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

Acute necrotizing pancreatitis associated with occult duodenal necrosis and perforation developed in 3 patients 2 to 4 weeks after initially successful treatment of hemorrhagic pancreatitis. Exploration was required for fever, abdominal mass, or X-ray findings of an intra-abdominal abscess. At operation all pancreatic and retroperitoneal abscesses were drained with sump tubes, and the duodenal fistula was closed. An intraluminal tube, placed via a gastrostomy, was used for decompression of the duodenum. Postoperative management included total parenteral nutrition, antibiotics specific for aerobic and anaerobic flora, and frequent X-rays to locate new intra-abdominal abscesses. One to 4 reoperations were necessary because of continuing pancreatic necrosis and abscess formation in each patient. Necrotizing pancreatitis with unrelenting retroperitoneal sepsis and fistula formation results in serious morbidity, hospital stays of several months, and is now the major cause of death in patients with pancreatitis. Survival of all 3 patients resulted from drainage of evolving retroperitoneal abscesses and improvement in our technique for management of large duodenal fistulas.
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PMID:Survival of patients with duodenal fistulas from necrotizing pancreatitis. 86 47

Acute necrotizing pancreatitis induced by infusion of bile salt into the pancreatic duct in rats is consistently associated with acute lung injury similar to the adult respiratory distress syndrome. The role of platelet-activating factor (PAF) in this pancreatitis-associated remote organ failure (lung injury) was investigated. Pulmonary tissue levels of PAF were increased gradually and reached a level of 1345 +/- 455 pg/g (6 times the control level) at 12 hours after induction of pancreatitis, whereas pancreatic PAF levels were undetectable and blood PAF remained unchanged. This local pulmonary PAF accumulation occurred at approximately the same time as the progression of lung injury. Pulmonary responses detected (i.e., eicosanoid production, leukocytic infiltration, Evan's blue extravasation, beta-glucuronidase release) were attenuated to varying degrees by treatment of rats in which pancreatitis was initiated with the PAF receptor antagonists (WEB2170 and BN52021). Rat lung lavages were examined after a 12-hour course of pancreatitis and no changes in PAF concentration, surfactant content, and phospholipase A2 (PLA2) activity were noted. Intravenous administration of PLA2 promoted pulmonary PAF production in experimental rats with pancreatitis but not in normal rats. This observation indicates that PLA2, which was determined to be elevated in plasma during pancreatitis, may be responsible for the accumulation of PAF in the lung. In conclusion, pancreatitis-associated lung injury appears to result from an endogenous inflammatory response in which PAF may play an important role.
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PMID:Role of platelet-activating factor in pancreatitis-associated acute lung injury in the rat. 156 55

Conservative treatment for an attack of acute pancreatitis still takes priority. The treatment of choice in biliary pancreatitis is endoscopic papillotomy with extraction of any bile duct stones. After this procedure the patient usually recovers quickly and cholecystectomy should be done as an interval operation. An early operation has to be done when conservative treatment fails and organ failure occurs. The 'gold standard' of surgical therapy today is the opening of the lesser sac with continuous postoperative lavage and drainage, digital elimination of necrotic tissue and drainage of the paracolic areas. Other described surgical procedures do not produce significantly better results. Necrotizing pancreatitis still has a high mortality in contrast to mild oedematous pancreatitis, which is rarely a problem.
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PMID:Acute pancreatitis: the role of early surgery. 176 23

Serum lipid (triglycerides and cholesterol) concentrations were studied in 49 patients with acute pancreatitis (AP). The aims of the study were to investigate the prevalence of hyperlipidemia (HL) in patients with AP according to etiology and to evaluate whether HL precedes or is a consequence of AP. Moreover, we analyzed the relationship between HL and the development of pancreatic necrosis. At admission, 23 patients (47%) had HL: 9 of 19 patients with alcoholic pancreatitis, 5 of 18 patients with biliary pancreatitis, and 9 of 12 patients with AP of miscellaneous etiologies (p less than 0.05). Severe HL (serum triglycerides greater than 20 mmol/L) was observed in five patients. Serum lipid levels in patients with AP and HL decreased markedly during the first 72 h of evolution, but remained slightly above the upper normal limit in most of them after 15 d. The prevalence of HL was similar in edematous and necrotizing pancreatitis. Necrotizing pancreatitis was significantly associated with the presence of hypertriglyceridemia in conjunction with hypercholesterolemia (p less than 0.05). The observations that a) hyperlipidemia is an early event in acute pancreatitis, (b) serum lipid values decrease during the acute phase of the disease, (c) hyperlipidemia has a different prevalence in different etiologies, and (d) high serum lipid levels are not always associated to pancreatic necrosis suggest that HL is a preexistent metabolic abnormality with respect to AP. On the other hand, HL may play a role in aggravating AP.
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PMID:Hyperlipidemia in acute pancreatitis. Relationship with etiology, onset, and severity of the disease. 178 37

