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2018-11-23T06:52:18Z

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==Hyperbaric oxygen therapy improved intracranial pressure and multiple markers of cerebral metabolic function when added to a comprehensive intensive treatment protocol for acute traumatic brain injury ==
==Clinical bottom line:==
{|
| '''1. There were improvements in multiple indicators of cerebral metabolic function and oxygenation following HBO2.''' '''2. ICP decreased significantly following HBO2.''' '''3. These improvements persisted for several hours.''' 
|-
|}
'''Citation/s:'''1. Rockswold SB, Rockswold GL, Zaun DA, Zhang X, Cerra CE, Bergman TA, Liu J. A prospective, randomized clinical trial to compare the effect of hyperbaric to normobaric hyperoxia on cerebral metabolism, intracranial pressure, and oxygen toxicity in severe traumatic brain injury. Journal of Neurosurgery 2010;112:1080-1094. 
'''Lead author's name and fax:''' [[mailto:gaylan.rockswold@hcmed.org | gaylan.rockswold@hcmed.org]] 

'''Three-part Clinical Question:''' For patients with severe traumatic brain injury, does the addition of hyperbaric oxygen therapy to an intensive treatment regimen result in any improvement in cerebral metabolism and oxygenation? 
'''Search Terms:''' Traumatic brain injury, cerebral metabolism, intracranial pressure 

'''The Study:'''Non-blinded randomised controlled trial with intention-to-treat.
'''The Study Patients:''' Adult patients with acute traumatic brain injury (within 24 hrs) and GCS <9 admitted to a neurosurgical intensive care setting
'''Control group''' (N = 21; 21 analysed): Intensive neurosurgical care according to current guidelines of Brain Trauma Foundation and 100% oxygen at 1 ATA for 3 hours daily (normobaric arm in this study). There was also a control of intensive neurosurgical care without extra oxygen.
'''Experimental group''' (N = 26; 26 analysed): As above plus 100% oxygen at 1.5 ATA for one hour daily for three days. 

'''The Evidence:'''
{|
| '''Outcome''' || '''Time to Outcome''' || '''NBO rate''' || '''HBO rate''' || '''Relative risk reduction''' || '''Absolute risk reduction''' || '''NNT'''
|-
| '''Brain PO2 >200mmHg for 15 minutes at any time''' || 3 days || .05 || .51 || 920% || 0.460 || 2
|-
|^ |||||| 95% CI: || 493% to 1347% || 0.25 to 0.67 || 1 to 4
|-
|}

{|
| '''Measure''' |||| '''Control Group''' |||| '''Experimental Group''' || '''Difference''' || '''P-value or 95% CI'''
|-
|^ || '''Mean''' || '''SD''' || '''Mean''' || '''SD''' ||^ ||^
|-
| '''Intracranial pressure (cm H2O)''' || -0.25 || || +0.67 || || 0.92 || P = 0.001
|-
| '''Brain PO2 (mmHg)''' || 223 || 29 || 86 || 12 || 137 || 124.6 to 149.4
|-
| '''CMRO2 (Ratio post/pre-treatment) ''' || 0.93 || || 1.25 || || 0.32 || P = 0.01
|-
|}

'''Comments:'''
1. Small study designed mainly to prove this regimen was possible and to demonstrate some improvement in markers of cerebral well-being.
2. The authors identified a 'critical' oxygen level of 200 mmHg above which the other benefits shown were much more likely, and this level was achieved more often with HBO2 than normobaric oxygen.
3. These authors are planning a larger clinical study based on this work. 

'''Appraised by:''' Mike Bennett, Prince of Wales Hospital, Sydney. ; Friday, 13 April 2012
Email: [[mailto:m.bennett@unsw.edu,au | m.bennett@unsw.edu,au]]

'''Kill or Update By:''' November 2021


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