Impact of a goal-directed factor-based coagulation management on thromboembolic events following major trauma

Stein, Anais L.; Rössler, Julian; Braun, Julia; Sprengel, Kai; Beeler, Patrick E.; Spahn, Donat R.; Kaserer, Alexander; Stein, Philipp

doi:10.1186/s13049-019-0697-0

Cited by 10 publications

(6 citation statements)

References 34 publications

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“…Analyses of the US National Trauma Data Bank showed in-hospital VTE rates of around 1% 194,302,303 . In a Swiss trauma centre, VTE rates were in the range 7-10% 304 , and in Germany a rate of 2% was reported 305 . A higher VTE incidence has been reported in a military population than in civilians (22% and 2%, respectively) [306][307][308] .…”

Section: Quality Of Lifementioning

confidence: 99%

Trauma-induced coagulopathy

Moore

Kornblith

et al. 2021

Nat Rev Dis Primers

445

464

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Injury is the fourth leading cause of mortality worldwide, accounting for 9% of deaths globally (4.9 million people) in 2016 (ref. 1 ). Moreover, the burden is highest in individuals <50 years of age, among whom injury as a cause of death is second only to infectious diseases. Early preventable deaths after injury in civilian 2 and military 3 settings are primarily attributable to uncontrolled haemorrhage 2-8 , whereas later preventable deaths are typically due to hypercoagulability 9 . Consequently, there is intense interest worldwide in the pathogenesis of trauma-induced coagulopathy (TIC) to attenuate its adverse effects on the outcomes of seriously injured patients.Impaired coagulation following sudden death from injury has been observed for centuries 10 and, in the 1960s, the first clinical laboratory documentation of the temporal changes in coagulation following severe injury were documented 11 . However, early endogenous drivers of coagulopathy were not specifically investigated until 1982, when a case series of patients with major abdominal vascular injuries highlighted TIC as a common direct cause of early post-injury mortality: 89% of the deaths were bleeding-related, yet half occurred after mechanical control of bleeding sites -in other words, they were due to coagulopathy 12 . The remaining ongoing quagmire is the inability to distinguish between patients with exsanguinating injuries whose TIC is the result of metabolic failure (that is, who are bleeding because they are dying) from patients whose TIC is the cause of the ongoing blood loss (that is, who are dying because they are bleeding) 13 . Furthermore, not all patients with abnormalities in laboratory coagulation tests are bleeding 14 .Despite the long-term fascination with changes in coagulation resulting from shock and tissue injury 15 , there is no standard definition of TIC, which refers to abnormal coagulation capacity attributable to trauma. The term TIC was established during the Trans-Agency Consortium for Trauma Induced Coagulopathy Workshop conducted by the National Institutes of Health in April 2010 to describe the variety of phenomena that characterize this condition. TIC can manifest as a spectrum of phenotypes from hypocoagulation to hypercoagulation (fig. 1), as a function of several interactive factors, including (but not limited to) tissue injury, presence of shock and, in particular, time from injury (fig. 2).

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Section: Quality Of Lifementioning

confidence: 99%

Trauma-induced coagulopathy

Moore

Kornblith

et al. 2021

Nat Rev Dis Primers

445

464

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“…Existing protocols for such goal-driven trauma treatment 37 – 40 use thromboelastometry, a viscoelastic coagulation assay, but this assay is time-consuming at typically about an hour per run. These protocols are non-quantitative, rely on clinical intuition and older standard procedures, and only correct for a small number of coagulation factors and/or their interactions.…”

Section: Introductionmentioning

confidence: 99%

Personalized modulation of coagulation factors using a thrombin dynamics model to treat trauma-induced coagulopathy

2021

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Current trauma-induced coagulopathy resuscitation protocols use slow laboratory measurements, rules-of-thumb, and clinician gestalt to administer large volumes of uncharacterized, non-tailored blood products. These one-size-fits-all treatment approaches have high mortality. Here, we provide significant evidence that trauma patient survival 24 h after hospital admission occurs if and only if blood protein coagulation factor concentrations equilibrate at a normal value, either from inadvertent plasma-based modulation or from innate compensation. This result motivates quantitatively guiding trauma patient coagulation factor levels while accounting for protein interactions. Toward such treatment, we develop a Goal-oriented Coagulation Management (GCM) algorithm, a personalized and automated ordered sequence of operations to compute and specify coagulation factor concentrations that rectify clotting. This novel GCM algorithm also integrates new control-oriented advancements that we make in this work: an improvement of a prior thrombin dynamics model that captures the coagulation process to control, a use of rapidly-measurable concentrations to help predict patient state, and an accounting of patient-specific effects and limitations when adding coagulation factors to remedy coagulopathy. Validation of the GCM algorithm’s guidance shows superior performance over clinical practice in attaining normal coagulation factor concentrations and normal clotting profiles simultaneously.

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“…Altogether, the transfer of our data into a clinical context must therefore be done very carefully. All factor components of CRFs have previously been safely administered in loose compositions for the management of bleeding associated coagulopathy 43 . PCCs show a reliable safety pro le and are now the treatment of choice for the emergency reversal of Vitamin K antagonists 44,45 .…”

Section: Discussionmentioning

confidence: 99%

Normalization Of Blood Clotting Characteristics Using Prothrombin Complex Concentrate, Fibrinogen And FXIII In An Albumin Based Fluid: Experimental Studies In Thromboelastometry.

Koller

Kinast

Castellanos

et al. 2021

Preprint

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Background: Colloid fluids supplemented with adequate combinations of coagulation factor concentrates with the capability to restore coagulation could be a desirable future treatment component in massive transfusion.Methods: Starting from a coagulation factor and blood cell-free albumin solution we added Prothrombin Complex Concentrate, Fibrinogen Concentrate and Factor XIII in different combinations and concentrations to analyze their properties to restore thromboelastometry parameters without the use of plasma. Further analysis under the presence of platelets was performed for comparability to whole blood conditions.Results: Albumin solutions enriched with Fibrinogen Concentrate, Factor XIII and Prothrombin Complex Concentrate at optimized concentrations show restoring coagulation potential. Prothrombin Complex Concentrate showed sufficient thrombin formation for inducing fibrinogen polymerization. The combination of Prothrombin Complex Concentrate and Fibrinogen Concentrate led to the formation of a stable in vitro fibrin clot. Fibrinogen and Factor XIII showed excellent capacity to improve fibrin clot firmness expressed as Amplitude at 10 minutes and Maximal Clot Firmness. Fibrinogen alone, or in combination with Factor XIII, was able to restore normal Amplitude at 10 minutes and Maximal Clot Firmness values. In the presence of platelets, the thromboelastometry surrogate parameter for thrombin generation (Clotting Time) improves and normalizes when compared to whole blood.Conclusions: Combinations of coagulation factor concentrates suspended in albumin solutions can restore thromboelastometry parameters in the absence of plasma. This kind of artificial colloid fluids with coagulation-restoring characteristics might offer new treatment alternatives for massive transfusion.Trial registration: Study registered at the institutional ethic committee “Institut de Recerca, Hospital Santa Creu i Sant Pau, with protocol number IIBSP-CFC-2013-165.

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Impact of a goal-directed factor-based coagulation management on thromboembolic events following major trauma

Cited by 10 publications

References 34 publications

Trauma-induced coagulopathy

Trauma-induced coagulopathy

Personalized modulation of coagulation factors using a thrombin dynamics model to treat trauma-induced coagulopathy

Normalization Of Blood Clotting Characteristics Using Prothrombin Complex Concentrate, Fibrinogen And FXIII In An Albumin Based Fluid: Experimental Studies In Thromboelastometry.

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