Hemorrhagic blood failure: Oxygen debt, coagulopathy, and endothelial damage

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Trauma is responsible for 1 in 10 deaths worldwide and is the leading cause of death of people less than 45 years old.1 The two most common causes of death in trauma victims are brain injury and hemorrhage.2 Hemorrhage accounts for the preponderance (~60%) of deaths in patients with potentially salvageable injuries (~50% of those injured), amounting to about one third of trauma deaths.1 Over 90% of potentially survivable US military combat deaths are attributed to hemorrhage.3 The majority of all victims who die from hemorrhage will die within the first several hours after injury, indicating that a great number of them could be rescued if hemorrhage could be stopped quickly.4,5
Impaired clot formation, or coagulopathy, that increases bleeding is also present in 20% to 30% of severely injured trauma patients immediately after injury and is associated with increased incidence of multi-organ failure, intensive care utilization, and death.6 Traumatic coagulopathy is a distinct and multilayered biochemical response to tissue injury and hemorrhagic shock.7 When present on arrival to the Emergency Department, coagulopathy is associated with four- to sixfold increased mortality.8 The pathophysiology of traumatic coagulopathy is now recognized to be multifactorial and networked in nature, consisting of contrasting coagulation states that produce an emergent syndrome that contributes to failure of the vital functions of the blood.
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