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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bowel necrosis is an uncommon complication of pancreatitis. Two patients are reported who developed ileocecal and descending colon changes as a result of ischemia following severe pancreatitis. Arteriography in one patient confirmed the presence of intraluminal thrombi.
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PMID:Colonic necrosis complicating pancreatitis. 61 98

The pancreas, like the kidney, is highly vulnerable to ischemic necrosis. This form of pancreatic injury may express itself as prolonged hyperamylasemia with only minimal signs or symptoms of inflammation, or may produce severe pancreatitis followed by abscesses and death. Autopsy examination of patients dying after oligemic shock showed a 9% incidence of major pancreatic injury if there was not concomitant acute renal tubular necrosis (ATN), but a 50% incidence in those with ATN. Similarly, among patients dying after non-oligemic shock, 12% of those without ATN had major pancreatic injury but 35% with ATN also had pancreatic ischemic injury. Among 13 selected patients examined prospectively after being in shock, pancreatic injury was indicated by hyperamylasemia, hyperlipasemia, elevated amylase/creatinine clearance ratio, and elevated circulating isoamylases specifically of pancreatic origin. Four of the 13 had clinical manifestations of pancreatitis. Not only must shock be added to this list of causes of pancreatitis, but pancreatic ischemia due to hypoperfusion may also be the critical factor which causes the progression from edema to necrosis in other forms of pancreatitis, including those associated with alcohol and biliary disease.
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PMID:Susceptibility of the pancreas to ischemic injury in shock. 68 87

Acute pancreatitis is a well known occurrence after upper gastrointestinal and biliary tract surgery when local trauma plays a major role in the pathogenesis of this complication. The incidence of pancreatitis after surgical procedures during which local trauma to the pancreas does not occur is extremely low (less than 0.1%). In the present study the incidence of unexplained pancreatitis in 182 patients who died after cardiac surgery was 16%. The role of ischemia in the pathogenesis of pancreatitis in this setting is evaluated.
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PMID:Pancreatitis after cardiac surgery; a morphologic study. 93 46

Twenty-four dogs were divided into five groups. Under pentothal sodium anesthesia, those in the control group received no further manipulation; another group underwent laparotomy only; and dogs in the last three groups had induced pancreatitis, intestinal ischemia and duodenal perforation, respectively. An analysis was made of serum and peritoneal lavage fluid in the dog of each group at 30 minute intervals for four and one-half hours. Parameters which were significantly elevated in dogs with pancreatitis compared with other groups included fluid amylase, lactate dehydrogenase, proteolytic activity and intestinal alkaline phosphatase and serum amylase. We judge that these biochemical differences in the lavage fluid, when taken with the physical characteristics of the fluid and the clinical symptoms, can significantly aid the clinician in arriving at the diagnosis of acute pancreatitis.
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PMID:Use of peritoneal lavage in the diagnosis of experimental acute pancreatitis. 112 80

Colonic strictures are an uncommon complication of pancreatitis. Three new cases are described and in each case the histological features strongly resemble those seen in strictures of ischemic origin. It is postulated that ischemia and not encircling pericolic inflammation, is the cause of strictures associated with pancreatitis.
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PMID:Etiology of strictures of the colon associated with pancreatitis. 119 Feb 3

The frequency of surgical complications after liver transplantation remains high. Sixty transplants were done in 48 patients during 4 years. Eleven patients were retransplanted (re-transplant rate, 20%) for primary nonfunction (6), arterial thrombosis (3), warm ischemia (1), and rejection (2). Right pleural effusions were drained in 13 patients and left ones in 2. Forty-eight re-explorations excluding retransplantation were performed in 20 patients. Twelve laparotomies were for control of postoperative intraabdominal bleeding. The majority of these patients (8/10, 80%) were transplanted with reduced-size grafts. Early postoperative vascular complications were detected in 12 grafts (5 portal vein occlusions, 7 arterial thromboses). All 5 patients with portal vein (PV) occlusions were reexplored, and PV flow was reestablished in all 5. Biliary leaks were diagnosed in 6 patients and were associated with arterial thromboses in 2 cases. Reoperation was required in 4 of 6 patients. Bowel perforation occurred in 4 patients; 2 small bowel, 1 duodenum, and 1 colon. There was 1 postoperative bowel obstruction requiring laparotomy. Two splenectomies were required in 4 patients with splenic infarction. Resection of part of a transplanted liver was done in 1 patient to exclude septic infarcts. Pancreatitis was diagnosed in 4 patients and one required laparotomy for control of pancreatic hemorrhage. Intraabdominal abscesses required open drainage in 2 patients and percutaneous drainage in 4. Seven thoracotomies were done in 6 patients: 5 open lung biopsies, 1 for control of hemorrhage, and 1 for diaphragmatic plication. The current high survival rates following liver transplantation require aggressive surgical management of a myriad of complications and numerous procedures are necessary both as treatment modalities and as diagnostic aids.
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PMID:Surgical complications in children after liver transplantation. 147 91

