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DOI: 10.1055/s-0044-1782609
Role of Hyperbaric Oxygen Therapy in Traumatic Brain Injury: A Systematic Review of Randomized Controlled Trials
Authors
Abstract
Background
Traumatic brain injury (TBI) is a significant public health concern. Standard care involves conservative management and pharmacological and surgical interventions. Hyperbaric oxygen therapy (HBOT) has emerged as a potential treatment for TBI, with varied findings in the literature. Our systematic review aims to comprehensively assess the efficacy and safety of HBOT in TBI management, addressing existing knowledge gaps and providing insights for clinical practice and future research.
Materials and Methods
A systematic literature search was performed in PubMed, SCOPUS, Central Cochrane Registry of Controlled Trials (The Cochrane Library), and ScienceDirect databases for the role of HBOT in TBI. We included studies involving randomized controlled trials (RCTs). Quasi-randomized controlled studies, prospective, retrospective observational studies, case series, case reports, letters, editorials, comments, animal studies, and studies from non-English literature were excluded.
Results
After identifying 306 articles, we narrowed it to 8 for qualitative synthesis. The studies were categorized into subgroups: those on patients with an acute history of cerebral injury and those with a history of mild TBI. The combined RCTs involved 651 patients (326 in the first subgroup, 325 in the second). Despite a uniform HBOT session duration of 60 minutes, variations in compression, decompression phases, and pressure used (1.5ATA to 2.5ATA) hindered meta-analysis comparability. Outcome measures differed, complicating comparisons. Overall, HBOT appears beneficial in the first group and less so in the second. Complications are primarily pulmonary, which include dyspnea, cyanosis, hyperoxic pneumonia, and increased fraction of inspired oxygen requirement.
Conclusion
Our study encountered challenges in reaching definitive conclusions due to outcome variability among the included studies. Despite mixed results, HBOT shows potential benefits for acute TBI patients. Conversely, our findings suggest the limited efficacy of HBOT for chronic traumatic brain injury patients. Further research is crucial, particularly exploring diverse HBOT treatment protocols to establish optimal pressure levels and the required number of sessions for effective outcomes
Introduction
Traumatic brain injury (TBI) represents a significant public health concern, characterized by substantial morbidity and mortality, imposing a considerable burden on affected families.[1] Notably, a considerable proportion of TBIs is attributed to road traffic accidents.[2] Current standard care for TBI primarily involves conservative management, encompassing crucial interventions such as intracranial pressure monitoring, maintenance of hemodynamic stability, and pharmacological measures involving antihypertensives and antiepileptics.[3] [4] Additionally, efforts to prevent secondary injury by minimizing factors such as hypoxia, hypercapnia, and systemic hypotension are integral components of routine TBI treatment.[5] [6] [7] One therapeutic option that gained attention in the context of TBI is hyperbaric oxygen therapy (HBOT). Originally designed to mitigate secondary damage associated with hypoxia, HBOT is believed to enhance oxygen delivery to injured tissues, reduce inflammation, and foster the healing of damaged brain tissue.[2] In animal models, it has been shown that hyperbaric oxygen can prevent the release of plasma endothelins[8] or alter the levels of matrix metalloproteinase-9 [9] or change in cyclooxygenase 2 expression[10] and thus reducing the impact of secondary brain injury. The existing literature on HBOT for TBI presents a spectrum of findings, with both positive outcome studies and those reporting no significant effects.[11] [12] [13] [14] [15] [16] Considering the varied evidence and potential gaps in understanding the role of HBOT in TBI treatment, our systematic review aims to comprehensively address this issue. By synthesizing and analyzing the available evidence, our review seeks to provide a more nuanced understanding of the efficacy and potential benefits of HBOT in the management of TBI. This systematic review is undertaken with the goal of bridging existing knowledge gaps and offering valuable insights that may inform clinical practice and guide future research in this critical area.
Materials and Methods
We used the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines for conducting the present review.[17]
Patient, Intervention, Comparison/comparator and Outcome (PICO) Question
In this systematic review, we investigated articles focusing on the utilization of HBOT in the management of TBI among adults. Our primary objective was to gather evidence on the effectiveness of HBOT in the treatment of TBI, while also assessing its safety profile and potential complications.
Search Strategy
A systematic literature search was conducted across PubMed, SCOPUS, Central Cochrane Registry of Controlled Trials (The Cochrane Library), and ScienceDirect databases, using the search terms outlined in [Table 1]. Additionally, the reference lists of included studies were reviewed for potentially relevant studies. Three investigators independently screened abstracts, with selected articles undergoing full-text evaluation. Conflicts were resolved through consensus, resulting in a final list of studies.
