Decompression Illness

Venous gas bubbles in breath hold divers

Venous gas bubbles in breath hold divers remained a focus of researchers this year, with a notable presentation coming from Danilo Cialoni and his EDAN team1.  At EUBS 2017 they presented the extension of study previously reported and described in this blog. After discovering post-dive VGE in one breath hold diver, they studied VGE in 37 elite breath hold divers during their training in 42 meter deep pool with water temperature  of 32 oC.

Divers underwent echocardiographic Going downmonitoring before the series of dives, after a number of training dives, and every 15 minutes for up to 90 minutes after the last dive. Bubbles were detected in 39% of divers (28% low VGE grade and 11%  high VGE grade). Bubblers did significantly longer and deeper dives with shorter surface intervals. The data from this study will be used to correct the decompression algorithms for breath hold divers, which primarily means extending the time between the dives to prevent carrying over dissolved gas from one dive to another. Four divers did develop neurological symptoms of taravana during the study. All symptoms were mild and divers recovered after breathing oxygen at surface. Most notably, in one diver with taravana, bubbles were not discovered.

Another taravana case unrelated to this study was presented by another group2. A 39 year old diver performed about 30 dives over the course of 5 hours to depths between 29 and 32 meters, with dive times between 2 and 2.5 minutes each. A few minutes after his last dive the individual developed expressive aphasia (difficulty speaking and expressing thoughts) and a headache. The aphasia resolved shortly but the headache persisted and diver was admitted to an emergency department 48 hours post dive. The diagnostic workup included the brain MRI which revealed a brain injury. The patient was treated with one Table 6 and five HBO treatments at 2.5 ATA on the following days. His conditions significantly improved after the treatment and at 2 months follow up he was completely recovered.

Competitive breath hold divers should be aware that post-dive symptoms may be caused by brain injury and regardless of assumed cause (decompression or hypoxic) they need neurological examination and treatment in case of confirmed injury.


  1. Cialoni,D. et al. Prevalence of venous gas emboli in repetitive breath hold diving. Proposal for a new decompression algorithm. P 17
  2. Guerreiro F, et al. Decompression illness in extreme breath hold dive (Taravana syndrome) – A case report. P 47

What’s Left to Learn about Bubbles?



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


Outcomes of Decompression Illness

Recompression treatment and hyperbaric oxygen (HBOT) are standard treatment for decompression illness. While it is generally accepted that sooner recompression is associated with better outcomes, the urgency of treatment may not be same for all cases. Looking for practical guidelines we regularly consult published case series. Three case series presented at EUBS 2017 may be used to illustrate problems with such approach.

In the first paper1, authors compare outcomes in 24 mild cases of DCS treated in an on-site facility with an average delay to treatment 7.8 hours, to outcomes of 29 mild cases treated at an off-site facility with an averaged delay of 42 hours. Cases treated on-site almost all resolved completely after a single recompression (US Navy Table 6 or US Navy Table 5) and only one case needed an additional treatment. Of 29 cases treated off-site, only 17 resolved after first recompression, eight resolved after additional 1 to 5 tailing treatments, and four were left with some residual symptoms after tailing treatments. The authors suggest that this data supports rapid on-site treatment for all cases. In my opinion, there are two issues with this data.


First, the two datasets may not be comparable. Diagnostic criteria and outcome evaluation methods were not explicitly reported and may have been different in two facilities. Cases treated off-site may have left the site before symptom onset and travel may have contributed to the DCS. Second, the sample size is small enough that apparent differences may have been effected by chance.

The second reported case series2 includes 31 divers treated for DCS or AGE. Patients were thoroughly evaluated after the treatment and two to three months later. The evaluation included explicit inquiry about 20 separate symptoms and overall quality of life (VAS scale 1 – 100). At discharge and follow up 45% and 46% of patients respectively were free of symptoms. The most frequent persisting symptoms were tiredness, tingling, difficulty concentrating, and ear ringing.

The third presented series included 12 cases of inner ear DCS3. All patient were harvester divers and most dives included some omitted decompression time. The average time to treatment was 11 hours (5 – 72). Some cases received an on-site in-water recompression but still needed repeated HBOT. Patients received between 1 and 25 HBOT sessions. Eight cases recovered completely, three had residual symptoms and one was lost to follow up. Interestingly, the outcome was not apparently affected by the time to treatment.

These three case series with different case mixes could not be compared directly to each other, but they are a good reminder that the ability to generalize findings from small case series is questionable, particularly when it comes to the question of how the delay to treatment affects the outcome. This research also supports the call for a more standard and thorough description of case series, so we can better compare case studies, and evaluate the data.


  1. Wang Z. Efficacy of early treatment of decompression sickness in an on-site facility vs. delayed treatment of decompression sickness in an off-site facility. P 49.
  2. Johnsson J, et al. Recompression treated decompression illness signs and symptoms – initial findings and 2-3 months follow-up. P 72.
  3. Calderon J. et all. 12 cases of vestibular decompression sickness with clinical monitoring and recording of video. Hospital Ancud, Chile.

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.


  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

Can drinking wine provide benefits for divers?

