Cerebral autoregulation may be altered after traumatic brain injury (TBI). Recent evidence suggests that patients' autoregulatory status following severe TBI may influence cerebral perfusion pressure management. The authors evaluated the utility of incorporating a recently upgraded parenchymal thermal diffusion probe for the measurement of cerebral blood flow (CBF) in the neurointensive care unit for assessing cerebral autoregulation and vasoreactivity at bedside.
The authors evaluated 20 patients with severe TBI admitted to San Francisco General Hospital who underwent advanced neuromonitoring. Patients had a parenchymal thermal diffusion probe placed for continuous bedside monitoring of local CBF (locCBF) in addition to the standard intracranial pressure and brain tissue oxygen tension (PbtO2) monitoring. The CBF probes were placed in the white matter using a separate cranial bolt. A pressure challenge, whereby mean arterial pressure (MAP) was increased by about 10 mm Hg, was performed in all patients to assess autoregulation. Cerebral CO2 vasoreactivity was assessed with a hyperventilation challenge. Local cerebral vascular resistance (locCVR) was calculated by dividing cerebral perfusion pressure by locCBF. Local cerebral vascular resistance normalized to baseline (locCVRnormalized) was also calculated for the MAP and hyperventilation challenges.
In all cases, bedside measurement of locCBF using a cranial bolt in patients with severe TBI resulted in correct placement in the white matter with a low rate of complications. Mean locCBF decreased substantially with hyperventilation challenge (−7 ± 8 ml/100 g/min, p = 0.0002) and increased slightly with MAP challenge (1 ± 7 ml/100 g/min, p = 0.17). Measurements of locCBF following MAP and hyperventilation challenges can be used to calculate locCVR. In 83% of cases, locCVR increased during a hyperventilation challenge (mean change +3.5 ± 3.8 mm Hg/ml/100 g/min, p = 0.0002), indicating preserved cerebral CO2 vasoreactivity. In contrast, we observed a more variable response of locCVR to MAP challenge, with increased locCVR in only 53% of cases during a MAP challenge (mean change −0.17 ± 3.9 mm Hg/ml/100 g/min, p = 0.64) indicating that in many cases autoregulation was impaired following severe TBI.
Use of the Hemedex thermal diffusion probe appears to be a safe and feasible method that enables continuous monitoring of CBF at the bedside. Cerebral autoregulation and CO2 vasoreactivity can be assessed in patients with severe TBI using the CBF probe by calculating locCVR in response to MAP and hyperventilation challenges. Determining whether CVR increases or decreases with a MAP challenge (locCVRnormalized) may be a simple provocative test to determine patients' autoregulatory status following severe TBI and helping to optimize CPP management.