Eligibility Criteria
Randomized controlled trials (RCTs) meeting the inclusion criteria, which focused on ultrasound-guided procedures for postoperative analgesia in pediatric abdominal surgeries, were included. Quasi-randomized controlled studies, prospective and retrospective observational studies, case series, case reports, letters, editorials, comments, animal studies, and non-English literature studies were excluded.
Data Extraction
Three investigators independently assessed studies and extracted data using a predesigned proforma based on inclusion criteria. Extracted details included study author, publication year, country, sample size, type of block, type of surgery, reported outcomes, and any complications. Authors were contacted for missing data, and discrepancies were resolved through consensus. The PRISMA flowchart illustrating the study selection process is presented in [Fig. 1]. We employed the revised Joanna Briggs Institute (JBI) critical appraisal tool to assess the risk of bias in RCTs.[18]


Results
With our search criteria, a total of 306 records were identified. After removing duplicates, 287 articles were screened, leading to 17 articles for full-text review. Out of these, 11 articles were excluded with reasons as mentioned in [Table 2].[2] [8] [9] [10] [19] [20] [21] [22] [23] [24] [25] The remaining six articles were included in the qualitative synthesis ([Table 3]).[11] [12] [13] [14] [15] [16] Of these six articles, two studies reported adverse events from three RCTs.[20] [25] Out of these studies, four studies were conducted on military personnel with a history of TBI—mild severity, while four studies were conducted on patients with an acute history of cerebral injury. Four studies originated from the United States, two from China, one from South America, and one from France. A total of 651 patients were included in all the combined RCTs. Of these, 325 were military personnel with chronic TBI, and 326 patients had acute cerebral injury. HBOT was administered to 286 patients, with one study not specifying the exact number of patients, and the remaining served as controls. The age of the participants ranged from 26 to 70 years. We categorized our review into two subgroups: one with acute cerebral injury with poor Glasgow Coma Scale (GCS) and the other with chronic TBI.
Study author (Year) |
Reason for exclusion |
---|---|
Barrett et al 2004[19] |
Pilot study—nonrandomized |
Churchill et al 2019 [20] |
The authors analyze the data pooled from other two clinical trials[27] [28] |
Hu et al 2008 [9] |
Animal model |
Hu et al 2010 [21] |
Animal model |
Jin et al 2006 [10] |
Animal model |
Liu and Shang 2023 [2] |
Study group and control group both received hyperbaric O2, no nonhyperbaric O2 group |
Mao et al 2010 [22] |
Article in Chinese |
Nelson et al 1994 [23] |
Animal model |
Rasmussen et al 2015 [24] |
Animal model |
Wang et al 2004 [8] |
Animal model |
Wolf et al 2012[25] |
Study is only reported adverse events in already performed RCT's. /post hoc analysis. Original study reference is not available. |
Study author (Year) |
Country |
Sample |
HBOT/Control |
Age (mean) |
Sex (M/F) |
Inclusion criteria |
Exclusion criteria |
HBOT |
Outcomes |
Complications |
Conclusion |
|||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
Type of injury |
Grade of injury |
Started at |
Session- C/M/D |
Sessions frequency |
Total duration |
Pressure |
||||||||||
Artru et al 1976[11] |
France |
60 |
31/29 |
30 |
NA |
Trauma |
Severity of coma- JOUVET scale all |
Severe chest injury, open brain wound |
NA |
10/60/20 |
1/day |
10 session+ 4 day pause- till recovery or death |
2.5 ATA |
Mortality no difference, mean duration of coma no difference, brainstem contusion without supratentorial mass, better rate of recovery at 1month |
Dyspnea, cyanosis, hyperoxic pneumonia (n = 11) |
Besides the toxic action on normal nervous tissue, HBOT can counteract edema and ischemia in the zones of brain injuries |
Cifu et al 2014 [12] |
Colombia, South America |
61 |
NA |
23 |
NA |
Trauma |
TBI mild |
Disorders contraindication for HBOT |
>8 months |
3/60/3 |
1/day |
40 sessions over 10 weeks |
2.0 ATA |
Posttraumatic disorder checklist military version no significance, Rivermead postconcussion symptoms questionnaire no significance |
NA |
No effect on postconcussion symptoms after mild traumatic brain injury |
with sham compression |
||||||||||||||||
Ren et al 2023[13] |
China |
40 |
20/20 |
46–70 |
Not clear |
Trauma |
GCS 3-12 |
