School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA.
Department of Surgery, Georgetown University School of Medicine, Washington DC 20007, USA; The Burn Center, MedStar Washington Hospital Center, Georgetown University School of Medicine, Washington DC 20007, USA.
Burns. 2022 Dec;48(8):1805-1815. doi: 10.1016/j.burns.2022.08.016. Epub 2022 Aug 29.
Various studies have reported discordant results on the magnitude and direction of burn-induced coagulopathy (BIC), which has recently been associated with multiple organ dysfunction syndrome (MODS) and death. The increased mechanistic understanding of BIC is due, in part, to novel assays that have expanded the armamentarium beyond traditional tests like PT and aPTT. Still, BIC is a dynamic process, and the progression is difficult to define in the thermally-injured. To this end, we aimed to enhance the understanding of burn-induced coagulation abnormalities by employing functional assessments of platelet aggregation, viscoelastic kinetics, and thrombin generation in an extensive burn model in swine. Anesthetized Yorkshire pigs sustained 40% total body surface area (TBSA) full-thickness contact burns and recovered in metabolic cages. Blood was collected at baseline (BL), as well as 6, 24, and 48 h after injury. A significant effect of burn (P < 0.0001) was seen on platelets, with mild thrombocytopenia apparent at 24 h. While slight decreases in aPTT were not significant, rotational thromboelastometry (ROTEM) analysis revealed hypercoagulation 6 and 24 h after burn by a decreased clotting time. Maximum clot firmness increased after burn, but was not statistically significant until 48 h. Hypercoagulation was not supported by platelet aggregation, as the response to ADP was greatly and persistently diminished, and the response to collagen was unchanged. Endogenous thrombin potential was significantly reduced at 6 and 24 h after burn (P < 0.0001), and also correlated with a number of ROTEM parameters and collagen-induced platelet aggregation. In contrast, PT was not correlated with other measured parameters. Taken together, novel coagulation parameters may be more sensitive than PT in characterizing coagulopathy in the setting of burns. The data presented herein makes initial strides to report the natural history of several of these variables over time in a large animal model of extensive burns, indicating early hypercoagulability followed by hypocoagulation. Future work will elucidate the effects of standard of care.
各种研究报告了烧伤诱导性凝血障碍（BIC）的幅度和方向的不一致结果，最近与多器官功能障碍综合征（MODS）和死亡有关。对 BIC 的机械理解的增加部分是由于新的检测方法，这些方法扩展了除了传统的 PT 和 aPTT 测试之外的武器。尽管如此，BIC 是一个动态过程，在热损伤中很难定义其进展。为此，我们旨在通过在猪的广泛烧伤模型中使用血小板聚集、粘弹性动力学和凝血酶生成的功能评估来增强对烧伤诱导性凝血异常的理解。麻醉的约克夏猪承受 40%的全身体表面积（TBSA）全厚接触烧伤，并在代谢笼中恢复。在基线（BL）以及受伤后 6、24 和 48 小时采集血液。烧伤（P < 0.0001）对血小板有显著影响，24 小时时明显出现轻度血小板减少症。尽管 aPTT 的轻微下降没有意义，但旋转血栓弹性测定（ROTEM）分析显示烧伤后 6 和 24 小时的高凝状态通过凝血时间缩短来表示。烧伤后最大血凝块硬度增加，但直到 48 小时才具有统计学意义。血小板聚集不支持高凝状态，因为 ADP 的反应大大且持续减弱，而对胶原的反应不变。烧伤后 6 和 24 小时，内源性凝血酶潜能显著降低（P < 0.0001），并且与一些 ROTEM 参数和胶原诱导的血小板聚集相关。相比之下，PT 与其他测量参数不相关。总的来说，新型凝血参数可能比 PT 更敏感，能够在烧伤情况下更准确地描述凝血障碍。本文提供的资料首次在大型动物广泛烧伤模型中报告了这些变量中的一些随时间变化的自然史，表明早期高凝状态后出现低凝状态。未来的工作将阐明标准治疗的影响。
