Venous gas embolism as a predictive tool for improving CNS decompression safety

A key process in the pathophysiological steps leading to decompression sickness (DCS) is the formation of inert gas bubbles. The adverse effects of decompression are still not fully understood, but it seems reasonable to suggest that the formation of venous gas emboli (VGE) and their effects on the endothelium may be the central mechanism leading to central nervous system (CNS) damage. Hence, VGE might also have impact on the long-term health effects of diving. In the present review, we highlight the findings from our laboratory related to the hypothesis that VGE formation is the main mechanism behind serious decompression injuries. In recent studies, we have determined the impact of VGE on endothelial function in both laboratory animals and in humans. We observed that the damage to the endothelium due to VGE was dose dependent, and that the amount of VGE can be affected both by aerobic exercise and exogenous nitric oxide (NO) intervention prior to a dive. We observed that NO reduced VGE during decompression, and pharmacological blocking of NO production increased VGE formation following a dive. The importance of micro-nuclei for the formation of VGE and how it can be possible to manipulate the formation of VGE are discussed together with the effects of VGE on the organism. In the last part of the review we introduce our thoughts for the future, and how the enigma of DCS should be approached

Could some aviation deep vein thrombosis be a form of decompression sickness?

© 2016, Springer Science+Business Media New York. Aviation deep vein thrombosis is a challenge poorly understood in modern aviation. The aim of the present project was to determine if cabin decompression might favor formation of vascular bubbles in commercial air travelers. Thirty commercial flights were taken. Cabin pressure was noted at take-off and at every minute following, until the pressure stabilized. These time–pressure profiles were imported into the statistics program R and analyzed using the package SCUBA. Greatest pressure differentials between tissues and cabin pressures were estimated for 20, 40, 60, 80 and 120 min half-time compartments. Time to decompress ranged from 11 to 47 min. The greatest drop in cabin pressure was from 1022 to 776 mBar, equivalent to a saturated diver ascending from 2.46 msw depth. Mean pressure drop in flights >2 h duration was 193 mBar, while mean pressure drop in flights <2 h was 165 mBar. The greatest drop in pressure over 1 min was 28 mBar. Over 30 commercial flights it was found that the drop in cabin pressure was commensurate with that found to cause bubbles in man. Both the US Navy and the Royal Navy mandate far slower decompression from states of saturation, being 1.7 and 1.9 mBar/min respectively. The median overall rate of decompression found in this study was 8.5 mBar/min, five times the rate prescribed for USN saturation divers. The tissues associated with hypobaric bubble formation are likely slower than those associated with bounce diving, with 60 min a potentially useful index