Introduction:
Outcome prediction after diffuse hypoxic-ischemic brain injury (HIBI), which most commonly occurs after sudden cardiac arrest, remains fraught with uncertainty. Cerebral autoregulation (CA) normally limits fluctuations in cerebral blood flow through pressure induced changes in cerebral arteriolar diameter. CA is disrupted after brain injury, and the degree of autoregulatory failure correlates with the severity of brain injury. CA measurements may thus enable more accurate outcome prediction after HIBI.
Hypothesis:
We hypothesized that the degree of impairment in cerebrovascular pressure reactivity, one of the principle mechanisms of CA, correlates with the extent of HIBI and can predict outcome.
Methods:
Intracranial pressure (ICP) and mean arterial pressure (MAP) were continuously recorded for all subjects. The Pressure Reactivity Index (PRx) was calculated as a moving linear correlation coefficient between ICP and MAP for each 30 sec data epoch. PRx is positive when ICP increases in concert with MAP and implies impaired pressure reactivity. For each subject, both the mean PRx for the entire recording session as well as the proportion of PRx values > 0.2 (previously found to predict poor outcome in TBI) were calculated.
Results:
We included 22 consecutive patients with HIBI who underwent invasive ICP monitoring in this single center observational study between 02/2016-02/2018. Median age was 41 (range 20-77), 36% (8/22) survived to hospital discharge, and 18% (4/22) had return of consciousness. The median time of ICP monitoring was 101 hr (range 8-381 hr). HIBI was due to cardiac arrest in 19/22 patients and prolonged hypoxia in 3/22. Mean PRx was significantly higher in patients without return of consciousness (0.49 ± 0.05 vs. 0.036 ± 0.032, p = 0.001), as was the proportion of PRx values > 0.2 (0.73 ± 0.037 vs 0.34 ± 0.058, p < 0.001). All patients with return of consciousness had mean PRx < 0.2. Using this cutoff value, PRx had a 94% sensitivity and 100% specificity for predicting death or vegetative state.
Conclusions:
Continuous pressure reactivity measurements correlate with outcome after HIBI, and may be a useful adjunct for neuroprognostication. Future studies are needed to validate these findings in larger cohorts.
Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a “two-hit” model