Active bleeding, unstable vital signs and CSF leak, skull base fracture, thoracic and abdominal injuries |
>24 hours |
20/60/20 |
1/day |
10 days |
0.2 Mpa |
Serum levels of superoxide dismutase significant decrease P,0.05, endothelium derived relaxing factor—nitric oxide significantly decreased, nerve growth factor significantly decreased, serum malondialdehyde significantly decreased |
NA |
HBOT can effectively inhibit the oxidative stress response of the body, enhance the survival of damaged neurons, and accelerate the recovery |
Rockswold et al 1992 [14] |
Minnesota, USA |
166 |
84/82 |
32 |
65/19 |
Trauma, surgical mass lesions |
GCS ≤9 |
Not clear |
26 hours |
x/60/x |
3/day |
2 weeks/ till brain dead/ awake |
1.5 ATA |
Mortality HBOT (17%) vs. controls (32%) in trauma p = 0.02, mortality HBOT (17%) vs. controls (32%) in mass lesions p = 0.09, Glasgow Outcome Scale no difference |
Increased FiO2 requirement and chest infiltrates needed termination of treatment (n = 10), seizures (n = 2), hemotympanum (n = 2) |
50% reduction in the mortality rate of patients with GCS scores of 4 to 6. The functional recovery of the salvaged patients was not satisfactory |
Walker et al 2018[15] |
USA |
71 |
36/35 |
33 |
70/1 |
Trauma |
TBI mild |
Moderate-to-severe TBI, disorders contraindication for HBOT |
>1 year post-injury |
60 minutes |
NA |
40 sessions-12 weeks |
1.5 ATA |
Sleep by actigraphy—no improvement, sleep by self-reports—no improvement |
NA |
HBOT improved some self-report measures of sleep on the |
PSQI, but overall extremely poor |
||||||||||||||||
Xie et al 2007[16] |
China |
60 |
30/30 |
26 |
37/23 |
h/o craniocerebral injury |
GCS 3-12 |
Trauma to chest and abdomen, active hemorrhage, lung pathology, arrythmias, ear disease, pregnancy |
1–10 days |
15/70/15 |
1-10/day |
1 |
0.2–0.25 Mpa |
CRP before and after p < 0.01, GCS before and after p < 0.01 |
NA |
HBOT decrease -plasma CRP in patients with craniocerebral injury |
Abbreviations: CRP, C-reactive protein; CSF, cerebrospinal fluid; FiO2, fraction of inspired oxygen; GCS, Glasgow Coma Scale; HBOT, hyperbaric oxygen therapy; NA, not available; PSQI, Pittsburgh Sleep Quality Index; TBI, traumatic brain injury;
For patients with acute cerebral injury with poor GCS, the inclusion criteria were TBI with poor GCS, ranging from 3 to 12. Common exclusion criteria across all studies included concomitant trauma to the chest and abdomen, active hemorrhage, lung pathology, open brain wound, skull base fractures, cerebrospinal fluid (CSF) leak, unstable vital signs, arrhythmias, ear diseases, and pregnancy. There was no uniformity in delivering HBOT therapy in all these studies. Therapy was initiated after 24 hours in all the studies, with session durations consisting of compression, maintenance, and decompression phases. The compression phase was mentioned in three out of the four RCTs, ranging from 10 to 20 minutes. Rockswold et al[14] did not provide this information. The maintenance phase lasted about 60 to 70 minutes, and the decompression phase lasted about 15 to 20 minutes. Rockswold et al[14] did not mention the decompression phase. The pressure used was reported in atmospheric pressure absolute in two studies and megapascals in two studies. Artru et al[11] and Rockswold et al,[14] 1992, used 2.5 ATA and 1.5 ATA, respectively, while Xie et al[16] and Ren et al[13] used 0.2 MPa, corresponding to approximately 2 ATA. The frequency of sessions per day varied from one to ten sessions per day by Xie et al,[16] to one per day by Artru et al.[11] The total sessions/total duration of therapy varied from 10 sessions,[11] [13] [16] to sessions till death or awakening,[11] [14] restarted sessions after 10 with a 4-day pause until recovery or death.
The outcomes measured were different in all the studies. Xie et al[16] measured C-reactive protein (CRP) concentrations and GCS before and after therapy, showing significant improvement. Ren et al[13] measured levels of superoxide dismutase (SOD), nitric oxide (NO), nerve growth factor, and malondialdehyde, demonstrating a significant decrease with HBOT therapy. Rockswold et al[14] measured mortality, showing significant improvement, but with the Glasgow Outcome Scale, there was not much difference, indicating that functional recovery in salvaged patients was not satisfactory. Artru et al[11] measured mortality and mean duration of coma, which showed no significant difference; however, there was better recovery at 1 month in a subgroup of patients with brain stem contusion without supratentorial mass lesion.
