Pericolic abscess due to Streptococcus pyogenes: report of a case that clinically mimicked acute cholecystitis.
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Abscess↗
Biomedical subjects
T N Pappas
Publications and source records attributed to T N Pappas.
Mechanisms of gastric and esophageal perforations during laparoscopic Nissen fundoplication.
OBJECTIVE: The purpose of this study was to determine possible mechanisms of 17 gastric and esophageal perforations that occurred during laparoscopic Nissen fundoplication. METHODS: Specific details of each perforation relating to mechanism of injury, surgeon experience, diagnosis, treatment, and outcome were obtained. For each perforation, an attempt was made to accurately determine the mechanism of perforation. RESULTS: Three mechanisms accounted for the 17 perforations, the majority of which occurred within the first ten laparoscopic Nissen fundoplications performed by the surgeon. Ten perforations resulted from injuries related to improper retroesophageal dissection, five occurred during passage of the bougie dilator or nasogastric tube, and two occurred after surgery secondary to suture pullthrough. Six patients received a delayed diagnosis, which adversely affected outcome. Most of the perforations were successfully managed by primary closure and wrap to include the repair. Morbidity was significantly increased for perforations recognized late. One death, attributed to sepsis, occurred in association with a delay in diagnosis. CONCLUSIONS: Gastric and esophageal perforations are serious complications of the new laparoscopic method of Nissen fundoplication. The mechanisms of these complications are specifically related to limitations of the laparoscopic technique. Prevention of these potentially lethal complications requires a full understanding of the detailed anatomy of the gastroesophageal region and awareness of the recognized mechanisms of perforation.
Adult↗
Quality of life after treatment for pancreatitis.
OBJECTIVE: The authors evaluated the morbidity, mortality, and quality of life after pancreatic debridement for necrosis and compared these values to those for quality of life after elective medical and surgical management for chronic pancreatitis. SUMMARY BACKGROUND DATA: Quality of life after pancreatic debridement for necrosis has received little attention. Although quality of life after other pancreatic surgery has been evaluated and is though to be good, management of patients with pancreatic necrosis can be labor intensive and require extraordinary resources. Therefore, further evaluation of the quality of life achieved after treatment is appropriate. METHODS: Forty patients (group 1) underwent operative debridement for necrosis between 1986 and 1994. Medical records of these patients were reviewed for morbidity, mortality, and in-hospital costs. Follow-up of quality of life was assessed by the Short Form-36 Health Survey. Patients in group 2 (n = 89) underwent medical management of chronic pancreatitis. Group 3 included 47 patients who underwent elective operations for ductal abnormalities. The Short Form-36 Health Surveys were administered to all three groups and compared statistically. RESULTS: Mortality and morbidity from pancreatic debridement was 18% and 77%, respectively. Quality-of-life evaluations in groups 1 through 3 and age-matched controls were statistically similar. CONCLUSIONS: Pancreatic debridement for necrosis requires intense application of resources and is associated with a high mortality and morbidity. Long-term follow-up shows good quality of life for patients who survive this morbid disease. This study supports the continued aggressive approach to the management of pancreatic necrosis, given that long-term outcome about quality of life is good.
Chronic Disease↗
The management of tumors of the ampulla of Vater by local resection.
OBJECTIVE: The authors report on indications and results of local excision of tumors of the ampulla of Vater. SUMMARY BACKGROUND DATA: Local excision of ampullary tumors has been performed for nearly a century but remains controversial. The use of this procedure for benign conditions is clear, but its place, if any, in the management of ampullary malignancy is debated. METHODS: The presentation, evaluation, and treatment of 26 patients who underwent local resection of ampullary tumors between January 1987 and November 1994 are reviewed. RESULTS: There were 16 men and 10 women, with a median age of 58 years. Eighteen patients had adenomas, whereas 8 patients had adenocarcinomas. Patients presented predominantly with jaundice (50%), pain (35%), and pancreatitis (27%) and were evaluated with endoscopic retrograde cholangiopancreatography and biopsy. All patients with benign lesions had accurate preoperative biopsies. Two of eight patients shown intraoperatively to have malignant lesions had preoperative biopsies read as benign. There were no deaths. Postoperative complications included two wound infections and one episode each of cholangitis, lower gastrointestinal bleeding, and adhesive gastrointestinal obstruction. All patients had prompt resolution of jaundice if present before surgery, and the mean postoperative stay was 7.5 days. Six of eight patients with malignant lesions have had recurrent disease. CONCLUSIONS: Local excision of malignant ampullary tumors is effective palliative therapy when the patient is unfit for the Whipple procedure. Ampullary resection usually is curative for patients with benign lesions without a polyposis syndrome. In this series, intraoperative frozen section routinely was accurate.
