Hypothermia in multisystem trauma

Abstract

Exsanguinating hemorrhage is a common clinical feature of multisystem trauma that results in death or severe disability. Cardiovascular collapse resulting from hemorrhage is unresponsive to conventional methods of cardiopulmonary resuscitation. Even when bleeding is controlled rapidly, adequate circulation cannot be restored in time to avoid neurologic consequences that appear after only 5 mins of cerebral ischemia and hypoperfusion. Reperfusion adds further insult to injury. A novel solution to this problem would be to institute a therapy that makes cells and organs more resistant to ischemic injury, thereby extending the time they can tolerate such an insult. Hypothermia can attenuate some effects of ischemia and reperfusion. Accumulating preclinical data demonstrate that hypothermia can be induced safely and rapidly to achieve emergency preservation for resuscitation during lethal hemorrhage. Hypothermia may be an effective therapeutic approach for otherwise lethal traumatic hemorrhage, and a clinical trial to determine its utility is warranted.

Pre-Hospital Hypothermia is Not Associated with Increased Survival After Traumatic Brain Injury

“…In fact, the majority of systematic reviews examining the effects of induced hypothermia after TBI have failed to note a consistent benefit in terms of functional outcomes or survival [43][44][45][46]. While induced hypothermia is associated with normal cellular energy reserves, spontaneous hypothermia that develops in trauma patients is usually caused by severe tissue ischemia, environmental exposure, infusion of cold intravenous fluids/blood products, and heat loss from open body cavities [9,10]. Spontaneous hypothermia in the setting of trauma is frequently an ominous sign and has been well described in the literature as part of the lethal triad (hypothermia, acidosis, and coagulopathy) [9,10,12,[47][48][49].…”

“…Spontaneous hypothermia in the setting of trauma is frequently an ominous sign and has been well described in the literature as part of the lethal triad (hypothermia, acidosis, and coagulopathy) [9,10,12,[47][48][49]. Its presence signifies advanced tissue ischemia, depletion of energy substrates, failed homeostatic mechanisms to maintain normothermia, as well as impending development of recalcitrant coagulopathy due to increased fibrinolysis, thrombocytopenia, platelet dysfunction, and endothelium abnormalities [9,12]. Uncontrolled hypothermia could exacerbate the early and deadly coagulopathy that has been documented to occur in patients with TBI, particularly when hypoperfusion is present [50,51].…”

“…While induced hypothermia is associated with normal cellular energy reserves, spontaneous hypothermia that develops in trauma patients is usually caused by severe tissue ischemia, environmental exposure, infusion of cold intravenous fluids/blood products, and heat loss from open body cavities [9,10]. Spontaneous hypothermia in the setting of trauma is frequently an ominous sign and has been well described in the literature as part of the lethal triad (hypothermia, acidosis, and coagulopathy) [9,10,12,[47][48][49]. Its presence signifies advanced tissue ischemia, depletion of energy substrates, failed homeostatic mechanisms to maintain normothermia, as well as impending development of recalcitrant coagulopathy due to increased fibrinolysis, thrombocytopenia, platelet dysfunction, and endothelium abnormalities [9,12].…”

“…Induced hypothermia is implemented in a controlled fashion for cytoprotection during ischemia and reperfusion, and has been documented in neurosurgical and cardiovascular surgery, as well as post-cardiac arrest patients [9][10][11][12][13][14].…”

Potential role of therapeutic hypothermia in the salvage of traumatic hemorrhagic shock

“…Up to now, it has been broadly used in cardiovascular surgery but has also been recommended for treatment of cardiac arrest, severe traumatic brain injury, near-drowning, ischemic stroke, neonatal hypoxic-ischemic encephalopathy, and spinal cord injury [8,9]. Recent studies have focused on its potential role in traumatic HS [10,11]. However, due to differences in methodology and animal models, the results remain inconclusive.…”