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A new technique (using readily available materials) for passing any single lumen tube into the duodenum is presented. This procedure usually greatly reduces the time and effort required to pass an intestinal tube through the pylorus. Once passed, the tube functions normally, without the limitations posed by duodenal tubes.
AIM OF THE STUDY: We describe a new endoscopic procedure for membranectomy of fenestrated duodenal membranes. METHODS: With the patients under general anesthesia and tracheally intubated, a flexible video-panendoscope was introduced into the second portion of the duodenum. The fenestrated membrane was visualized and a triple-lumen stone extraction balloon of 15 mm was inserted through the fenestration. After the balloon was insufflated, gentle traction was performed in order to expose the fenestrated membrane and differentiate it from the normal duodenal wall. The orifice was dilated in order to introduce the endoscope and localize the Vater's ampulla. A sphincterotome was used to carry out one or two incisions of 1.5 to 2 cm in the membrane in the opposite direction to the ampulla. RESULTS: The procedure was successfully performed in five patients with a mean surgical time of 50 minutes. None of the patients complained of postoperative pain. Peristalsis was not affected, and patients started intake of oral fluids at approximately 24 hours. On discharge patients were completely asymptomatic, and four patients were followed up for one year following the procedure and remained asymptomatic. One patient who was also asymptomatic did not continue follow-up longer than two weeks after the procedure. CONCLUSION: Endoscopic membranectomy of duodenal membranes is a safe and effective procedure that reduces surgical times, postoperative fasting times and the length of hospitalization, and probably has no postoperative complications.
To determine the effects of luminal protease inhibition on duodenal delivery and the intraluminal fate of pancreatic enzymes, six healthy subjects were intubated with an oro-ileal multilumen tube assembly. By using nonabsorbable markers, cumulative trypsin, chymotrypsin, lipase, and amylase activities were measured as delivered to duodenum, midjejunum, and distal ileum, with or without simultaneous duodenal perfusion of the protease inhibitor camostat at graded doses. Compared with saline, camostat (a) inhibited trypsin activity in the entire small intestinal lumen by up to 99%, and significantly reduced chymotrypsin activity by up to 89%; (b) significantly increased duodenal deliveries of lipase activity, amylase activity and volume; (c) did not influence plasma cholecystokinin concentrations; and (d) significantly increased jejunal and ileal deliveries of lipase but not amylase activity. Small intestinal transit and motility were not affected by camostat. In additional in vitro studies, camostat significantly reduced the spontaneous decline in lipase activity in fresh human duodenal juice incubated at 37 degrees C. These findings demonstrate that duodenal deliveries of lipase and amylase activities increase when intraluminal protease activity is decreased; they suggest that this increase is not caused by slower proteolytic destruction of enzyme protein but by stimulation of pancreatic secretion. Thus, luminal protease-mediated feedback regulation of pancreatic secretion may be operative in humans. Because plasma cholecystokinin concentrations were not affected, these effects may in part be independent of cholecystokinin. The data further suggest that proteolytic digestion plays a major role in the rapid loss of luminal lipase activity on small intestinal transit.
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A two-marker technique avoiding transpyloric intubation was used to measure the volume of gastric secretion, the rate of gastric emptying and the degree of postprandial duodenogastric reflux in 8 dogs, 5 without and 3 with Heineke-Mikulicz pyloroplasties. The stomach emptied after a liquid fatty meal at an overall rate of 4.9 ml/min +/- 0.2 s.e.m. in animals with a normal pylorus and 5.7 +/- 0.2 ml/min in those with pyloroplasties (P less than 0.05). Though mean fractional emptying rates were similar, the fractional emptying rate was greater in animals with pyloroplasties than in those without in the first 10 and in the last 20 minutes. The rate of duodenogastric reflux was likewise greater in animals with pyloroplasties than in those without (1.8 +/- 0.2 ml/min and 0.7 +/- 0.2 ml/min respectively, P less than 0.05). The rates of gastric secretion did not differ materially (2.2 +/- 0.3 ml/min and 2.1 +/- 0.2 ml/min), but a greater proportion of the gastric contents was emptied more than once in animals with pyloroplasties than in those without (7.7 +/- 1.5 per cent and 2.3 +/- 1.0 per cent, P less than 0.05).
An investigation of changes in duodenal metallothionein (MT) levels following zinc exposure was conducted. Mice fed zinc-deficient (less than 1 ppm zinc) or zinc-supplemented (50 ppm) diets showed no increase in duodenal MT levels 24 hours after exposure to 17 mumol/kg zinc by gastric intubation. However, both MT induction and zinc incorporation were measured in the liver indicating transport of zinc via the intestinal mucosa. Only a small increase in [35S]cystine was observed to be incorporated into the MT fractions of duodenal homogenate obtained from zinc-exposed mice. Thus no statistically significant increase in duodenal MT was detected on single oral exposure of mice to zinc sulfate. Repetitive parenteral or enteral doses of zinc sulfate spaced 12 hours apart resulted in significant increases in duodenal MT. However, increases in MT by dietary zinc were not found until a 300 ppm zinc diet was used. No difference could be detected in duodenal MT levels of pair-fed animals fed zinc-deficient or 50 ppm zinc diet for 14 days. Similarly, no statistically significant difference in 65Zn uptake by in situ perfused duodenal sections could be detected in mice maintained on zinc-deficient or 100 ppm zinc diet for 1 month. These findings suggest that intestinal MT functions as a rapidly turned over zinc storage protein rather than a zinc regulatory protein.
BACKGROUND: The mortality rate associated with postoperative peritonitis remains high, especially when the source of infection cannot be eradicated. Such is the case with peritonitis arising from the duodenum, as primary closure is futile and intubation alone may be followed by local complications. METHODS: Forty-nine consecutive patients with postoperative peritonitis originating from a duodenal leak and a mean Acute Physiology And Chronic Health Evaluation II score of 17.7 were treated according to the following procedure: a three-channelled spiral drain was inserted through the leak and extraluminal drains were placed near the duodenal defect. Intraluminal irrigation was undertaken immediately through the infusion channel of the spiral drain. RESULTS: Eleven patients died and 26 suffered complications. The mean duration of intubation was 21 days. CONCLUSION: Intubation with intraluminal irrigation has proved effective in a homogeneous group of patients with peritonitis due to duodenal leakage.
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CONCLUSION: Ileal inhibitory effects on pancreatic enzyme output are also demonstrable during exogenous, cholinergic stimulation of exocrine pancreatic secretion. These findings support the hypothesis that direct inhibition of cholinergic systems may be involved in the ileal inhibitory effects on pancreatic enzyme secretion. Furthermore, glucagon-like peptide-1 (GLP-1) may play a role in the mediation of the ileum-induced effects. BACKGROUND: Ileal carbohydrate perfusion inhibits endogenously stimulated exocrine pancreatic secretion in humans. Our aim was to investigate if ileal perfusion of carbohydrates exerts similar effects on exogenously stimulated pancreatic enzyme output, i.e., if the inhibitory mechanisms are reproducible during direct, cholinergic stimulation of the exocrine pancreas. Furthermore, we sought to clarify the role of the potential humoral mediators (GLP-1) and peptide YY (PYY). METHODS: Eight healthy fasting volunteers were intubated with an oroileal multilumen tube system for aspiration of duodenal juice and perfusion of test solutions. Exocrine pancreatic secretion was stimulated by a continuous i.v. infusion of the cholinergic agonist carbachol. Additionally, the ileum was perfused for 15-min intervals with either carbohydrates (total load: 18 g) or saline as control. Blood samples for determination of GLP-1 and PYY were taken before the beginning of exogenous stimulation and before and after ileal perfusion. RESULTS: Exogenously stimulated pancreatic enzyme secretion was significantly inhibited by additional ileal carbohydrate perfusion (p < 0.05), whereas ileal saline had no effect. Moreover, plasma levels of GLP-1 increased significantly (p = 0.004) after ileal perfusion of carbohydrates, but not after saline. PYY plasma concentrations remained unchanged after both ileal perfusates.
In a layer juxtaposed to the mucosal surface of distal duodenum and of jejunum, and designated as "acid microclimate," the proton concentration is significantly higher than in the bulk phase of the intestinal lumen. The aim of the present study was to quantify the effect of different sugars on the mucosal surface pH value when these substrates were either added to the in vitro preparation of rat distal duodenal and mid-jejunal segments or administered by intragastric intubation and by i.v. infusion. All pH measurements were carried out in vitro by surface microelectrodes in oxygenated phosphate buffer. Glucose, fructose, mannose, galactose and 3-O-methylglucose were applied in vitro, glucose, maltose, fructose, galactose, 3-O-methylglucose and whey protein for the intragastric intubation and glucose, fructose and galactose for the intravenous infusion. Only substrates that could be metabolized in the intestinal epithelia were able to depress surface pH to a considerable extent. Substrate concentration at which half-maximum decrease of surface pH was obtained (K delta pH) was calculated to be 4.5 mM for glucose, 14.5 mM for fructose and 34.5 mM for mannose. The study was the first to demonstrate that metabolizable sugars are not only able to lower surface pH of intestinal epithelia when they are added in vitro but that they are also effective after intragastric intubation or i.v. infusion. It is plausible that generation of the protons, which are secreted into the acid microclimate zone, is closely related to the intracellular metabolization of glucose. The existence of a high proton concentration on the immediate mucosal surface could be of considerable significance for the absorption of weak electrolytes, a group to which different nutrients belong.
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Using Fordtran's technique but substituting the meat extract Oxo for the steak meal we investigated gastric acid secretion in eight control subjects and nine patients with chronic duodenal ulcer. Intragastric titration was performed using a double lumen tube measuring the pH in the stomach every three minutes and adjusting it to 5.5 throughout the test by infusing 0.3-M sodium bicarbonate. On a separate day a pentagastrin test was performed using a conventional gastric aspiration technique. In the eight control subjects the mean acid output after pentagastrin was 13.7 +/- 2.1 (SEM) mmol/h, whereas the mean hourly acid output measured by intragastric titration was 20.1 +/- 3.1. The greater response to Oxo than to pentagastrin in the controls (deltaAO = + 46%) was significant (P less than 0.01). This is in contrast with our duodenal ulcer patients whose mean hourly acid outputs were 22.7 +/- 4.4 and 23.0 +/- 4.4 mmol/h in response to pentagastrin and Oxo respectively (r = 0.95). The findings, while clearly at variance with those of Fordtran and Walsh (1973), are more in keeping with the concept of increased endogenous secretory drive in duodenal ulcer patients compared to normal subjects.
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