Adenocarcinoma↗
Apolipoprotein A-IV acts in the brain to inhibit gastric emptying in the rat.
We have very recently shown that intracisternal injection of apolipoprotein A-IV (apo A-IV), a glycoprotein produced in the small intestine by fat, dose-dependently inhibited gastric acid secretion in pylorus-ligated conscious rats. These results suggest that apo A-IV acts centrally as a neuromodulator to inhibit gastric secretion. The present study was carried out to examine the hypothesis that apo A-IV acts centrally to alter gastric emptying. Rats fasted 24 h received intracisternal injection of apo A-IV and a liquid meal by oral intubation under brief isoflurane anesthesia. Gastric emptying of a liquid meal was determined by the phenol red method. Intracisternal injection of apo A-IV inhibited gastric emptying of a liquid meal in a dose-dependent manner (1.0-4.0 micrograms). On the other hand, apo A-I in a dose of 4 micrograms failed to change gastric emptying. Gastric emptying was not altered by intraperitoneal administration of apo A-IV in a dose of 15 micrograms. These results suggest that apo A-IV acts centrally to delay gastric emptying of a liquid meal. Together with our recent finding that apo A-IV acts centrally to inhibit gastric acid secretion, the present study supports our hypothesis that apo A-IV may be involved in lipid-induced inhibition of gastric function.
Animals↗
Intracisternal injection of TRH antibody blocks gastric emptying stimulated by 2-deoxy-D-glucose in rats.
We evaluated the effect of 2-deoxy-D-glucose (2-DG) on gastric emptying of a non nutrient solution in conscious rats using a Phenol red method. Intravenous injection of 2-deoxy-D-glucose dose-dependently increased the rate of gastric emptying. This stimulatory action of 2-DG was abolished by subdiaphragmatic vagotomy. Intracisternal injection of thyrotropin-releasing hormone (TRH) antibody blocked intracisternal TRH and intravenous 2-DG-induced enhancement of gastric emptying but not the stimulation of gastric emptying induced by intracisternal pancreatic polypeptide. The TRH antibody injected intraperitoneally had no effect. These results suggest that endogenous TRH in the brain is involved in vagal-dependent stimulation of gastric emptying by 2-DG.
Animals↗
Apolipoprotein A-IV acts centrally in the brain to reduce the severity of gastric ulceration in the rat.
We have recently reported that apolipoprotein A-IV (apo A-IV), a protein associated with lipoproteins, acts in the brain to inhibit gastric acid secretion. In the present study, we determined whether or not apo A-IV has an anti-ulcer action via the central nervous system using Sprague-Dawley rats. Intracisternal injection of apo A-IV dose-dependently (2.0-4.0 micrograms/rat) reduced the severity of gastric mucosal lesions induced by intravenous injection of 2-deoxy-D-glucose or subcutaneous administration of indomethacine. A higher dose (15 micrograms) of apo A-IV injected intraperitoneally failed to inhibit the development of gastric mucosal damage evoked by these ulcerogenic agents. These results suggest for the first time that apo A-IV has an anti-ulcer action through a central mechanism.
Animals↗
Gastric mucosal damage induced by 2-deoxy-D-glucose involves medullary TRH in the rat.
These studies examined the effect of 2-deoxy-D-glucose (2-DG) on gastric mucosal integrity. Intravenous administration of 2-DG in doses of 100 and 125 mg/kg dose-dependently produced multiple, hemorrhagic gastric mucosal lesions while 75 mg/kg of 2-DG failed to induce gastric lesions. Intracisternal injection of 2-DG in doses of 10 and 20 mg/kg also induced gastric mucosal damage in a dose-dependent manner whereas the injection of 5 mg/kg of 2-DG intracisternally did not induce the development of gastric lesions. Gastric mucosal damage by intravenous 2-DG was completely blocked by bilateral gastric branch vagotomy. Intracisternal but not intraperitoneal injection of anti-TRH antibody 8964 significantly reduced the severity of gastric mucosal lesions evoked by intravenous administration of 2-DG. These results suggest that 2-DG acts in the brain to induce gastric mucosal damage through vagal dependent pathways. Endogenous TRH in the central nervous system may be involved in the production of gastric mucosal damage by 2-DG.
