Possible central nervous system oxygen toxicity seizures among US recreational air or enriched air nitrox open circuit diving fatalities 2004–2013

© 2017 Taylor & Francis Group, LLC. Background: The first diver certification programme for recreational ‘enriched air nitrox’ (EAN) diving was released in 1985. Concerns were expressed that many EAN divers might suffer central nervous system (CNS) oxygen toxicity seizures and drown. Methods: US fatalities on open-circuit scuba occurring between 2004–2013, where the breathing gas was either air or EAN, were identified. Causes of death and preceding circumstances were examined by a medical examiner experienced in diving autopsies. Case notes were searched for witnessed seizures at elevated partial pressures of oxygen. Results: The dataset comprised 344 air divers (86%) and 55 divers breathing EAN (14%). EAN divers’ fatal dives were deeper than air divers’ (28 msw vs 18 msw, p < 0.0001). Despite this, of the 249 cases where a cause of death was established, only three EAN divers were considered to have possibly died following CNS oxygen toxicity seizures at depth (ppO2 132, 142 and 193 kPa). Conclusion: The analysis of recreational diving fatalities in the US over 10 years found just one death likely from CNS oxygen toxicity among EAN divers. A further two possible, although unlikely, cases were also found. Fears of commonplace CNS oxygen toxicity seizures while EAN diving have not apparently been realized

Association of microparticles and neutrophil activation with decompression sickness.

Decompression sickness (DCS) is a systemic disorder, assumed due to gas bubbles, but additional factors are likely to play a role. Circulating microparticles (MPs)--vesicular structures with diameters of 0.1-1.0 μm--have been implicated, but data in human divers have been lacking. We hypothesized that the number of blood-borne, Annexin V-positive MPs and neutrophil activation, assessed as surface MPO staining, would differ between self-contained underwater breathing-apparatus divers suffering from DCS vs. asymptomatic divers. Blood was analyzed from 280 divers who had been exposed to maximum depths from 7 to 105 meters; 185 were control/asymptomatic divers, and 90 were diagnosed with DCS. Elevations of MPs and neutrophil activation occurred in all divers but normalized within 24 h in those who were asymptomatic. MPs, bearing the following proteins: CD66b, CD41, CD31, CD142, CD235, and von Willebrand factor, were between 2.4- and 11.7-fold higher in blood from divers with DCS vs. asymptomatic divers, matched for time of sample acquisition, maximum diving depth, and breathing gas. Multiple logistic regression analysis documented significant associations (P < 0.001) between DCS and MPs and for neutrophil MPO staining. Effect estimates were not altered by gender, body mass index, use of nonsteroidal anti-inflammatory agents, or emergency oxygen treatment and were modestly influenced by divers' age, choice of breathing gas during diving, maximum diving depth, and whether repetitive diving had been performed. There were no significant associations between DCS and number of MPs without surface proteins listed above. We conclude that MP production and neutrophil activation exhibit strong associations with DCS.info:eu-repo/semantics/publishe