Pancreatic necrosis

Discuss the clinical implications of pancreatic fluid collections, pancreatic abscess, and pancreatic necrosis in acute pancreatitis. 

Pancreatic necrosis occurs within the first 2 weeks of acute pancreatitis and develops in 10% to 30% of patients with acute pancreatitis. 

Acute pancreatitis can progress to several distinct consequences. Pancreatic fluid collections and pancreatic abscesses can form during the course of acute pancreatitis. Pancreatic necrosis can occur when pancreatic enzymes damage the pancreatic tissue or when pancreatic abscesses become secondarily infected. This infection is usually due to bacteria that are normally found in the gastrointestinal tract, including Escherichia coli, Enterobacteriaceae, Staphylococcus aureus, viridans group streptococci, and anaerobes. 

Patients at greatest risk for mortality from acute pancreatitis are those who have multi-organ failure (e.g., hypotension, respiratory failure, or renal failure), pancreatic necrosis, obesity, volume depletion, greater than 70 years of age, and an elevated APACHE II score.3,4 The Acute Physiology, Age, and Chronic Health Evaluation (APACHE) II score is a rating scale of disease severity in critically ill patients. 

Pancreatic necrosis is a diffuse inflammation of the pancreas with infectious etiology. Pancreatic necrosis occurs within the first 2 weeks of acute pancreatitis and develops in 10% to 30% of patients with acute pancreatitis. The necrotic pancreas can become secondarily infected with enteric gramnegative bacteria (such as E. coli), and disseminated infection may result from pancreatic necrosis.7,8... 

Pancreatic abscess is a collection of pus that forms in the pancreas 4 to 6 weeks after acute pancreatitis. Pancreatic abscess is usually less life-threatening than pancreatic necrosis or pancreatic pseudocyst and can be managed with percutaneous drainage.5... 

Antibiotics are appropriate for pancreatic necrosis, which can be infected initially or be susceptible to a secondary infection.21 Selected intravenous antibiotic regimens are shown in Table 20-2. If necrosis is confirmed, antibiotics are insufficient as sole therapy surgical debridement is necessary for cure. 

TABLE 20-2. Intravenous Antimicrobial Regimens for Pancreatic Necrosis... 

The patient has been transferred from the CT scanner to the surgical intensive care unit for mechanical ventilation, blood pressure support, and surgical evaluation. A diagnosis of acute pancreatitis with pancreatic necrosis is made. 

Isenmann R, Beger HG Bacterial infection of pancreatic necrosis Role of bacterial translocation, impact of antibiotic treatment. Pan-creatology 2001 1 79-89. 

Local complications in severe AP may include acute fluid collection, pancreatic necrosis, abscess, pseudocyst formation, and pancreatic ascites. 

Treatment of AP is aimed at relieving abdominal pain and nausea, replacing fluids, minimizing systemic complications, and preventing pancreatic necrosis and infection. 

Savelyev VS, Kubishkin VA (1993) Pancreatic necrosis State of the problem and prospec-tives. Khirurgiia 6 22-29... 

Pancreatic necrosis A diffuse or focal area(s) of nonviable pancreatic parenchyma, typically associated with peripancreatic fat necrosis. 

Pancreatic abscess A circumscribed intraabdominal collection of pus, usually in proximity to the pancreas, containing little or no pancreatic necrosis, which arises as a consequence of acute pancreatitis or pancreatic trauma. 

Based on the studies that indicated the relationship between a decrease in vitamin C concentration and morphological changes within the pancreas, it was suggested that assaying the level of vitamin C can constitute a useful indicator of pancreatic necrosis. 

As new imaging tools have become available, such as CT and MRI, many attempts have been made to evaluate imaging criteria for assessing the severity of acute pancreatitis. The first severity index of acute pancreatitis was developed in 1990 by Balthazar et al. (B2). The CT Scoring Index (CTSI) is a 10-point system based on the degree and the type of changes in pancreatic parenchyma and peripancreatic tissues as well as the extent of pancreatic necrosis. The majority of studies confirm its clinical utility for prediction of severity of AP (K6, LI, M20, S14, VI) however, some authors report CT to be ineffective (L13, L14). 

L3. Lankisch, P. G., Struckmann, K., Assmus, C., Lehnick, D., Maisonneuve, P., andLowenfels, A. B., Do we need a computed tomography examination in all patients with acute pancreatitis within 72 h after admission to hospital for the detection of pancreatic necrosis Scand. J. Gastroenterol. 36, 432-436 (2001). 

Nl. Naskalski, J. W., Determination of ribonuclease activity in serum of patients with pancreatic necrosis. Lab. Diag. 30,425—430 (1989). 

There have been over 50 published reports of acute pancreatitis associated with valproate (SEDA-18, 70) (84), including several confirmed by rechallenge. Deaths have occurred from hemorrhagic pancreatic necrosis complications can include pleural and pericardial effusions, coagulopathy, pseudocyst, ascites, wound infection, and pneumonia (SED-13, 151) (85). Hepatotoxicity can coexist. There is suggestive evidence that end-stage renal insufficiency (SEDA-22, 92) and mental retardation (84) can be predisposing factors. 

Ethionine is an acutely toxic compound that targets the liver and pancreas in animals, and possibly humans. Ethionine inhibits intracellular S-adenosy-Imethionine mediated methylation, and cause widespread liver and pancreatic necrosis. 

Hong, J.R., Y.L. Hsu and J.L. Wu. Infectious pancreatic necrosis induces apoptosis due to down-regulation of survival factor MCL-1 protein expression in a fish cell line. Virus Res. 63 75-83, 1999. 

Antibiotics should not be used in the absence of signs of infection except in patients with severe acute pancreatitis when pancreatic necrosis is present. 

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