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

A large retrospective autopsy study of patients was analyzed to evaluate the major etiologic and pathologic factors contributing to fatal acute pancreatitis (AP). From an autopsy population of 50,227 patients, 405 cases were identified where AP was defined as the official primary cause of death. AP was classified according to morphological and histological, but not biochemical, criteria. Patients with AP died significantly earlier than a control autopsy population of 38,259 patients. Sixty percent of the AP patients died within 7 days of admission. Pulmonary edema and congestion were significantly more prevalent in this group, as was the presence of hemorrhagic pancreatitis. In the remaining 40% of patients surviving longer than 7 days, infection was the major factor contributing to death. Major etiologic groups in AP were chronic alcoholism; postabdominal surgery; common duct stones; a small miscellaneous group including viral hepatitis, drug, and postpartum cases; and a large idiopathic group comprising patients with cholelithiasis, diabetes mellitus, and ischemia. The prevalence of established diabetes mellitus in the AP group was significantly higher than that observed in the autopsy control series, suggesting that this disease should be considered as an additional risk factor influencing survival in AP. Pulmonary complications, including pulmonary edema and congestion, appeared to be the most significant factor contributing to death and occurred even in those cases where the pancreatic damage appeared to be only moderate in extent. Emphasis placed on the early recognition and treatment of pulmonary edema in all cases of moderate and severe AP should contribute significantly to an increase in survival in this disease.
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PMID:Death due to acute pancreatitis. A retrospective analysis of 405 autopsy cases. 389

Extrahepatic manifestations due to an immunologic response to a surface antigen of hepatitis B virus have been identified. These include a serum sicknesslike syndrome and a necrotizing vasculitis. The latter is far more important and in indistinguishable histologically from nonhepatitis related polyarteritis. At least 90 cases have been reported in the decade since 1970, and five are added here. The necrotizing vasculitis syndrome results from fibrinoid necrosis and inflammation of small and medium-sized arterial walls recognizable angiographically by arterial microaneurysms and often by visceral infarction and hemorrhage. Renal failure is common and often associated with pulmonary edema. Gastrointestinal symptoms are a prominent feature due to bowel ischemia. Infarction and perforation are significant causes of morbidity and mortality. Necrotizing vasculitis is also one cause of pancreatitis and of cholecystitis. Plain films, contrast studies, computed tomography, and sonography have been shown to be useful in the recognition of these complications.
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PMID:Radiologic recognition of extrahepatic manifestations of hepatitis B antigenemia. 611 55

The symptoms and signs of 51 patients with a history of scorpion sting were studied. Acute pulmonary oedema with peripheral circulatory failure due to myocarditis developed in 10. Pulmonary oedema appeared within thirty minutes to ten hours after the sting. 5 out of 7 male patients in whom pulmonary oedema subsequently developed presented with priapism. Profuse sweating, mydriasis, vomiting, and peripheral circulatory failure were also seen, and, in 1 patient, the clinical picture was suggestive on pancreatitis. The remaining 40 patients has severe local pain only and no subsequent cardiac manifestations. There appears to be a positive correlation between occurrence of priapism in a male and the later development of cardiac manifestations after a scorpion sting.
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PMID:Diagnostic cardiac premonitory signs and symptoms of red scorpion sting. 612 Apr 3

The authors report a case of severe hypertriglyceridemia (148.5 mmol/l) in a 27-year-old woman admitted for coma of unknown origin. Initial investigations revealed ketoacidosis, pancreatitis and noncardiogenic pulmonary edema. The diabetes was unknown. Ketoacidosis was rapidly controlled. The hypertriglyceridemia was corrected by one course of plasma exchange (4,400 ml) during which the patient returned to consciousness. The patient recovered without any sequelae. Only 2 similar cases, treated by plasma exchange, have been reported in the literature until now.
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PMID:Treatment by plasma exchange of a patient with hyperlipidemia and diabetic ketoacidosis with lesional pulmonary edema and acute pancreatitis. 681 94

A retrospective study of severity symptoms in a series of 102 patients operated upon for acute haemorrhagic pancreatitis showed that the risk of death was much significantly higher when shock (p less than 0,00001) and renal failure (p less than 0,0001) were present. The association, during the post-operative period, of shock and renal failure with one of the following symptoms: digestive haemorrhage, psychic disorders, pulmonary oedema, post-operative peritonitis and evisceration invariably proved fatal. It is suggested that controlled therapeutic trials should be carried out in patients presenting with these complications.
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PMID:[Acute haemorrhagic pancreatitis. Criteria of letality (author's transl)]. 696 96

Myocardial depression (measured by ventricular function curves on response to a fluid load) has been shown in 10 patients with acute hemorrhagic pancreatitis. Significant inadequate responses were found on evaluation of both the left and right heart. The increased pulmonary vascular resistance associated with adult respiratory distress syndrome (ARDS) of this disease was shown to correlate inversely with pulmonary wedge pressure, thereby excluding myocardial failure and pulmonary edema as mechanisms for the production of the ARDS.
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PMID:The myocardial depressant factor (MDF) in acute hemorrhagic pancreatitis. 724 73

