Serial experimental and clinical studies on the pathogenesis of multiple organ dysfunction syndrome (MODS) in severe burns

These serial clinical and experimental studies were designed to clarify the pathogenesis of postburn MODS. Both animal and clinical studies were perfo rmed. In animal experiments, 46 male cross-bred dogs were cannulated with S wan-Ganz catheters and 39 of them were inflicted with 50% TBSA third degree burns (7 were used as controls). The burned dogs were randomly divided int o 4 groups: immediate infusion, delayed infusion, delayed fast infusion and delayed fast infusion combined with ginsenosides. All dogs were kept under constant barbiturate sedation during the whole study period. Hemodynamics, visceral MDA, mitochondrial respiratory control rate (RCR) and ADP/O ratio , ATP, succinic dehydrogenase (SDH), organ water content as well as light a nd electron microscopy of visceral tissues were determined. In the clinical study, 61 patients with extensive deep burns were chosen, of which 16 sust ained MODS. Plasma TXB2/6-keto-PGF1 alpha ratio, TNF, SOD, MDA, circulatory platelet aggregate ratio (CPAR), PGE(2), interleukin-l, total organ water content and pathological observations of visceral tissues from patients who died of MODS were carried out. Results demonstrated that ischemic-reperfus ion damage due to severe shock, sepsis and inhalation injury are three main causes of postburn death. All inflammatory mediators increased markedly in both animals and patients who sustained organ damage or MODS. SDH, RCR, AD P/O and ATP decreased significantly. These findings suggested that ischemic damage and systemic inflammatory response syndrome (SIRS) initiated by med iators or cytokines might be important in the pathogenesis of postburn MODS . (C) 1998 Elsevier Science Ltd for ISBI. All rights reserved.