include acute respiratory distress syndrome (ARDS), multiple organ dysfunction syndrome, disseminated intravascular coagulation (DIC), hypocalcemia (from fat saponification), hyperglycemia and insulin dependent diabetes mellitus (from pancreatic insulin-producing beta cell damage), malabsorption due to exocrine failure Metabolic Hypocalcemia, hyperglycemia, hypertriglyceridemia Respiratory Hypoxemia, atelectasis, effusion, pneumonitis, acute respiratory distress syndrome Renal Renal artery or vein thrombosis Kidney failure Circulatory Arrhythmias Hypovolemia and shock Myocardial infarction Pericardial effusion Vascular thrombosis Gastrointestinal Gastrointestinal hemorrhage from stress ulceration Gastric varices (secondary to splenic vein thrombosis) Gastrointestinal obstruction Hepatobiliary Jaundice Portal vein thrombosis Neurologic Psychosis or encephalopathy (confusion, delusion and coma) Cerebral Embolism Blindness (angiopathic retinopathy with hemorrhage) Hematologic Anemia Disseminated intravascular coagulation Leucocytosis Dermatologic Painful subcutaneous fat necrosis Miscellaneous Subcutaneous fat necrosis Arthalgia Causes Most common Biliary pancreatitis due to gallstones or constriction of ampulla of Vater in 40% of cases Alcohol in 30% of cases Idiopathic in 15-25% of cases Metabolic disorders: hereditary pancreatitis, hypercalcemia, elevated triglycerides, malnutrition Post-endoscopic retrograde cholangiopancreatography Abdominal trauma Penetrating ulcers Carcinoma of the head of pancreas, and other cancer Drugs: diuretics (e.g., thiazides, furosemide), gliptins (e.g., vildagliptin, sitagliptin, saxagliptin, linagliptin), tetracycline, sulfonamides, estrogens, azathioprine and mercaptopurine, pentamidine, salicylates, steroids, Depakote Infections: mumps, viral hepatitis, coxsackie B virus, cytomegalovirus, Mycoplasma pneumoniae, Ascaris Structural abnormalities: choledochocele, pancreas divisum Radiotherapy Autoimmune pancreatitis Severe hypertriglyceridemia Less common Scorpion venom Chinese liver fluke Ischemia from bypass surgery Heart valve surgery Fat necrosis Pregnancy Infections other than mumps, including varicella zoster Hyperparathyroidism Valproic acid Cystic fibrosis Anorexia or bulimia Codeine phosphate reaction Pathology Pathogenesis Acute pancreatitis occurs when there is abnormal activation of digestive enzymes within the pancreas. This occurs through inappropriate activation of inactive enzyme precursors called zymogens (or proenzymes) inside the pancreas, most notably trypsinogen. Normally, trypsinogen is converted to its active form (trypsin) in the first part of the small intestine (duodenum), where the enzyme assists in the digestion of proteins. During an episode of acute pancreatitis, trypsinogen comes into contact with lysosomal enzymes (specifically cathepsin), which activate trypsinogen to trypsin. The active form trypsin then leads to further activation of other molecules of trypsinogen. The activation of these digestive enzymes lead to inflammation, edema, vascular injury, and even cellular death. The death of pancreatic cells occurs via two main mechanisms: necrosis, which is less organized and more damaging, or apoptosis, which is more controlled. The balance between these two mechanisms of cellular death is mediated by caspases which regulate apoptosis and