Cerebrovascular reactivity during hypothermia and rewarming

Background. Experimental evidence from a murine model of traumatic brain injury (TBI) suggests that hypothermia followed by fast rewarming may damage cerebral microcirculation. The effects of hypothermia and subsequent rewarming on cerebral vasoreactivity in human TBI are unknown. Methods. This is a retrospective analysis of data acquired during a prospective, observational neuromonitoring and imaging data collection project. Brain temperature, intracranial pressure (ICP), and cerebrovascular pressure reactivity index (PRx) were continuously monitored. Results. Twenty-four TBI patients with refractory intracranial hypertension were cooled from 36.0 (0.9) to 34.2 (0.5)degrees C [mean (SD), P < 0.0001] in 3.9 (3.7) h. Induction of hypothermia [average duration 40 (45) h] significantly reduced ICP from 23.1 (3.6) to 18.3 (4.8) mm Hg (P < 0.05). Hypothermia did not impair cerebral vasoreactivity as average PRx changed non-significantly from 0.00 (0.21) to -0.01 (0.21). Slow rewarming up to 37.0 degrees C [rate of rewarming, 0.2 (0.2)degrees C h(-1)] did not increase ICP [18.6 (6.2) mm Hg] or PRx [0.06 (0.18)]. However, in 17 (70. 1%) out of 24 patients, rewarming exceeded the brain temperature threshold of 37 degrees C. In these patients, the average brain temperature was allowed to increase to 37.8 (0.3)degrees C (P < 0.0001), ICP remained stable at 18.3 (8.0) mm Hg (P = 0.74), but average PRx increased to 0.32 (0.24) (P < 0.0001), indicating significant derangement in cerebrovascular reactivity. After rewarming, PRx correlated independently with brain temperature (R = 0.53; P < 0.05) and brain tissue O-2 (R=0.66; P < 0.01). Conclusions. After moderate hypothermia, rewarming exceeding the 37 degrees C threshold is associated with a significant increase in average PRx, indicating temperature-dependent hyperaemic derangement of cerebrovascular reactivity.