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1/37. Acute pancreatitis as a complication of polyarteritis nodosa.

    CONCLUSIONS: polyarteritis nodosa (PAN) must be considered as one of the rare causes of "idiopathic" acute necrotizing pancreatitis. BACKGROUND: PAN is characterized by panmural inflammation of arterioles causing arteriolar ectasia, aneurysm formation, and thrombosis, resulting in organ ischemia. methods: We report a case of necrotizing pancreatitis associated with segmental necrosis of the liver and spleen due to polyarteritis nodosa. RESULTS: Five previously reported cases of documented acute pancreatitis secondary to PAN have been identified from the English literature. The mechanism through which pancreatic ischemia results in acute pancreatitis is unknown. Although limited pancreatic infarction is common in PAN, necrotizing pancreatitis is rare, and the poor overall prognosis of PAN is owing largely to other organ complications.
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2/37. stenotrophomonas (xanthomonas) maltophilia infection in necrotizing pancreatitis.

    CONCLUSION: Although the therapy of infected pancreatic collections or organized pancreatic necrosis remains surgical, we have demonstrated that infected organized pancreatic necrosis can be treated endoscopically. BACKGROUND: stenotrophomonas (xanthomonas) maltophilia has been increasingly recognized as a nosocomial pathogen associated with meningitis, pneumonia, conjunctivitis, soft tissue infections, endocarditis, and urinary tract infections. This organism is consistently resistant to imipenem, a drug commonly employed in patients with necrotizing pancreatitis to prevent local and systemic infections. methods AND RESULTS: We report the first case of infected pancreatic necrosis by S. (X.) maltophilia. Our patient was treated successfully with endoscopic drainage of the pancreatic fluid collection and appropriate antibiogram-based antibiotic therapy. Endoscopic drainage has emerged as one of the treatment modalities for pancreatic fluid collections.
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3/37. Postoperative acute pulmonary thromboembolism in patients with acute necrotizing pancreatitis with special reference to apheresis therapy.

    Eight patients with pancreatic abscesses secondary to acute necrotizing pancreatitis underwent drainage of their abscesses under laparotomy. Two of them died of acute pulmonary thromboembolism (PTE) within 1 week. autopsy revealed a large thrombus at the main trunk of the pulmonary artery and in the left common iliac vein. Femoral catheter insertion/indwelling, immobilization, surgery, increased trypsin/kinin/kallikrein, increased endotoxin, and decreased antithrombin-III (AT-III) were present following drainage of the pancreatic abscesses. With respect to the bedside diagnosis of acute PTE, alveolar-arterial oxygen gradients obtained by blood gas analysis and mean pulmonary artery pressure estimated by pulsed Doppler echocardiography are very useful. In terms of the treatment, attention should be paid to the following to prevent deep venous thrombosis: prophylactic administration of low molecular weight heparin and administration of AT-III (AT-III > or = 80%), use of the subclavian vein whenever possible as blood access for apheresis therapy, as short a compression time as possible after removing the blood access catheter (< or =6 h), and application of intermittent pneumatic compression devices or elastic compression stockings on the lower extremities.
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4/37. Experience with duodenal necrosis. A rare complication of acute necrotizing pancreatitis.

    Duodenal necrosis is a rare, but very serious complication of acute necrotizing pancreatitis that most likely is the result of vascular compromise and ischemia of the peri-Vaterian aspect of the duodenal wall. In this article, we present three patients with duodenal necrosis complicating acute necrotizing pancreatitis. The diagnosis was made at the time of necrosectomy. Management options of this challenging complication of necrotizing pancreatitis are discussed.
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5/37. Case report: inappropriate use of percutaneous drainage in the management of pancreatic necrosis.

    We describe three cases of severe necrotizing pancreatitis, with apache II scores of 11, 17 and 22, respectively. There was no significant pancreatic parenchymal perfusion in any of the three patients on contrast-enhanced computed tomography. All three patients were primarily treated with percutaneous drains and all three subsequently required open laparotomies. We do not recommend percutaneous drainage as a definitive therapy for severe necrotizing pancreatitis.
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6/37. Polyarticular heterotopic ossification complicating critical illness.

    A patient with generalized heterotopic ossification (HO) complicating critical illness due to necrotizing pancreatitis is described; data on two other cases with HO are briefly presented. The clinical features, prevention and therapy of HO are discussed. The effect of surgical therapy of the HO in our three patients was good.
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7/37. Ischaemic necrotizing pancreatitis after cardiac surgery. A case report and review of the literature.

