As part of the initial injury there is an extensive inflammatory response due to pancreatic cells synthesizing and secreting inflammatory mediators: primarily TNF-alpha and IL-1. A hallmark of acute pancreatitis is a manifestation of the inflammatory response, namely the recruitment of neutrophils to the pancreas. The inflammatory response leads to the secondary manifestations of pancreatitis: hypovolemia from capillary permeability, acute respiratory distress syndrome, disseminated intravascular coagulations, renal failure, cardiovascular failure, and gastrointestinal hemorrhage. Histopathology
The acute pancreatitis (acute hemorrhagic pancreatic necrosis) is characterized by acute inflammation and necrosis of pancreas parenchyma, focal enzymic necrosis of pancreatic fat and vessel necrosis (hemorrhage). These are produced by intrapancreatic activation of pancreatic enzymes. Lipase activation produces the necrosis of fat tissue in pancreatic interstitium and peripancreatic spaces as well as vessel damage. Necrotic fat cells appear as shadows, contours of cells, lacking the nucleus, pink, finely granular cytoplasm. It is possible to find calcium precipitates (hematoxylinophilic). Digestion of vascular walls results in thrombosis and hemorrhage. Inflammatory infiltrate is rich in neutrophils. Due to the pancreas lacking a capsule, the inflammation and necrosis can extend to include fascial layers in the immediate vicinity of the pancreas. Diagnosis
Acute pancreatitis is diagnosed using clinical history and physical examination, based on the presence of at least 2 of 3 criteria: abdominal pain, elevated serum lipase or amylase, and abdominal imaging findings consistent with acute pancreatitis. Additional blood studies are used to identify organ failure, offer prognostic information, and determine if fluid resuscitation is adequate and whether ERCP is necessary.
Complications
Locoregional complications include pancreatic pseudocyst (most common, occurring in up to 25% of all cases, typically after 4–6 weeks) and phlegmon/abscess formation, splenic artery pseudoaneurysms, hemorrhage from erosions into splenic artery and vein, thrombosis of the splenic vein, superior mesenteric vein and portal veins (in descending order of frequency), duodenal obstruction, common bile duct obstruction, progression to chronic pancreatitis, pancreatic ascites, pleural effusion, sterile/infected pancreatic necrosis.Systemic complications include ARDS, multiple organ dysfunction syndrome, DIC, hypocalcemia (from fat saponification), hyperglycemia and insulin dependent diabetes mellitus (from pancreatic insulin-producing beta cell damage), malabsorption due to exocrine failure

MetabolicHypocalcemia, hyperglycemia, hypertriglyceridemiaRespiratoryHypoxemia, atelectasis, Effusion, pneumonitis, Acute respiratory distress syndrome (ARDS)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
DIC
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-ERCP
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.