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

Pancreatic necrosis is a principal determinant of the severity, duration, and infectious complications of acute pancreatitis. There has been no objective index for pancreatic necrosis, and its recognition has necessarily rested upon nonspecific clinical signs, including later deterioration or appearance of sepsis. In search of such an index, we have measured serum levels of a poly-[C]-specific acid ribonuclease (RNase) in 38 patients with acute pancreatitis, 12 patients with chronic pancreatitis, and 50 control patients. The values in chronic pancreatitis (mean, 52 units; range, 33 to 80 units) were within observed normal limits (mean, 51; range, 17 to 94). The values in acute pancreatitis segregated into two groups, normal values (group A) and high values (group B). Of 25 patients in group A (mean, 46; range, 19 to 87), only one developed evidence of pancreatic necrosis or abscess. In contrast, of the 13 patients in group B (mean, 192, range, 98 to 385), 11 required surgical debridement/drainage for pancreatic necrosis (six) or abscess (five) (P less than 0.001). Each of the other two patients had prolonged pancreatic inflammation with fever and a pancreatic mass which persisted for more than 2 weeks. RNase levels in group B patients rose within a few days after onset of pancreatitis and tended to parallel the clinical course. These findings suggest that measurement of serum RNase in acute pancreatitis gives a reliable indication of pancreatic necrosis. Therefore RNase determinations should be of value for earlier identification and monitoring of patients at high risk of late complications, and for helping to select those who will benefit from early debridement before secondary infection occurs.
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PMID:Serum ribonuclease elevations and pancreatic necrosis in acute pancreatitis. 46 72

Acute pancreatitis is often a mild, self-limiting illness that responds to simple supportive therapy in the form of intravenous fluids and analgesics. More severe attacks may result in organ failure or pancreatic necrosis. Such patients should be identified early in the course of an attack and actively monitored within an intensive care unit or high dependency area. Supportive therapy remains the basis of management. Attention to the adequacy of the fluid balance and oxygenation are of prime importance and supportive therapy may include inotropic support, assisted ventilation and renal dialysis. Pancreatic necrosis should be sought by contrast-enhanced computed tomography (CT) scanning, and surgical intervention may be required if the patient's clinical condition continues to deteriorate. Surgery should ideally be delayed until the second or subsequent week when necrosectomy (debridement of necrotic pancreatic tissue) may be possible rather than formal pancreatic resection. The role of various drugs to suppress pancreatic secretion and inhibit pancreatic enzymes, although shown to be consistently effective in experimental pancreatitis, has not been established by controlled clinical trials in humans. Recent controlled studies examining peritoneal lavage in humans have failed to confirm the beneficial results suggested in earlier studies. Early endoscopic sphincterotomy for patients with severe gallstone pancreatitis and ductal calculi has been reported to reduce mortality and morbidity in one controlled clinical trial and may prove to be an important advance.
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PMID:Current concepts in the management of pancreatitis. 171 43

The earliest echographic manifestations of developing pancreatitis or pancreatic necrosis were studied experimentally in five dogs (Beagles). Fifteen minutes after induction of pancreatitis the pancreas was removed and accurately corresponding histological and sonographic serial sections were prepared. Pancreatic necrosis up to 25% was not apparent sonographically. 50% pancreatic necrosis manifested various echo patterns (low echoes, focal hyperechogenicity). 75% and 100% pancreatic necrosis showed characteristic sonographic appearances of focal-nodular hyperechogenicity on an hypo-echogenic background. The study has shown that sonography is a highly sensitive method for recognizing even the earliest stages of acute necrotizing pancreatitis.
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PMID:[Experimental studies on the earliest echographic manifestations of incipient pancreatitis and pancreatic necrosis]. 284 85

Pancreatic necrosis and sepsis are the major causes of death in instances of acute pancreatitis. No widely accepted definition of these conditions in individuals exists, and, yet, accurate differentiation is mandatory for effective therapy. A series of operational definitions conforming to known clinopathologic factors are proposed for the necrotizing septic complications of acute pancreatitis. These complications, as distinguished from acute interstitial pancreatitis, are fat sequestra, pancreatic necrosis, infected pancreatic necrosis, pancreatic abscess and acute pseudocyst. Imprecise definitions of these complications of necrotizing pancreatitis make inter-institutional comparisons of previously identified data dubious.
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PMID:Progress in acute pancreatitis. 304 92

Inhibition of pancreatic secretion is a widely accepted therapeutical principle of acute pancreatitis. However, stimulation of water and bicarbonate secretion may be beneficial by washing out the ductular system in pancreatitis. Secretin (2 and 16 CU/kg body weight) or saline were given to rats at different time intervals after induction of sodium taurocholate pancreatitis. Pancreatic necrosis and edema were slightly more marked after secretin but secretin had no influence on the survival time and rate or enzymatic parameters. It is concluded that in the rat secretin-induced pancreatic secretion does not alter the course of acute pancreatitis.
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PMID:Influence of secretin on the course of acute experimental pancreatitis in rats. 687 5

To determine the incidence and severity of drug induced acute pancreatitis, data from 45 German centres of gastroenterology were evaluated. Among 1613 patients treated for acute pancreatitis in 1993, drug induced acute pancreatitis was diagnosed in 22 patients (incidence 1.4%). Drugs held responsible were azathioprine, mesalazine/sulfasalazine, 2',3'-dideoxyinosine (ddI), oestrogens, frusemide, hydrochlorothiazide, and rifampicin. Pancreatic necrosis not exceeding 33% of the organ was found on ultrasonography or computed tomography, or both, in three patients (14%). Pancreatic pseudocysts did not occur. A decrease of arterial PO2 reflecting respiratory insufficiency, and an increase of serum creatinine, reflecting renal insufficiency as complications of acute pancreatitis were seen in two (9%) and four (18%) patients, respectively. Artificial ventilation was not needed, and dialysis was necessary in only one (5%) case. Two patients (9%) died of AIDS and tuberculosis, respectively; pancreatitis did not seem to have contributed materially to their death. In conclusion, drugs rarely cause acute pancreatitis, and drug induced acute pancreatitis usually runs a benign course.
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PMID:Drug induced acute pancreatitis: incidence and severity. 880 Dec 18

Acute pancreatitis is in the majority of patients a mild, self-limiting illness. Five to fifteen percent of the patients develop acute necrotizing pancreatitis, a severe illness with a high morbidity and mortality. Secondary infection of the pancreatic necrosis (infected pancreatic necrosis) is the main cause of death. Pancreatic necrosis is identified with a high accuracy by contrast-enhanced computed tomography. The differentiation between sterile and infected necrosis requires demonstration of bacteria or fungi isolated from the necrosis. Surgical treatment of a sterile necrosis remains controversial, but there is a tendency towards conservative non-operative treatment. Infected pancreatic necrosis is regarded as an absolute indication for surgery, untreated the mortality is approximately 100%. The aim of modern treatment is to remove the pancreatic necrosis continuously. This has successfully been done by the open packing method, with or without subsequent drainage. At present no randomized trials comparing the different treatment modalities are available. The question of prophylactic antibiotics still remains unanswered. For the present imipenem 0,5 g x 3 is recommended.
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PMID:[Necrotizing pancreatitis]. 757 Oct 95

Pancreatic necrosis is a well-known risk factor for infectious complications in the patients affected with acute pancreatitis. Dynamic CT with i.v. administration of a large bolus of contrast medium can establish the diagnosis of necrotizing pancreatitis. A series of 49 cases of severe acute pancreatitis was reviewed, and early CT investigations were seen to fail to detect pancreatic necrosis in 22 instances, versus 27 positive cases. In the group of patients with no necrosis, the clinical course was uneventful or characterized by mild complications which regressed spontaneously or by means of adjuvant medical treatment. On the contrary, 17 patients with necrotizing pancreatitis developed severe complications requiring intensive treatment. These complications occurred in 50% of the patients with < 50% of pancreatic necrosis, while the figure rose to 77% whenever more extensive involvement was observed. Our results show that the presence and extent of pancreatic necrosis must be diagnosed as early as possible for prognostic and therapeutic purposes; this can be done by the routinary use of dynamic CT with the administration of large amounts of contrast media at high flow rates.
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PMID:[Dynamic computed tomography in the prognostic assessment of acute pancreatitis]. 849 70

