摘要
我们连续观察51例烧伤面积30%以上病人,17例并发 MOF,死亡12例(70.6%)。衰竭脏器越多,病死率越高。肺功能衰竭发病率最高,肾功能衰竭的病死率最高.休克与感染是其主要:发病因素。氧自由基介导的损害参与了烧伤后 MOF 的发生与发展。烧伤后抗氧化能力下降,氧自由基增多及脂质过氧化增强,其损害程度有功能衰竭者比无功能衰竭者重,死亡者比存活者重.烧伤后 HX-HO系统反应亢进,表明缺血组织是伤后氧自由基的重要来源。烧伤后血栓素与前列环素的变化,在 MOF发病中,也有重要作用,伤后 TXA_2-PGI_2均明显增高,但 TXA_2增高的幅度更大,因而 TXA_2/PGI_2比值睨显增高,MOF 病人高于无 MOF 者,且随病情恶化而增加,其机理主要在于促使形成微聚物和血栓,导致脏器损害.
31 burned patients with TBSA over 30% were studied prospectively.MOF developed in 17 of them.Postburn MOF occurred mainly in those with TBSA over 70%.Mortality of MOF was directly proportional to the number of organs involved.The incidence of pulmon- ary failure was the highest,and the highest mortality was attributed to renal failure.MOF occurring in the early stage was more related to burn shock,and those occurring in the late stage was predisposed mainly by infection.Oxygen free radicals play an important role in the genesis and development of postburn MOF.In this study,it was revealed that antipero- xidation ability declined,active oxygen was increased,and lipid peroxidation became excess- ive after the burn injury.It was also found that oxygen free radical-mediated effects pro- duced more serious damages in patients with MOF than those without,and also more in tho- se died than the survivors.The hypoxanthine-xanthine oxidase system was a significant sour- ce of oxygen radicals after the burn injury.There were also significant changes in plasma TXA_2 and PGI_2 levels postburn.The marked increase in TXA_2/PGI_2 ratio indicated imbalance between TXA_2 and PGI_2,which was correleted well with burn size and closely related to the development of postburn MOF.The excessive production of TXA_2 might trigger or accelerate the formation of microaggregates and thromboxin,subsequently leading to visceral damages and failure.