The complications encountered were reported in only two studies.[11] [14] The reported complications in these studies can be divided into pulmonary and nonpulmonary. The pulmonary complications reported included dyspnea, cyanosis, hyperoxic pneumonia, and increased fraction of inspired oxygen (FiO2) requirement, totaling 21 patients out of 115. Some patients required termination of treatment due to pulmonary complications. Nonpulmonary complications reported included seizures (n = 2) and hemotympanum (n = 2).
In the subgroup of patients with chronic TBI, primarily involving military personnel with history of mild TBI, four studies were identified, of which only two reported adverse events.[20] [25] Churchill et al[20] reported adverse events from two studies, namely the Hyperbaric Oxygen for Persistent Post-Concussive Symptoms (HOPPS) study and The Brain Injury and Mechanism of Action of Hyperbaric Oxygen for Persistent Post-Concussive Symptoms after Mild Traumatic Brain Injury (mTBI) (BIMA) study, while Wolf et al[25] reported adverse events from the HBO-TBI study. Therefore, a total of five RCTs are included in this subgroup. The total number of patients studied in this subgroup was 325, with only seven being females. Among these patients, 145 received HBOT; however, Cifu et al[12] did not specify the number of subjects who received therapy versus controls. The age of participants ranged from 23 to 33 years. All patients included in these studies had mild TBI, and the exclusion criteria were like the first group mentioned above, excluding those with moderate-to-severe TBI and contraindications for HBOT.
Therapy in all the studies commenced between 8 months and 1 year after the TBI. The duration of the maintenance phase in all studies was 60 minutes, with the compression and decompression phases lasting about 3 to 5 minutes each. Walker et al[15] and Wolf et al[25] did not specify the duration of the compression and decompression phases. A total of 40 sessions were administered in all studies, distributed over 10 to 12 weeks. The pressure used varied from 1.5 to 2.4 ATA. The outcomes measured included sleep, assessed by actigraphy (objective) and self-reports (subjective) in the study by Walker et al,[15] which showed no improvement. The posttraumatic disorder checklist military version and the Rivermead Post Concussion Symptoms Questionnaire were utilized by Cifu et al,[12] revealing no significant differences. Complications reported from the HOPPS study and BIMA study[20] and the HBO-TBI study[25] included common occurrences such as ear barotrauma (n = 33), sinus pain (n = 10), vision changes (n = 3), headache (n = 10), among 193 patients. The details of risk of bias assessment with JBI tool are shown in [Table 4].
Study ID |
P1 |
P2 |
P3 |
P4 |
P5 |
P6 |
P7 |
P8 |
P9 |
P10 |
P11 |
P12 |
P13 |
---|---|---|---|---|---|---|---|---|---|---|---|---|---|
Artru et al 1976[11] |
Unclear |
Unclear |
Yes |
Unclear |
Unclear |
Yes |
No |
Yes |
Yes |
Yes |
Yes |
Yes |
Yes |
Cifu et al 2014[12] |
Yes |
Yes |
Yes |
Yes |
Yes |
Yes |
Yes |
Yes |
Yes |
Yes |
Yes |
Yes |
Yes |
Ren et al 2023[13] |
Yes |
Unclear |
Unclear |
Unclear |
No |
Yes |
No |
Yes |
Yes |
Yes |
Yes |
Yes |
Yes |
Rockswold et al 1992[14] |
Unclear |
Unclear |
Yes |
No |
No |
Yes |
Yes |
Yes |
Yes |
Yes |
Yes |
Yes |
Yes |
Walker et al 2018[15] |
Yes |
Yes |
Yes |
Yes |
Yes |
Yes |
Yes |
Yes |
Yes |
Yes |
Yes |
Yes |
Yes |
Xie et al 2007[16] |
Unclear |
Unclear |
Yes |
Unclear |
No |
Yes |
Unclear |
Yes |
Yes |
Unclear |
Yes |
Yes |
Yes |
Abbreviation: RCT, randomized controlled trial.
Discussion
TBI can lead to hypoxic injury, which may progress or occur days after the injury. This is in contrast to acute cerebrovascular occlusion, which causes immediate damage.[14] The mechanism of action of HBOT is not fully understood, but possible mechanisms include the correction of hypoxia, as evidenced by an increase in partial pressure of oxygen in CSF,[11] correction of ischemia by decreasing intracranial pressure or by shifting blood from normal to ischemic areas (the reverse steal phenomenon), and correction of acidosis and cerebral edema. HBOT can also act as an antioxidant, preventing oxidative stress in hypoxic-injured cells.[14] However, there are potential negative side effects of HBOT. The oxygen toxicity on the brain is referred to as the Paul Bert effect, while oxygen toxicity on the lungs is known as the Smith effect.[26] Both effects become evident at very high pressures (15–20 ATA) or when the pressure is used for a longer duration. Possible side effects include an increase in cerebral edema, seizures, dyspnea, cyanosis, hyperoxic pneumonia, and an increase in FiO2 requirement. The positive or negative effects will depend on pressure, the duration, and pathophysiological condition of the brain.
