Aneirin
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Joined: 3/18/2006 From: Tamaris Status: offline
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quote:
ORIGINAL: Icarys 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 Clinical articleSarah B. Rockswold, M.D.1,2, Gaylan L. Rockswold, M.D., Ph.D.2,3, David A. Zaun, M.S.4, Xuewei Zhang, M.D.2, Carla E. Cerra, R.N., B.A.N.2, Thomas A. Bergman, M.D.2,3, and Jiannong Liu, Ph.D.4 1Department of Physical Medicine and Rehabilitation; 2Division of Neurosurgery, Department of Surgery, Hennepin County Medical Center; 3Department of Neurosurgery, University of Minnesota; and 4Analytical Services, Chronic Disease Research Group, Minneapolis Medical Research Foundation, Minneapolis, Minnesota Abbreviations used in this paper: AVDO2 = arteriovenous differences in oxygen; BAL = bronchial alveolar lavage; CBF = cerebral blood flow; CMRO2 = cerebral metabolic rate of oxygen; FiO2 = fraction of inspired oxygen; GCS = Glasgow Coma Scale; HBO2 = hyperbaric oxygen; ICP = intracranial pressure; ICU = intensive care unit; IL = interleukin; L/P = lactate/pyruvate; NBH = normobaric hyperoxia; OEF = oxygen extraction fraction; PEEP = positive end expiration pressure; P/F = PaO2/FiO2; PvO2 = partial pressure of venous oxygen; ROS = reactive oxygen species; TBI = traumatic brain injury; TIL = therapeutic intensity level; UPTD = unit pulmonary toxicity dose. Address correspondence to: Gaylan L. Rockswold, M.D., Ph.D., Department of Surgery, Hennepin County Medical Center, 701 Park Avenue, Minneapolis, Minnesota 55415. email: [email protected]. Please include this information when citing this paper: published online October 23, 2009; DOI: 10.3171/2009.7.JNS09363.DOI: 10.3171/2009.7.JNS09363 Object Oxygen delivered in supraphysiological amounts is currently under investigation as a therapy for severe traumatic brain injury (TBI). Hyperoxia can be delivered to the brain under normobaric as well as hyperbaric conditions. In this study the authors directly compare hyperbaric oxygen (HBO2) and normobaric hyperoxia (NBH) treatment effects. Methods Sixty-nine patients who had sustained severe TBIs (mean Glasgow Coma Scale Score 5.8) were prospectively randomized to 1 of 3 groups within 24 hours of injury: 1) HBO2, 60 minutes of HBO2 at 1.5 ATA; 2) NBH, 3 hours of 100% fraction of inspired oxygen at 1 ATA; and 3) control, standard care. Treatments occurred once every 24 hours for 3 consecutive days. Brain tissue PO2, microdialysis, and intracranial pressure were continuously monitored. Cerebral blood flow (CBF), arteriovenous differences in oxygen, cerebral metabolic rate of oxygen (CMRO2), CSF lactate and F2-isoprostane concentrations, and bronchial alveolar lavage (BAL) fluid interleukin (IL)–8 and IL-6 assays were obtained pretreatment and 1 and 6 hours posttreatment. Mixed-effects linear modeling was used to statistically test differences among the treatment arms as well as changes from pretreatment to posttreatment. Results In comparison with values in the control group, the brain tissue PO2 levels were significantly increased during treatment in both the HBO2 (mean ± SEM, 223 ± 29 mm Hg) and NBH (86 ± 12 mm Hg) groups (p < 0.0001) and following HBO2 until the next treatment session (p = 0.003). Hyperbaric O2 significantly increased CBF and CMRO2 for 6 hours (p ≤ 0.01). Cerebrospinal fluid lactate concentrations decreased posttreatment in both the HBO2 and NBH groups (p < 0.05). The dialysate lactate levels in patients who had received HBO2 decreased for 5 hours posttreatment (p = 0.017). Microdialysis lactate/pyruvate (L/P) ratios were significantly decreased posttreatment in both HBO2 and NBH groups (p < 0.05). Cerebral blood flow, CMRO2, microdialysate lactate, and the L/P ratio had significantly greater improvement when a brain tissue PO2 ≥ 200 mm Hg was achieved during treatment (p < 0.01). Intracranial pressure was significantly lower after HBO2 until the next treatment session (p < 0.001) in comparison with levels in the control group. The treatment effect persisted over all 3 days. No increase was seen in the CSF F2-isoprostane levels, microdialysate glycerol, and BAL inflammatory markers, which were used to monitor potential O2 toxicity. Conclusions Hyperbaric O2 has a more robust posttreatment effect than NBH on oxidative cerebral metabolism related to its ability to produce a brain tissue PO2 ≥ 200 mm Hg. However, it appears that O2 treatment for severe TBI is not an all or nothing phenomenon but represents a graduated effect. No signs of pulmonary or cerebral O2 toxicity were present.KEYWORDS:hyperbaric oxygen; normobaric hyperoxia; oxygen toxicity; traumatic brain injury; cerebral metabolism; intracranial pressure.Cited byShelly D. Timmons. (2010) Current trends in neurotrauma care. Critical Care Medicine 38, S431-S444 Sorry, the article construction is lost on me, as one of my asd related problems is a failure to be able to read anything where the structure of any wording is heavy. The above is heavy to me, too many words and symbols all together, it is why I write the way I do, in very short paragraphs with decent spacing in between. Another subject or train of thought deserves a new paragraph. It is also why some on here may accuse me of not reading what they have quoted, for if I perceive heavy, I skip by as I know I will get confused and end up reading the same sentence somewhere in the middle over and over again until I get frustrated and give up. This problem has taken three years for my tutors at college to understand, understand why I failed to read what has been set, for the structure is a problem to me, but now they and I know, I am not lazy, just challenged and so I have been awarded a bunch of learning aides to help me in my analysis of what I have to do.
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Everything we are is the result of what we have thought, the mind is everything, what we think, we become - Guatama Buddha Conservatism is distrust of people tempered by fear - William Gladstone
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