Akute Pankreatitis I: Einführung

Acute pancreatitis develops when digestive enzymes activate prematurely within the pancreas, causing autodigestion of pancreatic tissue. Common causes include gallstones obstructing the ampulla of Vater, chronic alcohol use damaging acinar cells, hypertriglyceridemia impairing microcirculation, abdominal trauma, viral infections like mumps, and certain medications such as azathioprine. ERCP procedures can also trigger inflammation through mechanical trauma or chemical irritation.

Gallstones obstruct the ampulla of Vater, the opening where pancreatic and bile ducts enter the small intestine. This obstruction causes a backup of bile and pancreatic enzymes into the pancreatic duct system. The accumulated enzymes activate prematurely within the gland, initiating inflammation and tissue damage characteristic of acute pancreatitis.

Acute pancreatitis typically presents with constant epigastric or upper abdominal pain that may radiate to the back and worsen after eating. Accompanying symptoms include nausea, vomiting, bloating, and fever. As inflammation progresses, patients may develop jaundice, hypotension, and tachycardia. In severe cases, systemic inflammatory response syndrome or multi-organ failure can occur, significantly increasing mortality risk.

Chronic alcohol use damages pancreatic acinar cells and disrupts the normal regulation of digestive enzymes. This cellular injury impairs the pancreas's ability to control enzyme activation, leading to premature enzyme activation within the gland. Alcohol-related pancreatitis often causes recurrent episodes and can progress to chronic inflammation if alcohol consumption continues.

Metabolic factors like hypertriglyceridemia and hypercalcemia contribute to acute pancreatitis through distinct mechanisms. Hypertriglyceridemia impairs pancreatic microcirculation and promotes premature enzyme activation. Hypercalcemia directly stimulates early activation of digestive enzymes within the pancreatic ducts. Both conditions disrupt normal pancreatic function and trigger inflammatory responses characteristic of acute pancreatitis.

Yes, certain medications can trigger acute pancreatitis through drug-induced mechanisms. Common culprits include azathioprine, thiazide diuretics, corticosteroids, and chemotherapeutic agents. These drugs can directly injure pancreatic tissue or disrupt enzyme regulation, leading to premature enzyme activation and inflammation. Drug-induced pancreatitis should be considered when evaluating patients with acute pancreatic inflammation.

Severe acute pancreatitis can progress to systemic inflammatory response syndrome and multi-organ failure, significantly increasing mortality risk. As pancreatic enzymes leak into surrounding tissues and the bloodstream, widespread inflammation develops. Complications include hypotension, tachycardia, jaundice from bile duct involvement, and dysfunction of vital organs. Early recognition of severe disease is critical for patient outcomes.