Hyperbaric oxygen therapy effects on pulmonary functions: a prospective cohort study.

BACKGROUND: Oxygen toxicity is one potential side effect of hyperbaric oxygen therapy (HBOT). Previous small studies showed mild reductions in pulmonary functions reflecting reductions in small airway conductance after repetitive hyperbaric oxygen sessions. However, there are no updated data with well performed pulmonary tests that address the pulmonary effect of the currently used HBOT protocols. The aim of this study was to evaluate the effect of HBOT on pulmonary functions of patients receiving the currently used HBOT protocol. METHODS: Prospective analysis included patients, 18 years or older, scheduled for 60 daily HBOT sessions between 2016 and 2018. Each session was 90 min of 100% oxygen at 2 ATA with 5 min air breaks every 20 min, 5 days per week. Pulmonary functions, measured at baseline and after HBOT, included forced vital capacity (FVC), forced expiratory volume in 1 sec (FEV1) and peak expiratory flow rate (PEF). RESULTS: The mean age was 60.36 ± 15.43 and 62.5% (55/88) were males. Most of the patients (83/88, 94.3%) did not have any pulmonary disease prior to inclusion and 30.7% (27/88) had a history of smoking. Compared to baseline values, at the completion of 60 HBOT sessions, there were no significant changes in FEV1 (0.163), FEV1/FVC ratio (0.953) and FEF25-75% (0.423). There was a statistically significant increase though not clinically relevant increase in FVC (0.1 ± 0.38 l) and PEF (0.5 ± 1.4 l) with a 0.014 and 0.001 respectively. CONCLUSION: Regarding pulmonary functions, repeated hyperbaric oxygen exposure based on the currently used HBOT protocol is safe. Surprisingly, there was a modest non clinically significant though statistically significant improvement in PEF and FVC in the current cohort of patients who were without chronic lung diseases. TRIAL REGISTRATION: Clinicaltrials.gov, trial ID: NCT03754985 , (Nov 2018) Retrospectively registered.

Correction: Hyperbaric oxygen can induce angiogenesis and recover erectile function.

This has been corrected in both the PDF and HTML versions of the Article.

Hyperbaric oxygen can induce angiogenesis and recover erectile function.

Erectile dysfunction (ED) is caused by microvascular or macrovascular insufficiency in the majority of patients. Recent studies have shown that hyperbaric oxygen therapy (HBOT) can induce angiogenesis in different body organs. The effect of HBOT on the non-surgery-related ED has not been investigated yet. The aim of the current study was to evaluate the effects of HBOT on sexual function and penile vascular bed in non-surgical ED patients. A prospective analysis of patients suffering from chronic ED treated with 40 daily HBOT sessions. Clinical efficacy was assessed using the International Index of Erectile Function questionnaire (IIEF) and a global efficacy question (GEQ). The effect on the penile vascular bed was evaluated by perfusion MRI. Thirty men (mean age of 59.2 ± 1.4) suffering from ED for 4.2 ± 0.6 years completed the protocol. HBOT significantly improved all IIEF domains by 15-88% (p < 0.01). Erectile function improved by 88% (p < 0.0001) and 80% of the patients reported positive outcome according to the GEQ. Angiogenesis was indicated by perfusion MRI that showed a significant increase by 153.3 ± 43.2% of K-trans values in the corpous cavernous (p < 0.0001). HBOT can induce penile angiogenesis and improve erectile function in men suffering from EcD. HBOT reverses the basic common pathophysiology, atherosclerosis and decreased penile perfusion, responsible for most cases of ED.

Reversibility of retinal ischemia due to central retinal artery occlusion by hyperbaric oxygen.

PURPOSE: Ischemic retinal damage can be reversed by hyperbaric oxygen therapy (HBOT) as long as irreversible infarction damage has not developed. However, the time window till irreversible damage develops is still unknown. The study aim was to evaluate the effect of HBOT and determine possible markers for irreversible retinal damage. MATERIALS AND METHODS: Retrospective analysis of 225 patients treated with HBOT for central retinal artery occlusion (CRAO) in 1999-2015. One hundred and twenty-eight patients fulfilled inclusion/exclusion criteria: age >18 years, symptoms <20 hours, and best-corrected visual acuity (BCVA) <0.5 logMAR. RESULTS: Time delay from symptoms to treatment was 7.8±3.8 hours. The BCVA was significantly improved after HBOT, from 2.14±0.50 to 1.61±0.78 (P<0.0001). The proportion of patients with clinically meaningful visual improvement was significantly higher in patients without cherry-red spot (CRS) compared to patients with CRS at presentation (86.0% vs 57.6%, P<0.0001). The percentage of patients with final BCVA better than 1.0 was also significantly higher in patients without CRS vs patients with CRS at presentation (61.0% vs 7.1%, P<0.0001). There was no correlation between CRS and the time from symptoms. HBOT was found to be safe, and only 5.5% of patients had minor, reversible, adverse events. CONCLUSION: HBOT is an effective treatment for non-arteritic CRAO as long as CRS has not formed. The fundus findings, rather than the time delay, should be used as a marker for irreversible damage.

