The most common predisposing factors are gallstones and alcohol abuse. Although the term pancreatitis suggests an infection, in most patients no infection is identified, although one may occur as a complication.
Besides producing insulin, glucagon, and somatostatin, the pancreas produces and releases the digestive enzymes lipase, trypsin, and amylase. Normally, these enzymes aren’t activated until they’re secreted into the small intestine during digestion.But in pancreatitis, some or all of these enzymes are activated before they leave the organ, and begin to destroy the pancreas. Called autodigestion, this process can lead to erosion through the pancreas and out into the abdominal cavity, producing profound inflammation, fluid shifts, hypovolemia, and hemorrhage. It also may cause abdominal compartment syndrome and affect the pancreas’ glucose-regulating ability, triggering hyperglycemia.
Nearly all patients with acute pancreatitis complain of severe abdominal or epigastric pain of sudden onset—perhaps as quickly as 60 minutes. The patient may describe it as a burning or boring pain that radiates to the back. Position changes don’t relieve it; consuming alcohol or high-fat foods may worsen it. Other common signs and symptoms are nausea and vomiting.On physical examination, expect to detect a firm, distended, diffusely tender abdomen and possibly rebound tenderness. Absent bowel sounds may indicate paralytic ileus. A patient with intra-abdominal bleeding may exhibit Cullen’s sign (bruising around the umbilical area from intraperitoneal bleeding) or Grey-Turner’s sign (flank bruising from retroperitoneal bleeding), along with a low hemoglobin and hematocrit.
Diagnosis of acute pancreatitis hinges on the patient’s history, blood test results, pancreatic ultrasonography to identify gallstones, and perhaps a computed tomography scan of the abdomen. Blood tests typically include a complete blood count, serum electrolytes, blood urea nitrogen, serum creatinine, liver enzymes, serum and urine amylase, serum lipase, triglycerides, total protein, serum albumin, bilirubin, coagulation panel, and arterial blood gases.
Rating severity of the condition
Clinicians use several methods to rate the severity of acute pancreatitis:
• Ranson’s criteria. On admission, these include age, white blood cell (WBC) count, and glucose, lactate dehydrogenase, and aspartate aminotransferase levels. At 48 hours, the criteria include hematocrit, blood urea nitrogen, calcium, partial pressure of arterial oxygen, base deficit, and estimated third-space fluid.
• APACHE II, a physiologic scoring system which consists of 16 criteria; it may be used daily
• modified Glasgow scale, assessed at 48 hours.
Treatment is supportive, aimed at relieving symptoms, returning the pancreas to normal function, and preventing complications. Reestablishing fluid balance is essential. A patient with significant hypovolemia may need to be admitted to the ICU for hemodynamic monitoring.Antibiotics aren’t recommended. Research shows that they don’t reduce morbidity or mortality when used in patients without a documented infection.
Many acute pancreatitis patients describe their pain level as 10 on a
1-to-10 scale, so pain management is crucial. Experts recommend I.V. analgesia (preferably patient-controlled). Historically, clinicians have avoided giving morphine because of the theoretical risk it could cause spasm of the sphincter of Oddi, leading in turn to additional pancreatic injury. However, most now prefer morphine over meperidine and other analgesics because it achieves greater pain control. Collaborate with the pain-management team to formulate interventions that maximize patient comfort.
Expect to withhold oral intake during the acute phase. As prescribed, administer antiemetics to relieve nausea and vomiting. The physician may order placement of a nasogastric tube to decompress the stomach.Although total parenteral nutrition (TPN) has traditionally been the preferred nutritional method for patients with acute pancreatitis, new research favors placement of an enteral feeding tube into the jejunum to avoid stimulating pancreatic enzyme release—even in patients without bowel sounds. Enteral feeding also is cheaper and causes fewer complications than TPN. However, severe ileus may necessitate TPN.
Acute pancreatitis may lead to such complications as pancreatic abscess or necrosis, organ failure, circulatory instability, and metabolic abnormalities. The most common complication is fluid collection within or around the pancreas. Such collections may be relatively benign, but drainage is needed if they become infected or grow large enough to compress surrounding tissue. Otherwise, sepsis, pancreatic pseudocysts, ascites, or pleural effusions may occur.Suspect pancreatic necrosis if the patient develops a fever not attributable to another cause, has an elevated WBC count, doesn’t improve, or deteriorates suddenly. Necrotic tissue stimulates additional inflammation, increases vascular permeability, and causes significant fluid shifts. Mortality for patients who develop pancreatic necrosis may be as high as 50%.
Complex but controllable
Acute pancreatitis is a complex condition whose management can be daunting. Supportive therapy usually controls mild forms. But for patients with a severe form, early recognition of deterioration and rapid transfer to the ICU are critical. To promote the best possible outcome, stay alert for signs of deterioration in your patient with acute pancreatitis. O
Amerine E. Get optimum outcomes for acute pancreatitis patients. Nurse Pract. 2007;32(6):44-48.Carroll J, Herrick B, Gipson T, Lee S. Acute pancreatitis: diagnosis, prognosis and treatment. Am Fam Physician. 2007;175(10):1513-1520.
535109. Accessed October 16, 2007.
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Deborah Pool is a residential faculty member at Glendale Community College in Glendale, Ariz.