The intercellular adhesion molecule-1 (ICAM-1), a membrane glycoprotein, is important in the adhesion of cytokine-stimulated leukocytes to the endothelium of microvessels and their transendothelial migration. Circulating isoforms of ICAM-1 (cICAM-1) are known to be elevated in human serum as an indirect consequence of inflammatory responses. The aim of this study was to investigate whether cICAM-1 levels are elevated in patients with acute pancreatitis within 48 h of the onset of abdominal pain and whether cICAM-1 levels correlate with the severity of the tissue damage. Twenty-five consecutive patients admitted to a medical ICU had elevated cCAM-1 concentrations of 548 +/- 68 ng/ml, significantly different when compared to a control group of 18 healthy subjects (343 +/- 29; p = 0.018). According to the findings of contrast-enhanced CT or laparotomy patients were further divided in a group with acute edematous pancreatitis and a group with acute necrotizing pancreatitis. Pancreatic necrosis was associated with cICAM-1 levels of 729 +/- 106 ng/ml, significantly different from patients with mild disease (367 +/- 48) and controls (p < 0.001). Plasma cICAM-1 levels were not significantly different between healthy subjects and patients with mild pancreatitis. A significant correlation was found between cICAM-1 and C-reactive protein, an acute phase reactant and marker of necrotizing pancreatitis (r = 0.62; p < 0.01). The sensitivity and specificity for the detection of edematous or necrotizing pancreatitis of cICAM-1 plasma concentrations (cutoff point at 500 ng/ml) were 75% and 85%, respectively. These results suggest an enhanced release of ICAM-1 into plasma in the early stage of acute necrotizing pancreatitis. Leukocyte-endothelial cell adhesion may be associated with the inflammatory process of necrotizing tissue damage in acute pancreatitis. It could thus serve as a marker or predictor of a severe clinical course of pancreatitis.
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PMID:Increased plasma concentrations of circulating intercellular adhesion molecule-1 (cICAM-1) in patients with necrotizing pancreatitis. 887 97

In a previous retrospective case-control study, hemoconcentration was associated with the development of pancreatic necrosis. The aim of the present study was to determine in a cohort study whether hemoconcentration is a marker for both organ failure and necrotizing pancreatitis. A cohort study was performed on patients admitted with acute pancreatitis from February 1996 to April 1997. Pancreatic necrosis was defined by findings on dynamic contrast-enhanced computed tomography scan or magnetic resonance imaging. Of 128 total patients with acute pancreatitis, 53 underwent computed tomography or magnetic resonance imaging. Eighteen of 53 had necrotizing pancreatitis. Logistic regression identified an admission hematocrit > or = 44% and a failure of admission hematocrit to decrease at 24 hours as the best binary predictors of necrotizing pancreatitis and organ failure. By 24 hours, 17 of 18 patients with necrotizing pancreatitis versus 11 of 35 with interstitial pancreatitis met one or the other criterion for necrosis (p < 0.001). By 24 hours, 13 of 15 with organ failure versus 36 of 104 without organ failure met one or the other criterion (p < 0.001). The negative predictive value by 24 hours was 96% for necrotizing pancreatitis and 97% for organ failure. Hemoconcentration with an admission hematocrit > or = 44% and/or failure of admission hematocrit to decrease at approximately 24 hours was associated with the development of necrotizing pancreatitis and organ failure. Patients who did not experience hemoconcentration were very unlikely to develop pancreatic necrosis or organ failure.
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PMID:Hemoconcentration is an early marker for organ failure and necrotizing pancreatitis. 1134 47


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