sphincter pressure (LESP), although their effect on esophageal peristalsis is unknown. We studied the effect of infusion of prostaglandin E1 (PGE1) or prostacyclin (PI) on esophageal peristalsis in the proximal and distal esophagus in the awake baboon. Peristalsis was recorded using a polyvinyl catheter and a pneumohydraulic perfusion system and was induced by wet swallows. PGE1 infusion significantly (P less than 0.01) diminished peristaltic amplitude in proximal and distal esophagus by 51% and 77%, respectively. The wave duration was significantly (P less than 0.001) shortened by PGE1 in the distal esophagus, but not in the proximal esophagus. Similarly, prostacyclin significantly (P less than 0.05) decreased peristaltic amplitude in proximal and distal esophagus by 31% and 67%, respectively. As seen with PGE1, PI decreased distal esophageal amplitude significantly (P less than 0.02) more than proximal esophageal amplitude. Equivalent decreases in mean arterial blood pressure seen during prostaglandin infusion were reproduced by bleeding with no changes in measurements of peristaltic activity. Decreased peristaltic wave amplitude and duration suggest that prostaglandins exert a modulating local effect on esophageal muscle. In addition, this effect appears to be more pronounced on distal smooth muscle than on proximal striated muscle in the baboon esophagus.