HBOT was used for patients with acute cerebral injury with poor GCS in four of the studies included in our review. Xie et al[16] utilized HBOT employing an iced-wheel four-door, two-cabin air compression chamber from 24 hours to 10 days after the injury. A pressure of 0.2 to 0.25 MPa was applied with a compression phase lasting 15 to 20 minutes, maintained for 70 to 80 minutes, and then decompressed over 20 minutes. A total of 10 daily sessions were administered. CRP and GCS were compared between the HBOT group and the control group. They observed a significant difference in the HBOT group (t = 9.21, p < 0.01), leading to the conclusion that HBOT can remarkably decrease the content of CRP in patients with cerebrovascular injury during stress phases.
Artru et al[11] administered HBOT at 2.5 ATA, involving a compression phase of 10 minutes, a maintenance phase of 60 minutes, and a decompression phase of 20 minutes. The therapy was delivered for 10 daily sessions, followed by a 4-day gap, and then continued with 10 daily sessions until the patient either regained consciousness or succumbed. The average initial treatment delay for starting HBOT was 4.5 days. Treatment was halted in five patients due to severe intolerance, suggesting impending hyperoxic pneumonia, and in six patients with severe pulmonary infections, fearing the exacerbation of lesions. Coma rate at 1 month and mortality rate were the measured outcomes. The study revealed no significant difference between the HBOT and control groups regarding the coma rate at 1 month and the mortality rates at 1 month and 1 year. However, in a subgroup analysis of patients under 30 years old with brain stem contusion who did not undergo surgery, a significant recovery of consciousness was observed. The researchers concluded that there is no significant difference in the overall mortality rate between HBOT and controls, but there were no detrimental effects found concerning the toxic effects of HBOT on the normal brain and lungs. They suggested that early treatment with less frequent interruptions might yield positive results, and any negative effects on the lungs could potentially be mitigated by using premedication with a neuroleptic or a benzodiazepine derivative.
Ren et al[13] employed HBOT daily for 10 days at a pressure of 0.2 MPa, with a pressurization period of 20 minutes, a plateau phase of 60 minutes, and a decompression period of 20 minutes. Oxidative stress indicators such as SOD, endothelium-derived relaxing factor—NO—and nerve growth factor were compared at the end of the therapy. They observed a significant improvement in SOD (p < 0.05), NO (p < 0.01), and malondialdehyde content (p < 0.05) in the HBOT group compared to the controls. The researchers concluded that HBOT can be utilized to reduce systemic oxidative stress response in patients with craniocerebral injury.
Rockswold et al[14] utilized HBOT through a monoplace hyperbaric chamber, maintaining a pressure of 1.5 ATA. The compression rate was set at 1 psi/min, held for 60 minutes, and then decompressed at the same rate. Sessions were conducted three times daily for 2 weeks or until the patient was brain dead or showed improvement in the GCS. Outcomes were assessed using the Glasgow Outcome Scale. The average time from injury to the first HBOT therapy was 26 hours. The most common complication encountered was pulmonary, leading to increased FiO2 requirements. The study revealed that the mortality rate was not significantly decreased compared to the control group (p = 0.037), and HBOT did not increase the number of patients in the favorable outcome category (decreased morbidity). However, the researchers suggested that employing a different HBOT protocol or incorporating 21-aminosteroid might have improved the quality of survival.
HBOT was employed for patients with chronic stable TBI in four of the eight studies reviewed. Two of these studies specifically focused on reporting adverse events from three RCTs. Walker et al[15] utilized HBOT, delivering forty 60-minute sessions at 1.5 ATA over 12 weeks. Sleep assessment through self-reports and actigraphy was used as an outcome measure. The study did not identify any statistically significant changes over time attributed to the intervention in most of the Pittsburgh Sleep Quality Index (PSQI) measures. However, an exception was noted for the PSQI component score related to habitual sleep efficiency, where significant changes over time in response to the intervention were observed. Cifu et al[12] employed HBOT through a multiplace chamber, administering a series of 40 once-a-day sessions over 10 weeks at a pressure of 2.0 ATA. The compression phase lasted 3 minutes, with a plateau of 60 minutes and a decompression phase of 3 minutes. They used the Posttraumatic Stress Disorder Checklist–Military Version (PCL-M) for assessing PTSD symptoms and the Rivermead Post Concussion Symptom Questionnaire (RPQ) for evaluating post-concussion symptoms both pre- and post-therapy. Their findings showed no significant difference between the group testing, leading to the conclusion that HBOT has no significant impact on postconcussion symptoms after mild TBI. Churchill et al[20] and Wolf et al[25] reported adverse effects from the RCTs, and these were detailed in the results section.
