Rush B F, Sori A J, Murphy T F, Smith S, Flanagan J J, Machiedo G W
Department of Surgery, UMD-New Jersey Medical School, East Orange.
Ann Surg. 1988 May;207(5):549-54. doi: 10.1097/00000658-198805000-00009.
Previous investigations of a treated model of hemorrhagic shock in the rat indicated the frequent occurrence of bacteremia that appeared to derive from the gut. This paper determines the incidence of bacteremia and endotoxemia during the acute shock period and compares this with similar observations in humans in varying degrees of shock. Studies in 26 rats indicated that bacteremia and endotoxemia was present in 50% and 87%, respectively, by the end of 2 hours at a mean arterial pressure of 30 mmHg. Observations in 50 patients admitted to the trauma unit showed that positive bacterial blood cultures were present in 56% when the admission systolic blood pressure was 80 mmHg or less (p less than 0.01 compared with either of the other groups). Endotoxemia was noticed in two such patients. Direct access of bacteria and endotoxin to the blood stream may occur during hemorrhagic or traumatic shock and is the probable cause of subsequent sepsis in traumatized patients when no other source is apparent.
先前对大鼠失血性休克治疗模型的研究表明,经常发生似乎源自肠道的菌血症。本文确定了急性休克期菌血症和内毒素血症的发生率,并将其与不同程度休克的人类患者的类似观察结果进行比较。对26只大鼠的研究表明,在平均动脉压为30 mmHg的2小时末,菌血症和内毒素血症的发生率分别为50%和87%。对50名入住创伤科的患者的观察表明,入院时收缩压为80 mmHg或更低时,56%的患者血培养细菌呈阳性(与其他两组相比,p均小于0.01)。在两名此类患者中发现了内毒素血症。在出血性或创伤性休克期间,细菌和内毒素可能直接进入血流,这可能是创伤患者在无其他明显感染源时随后发生败血症的原因。