The pathogenesis of acute pancreatitis is based on the following principles: 1. Biliary. In biliary pancreatitis there is a causal relationship between the induction of acute pancreatitis and the migration of gallstones. The basic pathomechanism seems to be a combination of an increase in permeability and pressure in the ductal system. 2. Intraacinar. Caerulein-pancreatitis is a well established experimental model which reflects the intracellular/interstitial type of activation. Basolateral secretion of pancreatic enzymes into the interstitial space represents the initial event. Intracellular activation of trypsin by the fusion of zymogen-granules and lysosomes has been advocated as an alternative mechanism. 3. Alcohol. The acute alcohol pancreatitis comprises a combined pathogenesis. Obstruction and reflux as well as the cytotoxic effect of alcohol seem to be the main principles. 4. Disturbance of pancreatic microcirculation. Ischemia of the pancreas seems to play a key role in the transition from pancreatic edema to necrosis. Improvement of capillary perfusion by isovolemic hemodilution with dextran 60 has been shown to be an efficient therapeutic tool.
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PMID:[Etiology and pathogenesis of acute pancreatitis]. 152 49

Local or generalized alteration of microcirculation may be expected in diseases of the pancreas. Changes may range from increased permeability of capillaries to hemorrhage. Tissue necrosis may result from prolonged ischemia owing to intravascular coagulation and severely impaired blood flow. It is possible to observe early microvascular changes by intravital microscopy. Klar and coworkers have demonstrated by this method that isovolemic hemodilution improves blood flow under conditions that would otherwise lead to tissue damage. This paper presents the basic microcirculation of the pancreas and the changes that accompany pancreatic disease. It emphasizes that concentration on the changes in microcirculation that accompany the early manifestations of pancreatic diseases, particularly pancreatitis, may reveal important clues to their pathogenesis.
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PMID:Microvasculature of the pancreas. Relation to pancreatitis. 152 46

In a variety of animal models of acute pancreatitis, cholecystokinin-receptor antagonists have ameliorated the injury response. These results suggest that cholecystokinin may play a primary role in the pathogenesis of pancreatitis initiated by multiple stimuli. In an effort to test this theory, a sensitive and high affinity cholecystokinin-receptor antagonist L364,718 was administered to four different models of acute pancreatitis that were produced in the ex vivo perfused canine pancreas preparation. The four models of pancreatitis were initiated by cerulein infusion, partial duct obstruction with secretin stimulation, oleic acid infusion, and a 2-hour period of ischemia. In each model, pancreatitis was manifest by edema formation, weight gain, and hyperamylasemia during a 4-hour perfusion. In cerulein infusion-induced pancreatitis L364,718 inhibited edema formation and weight gain (31 +/- 5 gm versus 7 +/- 6 gm; p less than 0.05) and significantly decreased plasma amylase activity (36,605 +/- 21,216 U/dl versus 9421 +/- 5149 U/dl; p less than 0.05). The acute pancreatitis induced by the other three stimuli was not ameliorated by L364,718 treatment. We conclude that in the ex vivo-perfused canine pancreas preparation cerulein-induced pancreatitis is mediated at least in part by the cholecystokinin receptor. Early blockade of the cholecystokinin receptor was of no benefit in treating the other models of pancreatitis, suggesting that cholecystokinin is not involved in the early pathogenesis.
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PMID:The role of cholecystokinin in the pathogenesis of acute pancreatitis in the isolated pancreas preparation. 170 26

The effect of allopurinol, a xanthine oxidase inhibitor, on canine experimental ischemic pancreatitis was studied. The animals were divided into nine groups: 1. Group 1. Control with pancreatic ischemia; 2. Group 2. Received allopurinol once, previous to ischemia; 3. Group 3. Received allopurinol once, immediately after ischemia; 4. Group 4. Received allopurinol immediately after ischemia and then daily; and 5. Groups 5, 6, and 7 were controls for the operation, allopurinol, and its vehicle, respectively; 6. Group 8 (pancreatic ischemia) and Group 9 (that received allopurinol after ischemia and daily) were also studied histologically. Serum amylase was determined in all animals. In Groups 1 and 5, following the ischemic period, hyperamylasemia developed and a peak was reached 24 h after ischemia. In Group 2, a significant decrease of amylase levels was found, compared to matched controls immediately after ischemia and then rose, reaching on the fifth day a peak that was less than the controls at 24 h. In Group 3, the serum amylase level increased immediately to values similar to controls; later, there was a drop to levels lower than those found in controls, followed by a peak on the fifth day. In Group 4, there was no significant elevation in the amylase values. Groups 6 and 7 showed no changes of amylasemia. In this experimental model, allopurinol blocked or ameliorated significantly cellular injury, as shown by a decrease of amylase levels in blood, and of histopathological changes, depending on dose and time of administration. These results offer the possibility of a prophylactic therapy for chronic relapsing and idiopathic pancreatitis.
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PMID:Effects of allopurinol on ischemic experimental pancreatitis. 171 Oct 87


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