Grading Clinical Coagulopathy and Predicting Massive Transfusion

Thorn, Sophie; Maegele, Marc

doi:10.1007/978-3-030-53606-0_15

Cited by 2 publications

(6 citation statements)

References 79 publications

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“…11 , 12 The risk of coagulopathy was considered high with a first observation of systolic blood pressure less than 70 mm Hg or a shock index (calculated as heart rate divided by systolic blood pressure) greater than 1.1. 13 Exclusion criteria were age younger than 18 years, refusal to participate, liberty deprivation, pregnancy, known allergy to amotosalen, prehospital administration of coagulation factors, initial cardiac arrest, or a known do-not-resuscitate status from the prehospital setting. We collected individual consent before inclusion if the patient’s state of consciousness allowed it.…”

Section: Methodsmentioning

confidence: 99%

“…The INR thresholds used to diagnose TIC vary from study to study. 5 , 13 In this trial, we used an INR threshold value of 1.2.…”

Section: Methodsmentioning

confidence: 99%

“…Prehospital physicians assessed severity using clinical, circumstantial, and Vittel kinetic criteria (physiological variables, anatomical injuries, prehospital resuscitation, patient predisposition, and kinetic components) that are close to the 2011 guidelines for field triage and commonly used in the French emergency medical response system . The risk of coagulopathy was considered high with a first observation of systolic blood pressure less than 70 mm Hg or a shock index (calculated as heart rate divided by systolic blood pressure) greater than 1.1 . Exclusion criteria were age younger than 18 years, refusal to participate, liberty deprivation, pregnancy, known allergy to amotosalen, prehospital administration of coagulation factors, initial cardiac arrest, or a known do-not-resuscitate status from the prehospital setting.…”

Section: Methodsmentioning

confidence: 99%

“…Median length of hospital stay was 9 (IQR, 3-24) days in the plasma group and 10 (IQR, 2-20) days in the control group (P = .80). Time to death after inclusion was 16 (IQR, 6-96) hours in the plasma group and 21 (IQR, [13][14][15][16][17][18][19][20][21][22][23][24] hours in the control group (P = .60).…”

Section: Jama Network Open | Emergency Medicinementioning

confidence: 99%

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Prehospital Lyophilized Plasma Transfusion for Trauma-Induced Coagulopathy in Patients at Risk for Hemorrhagic Shock

Jost

Lemoine

et al. 2022

JAMA Netw Open

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Key Points Question Does prehospital transfusion of lyophilized plasma result in a lower incidence of trauma-induced coagulopathy at hospital admission compared with standard care with normal saline infusion in patients at risk for hemorrhagic shock after trauma? Findings This multicenter randomized clinical trial included 150 patients with trauma who were treated in a prehospital setting. Median international normalized ratio at hospital admission, massive transfusion rate, 30-day survival, and adverse events did not significantly differ between lyophilized plasma transfusion and standard care. Meaning These findings suggest that prehospital lyophilized plasma transfusion is a feasible and safe procedure for patients who are at risk for hemorrhagic shock, although there is a lack of evidence regarding its ability to prevent trauma-induced coagulopathy.

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Section: Methodsmentioning

confidence: 99%

“…The INR thresholds used to diagnose TIC vary from study to study. 5 , 13 In this trial, we used an INR threshold value of 1.2.…”

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Jama Network Open | Emergency Medicinementioning

confidence: 99%

See 2 more Smart Citations

Prehospital Lyophilized Plasma Transfusion for Trauma-Induced Coagulopathy in Patients at Risk for Hemorrhagic Shock

Jost

Lemoine

et al. 2022

JAMA Netw Open

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“…VHAs assist the early detection of coagulopathies associated with SHINE when these patients are treated with plasma whether for trauma or sepsis (Thölking et al, 2015;Moore et al, 2018;Sperry et al, 2018;Pusateri et al, 2020). Recent trauma models adopting VHAs show promise for earlier identification of hemostatic derangement and SHINE, which predicts the need for MT in trauma patients (Thorn and Maegele, 2021). Likewise, early use of VHAs in SIC enables early detection of the depth and duration of shock prior to coagulopathic manifestation by conventional coagulation tests (CCTs) and other standard clinical and biologic markers (Pavoni et al, 2020).…”

Section: Pathophysiology Of Shinementioning

confidence: 99%

SHock-INduced Endotheliopathy (SHINE): A mechanistic justification for viscoelastography-guided resuscitation of traumatic and non-traumatic shock

Bunch

Chang²,

Moore³

et al. 2023

Front. Physiol.

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Irrespective of the reason for hypoperfusion, hypocoagulable and/or hyperfibrinolytic hemostatic aberrancies afflict up to one-quarter of critically ill patients in shock. Intensivists and traumatologists have embraced the concept of SHock-INduced Endotheliopathy (SHINE) as a foundational derangement in progressive shock wherein sympatho-adrenal activation may cause systemic endothelial injury. The pro-thrombotic endothelium lends to micro-thrombosis, enacting a cycle of worsening perfusion and increasing catecholamines, endothelial injury, de-endothelialization, and multiple organ failure. The hypocoagulable/hyperfibrinolytic hemostatic phenotype is thought to be driven by endothelial release of anti-thrombogenic mediators to the bloodstream and perivascular sympathetic nerve release of tissue plasminogen activator directly into the microvasculature. In the shock state, this hemostatic phenotype may be a counterbalancing, yet maladaptive, attempt to restore blood flow against a systemically pro-thrombotic endothelium and increased blood viscosity. We therefore review endothelial physiology with emphasis on glycocalyx function, unique biomarkers, and coagulofibrinolytic mediators, setting the stage for understanding the pathophysiology and hemostatic phenotypes of SHINE in various etiologies of shock. We propose that the hyperfibrinolytic phenotype is exemplified in progressive shock whether related to trauma-induced coagulopathy, sepsis-induced coagulopathy, or post-cardiac arrest syndrome-associated coagulopathy. Regardless of the initial insult, SHINE appears to be a catecholamine-driven entity which early in the disease course may manifest as hyper- or hypocoagulopathic and hyper- or hypofibrinolytic hemostatic imbalance. Moreover, these hemostatic derangements may rapidly evolve along the thrombohemorrhagic spectrum depending on the etiology, timing, and methods of resuscitation. Given the intricate hemochemical makeup and changes during these shock states, macroscopic whole blood tests of coagulative kinetics and clot strength serve as clinically useful and simple means for hemostasis phenotyping. We suggest that viscoelastic hemostatic assays such as thromboelastography (TEG) and rotational thromboelastometry (ROTEM) are currently the most applicable clinical tools for assaying global hemostatic function—including fibrinolysis—to enable dynamic resuscitation with blood products and hemostatic adjuncts for those patients with thrombotic and/or hemorrhagic complications in shock states.

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Grading Clinical Coagulopathy and Predicting Massive Transfusion

Cited by 2 publications

References 79 publications

Prehospital Lyophilized Plasma Transfusion for Trauma-Induced Coagulopathy in Patients at Risk for Hemorrhagic Shock

Prehospital Lyophilized Plasma Transfusion for Trauma-Induced Coagulopathy in Patients at Risk for Hemorrhagic Shock

SHock-INduced Endotheliopathy (SHINE): A mechanistic justification for viscoelastography-guided resuscitation of traumatic and non-traumatic shock

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