Conclusion
Our study faced challenges in drawing definitive conclusions due to the variability in reported outcomes across the included studies. Nonetheless, there appears to be potential benefit from HBOT in patients with acute TBI, despite mixed outcomes, including positive responses in two studies and negative responses in two studies. Conversely, our findings suggest that HBOT may not be beneficial for chronic TBI patients. It is crucial to emphasize the need for further research, specifically testing HBOT with diverse treatment protocols to determine optimal and safe pressure levels, as well as the total number of sessions required for effective outcomes.
Conflict of Interest
None declared.
Ethical Approval
The study was started after the approval from institutional ethical committee.
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References
- 1 Rockswold SB, Rockswold GL, Zaun DA, Liu J. A prospective, randomized Phase II clinical trial to evaluate the effect of combined hyperbaric and normobaric hyperoxia on cerebral metabolism, intracranial pressure, oxygen toxicity, and clinical outcome in severe traumatic brain injury. J Neurosurg 2013; 118 (06) 1317-1328
- 2 Liu H-y, Shang Y-h. Effect of guipizide maleate with hyperbaric oxygen therapy on neurophysiology and coagulation indices in patients with severe craniocerebral injury. Trop J Pharm Res 2023; 22 (07) 1483-1488
- 3 Konar S, Maurya I, Shukla DP. et al. Intensive care unit management of traumatic brain injury patients. Journal of Neurointensive Care. 2022; 5 (01) 1-8
- 4 Agrawal A, Savardekar A, Singh M. et al. Pattern of reporting and practices for the management of traumatic brain injury: an overview of published literature from India. Neurol India 2018; 66 (04) 976-1002
- 5 Hawryluk GWJ, Rubiano AM, Totten AM. et al. Guidelines for the management of severe traumatic brain injury: 2020 update of the decompressive craniectomy recommendations. Neurosurgery 2020; 87 (03) 427-434
- 6 Jha S, Ghewade P. Management and treatment of traumatic brain injuries. Cureus 2022; 14 (10) e30617
- 7 Vella MA, Crandall ML, Patel MB. Acute management of traumatic brain injury. Surg Clin North Am 2017; 97 (05) 1015-1030
- 8 Wang YH, Yang FY, Lian XY, Yang WJ. Effect of hyperbaric oxygen on the plasma endothelins in rats with severe head injury. Zhongguo Linchuang Kangfu 2004; 8 (01) 54-55
- 9 Hu SL, Hu R, Li F. et al. Hyperbaric oxygen preconditioning protects against traumatic brain injury at high altitude. Acta Neurochir Suppl (Wien) 2008; 105 (105) 191-196
- 10 Jin Z, Zhang ZJ, Bai Y. Intervention of hyperbaric oxygen treatment for the neuronal apoptosis and the expression of cyclooxygenase 2 in rats with head injury in an early period. Zhongguo Linchuang Kangfu 2006; 10 (38) 97-99
- 11 Artru F, Chacornac R, Deleuze R. Hyperbaric oxygenation for severe head injuries. Preliminary results of a controlled study. Eur Neurol 1976; 14 (04) 310-318
- 12 Cifu DX, Hart BB, West SL, Walker W, Carne W. The effect of hyperbaric oxygen on persistent postconcussion symptoms. J Head Trauma Rehabil 2014; 29 (01) 11-20
- 13 Ren B, Ye H, Shan W, Tao X, Ye Z. Effect of hyperbaric oxygen intervention on oxidative stress and expression of nerve growth factor in patients with craniocerebral injury. J Inflamm Res 2023; 16: 4925-4932
- 14 Rockswold GL, Ford SE, Anderson DC, Bergman TA, Sherman RE. Results of a prospective randomized trial for treatment of severely brain-injured patients with hyperbaric oxygen. J Neurosurg 1992; 76 (06) 929-934
- 15 Walker JM, Mulatya C, Hebert D, Wilson SH, Lindblad AS, Weaver LK. Sleep assessment in a randomized trial of hyperbaric oxygen in U.S. service members with post concussive mild traumatic brain injury compared to normal controls. Sleep Med 2018; 51: 66-79
