Abstract
Acute traumatic coagulopathy (ATC) is an acute and endogenous mechanism triggered by the association of trauma and hemorrhage. Several animal models have been developed, but some major biases have not yet been identified. Our aim was to develop a robust and clinically relevant murine model to study this condition. Anesthetized adult Sprague Dawley rats were randomized into 4 groups: C, control; T, trauma; H, hemorrhage; TH, trauma and hemorrhage (n = 7 each). Trauma consisted of laparotomy associated with four-limb and splenic fractures. Clinical variables, ionograms, arterial and hemostasis blood tests were compared at 0 and 90 min. ATC and un-compensated shock were observed in group TH. In this group, the rise in prothrombin time and activated partial thromboplastin was 29 and 40%, respectively. Shock markers, compensation mechanisms and coagulation pathways were all consistent with human pathophysiology. The absence of confounding factors, such as trauma-related bleeding or dilution due to trans-capillary refill was verified. This ethic, cost effective and bias-controlled model reproduced the specific and endogenous mechanism of ATC and will allow to identify potential targets for therapeutics in case of trauma-related hemorrhage.
Highlights
Every year, 5.6 million people die worldwide as a result of trauma
acute traumatic coagulopathy (ATC) is defined as an increase in prothrombin time (PT) and/or activated partial thromboplastin time due to the combination of trauma and hemorrhage
This coagulation disorder was induced by the association of trauma and hemorrhage because no statistical difference between C, T and H groups was retrieved for these variables (p > 0.05, Fig. 3A–D)
Summary
5.6 million people die worldwide as a result of trauma. The four leading causes of trauma are road traffic injuries, self-inflicted violence, inter personal violence and falls, responsible for 25, 16, 10 and 6% of death, respectively. If compensation mechanisms are overwhelmed, arterial blood pressure decreases and death occurs due to the inability to maintain tissue perfusion in critical organs. An acute traumatic coagulopathy (ATC) dramatically increases blood losses This specific coagulation disorder develops extremely quickly in the first 60 minutes after trauma and is detected in approximately one third of multiple injured patients upon hospital admission[7,8,9]. In one of them, ATC was triggered by a tissue factor infusion without trauma This mechanism was not similar to real-life patients[25]. They were not focused on the endogenous mechanism[26,27,33,34]
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