Endoscopic electrosurgical treatment for strictures of the gastrointestinal tract.
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Biomedical subjects
Publications and source records attributed to W J Hogan.
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In this study, we evaluated the effect of transsphincteric fluid flow on the rate of spike bursts in the opossum sphincter of Oddi (SO). For chronic studies in awake animals, bipolar electrodes were implanted on the SO, gastric antrum, duodenum, and jejunum. In group 1 animals, surgery was limited to electrode implantation. Subsequently, these animals underwent a cholecystectomy. Group 2 animals had electrode implantation without further surgery. In group 3 animals, bile flow was diverted around the SO, whereas in group 4 animals, pancreatic juice as well as bile was diverted around the SO. Multiple myoelectric recordings were obtained in each animal during fasting and after feeding. In fasted control animals, the rate of SO spike bursts showed cyclic increases synchronous with phase III of the duodenal migratory myoelectric complex. Feeding increased the rate of SO spike bursts. Cholecystectomy had no effect on SO spike bursts in fasted animals. Diversion of bile or bile and pancreatic juice around the SO did not alter the fasting pattern of SO spike bursts. However, flow diversion in the group 3 and group 4 animals did cause a modest decrease of SO spike bursts, from approximately 2/min to about 1/min, during phase I of the duodenal migrating myoelectric complex (p less than 0.05). Sphincter of Oddi spike-burst rate was not affected during the remainder of the migrating myoelectric complex cycle. Neither cholecystectomy nor flow diversion caused any change in the normal SO responses to feeding. Excitatory SO responses caused by motilin or by cholecystokinin-octapeptide were shown to be independent of changes in transsphincteric flow. We conclude that variations in transsphincteric flow cause only minimal alteration of the rate of spike bursts in the opossum SO during fasting. Therefore, factors other than transsphincteric flow, such as hormonal or neural influences, appear to be the major mechanism(s) that regulate the rate of SO contractions in awake opossums.
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Endoscopic sphincterotomy (ES) alters the structure and motor function of the sphincter of Oddi (SO). The magnitude and duration of these changes, however, have not been critically examined. Before ES, 22 patients with common bile duct stones were evaluated by endoscopic retrograde cholangiography. The pressure gradient between the common bile duct and the duodenum, the SO basal pressure, and the SO peak phasic pressures were obtained. After ES, the electrosurgical incision length was determined using the extended papillotome and an inflated Fogarty balloon as reference. A high correlation existed between the endoscopist's estimate of ES incision size using this technique and the actual length of simulated incisions fashioned in cardboard mounts. These studies were repeated in all 22 patients at 1-yr follow-up and in 8 of these patients at 2-yr follow-up. At 12 mo and 24 mo after ES, the common bile duct (CBD) to duodenal pressure gradient and the sphincter of Oddi basal pressure were virtually eliminated. The amplitude of SO phasic contractions was significantly diminished 12 mo after ES (124 +/- 16 mmHg to 37 +/- 10 mmHg; p less than 0.001), but 24 mo after ES, SO phasic contraction amplitude was not significantly different from the values before ES. Incision length at 1-yr follow-up was reduced in the group of 22 patients from 11.6 +/- 0.8 mm to 8.3 +/- 0.5 mm (p less than 0.001), and in the group of 8 patients from 11.0 +/- 1.5 mm to 7.5 +/- 0.7 mm (p less than 0.025). After an additional 12 mo, however, i.e., 24 mo after ES, the incision length was 6.5 +/- 0.7 mm. There was no significant difference in incision length between the 12-mo and 24-mo examinations. We conclude that after ES, incision length decreases during the first year. There appears to be no further significant reduction in incision length at 2 yr. In addition, the reduction of the CBD to duodenal pressure gradient and the SO basal pressure remain unchanged for at least 2 yr. These manometric findings support the observation that after ES the enlarged opening of the CBD into the duodenum remains open for at least 2 yr.
