Treatment of children with hyperbaric oxygenation (HBOT): a Europe-wide survey.

BACKGROUND: Hyperbaric oxygenation therapy (HBOT) is used as emergency treatment for decompression sickness, gas embolism, carbon monoxide intoxication, and necrotizing fasciitis. There is low evidence and little clinical knowledge about the treatment of children with HBOT. METHODS: We sent an internet-based questionnaire to HBO centers in Europe to gain information about their experience with children and HBOT. RESULTS: Out of all HBO-centers who participated in the questionnaire 90% treat children analogue to adults about indication and HBOT protocol. Most treated children had life-threatening indications or the risk of organ loss. The reported rate of side effects was: 6.8% anxiety, 2.4% barotrauma, 0.9% seizure, 0.2% retinopathy and no case of pulmonary barotrauma or oxygen toxicity. CONCLUSIONS: HBO therapy for children is present in European HBO centers. The rate of severe side effects is as low to the rates in adults; apart from this, oxygen-related seizures and anxiety are more frequent. A special focus seems necessary on the psychological management of the children, because anxiety is common depending on the age of the children. Especially for smaller children, an adequate psychological support seems essential. Prospective observational or controlled studies in children seem necessary to create relevant clinical evidence for HBOT and to observe the rate of side-effects.

The Effect of Hyperbaric Oxygen Therapy on Human Adipose-Derived Stem Cells.

BACKGROUND: Adipose-derived stem cells are considered as candidate cells for regenerative plastic surgery. Measures to influence cellular properties and thereby direct their regenerative potential remain elusive. Hyperbaric oxygen therapy-the exposure to 100% oxygen at an increased atmospheric pressure-has been propagated as a noninvasive treatment for a multitude of indications and presents a potential option to condition cells for tissue-engineering purposes. The present study evaluates the effect of hyperbaric oxygen therapy on human adipose-derived stem cells. METHODS: Human adipose-derived stem cells from healthy donors were treated with hyperbaric oxygen therapy at 2 and 3 atm. Viability before and after each hyperbaric oxygen therapy, proliferation, expression of surface markers and protein contents of transforming growth factor (TGF)-ß, tumor necrosis factor-α, hepatocyte growth factor, and epithelial growth factor in the supernatants of treated adipose-derived stem cells were measured. Lastly, adipogenic, osteogenic, and chondrogenic differentiation with and without use of differentiation-inducing media (i.e., autodifferentiation) was examined. RESULTS: Hyperbaric oxygen therapy with 3 atm increased viability, proliferation, and CD34 expression and reduced the CD31/CD34/CD45 adipose-derived stem cell subset and endothelial progenitor cell population. TGF-ß levels were significantly decreased after two hyperbaric oxygen therapy sessions in the 2-atm group and decreased after three hyperbaric oxygen therapy sessions in the 3-atm group. Hepatocyte growth factor secretion remained unaltered in all groups. Although the osteogenic and chondrogenic differentiation were not influenced, adipogenic differentiation and autodifferentiation were significantly enhanced, with osteogenic autodifferentiation significantly alleviated by hyperbaric oxygen therapy with 3 atm. CONCLUSION: Hyperbaric oxygen therapy with 3 atm increases viability and proliferation of adipose-derived stem cells, alters marker expression and subpopulations, decreases TGF-ß secretion, and skews adipose-derived stem cells toward adipogenic differentiation. CLINICAL QUESTION/LEVEL OF EVIDENCE: Therapeutic, V.

Development of visual acuity under hyperbaric oxygen treatment (HBO) in non arteritic retinal branch artery occlusion.

