• Zh Vopr Neirokhir Im N N Burdenko · Jan 2014

    Clinical Trial

    [The use of intravascular hypothermia to correct intracranial hypertension in patients with severe traumatic brain injury].

    • A V Oshorov, K A Popugaev, I A Savin, A Yu Lubnin, A G Gavrilov, L B Likhterman, A D Kravchuk, and A A Potapov.
    • Zh Vopr Neirokhir Im N N Burdenko. 2014 Jan 1;78(5):41-7; discussion 47-8.

    ObjectiveAssess to impact hypothermia on ABP, CPP, ICP and cerebral autoregulation. Material and methods. 14 patients with TBI (GOS<9) underwent hypothermia by Thermogard system within 32-35 °C (Zoll, USA). ICP was measured intraparenchymal by Codman sensor. Cerebral autoregulation was estimated by correlation coefficient Prx (Soft ICM Plus, Cambridge, UK). Temperature was measured in urinary bladder. There were selected five time periods: 1 - phase of initial state, 2 - phase of induction hypothermia, 3 - phase of hypothermia, 4 - phase of rewarming, 5 - phase after finishing hypothermia. All data preset as Mediana (min; max). Stat analysis was perfomed using Soft Statistica 10.0. Results. Phase 1 lasted nearly 7 (2; 12) h, ABP 94 (81; 102), CPP - 73 (52; 87), ICP 27 (16; 45) mm Hg, Prx 0,25 (-0,15; 0,7), temperature 38,2 °C (37; 39,8). Phase 2: 5 (2; 12) h, ABP 95 (85; 114), CPP 80 (65; 96), ICP 18 (10; 22) mm Hg, Prx -0,055 (-0,15; 0,7), temperature 35,2 °C (34,5; 35,5). Phase 3: 55 (20; 100) h, there were not significant changed ABP, CPP, Prx, ICP 15 (10; 18) mm Hg, temperature was 33,5 °C (32; 34,7). Phase 4: 17 (8; 24) h, ABP 90 (70; 100), CPP 77 (55; 85), ICP 15 (9; 27) mm Hg and Prx 0,2 (-0,2; 0,32). Temperature 36,9 °C (35,9; 38,5). Phase 5: 20 (6; 240) h, ABP 87(53; 110), CPP 72 (47; 107), ICP 17 (10; 32) mm Hg and Prx 0,2 (-0,2; 0,6). Temperature 37,7 °C (36,7; 39,0). Conclusion. Hypothermia is an effective method for correction of intracranial hypertension. Hypothermia can use as a additional option of intensive care during refractory intracranial hypertension. Rewarming phase is the most dangerous time on the re-development of intracranial hypertension and disruption of autoregulation.

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