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Pancreatitis The Journal of the American Medical Association says Acute pancreatitis is an inflammation of the pancreas that produces exocrine and endocrine dysfunction that may involve surrounding tissues and/or remote organ systems. (Torpy, J.M. 2012). The clinical course can range from a mild, self-limiting disease to a systemic process characterized by organ failure, sepsis, and death. In approximately eighty percent of patients it takes a milder form of endematous interstitial pancreatitis, whereas the other twenty percent develop severe acute necrotizing pancreatitis. Reported mortality rates for acute pancreatitis vary, but range from two to fifteen percent overall from twenty to fifty percent in patients with severe disease. Several prognostic scoring systems have been developed to predict the severity of acute pancreatitis. One of the most commonly used is Ransons criteria. If the patient has zero to two factors present, predicted mortality is 2 percent; with three to four factors, fifteen percent mortality; with five to six factors, forty percent mortality; and with seven to eight factors, predicted mortality is onehundred percent. (Urden, Stacy & Lough 2007). The following is Ransons criteria for estimating the severity of acute pancreatitis. At Admission: Age >55, Hypotension, Abnormal Pulmonary findings, Abnormal mass, Hemorrhagic or discolored peritoneal fluid, increased serum LDH (>350u/L), AST > 250u/L, leukocytosis (>16,000/mm3), Hyperglycemia (>200mg/dl; no diabetic hx) Neurologic deficit (confusion) . (Urden, Stacy & Lough 2007).

During initial 48 hrs. Of hospitalization: Fall in HCT >10% with hydration or HCT <30%, Hypocalcemia (<8mg/dl), arterial Po2 < 60mm Hg, Hypoalbuminemia (<3.2mg/dl) Base Deficit >4 mEq/L. . (Urden, Stacy & Lough 2007).

Approximately 185,000 cases of acute pancreatitis occur in the United States each year, of which 150,000 are the result of cholelithiasis (gallstones) or sustained alcohol abuse. Mild acute pancreatitis is characterized by edema and inflammation confined to the pancreas. Minimal organ dysfunction is present, and return to normal function usually occurs within six months. Although this is considered a milder form of pancreatitis, the patient is acutely ill and at risk for hypovolemic shock, fluid and electrolyte disturbances, and sepsis. A more widespread and complete enzymatic digestion of the gland characterizes severe acute pancreatitis. Enzymes damage the local blood vessels, and bleeding and thrombosis can occur. The tissue may become necrotic, with damage extending into the retroperitoneal tissues. Local complications include pancreatic cysts or abscesses and acute fluid collections in or near the pancreas. Patients who develop systemic complications with organ failure, such as pulmonary insufficiency with hypoxia, shock, renal failure, and GI bleeding, are also characterized as having severe acute pancreatitis. (Smeltzer, Bare, Hinkle & Cheever, 2010). In acute pancreatitis the normally inactive digestive enzymes become prematurely activated within the pancreas itself, leading to autodigestion of pancreatic tissue. The enzymes become activated through various mechanisms, including the obstruction of or damage to the

pancreatic duct system, alterations in the secretory processes of the acinar cells, infection, ischemia, and/or other known factors. . (Urden, Stacy & Lough 2007). Trypsin is the enzyme that becomes activated first and initiates the auto digestion process by triggering the secretion of proteolytic enzymes such as kallikrein, chymotrypsin, elastase, phospholipase A, and lipase. Release of kallikrein and chymotrypsin result in increased capillary membrane permeability, leading to the leakage of fluid into the interstitium and the development of edema and related Hypovolemia. Elastase is the most harmful enzyme in terms of direct cell damage. It causes dissolution of the elastic fibers of blood vessels and ducts, leading to hemorrhage. Phospholipase A, in the presence of bile, destroys the phospholipids of cell membranes, causing severe pancreatic and adipose tissue necrosis. Lipase flows into damaged tissue and is absorbed into the systemic circulation, resulting in fat necrosis of the pancreas and surrounding tissues. (Smeltzer, Bare, Hinkle & Cheever, 2010). The extent of injury to the pancreatic cells determines which form of acute pancreatitis will develop. If injury to the pancreatic cells is mild and without necrosis, edematous pancreatitis develops. The acinar cells appear structurally intact and blood flow is maintained through capillaries and venules. This form of acute pancreatitis is self-limiting. If injury to the pancreatic cells is severe, acute necrotizing pancreatitis develops. Cellular destruction in pancreatic injury results in the release of toxic enzymes and inflammatory mediators into the systemic circulation and causes injury to the vessels and other organs distant from the pancreas; this may result in systemic inflammatory response syndrome (SIRS), multiorgan failure and/or death. Local tissue injury results in infection, abscess and pseudocyst formation, disruption of

the pancreatic duct, and severe hemorrhage with shock. (Smeltzer, Bare, Hinkle & Cheever, 2010).