Abstract

Accidental hypothermia is a common complication in severely injured patients. Risk factors include environmental exposure of the patient at the accident site or in the clinic, infusion of cold fluids, hemorrhagic shock and anesthetics which influence thermoregulation. In contrast to animal studies, human studies and clinical experiences have identified accidental hypothermia of the severely injured patient to be associated with increased complication and mortality rates. As a consequence, hypothermia together with acidosis and coagulopathy, have been coined the lethal triad in severely injured patients. On a cellular level hypothermia reduces cellular activity and metabolism resulting in reduced oxygen consumption, which is therapeutically used in patients following cardiac arrest. However, the activity of important enzymes, such as those of the coagulation pathway, is simultaneously down regulated. Hypothermia-induced coagulopathy, which is refractory to substitution of coagulation factors, is a major complication of hypothermia in traumatized patients. Therefore, hypothermic trauma patients with hemodynamic instability require aggressive rewarming.

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