Thirty-five patients with acute pancreatitis underwent serum monitoring of alpha-1-protease inhibitor, alpha-2-macroglobulin, complement factors C3 + C4, and C-reactive protein (CRP). Edematous interstitial pancreatitis was shown to be present in 13 patients by contrast-enhanced computed tomography (CT) and laparotomy (n = 3). Necrotizing pancreatitis was confirmed by laparotomy (n = 21) and contrast-enhanced CT. There were significant differences between the serum values of all measured parameters in the two morphologically defined pancreatitis groups. The best discriminating factors were CRP and alpha-2-macroglobulin, showing 95% and 85% overall detection rates for pancreatic necrosis, respectively.
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PMID:Sensitivity of antiproteases, complement factors and C-reactive protein in detecting pancreatic necrosis. Results of a prospective clinical study. 244 67

The mechanism that explains the association between corticoids and acute pancreatitis is unknown. Our hypothesis was that chronic glucocorticoid treatment could adversely affect the course of hemorrhagic pancreatitis by acting through cholecystokinin (CCK) receptors. Acute necrotizing pancreatitis was induced by feeding young female mice a choline-deficient, ethionine-supplemented (CDE) diet for 60 hours. Treatment with hydrocortisone (10 mg/kg/day) was begun 1 week before pancreatitis. At the onset of the CDE diet, a group of hydrocortisone-treated mice were also given the CCK receptor antagonist CR-1409 (5 mg/kg three times a day). Control mice received injections of saline solution. A follow-up of 336 hours was conducted for survival analysis. Hydrocortisone given alone did not produce pancreatitis. Hydrocortisone, however, did increase the pancreatic necrosis caused by the CDE diet (from 40% to 70%) and significantly reduce survival (from 40% to 9%). CR-1409 completely abolished the adverse effects of hydrocortisone on pancreatitis. We measured amylase release by dispersed pancreatic acini from mice chronically treated with hydrocortisone in response to CCK-8. Treatment with hydrocortisone increased both the sensitivity and the responsiveness of the pancreas to CCK-8. We conclude that glucocorticoids alone may not induce acute pancreatitis, but they can increase the risk of a more severe form of pancreatitis developing. The glucocorticoid effect appears to be attributable to a CCK receptor-mediated sensitization of the pancreas to endogenous CCK. Thus, CCK-receptor blockade may improve survival in necrotizing pancreatitis associated with chronic glucocorticoid treatments.
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PMID:Involvement of cholecystokinin receptors in the adverse effect of glucocorticoids on diet-induced necrotizing pancreatitis. 247 63

