[Systemic inflammatory response syndrome in pancreatic necrosis: triggers and organ damage]

To determine the main trigger mechanisms of multiple organ failure in acute severe pancreatitis.

An experimental study included 26 dogs with pancreatic necrosis. We assessed homeostasis disorders and functional changes in the pancreas, bowel, liver, kidneys, lungs and heart. Forty-six patients with severe acute pancreatitis were examined. We studied homeostasis disorders and functional state of the organs, endotoxemia, lipid peroxidation, phospholipase activity, coagulation system and hypoxia.

Injury of various organs and systems due to systemic inflammatory response at the early stage of disease is an important aspect in progression of acute pancreatitis. Membrane destabilizing phenomena and disturbances in tissue component of coagulation system are the most significant factors. Patients with severe acute pancreatitis had significant changes in homeostasis. We distinguished two subgroups of patients. The course of disease was different. In the first subgroup, changes in homeostatic parameters were 15.4-24.2% less than in the second subgroup. This largely determined treatment outcomes as a whole. In the first subgroup, therapy was effective in most cases, in the second one - less effective that required surgical interventions. In the first subgroup, mortality and hospital-stay were less compared to the second subgroup.

Oxidative stress, hypoxia, activation of phospholipases, and coagulation abnormalities are important in the development of systemic inflammatory response syndrome following acute pancreatitis. These factors are triggers for a cascade of the same kind of pathophysiological phenomena contributing to multiple organ failure and pancreatitis. In the tissues of various organs, proportional growth of these markers is observed until the 6^th day, while in the blood - until the 4^th day.