Acute pancreatitis is an inflammatory process of the pancreas that is caused by the premature activation of pancreatic enzymes. These enzymes are normally secreted in an inactive form for the digestion of fats, carbohydrates, and proteins. The origin of this premature activation can be multifactorial; the cause remains unclear, but obstruction or trauma of the ampulla of Vater of the common bile duct, chronic alcoholism, viral sources, and toxicity caused by other agents have been proposed as causative events. In acute pancreatitis, autodigestion of the pancreatic tissue by proteolytic enzymes (trypsinogen, chymotrypsinogen, proelastase, and phospholipase A) occurs when enzymes are activated in the pancreas rather than in the intestinal lumen (Greenberger & Toskes, 2005). Depending on the degree and extent of pancreatic inflammatory involvement or necrosis, the intensity of disease ranges from mild to severe. Two types of acute pancreatitis can be distinguished morphologically: edematous, or interstitial pancreatitis, and necrotizing pancreatitis (Friedman, 2005; Greenberger & Toskes, 2005).

Edematous or interstitial acute pancreatitis is characterized by interstitial edema, engorgement of capillaries, and dilation of lymphatic vessels. Necrotizing pancreatitis is characterized by pancreatic cell death and may initiate an inflammatory response that extends beyond the pancreas. Surrounding blood vessels may rupture, or the exudate of peritoneal fluid may sequester and become infected, leading to tissue necrosis, peritonitis, shock, and death. Distinction between the two morphologic types is essential for predicting the severity of the course of disease, as well as the outcome. Factors responsible for the transformation of edematous pancreatitis to the necrotizing form are largely unknown (Friedman, 2005; Greenberger & Toskes, 2005).

The pathophysiology of severe pancreatitis can be traced to the extravasation of pancreatic enzymes. These toxic proteolytic enzymes cause widespread chemical inflammation of tissue. As a result, considerable loss and sequestration of protein-rich fluid from the vascular space occurs, leading to hypovolemia, hypotension, and systemic hypoperfusion. Systemic inflammatory response syndrome (SIRS) can occur with the release of systemic inflammatory mediators as a result of pancreatic injury (Greenberger & Toskes, 2005).

Multisystem complications of acute pancreatitis involve almost every organ system and significantly affect the morbidity and mortality associated with this disease. These complications can occur early in the course of the disease or as late as 2 weeks after resolution of the acute phase. The causes of these complications range from enzyme impairment of pancreatic function to pancreatic tissue necrosis (Table 1-1).

Differential diagnosis can be difficult, so it is necessary for the clinician to look at the total picture of physical symptoms, laboratory data, and radiologic tests. The goals of treatment are to rest the pancreas, relieve pain, and maintain intravascular fluid volume. Management of secondary complications varies according to the organ system involved. The nurse’s role is to provide supportive care and to assess for signs and symptoms of complications (see Table 1-1).

The annual incidence of acute pancreatitis in the general population is 5 to 10 people per 100,000; thus, the disorder is relatively common (Turner, 2003) and its occurrence has been increasing. Between 1960 and 1980, the incidence of acute pancreatitis has increased 10-fold (Munoz & Katerndahl, 2006). Up to 25% of patients who develop acute pancreatitis have severe or life-threatening complications (Hale, Moseley, & Warner, 2000); within this percentage, between 2% and 10% of events can be fatal (Munoz & Katerndahl, 2006; Despins, 2005). Necrotizing pancreatitis contributes to the occurrence of acute pancreatitis in 3% to 5% of all patients in whom the condition has been diagnosed; a mortality rate of 50% has been reported (Greenberger & Toskes, 2005). The two major causative factors known to be responsible for acute pancreatitis are intake of alcohol and cholelithiasis. Pancreatitis in the oncology patient is likely to be caused by these same factors, but it also can result from direct tumor infiltration into the gland, metastasis to regional lymph nodes producing ductal obstruction, the complication of tumor lysis syndrome, a presenting manifestation of immunoblastic lymphoma, or complications resulting from medical or surgical therapy (Greenberger & Toskes, 2005; Yahanda & Chang, 2005; Yeo et al., 2005; Sinicrope & Levin, 2000). Other causes of pancreatitis include toxins, biliary obstruction, drugs (Box 1-1), hyperparathyroidism, hyperlipidemia, infection, trauma, ischemia, transplant, vasculitis, and autoimmune disorders (Friedman, 2005; Greenberger & Toskes, 2005).

Obstruction of the pancreatic ducts: Cholelithiasis caused by gallstones is the most common cause. Other causes of pancreatic duct obstruction include sphincter of Oddi stenosis, impaction of a stone at the ampulla, and occasionally microlithiasis or biliary sludge. In the oncology patient, primary adenocarcinoma of the pancreas is seldom a cause; however, metastases may cause obstruction, and this event is seen in cases of renal cell carcinoma, melanoma, and cancer of the prostate, breast, and lung (Yahanda & Chang, 2005; Yeo et al., 2005).

Alcohol consumption and abuse: The amount of daily consumed alcohol that is estimated to cause pancreatitis is 50 to 150 g (50 g is equivalent to four 12-oz servings of beer with 3% to 5% alcohol content). The average onset of alcohol-related pancreatitis occurs after 4 to 7 years of drinking (Munoz & Katerndahl, 2000).

Chemotherapy and biotherapy: L-asparaginase produces the highest incidence, reportedly with rates as high as 16% (Yahando & Chang, 2005), but numerous chemotherapy and biotherapy agents may be causative (Box 1-2).

Medications: See Box 1-1.

Manipulation of ampulla of Vater/pancreas: Endoscopic retrograde cholangiopancreatography (ERCP), pancreatectomy, splenectomy, trauma, and placement of intrahepatic catheter (Friedman, 2005; Greenberger & Toskes, 2005).

Metabolic abnormalities: Tumor lysis syndrome (TLS), hyperlipidemia, hyperparathyroidism, hypercalcemia, and end-stage renal disease (Friedman, 2005; Yeo et al., 2005; Sinicrope & Levin, 2000).

Infection: Parasitic infection, adenoviruses, mumps, coxsackieviruses, Staphylococcus, scarlet fever, hepatitis B, Campylobacter, Mycoplasma, rubella, Epstein-Barr virus, cytomegalovirus, and human immunodeficiency virus (HIV) (Sekimoto et al., 2006; Friedman, 2005; Greenberger & Toskes, 2005).

Dietary: High-fat diet (leading to cholelithiasis) and long-term hyperalimentation (biliary sludge) (Sekimoto et al., 2006; Greenberger & Toskes, 2005; Turner, 2003).

Vascular problems: Ischemia, systemic lupus erythematosus and shock states (Friedman, 2005).

Miscellaneous: Post bone marrow transplant, graft-versus-host disease, ectopic pregnancy, pregnancy, ovarian cyst, hypothermia, hereditary pancreatitis, scorpion venom, perforated peptic ulcer, Crohn’s disease, and Reye’s syndrome (Sekimoto et al., 2006; Friedman, 2005; Greenberger & Toskes, 2005; Yahanda & Chang, 2005; Yeo et al., 2005).

The prognosis is determined through assessment of morphologic involvement, which may be seen as edematous interstitial pancreatitis or necrotizing fulminant pancreatitis. The mechanism of action that determines which form will predominate remains unclear. The edematous interstitial form is usually a mild case that is self-limiting. In 5% to 15% of all cases, the disease takes the fulminant course (Munoz & Katerndahl, 2006; Despins, 2005). Prognosis can be predicted by the morphologic type and the presence of the following systemic complications: