Defining the Lethal Triad

Abstract

Worldwide, trauma leads to millions of deaths and severe injuries each year. Analysis of the leading causes of death in trauma patients reveals that hemorrhage is one of the most common and preventable etiologies in the acute period [1]. For those that survive the initial insult, the cause of both morbidity and late mortality after trauma is, in part, excessive inflammation and a vicious cascade of coagulation abnormalities. Thus, traumatic hemorrhage can be broadly categorized into two groups: (1) early surgical bleeding and (2) coagulopathy. Surgical bleeding is secondary to the injury (e.g., splenic laceration, femur fracture), and treatment often involves mechanical control through surgical or interventional procedures. Coagulopathy following trauma presents in two distinct forms. It is now widely recognized that severe injury is characterized by a unique, endogenous coagulopathy, referred to as the acute traumatic coagulopathy (ATC) that may be present on admission in as many as 30% of injured patients [2]. This devastating condition presents a major obstacle in the care of trauma patients and is an evolving area of active research. The second form of coagulopathy following trauma is a consequence of iatrogenic factors and resuscitation. Previous resuscitation strategies involving large volumes of crystalloid and/or packed red blood cells in isolation (without blood component therapy) led to a dilutional coagulopathy. Although this remains a clinically important challenge, modern resuscitation strategies that limit crystalloid and focus on 1:1:1 ratio-based transfusion have limited this component substantially [3, 4]. In this chapter, we will focus on the previously named “lethal triad” which links coagulopathy with hypothermia and acidosis as major contributors to the ongoing hemorrhage despite control of surgical bleeding.