首页> 美国卫生研究院文献>Annals of Surgery >Cytokine patterns in patients after major vascular surgery hemorrhagic shock and severe blunt trauma. Relation with subsequent adult respiratory distress syndrome and multiple organ failure.
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Cytokine patterns in patients after major vascular surgery hemorrhagic shock and severe blunt trauma. Relation with subsequent adult respiratory distress syndrome and multiple organ failure.

机译:大血管手术失血性休克和严重钝性创伤后患者的细胞因子类型。与随后的成人呼吸窘迫综合征和多器官衰竭的关系。

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摘要

OBJECTIVE: This study investigates the course of serum cytokine levels in patients with multiple trauma, patients with a ruptured abdominal aortic aneurysm (AAA), and patients undergoing elective AAA repair and the relationship of these cytokines to the development of adult respiratory distress syndrome (ARDS) and multiple organ failure (MOF). SUMMARY BACKGROUND DATA: Severe tissue trauma, hemorrhagic shock, and ischemia-reperfusion injury are pathophysiologic mechanisms that may result in an excessive uncontrolled activation of inflammatory cells and mediators. This inflammatory response is thought to play a key role in the development of (remote) cell and organ dysfunction, which is the basis of ARDS and MOF. METHODS: The study concerns 28 patients with multiple trauma, 20 patients admitted in shock because of a ruptured AAA, and 18 patients undergoing elective AAA repair. Arterial blood was serially sampled from admission (or at the start of elective operation) to day 13 in the intensive care unit, and the serum concentrations of tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1 beta, and IL-6 were determined. RESULTS: Twenty-two patients died, 15 within 48 hours and 7 after several weeks, as a result of ARDS/MOF. At hospital admission and after 6 hours, these nonsurvivors had significantly higher plasma TNF-alpha and IL-1 beta levels than did the survivors. At the same measuring points, TNF-alpha and IL-1 beta were significantly more elevated in patients with ruptured AAA than in traumatized patients. However, IL-6 was significantly higher in the traumatized patients. In 10 patients, ARDS/MOF developed, and 41 had an uncomplicated course in this respect. Those with ARDS/MOF exhibited significantly different cytokine patterns in the early postinjury phase. TNF-alpha and IL-1 beta levels were higher mainly on the first day of admission; IL-6 concentrations were significantly elevated in patients with ARDS/MOF from the second day onward. The latter cytokine showed a good correlation with the daily MOF score during the whole 2-week observation period. CONCLUSIONS: In the early postinjury phase, higher concentrations of these cytokines are associated, not only with an increased mortality rate, but also with an increased risk for subsequent ARDS and MOF. These data therefore support the concept that these syndromes are caused by an overwhelming autodestructive inflammatory response.
机译:目的:本研究调查了多发性创伤患者,腹主动脉瘤破裂(AAA)和择期AAA修复患者的血清细胞因子水平变化过程,以及这些细胞因子与成人呼吸窘迫综合征(ARDS)发展的关系。 )和多器官功能衰竭(MOF)。摘要背景数据:严重的组织创伤,失血性休克和缺血再灌注损伤是可能导致炎症细胞和介质过度失控活化的病理生理机制。该炎症反应被认为在(远程)细胞和器官功能障碍的发展中起关键作用,这是ARDS和MOF的基础。方法:该研究涉及28例多发性创伤患者,20例因AAA破裂而休克的患者以及18例接受AAA择期修复的患者。从入院(或择期手术开始)至第13天,对动脉血进行连续采样,并采集血清肿瘤坏死因子-α(TNF-alpha),白介素(IL)-1 beta和测定IL-6。结果:ARDS / MOF导致22例患者死亡,其中48小时内死亡15例,数周后死亡7例。入院时和6小时后,这些非幸存者的血浆TNF-alpha和IL-1 beta水平明显高于幸存者。在相同的测量点上,AAA破裂的患者的TNF-α和IL-1β明显高于受创伤的患者。但是,在受创伤的患者中,IL-6明显更高。在10例患者中,发展了ARDS / MOF,并且有41例患者在这方面的病程简单。患有ARDS / MOF的患者在损伤后早期表现出明显不同的细胞因子模式。 TNF-α和IL-1β水平主要在入院第一天较高;从第二天起,ARDS / MOF患者的IL-6浓度显着升高。在整个2周的观察期内,后一种细胞因子与每日MOF得分表现出良好的相关性。结论:在损伤后早期,这些细胞因子的较高浓度不仅与死亡率增加有关,而且与随后的ARDS和MOF风险增加有关。因此,这些数据支持了这些综合征是由压倒性的自毁性炎症反应引起的概念。

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