Ronit Kar , Erin V. Feeney , Jack R. Killinger , Katrina M. Morgan , Devin M. Dishong , Katelin C. Rahn , Rassam M.G. Rassam , Grace A. Ballentine , Philip C. Spinella , Matthew D. Neal , Barbara A. Gaines , Susan M. Shea , Christine M. Leeper
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For the control cohort, outpatient blood samples were collected, and for the trauma cohort, blood was collected in the trauma bay for conventional coagulation tests, thromboelastography, von Willebrand factor A1 domain activity, and a microfluidic assay using a stenotic channel (shear rate = 3500 s<sup>−1</sup>).</div></div><div><h3>Results</h3><div>The trauma cohort characteristics were 67% male, median (IQR) age 6 years (4-12), median (IQR) injury severity score 17 (9-26), and 78% blunt mechanism. In total, 50% required blood transfusion and 11% (2/18) died. While thromboelastography maximum amplitude (59.9 ± 6.1 mm) and platelet counts (306.3 ± 111.1 × 10<sup>3</sup> cells/μL) were within normal limits, the microfluidic assay revealed significantly lower platelet deposition in the trauma cohort versus the control cohort (1.18 ± 0.25 vs 3.06 ± 0.82 mean fluorescence intensity fold change; <em>P</em> < .0001). Lower levels of platelet deposition correlated with receipt of blood transfusion within 6 hours of arrival (<em>r</em> = −0.44, <em>P</em> = .048). von Willebrand factor A1 domain activity was not different between groups and was not correlated with platelet deposition based on mean fluorescence intensity fold change (<em>R</em><sup>2</sup> < 0.0001).</div></div><div><h3>Conclusion</h3><div>Posttraumatic platelet dysfunction was observed by utilizing a microfluidic assay in a pediatric trauma cohort. Further study is needed to understand the underlying mechanisms and significance of posttraumatic platelet dysfunction in children.</div></div>","PeriodicalId":20893,"journal":{"name":"Research and Practice in Thrombosis and Haemostasis","volume":"9 6","pages":"Article 103160"},"PeriodicalIF":3.4000,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Beyond the count: platelet dysfunction profile in pediatric trauma patients\",\"authors\":\"Ronit Kar , Erin V. Feeney , Jack R. Killinger , Katrina M. Morgan , Devin M. Dishong , Katelin C. Rahn , Rassam M.G. Rassam , Grace A. Ballentine , Philip C. Spinella , Matthew D. Neal , Barbara A. Gaines , Susan M. Shea , Christine M. Leeper\",\"doi\":\"10.1016/j.rpth.2025.103160\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Background</h3><div>Existing clinical coagulation assays are inadequate to evaluate posttraumatic platelet dysfunction in children.</div></div><div><h3>Objectives</h3><div>To elucidate changes in flow-dependent platelet function after injury in children using a microfluidic assay.</div></div><div><h3>Methods</h3><div>We enrolled 18 children who presented with highest-acuity trauma activation and 10 healthy children at an academic pediatric center. For the control cohort, outpatient blood samples were collected, and for the trauma cohort, blood was collected in the trauma bay for conventional coagulation tests, thromboelastography, von Willebrand factor A1 domain activity, and a microfluidic assay using a stenotic channel (shear rate = 3500 s<sup>−1</sup>).</div></div><div><h3>Results</h3><div>The trauma cohort characteristics were 67% male, median (IQR) age 6 years (4-12), median (IQR) injury severity score 17 (9-26), and 78% blunt mechanism. In total, 50% required blood transfusion and 11% (2/18) died. While thromboelastography maximum amplitude (59.9 ± 6.1 mm) and platelet counts (306.3 ± 111.1 × 10<sup>3</sup> cells/μL) were within normal limits, the microfluidic assay revealed significantly lower platelet deposition in the trauma cohort versus the control cohort (1.18 ± 0.25 vs 3.06 ± 0.82 mean fluorescence intensity fold change; <em>P</em> < .0001). Lower levels of platelet deposition correlated with receipt of blood transfusion within 6 hours of arrival (<em>r</em> = −0.44, <em>P</em> = .048). von Willebrand factor A1 domain activity was not different between groups and was not correlated with platelet deposition based on mean fluorescence intensity fold change (<em>R</em><sup>2</sup> < 0.0001).</div></div><div><h3>Conclusion</h3><div>Posttraumatic platelet dysfunction was observed by utilizing a microfluidic assay in a pediatric trauma cohort. 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引用次数: 0
摘要
现有的临床凝血试验不足以评估儿童创伤后血小板功能障碍。目的应用微流控法研究儿童损伤后血流依赖性血小板功能的变化。方法我们在一家学术儿科中心招募了18名表现为最高急性创伤激活的儿童和10名健康儿童。对于对照组,采集门诊血液样本,对于创伤组,在创伤室采集血液进行常规凝血试验、血栓弹性成像、血管性血液病因子A1结构域活性和使用狭窄通道(剪切速率= 3500 s−1)的微流控分析。结果创伤队列特征67%为男性,中位(IQR)年龄6岁(4-12岁),中位(IQR)损伤严重程度评分17分(9-26分),78%为钝性机制。总共有50%需要输血,11%(2/18)死亡。虽然血栓弹性成像最大振幅(59.9±6.1 mm)和血小板计数(306.3±111.1 × 103个细胞/μL)在正常范围内,但微流控分析显示,创伤组血小板沉积明显低于对照组(平均荧光强度变化1.18±0.25 vs 3.06±0.82;P < 0.0001)。血小板沉积水平较低与到达后6小时内接受输血相关(r = - 0.44, P = 0.048)。血管性血癌因子A1结构域活性各组间无差异,且基于平均荧光强度折叠变化与血小板沉积无相关性(R2 < 0.0001)。结论应用微流控法观察儿童创伤后血小板功能障碍。需要进一步研究了解儿童创伤后血小板功能障碍的潜在机制和意义。
Beyond the count: platelet dysfunction profile in pediatric trauma patients
Background
Existing clinical coagulation assays are inadequate to evaluate posttraumatic platelet dysfunction in children.
Objectives
To elucidate changes in flow-dependent platelet function after injury in children using a microfluidic assay.
Methods
We enrolled 18 children who presented with highest-acuity trauma activation and 10 healthy children at an academic pediatric center. For the control cohort, outpatient blood samples were collected, and for the trauma cohort, blood was collected in the trauma bay for conventional coagulation tests, thromboelastography, von Willebrand factor A1 domain activity, and a microfluidic assay using a stenotic channel (shear rate = 3500 s−1).
Results
The trauma cohort characteristics were 67% male, median (IQR) age 6 years (4-12), median (IQR) injury severity score 17 (9-26), and 78% blunt mechanism. In total, 50% required blood transfusion and 11% (2/18) died. While thromboelastography maximum amplitude (59.9 ± 6.1 mm) and platelet counts (306.3 ± 111.1 × 103 cells/μL) were within normal limits, the microfluidic assay revealed significantly lower platelet deposition in the trauma cohort versus the control cohort (1.18 ± 0.25 vs 3.06 ± 0.82 mean fluorescence intensity fold change; P < .0001). Lower levels of platelet deposition correlated with receipt of blood transfusion within 6 hours of arrival (r = −0.44, P = .048). von Willebrand factor A1 domain activity was not different between groups and was not correlated with platelet deposition based on mean fluorescence intensity fold change (R2 < 0.0001).
Conclusion
Posttraumatic platelet dysfunction was observed by utilizing a microfluidic assay in a pediatric trauma cohort. Further study is needed to understand the underlying mechanisms and significance of posttraumatic platelet dysfunction in children.