EUBS 2017 has left us with more questions than answers, on the topic of post-dive bubbles.
Ballestra presented the preliminary results of an exploratory study of the effects of sonic vibrations on post-dive venous gas emboli detected by transthoracic echocardiography1. (more…)
Decompression sickness is caused by gas bubbles that form in the body during and after decompression. The current thought is that gas bubbles originate on the venous side and pass to the arterial side either through intra-cardiac (PFO) or intra-pulmonary shunt (arteriovenous anastomoses). A group of scientists proposed recently a third mechanisms: the evolution of bubbles in the distal arteries, independent of venous gas bubbles.(1) They presented their work at the EUBS 2017 meeting (2) in Ravenna. (more…)
It is well known that compressed gas diving may result in acute decompression sickness and cause permanent injury to the brain and spinal cord. However, the risk of possible injury to the brain in the absence of acute decompression illness is less clear. Because of the controversy over the subject, and the lack of definitive evidence, DAN recently enlisted the help of a group of industry respected experts to provide their insight into the subject and published the results in Alert Diver (1).
The agents of neurologic decompression injuries are gas bubbles (emboli) that occur in tissue, travel with venous blood and may pass from venous circulation into the arterial system. Detectable venous gas emboli are often present after a dive, but they are usually removed through pulmonary capillary filtration. When the emboli pass to the arterial side, they may block arterial flow, causing tissue hypoxia in watershed areas and sometimes damage. The risk of arterialization increases in divers with a large PFO, but it can also occur through pulmonary arteriovenous shunts when there is high load of VGE. For decades this has been raising concern that brain injuries in divers may be more prevalent than previously thought and could potentially occur without a manifestation of acute decompression illness.
A recent paper published by our colleagues Balestra and Germonpre (2) seems to provide a quite clear answer to the question. The two researchers recruited 200 recreational divers who had never had DCS, and then randomly selected from among them 50 divers for further studies. In addition, they maintained a control group of subjects who had never been diving, and another control group of subjects who had been exposed to neurotoxic solvents. The aim of the study was to establish whether divers have more asymptomatic brain injuries than non-divers, review how divers perform on psychometric tests in comparison to non-divers, and research the possible effect of the presence of a PFO.
Balestra and Germonpre(2) used magnetic resonance imaging (MRI) to evaluate subjects for signs of asymptomatic brain injuries (unidentified bright objects – UBOs), performed echocardiographic tests for PFOs, and gave the subjects a battery of four neuro-psychometric tests. Divers who did not complete all studies were excluded, but 42 of the initial 50 remained in the study.
A significant PFO was detected in 38% of divers. UBOs were detected in 5 (12%) divers. Importantly, there was no correlation between the presence of a PFO and the ending or extent of UBO’s. That is the good news: diving without acute decompression illness does not cause UBOs, which were of concern to many divers and researchers.
Neuro-psychometric testing, however, produced inferior results for divers in two tests in comparison to non-divers, and similar results in comparison to the group exposed to neurotoxic solvents. On two other tests, divers did significantly better than the solvent group. This was not correlated with the presence of PFO. In summary, it appears that divers with five or more years of experience and at least 200 dives, have decreased short term memory and visual-motor performance, which could be a bad news if further studies confirm it.
Another interesting point from this study is that the prevalence of PFOs among study subjects was higher than in general population. The authors hypothesize that this may be due to strenuous intra-thoracic pressure changing activities, such as those encountered in diving, which may “open-up” previously sealed or microscopically small PFO. However, there are many other everyday life situations that raise intrathoracic pressure in similar manner as some dive maneuvers. In our opinion, this finding is of concern when discussing the prevalence of PFO in DCS case series. Even divers without a history of DCS may have greater prevalence of PFO than the general population.
This paper is worth reading and is available for free online at:http://journal.frontiersin.org/article/10.3389/fpsyg.2016.00696/full
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. (more…)
Cutaneous decompression sickness (DCS), or “skin bends,” most often manifests as skin mottling on the torso, upper arms and buttocks to various degrees. An associated marbled look to the skin is sometimes referred to as cutis marmorata. While cutaneous DCS is most likely related to gas occurring in body — after decompression or due to lung barotrauma or some medical procedures — there generally is no accepted explanation how the free gas is related to skin changes.
Possible explanations include the occurrence of gas bubbles in subcutaneous tissues, occlusion of subcutaneous arteries with circulating bubbles bypassing the lung filter (as with a patent foramen ovale), inflammatory reaction bubbles present locally or bubbles causing endothelial injury at remote locations.
Are some divers prone — or resistant — to gas bubbles after diving?
Decompression sickness (DCS), which may occur in divers after decompression from a dive, is dependent on the combined dose of gas saturation during the dive and the rate and magnitude of decompression. However, there is a great variability of outcomes in subjects exposed to the same dive profiles. The variability decreases as the severity of exposure increases.
DCS is correlated with the degree of venous gas emboli (VGE), or “bubbles”, in circulation after a dive. Generally, the higher the VGE grade (more bubbles) the greater the probability of DCS, and vice versa. Similar to DCS, there is a great variance in the probability of VGE appearing postdive. Some researchers who practice VGE detection have hinted that some divers bubble after most dives and may exhibit a high bubble grade (HBG) and others tend not to bubble at all or rarely exhibit HBG. The former are often labeled as bubblers (or high bubblers), while the latter are labeled as nonbubblers (or low bubblers).
Phosphodiesterase type 5 (PDE5) inhibitors — such as Viagra, Cialis, Levitra, Vivanza, Mvix and Lodenafil — are a class of popular drugs prescribed to treat erectile dysfunction and are often sold on the black market as sexual-function enhancers. It is reasonable to assume that many divers use PDE5 inhibitors while on a diving vacation, although the drugs’ possible effects on decompression safety have not been studied previously. In a recent paper, Blatteau et al.1 presented the results of a study on rats treated with sildenafil (Viagra) and then exposed to a simulated dive.
Venous gas embolism (VGE), or bubbles, in divers postdive indicates that their decompression was too fast, their bodies became supersaturated and free gas emerged from solution in tissues. The occurrence of free gas is considered a necessary condition for decompression sickness (DCS), which can happen even without VGE. However, the presence of VGE increases the number and types of possible harms to the body and thus the probability of DCS.
A number of studies indicate variability in proneness to DCS among divers; however, the question of whether divers who have suffered DCS produce bubbles more readily in general has not been answered yet. To answer this question, researchers would need to identify “bubblers” and “nonbubblers” and observe the outcomes of their dives over some period of time, which would require a lot of resources and time.
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