Therapeutic Hypothermia in Trauma Management: New Tricks for an Old Dog?
Neurologic injury is the most common cause of death in patients with out-of-hospital cardiac
arrest (OHCA) and contributes to the mortality of in-hospital cardiac arrest.
Neural tissue is damaged in traumatic injury as well. Traumatic brain injury
(TBI) may be classified based on severity, ranging from ‘mild’ to ‘severe’, most commonly
based on the Glasgow Coma Scale (GCS). There are two injury phases in TBI.
Primary injury occurs immediately at the time of impact, and includes the tear,
shear or hemorrhage due to the acceleration-deceleration
or rotational forces.
The process triggers multiple biochemical cascades in hours or days, which is
termed secondary brain injury.
Evolution of secondary damage mechanisms has been studied many times in the experimental
setting, and can be divided into three distinct phases: acute, sub-acute and chronic.
In another point of view, these hazards include ischaemic, cytotoxic and
inflammatory processes.
The immediate interventions in TBI comprise ensuring maintenance of perfusion of
the brain with oxygenated blood. ‘Airway, breathing, circulation’ confers to this prioritization.
Post-TBI cerebral ischemia may occur due to a combination of mechanical vessel distortion,
hypotension, loss of cerebral blood flow autoregulation, insufficient nitric oxide or vasospasm.
Therapeutic hypothermia may offer the prospect of an extended window
to restore the integrity of circulation,
with the brain maintained in a protective,
hypometabolic state.
The promising idea of ‘human refrigeration’ was advocated first for the management
of TBI and brain tumours by Fay in the 1940’s who reported its application in 124 cases.
Emerg Med Open J. 2017; 3(2): 30-37. doi: 10.17140/EMOJ-3-137
