1. 1
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 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 to
six 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 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).

2. 2
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

3. 3
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

4. 4
the pancreatic duct, and severe hemorrhage with shock.(Smeltzer, Bare, Hinkle & Cheever,
2010).