    Ischaemia is a rare but often lethal aetiology of pancreatitis. A 67-year-old man underwent aortocoronary by-pass. Postoperatively, he developed atrial fibrillation and possibly acute myocardial infarction. Later, he had acute pancreatitis and underwent laparotomy for purulent peritonitis due to a ruptured pancreatic abscess. Cholesterolosis was found but no gallstones. The postoperative period was heavily complicated and the patient eventually died due to multiorgan failure. The occurrence of ischaemic pancreatitis should be more readily suspected in patients with abdominal symptoms following surgery that induces ischaemia of the pancreas. It is possible that delay in diagnosis accounts for the high death rate of such postoperative complication.
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8/37. Pancreatic injury following acute methanol poisoning.

    BACKGROUND: methanol ingestion is a cause of potentially life-threatening poisoning with numerous systemic manifestations. Clinicians may overlook the possibility of acute pancreatitis in this setting. The objective of this paper is to document the incidence of this complication in a series of 22 patients and to discuss the respective role of methanol and ethanol in its pathogenesis. CASE REPORT: A 54-year-old woman developed acute necrotizing pancreatitis following acute methanol poisoning. She was treated by hemodialysis, ethanol infusion, and folinic acid, but, despite maximal supportive therapy, she died from multiple organ failure 54 hours after the ingestion. CASE SERIES: In a series of 22 consecutive patients admitted with a diagnosis of acute methanol poisoning, we found evidence of pancreatic damage in 11 patients. The abnormalities were present from admission and before ethanol therapy in 7 cases and developed after ethanol therapy in 4 cases. Seven patients had a history of chronic ethanol abuse, but no patient had previously suffered from acute or chronic pancreatitis. Three patients presented moderate-to-severe acute pancreatitis according to clinical and radiological criteria and required aggressive supportive therapy including peritoneal dialysis. One patient died from the direct consequences of acute necrotizing pancreatitis and 2 fully recovered from this event. Three patients evolved to brain death; autopsy revealed hemorrhagic lesions in the pancreas in only 1 case. CONCLUSIONS: Clinical, biological, and radiographic signs of acute pancreatic injury may be more common than previously realized. Acute methanol poisoning appears to produce pancreatic injury, although antidotal treatment with ethanol or prior chronic ethanol abuse may be contributing factors. Because ethanol treatment may complicate the pancreatic injury, fomepizole (4-methylpyrazole) may be the preferable antidote in acute methanol poisoning.
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9/37. succinylcholine-induced hyperkalemia and rhabdomyolysis in a patient with necrotizing pancreatitis.

    IMPLICATIONS: Commonly used muscle relaxants may have serious side effects when used in critically ill patients. This case report relates some of these side effects and reviews the mechanisms by which they are thought to occur.
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10/37. pancreatitis associated with simvastatin plus fenofibrate.

    OBJECTIVE: To report a case of acute necrotizing pancreatitis associated with simvastatin and fenofibrate use. CASE SUMMARY: A 70-year-old white man presenting with rapid onset of abdominal pain, nausea, and vomiting was diagnosed with acute pancreatitis. On bowel rest, his condition deteriorated secondary to systemic inflammatory response syndrome, and he was transferred to a tertiary hospital's intensive care unit (ICU). He had been taking fenofibrate for 1 year; 6 months prior to this admission, he had been taking simvastatin 3 days of the week and fenofibrate the other 4 days of the week. The pancreatic tissue became necrotic, requiring surgical debridement. After a hospital stay of 121 days, including multiple ICU admissions, the patient died secondary to a bowel perforation. DISCUSSION: Although idiopathic pancreatitis cannot be ruled out in this patient, no causes of pancreatitis were identified other than drug induced. Five cases of acute pancreatitis caused by simvastatin have been reported; no case reports were found for fenofibrate. The onset of pancreatitis relative to the duration of therapy with simvastatin supports this medication as a possible cause of the pancreatitis. CONCLUSIONS: Drug-induced pancreatitis is well established as an adverse effect of some medications, although most are substantiated only with case reports. Given the absence of other apparent causes, simvastatin and fenofibrate should be considered as possible causes of pancreatitis in this patient.
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