• Critical care medicine · Jul 2024

    Effect of Increasing Blood Pressure on Brain Tissue Oxygenation in Adults After Severe Traumatic Brain Injury.

    • Thitikan Kunapaisal, Abhijit V Lele, Courtney Gomez, Anne Moore, Marie Angele Theard, and Monica S Vavilala.
    • Department of Anesthesiology and Pain Medicine, University of Washington, Seattle, WA.
    • Crit. Care Med. 2024 Jul 1; 52 (7): e332e340e332-e340.

    ObjectivesTo examine if increasing blood pressure improves brain tissue oxygenation (PbtO 2 ) in adults with severe traumatic brain injury (TBI).DesignRetrospective review of prospectively collected data.SettingLevel-I trauma center teaching hospital.PatientsIncluded patients greater than or equal to 18 years of age and with severe (admission Glasgow Coma Scale [GCS] score < 9) TBI who had advanced neuromonitoring (intracranial blood pressure [ICP], PbtO 2 , and cerebral autoregulation testing).InterventionsThe exposure was mean arterial pressure (MAP) augmentation with a vasopressor, and the primary outcome was a PbtO 2 response. Cerebral hypoxia was defined as PbtO 2 less than 20 mm Hg (low).Main ResultsMAP challenge test results conducted between ICU admission days 1-3 from 93 patients (median age 31; interquartile range [IQR], 24-44 yr), 69.9% male, White ( n = 69, 74.2%), median head abbreviated injury score 5 (IQR 4-5), and median admission GCS 3 (IQR 3-5) were examined. Across all 93 tests, a MAP increase of 25.7% resulted in a 34.2% cerebral perfusion pressure (CPP) increase and 16.3% PbtO 2 increase (no MAP or CPP correlation with PbtO 2 [both R2 = 0.00]). MAP augmentation increased ICP when cerebral autoregulation was impaired (8.9% vs. 3.8%, p = 0.06). MAP augmentation resulted in four PbtO 2 responses (normal and maintained [group 1: 58.5%], normal and deteriorated [group 2: 2.2%; average 45.2% PbtO 2 decrease], low and improved [group 3: 12.8%; average 44% PbtO 2 increase], and low and not improved [group 4: 25.8%]). The average end-tidal carbon dioxide (ETCO 2 ) increase of 5.9% was associated with group 2 when cerebral autoregulation was impaired ( p = 0.02).ConclusionsMAP augmentation after severe TBI resulted in four distinct PbtO 2 response patterns, including PbtO 2 improvement and cerebral hypoxia. Traditionally considered clinical factors were not significant, but cerebral autoregulation status and ICP responses may have moderated MAP and ETCO 2 effects on PbtO 2 response. Further study is needed to examine the role of MAP augmentation as a strategy to improve PbtO 2 in some patients.Copyright © 2024 by the Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.

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