- 16 Xie Z, Zhuang M, Lin L, Xu H, Chen L, Hu L. Changes of plasma C-reactive protein in patients with craniocerebral injury before and after hyperbaric oxygenation: a randomly controlled study. Neural Regen Res 2007; 2 (05) 314-317
- 17 Page MJ, McKenzie JE, Bossuyt PM. et al. The PRISMA 2020 statement: an updated guideline for reporting systematic reviews. BMJ 2021; 372 (71) n71
- 18 Barker TH, Stone JC, Sears K. et al. The revised JBI critical appraisal tool for the assessment of risk of bias for randomized controlled trials. JBI Evid Synth 2023; 21 (03) 494-506
- 19 Barrett KF, Masel B, Patterson J, Scheibel RS, Corson KP, Mader JT. Regional CBF in chronic stable TBI treated with hyperbaric oxygen. Undersea Hyperb Med 2004; 31 (04) 395-406
- 20 Churchill S, Deru K, Weaver LK. et al. Adverse events and blinding in two randomized trials of hyperbaric oxygen for persistent post-concussive symptoms. Undersea Hyperb Med 2019; 46 (03) 331-340
- 21 Hu S, Li F, Luo H. et al. Amelioration of rCBF and PbtO2 following TBI at high altitude by hyperbaric oxygen pre-conditioning. Neurol Res 2010; 32 (02) 173-178
- 22 Mao JH, Sun ZS, Xiang Y. Observation of curative effects of hyperbaric oxygen for treatment on severe craniocerebral injury. J Clin Neurol 2010; 23 (05) 386-388
- 23 Nelson AG, Wolf Jr EG, Li B. Influence of delayed hyperbaric oxygenation on recovery from mechanically induced damage. Undersea & Hyperbaric Medicine 1994; 21 (02) 185-191
- 24 Rasmussen VM, Borgen AE, Jansen EC, Rotbøll Nielsen PH, Werner MU. Hyperbaric oxygen therapy attenuates central sensitization induced by a thermal injury in humans. Acta Anaesthesiol Scand 2015; 59 (06) 749-762
- 25 Wolf EG, Prye J, Michaelson R, Brower G, Profenna L, Boneta O. Hyperbaric side effects in a traumatic brain injury randomized clinical trial. Undersea Hyperb Med 2012; 39 (06) 1075-1082
- 26 Chawla A, Lavania AK. Oxygen toxicity. Med J Armed Forces India 2001; 57 (02) 131-133
- 27 Hyperbaric Oxygen Therapy (HBO2) for Persistent Post-concussive Symptoms After Mild Traumatic Brain Injury (mTBI) | ClinicalTrials.gov.
- 28 mTBI Mechanisms of Action of HBO2 for Persistent Post-Concussive Symptoms | ClinicalTrials.gov.
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04. Juni 2024
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References
- 1 Rockswold SB, Rockswold GL, Zaun DA, Liu J. A prospective, randomized Phase II clinical trial to evaluate the effect of combined hyperbaric and normobaric hyperoxia on cerebral metabolism, intracranial pressure, oxygen toxicity, and clinical outcome in severe traumatic brain injury. J Neurosurg 2013; 118 (06) 1317-1328
- 2 Liu H-y, Shang Y-h. Effect of guipizide maleate with hyperbaric oxygen therapy on neurophysiology and coagulation indices in patients with severe craniocerebral injury. Trop J Pharm Res 2023; 22 (07) 1483-1488
- 3 Konar S, Maurya I, Shukla DP. et al. Intensive care unit management of traumatic brain injury patients. Journal of Neurointensive Care. 2022; 5 (01) 1-8
- 4 Agrawal A, Savardekar A, Singh M. et al. Pattern of reporting and practices for the management of traumatic brain injury: an overview of published literature from India. Neurol India 2018; 66 (04) 976-1002
- 5 Hawryluk GWJ, Rubiano AM, Totten AM. et al. Guidelines for the management of severe traumatic brain injury: 2020 update of the decompressive craniectomy recommendations. Neurosurgery 2020; 87 (03) 427-434
- 6 Jha S, Ghewade P. Management and treatment of traumatic brain injuries. Cureus 2022; 14 (10) e30617
- 7 Vella MA, Crandall ML, Patel MB. Acute management of traumatic brain injury. Surg Clin North Am 2017; 97 (05) 1015-1030
