A review of transfusion- and trauma-induced hypocalcemia: Is it time to change the lethal triad to the lethal diamond?
A review of transfusion- and trauma-induced hypocalcemia: Is it time to change the lethal triad to the lethal diamond?
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DOI：
10.1097/ta.0000000000002570
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发表时间：
2020-03-01
影响因子：
3.4
通讯作者：
Siegler, Jeffrey
中科院分区：
文献类型：
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作者：
Ditzel, Ricky Michael, Jr.;Anderson, Justin Lee;Siegler, Jeffrey
失血性休克患者的管理原则随着时间的推移而演变。有充分证据表明，持续遭受休克或灌注不足的患者因低温、凝血病和酸中毒引起的血液衰竭而发病和死亡的风险更大。1这三种情况-体温过低、凝血病和酸中毒-统称为致死三联征，作为描述弥散性血管内凝血病作用机制的基础生理损伤，并推动当前出血性休克复苏的努力。2，3低温，定义为低于35 ℃的核心温度，通过抑制血栓素A2对止血产生有害影响，除了改变整个凝血级联中酶促过程发生的速率外，还导致损伤部位局部血管收缩和血小板聚集的减少。此外，体温过低与氧-血红蛋白解离曲线的负移和心肌收缩力的降低有关，这两者都导致组织氧合减少和氧债状态增加。上述机制与凝血障碍和酸中毒直接相关，因为不可逆性休克在整个致死三联征中进展。凝血病，传统上被认为是国际标准化比值（INR）1.5或更高的急性设置，可能会额外加剧血液稀释血小板和凝血因子通过晶体输注。4，5最后，酸中毒或血清pH值低于7.36与凝血因子活性降低、纤维蛋白降解速率和凝血时间增加相关，进一步加重创伤性出血诱导的凝血病。[6]正是通过这些机制，致命三联体中的每一个要素与其他要素重叠。虽然全血（WB）和血液制品的使用有助于降低死亡率的患者患有致命的三联体，本综述的作者认为，仍然存在差距，在创伤引起的凝血功能障碍的管理。本文献综述的目的是通过对以往研究的检查来证明创伤中低钙血症的患病率，以及在严重创伤患者的管理中解决这一缺陷的必要性。因此，我们希望促进创伤低钙血症管理的有针对性的研究，并支持最近发表的创伤管理指南，解释创伤诱导凝血功能障碍的这一差距。我们认为，早期识别和纠正低钙血症，在这个病人群体中可能是一个缺失的环节管理和预防创伤引起的凝血功能障碍，并有效地改变描述符从致命的三联体致命的钻石。
The principles of managing patients suffering from hemorrhagic shock have evolved over time. It is well supported that patients who continue to suffer from shock or hypoperfusion are at greater risk of morbidity and mortality attributable to blood failure precipitated by hypothermia, coagulopathy, and acidosis. 1 These three conditions—hypothermia, coagulopathy, and acidosis—collectively known as the lethal triad, serve as the foundational physiologic insults that describe the mechanisms of action of disseminated intravascular coagulopathy and drive the current hemorrhagic shock resuscitation efforts. 2, 3 Hypothermia, defined as a core temperature under 35 C, exerts deleterious effects on hemostasis by inhibiting thromboxane A 2, causing a reduction in local vasoconstriction and platelet aggregation at the site of injury in addition to altering the rate at which enzymatic process occurs throughout the clotting cascade. Moreover, hypothermia is associated with a leftward shift of the oxygen-hemoglobin dissociation curve and a reduction in myocardial contractility, both leading to reduced tissue oxygenation and an increased state of oxygen debt. These mechanisms described previously directly correlate with coagulopathy and acidosis as irreversible shock progresses throughout the lethal triad. Coagulopathy, traditionally regarded as an international normalized ratio (INR) of 1.5 or greater in an acute setting, may additionally be exacerbated by hemodilution of platelets and clotting factors through crystalloid infusions. 4, 5 Lastly, acidosis or serum pH of less than 7.36 is associated with a reduction in coagulation factor activity and increases in fibrin degradation rate and coagulation times, further exacerbating the traumatic hemorrhage induced coagulopathy. 6 It is through these mechanisms by which each element of the lethal triad overlaps upon the others. Although the use of whole blood (WB) and blood products has assisted in decreasing mortality for patients suffering from the lethal triad, the authors of this review believe that there are still gaps in the management of trauma-induced coagulopathy. The goal of this literature review was to demonstrate through examination of previous studies the prevalence of hypocalcemia in trauma and the need to address this deficiency in management of severely injured patients. From this, we hope to promote targeted research in the management of hypocalcemia in trauma and support recently published guidelines in trauma management that accounts for this gap in trauma-induced coagulopathy. We believe that early identification and correction of hypocalcemia in this patient population could be a missing link to the management and prevention of trauma-induced coagulopathy and effectively change the descriptor from the lethal triad to the lethal diamond.