Real-world effectiveness of hyperbaric oxygen therapy for delayed neuropsychiatric sequelae after carbon monoxide poisoning.

To assess real-world effectiveness of hyperbaric oxygen therapy (HBOT) on delayed neuropsychiatric sequelae (DNS) after carbon monoxide (CO) poisoning we conducted a retrospective review of patients with CO poisoning admitted to Linkou Chang-Gung Memorial Hospital, Taiwan's largest medical center, during 2009-2015. We included patients developing DNS after CO poisoning and compared improvements in neuropsychiatric function, with and without HBOT, after 12 months post-DNS to understand differences in recovery rates. DNS improvement-associated factors were also evaluated. We used receiver operating characteristic (ROC) curve analysis to assess the role of time elapsed between DNS diagnosis and HBOT initiation in predicting DNS improvement. A total of 62 patients developed DNS, of whom 11 recovered while the rest did not. Possible factors predicting DNS improvement included receiving HBOT post-DNS (72.7% vs 25.5%; P = 0.006), and treatment with more than three HBOT sessions during acute stage CO poisoning (81.8% vs 27.5%; P = 0.003). The relevant area under the ROC curve was 0.789 (95% CI 0.603-0.974), and the best cut-off point was 3 days post-DNS diagnosis, with 87.5% sensitivity and 61.5% specificity. Early HBOT in patients who developed DNS after CO poisoning significantly improved their DNS symptoms, with treatment effects sustained for 1 year after DNS diagnosis.

Targeting optimal time for hyperbaric oxygen therapy following carbon monoxide poisoning for prevention of delayed neuropsychiatric sequelae: A retrospective study.

OBJECTIVES: Delayed neuropsychiatric sequelae (DNS) are serious complications of carbon monoxide poisoning; neuropsychiatric disorders can occur within a few days of recovery from acute poisoning. Hyperbaric oxygen therapy (HBOT) has been the main treatment of carbon monoxide (CO) poisoning and was recommended as the treatment choice for CO poisoning by the American Undersea and Hyperbaric Medical Society and the Tenth European Consensus Conference on Hyperbaric Medicine of the European Underwater and Baromedical Society. However, the optimal timing for commencing HBOT in patients with CO poisoning remains unknown. We therefore conducted a retrospective study in an attempt to target the optimal time of HBOT for DNS prevention. METHODS: A retrospective review of patient files/medical records was conducted on all patients with CO poisoning admitted to the Emergency Department of Linkou Chang-Gung Memorial Hospital, Taiwan between January 1, 2009 and December 31, 2015. A total of 279 patients who received HBOT were eligible for further DNS detection. DNS was defined as the presence of one of the following neurological, cognitive, or psychological sequelae that were documented in the medical record during hospital stay or outpatient clinic follow-up for at least 6 months. A multivariable logistic regression analysis was employed to identify potential determinants of DNS after receiving HBOT for CO poisoning. A receiver operating characteristic (ROC) curve was used to analyse the influence of duration from CO exposure to HBOT on DNS development. RESULTS: A Glasgow coma score of <9 (odds ratio [OR], 3.20; 95% confidence interval [CI], 1.19-8.60) and a longer duration from CO exposure to HBOT (OR, 1.06; 95% CI, 1.03-1.09) were associated with a higher risk of DNS. By contrast, the presence of multiple victims from the same incident was associated with a lower risk of DNS. The ROC curve for the duration between CO exposure and HBOT in predicting DNS development demonstrated an area under the curve of 0.638 (95% CI, 0.575-0.698). The optimal cut-off point according to the Youden index was 22.5 h, with a sensitivity of 41.7% and a specificity of 85.9%. We also stratified the duration from CO exposure to HBOT into 5 intervals (< 6 h, 6-11 h, 12-23 h, 24-47 h and ≥ 48 h) and revealed a trend of increasing DNS risk with time. CONCLUSIONS: We identified several potential predictors of DNS in patients with CO poisoning who received HBOT. Multivariable logistic regressions further revealed that longer duration from CO exposure to HBOT, loss of consciousness, and the presence of multiple victims were independent predictors of DNS development. HBOT should be performed as early as possible and preferably within 22.5 h after CO poisoning.

Top-cited articles on hyperbaric oxygen therapy published from 2000 to 2010.

OBJECTIVE: Hyperbaric oxygen therapy (HBO2T) is a specialty with wide clinical applications and study fields. An evaluation of the major research direction of HBO2T studies would be helpful for researchers in this field. In this study, we identified the most frequently cited HBO2T articles to analyze the study focus of HBO2T research in the past 10 years. METHODS: "Hyperbaric oxygen" was used as the keyword to search articles in PubMed between January 2000 and November 2010. The cited times of an article were tracked in Google Scholar. The top 100 most-cited articles were identified and their publication year, author nationalities, journal, study field and style were recorded and analyzed. RESULTS: In total, 2,362 HBO2T-related articles were retrieved. The number of HBO2T articles published per year has been increasing during the past 10 years. More than half of the top-cited articles (52/100) were from studies in the United States. Studies focusing on stroke (20), radiation injury (11), carbon monoxide (10), and wounds (9) accounted for 50% of the top-cited articles. CONCLUSION: HBO2T has been a field of increasing scientific publications in the past 10 years. The focus of research fields were stroke, radiation injury, carbon monoxide and wounds. The United States maintains an important influence on HBO2T studies.

Pulmonary perfusion with L-arginine ameliorates post-cardiopulmonary bypass lung injury in a rabbit model.

