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Query: UMLS:C0036690 (sepsis)
 59,461 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

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

We have described a 45-year-old obese white man found to have myeloperoxidase (MPO) deficiency of the granulocytic and monocytic series. Pancreatic necrosis due to bacterial infection developed as a complication of acute pancreatitis. Subsequently, he died of sepsis. MPO staining of terminal antemortem blood smears and postmortem bone marrow aspirates showed absence of MPO in cells of the myelocytic and monocytic series. Family members' neutrophils and monocytes stained positive for MPO. MPO deficiency associated with severe sepsis is rarely reported. This case serves as a review of the association between hereditary and acquired MPO deficiency and severe infection.
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PMID:Myeloperoxidase deficiency and severe sepsis. 839 23

The pathophysiology of severe acute pancreatitis (AP) resembles other conditions with systemic inflammatory response syndrome (SIRS) such as sepsis predisposing to remote organ failure. Because extracellular phospholipases A2 (PLA2) have been implicated in AP, their serum concentrations were analyzed with respect to SIRS and systemic complications in patients with severe AP. The serum samples were collected daily for 12 days in 57 patients with severe AP. SIRS, early organ complications, local complications, and outcome of AP were recorded. Time-resolved fluoroimmunoassays were used for group I and group II PLA2 measurements. Thirty-nine (68.4%) patients fulfilled the criteria of SIRS within 12 days from admission. Pancreatic necrosis was detected in 43 (75.4%) patients. Infected necrosis was found preoperatively or at operation in five (8.8%) patients. Twenty-six (45.6%) and eight (14.0%) patients had respiratory or renal failure, respectively. Seven (12.3%) patients died of their disease. All patients with systemic complications fulfilled the criteria of SIRS. The increasing number of positive SIRS criteria was associated with increased frequency of systemic complications. Pancreatic necrosis was not significantly associated with SIRS. The serum concentration of group II PLA2 was significantly higher in patients with SIRS (p < 0.05) compared with patients without from day 7 onward. The concentration of group II PLA2 increased (p < 0.01) in patients with SIRS but decreased in patients without. The serum concentration of group II PLA2 did not differ significantly with respect to systemic complications. The concentration of group I PLA2 decreased (p < 0.05) similarly in patients with and without SIRS or systemic complications during follow-up, respectively. Early systemic complications of severe AP are associated with SIRS with increasing frequency as the number of positive SIRS criteria increases. Group II PLA2 but not group I PLA2 may have pathophysiologic importance in severe AP-associated SIRS. Increasing serum concentration of group II PLA2 seems to reflect the ongoing systemic inflammation in severe AP-associated SIRS.
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PMID:Extracellular phospholipases A2 in relation to systemic inflammatory response syndrome (SIRS) and systemic complications in severe acute pancreatitis. 1023 44

A patient who had undergone failed transgastric placement of two cystgastrostomy stents referred to the regional pancreatic unit with ongoing sepsis for further management. Following stabilisation, percutaneous minimally invasive necrosectomy (MIN) was performed. MIN resulted in sustained clinical resolution of the sepsis and normalisation of serum C reactive protein levels. The transgastric drains were removed by MIN and, importantly, the patient did not develop a gastric fistula. To our knowledge, this is the first report of MIN following endoscopic cystgastrostomy stent placement. Pancreatic necrosis progresses from solid to semisolid to liquid states over a period of several months. Transgastric drainage should be reserved for subjects with either a pancreatic abscess or predominantly liquid necrosis reserving MIN for patients with systemic sepsis and those with semisolid necrosis. As increasing strategies to treat pancreatic necrosis become available clinicians must be alert to the development of new complications of these treatments.
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PMID:Percutaneous minimally invasive necrosectomy following endoscopic transgastric drainage in acute necrotising pancreatitis. 2308 67

Summary. Infection frequently complicates the course of severe acute pancreatitis and might manifest as infected pancreatic necrosis, pancreatic abscess or an infected peripancreatic fluid collection. Pancreatic necrosis occurs in roughly 21% of all cases of pancreatitis. In patients with necrosis involving more than one-half of the pancreas, the incidence of subsequent infection is as high as 40%-70%. More than 50% of these infection yield a polymicrobial isolate with predominance of enteric bacteria but recently, the microbiologic pattern has shifted toward more resistant gram-negative bacilli, gram-positive cocci and yeast, a reflection of exposure to broad-spectrum antimicrobial agents. Given the morbidity associated with infection, many commentators have advocated prophylactic antimicrobial therapy in patients with necrosis to the point that this measure has been incorporated into routine practice. However, there is controversy over the risks and potential benefit. Currently, advise against the routine use of prophylactic systemic antibiotics and antifungals (side-effect selection of resistant microbes and fungi). However, there may be some patients who benefit from prophylaxis, and additional studies and investigations are ongoing. Antibiotics should not be given early in the disease course because most symptoms are due to the inflammatory response, not an infectious etiology. Antibiotics are indicated when CT scans indicate a pancreatic phlegmon, empirically in the case of severe pancreatitis associated with septic shock, or with documented fine - needle aspiration biopsy identification of bacteria. Under those circumstances, antibiotic coverage is warranted to prevent systemic gram-negative sepsis. Infected pancreatic necrosis should be treated with carbapenems because they can effectively penetrate pancreatic tissue. Other conditions, such as biliary pancreatitis associated with cholangitis, mandate antibiotic coverage.
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PMID:[Antibiotics for pancreatitis--still controversial?]. 2312 Aug 50