Choledochocele is a rare abnormality involving the intramural segment of the common bile duct. It may present clinically as recurrent acute pancreatitis, biliary colic, or cholestatic jaundice. A choledochocele may be easily overlooked by the conventional diagnostic methods, such as upper gastrointestinal series, intravenous cholangiogram, abdominal ultrasound, and computed tomography. Endoscopic retrograde cholangiopancreatography is helpful in demonstrating a choledochocele. Additionally, in selected cases, a choledochocele may be effectively managed by endoscopic sphincterotomy. We present the clinical, endoscopic, and radiographic findings in a series of 8 patients with choledochocele. The radiologic technique most useful in demonstrating a choledochocele at the time of endoscopic retrograde cholangiopancreatography is detailed. The pathogenesis, differential diagnosis, and relevant current literature pertaining to choledochocele are discussed.
The combination of a normal oral cholecystogram and ultrasound study of the gallbladder is considered adequate evidence to exclude cholelithiasis as a cause of biliarylike pain. We examined 206 patients with biliarylike pain and normal findings on cholecystogram and ultrasound study of the gallbladder by endoscopic retrograde cholangiopancreatography (ERCP). Of the 195 patients who had successful ERCP, 32 patients (group 1) had mild, transient abnormalities in liver function tests and 163 (group 2) had normal liver function test results. Small gallstones were demonstrated on ERCP examination in 25 of 32 group 1 patients and in four of 163 group 2 patients, all confirmed at surgery or endoscopic sphincterotomy. In conclusion, despite negative results on cholecystogram and ultrasound study of the gallbladder, patients with biliarylike pain and abnormal liver function test results should be evaluated further by diagnostic ERCP examination.
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Therapeutic endoscopy of the GI tract is emerging as a new discipline. Its use for such procedures as foreign body removal, polypectomy, and papillotomy is widely accepted, but newer applications--including endoscopic hemostasis and injection sclerotherapy of esophageal varices--are still controversial. An overview of therapeutic guidelines and state-of-the-art technique is presented.
We studied the effect of motilin on myoelectric activity of the sphincter of Oddi (SO) and upper gastrointestinal tract in conscious opposums. In 17 animals, bipolar electrodes were implanted on the gastric antrum, SO, duodenum, and jejunum. Subsequent 8-h recordings reconfirmed our previous findings that SO spike burst rate changed with interdigestive cycles of the gastrointestinal migrating myoelectric complex (MMC), becoming maximal during passage of phase III activity through the duodenum. In eight animals, peak motilin levels were shown to occur concurrently with maximal SO spike burst rate and MMC phase III activity in the duodenum. Motilin infusion (0.3 and 0.9 micrograms X kg-1 X h-1), given for 30-60 min starting 10 min after duodenal phase III, elicited premature MMC activity that originated in the stomach. Maximal SO activity occurred coincident with passage of premature phase III activity through the duodenum. Pulse intravenous doses of motilin (25-1,600 ng/kg) generally caused an immediate increase in spike burst activity in the gastric antrum, duodenum, and SO that lasted 3-5 min and was often followed by a premature MMC, usually starting in the antrum and progressing through the duodenum and jejunum. Increases in SO spike burst rate also occurred concurrent with motilin-induced, premature duodenal phase III. Motilin given at 5-60% of the duodenal MMC cycle length elicited premature MMCs at 10-60% of the cycle, but no premature MMCs were elicited by any of the motilin doses at the 5% intervals.(ABSTRACT TRUNCATED AT 250 WORDS)
