Necrosis, acute pancreatitis

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. 

A patient with acute pancreatitis may develop many severe local and systemic complications. Local complications involve fluid collection, necrosis, or abscess in the pancreas. A pancreatic fluid collection (or pancreatic pseudocyst) is a collection of tissue, pancreatic enzymes, and blood that forms weeks after acute pancreatitis. Many pancreatic pseudocysts resolve spontaneously, but some require surgical drainage.5 Rupture of a pancreatic pseudocyst with associated erosion and hemorrhage of major abdominal blood vessels can have a mortality approaching 60% thus, continued monitoring of a pseudocyst is prudent.6... 

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... 

Empiric antibiotics are not necessary if the patient has mild disease or a non-infectious etiology of acute pancreatitis. Antibiotics have not been shown to prevent the formation of pancreatic abscess or necrosis when given early in the course of acute pancreatitis. 

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. 

Severe acute pancreatitis Acute pancreatitis associated with organ failure and/or local complications, such as necrosis, abscess, or pseudocyst. 

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. 

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). 

Computed tomography is undoubtedly the most accurate method for determining the extent of necrosis in acute pancreatitis debate exists, however, regarding patient selection and the optimal timing of CT (M20, L3), especially in the patients with Ranson score below 2. 

B12. Block, S., Maier, W., Bittner, R., Biichler, M., Malfertheiner, P., and Beger, H. G., Identification of pancreas necrosis in severe acute pancreatitis Imaging procedures versus clinical staging. Gut 27, 1035-1042 (1986). 

E2. Exley, A. R., Leese, T., Holliday, M. P., Swann, R. A., and Cohen, J., Endotoxemia and serum tumour necrosis factor as prognostic markers in severe acute pancreatitis. Gut 33, 1126-1128 (1992). 

F3. Fitz, R. H., Acute pancreatitis A consideration of pancreatic hemorrhage, hemorrhagic suppurative and gangrenous pancreatitis and of disseminated fat necrosis. Boston Med. Surg. 120, 181-187 (1889). 

G4. Grewal, H. P., Kotb, M., Mohey ElDin, A., Ohman, M., Salem, A., Gaber, L., and Gaber, O., Induction of tumor necrosis factor in severe acute pancreatitis and its subsequent reduction after hepatic passage. Surgery 115,213—221 (1994). 

H8. Hughes, C. B., Gaber, L. W., and Kolb, M., Induction of acute pancreatitis in germ-free rats Evidence of a primary role for tumor necrosis factor alpha. Surgery 117, 201-205 (1995). 

K5. Kedra, B., Popiela, T., and Naskalski, J., Poly-C ribonuclease in acute pancreatitis. Part 1. Is blood serum poly-C ribonuclease activity an efficient necrosis indicator in acute pancreatitis [in Polish], Pol. Przegl. Chir. 66, 1237-1243 (1994). 

K6. Kemppainen, E., Sainio, V., Haapiainen, R., Kivisaari, L., Kivilaakso, E., and Puolakkainen, P., Early localization of necrosis by contrast-enhanced computed tomography can predict outcome in severe acute pancreatitis. Br. J. Surg. 83,924—929 (1996). 

L2. Lankisch, P. G., Pfichthofer, D., and Lehnik, D., No strickt correlation between necrosis and organ failure in acute pancreatitis. Pancreas 20, 319 (2000). 

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). 

M19. Muller, C. A., Uhl, W., Printzen, G., Gloor, B., Bischofberger, H., Tcholakov, O., and Biichler, M. W., Role of procalcitonin and granulocyte colony stimulating factor in the early prediction of infected necrosis in severe acute pancreatitis. Gut 46,233—238 (2000). 

N7. Norman, J. G., Fink, G. W., and Franz, M. G., Acute pancreatitis induces intrapancreatic tumor necrosis factor gene expression. Arch. Surg. 130, 966—971 (1995). 

PI. Paajanen, H., Laato, M., Jaakkola, M., Pulkki, K., Ninikoski, J., and Nordback, I., Serum tumour necrosis factor compared with C-reactive protein in the early assessment of severity of acute pancreatitis. Br. J. Surg. 82,271—273 (1995). 

T4. Tenner, S., Sica, G., Hughes, M., Noordhoek, E., Feng, S., Zinner, M., and Banks, P. A., Relationship of necrosis to organ failure in severe acute pancreatitis. Gastroenterology 113,899—903... 

Ul. Uhl, W., and Biichler, M., PMN-elastase in comparison with CRP, antiproteases, and LDH as indicators of necrosis in human acute pancreatitis. Pancreas 6, 253 (1991). 

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