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Burn injury is traditionally referred to as a common triggering cause of acute coagulopathy, ranging from subclinical activation of coagulation to fulminant overt Disseminated Intravascular Coagulation (DIC). Coagulopathy associated with burn injury was well recognized as early as the 1970s.1,2 Coagulopathy in burn patients is considered to be driven by an endothelial injury, release of tissue factor and inflammatory cytokines.3 Blood loss, hypovolaemia or excessive volume expansion, hypothermia and acidosis further aggravate the situation.4-6 Coagulation system activation is characterized initially by thrombin generation, hypercoagulability and hyperfibrinosysis.7 Activation of both thrombosis and fibrinolysis and increased consumption of coagulation factors leads thereafter to the development of consumption coagulopathy.3,6-8 The coagulation system abnormalities may be further enhanced by surgery; wound excision may be associated with extensive blood loss, dilution and consumption of coagulation factors which may have an additional negative impact on the coagulation system. Additionally, the activation of inflammatory and coagulation cascade in septic burn patients can lead to microvascular injury and subsequent multiple organ dysfunction or failure.3,6 The literature on coagulopathy in burn patients is relatively Annals of Burns and Fire Disasters Pending Publication