Pancreatitis急性胰腺炎ppt课件.ppt

In the early stages of pancreatic injury and inflammation, proinflammatory cytokines, such as interleukin (IL)-1, IL-6, IL-8, and tumor necrosis factor (TNF)-A, appear to be released from tissue macrophages within the pancreas. Neutrophil activation likely results from release of IL-8 from macrophages and endothelial cells and release of platelet-activating factor (PAF) from endothelial cells. Later in the process, release of cytokines from T-helper lymphocytes (eg, IL-2, interferon- C) may also participate in the inflammatory response [3] Resent data has curbed some of the excitement re: use of APACHE in early pancreatitis. In short, prediction of severity is sub optimal at the present time. So, even if we can’t identify severe cases sooner, the CT index appears to be the best way to judge severity. intestinal decontamination study – no improvement CT Severity Index appearance normal enlarged inflamed 1 fluid collection 2 or more collections grade A B C D E score 0 1 2 3 4 necrosis none 33% 33-50% 50% score 0 2 4 6 score morbidity mortality 1-2 4% 0% 7-10 92% 17% Balthazar et al. Radiology 1990. Severe Acute Pancreatitis Scoring systems ? 3 Ranson criteria ? 8 APACHE II points ? 5 CT points Organ failure shock (SBP 90 mmHg) pulmonary edema / ARDS (PaO2 60 mmHg) renal failure (Cr 2.0 mg/dl) Local complications fluid collections ? pseudocysts necrosis (mortality 15% if sterile, 30-35% if infected) abscess Goals of Treatment Limit systemic injury support and resuscitation – effective decrease pancreatic secretion – ineffective / harmful? inhibit inflammatory mediators – ineffective inhibit circulating trypsin – ineffective (too late) removing gallstones – mostly ineffective Prevent necrosis – how? Prevent infection antibiotics (imipenem and ciprofloxacin) – probably effective in necrotic pancreatitis prevent colonic bacterial translocation removing gallstones – variably effective Treatment of Mild Pancreatitis Pancreatic rest Supportive care fluid resuscit