Physiologic and biochemical rationale for treating COVID-19 patients with hyperbaric oxygen.

The SARS-Cov-2 (COVID-19) pandemic remains a major worldwide public health issue. Initially, improved supportive and anti-inflammatory intervention, often employing known drugs or technologies, provided measurable improvement in management. We have recently seen advances in specific therapeutic interventions and in vaccines. Nevertheless, it will be months before most of the world's population can be vaccinated to achieve herd immunity. In the interim, hyperbaric oxygen (HBO2) treatment offers several potentially beneficial therapeutic effects. Three small published series, one with a propensity-score-matched control group, have demonstrated safety and initial efficacy. Additional anecdotal reports are consistent with these publications. HBO2 delivers oxygen in extreme conditions of hypoxemia and tissue hypoxia, even in the presence of lung pathology. It provides anti-inflammatory and anti-proinflammatory effects likely to ameliorate the overexuberant immune response common to COVID-19. Unlike steroids, it exerts these effects without immune suppression. One study suggests HBO2 may reduce the hypercoagulability seen in COVID patients. Also, hyperbaric oxygen offers a likely successful intervention to address the oxygen debt expected to arise from a prolonged period of hypoxemia and tissue hypoxia. To date, 11 studies designed to investigate the impact of HBO2 on patients infected with SARS-Cov-2 have been posted on clinicaltrials.gov. This paper describes the promising physiologic and biochemical effects of hyperbaric oxygen in COVID-19 and potentially in other disorders with similar pathologic mechanisms.

Hyperbaric medicine simulation education curriculum: CNS toxicity during Treatment Table 6 and intubated ICU patient with mucous plugging.

INTRODUCTION/BACKGROUND: The incidence of complications and number of critically ill patients in hyperbaric medicine is relatively low [1]. This poses a challenge to those tasked with educating trainees as well as maintaining the skills of staff. Hyperbaric medicine fellows may not be exposed to critical patient scenarios or complications of hyperbaric medicine during a one-year fellowship. Additional staff may be unfamiliar with these situations as well. The purpose of hyperbaric simulation curriculum is to train health care providers for rare situations. To our knowledge, this hyperbaric simulation curriculum is the first published use of simulation education in the specialty of undersea and hyperbaric medicine. MATERIALS AND METHODS: Two simulation cases have been developed that involve a patient with oxygen toxicity during hyperbaric treatment as well as an ICU patient with mucous plugging. RESULTS: Medical training simulations are an effective method of teaching content and training multiple roles in Undersea and Hyperbaric Medicine. SUMMARY/CONCLUSIONS: A hyperbaric simulation curriculum is an achievable educational initiative that is able to train multiple team members simultaneously in situations that they may not encounter on a regular basis. We believe that this could be easily exported to otherinstitutions for further education.

Side effects of hyperbaric oxygen therapy.

Several side effects and complications from hyperbaric oxygen (HBO2) therapy have been described, with varying degrees of seriousness. By far, the two most frequent and benign side effects comprise middle ear barotrauma, which has been noted in up to 2% of treated patients, and can be prevented or minimized by teaching autoinflation techniques, or by inserting tympanostomy tubes. Another frequent complaint is claustrophobia, both during multiplace and monoplace chamber compression, requiring reassurance, coaching and, at times, sedation. Other more rare, but more severe side effects derive from oxygen (O2) toxicity, from the multiple exposures required for chronic treatments, especially progressive myopia, usually transient and reversible after stopping HBO2 sessions, or pulmonary dyspnea, with cough and inspiratory pain. More serious O2-induced seizures happen rarely, at higher O2 pressures, and often during acute treatments in acidotic patients (carbon monoxide poisoning).

Seizure incidence by treatment pressure in patients undergoing hyperbaric oxygen therapy.

INTRODUCTION: Hyperbaric oxygen (HBO2) therapy uses different maximum treatment pressures. A side effect of HBO2 is oxygen toxicity seizure. The purpose of this study was to determine the overall incidence of oxygen toxicity seizure and assess risk at different treatment pressures. METHOD: A retrospective chart review was performed on patients who underwent HBO2 at a university hospital and at an outpatient center. Statistical analysis was performed to determine overall incidence of seizure and identify risk factors including maximum treatment pressure. RESULTS: A total of 931 patients were identified representing a total of 23,328 treatments. The overall incidence of seizure was one in 2,121 treatments (five per 10,000). There were zero per 10,000 at 2.0 atmospheres absolute/atm abs (0/16,430), 15 per 10,000 at 2.4/2.5 atm abs (1/669) and 51 per 10,000 at 2.8 atm abs (1/197). There was a statistically significant difference for seizure between the different pressures (χ2 (2, 23,540) = 31.38, p < .001). DISCUSSION: The overall incidence of oxygen toxicity seizure in this study is consistent with recent reports. This study demonstrated a statistically significant increased risk of seizure with increasing treatment pressure. Treatment at higher pressure should be chosen based on demonstrable benefit with a clear understanding of increased risk with higher pressure.

Incidence of DCS and oxygen toxicity in chamber attendants: a 28-year experience.