We studied the opossum sphincter of Oddi (SO) because in this species the SO is approximately 3 cm in length and its extraduodenal location permits recording of motor activity with negligible interference from duodenal motor activity. The SO segment of 120 animals was evaluated by one or more of the following: (a) intraluminal manometry; (b) electromyography; (c) common bile duct (CBD) flow monitored by a drop counter; (d) cineradiography of intraductal contrast medium; and (e) histologic examination. SO pull-throughs using an infused catheter of 0.6-mm o.d. invariably showed a high pressure zone (HPZ) of 18 +/- 3 SE mm Hg in the terminal 4-5 mm of the SO segment. This HPZ had a narrow lumen, 0.5-0.7 mm in diam, and prominent circular muscle. The HPZ in the terminal SO had both active and passive components. HPZ with minimal amplitude and a paucity of underlying smooth muscle were present inconstantly at the junction of the SO segment with the CBD and pancreatic duct, respectively. The dominant feature of the SO segment was rhythmic peristaltic contractions that originated in the proximal SO and propagated toward the duodenum. These contractions occurred spontaneously at a rate of 2-8/min, ranged up to 200 mm Hg in magnitude, had a duration of approximately 5 s and were not abolished by tetrodotoxin. Concurrent myoelectric and manometric recordings showed that each phasic contraction was immediately preceded by an electrical spike burst. Simultaneous recordings of cineradiography, CBD inflow of contrast medium, SO manometry, and SO electromyography indicated that rhythmic peristaltic contractions stripped contrast medium from the SO into the duodenum. During SO systole, CBD emptying was transiently interrupted, whereas SO filling occurred during the diastolic interval between SO peristaltic contractions. SO distention increased the frequency of SO peristalsis. We conclude that (a) the dominant feature of the opossum SO is rhythmic peristaltic contractions that originate in the proximal SO and propagate toward the duodenum; (b) these forceful SO peristaltic contractions are myogenic in origin and serve as a peristaltic pump that actively empties the SO segment; (c) CBD outflow occurs passively during SO diastole, but is interrupted transiently during each SO peristaltic contraction; and (d) a short HPZ with active as well as passive components exists in the distal SO segment and acts as a variable resistor to SO outflow.
In this study we evaluated the effect of enteric hormones on sphincter of Oddi and gastrointestinal spike burst frequency in fasted conscious opossums. A chronic model for obtaining multiple long-term recording of sphincter of Oddi and gastrointestinal myoelectric activity was prepared in 12 animals by implanting bipolar electrodes in the gastric antrum, duodenum, sphincter of Oddi, jejunum, and ileum. Subsequently, 8-18 recording session, 6-8 h in length, were obtained in each animal. Each study was preceded by a 15-h fast. After recording two cycles of the interdigestive migratory myoelectric complex, a 60-min infusion of saline, cholecystokinin-octapeptide, pentagastrin, glucagon, or secretin was begun early in the quiescent period of duodenal activity, 10 min after termination of phase 3 of the migratory myoelectric complex activity. Cholecystokinin-octapeptide (10-80 ng/kg . min) and pentagastrin (25-200 ng/kg . min) increased sphincter of Oddi spike burst frequency while converting interdigestive gastrointestinal myoelectric activity to a fed-like pattern of continuous, irregular spike bursts. Glucagon at high doses of 500 and 1000 ng/kg . min depressed sphincter of Oddi and gastrointestinal spike burst activity, whereas lower doses of glucagon and secretin (3-12 CU/kg . h) had no effect. We conclude that in the opossum, relatively low doses of cholecystokinin-octapeptide and pentagastrin stimulate sphincter of Oddi and gastrointestinal spike burst activity while disrupting the cyclic pattern of sphincter of Oddi and gastrointestinal spike burst activity present during fasting. The physiological significance of these findings remains to be determined.