Hyperbaric oxygen therapy can diminish fibromyalgia syndrome--prospective clinical trial.

BACKGROUND: Fibromyalgia Syndrome (FMS) is a persistent and debilitating disorder estimated to impair the quality of life of 2-4% of the population, with 9:1 female-to-male incidence ratio. FMS is an important representative example of central nervous system sensitization and is associated with abnormal brain activity. Key symptoms include chronic widespread pain, allodynia and diffuse tenderness, along with fatigue and sleep disturbance. The syndrome is still elusive and refractory. The goal of this study was to evaluate the effect of hyperbaric oxygen therapy (HBOT) on symptoms and brain activity in FMS. METHODS AND FINDINGS: A prospective, active control, crossover clinical trial. Patients were randomly assigned to treated and crossover groups: The treated group patients were evaluated at baseline and after HBOT. Patients in the crossover-control group were evaluated three times: baseline, after a control period of no treatment, and after HBOT. Evaluations consisted of physical examination, including tender point count and pain threshold, extensive evaluation of quality of life, and single photon emission computed tomography (SPECT) imaging for evaluation of brain activity. The HBOT protocol comprised 40 sessions, 5 days/week, 90 minutes, 100% oxygen at 2ATA. Sixty female patients were included, aged 21-67 years and diagnosed with FMS at least 2 years earlier. HBOT in both groups led to significant amelioration of all FMS symptoms, with significant improvement in life quality. Analysis of SPECT imaging revealed rectification of the abnormal brain activity: decrease of the hyperactivity mainly in the posterior region and elevation of the reduced activity mainly in frontal areas. No improvement in any of the parameters was observed following the control period. CONCLUSIONS: The study provides evidence that HBOT can improve the symptoms and life quality of FMS patients. Moreover, it shows that HBOT can induce neuroplasticity and significantly rectify abnormal brain activity in pain related areas of FMS patients. TRIAL REGISTRATION: ClinicalTrials.gov NCT01827683.

Delayed recompression for decompression sickness: retrospective analysis.

INTRODUCTION: Most cases of decompression sickness (DCS) occur soon after surfacing, with 98% within 24 hours. Recompression using hyperbaric chamber should be administrated as soon as feasible in order to decrease bubble size and avoid further tissue injury. Unfortunately, there may be a significant time delay from surfacing to recompression. The time beyond which hyperbaric treatment is non effective is unclear. The aims of the study were first to evaluate the effect of delayed hyperbaric treatment, initiated more than 48 h after surfacing for DCS and second, to evaluate the different treatment protocols. METHODS: From January 2000 to February 2014, 76 divers had delayed hyperbaric treatment (≥48 h) for DCS in the Sagol center for Hyperbaric medicine and Research, Assaf-Harofeh Medical Center, Israel. Data were collected from their medical records and compared to data of 128 patients treated earlier than 48 h after surfacing at the same hyperbaric institute. RESULTS: There was no significant difference, as to any of the baseline characteristics, between the delayed and early treatment groups. With respect to treatment results, at the delayed treatment divers, complete recovery was achieved in 76% of the divers, partial recovery in 17.1% and no improvement in 6.6%. Similar results were achieved when treatment started early, where 78% of the divers had complete recovery, 15.6% partial recovery and 6.2% no recovery. Delayed hyperbaric treatment using US Navy Table 6 protocol trended toward a better clinical outcome yet not statistically significant (OR=2.786, CI95%[0.896-8.66], p=0.07) compared to standard hyperbaric oxygen therapy of 90 minutes at 2 ATA, irrespective of the symptoms severity at presentation. CONCLUSIONS: Late recompression for DCS, 48 hours or more after surfacing, has clinical value and when applied can achieve complete recovery in 76% of the divers. It seems that the preferred hyperbaric treatment protocol should be based on US Navy Table 6.

Hyperbaric oxygen therapy can improve post concussion syndrome years after mild traumatic brain injury - randomized prospective trial.

