Acute pancreatitis presents with relatively rapid onset of pain, usually in the epigastric region. The pain may radiate to the back and is nearly always aggravated by eating. The patient moves frequently to find a position of comfort. Nausea and vomiting occur in most cases. Pain is typically continuous and quite severe, usually requiring narcotics. Severe pancreatitis can lead to hemorrhage, visible as ecchymoses in the flanks (Grey Turner sign) or periumbilical region (Cullen sign). Rupture of a minor pancreatic duct can lead to development of a pancreatic pseudocyst, characterized by persistent severe pain and tenderness and a palpable mass. With necrosis and fluid collections, patients experiencing severe pancreatitis are prone to infectious complications, and the clinician must be alert for fever and signs of sepsis.
Acute pancreatitis can be difficult to diagnose. Elevations in total serum amylase or lipase support the diagnosis. These pancreatic enzymes are released into the blood during pancreatic injury. Nonspecific elevations of the enzymes are common, however. As acute pancreatitis progresses, the amylase level tends to decline faster than lipase, making the latter a
Cholelithiasis and biliary sludge Choledochal cyst Pancreas divisum Anomalous junction of biliary and pancreatic ducts Annular pancreas Ampullary obstruction (mass, inflammation from Crohn’s disease) Ascaris infection good choice for diagnostic testing late in the course of the disease.
Serial measurement of laboratory studies is importantto monitor for severe complications. At diagnosis, baseline complete blood count, C-reactive protein, electrolytes,blood urea nitrogen, creatinine, glucose, calcium, and phosphorus should be obtained. These should be measured atleast daily, along with amylase and lipase, until the patienthas recovered.
Because enzyme levels are not 100% sensitive or specific,imaging studies are important for the diagnosis of pancreatitis. In acute pancreatitis, edema is present in all but themildest cases. Ultrasound is capable of detecting this edemaand should be performed as part of the overall diagnosticapproach. If overlying bowel gas obscures the pancreas, acomputed tomography (CT) scan allows complete visualization of the gland. CT scans should be done with oral andintravenous (IV) contrast agents to facilitate interpretation.Ultrasound and CT also can be used to monitor for the development of pseudocysts and for evidence of ductal dilation secondary to obstruction. The other important reason toperform imaging studies early in the course of pancreatitis isto rule out gallstones; the liver, gallbladder, and common bileduct all should be visualized. Magnetic resonance cholangiopancreatography may be used to detect anatomic variantscausing pancreatitis.
There are no proven specific therapies for acute pancreatitis. If a predisposing etiology is found, such as a drug reaction or a gallstone obstructing the sphincter of Oddi, this should be specifically treated. Initially, oral intake is prohibited, an acid-blocking drug is prescribed, and (except in mild cases) nasogastric suction is begun. Fluid resuscitation is necessary because of vomiting and third space losses. Pain relief should be provided. Meperidine, fentanyl, and hydromorphone are most commonly used. Nutritional support should be provided early in the course if the patient will be nothing by mouth (NPO) for extended periods. Feedings can begin once pain subsides or can be administered downstream from the duodenum. If this is not possible, parenteral nutrition is an option. Fewer complications and more rapid recovery occur with jejunal feedings compared with parenteral nutrition. Antibiotics should be considered if the patient is febrile, has extensive pancreatic necrosis, or has laboratory evidence of infection. A broad-spectrum antibiotic, such as imipenem, is considered the best choice.