Decompression sickness has been the suspected cause of the post-dive symptoms of brain injury in breath-hold divers for a long time, and the quest for the proof of culprit has been ongoing, but without success. In the meantime, many possible explanations of neurological symptoms in breath-hold divers were proposed, including in-situ bubble development, lung barotrauma and consequent gas embolization, atherosclerosis, small vessel disease, transitory extreme elevation of blood pressure, and repeated hypoxic injury.
Several researchers have studied venous gas emboli in breath-hold divers, but their results have been mixed. Spencer reported in 1972 positive finding of VGE in Ama divers of Japan after repetitive breath-hold diving. Lamaitre reported in 2009 finding of the lowest VGE grade in one out of twelve Ama divers. On the other hand, Boussuges could not find any bubbles in ten divers diving repeatedly for two to six hours up to 34 meter depth. More details on those studies can be found in another post on this blog, in which I admit that clinical documentation of decompression sickness-like symptoms and signs appears supportive of a DCS diagnosis. The bulk of material presented by the researchers was, however, more circumstantial than crucial evidence.
Recently Cialoni and co-authors (1) published in UHMS a report about finding high grade bubbles in breath-hold divers lasting for 45 minutes post dive and declining over the following 90 minutes. This diver did not have any symptoms, but the bullets were flying around and there was a potential for arterialization of bubbles and, if the diver had a PFO, embolization of the brain. This outstanding finding, they explain, is a result of 14 deep dives (40 m) and long bottom times (141+-42 seconds), typical for advance spearfishing divers.
However, another outstanding circumstance is that these dives were conducted in warm water (33 0C; 91.4 0F), which was uniform throughout the water column, which is higher than usual water temperature where the spearfishing occur. It was shown previously that diving in warm water increases the bubble grade three-fold (2), and may increase an individual’s risk of DCS.
Regardless of the circumstances, the finding of Cialoni and coauthors is the proof of hypothesis that breath-hold diving may generate venous gas bubbles. The true relationship of VGE and post-dive neurological symptoms is not known. The VGE may not be necessary for cerebral decompression sickness. Finally, the DCS may not be the only cause of cerebral symptoms occurring after deep and repeated breath-hold dives. More investigation on the topic is necessary, and some studies are ongoing and we hope that more results will come soon.
- Cialoni D., et al. Detection of venous gas emboli after repetitive breath-hold dives: case report. Undersea Hyperb Med 2016;43(4):449-455
- Dunford R. Hayward J. Venous gas bubble production following cold stress during a no-decompression dive. Undersea Biomed Res, 1981;8(1):41-49.
- Gerth WA. On diver thermal status and susceptibility to decompression sickness. Diving Hyperb Med. 2015 Sep;45(3):208.