The effect of cerebral perfusion pressure guided therapy on acute respiratory distress syndrome in traumatic brain injury
CCCF ePoster library. Thiara S. Oct 3, 2017; 198123; 57
Sonny Thiara
Sonny Thiara
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The effect of cerebral perfusion pressure guided therapy on acute respiratory distress syndrome in traumatic brain injury

Thiara, Sonny 1; Griesdale, Donald E 1,3,4; Henderson, Wiliiam R 2; Sekhon, Mypinder S 1.



1Department of Medicine, Division of Critical Care Medicine, Vancouver General Hospital, West 12th Avenue, University of British Columbia, Vancouver, BC, Canada, V5Z 1M9.

2Department of Emergency Medicine, Division of Critical Care Medicine, Vancouver General Hospital, West 12th Avenue, University of British Columbia, Vancouver, BC, Canada, V5Z 1M9.

3Department of Anaesthesiology, Pharmacology and Therapeutics, Vancouver General Hospital, West 12th Avenue, University of British Columbia, Vancouver, BC, Canada, V5Z 1M9.

4Centre for Clinical Epidemiology and Evaluation, Vancouver Coastal Health Research Institute,899 West 12th Avenue, University of British Columbia, Vancouver, BC, Canada, V5Z 1M9.

 


Introduction: Previously, increased cerebral perfusion pressure (CPP) > 70mmHg has been associated with the onset of acute respiratory distress (ARDS) after traumatic brain injury (TBI).  Recently, the concept of individualized perfusion targets using real time autoregulation assessment has emerged and at times, requires CPP titration > 70mmHg.  Given historical concerns with increased incidence of ARDS, the association between ARDS and increased CPP requires further research.
 
Objectives: To investigate the relationship between increased cerebral perfusion pressure in traumatic brain injury patients who develop acute respiratory distress syndrome versus those who do not.

Methods: We conducted a single center retrospective cohort study investigating the association of increased CPP in patients who developed ARDS versus those who did not.  We collected demographic data pertaining to age, gender, GCS motor score, Rotterdam CT score and mechanism of injury.  We also collected physiologic data for CPP, intracranial pressure, ventilation parameters, cumulative fluid balance and delta pressure.  Finally, we collected outcomes measures pertaining to duration of ventilation, length of ICU admission, length of hospitalzation and six month neurological outcome.
 
Results:  We conducted a retrospective analysis of 113 patients with severe TBI who underwent multimodal neuromonitoring.  The mean age was 39 years (SD 17) and 26 / 113 (23%) were female gender.  The median motor score was 3 (IQR 1 - 4).  The median Rotterdam score was 3 (IQR 3 - 4).  Sixteen patients (14%) developed ARDS according to the Berlin definition.  There was no difference in the mean CPP during the first 7 days of admission between patients who developed ARDS (74mmHg SD 18 vs. 73mmHg SD 18, p=0.86) versus those who did not.  There were no differences with respect to duration of mechanical ventilation, ICU length of stay, hospitalization or neurological outcome in both groups.
 
Conclusion: In our cohort of severe TBI patients who underwent invasive neuromonitoring, we did not observe an association between increased CPP in patients who developed ARDS versus those who did not.

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