The Incidence and Magnitude of Cerebral Desaturation in Traumatic Brain Injury (TBI) Patients

In patients who have suffered a traumatic brain injury, the current management strategies focus on the maintenance of normotension and normoxia and a normalized intracranial pressure (ICP). Recent evidence calls into question the utility of ICP monitoring in these patients. More advanced cerebral monitoring such as the use of invasive brain tissue oxygen monitors have not found their way into widespread clinical practice. Cerebral oximetry monitoring utilizes the different absorption characteristics of oxygenated and deoxygenated blood to measure global brain oxygen levels.

While clinicians have no ability to reverse the primary brain injury, they can mitigate the secondary injury effects, namely hypoxia and hypotension. It is well known that maintaining normal blood pressure and oxygen saturation can prevent secondary brain injury. However, it is also known that despite the appearance of normal hemodynamics, brain oxygen delivery in the ischemic penumbra may be inadequate. This secondary brain injury is likely related to decreases in cerebral oxygenation (rSO2).

There have been a number of studies that have examined a link between intraoperative decreases in rSO2 and adverse perioperative outcome. These studies suggest that decreases in rSO2 may be related to both adverse neurologic and non-neurologic sequelae. All of these studies suffer from similar flaws, however. They are typically small in size, have varying definitions of what constitutes a cerebral desaturation event, and have incompletely, or poorly defined complications. Also lacking is a mechanistic explanation for the cerebral desaturations as peripheral oxygen saturation typically remains near normal.

The brain can be considered the organ of highest priority when it comes to tissue hypoperfusion during shock states. When oxygen delivery to the brain is decreased below a critical value, cerebral desaturations occur. In the context of TBI, cerebral desaturation may be the hallmark of secondary injury. Consistent with this hypothesis, in the largest cerebral oximetry trial to date, Murkin and colleagues discovered that the incidence and magnitude of cerebral desaturations was related to major non-neurologic organ morbidity.

Two questions arise in relation to this prior research. First, are these cerebral desaturations causative of the adverse outcomes, and second if these desaturations were treated (i.e. if cerebral oxygenation was normalized) would outcome be improved (i.e. or are cerebral desaturations merely an epiphenomenon)?