Speakers
Dr. Raymond Siu-Ming WONG
Hong Kong
Dr. Raymond Wong is Consultant in the Department of Medicine & Therapeutics at the Prince of Wales Hospital and the Head of the Cluster Clinical Haematology Unit of the New Territories East Cluster, Hospital Authority. He is also Honorary Clinical Associate Professor and Head of the Division of Haematology at the Department of Medicine & Therapeutics of the Chinese University of Hong Kong.
Dr. Wong has been playing a pivotal role in haematology and transfusion practice in the public hospital system in Hong Kong. He is currently the Convenor of the Haematology Working Group and the Chairman of the Central Committee on Transfusion Service. He is also the co-chairperson of the Expert Panel on Patient Blood Management.
Dr. Wong is the President-elect of the Asia-Pacific Society on Thrombosis & Hemostasis. He is author or co-author of more than 150 peer-reviewed articles published in international journals including Blood, Circulation, JAMA and the New England Journal of Medicine.
Trauma-induced coagulopathy describes abnormal coagulation processes that are attributable to trauma. In the early hours of development, hypocoagulability is typically present, resulting in bleeding, whereas later stage is characterized by a hypercoagulable state associated with venous thromboembolism and multiple organ failure. Several pathophysiological mechanisms including tissue injury and shock synergistically provoke endothelial, immune system, platelet and clotting, underlie trauma-induced coagulopathy. Haemostatic abnormalities include fibrinogen depletion, inadequate thrombin generation, impaired platelet function and dysregulated fibrinolysis.
The acute coagulopathy after trauma has several “exogenous” causes: firstly, loss and consumption of coagulation factors due to bleeding; secondly, dilution of coagulation factors due to fluid therapy; and thirdly, dysfunction of coagulation factors due to hypothermia and acidosis. The trauma-induced coagulopathy of “endogenous” origin is considered to be triggered by the release of tissue factor from traumatized tissue, causing localized activation of coagulation factors with accompanying consumption of platelets and fibrinogen. Additionally, impaired tissue perfusion triggers an increased expression of thrombomodulin and thus activity of protein C, resulting in systemic anticoagulation and increased fibrinolysis. Fibrinogen is central to trauma-induced coagulopathy and low level is related to the grade of injury, shock, blood loss, and mortality.
Trauma-induced coagulopathy is not a uniform phenotype but a spectrum ranging from thrombotic to bleeding phenotypes. Advances in point-of-care coagulation testing, and availability of coagulation factors and fibrinogen concentrates allows clinicians to employ a more goal-directed approach.