We have described a spectrum of pancreatic surgery after cardiopulmonary bypass. At one end is a subclinical lesion which was manifested only by elevations in serum isoamylase levels (27 percent of patients) and increased ribonuclease levels (13 percent of patients) in asymptomatic patients followed after cardiac surgery. At the other end is a severe and often lethal necrotizing pancreatitis. Acute necrotizing pancreatitis was found at autopsy in 25 percent of 138 patients who died after cardiac surgery, and it correlated strongly with low output, acute tubular necrosis, and infarction of the liver, spleen, or bowel. It was the principal cause of death in 4 percent of these patients. In addition, 24 percent of 38 nonsurgical patients who died from cardiac failure and hypoperfusion had acute pancreatitis at autopsy, whereas acute pancreatitis was not observed in 55 nonsurgical patients who died without a significant period of low output. Acute pancreatitis was recognized postoperatively in 12 patients (0.2 percent). Three had mild pancreatitis, and all responded well to conservative therapy. In nine patients, fulminant necrotizing pancreatitis developed. Their courses were characterized by significant early postoperative hemodynamic compromise, abdominal distention, ileus, fever, and episodes of late vascular instability associated with hypocalcemia. The diagnosis of pancreatitis was usually missed because of the absence of pain, tenderness and hyperamylasemia. The diagnosis was confirmed at laparotomy in eight patients and at autopsy in one. The only two survivors among the nine with severe cases had aggressive mobilization, debridement, and wide drainage of the necrotic pancreas. We suggest that a mild subclinical injury to the pancreas may occur as a consequence of cardiopulmonary bypass and may progress to severe ischemic necrosis if hypoperfusion follows in the postoperative period, the presentation of necrotizing pancreatitis may be atypical in the cardiac surgical patient and should be considered if nonspecific abdominal symptoms are present, and aggressive debridement and drainage may be the optimal treatment for aggressive forms of this disease.
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PMID:Acute pancreatitis after cardiopulmonary bypass. 258 Apr 53

Acute necrotising pancreatitis in rats was induced by injecting 5% sodium taurocholate into the pancreatic duct. Prostaglandin E2 (100 micrograms/kg subcutaneously twice) decreased the mortality rate from 100% to 60% (NS). When treatment with prostaglandin E2 was combined with simultaneous administration of either dazmegrel (UK 38,485, 50 mg/kg bodyweight) or Sibelium (Flunarizine R 14,950, 0.2 mg/kg body weight) a significant decrease in the mortality rate (p less than 0.05) was recorded. Dazmegrel is a selective thromboxane A2 synthetase inhibitor and prevents the formation of thromboxane A2. Flunarizine (a calcium entry blocker) decreases thromboxane A2 formation and also inhibits the effects of raised thromboxane A2 concentrations. As plasma thromboxane B2 (the stable metabolite of thromboxane A2) concentrations increase and the plasma prostaglandin E2 concentrations decrease in acute necrotising pancreatitis in rats, the results of the present study indicate that these prostaglandins play a role in the pathophysiology of the disease. It is suggested that restoration of the balance in prostanoid concentrations will have a beneficial effect on the course of acute necrotising pancreatitis.
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PMID:Significance of prostaglandin E2 in acute necrotising pancreatitis in rats. 273 61

The authors report their experience with surgical treatment of acute necrotizing pancreatitis. 207 of 411 patients with acute pancreatitis were operated upon. Acute necrotizing pancreatitis was found in 126 individuals. The following surgical procedures were used: subtotal spleno-pancreatectomy in 26 cases (20.6 per cent), necrectomy or sequestrectomy in 25 cases (19.7 per cent), and conservative procedures, including drainage or incision of the pancreatic capsule, in 76 cases (70.6 per cent). Most of the operations were delayed emergency interventions. The authors found adequate exposure of the pancreas as well as on proper drainage of the lesser sac and retroperitoneal areas essential. This can be accomplished by means of the authors' procedure called "intraperitonealisation" of the pancreas and by multiple coeliostomy.
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PMID:Intraperitonealisation of pancreas and multiple coeliostomy--a possible approach to reduce mortality of acute necrotizing pancreatitis. 292 71

Necrotizing pancreatitis has a formidable mortality that may exceed 55% even when treated by surgical drainage. Standard surgical techniques for controlling pancreatic sepsis are often inadequate because the unique chronicity of pancreatitis results in persistent and ongoing inflammation and sloughing of necrotic retroperitoneal tissue that promotes further sepsis. Ten consecutive high-risk patients in whom standard surgical debridement and drainage had failed were treated with open packing of the pancreatic bed. This was followed by daily debridement dressing changes at the bedside in the surgical intensive care unit. Management of the open abdomen in the surgical intensive care unit using standard surgical techniques ensured optimum wound toilet, prevented recurrent intra-abdominal sepsis, was logistically acceptable, was well tolerated by critically ill patients, and allowed a higher salvage rate (80%) of high-risk patients than might otherwise be anticipated.
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PMID:Surgical management of necrotizing pancreatitis. 351 35


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