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The biggest contributor to coagulopathies after brain death is the release of thromboplastin. When brain death occurs, there is significant stimulation of the coagulation cascade, partly due to the release of tissue factor (also known as thromboplastin), which initiates the extrinsic pathway of coagulation. This release leads to the activation of various coagulation factors, resulting in a hypercoagulable state, and can eventually shift to a coagulopathy as the body responds to the imbalance, especially in cases where organ perfusion is compromised.

While blood loss can contribute to coagulopathies, it is not a primary factor immediately following brain death. Platelet dysfunction can occur, but it is not the initial trigger of coagulopathy in this context. Vitamin K deficiency, which affects the synthesis of certain clotting factors, generally takes time to develop and is not an immediate consequence after brain death. Thus, the release of thromboplastin stands out as the most significant factor influencing coagulopathies post-brain death.