Coagulation Perturbations After Severe Injury: Translational Approaches and the State of the Science

Abstract

Despite evidence of acute traumatic coagulopathy hiding in plain site for decades, coagulopathy after trauma was thought to result from the iatrogenic effects of otherwise well-intentioned resuscitation. The luminary shock research of the late 1960s and early 1970s combined with advances in blood banking result in a cold red blood cell and crystalloid-based resuscitation practice which prevailed for decades. Indeed, the initial groundbreaking work on hemorrhagic shock revealed that shocked patients required both oxygen carrying capacity and blood flow (pressure) for survival [1–3]. While much of this early work was done in the era of whole blood, this was largely forgotten as a result of the contemporaneously timed move away from whole blood transfusion toward component therapy. Beginning in the mid-1970s, the blood banking community realized that they could component separate whole blood thereby taking a unit of whole blood and converting it to components; one unit of packed red blood cells (PRBCs) one unit of fresh frozen plasma (FFP) some part of a unit of platelets with the remainder becoming cryoprecipitate consisting of concentrated factors and fibrinogen. The white blood cells were spun or filtered off variably during the process. These changes which were initially made for resource allocation and financial reasons were solidified in the early 1980s by the emergence of HIV and concerns about the safety of the blood supply. Hence the new understanding from research on shock that our patients need oxygen carrying capacity and flow and left with components in the blood bank and crystalloid on the shelf our resuscitation practices evolved toward the delivery of large volumes of cold packed red blood cells and many liters of salt water. It was for decades common to resuscitate severely injured patients with multiple units of packed red blood cells and many liters of crystalloid with little to no attention paid to coagulation measures or any need for plasma or platelets. These resuscitation practices resulted in the creation of or exacerbation of iatrogenic coagulopathy characterized by dilution, hypothermia, and acidosis described below.