Prevailing over acute pancreatitis

An inflammatory condition, acute pancreatitis runs the gamut from mild to severe. In the United States, it accounts for about 150,000 to 225,000 hospital admissions each year, at an estimated cost of $3 to $6 billion. Diagnosing and managing this complex condition can be challenging.
In about 80% of cases, acute pancreatitis is mild, marked by inflammation and edema of the pancreas and biliary system. Usually, this mild form is self-limiting, resolving within 5 to 7 days without complications.But roughly 15% to 20% of patients develop severe acute pancreatitis, experiencing life-threatening hypotension from third-space fluid losses and hemorrhage. Vulnerable to such complications as pancreatic abscess or necrosis, pseudocysts, sepsis, and multiple organ dysfunction syndrome, they must be treated in an intensive care unit (ICU).
The risk of death from acute pancreatitis depends on the patient’s condition before onset, as well as severity of inflammation and development of complications. In severe acute pancreatitis, mortality can reach 30%.

Predisposing factors
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.

How pancreatitis arises
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.
With severe inflammation, so much fluid may be displaced into the abdominal cavity that intravascular fluid deficits and even hypo­-volemic shock occur. In some patients, coagulation is altered, increasing the bleeding risk.
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.
Serum amylase of three times the normal level is diagnostic. How-­ever, if the patient waits 2 to 3 days before seeking medical care, the level may have returned to near normal by the time of diagnosis. Serum lipase is a more sensitive test of pancreatic function; levels rise in 3 to 4 hours, peak in 24 hours, and stay high for up to 2 weeks.
Some facilities measure C-reactive protein. An increased level indicates inflammation; a level above 150 mg/L 48 hours after symptom onset reflects severe acute pancreatitis.

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.
Fluid replacement consists mainly of crystalloids (such as normal saline solution, lactated Ringer’s solution, or both) and is guided by the patient’s clinical condition. In hemorrhagic pancreatitis, blood transfusions may be warranted. A significantly decreased albumin level may indicate the need for albumin replacement. To monitor the patient’s fluid status, measure fluid intake and output carefully and obtain daily weights.
Hyperglycemia (from diminished or absent insulin secretion) can cause additional fluid loss and increase serum osmolality. The patient may need a continuous insulin infusion, or may be managed by a sliding scale, in which the insulin dosage is titrated to the patient’s blood glucose level. Be sure to monitor serum glucose levels carefully to prevent accidental hypoglycemia.

Controlling pain
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.

Other nursing interventions
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.
Additional interventions may include administering oxygen to correct hypoxia stemming from pain or pulmonary complications, and giving histamine2 blockers to minimize the risk of stress ulcers.
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

Selected references
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.
Draganov P, Forsmark C. Diseases of the pancreas: Acute and chronic pancreatitis. In Dale D, Federman D, eds. ACP Medicine Online.
535109. Accessed October 16, 2007.
Sargent S. Pathophysiology, diagnosis and management of acute pancreatitis. Br J Nurs. 2006;15(18):999-1005.
Whitcomb D. Acute pancreatitis. N Engl J Med. 2006;354:2142-2150.
For a complete list of selected references, visit

Deborah Pool is a residential faculty member at Glendale Community College in Glendale, Ariz.

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