Animals↗
The use of pancreatic ductoscopy in the operative management of benign and malignant pancreatic disorders.
Direct visualization of the pancreatic duct was helpful in decision making during complex pancreaticobiliary operations. Two-, 3-, or 5-mm scopes were introduced into the pancreatic ducts of 32 patients with pancreatic disorders. Scopes were passed into the ductal system of: (1) 16 patients undergoing pancreaticojejunostomy; (2) six patients undergoing pancreaticoduodenectomy; (3) four patients with pancreatic pseudocysts or choledochal cysts: (4) two patients undergoing resection of the pancreatic tail; and (5) two patients undergoing accessory ductoplasty for pancreas divism or stricture. Eight patients had calculi removed utilizing the scope, and multiple strictures were identified and filleted. Pancreatic ductoscopy was used in two patients to document successful sphincteroplasty of an accessory duct. In two instances benign pancreatic duct tumors were removed. Pancreatic ductoscopy was used to search for coexistent duct neoplasms in the eight patients who underwent resection. The technique permits intraoperative inspection, biopsy, and removal of lesions intrinsic to the ductal system. Combined with surgical procedures this endoscopic method proved a useful adjunct in difficult cases.
Adult↗
Differential expression of substance P receptors in patients with Crohn's disease and ulcerative colitis.
BACKGROUND & AIMS: Although clinical and pathological differences exist between Crohn's disease (CD) and ulcerative colitis (UC), distinguishing features are often absent, making diagnosis and treatment problematic. This study evaluated the differences in the expression of substance P (SP) receptors in patients with CD or UC. METHODS: Tissue samples from patients with inflammatory bowel disease or control patients were obtained at surgery, processed for 125I-SP binding, and analyzed by quantitative autoradiography. RESULTS: Patients with CD showed a massive increase in SP receptors in lymphoid aggregates, small blood vessels, and enteric neurons of the small and large bowel relative to controls. Six of 16 CD specimens had no pathological evidence of CD yet continued to express high concentrations of SP receptors. Pathologically positive patients with UC showed high concentrations of SP receptors on colonic lymphoid aggregates and small blood vessels but not enteric neurons. No increased SP binding was evident in clinically and pathologically quiescent UC colons and normal UC ileostomy samples. CONCLUSIONS: The increased expression of SP receptors on the enteric neurons of patients with CD distinguishes CD from UC. The persistent increased SP binding in pathologically normal CD tissue may indicate a subclinical disease state. SP receptor expression may have important diagnostic, etiologic, and therapeutic usefulness in inflammatory bowel disease.
Adult↗
Mechanism of action of intracisternal apolipoprotein A-IV in inhibiting gastric acid secretion in rats.
BACKGROUND & AIMS: We recently showed that intracisternal injection of apolipoprotein A-IV (apo A-IV), a protein produced by the small intestine in response to fat, inhibits gastric acid secretion. The aim of this study was to investigate the mechanism of acid inhibition by central apo A-IV. METHODS: Gastric acid secretion was determined in pylorus-ligated conscious rats. The effect of intracisternal injection of apo A-IV on gastric acid secretion stimulated by pentagastrin, bethanechol, or intracisternal thyrotropin-releasing hormone (central vagal stimulant) was examined. The effects of vagotomy, indomethacin, and adrenergic blockers on the acid inhibition of apo A-IV were examined to investigate the role of the vagal system, prostaglandin pathways, and adrenergic system. RESULTS: Intracisternal apo A-IV significantly inhibited pentagastrin-, bethanechol-, and thyrotropin-releasing hormone-stimulated gastric acid secretion in a similar fashion. Inhibition of pentagastrin-stimulated acid secretion by apo A-IV still occurred even in vagotomized rats. Yohimbine but not indomethacin or propranolol eliminated apo A-IV--induced inhibition of acid. CONCLUSIONS: Intracisternal apo A-IV inhibits gastric acid secretion through alpha 2-adrenergic receptors. The vagal pathway and the prostaglandin system are not involved in apo A-IV--induced acid inhibition.
Adrenergic beta-Antagonists↗
Pancreatic polypeptide microinjection into the dorsal motor nucleus inhibits pancreatic secretion in rats.
