Acidosis, coagulopathy, and hypothermia occurring together in a trauma casualty is referred to as the lethal triad.

Acidosis is most commonly the result of lactic acid buildup as cells revert to anaerobic processes in the absence of adequate cellular oxygenation (or shock). Sometimes there is a respiratory contribution if the respiratory drive is blunted and there is a buildup of carbon dioxide, but the metabolic acidosis from lactic acid buildup in trauma tends to be the predominant issue.

Coagulopathy can result from direct losses of clotting factors and platelets due to massive hemorrhage but can be accentuated by hemodilution if fluids are replaced by crystalloid or colloid fluids that do not replace clotting factors and platelets like you would get from using whole blood transfusions as fluid replacement therapy. Additionally, the function of clotting factors is temperature-dependent and hypothermia leads to clotting factor dysfunction, even if there is an adequate quantity.

Hypothermia results from a combination of environmental factors (exposure, even in warmer climates) and physiologic responses to blood loss. As mentioned previously, the functions of the clotting cascade are impaired in hypothermia, and further blood loss from coagulopathy leads to increasing hypothermia. This vicious cycle of acidosis, hypothermia, and coagulation (or the lethal triad) requires prevention management strategies at each level.

In other words, prevent and/or treat hypothermia, as we’ll discuss in module 12, prevent acidosis by correcting hypovolemia with fluids that support increased oxygenation (in particular, blood products), and prevent coagulopathy by decreasing direct losses from hemorrhage and clotting factor dysfunction by treating hypothermia.