Platelet aggregation after blunt trauma is associated with the acute respiratory distress syndrome and altered by cigarette smoke exposure.
Platelet aggregation after blunt trauma is associated with the acute respiratory distress syndrome and altered by cigarette smoke exposure.
复制标题
钝性创伤后的血小板聚集与急性呼吸窘迫综合征有关，并会因暴露于香烟烟雾而改变。
DOI：
10.1097/ta.0000000000001738
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发表时间：
2018
期刊：
影响因子：
--
通讯作者：
Calfee,CarolynS
中科院分区：
文献类型：
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作者：
Moazed,Farzad;Hendrickson,Carolyn;Nelson,Mary;Conroy,Amanda;Cohen,MitchellJ;Calfee,CarolynS
被动吸烟者和主动吸烟者在钝伤后发生急性呼吸窘迫综合征（ARDS）的风险增加。然而，负责的机制，包括血小板聚集的作用，为这种association. METHODS的作用，我们分析了215例严重钝性创伤从一个前瞻性观察队列在一级创伤中心2010年和2015年之间。受试者接受了基于阻抗的血小板聚集测定法，以响应血小板激动剂花生四烯酸、二磷酸腺苷、胶原蛋白和凝血酶受体激活肽-6。采用柏林标准判定入院前8天内的急性呼吸窘迫综合征。测量血浆可替宁以评估香烟烟雾暴露。回归分析用于评估（1）血小板聚集与ARDS和（2）香烟烟雾暴露与血小板聚集之间的关系。在0小时和24小时，受损的血小板聚集与发生ARDS的几率增加相关。吸烟暴露与到达急诊室后血小板聚集增加相关。然而，在24小时，香烟烟雾暴露与血小板聚集的损害增加有关，反映了创伤后最初24小时血小板聚集的统计学显著下降。血小板聚集性下降与ARDS之间的关系因吸烟状态而异，表明血小板活化受损对吸烟暴露者的ARDS风险有不同影响（花生四烯酸，相互作用p：0.005，胶原蛋白相互作用p：0.02，腺苷二磷酸，相互作用p：结论严重钝伤后0小时和24小时血小板聚集功能受损与发生ARDS的风险增加有关。暴露于香烟烟雾的患者在入院后的前24小时内更容易发生血小板聚集受损，这可能导致他们患ARDS的风险增加。
BACKGROUNDThe risk of the acute respiratory distress syndrome (ARDS) is increased in passive and active smokers after blunt trauma. However, the mechanisms responsible, including the role of platelet aggregation, for this association are unknown.METHODSWe analyzed 215 patients with severe blunt trauma from a prospective observational cohort at a Level I trauma center between 2010 and 2015. Subjects underwent impedance-based platelet aggregometry in response to platelet agonists arachidonic acid, adenosine diphosphate, collagen, and thrombin receptor activating peptide-6. Acute respiratory distress syndrome within the first 8 days of admission was adjudicated using Berlin criteria. Plasma cotinine was measured to assess cigarette smoke exposure. Regression analyses were used to assess the relationship between (1) platelet aggregation and ARDS and (2) cigarette smoke exposure and platelet aggregation.RESULTSAt both 0 hour and 24 hours, impaired platelet aggregation was associated with increased odds of developing ARDS. Cigarette smoke exposure was associated with increased platelet aggregation upon arrival to the emergency department. However, at 24 hours, cigarette smoke exposure was associated with increased impairment in platelet aggregation, reflecting a statistically significant decline in platelet aggregation over the initial 24 hours after trauma. The relationship between this decline in platelet aggregation and ARDS differed by cigarette smoke exposure status, suggesting that impaired platelet activation differentially affects the risk of ARDS in those with cigarette smoke exposure (arachidonic acid, p for interaction: 0.005, collagen p for interaction: 0.02, adenosine diphosphate, p for interaction: 0.05).CONCLUSIONImpaired platelet aggregation at 0 hour and 24 hours is associated with an increased risk of developing ARDS after severe blunt trauma. Cigarette smoke–exposed patients are more likely to develop impaired platelet aggregation over the first 24 hours of admission, which may contribute to their increased risk of ARDS.