Influence of the COVID-19 pandemic on causes for the development of carbon monoxide intoxications.

Introduction: Several causes can lead to carbon monoxide (CO) intoxication. A first-line treatment option for such intoxications is hyperbaric oxygenation (HBO2) therapy. The COVID-19 pandemic has been changing everyday life in Germany since March 2020, mainly caused by statutory provisions. Our aim was to review whether these changes have an influence on the causes and frequency for the development of CO intoxication. Methods: We retrospectively analyzed the data of patients who were treated for CO intoxication in our institution between April 2019 and March 2021. Besides demographic data, we compared the overall number and documented causes for each CO intoxication in the period of April 2020 to March 2021 with the period between April 2019 and March 2020. Results: After applying inclusion and exclusion criteria, 139 patients were included. We found a significant decrease in the overall number of patients who needed treatment since the beginning of the COVID-19 pandemic. However, the share of CO intoxication caused by the indoor use of coal stoves, coal barbecue, or suicide attempts increased. In contrast, the share of cases caused by apartment or house fire, smoking waterpipe, or gas stoves decreased. Conclusion: The COVID-19 pandemic and the associated restrictions lead to a significant reduction in the number of patients in need for HBO2 therapy due to CO-Intoxication. The causes leading to CO intoxication also changed since the beginning of the COVID-19 pandemic. We observed a shift toward causes related to the indoor use of coal-fired stoves and barbecues as well as suicide attempts.

Long-term experience of hyperbaric oxygen therapy for refractory radio- or chemotherapy-induced haemorrhagic cystitis.

BACKGROUND: Radiotherapy and cyclophosphamide-induced haemorrhagic cystitis are rare but severe complications occurring in 3-6% of patients. Hyperbaric oxygen treatment (HBOT) has been demonstrated to be an effective treatment for haematuria not responding to conventional management. Only very few data exist for long-term follow-up after HBOT. METHODS: We retrospectively reviewed 15 patients referred for HBOT for haemorrhagic cystitis (HC). HBOT was performed for 130 min/day at a pressure of 2.4 atmospheres. We evaluated patient demographics, type of radio- and chemotherapy and characteristics of haematuria. The effect of HBOT was defined as complete or partial resolution of hematuria according to the RTOG/EORTC grade and Gray score. RESULTS: A total of 15 patients (12 after radiotherapy, two after chemotherapy and one patient with a combination of both) were treated with a median of 34 HBO treatments. Radiotherapy patients received primary, adjuvant, salvage and HDR radiotherapy (60 - 78 Gy) for prostate, colon or cervical cancer. The patient with combination therapy and both of the chemotherapy patients were treated with cyclophosphamide. First episodes of haematuria occurred at a median of 48 months after completion of initial therapy. The first HBOT was performed at a median of 11 months after the first episode of hematuria. After a median of a 68-month follow-up after HBOT, 80% experienced a complete resolution and two patients suffered a singular new minor haematuria (p < 0.00001). A salvage-cystectomy was necessary in one patient. No adverse effects were documented. CONCLUSIONS: Our experience indicate that HBOT is a safe and effective therapeutic option for treatment-resistant radiogenic and chemotherapy-induced haemorrhagic cystitis. For a better evaluation prospective clinical trials are required.

Assessment of hemostaseologic alterations induced by hyperbaric oxygen therapy using point-of-care analyzers.

BACKGROUND: Exposure to hyperbaric conditions influences the coagulation system. Thromboembolic events and disseminated intravascular coagulation were observed. OBJECTIVES: To detect the effects of a hyperbaric environment on the human coagulation system using the point-of-care coagulation analyzers Multiplate and ROTEM. PATIENTS/METHODS: 20 patients were included. Each received 90 minutes of oxygen intermittently at 2.4 atmospheres absolute, as per the TS 240-90 wound-healing protocol. Blood samples were taken before and after hyperbaric exposure and ROTEM, Multiplate and standard laboratory assays were subsequently performed. RESULTS: ROTEM showed a significant increase of the maximum clot firmness (EXTEM MCF; p < 0.05) and the thromboelastometric platelet component of the clot firmness (MCF(EXTEM) - MCF(FIBTEM); p < 0.01). Multiplate showed a platelet activation mediated by thrombin (AU TRAP-test; p < 0.05) and by arachidonic acid (AUC ASPI-test; p < 0.01). Standard laboratory assays revealed a lower activated partial thromboplastin time (p < 0.05) and a higher leukocyte count (p < 0.05). No further changes were detected. A t-test was performed after testing if data followed normal distribution. CONCLUSIONS: ROTEM and Multiplate were able to detect an activation of platelets after HBO2 therapy via thrombin and arachidonic acid pathways. Previously reported fibrinolysis could not be confirmed.

Oxygen therapy improves energy metabolism in focal cerebral ischemia.

Oxygen therapy (OT) with hyperbaric oxygen (HBO) or normobaric hyperoxia (NBO) improves the oxygenation of penumbral tissue in experimental ischemic stroke. However, whether this results in the improvement of energy metabolism is unclear. We investigated the effect of both OTs on tissue acidosis and on ATP production. Beginning 25 min after filament middle cerebral artery occlusion (MCAO), mice breathed either air, 100% O2 (NBO), or 100% O2 at 3 ata (HBO) for 60 min. Regional tissue pH was measured using the umbelliferone fluorescence. Regional ATP concentration was depicted by substrate-specific bioluminescence. Severity of ischemia did not differ among groups in laser-Doppler flowmetry. Both NBO (70.1±14.0 mm³) and, more effectively, HBO (57.2±11.9 mm³) significantly reduced volume of tissue acidosis compared to air (89.4±4.0 mm³), p<0.05). Topographically, acidosis was less pronounced in the medial striatum and in the cortical ischemic border areas. This resulted in significantly smaller volumes of ATP depletion (77.8±7.7 mm³ in air, 61.4±15.2 mm³ in NBO and 51.2±14.4 mm³ in HBO; p<0.05). In conclusion, OT significantly improves energy metabolism in the border zones of focal cerebral ischemia which are the areas protected by OT in this model.