ACUTE-PANCREATITIS AS A MODEL OF SEPSIS

Severe acute pancreatitis has many similarities to sepsis syndrome and septic shock. The haemodynamic features of cardiovascular instability , reduced ejection fraction and decreased systemic vascular resistance are indistinguishable in each of these conditions. In addition there are many striking similarities in the cytokine and inflammatory mediat or profiles, suggesting that the haemodynamic abnormalities may result from the same pathogenic mechanisms, albeit as a result of different inflammatory stimuli. Although septic complications of severe acute pa ncreatitis do arise these are usually late features and in the early p hase of a severe attack there is sterile pancreatic necrosis. Evidence suggests that the important cytokines in the development of complicat ions and multiple organ failure in severe acute pancreatitis are tumou r necrosis factor-alpha, interleukin-1, interleukin-6 and interleukin- 8. In addition, endotoxin and other important inflammatory mediators i ncluding platelet activating factor and phospholipase A(2) are implica ted in the development of complications in both severe acute pancreati tis and sepsis. Patients with severe acute pancreatitis are not an ent irely homogeneous group but in terms of pathogenesis and complications of their disease they have much more in common with each other than t he patients who are collected under the unifying diagnosis of 'sepsis' . The similar clinical and biochemical features between severe acute p ancreatitis and sepsis make the former an excellent model for studying the pathogenesis of the sepsis syndrome.