gastrointestinal disorders
Acute Pancreatitis
Diagnosis of Acute Pancreatitis
Serum markers (amylase, lipase) Imaging studies Pancreatitis is suspected whenever severe unexplained abdominal pain occurs, especially in a patient with significant alcohol use or known gallstones. The diagnosis of acute pancreatitis is established by the presence of at least 2 of the following: Abdominal pain consistent with the disease Serum amylase and/or lipase > 3 times the upper limit of normal (normal range of amylase and lipase levels can differ depending on the assay used) Characteristic findings on contrast-enhanced cross-sectional imaging studies Thedifferential diagnosisof the symptoms of acute pancreatitis includes Perforated gastric or duodenal Diagnosis None Mesenteric infarction Intestinal Obstruction None Overview of Aortic Aneurysms None Biliary colic Appendicitis None Colonic Diverticulitis None Inferior wall Acute Myocardial Infarction (MI) None Hematoma of the abdominal muscles or spleen To exclude other causes of abdominal pain and to diagnose metabolic complications of acute pancreatitis, a broad range of tests is usually done at initial evaluation. These include laboratory and imaging tests. Serum amylase and lipase concentrations increase on the first day of acute pancreatitis and return to normal in 3 to 7 days. Lipase is more specific for pancreatitis, but both enzymes may be increased in renal failure and various abdominal conditions (eg, perforated ulcer, mesenteric vascular occlusion, intestinal obstruction). Other causes of increased serum amylase include salivary gland dysfunction, macroamylasemia, and tumors that secrete amylase. Fractionation of total serum amylase into pancreatic type (p-type) isoamylase and salivary-type (s-type) isoamylase increases the accuracy of serum amylase. Both amylase and lipase levels may remain normal if destruction of acinar tissue during previous episodes precludes release of sufficient amounts of enzymes. The normal range of amylase and lipase levels can differ depending on the assay used. The serum of patients with hypertriglyceridemia may contain a circulating inhibitor that must be diluted before an elevation in serum amylase can be detected. Serum amylase levels may be chronically elevated in macroamylasemia where amylase is bound to a serum immunoglobulin to form a complex that is filtered slowly from the blood by the kidneys. Amylase:creatinine clearance ratio does not have sufficient sensitivity or specificity to diagnose pancreatitis. It is generally used to diagnose macroamylasemia when no pancreatitis exists. A urine dipstick test for trypsinogen-2 has sensitivity and specificity of>90% for acute pancreatitis. The white blood cell count usually increases to 12,000 to 20,000/mcL (12 to 20 × 109/L). Third-space fluid losses may increase the hematocrit to as high as 50 to 55% and elevate the bloodureanitrogen (BUN), indicating severe inflammation. Persistent elevation in BUN despite resuscitation is an indicator of increased morbidity and mortality. Hyperglycemia and hypocalcemia may occur. Patients may have abnormal liver function test results, including elevated serum bilirubin, due to a retained stone in the bile duct or compression of the bile duct by pancreatic edema. Patients with shock may have an elevated anion gap metabolic acidosis or other electrolyte abnormalities. Hypomagnesemia needs to be excluded in patients with hypocalcemia. CT with IV contrastis the imaging study of choice to establish the diagnosis of acute pancreatitis and to assess for local complications. It is done early in the disease course if the diagnosis of acute pancreatitis is uncertain or to exclude other causes for the patient's symptoms. Also, once pancreatitis has been diagnosed, CT is done later in the disease course to identify the complications of acute pancreatitis such as necrosis, fluid collection, or pseudocysts, particularly if abdominal symptoms persist. Necrotic pancreatic tissue does not enhance after IV contrast is given. Generally, MRI outperforms CT for detecting choledocholithiasis and pancreatic necrosis and should be done in patients in whom other tests for choledocholithiasis were indeterminate and in patients who are considered likely to need a pancreatic drainage procedure. Abdominal ultrasonographyshould be done if gallstone pancreatitis is suspected (and another cause is not obvious) to detect gallstones or dilation of the common bile duct, which indicates biliary tract obstruction. Edema of the pancreas may be visible, but overlying gas frequently obscures the pancreas. If done,plain x-rays of the abdomenmay disclose calcifications within pancreatic ducts (evidence of prior inflammation and hence chronic pancreatitis), calcified gallstones, localized ileus of a segment of small intestine in the left upper quadrant or the center of the abdomen (a “sentinel loop”), or the colon cutoff sign (absence of air in left colonic flexure or descending colon) in more severe disease. However, the value of routine abdominal x-rays is controversial. Chest x-rayshould be done and may reveal atelectasis or a pleural effusion (usually left-sided or bilateral but rarely confined to the right pleural space), which are signs of severe disease. The role ofendoscopic ultrasonographyis limited in acute pancreatitis. Endoscopic ultrasonography has a comparable sensitivity to magnetic resonance cholangiopancreatography (MRCP) for detecting common bile duct stones, but MRCP has the advantage of being noninvasive. MRCP is done if liver tests, particularly direct bilirubin and alanine aminotransferase (ALT), are elevated from their baseline and abdominal ultrasonography does not exclude gallstones in the common bile duct as the etiology for gallstone acute pancreatitis. Endoscopic retrograde cholangiopancreatography(ERCP) to relieve bile duct obstruction should be done expeditiously in patients with gallstone pancreatitis who have increasing serum bilirubin and signs of cholangitis. 