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. 2010;1(1):12-21.

Acute traumatic coagulopathy: Incidence, risk stratification and therapeutic options

Affiliations

Acute traumatic coagulopathy: Incidence, risk stratification and therapeutic options

Marc Maegele. World J Emerg Med. 2010.

Abstract

Background: Uncontrolled hemorrhage is responsible for over 50% of all trauma-related deaths within the first 48 hours after admission. Clinical observations together with recent research resulted in an appreciation of the central role of coagulopathy in acute trauma care. A synopsis is presented of different retrospective analyses based upon datasets from severe multiply injured patients derived from the TR-DGU database (Trauma Registry of the Deutsche Gesellschaft fur Unfallchirurgie (DGU)/ German Society of Trauma Surgery) with respect to frequency, risk stratification and therapeutic options of acute traumatic coagulopathy (ATC).

Methods: The synopsis of different analyses based upon the datasets from severe multiply injured patients derived from the TR-DGU database and development/validation of a scoring system (TASH-score = Trauma Associated Severe Hemorrhage) that allows an early and reliable estimation for the probability of massive transfusion as a surrogate for life-threatening hemorrhage after severe multiple injuries.

Results: The high frequency of ATC upon emergency room admission is associated with significant morbidity and mortality in multiply injured patients. The TASH-score is recognized as an easy-to-calculate and valid scoring system to predict the individual's probability for massive transfusion and thus ongoing life-threatening hemorrhage at a very early stage after severe multiple injuries.

Conclusion: An early aggressive management of ATC including a more balanced administration of blood products to improve outcome is advocated.

Keywords: Coagulopathy; Epidemiology; Management; Risk stratification; Trauma.

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Conflict of interest statement

Competing interest: There are no conflicts of interest associated with this article.

Figures

Figure 1
Figure 1
Potential mechanisms underlying ATC. Besides dilutional coagulopathy, hemorrhage may also induce shock followed by acidemia and hypothermia, further triggering coagulopathy to form the so-called “lethal triad”. Trauma with shock, hypoperfusion and hypoxia can also cause ATC associated with further consumption and hyperfibrinolysis. The clinical importance of inflammation for the development of ATC has not yet been fully understood.[4]
Figure 2
Figure 2
The incidence of ATC in subgroups according to ISS (4 subgroups) and intravenous fluids administered during the pre-hospital phase of care (5 subgroups). Each line represents a group of patients with a similar ISS score, while each vertical group represents patients who had received comparable amounts of intravenous fluids during the pre-hospital phase of care. Sample sizes for the groups ranged between 68 and 1439 patients.
Figure 3
Figure 3
The mortality of patients with and without ATC on ER arrival according to the severity of injury as reflected by ISS.
Figure 4
Figure 4
Incidence of ATC as a function of BE on ER arrival.
Figure 5
Figure 5
TASH-score. The TASH-score of 18 equals to a 50% risk for massive transfusion (MT) after severe multiple injuries.
Figure 6
Figure 6
An example for the clinical application of the TASH-score to identify patients at risk for MT.
Figure 7
Figure 7
Clinical strategy for blood volume replacement during the first 24 hours after injury including triggering values for the administration of specific blood components. Recent studies have suggested a more aggressive coagulation management with different components administered early and in a balanced ratio. Antifibrinolytic agents (e.g. tranexamic acid, e-aminocaproic acid) should be considered in the treatment of the bleeding trauma patient but should be stopped once the bleeding is adequately controlled. PCC should be used for the emergency reversal of vitamin-K-dependent oral anticoagulants only; there is no place for the use of AT III in the treatment of the bleeding trauma patient. FFP:fresh frozen plasma; Fg: fibrinogen; Hb:haemoglobin; Hct:hematocrit; Plts:platelets; pRBC:packed red blood cells; PT:prothrombin time; aPTT:activated partial thromboplastin time; rFVIIA:recombinant factor Vila; TBI:traumatic brain injury (adopted/modified from[14])
Figure 8
Figure 8
Mortality rates for patients transfused at different pRBC:FFP ratios during acute care. Early (< 6-hour and < 24-hour) and 30-day mortality rates in percent (%) for patients transfused at a pRBC:FFP ratio of > 1:1, a pRBC:FFP ratio of 0.9-1.1 (1:1), and a pRBC:FFP ratio of < 0.9 during immediate care.

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