Serum amylase. Even though there is no definite correlation between the severity of pancreatitis and the degree of serum amylase elevation, serum amylase elevation is commonly equated to the presence of pancreatitis. However, hyperamylasemia may be present in many other conditions. Amylase is found in many organs, including salivary glands, liver, small intestine, kidney, and fallopian tubes, and in various tumors such as carcinoma of the esophagus, lung, and ovary.
In 75% of the patients with acute pancreatitis, the serum amylase is elevated. Hyperamylasemia is noted within the first 24 hours and persists for 3 to 5 days. Amylase levels normalize unless there is extensive pancreatic necrosis, ductal obstruction, or pseudocyst formation. Serum amylase levels may be spuriously normal in patients with hypertriglyceridemia and in patients with recurrent alcoholic pancreatitis.
Serum lipase levels are elevated in approximately 70% of patients. When both serum amylase and serum lipase are determined, one enzyme is elevated in 80% to 85% of the patients with acute pancreatitis, thus increasing the diagnostic yield.
Urine amylase is increased in acute pancreatitis and may remain elevated for 7 to 10 days after serum levels have returned to normal.
|TABLE. CAUSES OF HYPERAMYLASEMIA|
Leukocytosis (10,000-20,0000/ВµL) is frequent.
Hemoconcentration due to third-space fluid sequestration may lead to hematocrit elevation to greater than 50%.
Hyperglycemia is not uncommon and may result from decreased insulin and increased glucagon, catecholamine, and glucocorticoid release.
Hypocalcemia occurs in about 25% of patients. its pathogenesis is multifactorial and most likely results from sequestration of calcium in saponified fats as well as the presence of elevated levels of glucagon and calcitonin.
Serum bilirubin, alkaline phosphatase, and aminotransferase (alanine [alanine aminotransferase], aspartate [aspartate aminotransferase]) levels may be transiently elevated and return to normal in 4 to 7 days unless there is persistent biliary obstruction from gallstones or other causes.
Arterial hypoxemia may be present in 25% of patients. In some patients, adult respiratory distress syndrome may develop. Cardiovascular and electrocardiographic abnormalities may also occur, especially in severely ill patients.
Radiologic studies. Several radiologic studies are useful in the diagnosis and management of acute pancreatitis. These include flat film (kidneys, ureters, and bladder [KUB]) of the abdomen, chest x-rays, ultrasonography, computed tomography (computed tomography), and endoscopic retrograde cholangiopancreatography.
The plain films are useful in excluding other diagnoses, such as perforated viscus, mesenteric ischemia, or infarction. Findings suggestive of diffuse or localized ileus and presence of ascites are nonspecific.
Ultrasound and computed tomography scans are helpful in determining the size and appearance of the pancreas, the peripancreatic spread of the inflammation and phlegmon, and the condition of the biliary tract. These noninvasive techniques should be used to confirm clinically suspected disease and its complications such as cholecystitis, choledocholithiasis, tumor, pseudocyst, and ascites.
When ileus is present, the Ultrasound waves are scattered by the air in the intestinal lumen, and a clear picture of the pancreas cannot be obtained. However, Ultrasound is the test of choice for documenting cholelithiasis and biliary ductal dilatation. Computed tomography scan of the abdomen gives a clearer picture of the pancreas and the surrounding areas than Ultrasound does and should be obtained when there is a likelihood of severe pancreatitis (e.g., multiple positive Ranson’s signs during the first 48 hours). If the computed tomography scan is normal or shows mild pancreatic edema, the likelihood of a severe complication is remote even if many of Ranson’s signs are positive.
When a markedly swollen pancreas is seen with or without fluid collections, the presence of extensive necrotic areas within the pancreas (necrotizing pancreatitis) predisposes the patient to secondary infection and higher risk of mortality. The distinction between acute interstitial and necrotizing pancreatitis can be made if a computed tomography scan is obtained following the administration of intravenous contrast medium (dynamic computed tomography scan). In acute interstitial pancreatitis, the pancreas is well perfused and uniformly enhanced by the intravascular contrast agent. If necrosis is present, the areas of devitalized tissue are not perfused and are not enhanced.
The presence of air bubbles in the pancreatic and peripancreatic region is strong evidence of pancreatic infection. When fever, elevated white blood count, and clinical toxicity are associated with computed tomography scan evidence of either fluid collections or necrotizing pancreatitis, computed tomography-guided percutaneous aspiration, staining, and culture of the obtained fluid may help to distinguish sterile pancreatitis from pancreatic infection. When infection is suspected or proved, surgical debridement may be lifesaving.
Endoscopic retrograde cholangiopancreatography is generally contraindicated in patients with acute pancreatitis except when an impacted common bile duct stone may be the cause of the pancreatitis. Endoscopic sphincterotomy in these very ill patients may be immediately therapeutic. Endoscopic retrograde cholangiopancreatography is also useful in establishing the diagnosis of pancreas divisum; annular pancreas; pancreatic cancer; periampullary, ampullary, and pancreatic ductal abnormalities; and the possible communication of the pancreatic duct with pseudocysts. These studies are usually performed after the patient has been clinically stabilized.