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|NI FEATURE: THE EDITORIAL DEBATE II-- PROS AND CONS
|Year : 2019 | Volume
| Issue : 3 | Page : 653-654
Hyperbaric oxygen therapy in ischemic stroke management: Standardized consensus-based therapeutic protocol
Guru Dutta Satyarthee
Department of Neurosurgery, Neurosciences Centre, All India Institute of Medical Sciences, New Delhi, India
|Date of Web Publication||23-Jul-2019|
Dr. Guru Dutta Satyarthee
Department of Neurosurgery, Room No. 714, Neurosciences Centre, All India Institute of Medical Sciences, New Delhi
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Satyarthee GD. Hyperbaric oxygen therapy in ischemic stroke management: Standardized consensus-based therapeutic protocol. Neurol India 2019;67:653-4
Hyperbaric oxygen treatment (HBOT) is a non-invasive method of administering pure oxygen at above-normal atmospheric pressure in the pressurized chamber. It may lead to an improvement in tissue oxygenation by increasing oxygen content in the arterial blood as well as interstitial tissue., The authors reported that the patients receiving hyperbaric oxygen within three months of sustaining a hypoxic-ischemic insult showed a better improvement involving their motor, visual and auditory functions and also gained the capability to express themselves.
The primary aim of the procedure is to increase oxygenation in the ischemic cerebral region in order to limit the secondary tissue damage. However, the efficacy of therapy is dependent on various factors that influence the protocol, including the timing of initiation of therapy, the duration of the session, the presence of a single session or multiple sessions and the level of atmospheric pressure. The role of hyperbaric oxygen therapy is explored in different diseases. A common session of HBOT treatment is carried out usually at 2.5 atmospheric pressure in a chamber over a session period of 60-90 minutes but variable protocols exist at different centres.
There is a lack of consensus regarding the atmospheric pressure to be sustained, the time window for which it is to be administered and the number of sessions of therapy needed. However, an earlier initiation of therapy is often believed to lead to a better improvement in the neurological outcome. The efficacy appears to attenuate significantly as the treatment initiation is delayed after the onset of acute stroke. An ultra-early initiation within 60 min of stroke was reported to cause a marked reduction in the infarct volume along with improvement in the behavioural scores.
Yin et al., observed the initiation of therapy at six hours following stroke at 2.5 atmospheric pressure with two-hour sessions. This led to a neurological improvement. Lou et al., observed that when the treatment was started upto 6-h post-stroke with a 1h session at three atmospheric pressure, the procedure led to an improved outcome. However, the technique could not be recommended at 12 h post-stroke.
Regarding the consideration of single or multiple sessions, in 2008, Xue et al., observed that even a single-session therapy was effective when initiated at 18 h post-stroke; and, in 2013, Mu et al., after 48 h of stroke, found the therapy to be of therapeutic value. The latter study led to the expansion of the therapeutic window period for upto 48 h. However, the authors recommended the need for a revised therapeutic protocol. Veltkamp et al., advocated that even a single session therapy started after 72 h of stroke onset, comprising of 1h sessions, led to neurological improvement.
There is a lack of clear consensus regarding the role of multiple session therapy. Yin et al., noted that cases receiving repeated sessions over six consecutive days had a reduction in their infarct size and improvement in neurological deficits. Further, Lee at al., in 2013, also supported a multiple session therapy starting within 24 h after stroke, comprising a total of 15 sessions, with each session of 90 min duration with a frequency of three sessions in a week over a total of a three week period, at two and a half atmospheric pressure [this pressure led to a significant improvement in the neurological and behavioural effects].
There is still ambiguity about the ideal atmospheric pressure level. There is controversy regarding the start of therapy either at 2,2.5 or 3 atmospheric pressure. The adverse effects include ear barotrauma if the pressure exceeds three atmospheric pressure, and there is an increased risk of seizure. However, a large study with a standardized protocol is the need of the hour and a consensus should be aimed at, since the prevalence of ischemic stroke is still alarmingly high.
| » References|| |
Sankaran R, Radhakrishnan K, Sundaram KR. Hyperbaric oxygen therapy in patients with hypoxic ischemic encephalopathy. Neurol India 2019;67:728-31. [Full text]
Ostrowski RP, Stepien K, Pucko E, Matyja E. Hyperbaric oxygen modalities are differentially effective in distinct brain ischemia models. Med Gas Res 2016;6:39-47.
] [Full text]
Hu Q, Liang X, Chen D, Chen Y, Doycheva D, Tang J, et al
. Delayed hyperbaric oxygen therapy promotes neurogenesis through reactive oxygen species/hypoxia-inducible factor-1alpha/beta-catenin pathway in middle cerebral artery occlusion rats. Stroke 2014;45:1807-14.
Yin D, Zhou C, Kusaka I, Calvert JW, Parent AD, Nanda A, et al
. Inhibition of apoptosis by hyperbaric oxygen in a rat focal cerebral ischemic model. J Cereb Blood Flow Metab 2003;23:855-64.
Lou M, Eschenfelder CC, Herdegen T, Brecht S, Deuschl G. Therapeutic window for use of hyperbaric oxygenation in focal transient ischemia in rats. Stroke 2004;35:578-83.
Xue L, Yu Q, Zhang H, Liu Y, Wang C, Wang Y. Effect of large dose hyperbaric oxygenation therapy on prognosis and oxidative stress of acute permanent cerebral ischemic stroke in rats. Neurol Res 2008;30:389-93.
Mu J, Ostrowski RP, Soejima Y, Rolland WB, Krafft PR, Tang J, et al
. Delayed hyperbaric oxygen therapy induces cell proliferation through stabilization of cAMP responsive element binding protein in the rat model of MCAo-induced ischemic brain injury. Neurobiol Dis 2013;51:133-43.
Veltkamp R, Siebing DA, Sun L, Heiland S, Bieber K, Marti HH, et al
. Hyperbaric oxygen reduces blood-brain barrier damage and edema after transient focal cerebral ischemia. Stroke 2005;36:1679-83.
Yin D, Zhang JH. Delayed and multiple hyperbaric oxygen treatments expand therapeutic window in rat focal cerebral ischemic model. Neurocrit Care 2005;2:206-11.
Lee YS, Chio CC, Chang CP, Wang LC, Chiang PM, Niu KC, et al
. Long course hyperbaric oxygen stimulates neurogenesis and attenuates inflammation after ischemic stroke. Mediators Inflamm 2013;2013:512978.
Liska GM, Lippert T, Russo E, Nieves N, Borlongan CV. A dual role for hyperbaric oxygen in stroke neuroprotection: Preconditioning of the brain and stem cells. Cond Med 2018;1:151–66.