Short- and long-term survival after severe acute pancreatitis: A retrospective 17 years' cohort study from a single center.

PURPOSE: To study mortality in severe acute pancreatitis (SAP) and to identify risk factors for mortality. MATERIALS AND METHODS: A retrospective 17-years' cohort study of 435 consecutive adult patients with SAP treated at intensive care unit of a university hospital. RESULTS: Overall, 357 (82.1%) patients survived at 90 days follow-up. Three-hundred six (89.5%) patients under 60 years, 38 (60.3%) patients between 60 and 69 years, and 13 (43.3%) patients over 69 years of age survived at 90 days follow-up. Independent risk factors for death within 90-days were: 60 to 69 years of age (odds ratio [OR] 5.1), >69 years of age (OR 10.4), female sex (OR 2.0), heart disease (OR 2.9), chronic liver failure (OR 12.3), open abdomen treatment (OR 4.4) and sterile necrosectomy within 4 weeks (OR 14.7). The 10-year survival estimate was <70% in patients under 60 years and <30% in patients over 60 years. Underlying cause of death after the initial 90-day follow-up period was alcohol-related in 48 (57.1%) patients, and all of them had suffered from alcoholic SAP. CONCLUSIONS: Although younger patients have excellent short-term survival after SAP, the long-term survival estimate is disappointing mostly due to alcohol abuse.

Inflammation and immunosuppression in severe acute pancreatitis.

Acute pancreatitis (AP) is a common disease, which usually exists in its mild form. However, in a fifth of cases, the disease is severe, with local pancreatic complications or systemic organ dysfunction or both. Because the development of organ failure is the major cause of death in AP, early identification of patients likely to develop organ failure is important. AP is initiated by intracellular activation of pancreatic proenzymes and autodigestion of the pancreas. Destruction of the pancreatic parenchyma first induces an inflammatory reaction locally, but may lead to overwhelming systemic production of inflammatory mediators and early organ failure. Concomitantly, anti-inflammatory cytokines and specific cytokine inhibitors are produced. This anti-inflammatory reaction may overcompensate and inhibit the immune response, rendering the host at risk of systemic infection. At present, there is no specific treatment for AP. Increased understanding of the pathogenesis of systemic inflammation and development of organ dysfunction may provide us with drugs to ameliorate physiological disturbances.