- 8 Wang YH, Yang FY, Lian XY, Yang WJ. Effect of hyperbaric oxygen on the plasma endothelins in rats with severe head injury. Zhongguo Linchuang Kangfu 2004; 8 (01) 54-55
- 9 Hu SL, Hu R, Li F. et al. Hyperbaric oxygen preconditioning protects against traumatic brain injury at high altitude. Acta Neurochir Suppl (Wien) 2008; 105 (105) 191-196
- 10 Jin Z, Zhang ZJ, Bai Y. Intervention of hyperbaric oxygen treatment for the neuronal apoptosis and the expression of cyclooxygenase 2 in rats with head injury in an early period. Zhongguo Linchuang Kangfu 2006; 10 (38) 97-99
- 11 Artru F, Chacornac R, Deleuze R. Hyperbaric oxygenation for severe head injuries. Preliminary results of a controlled study. Eur Neurol 1976; 14 (04) 310-318
- 12 Cifu DX, Hart BB, West SL, Walker W, Carne W. The effect of hyperbaric oxygen on persistent postconcussion symptoms. J Head Trauma Rehabil 2014; 29 (01) 11-20
- 13 Ren B, Ye H, Shan W, Tao X, Ye Z. Effect of hyperbaric oxygen intervention on oxidative stress and expression of nerve growth factor in patients with craniocerebral injury. J Inflamm Res 2023; 16: 4925-4932
- 14 Rockswold GL, Ford SE, Anderson DC, Bergman TA, Sherman RE. Results of a prospective randomized trial for treatment of severely brain-injured patients with hyperbaric oxygen. J Neurosurg 1992; 76 (06) 929-934
- 15 Walker JM, Mulatya C, Hebert D, Wilson SH, Lindblad AS, Weaver LK. Sleep assessment in a randomized trial of hyperbaric oxygen in U.S. service members with post concussive mild traumatic brain injury compared to normal controls. Sleep Med 2018; 51: 66-79
- 16 Xie Z, Zhuang M, Lin L, Xu H, Chen L, Hu L. Changes of plasma C-reactive protein in patients with craniocerebral injury before and after hyperbaric oxygenation: a randomly controlled study. Neural Regen Res 2007; 2 (05) 314-317
- 17 Page MJ, McKenzie JE, Bossuyt PM. et al. The PRISMA 2020 statement: an updated guideline for reporting systematic reviews. BMJ 2021; 372 (71) n71
- 18 Barker TH, Stone JC, Sears K. et al. The revised JBI critical appraisal tool for the assessment of risk of bias for randomized controlled trials. JBI Evid Synth 2023; 21 (03) 494-506
- 19 Barrett KF, Masel B, Patterson J, Scheibel RS, Corson KP, Mader JT. Regional CBF in chronic stable TBI treated with hyperbaric oxygen. Undersea Hyperb Med 2004; 31 (04) 395-406
- 20 Churchill S, Deru K, Weaver LK. et al. Adverse events and blinding in two randomized trials of hyperbaric oxygen for persistent post-concussive symptoms. Undersea Hyperb Med 2019; 46 (03) 331-340
- 21 Hu S, Li F, Luo H. et al. Amelioration of rCBF and PbtO2 following TBI at high altitude by hyperbaric oxygen pre-conditioning. Neurol Res 2010; 32 (02) 173-178
- 22 Mao JH, Sun ZS, Xiang Y. Observation of curative effects of hyperbaric oxygen for treatment on severe craniocerebral injury. J Clin Neurol 2010; 23 (05) 386-388
- 23 Nelson AG, Wolf Jr EG, Li B. Influence of delayed hyperbaric oxygenation on recovery from mechanically induced damage. Undersea & Hyperbaric Medicine 1994; 21 (02) 185-191
- 24 Rasmussen VM, Borgen AE, Jansen EC, Rotbøll Nielsen PH, Werner MU. Hyperbaric oxygen therapy attenuates central sensitization induced by a thermal injury in humans. Acta Anaesthesiol Scand 2015; 59 (06) 749-762
- 25 Wolf EG, Prye J, Michaelson R, Brower G, Profenna L, Boneta O. Hyperbaric side effects in a traumatic brain injury randomized clinical trial. Undersea Hyperb Med 2012; 39 (06) 1075-1082
- 26 Chawla A, Lavania AK. Oxygen toxicity. Med J Armed Forces India 2001; 57 (02) 131-133
- 27 Hyperbaric Oxygen Therapy (HBO2) for Persistent Post-concussive Symptoms After Mild Traumatic Brain Injury (mTBI) | ClinicalTrials.gov.
- 28 mTBI Mechanisms of Action of HBO2 for Persistent Post-Concussive Symptoms | ClinicalTrials.gov.

