Cerebral Oximetry and Perioperative Outcome in Non-Cardiac Surgery

There have been a number of studies that have examined a link between intraoperative decreases in rSO2 and adverse perioperative outcome3-7. These studies, the vast majority of which have been in the setting of cardiac surgery, suggest that decreases in rSO2 (as detected by near-infrared spectroscopy) may be related to both adverse neurologic and non-neurologic sequelae. Interestingly, and importantly, the studies examining cerebral desaturation in non-cardiac surgical patients (such as those undergoing major abdominal surgery, carotid endarterectomy, liver transplantation, and pulmonary resection) have also uncovered a link between cerebral desaturation and non-neurologic outcomes3,7-12. These small studies have reported preliminary correlates between decreases in rSO2 and various postoperative complications and prolonged length of stay. These studies have also shown that the changes in rSO2 are not correlated with changes in traditional hemodynamic parameters (mean arterial pressure (MAP) and heart rate).

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.

As a result, two natural questions arise in relation to this prior research. First, are these cerebral desaturations causative of the adverse outcomes (including non-neurologic complications), 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)? Numerous studies have demonstrated the poor correlation of traditional hemodynamic parameters (such as blood pressure and heart rate) to cardiac output and oxygen delivery13-17. Historically in the fields of anesthesiology and critical care, we have focused our monitoring and resuscitation targets on perfusion pressures rather than organ flows. Neglecting the fact that organs require flow as well as pressure has led to an over-reliance on normal vascular pressures (such as arterial, central venous, and pulmonary capillary wedge pressures) as a surrogate for adequate organ flow18.

It is entirely possible that monitoring cerebral oxygenation and discovering a link between desaturation and non-neurologic outcomes may show that the brain is an index organ for tissue perfusion monitoring. That is to say, since the perfusion of major organs are typically not monitored during anesthesia, cerebral oximetry is an excellent means to monitor global decreases in tissue oxygen delivery. 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 morbidity19.

The investigators will also be collecting blood samples preoperatively and at 24 hours postoperatively to determine if a panel of inflammatory biomarkers has the ability to predict postoperative complications.