Brain hypoxia associated with poor short-term outcome after severe TBI

Low oxygen supply (hypoxia) to vulnerable brain tissue is a major contributor to the risk of death or major disability after severe traumatic brain injury (TBI), reports a study in the November issue of Neurosurgery, official journal of the Congress of Neurological Surgeons. The journal is published by Lippincott Williams & Wilkins, a part of Wolters Kluwer Health.

Led by Dr. Mauro Oddo of University of Pennsylvania Medical Center, Philadelphia, the researchers write, "Brain hypoxia is associated with poor short-term outcome after severe TBI"—independent of other factors like intracranial pressure and cerebral perfusion pressure (i.e. brain blood flow). The results support a recent guideline revision calling for monitoring of brain oxygenation during intensive care for patients with severe head injury.

Brain Hypoxia Linked to Increased Risk of Death or Severe Disability
Dr. Oddo and colleagues looked at how brain hypoxia affected clinical outcomes in 103 patients with TBI. Most of the patients had bleeding within the brain after severe, blunt head trauma. In addition to sensors placed for routine monitoring of intracranial (within the skull) pressure and brain blood flow, all patients underwent monitoring of brain oxygenation.

If the oxygen supply fell below a certain critical level, the patient was considered to have brain hypoxia. The relationship between brain hypoxia and the outcomes of TBI was assessed. Forty-three percent of patients had poor outcomes: death or survival with severe disability or in a vegetative state.

The greater the drop in brain oxygenation, the higher the risk of poor outcomes. The average length of time with brain hypoxia was 8.3 hours for patients with poor outcomes after TBI, compared to 1.7 hours for those with good outcomes—survival with no or moderate disability.

High intracranial pressure is traditionally regarded as a bad prognostic sign for patients with TBI. Among the patients in the study with high intracranial pressure, only 46 percent of those with brain hypoxia had good outcomes, compared to 81 percent of those without brain hypoxia.

Brain oxygenation was also a stronger outcome predictor than cerebral perfusion pressure. Some patients had good brain oxygenation, despite reduced brain blood flow, while maintaining presently recommended levels of cerebral perfusion pressure was sometimes insufficient to avoid low brain oxygenation.

After adjustment for these and other important risk factors, brain oxygenation was a significant and independent predictor of patient outcomes. For each additional hour with brain hypoxia, the risk of poor outcomes increased by 11 percent.

Delayed brain damage occurring in the hours and days after TBI is a major contributor to death and disability. Recently revised guidelines have recommended that patients with severe TBI should undergo monitoring of brain oxygenation—technically called interstitial partial pressure of oxygen in brain tissue. However, it has been unclear whether this provides important additional information, beyond that supplied by monitoring intracranial pressure or brain blood flow—or whether hypoxia is just an indicator of more severe brain injury.

The new study strongly suggests that TBI patients with longer periods of brain hypoxia are more likely to have poor outcomes, independent of intracranial pressure, brain blood flow, and other risk factors. The findings support the recent recommendations adding brain oxygen monitoring after severe TBI, as part of an integrated monitoring strategy. However, more research will be needed to determine whether treatment adjustments in response to brain oxygenation monitoring lead to any improvement in patient outcomes.