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Uncontrolled hemorrhage is the most common cause of death in trauma patients admitted to the hospital, with a 30% mortality rate in those carrying the diagnosis. Additionally, nearly one in four trauma patients is coagulopathic upon arrival, making appropriate and expedient delivery of blood products and adjuncts paramount to their survival. As a result, most trauma centers have developed and maintain massive transfusion protocols (MTPs) that specify preset volumes and ratios of blood products to be rapidly available when needed. These protocols also contain standardized, efficient lines of communication between the emergency department, operating room, and blood bank. In this chapter, we will discuss the etiology of trauma-induced coagulopathy (TIC), blood typing and the implications of uncrossmatched blood transfusions, currently accepted ratios of blood products for transfusion, and possible adjuncts to blood products during massive transfusion.

Massive transfusion (MT) has many definitions in the literature, but the three most commonly agreed upon center around the amount of blood products given over a specified period of time. In adults, “massive transfusion” is diagnosed if any of the following criteria are met: transfusion of 10 or more units of packed red blood cells (PRBC) within 24 hours, transfusion of more than four units PRBCS in 1 hour with a need for ongoing transfusion, or replacement of 50% of the patient’s total blood volume (TBV) within 3 hours. The pediatric definitions of MT focus on TBV with the diagnosis established when one or more of the following occur: replacement of greater than 100% TBV within 24 hours, greater than 10% TBV per minute, or greater than 50% TBV within 3 hours defining massive transfusion.

The need for MT is more complicated than simple hemorrhagic, hypovolemic shock. Patients involved in major trauma also suffer from a multifactorial, trauma-induced coagulopathy. Previously this was attributed to a combination of hemodilution from crystalloids both prior to and following arrival in the emergency department, progressive hypothermia from patient exposure and large volume resuscitation without adequate fluid warming, and a persistent metabolic acidosis caused by end-organ hypoperfusion secondary to hypotension as well as the acidic nature of many resuscitation fluids. While these factors certainly contribute to trauma-induced coagulopathy, more extensive research demonstrates as many as 24%–56% of patients are coagulopathic on arrival to the hospital, even those who are initially hemodynamically stable and have not received crystalloid resuscitation.

The mechanism of this coagulopathy centers on impaired thrombus creation and stability. Hypoperfusion activates thrombomodulin expression on endothelial cells and Protein C activation from the subsequent thrombin–thrombomodulin complex results in inactivation of factors V and VIII by proteolysis, leading to decreased thrombus generation. Protein C also binds plasminogen activator inhibitor (PAI-1) which reduces t-PA inhibition and results in unregulated plasmin creation and subsequently to increased clot lysis. Decreased clot stability fuels a consumptive coagulopathy and a reduction in available clotting factors, fibrinogen, and platelets. The data also suggests that trauma may result in decreased ...

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