BACKGROUND/AIMS: Pancreatic polypeptide (PP), a hormone released from the pancreas, inhibits pancreatic secretion in vivo but not in vitro, suggesting that the inhibitory action of PP on pancreatic secretion is indirect. Circulating PP in physiological concentrations binds to specific receptors in the dorsal vagal complex in the brainstem. Therefore, the hypothesis of this study was that PP acts centrally and inhibits pancreatic secretion by modulating vagal tone. METHODS: The effects of microinjection of PP into the dorsal motor nucleus on 2-deoxy-D-glucose-stimulated and cholecystokinin octapeptide (CCK-8)-stimulated pancreatic secretion were examined in urethane-anesthetized rats. RESULTS: Microinjection of PP to the dorsal motor nucleus but not brainstem sites outside it inhibited 2-deoxy-D-glucose-stimulated pancreatic flow and protein output. CCK-8-stimulated pancreatic protein output was inhibited by PP in the dorsal motor nucleus in dose-dependent and site-specific manners. The inhibitory effect of PP on CCK-8-stimulated protein output was eliminated by vagotomy. CONCLUSIONS: The results suggest that PP acts in the dorsal motor nucleus to modulate vagal tone on the pancreas, thereby inhibiting pancreatic secretion. This study shows for the first time that the dorsal motor nucleus is involved in central feedback inhibition of the exocrine pancreas.
Analysis of Variance↗
Cystic duct patency in malignant obstructive jaundice. An ERCP-based study relevant to the role of laparoscopic cholecystojejunostomy.
OBJECTIVE: This endoscopic retrograde cholangiopancreatography-(ERCP)based study estimates the potential role of laparoscopic cholecystojejunostomy for palliation of patients with malignant obstructive jaundice. SUMMARY BACKGROUND DATA: Traditional treatment of malignant obstructive jaundice has used a standard bilioenteric anastomosis. Laparoscopic biliary bypass via a gallbladder conduit currently is an established technique; it provides a low initial morbidity alternative to open procedures, similar to endoscopic stenting. No study has specifically addressed anatomic factors relevant to cholecystojejunostomy, such as prior cholecystectomy, stricture location in reference to the hepatocystic junction, and cystic duct patency in patients with malignant obstructive jaundice. METHODS: Retrograde cholangiograms were reviewed from consecutive patients with malignant obstructive jaundice and a control group without biliary disease who underwent ERCP during a 2-year period. Patients with either prior biliary surgery or hilar tumors were excluded. The presence of gallbladder or cystic duct filling was assessed. In patients with patent cystic ducts, the distance from obstruction to the cystic duct takeoff was classified as either greater or less than 1 cm. RESULTS: Nearly half the patients with malignant obstructive jaundice were ineligible for cholecystojejunostomies because of prior biliary surgery (29%) or hilar tumors (17%). Half (50 of 101) of the remaining potential candidates had patent hepatocystic junctions. Patients with ampullary carcinoma and patent hepatocystic junctions (5 of 9) were all ideal candidates for cholecystojejunostomies, having biliary obstruction more than 1 cm from the cystic duct takeoff. Two thirds of the remaining eligible patients (28 of 45) had obstructions less than 1 cm from patent hepatocystic junctions. CONCLUSIONS: Palliation of malignant obstructive jaundice by laparoscopic cholecystojejunostomy should only be attempted after direct cholangiography demonstrates a patent hepatocystic junction that is well separated from the malignant stricture. The majority of patients with malignant obstructive jaundice are ineligible for cholecystojejunostomies because of prior cholecystectomies, hilar obstructions, or tumor involvement of the hepatocystic junction. Nonoperative treatments will continue to be indicated for the majority of patients with malignant obstructive jaundice.
Aged↗
Microinjection of TRH analogue into the dorsal vagal complex stimulates pancreatic secretion in rats.
