Acute traumatic coagulopathy: pathophysiology and resuscitation

Area of Science:

• Trauma and Emergency Medicine
• Hematology
• Physiology

Background:

• Acute traumatic coagulopathy (ATC) arises immediately post-trauma due to shock, hypoperfusion, and vascular damage.
• Key mechanisms include protein C activation, endothelial glycocalyx disruption, fibrinogen depletion, and platelet dysfunction.
• Hypothermia and acidaemia exacerbate ATC, leading to reduced clot strength, autoheparinization, and hyperfibrinolysis.

Purpose of the Study:

• To review normal hemostasis using the cell-based model.
• To elucidate the pathophysiology of ATC.
• To highlight critical goals and early identification triggers for massive transfusion in trauma care.

Main Methods:

• Review of normal coagulation and ATC pathophysiology.
• Identification of clinical triggers for massive transfusion (e.g., base deficit, INR, systolic blood pressure).
• Explanation of damage control resuscitation strategies.

Main Results:

• ATC involves multiple factors that decrease clot strength and promote bleeding.
• Early identification of massive transfusion needs is crucial for reducing trauma mortality.
• Damage control resuscitation (DCR) addresses hemostatic derangements.

Conclusions:

• ATC is a complex, multifactorial condition requiring prompt management.
• Developed trauma systems and early recognition of massive transfusion needs improve outcomes.
• Damage control resuscitation is a key strategy for managing severe hemorrhage in trauma patients.