PURPOSE: Nonperfusion of retinal tissue due to arterial occlusion leads inevitably to mostly irreversible retinal damage. Until today no evidence-based treatment exists. Inhalation of 100% oxygen at high atmospheric pressure causes an increased solubility of oxygen in the blood that helps the retinal tissue to survive through diffusion in case of an artery occlusion till vascular recanalization occurs. Hence the purpose of this study is to compare the visual outcome in patients with retinal branch artery obstruction treated with hyperbaric oxygen versus patients treated with hemodilution only. METHODS: Non-randomized, monocentric, retrospective study. Patients with diagnosis of non-arteritic retinal branch artery occlusion (BRAO) treated with hyperbaric oxygen therapy between 1997 and 2017. Exclusion criteria were central retinal artery occlusion, presence of a cilioretinal artery and arteritic cases. The control group was matched based on visual acuity (VA) at admission, age, and delay between symptoms and beginning of clinical care. RESULTS: The control group and the matching oxygen group contained 14 patients each. Initial VA in the matched HBO group was 0.18 ± 0.19 and 0.23 ± 0.19 in the control group (p = 0.57). Final VA at discharge was 0.69 ± 0.29 in the matched oxygen group and 0.32 ± 0.23 in the control group (p = 0.0009). HBO-treated patients had a significant visual increase compared with the control group. The most common comorbidities were arterial hypertension and vascular sclerosis. CONCLUSION: HBO treatment appears to have a beneficial effect on visual outcome in patients with retinal branch artery occlusion. HBO treatment could be a rescue therapy at an early stage of BRAO, especially to bridge the time of a potential reperfusion. However, further, prospective, randomized clinical trials are required to verify this assumption.

A single air dive induces apoptotic gene regulation but no increase in nucleosomes.

BACKGROUND: Oxidative stress caused by elevated partial pressure of oxygen during diving is a major contributor of inflammation and apoptosis. The underlying molecular mechanisms are poorly understood. The aim of the study was to describe apoptotic gene regulation induced by a single air dive. METHODS: 19 healthy volunteers were exposed to a 30-minute dive at 2.8 atmospheres (ATA) absolute in a pressure chamber in ambient air. Blood samples were obtained before, directly after and 24 hours after exposure. Gene expressions of Bcl-2, Bcl-xL and Bax were analyzed in mononuclear cell extracts by real-time polymerase chain reaction (PCR). Circulating nucleosomes were measured in serum before exposure and 24 hours afterward. RESULTS: The pro-apoptotic Bax expression was not significantly increased (p=0.74) directly after the dive but was induced (2.22 ± 0.85-fold) after 24 hours (p ≤ 0.01). Bcl-2 expression was not changed significantly directly after (p = 0.11) but was 1.88 ± 1.08-fold higher after 24 hours (p ≤ 0.01). Bcl-xL expression was not elevated significantly (p = 0.54) but was 2.04 ± 1.02-fold higher after 24 hours (p ≤ 0.01). The level of nucleosomes did not change after 24 hours compared to baseline. CONCLUSION: A single air dive at 2.8 ATA for 30 minutes causes an upregulation of pro- and anti-apoptotic genes but did not elevate circulating nucleosomes. In a single air dive the upregulation of anti-apoptotic Bcl-2 family members may counteract the pro-apoptotic potential of Bax.

Cerebral air embolism after pleural streptokinase instillation.

Iatrogenic pulmonary barotrauma and cerebral arterial gas embolism (CAGE) may complicate a variety of medical procedures, such as certain types of surgery, drug administration through thoracic drainage, pneumoperitoneum, cystoscopy, bronchoscopy, etc. Hyperbaric oxygen treatment following the guidelines for CAGE in diving is the treatment of choice. Pleural streptokinase instillation is a common treatment for parapneumonic pleural effusion and may lead to CAGE. We present such a complication in a 79-year-old woman with a left-sided empyema. Neurological recovery was reasonable, but a left hemiparesis persisted. Prompt treatment of CAGE is necessary to avoid permanent injury and severe disability.

Early hyperbaric oxygen treatment for nonarteritic central retinal artery obstruction.