BACKGROUND: Post-cardiopulmonary bypass (CPB) lung injury is the combination of whole body inflammatory response and local ischemia-reperfusion (IR) injury. We investigated the benefit of pulmonary perfusion with L-arginine in protection against post-CPB lung injury. METHODS: New Zealand white rabbits (n = 50, weight, 2.5-2.8 kg) were divided into five groups (n = 10 each): sham (sham sternotomy), CPB (CPB without pulmonary perfusion), perfusion (CPB with pulmonary perfusion), L-arginine (CPB with perfusion + L-arginine), and L-NAME (CPB with perfusion + L-NAME). The duration of CPB was 60 min followed by 2 h of reperfusion. Pulmonary perfusion was performed every 20 min through the pulmonary artery during CPB. Checking parameters included: (1) pulmonary vascular resistance, (2) pulmonary artery endothelium relaxation (organ chamber study), and (3) IR marker (myeloperoxidase) and inflammatory markers (TNF-α, IL-B, NF-κB). RESULTS: CPB induced pulmonary artery endothelium dysfunction manifested by increased pulmonary vascular resistance and impaired pulmonary artery relaxation. Pulmonary perfusion could significantly reverse the phenomenon (P < 0.01) while provision of NO precursor-L-arginine with pulmonary perfusion together further possessed significant relaxation ability for pulmonary arterial endothelium compared with perfusion alone (P < 0.05). Accordingly, lung parenchyma myeloperoxidase activity and inflammatory cytokine level were also markedly increased after CPB (P < 0.05). Pulmonary perfusion could partially decrease the response, whereas additional L-arginine further attenuated inflammatory cytokine release (P < 0.05). CONCLUSIONS: Pulmonary perfusion during CPB partially ameliorates CPB-induced lung injury. Pulmonary perfusion with L-arginine could further attenuate lung injury by restoring endothelial function and decreasing inflammatory response.

Immunomodulatory effects of Aureobasidium pullulans SM-2001 exopolymers on the cyclophosphamide-treated mice.

The immunomodulatory effects of exopolymers of Aureobasidium pullulans SM-2001 containing beta-1,3/1,6-glucan were evaluated on the cyclophosphamide (CPA)-treated mice. To induce immunosuppress, 150 and 110 mg/kg of CPA were intraperitoneally injected at 1 and 3 days before start of test material administrations, respectively. Exopolymers were subcutaneously or orally administered in a volume of 10 ml/kg, 4 times; 12-hr intervals from 24 hrs after second treatment of CPA. After treatment of exopolymers, the changes of thymus and spleen weights, splenic amounts of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta and IL-10, thymic and splenic CD3+, CD4+, CD8+ and TNF-alpha+ cells were monitored in CPA-treated mice. As results of CPA treatment, dramatical decreases of the CD3+, CD4+, CD8+ and TNF-alpha+ cells were detected in thymus and spleen with decreases of thymus and spleen weights. In addition, decreases of splenic TNF-alpha, IL-1beta and IL-10 contents were also detected at flow cytometrical observations. However, oral and subcutaneous treatment of exopolymers effectively reduced the immunosuppressive changes induced by CPA. Therefore, it is concluded that exopolymers of A. pullulans can be effectively prevent the immunosuppress mediated, at least partially, recruitment of T cells and TNF-alpha+ cells or enhancement of their activity, and can provide effective prevention or treat regimes for the immunosuppress and related diseases such as cancer, sepsis and high-dose chemotherapy or radiotherapy.

Micronucleus Test of Polycan™, ß-Glucan Originated from Aureobasidium, in Bone Marrow Cells of Male ICR Mice.

In this research the genotoxic effect of Polycan™ ß-glucans originated from Aureobasidium pullulans SM-2001, was evaluated using the mouse micronucleus test. Polycan™ was administered once a day for 2 days by oral gavage to male ICR mice at doses of 1000, 500 and 250 mg/kg. Cyclophosphamide was used as a known genotoxic agent in a positive control group. The appearance of a micronucleus is used as an index for genotoxic potential. The results obtained indicated that Polycan™ shows no genotoxicity effect up to 1000 mg/kg dosing levels. In addition, it is also considered that there were no problems from cytotoxicity of Polycan™ tested in this study because the polychromatic erythrocyte ratio was detected as > 0.47 in all tested groups.

Effects of beta-glucan from Aureobasidium pullulans on acute inflammation in mice.

The effects of beta-glucan isolated from Aureobasidium pullulans were observed on acute xylene-induced inflammation. beta-glucan at a dose of 62.5, 125 or 250 mg/kg were administered once orally to xylene-treated mice (0.03 mL of xylene was applied on the anterior surface of the right ear to induce inflammation), and the body weight change, ear weight, histological profiles and histomorphometrical analyses of ear were conducted upon sacrifice. The xylene was topically applied 30 min after dosing with beta-glucan. The results were compared to those of diclofenac, indomethacin and dexamethasone (15 mg/kg injected once intraperitoneally). All animals were sacrificed 2 h after xylene application. Xylene application resulted in marked increases in induced ear weights compared to that of intact control ear; hence, the differences between intact and induced ear were also significantly increased. The histological characteristics of acute inflammation, such as severe vasodilation, edematous changes of skin and infiltration of inflammatory cells, were detected in xylene-treated control ears with marked increase in the thickness of the ear tissues. However, these xylene-induced acute inflammatory changes were significantly and dose-dependently decreased by beta-glucan treatment. We conclude that beta-glucan from A. pullulans has a somewhat favorable effect in the reduction of the acute inflammatory responses induced by xylene application in mice.