The results of this study show that lower esophageal sphincter contractions occur during phases 2 and 3 of the gastric interdigestive migratory motor complex in humans. In one series of studies, esophageal, gastric, and duodenal pressures were monitored overnight for 12 h in 7 healthy, fasting subjects. A second group of 10 volunteers was studied for 12 h on two consecutive nights. Periods of gastric contraction that reached a maximum frequency of about 3/min were shown to be part of the migratory motor complex cycle because they occurred immediately before phase 3 migratory motor complex activity in the duodenum. In all subjects, gastric interdigestive contractions were accompanied by lower esophageal sphincter contractions that maintained a pressure barrier between the stomach and esophageal body. During late phase 2 and phase 3 gastric migratory motor complex activity, the lower esophageal sphincter contractions were especially vigorous. Mean basal lower esophageal sphincter pressure varied significantly during the interdigestive cycle. Lower esophageal sphincter pressure values were maximal during phase 3 of gastric migratory motor complex activity and minimal values occurred during phase 1. No episodes of gastroesophageal reflux occurred as a result of increase of intragastric pressure caused by interdigestive gastric contractions.
In this study, we evaluated factors that affect esophageal acid clearance in normal subjects. A 15-ml bolus of 0.1 N HCl (pH 1.2) was injected into the esophagus, and the subject then swallowed every 30 s. Manometric and pH monitoring demonstrated that esophageal acid clearance occurred by a series of step increases in pH, each associated with a swallow-induced peristaltic sequence. Between peristaltic sequences, pH increase was minimal. Saliva stimulation by oral lozenge greatly improved acid clearance, while oral aspiration of saliva abolished the step increases in esophageal pH and markedly delayed acid clearance. Replacement of aspirated saliva with a bicarbonate solution reproduced the step increases in esophageal pH and restored acid clearance toward normal, while replacement with water alone failed to improve acid clearance. Similar to the effect of the oral lozenge, bethanechol (5 mg subcutaneously) improved esophageal acid clearance, but this improvement was reversed by oral aspiration of saliva, which markedly delayed acid clearance. A change from the recumbent to the sitting position tended to improve acid clearance slightly, but this improvement was not statistically significant. We concluded that in normal subjects (a) swallowing carries saliva into the esophagus and peristalsis empties intraesophageal fluid into the stomach, (b) the neutralization of acid by saliva carried into the esophagus with each swallow accounts for the occurrence of acid clearance by step increases in pH, (c) the improvement in acid clearance with bethanechol is due to saliva stimulation, and (d) gravity contributes little to esophageal acid clearance in the presence of normal peristaltic stripping waves.
We evaluated the mechanisms of gastroesophageal reflux in 10 patients with reflux esophagitis and compared the results with findings from 10 controls. The patients had more episodes of reflux (35 +/- 15 in 12 hours, as compared with 9 +/- 8 in the controls) and a lower pressure of the lower esophageal sphincter (13 +/- 8 mm Hg as compared with 29 +/- 9 in the controls) (P less than 0.001). Reflux occurred by three different mechanisms: transient complete relaxation of the lower esophageal sphincter, a transient increase in intra-abdominal pressure, or spontaneous free reflux associated with a low resting pressure of the lower esophageal sphincter. In controls 94 per cent of reflux episodes were caused by transient sphincter sphincter relaxation. In the patients 65 per cent of episodes of reflux accompanied transient sphincter relaxation, 17 per cent accompanied a transient increase in intra-abdominal pressure, and 18 per cent occurred as spontaneous free reflux. The predominant reflux mechanism in individual patients varied: some had normal resting sphincter pressure and reflux that occurred primarily during transient sphincter relaxation, whereas others with low resting sphincter pressures had spontaneous free reflux or reflux that occurred during an increase in intra-abdominal pressure.
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The frequency and significance of pancreatic duct visualization by ultrasonography were correlated with endoscopic retrograde cholangiopancreatography or pancreatic computed tomography. The normal pancreatic duct was found to have parallel walls and to be less than 2 mm in internal diameter in the region of the body of the pancreas. The abdominal pancreatic duct had an internal diameter of 2 mm or greater or had walls that were nonparallel or convex outward (focal dilatation or beading). Pancreatic ducts were identified in approximately one-half of all patients evaluated. Failure to visualize an abnormally dilated pancreatic duct was secondary to distortion of pancreatic anatomy from large or multiple pseudocysts, calcific deposits within the pancreas, or technically poor visualization of the pancreas.