This study evaluated the effect of varying the synthesis of nitric oxide with sodium nitroprusside or N-nitro-L-arginine methyl ester (L-NAME) in a pancreatitis-lung injury model. Rats (n = 45) were randomized to control or caerulein-induced pancreatitis groups, treated with saline, sodium nitroprusside (0.4 micrograms/kg) or L-NAME (10 mg/kg). Myeloperoxidase activity was used as a measure of neutrophil infiltration. Wet to dry (W:D) lung weight and bronchoalveolar lavage (BAL) protein concentrations were used to assess vascular leakage. Pancreatitis was shown to induce pulmonary neutrophil influx: mean(s.e.m.) myeloperoxidase activity 6.79(0.5) units/g in caerulein-treated animals versus 2.08(0.5) units/g in controls (P < 0.001). Animals with pancreatitis showed increased microvascular leakage compared with controls (mean(s.e.m.) W:D lung weight 7.01(0.5) versus 2.85(0.2), P < 0.001; BAL protein concentration 2539(222) versus 347(32) micrograms/ml, P < 0.001). Compared with the saline-treated pancreatitis group, these changes were reduced by sodium nitroprusside (mean(s.e.m.) myeloperoxidase activity to 2.5(0.4) units/g, P < 0.001; W:D lung weight to 3.8(0.37), P < 0.001; BAL protein concentration 1389(182) micrograms/ml, P < 0.05). L-NAME exacerbated the pancreatitis-induced pulmonary oedema (W:D lung weight increased to 11.96(0.6), P < 0.001), protein leakage (BAL protein concentration rose to 3707(309) micrograms/ml, P < 0.05) and neutrophil infiltration (myeloperoxidase activity increased to 9.01(0.3) units/g, P < 0.05). These data suggest that, in vivo, nitric oxide inhibits pancreatitis-induced lung injury, possibly in part by inhibiting pulmonary neutrophil influx.
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PMID:Role of nitric oxide in lung injury associated with experimental acute pancreatitis. 764 71

Infusion of a supramaximally stimulating dose of the pancreatic secretagogue caerulein (10 micrograms.kg-1.h-1) for 4 h induces interstitial edematous acute pancreatitis in rats. This model of acute pancreatitis is associated with evidence of acute lung injury, including sequestered neutrophils within the pulmonary microvasculature, increased microvascular permeability, and interstitial pulmonary edema. Infusion of prostaglandin E1 (PGE1; 50 ng.kg-1.min-1) along with caerulein does not alter the severity of secretagogue-induced pancreatitis, but it does reduce the severity of pancreatitis-associated acute lung injury. The rise in lung weight, lung water content, and pulmonary microvascular permeability and the sequestration of neutrophils within the pulmonary microvasculature that accompany secretagogue-induced pancreatitis are all reduced by infusion of PGE1. Infusion of PGE1 does not interfere with polymorphonuclear neutrophil sequestration in the pancreas or reduce the enhanced expression of CD11b/c receptors on circulating neutrophils. Our observations indicate that PGE1 reduces the severity of pancreatitis-associated acute lung injury by preventing neutrophil sequestration within the lung. We speculate that PGE1 interferes with neutrophil sequestration by dilating pulmonary vasculature, increasing pulmonary flow rate, and reducing neutrophil-endothelial cell interaction and attachment.
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PMID:Protective effects of prostaglandin E1 on acute lung injury of caerulein-induced acute pancreatitis in rats. 903 72

We evaluated the effects of a protease inhibitor on the progression of acute pancreatitis in rats. The model was selected and modified to mimic an intermediate stage of the disease. The degree of microcirculatory derangement in the pancrease and of lung edema was determined to assess the effects of gabexate mesilate (ethyl-4-(6-guanidinohexanoyloxy) benzoate methane sulfonate), a synthetic antiprotease, in acute pancreatitis. Male Sprague-Dawley rats (225-275 g) were used. Experimental pancreatitis was established by four intramuscular injections of cerulein (50 micrograms/kg) at 1 hour intervals. Lipopolysaccharide (10 mg/kg) was injected intraperitoneally as an acute septic challenge. Gabexate mesilate was infused intravenously 6 hours after the initiation of induction of acute pancreatitis at doses of 0.01, 0.1, 1, or 10 mg/kg/h. Microcirculatory changes in the pancreas were studied using in vivo microscopy. All animals survived until the end of the experiments. Gabexate mesilate significantly improved pathologic criteria and decreased serum lipase levels at doses of 1 and 10 mg/kg/h. It significantly lessened the severity of lung edema and improved the microcirculatory environment in the pancreas by increasing flow velocity and reducing leukocyte sticking. These results indicate the beneficial effects of gabexate mesilate on pancreatic microcirculation and lung edema in the progression of acute pancreatitis with septic challenge in rats.
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PMID:Gabexate mesilate improves pancreatic microcirculation and reduces lung edema in a rat model of acute pancreatitis. 930 24

A 72-year-old man underwent resection of an infrarenal aortic aneurysm; during postoperative recovery, multiorgan failure developed secondary to cholesterol emboli in several arteries. The initial sign consisted of patches of livedo in the lower limbs with pedal pulses, hematuria and hyperdynamic shock with high cardiac output and reduced vascular resistance. The clinical picture progressed to multiple organ failure with non-cardiogenic pulmonary edema, oliguric kidney failure, coagulopathy, necrotizing pancreatitis and colic ischemia. The patient died 15 days after surgery. The formation of multiple cholesterol emboli is a rare complication after aortic surgery, vascular catheterization or anticoagulant treatment. It is caused by cholesterol crystals measuring 100 to 200 mu that embolize and block small arteries. Diagnosis is difficult because the organs involved can be many and various. No specific treatment is available and the rates of morbidity and mortality are high.
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PMID:[Multiple cholesterol athero-embolisms after resection of an abdominal aortic aneurysm]. 1117 70


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