BACKGROUND: Traumatic brain injury (TBI) is the leading cause of death and disability in the US. Approximately 70-90% of the TBI cases are classified as mild, and up to 25% of them will not recover and suffer chronic neurocognitive impairments. The main pathology in these cases involves diffuse brain injuries, which are hard to detect by anatomical imaging yet noticeable in metabolic imaging. The current study tested the effectiveness of Hyperbaric Oxygen Therapy (HBOT) in improving brain function and quality of life in mTBI patients suffering chronic neurocognitive impairments. METHODS AND FINDINGS: The trial population included 56 mTBI patients 1-5 years after injury with prolonged post-concussion syndrome (PCS). The HBOT effect was evaluated by means of prospective, randomized, crossover controlled trial: the patients were randomly assigned to treated or crossover groups. Patients in the treated group were evaluated at baseline and following 40 HBOT sessions; patients in the crossover group were evaluated three times: at baseline, following a 2-month control period of no treatment, and following subsequent 2-months of 40 HBOT sessions. The HBOT protocol included 40 treatment sessions (5 days/week), 60 minutes each, with 100% oxygen at 1.5 ATA. "Mindstreams" was used for cognitive evaluations, quality of life (QOL) was evaluated by the EQ-5D, and changes in brain activity were assessed by SPECT imaging. Significant improvements were demonstrated in cognitive function and QOL in both groups following HBOT but no significant improvement was observed following the control period. SPECT imaging revealed elevated brain activity in good agreement with the cognitive improvements. CONCLUSIONS: HBOT can induce neuroplasticity leading to repair of chronically impaired brain functions and improved quality of life in mTBI patients with prolonged PCS at late chronic stage. TRIAL REGISTRATION: ClinicalTrials.gov NCT00715052.

Hyperbaric oxygen induces late neuroplasticity in post stroke patients--randomized, prospective trial.

BACKGROUND: Recovery after stroke correlates with non-active (stunned) brain regions, which may persist for years. The current study aimed to evaluate whether increasing the level of dissolved oxygen by Hyperbaric Oxygen Therapy (HBOT) could activate neuroplasticity in patients with chronic neurologic deficiencies due to stroke. METHODS AND FINDINGS: A prospective, randomized, controlled trial including 74 patients (15 were excluded). All participants suffered a stroke 6-36 months prior to inclusion and had at least one motor dysfunction. After inclusion, patients were randomly assigned to "treated" or "cross" groups. Brain activity was assessed by SPECT imaging; neurologic functions were evaluated by NIHSS, ADL, and life quality. Patients in the treated group were evaluated twice: at baseline and after 40 HBOT sessions. Patients in the cross group were evaluated three times: at baseline, after a 2-month control period of no treatment, and after subsequent 2-months of 40 HBOT sessions. HBOT protocol: Two months of 40 sessions (5 days/week), 90 minutes each, 100% oxygen at 2 ATA. We found that the neurological functions and life quality of all patients in both groups were significantly improved following the HBOT sessions while no improvement was found during the control period of the patients in the cross group. Results of SPECT imaging were well correlated with clinical improvement. Elevated brain activity was detected mostly in regions of live cells (as confirmed by CT) with low activity (based on SPECT) - regions of noticeable discrepancy between anatomy and physiology. CONCLUSIONS: The results indicate that HBOT can lead to significant neurological improvements in post stroke patients even at chronic late stages. The observed clinical improvements imply that neuroplasticity can still be activated long after damage onset in regions where there is a brain SPECT/CT (anatomy/physiology) mismatch.

Effects of hyperbaric oxygen on blood glucose levels in patients with diabetes mellitus, stroke or traumatic brain injury and healthy volunteers: a prospective, crossover, controlled trial.

INTRODUCTION: A decrease in blood glucose levels (BGL) during hyperbaric oxygen treatment (HBOT) is a well-recognised phenomenon, but studies of this are limited and inconclusive. This study evaluated the effect of HBOT on BGL in patients with diabetes mellitus (DM), traumatic brain injury (TBI) or stroke and healthy volunteers in a prospective, open, controlled trial. METHODS: Thirty-nine participants were enrolled and evaluated twice: once during HBOT (90 minutes at 203 kPa), and once during a control session on normobaric air. Sessions were held up to two weeks apart and participants were instructed to eat the same diet. BGL was measured before, during and at the completion of each session. RESULTS: For the whole study group, there was a small but statistically significant decrease in BGL in both the HBOT (7.27 ± 3.66 mmol⁻¹ before to 6.71 ± 3.88 mmol ⁻¹ after, P = 0.037) and control (air) sessions (7.43 ± 3.49 mmol L⁻¹ before to 6.71 ± 3.77 mmol L⁻¹ after, P = 0.004). This fall did not differ between the two conditions (P = 0.59). Examining the three groups separately, BGL fell in all three subgroups, but this fall was only statistically significant for the air session in the diabetic group. There were no statistically significant differences in the BGL reduction when HBOT was compared to normobaric air in any of the three subgroups. CONCLUSIONS: BGL may decrease during HBOT and accordingly it should be monitored before entering the chamber. However, this decrease in BGL should probably not be attributed to the hyperbaric environment per se.