Objective 1

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Objective 1

  1. 1. 1 Pancreatitis The Journal of the American Medical Association says “Acute pancreatitis is aninflammation of the pancreas that produces exocrine and endocrine dysfunction that may involvesurrounding tissues and/or remote organ systems”. (Torpy, J.M. 2012). The clinical course canrange 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 ofendematous interstitial pancreatitis, whereas the other twenty percent develop severe acutenecrotizing pancreatitis. Reported mortality rates for acute pancreatitis vary, but range from twoto fifteen percent overall from twenty to fifty percent in patients with severe disease. Severalprognostic scoring systems have been developed to predict the severity of acute pancreatitis. Oneof the most commonly used is Ranson’s 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 tosix factors, forty percent mortality; and with seven to eight factors, predicted mortality is one-hundred percent. (Urden, Stacy & Lough 2007). The following is Ranson’s criteria for estimating the severity of acute pancreatitis.At Admission:Age >55, Hypotension, Abnormal Pulmonary findings, Abnormal mass, Hemorrhagic ordiscolored 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).
  2. 2. 2During 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 & Lough2007). 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. Mildacute pancreatitis is characterized by edema and inflammation confined to the pancreas.Minimal organ dysfunction is present, and return to normal function usually occurs within sixmonths. Although this is considered a milder form of pancreatitis, the patient is acutely ill and atrisk for hypovolemic shock, fluid and electrolyte disturbances, and sepsis. A more widespreadand complete enzymatic digestion of the gland characterizes severe acute pancreatitis. Enzymesdamage the local blood vessels, and bleeding and thrombosis can occur. The tissue may becomenecrotic, with damage extending into the retroperitoneal tissues. Local complications includepancreatic cysts or abscesses and acute fluid collections in or near the pancreas. Patients whodevelop systemic complications with organ failure, such as pulmonary insufficiency withhypoxia, shock, renal failure, and GI bleeding, are also characterized as having severe acutepancreatitis. (Smeltzer, Bare, Hinkle & Cheever, 2010). In acute pancreatitis the normally inactive digestive enzymes become prematurelyactivated within the pancreas itself, leading to autodigestion of pancreatic tissue. The enzymesbecome activated through various mechanisms, including the obstruction of or damage to the
  3. 3. 3pancreatic 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 processby 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 thedevelopment of edema and related Hypovolemia. Elastase is the most harmful enzyme in termsof 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 ofcell membranes, causing severe pancreatic and adipose tissue necrosis. Lipase flows intodamaged tissue and is absorbed into the systemic circulation, resulting in fat necrosis of thepancreas and surrounding tissues. (Smeltzer, Bare, Hinkle & Cheever, 2010). The extent of injury to the pancreatic cells determines which form of acute pancreatitiswill develop. If injury to the pancreatic cells is mild and without necrosis, edematouspancreatitis develops. The acinar cells appear structurally intact and blood flow is maintainedthrough capillaries and venules. This form of acute pancreatitis is self-limiting. If injury to thepancreatic cells is severe, acute necrotizing pancreatitis develops. Cellular destruction inpancreatic injury results in the release of toxic enzymes and inflammatory mediators into thesystemic 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/ordeath. Local tissue injury results in infection, abscess and pseudocyst formation, disruption of
  4. 4. 4the pancreatic duct, and severe hemorrhage with shock.(Smeltzer, Bare, Hinkle & Cheever,2010).

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