Traumatic brain injury
Brain tissue oxygen monitoring
M. Sean Grady
Ross P. Martini, Steven Deem, N. David Yanez, Randall M. Chesnut, Noel S. Weiss, Stephen Daniel, Michael Souter, and Miriam M. Treggiari
The authors sought to describe changes in clinical management associated with brain tissue oxygen (PbO2) monitoring and how these changes affected outcomes and resource utilization.
The cohort study comprised 629 patients admitted to a Level I trauma center with a diagnosis of severe traumatic brain injury over a period of 3 years. Hospital mortality rate, neurological outcome, and resource utilization of 123 patients who underwent both PbO2 and intracranial pressure (ICP) monitoring were compared with the same measures in 506 patients who underwent ICP monitoring only. The main outcomes were hospital mortality rate, functional independence at hospital discharge, duration of mechanical ventilation, hospital length of stay, and hospital cost. Multivariable regression with robust variance was used to estimate the adjusted differences in the main outcome measures between patient groups. The models were adjusted for patient age, severity of injury, and pathological features seen on head CT scan at admission.
On average, patients who underwent ICP/PbO2 monitoring were younger and had more severe injuries than patients who received ICP monitoring alone. Relatively more patients treated with PbO2 monitoring received osmotic therapy, vasopressors, and prolonged sedation. After adjustment for baseline characteristics, the hospital mortality rate was, if anything, slightly higher in patients undergoing PbO2-guided management than in patients monitored with ICP only (adjusted mortality difference 4.4%, 95% CI −3.9 to 13%). Patients who underwent PbO2-guided management also had lower adjusted functional independence scores at hospital discharge (adjusted score difference −0.75, 95% CI −1.41 to −0.09). There was a 27% relative increase (95% CI 6–53%) in the median hospital length of stay when the PbO2 group was compared with the ICP-only group.
The mortality rate in patients with traumatic brain injury whose clinical management was guided by PbO2 monitoring was not reduced in comparison with that in patients who received ICP monitoring alone. Brain tissue oxygen monitoring was associated with worse neurological outcome and increased hospital resource utilization.
Ross P. Martini, Jonathan Ward, Dominic A. Siler, Jamie M. Eastman, Jonathan W. Nelson, Rohan N. Borkar, Nabil J. Alkayed, Aclan Dogan, and Justin S. Cetas
Patients with aneurysmal subarachnoid hemorrhage (SAH) are at high risk for delayed cerebral ischemia (DCI) and stroke. Epoxyeicosatrienoic acids (EETs) play an important role in cerebral blood flow regulation and neuroprotection after brain injury. Polymorphisms in the gene for the enzyme soluble epoxide hydrolase (sEH), which inactivates EETs, are associated with ischemic stroke risk and neuronal survival after ischemia. This prospective observational study of patients with SAH compares vital and neurologic outcomes based on functional polymorphisms of sEH.
Allelic discrimination based on quantitative real-time polymerase chain reaction was used to differentiate wild-type sEH from K55R heterozygotes (predictive of increased sEH activity and reduced EETs) and R287Q heterozygotes (predictive of decreased sEH activity and increased EETs). The primary outcome was new stroke after SAH. Secondary outcomes were death, Glasgow Outcome Scale score, and neurological deterioration attributable to DCI.
Multivariable logistic regression models adjusted for age at admission and Glasgow Coma Scale scores revealed an increase in the odds of new stroke (OR 5.48 [95% CI 1.51–19.91]) and death (OR 7.52 [95% CI 1.27–44.46]) in the K55R group, but no change in the odds of new stroke (OR 0.56 [95% CI 0.16–1.96]) or death (OR 3.09 [95% CI 0.51–18.52]) in patients with R287Q genotype, compared with wild-type sEH. The R287Q genotype was associated with reduced odds of having a Glasgow Outcome Scale score of ≤ 3 (OR 0.23 [95% CI 0.06–0.82]). There were no significant differences in the odds of neurological deterioration due to DCI.
Genetic polymorphisms of sEH are associated with neurological and vital outcomes after aneurysmal SAH.