Pathophysiology

The cause of pancreatitis is multifactorial. Common causes include alcohol abuse, direct or indirect trauma to the pancreas, ulcerative penetration from adjacent structures (e.g., the duodenum), infectious processes, biliary tract disease, metabolic disorders (e.g., hyperlipidemia and hypercalcemia), and certain drugs (e.g., corticosteroids, furosemide, estrogens, and thiazide diuretics). Patients who have undergone extensive surgery involving mobilization of the abdominal viscera are at risk for development of postoperative pancreatitis, as are patients who have undergone procedures involving cardiopulmonary bypass.

Clinical manifestations

Acute pancreatitis is characterized as a severe chemical burn of the peritoneal cavity. Enzymes implicated as major culprits in the syndrome of pancreatitis are those activated by trypsin, enterokinase, and bile acids. Cardiovascular complications of acute pancreatitis can lead to pericardial effusions, alterations in cardiac rhythmicity, and signs and symptoms mimicking acute myocardial infarction, thrombophlebitis, and cardiac depression. Acute pancreatitis also predisposes patients to the development of acute respiratory distress syndrome and disseminated intravascular coagulopathy.

Pain is the foremost symptom of acute pancreatitis and may be variable in quality (i.e., localized or radiating, dull and tolerable, or severe and unremitting). Pancreatic pain may radiate from the midepigastric to the periumbilical region and may be more intense when the patient is in the supine position.

Abdominal distention is often seen and is largely attributable to the accumulation of intraperitoneal fluid and paralytic ileus. Nausea and vomiting and fever are common symptoms. Hypotension is seen in 40% to 50% of patients and is attributable to hypovolemia secondary to the loss of plasma proteins into the retroperitoneal space. Acute renal failure secondary to dehydration and hypotension may occur.

Hypocalcemia frequently develops in patients with acute pancreatitis, and this condition obviates monitoring the ECG for cardiac rhythm disorders (e.g., lengthened QT interval with possible reentry dysrhythmias). The clinician must also be observant for signs of tetany. Clinical shock may develop that is largely secondary to the effects of vasoactive kinin peptides (e.g., bradykinin) released during the inflammatory process; these peptides enhance vasodilation, vascular permeability, and leukocyte migration.

Elevated serum amylase levels are often present but do not necessarily indicate primary pancreatic disease; other intraabdominal disease processes result in such elevations, including biliary tract disease, tubo-ovarian disease, peptic ulcer disease, and acute bowel disease, including obstruction, inflammation, and ischemia. Elevated serum lipase levels may also be observed. Compressive obstruction of the common bile duct by an edematous head of the pancreas contributes to elevations in serum bilirubin and alkaline phosphatase levels.

Radiographic and ultrasonographic findings aid in the differential diagnosis of pancreatic disease. Evidence of free intraperitoneal air by radiography suggests the presence of a perforated viscus. CT is highly effective in the diagnosis of an enlarged, edematous pancreatic head, which is typically seen in patients with pancreatitis.

Treatment

Supportive therapy is initially undertaken in acute pancreatitis. This regimen usually includes intensive care unit admission and may involve implementation of invasive monitoring, fluid and hemodynamic resuscitation, and interventions necessary for the preservation of perfusion and function of the abdominal viscera. Severely ill, malnourished patients are often given parenteral nutritional support.

If the cause of pancreatitis is obstructive biliary disease caused by the presence of a stone in the common bile duct or by inflammation of the gallbladder, cholecystectomy and possibly common bile duct exploration are indicated.