Decompression sickness (DCS) and central nervous system oxygen toxicity are inherent risks for "inside" attendants (IAs) of hyperbaric chambers. At the Hyperbaric Medicine Center at the University of California San Diego (UCSD), protocols have been developed for decompressing IAs. Protocol 1: For a total bottom time (TBT) of less than 80 minutes at 2.4 atmospheres absolute (atm abs) or shallower, the U.S. Navy (1955) no-decompression tables were utilized. Protocol 2: For a TBT between 80 and 119 minutes IAs breathed oxygen for 15 minutes prior to initiation of ascent. Protocol 3: For a TBT between 120-139 minutes IAs breathed oxygen for 30 minutes prior to ascent. These protocols have been utilized for approximately 28 years and have produced zero cases of DCS and central nervous system oxygen toxicity. These results, based upon more than 24,000 exposures, have an upper limit of risk of DCS and oxygen toxicity of 0.02806 (95% CI) using UCSD IA decompression Protocol 1, 0.00021 for Protocol 2, and 0.00549 for Protocol 3. We conclude that the utilization of this methodology may be useful at other sea-level multiplace chambers.

Incidence of oxygen toxicity during the treatment of dysbarism.

Oxygen (O2) toxicity may result from exposure to partial pressures of O2 above 0.6ATA. Potential toxic exposure for divers occurs during the treatment of dysbarism. In the recompression chamber, PO2 may range from 0.9ATA to 3.3ATA depending upon the treatment table employed. This retrospective study examines the nature and incidence of O2 toxicity in 998 patients who underwent recompression treatment at our facility from 1983 through 2001. Only patients evaluated for diving related injury were considered for this study. Of 1189 charts reviewed, 998 patients received recompression and were entered into this study. The total number of treatment exposures was determined as was the total number of O2 toxicity events characterized as either pulmonary or CNS, and patients were divided into male/female analysis. Overall incidence as well as the incidence for both toxicity types was determined, and their occurrence in both male and female patients was ascertained. 2166 recompressions were undertaken, 449 female and 1717 male. The peak PO2 for these treatments ranged from 2.6ATA to 2.9ATA. 155 O2 toxicity events occurred in 152 patients, 49 females and 103 males. Three patients, 2 females and 1 male, had mixed events. Incidence of an O2 toxic event = 7.0 per 100 recompressions. Incidence of pulmonary toxicity overall = 5.0 per 100 recompressions, while CNS events = 2.0 per 100 recompressions with overall seizure rate = 0.6 per 100 recompressions. In females, pulmonary toxicity rate = 6.9 per 100 recompressions, CNS toxicity rate = 4.4 per 100 recompressions with seizures occurring at 1.3 per 100 recompressions. In males, pulmonary toxicity rate = 4.6 per 100 recompressions, CNS toxicity rate = 1.4 per 100 recompressions, and seizures at 0.4 per 100 recompressions.

[Experimental studies of Panax notoginseng saponins and Ginkgo biloba extracts on preventing acute oxygen toxicity].

AIM: To investigate the preventive effects of Panax notoginseng saponins (PNS) and Ginkgo biloba extracts (GbE) on acute oxygen toxicity and the possible mechanisms. METHODS: Mice were injected intraperitoneally with PNS and GbE for 5 days, then were exposed to 500 kPa hyperbaric oxygen (HBO) for 60 min, the convulsion latency, times and interval were observed. Moreover, reactive oxygen (RO) unit, MDA, NO, GSH levels and GSH-Px, CAT, MAO activities of mice brain were determined after they were exposed to HBO for 15 min. RESULTS: PNS and GbE could markedly prolong the convulsion latency and interval, reduce convulsion times, decrease contents of MDA and NO in mice brain, keep RO unit, GSH and GSH-Px at higher levels, but had no effects on CAT and MAO activities. CONCLUSION: PNS and GbE could effectively prevent acute oxygen toxicity, which were related to their antioxidant activities.

Central nervous system oxygen toxicity during routine hyperbaric oxygen therapy.

Hyperbaric oxygen therapy is associated with a recognized risk for clinically apparent central nervous system (CNS) toxicity. The risk for oxygen-induced convulsions during routine hyperbaric treatment of most routine conditions is extremely low. However, reports from the 1980's describing the incidence of CNS oxygen toxicity differ significantly from more recent reports since 1996. This retrospective study was conducted to determine the incidence of hyperbaric oxygen-induced seizures among patients treated at our facility for routine, non-emergent indications. In addition, the period studied was selected to examine the incidence of CNS oxygen toxicity between two brands of oxygen delivery hoods. We reviewed our treatment experience for approximately 10,000 routine patient treatments performed prior to and following a change in the brand of oxygen hoods used. Among 20,328 total patient treatments performed from 1992 to 2001, 6 patients experienced an oxygen-toxic seizure for an overall incidence of 1 in 3,388 treatments (0.03%). No difference in seizure incidence was seen between the two brands of oxygen hoods utilized. We conclude that the incidence of oxygen-toxic seizures in our patient population is approximately three-fold greater than historical reports and in agreement with more recent reports. The reason for this apparent increase in incidence of CNS oxygen toxicity is unknown.