Thyrotropin-releasing hormone (TRH) stimulates pancreatic exocrine secretion through the vagus nerve when injected into rat cerebrospinal fluid. However, little is known about the exact site of action of TRH in the brain to stimulate pancreatic secretion. Recent neuroimmunochemical and neurophysiological studies suggest that TRH could be a neurotransmitter in the dorsal vagal complex, which sends fibers to the pancreas through the vagus nerve. We therefore hypothesized that TRH may act centrally in the dorsal vagal complex to stimulate pancreatic exocrine secretion. To address this question, a TRH analogue, [1-methyl-(S)-4,5-dihydroorotyl]-L-histidyl-L-prolinamide- NH2, was microinjected into the dorsal vagal complex, and basal pancreatic fluid flow and protein secretion were measured in urethan-anesthetized rats. Microinjection of TRH analogue (0.2-2 ng/site) into the dorsal vagal complex significantly stimulated pancreatic flow and protein output in a dose-dependent manner. As a control, microinjection of the TRH analogue into the brain stem outside the vagal complex failed to stimulate pancreatic secretion. Either bilateral subdiaphragmatic vagotomy or atropine abolished the ability of the TRH analogue to stimulate pancreatic secretion. Our data suggest that TRH acts in the dorsal vagal complex to stimulate pancreatic secretion through vagus-dependent and cholinergic pathways. The dorsal vagal complex may play an important role as a central site for control of the exocrine pancreas.
Animals↗
Pancreatography and the surgical management of pseudocysts.
Endoscopic pancreatography has played a dominant role in the evolution of surgical treatment of pancreatic pseudocysts. This article presents an algorithm for the management of pseudocyst disease, focusing on pancreatography and elective treatment. Pancreatography's roles in refining operative strategies, identifying associated pancreatic and biliary disease, and predicting outcome of nonoperative treatment are reviewed.
Acute Disease↗
Substance P binding sites on intestinal lymphoid aggregates and blood vessels in inflammatory bowel disease correspond to authentic NK-1 receptors.
Previous reports have described the ectopic expression of substance P binding sites on lymphoid aggregates and small blood vessels in inflammatory bowel disease. In this report, three non-peptide NK-1 receptor antagonists, CP-96,345, RP-67,580, and L-703,606 abolished saturable 125I-Bolton-Hunter substance P binding to the ectopically expressed receptors in frozen sections of surgically resected bowel from five patients with either Crohn's disease or ulcerative colitis. The rank order of affinity was approximately substance P approximately CP-96,345 approximately L-703,606 > RP-67,580. These results suggest that: (i) the ectopically expressed substance P binding sites in inflammatory bowel disease are authentic NK-1 receptors, (ii) all ectopically expressed receptors on small blood vessels, and lymphoid aggregates as well as normally expressed receptors on the bowel circular muscle have similar receptor affinities and specificities for substance P and the non-peptide antagonists, and (iii) non-peptide antagonists may be therapeutically beneficial in inflammatory bowel disease by inhibiting the pro-inflammatory effects of substance P acting via the NK-1 receptor.
Binding Sites↗
Intracisternal injection of pancreatic polypeptide stimulates gastric emptying in rats.
In the present study, we evaluated the effects of central administration of pancreatic polypeptide (PP) on gastric emptying of a liquid meal in conscious rats using a phenol red method. Intracisternal injection of PP (0.5-2.0 micrograms) speeds gastric emptying of a test meal in a dose-dependent manner. In contrast, i.p. injection of PP at the same doses inhibited gastric emptying in a dose-related fashion. Bilateral gastric branch vagotomy abolished the increase in gastric emptying evoked by intracisternal PP. These results demonstrate that PP speeds gastric emptying through the vagal system when given centrally but slows emptying when given peripherally.
Animals↗
Neuropeptide Y functions as a physiologic regulator of cephalic phase acid secretion.
Neuropeptide Y (NPY) has been established as a potent orexigenic peptide, and recent studies suggest that NPY stimulates cephalic phase secretion as well. However, it is not known whether NPY's effects are pharmacologic or physiologic. In order to determine the physiologic significance of NPY, we examined the effects of two putative NPY receptor antagonists, PYX-1 and PYX-2, on sham feeding and gastric acid secretion in dogs. Our results demonstrate that intracerebroventricular (i.c.v.) injection of PYX-1 and PYX-2 at 1000 pmol/kg doses significantly suppresses the gastric acid response to sham feeding in dogs. The volumes sham fed were not significantly altered with i.c.v. administration of the antagonists. Peripheral administration did not affect acid secretion nor sham feeding volumes. Our data suggest that central administration of the novel NPY antagonists, PYX-1 and PYX-2, results in significant suppression of acid secretion in dogs. This supports our hypothesis that NPY functions as a physiologic modulator of cephalic phase acid secretion.
Animals↗