bubbles

What’s Left to Learn about Bubbles?

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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. Six divers performed dives to a depth of 33 meters depth for 20 minutes, in a fresh, warm water pool. Bubbles were detected in a standard way, with and without exposure to a sonic vibrations of 20 to 30 Hz. The amount of detected bubbles nearly doubled after sonic vibrations. If these preliminary result get confirmed, we will have to be concerned with post-dive exposure to a sonic noise from various sources, like music, helicopter vibrations and similar, and it is possible that we could find some convenient and fun ways to pre-condition our bodies before dives. This should be also considered in DCS cases in aircraft pilots.

In another study, the presenting author used contrast echocardiography, a standard clinical method, to monitor divers post-dive2. Unlike the more commonly used B-mode echocardiography,  which can detect circulating bubbles greater than 35 microns, the contrast echocardiography can detect much smaller bubbles (< 10 microns). Post-dive contrast echocardiography in seven divers did indeed show the presence of small bubbles in the right and left heart, even in absence of large bubbles detectable by standard B-mode echocardiography. Of particular note is the fact that the presence of small bubbles did not correlate with the amount of large bubbles detected.

The final study was a classical bubble study done by scientists from the Swedish Navy to evaluate the safety of the US Navy Diving Manual Revision 6 air decompression tables. Twenty-eight divers did 72 dives in controlled conditions with three different dive profiles at the no-D limit, or with one required decompression stop. Most dives resulted with VGE Spencer grade III or higher. Two divers were treated for limb DCS and four divers with high bubble load were given surface oxygen. This study confirms that high VGE grade correlates with the risk of DCS.

While the value of VGE monitoring for evaluation of decompression safety at the population level is not questionable, it does have clear limitations that are primarily reflected in great inter- and intra-individual variability. New technologies may help us to learn more about post-decompression bubbles dynamics and get closer to the personalized approach in prevention of DCS.

 

  1. Ballestra C., et al. Can sonic vibrations increase the number of decompression vascular gas emboli? P 12.
  2. Papadopoulou V., et al. Can current contrast mode echocardiography help estimate bubble opulation dynamics post-dive? P 18.
  3. Genser M., et al. Incdence of ost-dive bubbles and DCS usingthe US Navy Revison 6 ait tables. P 34

 

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New Decompression Model Based on Occurrence of Gas Bubbles in Small Arteries

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.

They base their theoretical work on previous experimental studies which identified so Blood cells backgroundcalled “active hydrophobic spots” (AHS) on inner surface of blood vessels.(3) Atomic force microscopy showed that on these spots tiny formations of gas bubbles, between 5 and 30 nm in diameter, were forming spontaneously. These formations are thousands of times smaller than venous gas bubbles, and if released into circulation they would probably be crushed immediately. However, in some specific conditions they could grow and reach the size of viable gas bubbles. This may happen in two stages.

The first stage of this condition occurs during decompression, when nano bubbles increase to the size of micro bubbles and are released into circulation. In the following second stage, bubbles grow due to simple diffusion of gas from the blood.  Favorable conditions for this may occur in small arteries with thin walls, through which inert gas from surrounding tissues may diffuse into the bloodstream. The smaller the artery, the more gas diffuses into it. These smaller arteries also have significantly slower blood flow, which enables an increase in the partial pressure of the inert gases. In normal conditions this contributes to a 1% increase of inert gas partial pressure in small cerebral arteries which does not cause much trouble. However, if the circulation slows down another 10%, the partial pressure increases by 44%, and this increase can contribute to a significant growth of microbubbles, occlusion of terminal arteries, and damage of the tissues manifesting as decompression sickness.

In the view of the authors, this proposed mechanism could explain some of the characteristics of DCS, like predominance of spinal cord DCS, effects of repetitive diving, variability of individual sensitivity to DCS, effects of aging and acclimation.

This is an interesting approach and we can expect significant results in this veign of research in the future. For now, those interested in decompression modelling should read the original papers, which are available online for free.

 

References
  1. Arieli R, Marmur A. A biophysical vascular bubble model for devising decompression procedures. Physiol Rep, 5 (6), 2017, e13191, doi: 10.14814/phy2.13191
  2. Arieli R. A new model of arterial decompression bubble development and spinal DCI. Abstract and Conference Book, EUBS 43 Annual Scientific Meeting, Ravenna (Italy), 12-18 September 2017, p 30.
  3. Arieli R. Nanobubbles Form at Active Hydrophobic Spots on the Luminal Aspect of Blood Vessels: Consequences for Decompression Illness in Diving and Possible Implications for Autoimmune Disease—An Overview. Front. Physiol. 8:591. doi: 10.3389/fphys.2017.00591

Does Diving Damage the Brain?

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.

bubblesA 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

  1. Willey J. Effects of diving on brain. Alertdiveronline. http://www.alertdiver.com/Brain
  2. Balestra C and Germonpré P (2016) Correlation between Patent Foramen Ovale, Cerebral “Lesions” and Neuropsychometric Testing in Experienced Sports Divers: Does Diving Damage the Brain? Front. Psychol. 7:696. doi: 10.3389/fpsyg.2016.00696

BREATH-HOLD DIVING, CIRCULATING GAS BUBBLES, AND NEUROLOGICAL SYMPTOMS

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 freediver-istock_webVGE 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.

References:

  1. Cialoni D., et al. Detection of venous gas emboli after repetitive breath-hold dives: case report. Undersea Hyperb Med 2016;43(4):449-455
  2. Dunford R. Hayward J. Venous gas bubble production following cold stress during a no-decompression dive. Undersea Biomed Res, 1981;8(1):41-49.
  3. Gerth WA. On diver thermal status and susceptibility to decompression sickness. Diving Hyperb Med. 2015 Sep;45(3):208.

Skin Mottling after Diving May Be Result of Brain Lesions Caused by Gas Bubbles

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.

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Can a Test Identify Divers Who May Be More Susceptible to DCS?

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).

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Do Viagra and other PDE5 Inhibitors Increase the Risk of DCS in Humans?

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.

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