PURPOSE: To compare hyperbaric oxygen treatment combined with hemodilution with hemodilution only in central retinal artery obstruction. DESIGN: Retrospective, nonrandomized case series. METHODS: We reviewed records of all our patients diagnosed with central retinal artery obstruction between 1997 and 2010. In these patients, hyperbaric oxygen and hemodilution therapy had been administered routinely (oxygen group). Where hyperbaric oxygenation could not be performed, patients were underwent hemodilution only (control group). Patients with presenting visual acuity (VA) of up to 20/200 within 12 hours of onset were included in our analysis. Exclusion criteria included cilioretinal vessels or arteritic occlusion. RESULTS: The oxygen group comprised 51 patients, and the control group comprised 29 patients. Mean baseline VA was counting fingers (oxygen group) and 20/1000 (control group; P = .1). Most other potential confounders, including duration of symptoms, also did not differ significantly at baseline. In the oxygen group, mean VA improvement was 3 lines (P < .0001). This was sustained over a follow-up of 3 months (P = .01). In the control group, mean improvement was 1 line (P = .23 at discharge, P = .17 at follow-up). Differences between both groups were not significant (P = .07 at discharge, P = .26 at follow-up). The number of patients gaining 3 lines or more was 38.0% versus 17.9% at discharge (P = .06) and 35.7% versus 30.8% at follow-up (P = .76). CONCLUSIONS: We saw significant VA improvement after the combined treatment, but not when using hemodilution only. Confirming superiority of the combination treatment requires a randomized, prospective trial. A high number of nonresponders highlights the need to improve our understanding and treatment of hypoxia-related metabolic insults after central retinal artery obstruction.

Hyperbaric oxygen induces apoptosis via a mitochondrial mechanism.

During therapeutic hyperbaric oxygenation lymphocytes are exposed to high partial pressures of oxygen. This study aimed to analyze the mechanism of apoptosis induction by hyperbaric oxygen. For intervals of 0.5-4 h Jurkat-T-cells were exposed to ambient air or oxygen atmospheres at 1-3 absolute atmospheres. Apoptosis was analyzed by phosphatidylserine externalization, caspase-3 activation and DNA-fragmentation using flow cytometry. Apoptosis was already induced after 30 min of hyperbaric oxygenation (HBO, P < 0.05). The death receptor Fas was downregulated. Inhibition of caspase-9 but not caspase-8 blocked apoptosis induction by HBO. Hyperbaric oxygen caused a loss of mitochondrial membrane potential and caspase-9 induction. The mitochondrial pro-survival protein Bcl-2 was upregulated, and antagonizing Bcl-2 function potentiated apoptosis induction by HBO. In conclusion, a single exposure to hyperbaric oxygenation induces lymphocyte apoptosis by a mitochondrial and not a Fas-related mechanism. Regulation of Fas and Bcl-2 may be regarded as protective measures of the cell in response to hyperbaric oxygen.

[Treatment of Acute Central Retinal Artery Occlusion (CRAO) by Hyperbaric Oxygenation Therapy (HBO)--Pilot study with 21 patients]. / Behandlung akuter retinaler Zentralarterienverschlüsse (ZAV) mit der hyperbaren Sauerstofftherapie (HBO)--Pilotstudie an 21 Patienten.

BACKGROUND: Central retinal artery occlusion causes severe loss of vision. Treatment trials include massage of the globe, paracentesis, antiglaucomatous eye drops, haemodilution or lysis therapy, which in individual cases did improve the visual outcome, although in general the prognosis remains poor. In this study we applied hyperbaric oxygenation treatment additionally to haemodilution to overcome retinal ischaemia until spontaneous recanalisation of the central retinal artery occurs. PATIENTS AND METHODS: Patients with central retinal artery occlusion and onset of symptoms up to 12 h were included. Following initial ocular massage and application of antiglaucomatous eyedrops, hyperbaric oxygenation treatment was performed twice daily for up to three days. RESULTS: 21 patients could be included. The time lag between onset of symptoms and admission was between 4 and 12 h. Initial visual acuity ranged from light perception to 0.08. On discharge 19 patients reported on a subjective visual improvement which could be confirmed in 13 patients. In 9 patients an initial increase of visual acuity under hyperbaric oxygenation treatment could be observed which however was again reduced by at least one line on discharge. No patient experienced vision loss below admission vision. CONCLUSIONS: Hyperbaric oxygenation treatment seems to improve the visual outcome in central retinal artery occlusion. Major parameters for visual prognosis are the time lag from the onset of symptoms to the beginning of hyperbaric oxygenation treatment and the time lag until retinal reperfusion begins. Hyperbaric oxygenation treatment can compensate retinal ischaemia; however, the lack of glucose and accumulation of toxic metabolites is not addressed. A combination of hyperbaric oxygenation treatment with administration of glutamate antagonists or intravitreal glucose application might further improve the visual outcome.