Acute pancreatitis

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Acute Pancreatitis is a nonbacterial inflammation of the pancreas caused by the activation, interstitial liberation and digestion of the gland by its own enzymes. It usually has a benign, self-limiting course, though overall mortality is approximately 10%, mostly due to complications. The mechanisms for tissue damage in acute pancreatitis are proteolysis (via trypsin and chymotrypsin), fat necrosis (via lipase and phospholipase), and blood vessel damage and hemmorhage (via elastase).

Biliary tract disease (gallstones; 45%) and alcoholism (35%) account for ≥ 80% of hospital admissions for acute pancreatitis. The remaining 20% are attributed to drugs (e.g., azathioprine, sulfasalazine, furosemide, valproic acid), estrogen use associated with hyperlipidemia, infection (e.g., mumps), hypertriglyceridemia, endoscopic retrograde pancreatography, structural abnormalities of the pancreatic duct, structural abnormalities of the common bile duct and ampullary region, surgery, vascular disease (especially severe hypotension), blunt and penetrating trauma, hyperparathyroidism and hypercalcemia, renal transplantation, hereditary pancreatitis, or are idiopathic, though 80% of idiopathic acute pancreatitis demonstrates microlithiasis (sludge and crystals).

Pathological findings in mild pancreatitis include peripancreatic fat necrosis and interstitial edema. In severe pancreatitis, there is extensive peripancreatic and intrapancreatic fat necrosis accompanied by parenchymal necrosis and hemorrhage, which leads to infection in 60% of cases. There is also a release of toxic factors into systemic circulation and peritoneal space. However, the severity of clinical features may not always correlate with the observed pathology.


Clinically, the patient may look well or premorbid. Patients may present with pain which may be epigastric, non-colicky, and constant, with radiation to the back that may improve when leaning forward. Patients may also have a tender rigid abdomen with guarding, nausea and vomiting accompanied with abdominal distension from paralytic ileus. Patients may also present with a chemical fever (i.e., not due to infection), jaundice due to a compression or obstruction of the bile duct and some other stuff.

The differential diagnosis would include:


Complications of acute pancreatitis include pancreatic abscess, pancreatic pseudocyst, and duodenal obstruction. Severe acute pancreatitis may lead to multiorgan failure. Hypocalcemia also occurs due to precipitation of calcium in areas of fat necrosis.