Historically, alcohol was used to treat bends in Greek sponge divers. In the late 1980s attempts to verify the possible beneficial effects of ethanol on prevention of DCS led to prevailing opinions that there was no proven benefit and that divers should not drink and dive. On the other hand, the assumption that wine drinking has beneficial effects on general health is still propagated.

wine_shutterstock_85339912The so called “French paradox” fueled a search for possible healthful components in wine that, as some researchers posted, protect French people from heart disease despite their fat rich diet and high blood cholesterol levels. Tannins and phenolics, a large group of substances that together make up to 0.1% of wine mass and determine the color and the taste of wine, were identified as beneficial substances. The most intriguing and studied phenolic is resveratrol which is now also sold as a dietary supplement.

Studies of resveratrol in vitro (on cellular cultures or in various models of biochemical systems) have shown anti-oxidant and other effects that with basic biological processes may provide protection against aging, various diseases and death. Further animal studies appeared to confirm beneficial effects. Some of the suspected mechanisms involving resveratrol included functions of endothelial cells (inner lining of blood vessels) and platelets which are also affected in diving. If resveratrol could prevent endothelial cell dysfunction and platelet aggregation, it may help to avoid decompression sickness. Recent resveratrol studies claimed several additional health benefits that could be appealing to divers.

The first claim is that resveratrol has beneficial effects on
skeletal and cardiac muscle functions similar to what is seen with endurance exercise training.1  Wouldn’t it be nice to work on your fitness by relaxing and sipping wine after a long workday rather than going to the gym and sweating?

The second claim is that resveratrol improves brain perfusion and provides neuroprotection2, both of which may be helpful in reducing risk of decompression sickness. Why not drink wine before or after diving?

Unfortunately, there is only one problem with all these studies; the amount of resveratrolDelicious  portion of  fresh salmon fillet  with aromatic herbs, used is equivalent to drinking 50 to 3000 liters of wine per day. It is far more than is needed to get drunk. It’s enough to dive in. Thus, drinking red wine does not seem to be a practical prophylaxis of decompression sickness.

But don’t despair. Even French Paradox is not due to wine drinking as was believed forty years ago. Most population studies indicate that health and longevity may be associated with overall diet. The benefits of French diets appear to come from plenty of fresh vegetables, moderate caloric intake and physical activity rather than just from wine. The French diet has a lot in common with the so called Mediterranean Diet which is widely considered most favorable. In fact, in 2010 it was acknowledged by UNESCO as an Intangible Cultural Heritage of Humanity. (

This story illustrates a common wisdom that there is no one single dietary supplement that could provide what mortals want. To stay healthy and fit for diving, adopt a healthy diet3 and, if you drink wine, limit yourself to one glass with your meal. More importantly, do not drink before the dive.

For quick orientation about healthy meal check MyPlate



  1. Dolinsky VW, Kelvin E. Jones EJ, Robinder S. Sidhu SS, Mark Haykowsky M, Michael P. Czubryt MP, Tessa Gordon T, and Jason Dyck   Improvements in skeletal muscle strength and cardiac function induced by resveratrol during exercise training contribute to enhanced exercise performance in rats. J Physiol 590.11 (2012) pp 2783–2799
  2. Otto MA. Resveratrol improves cerebral perfusion in type 2 diabetes. Clinical Endocrinology News Digital Network. January 17, 2016
  3. US Department of Health and Human Services and US Department of Agriculture 2005 – 2020 Dietary Guidelines for Americans. 8th December 2015. Available at

Validation of Tasmania’s Aquaculture Industry “Yo-Yo” Diving Schedules

Validation of Tasmania photo (3)

Office of Naval Research 2014

While vacationing in Croatia, I heard a story about a diver who fits the description of people I sometimes call “robo-divers.” The story’s hero is a famous Croatian sponge diver, with whom I share an acquaintance. My friend, who is one of his teammates, described this robo-diver’s practice, which is similar to previously described empirical dive practices of other local sponge divers: Reportedly, he does four descents per day to extreme depths, after each of which he ascends very slowly without decompression stops. After the last dive of the day, he quickly takes his boat to shallow waters (within approximately 10 minutes) and descends for about two hours of decompression, split between stops at nine, six and three meters (30, 20 and 10 feet).

I don’t know about his decompression sickness history, but I do know that he is 64 years old now, and the fact that he has survived this long following those types of dive practices make me think of him more as a robot than as a man of flesh and bone. At very least, it is unlikely that this diver has a PFO.


Using the Selfie as a Telemedical Tool

isolated hand holding smartphone or phone
Last April, a Canadian woman named Stacey Yepes experienced stroke symptoms, but by the time she made it to the hospital her symptoms were gone. Because her physicians could not find any signs of stroke, they believed that she was displaying symptoms of stress and released her home. A few days later, she had a similar attack and used her phone to tape herself during an episode in which she suffered from facial drooping and slurred speech. The video helped her doctors diagnose her with TIA (transient ischemic attack).

In many cases of diseases with transitory symptoms, physicians are unable to diagnose patients and opportunities for early treatments are missed. In the case of TIA, it is especially important to establish an early diagnosis and provide treatment to prevent the progression of symptoms and permanent loss of brain tissue. TIA can lead to blood clotting in the brain, but early administration of thrombolytic medication can prevent clotting and brain damage. Because of the transitory nature of TIA symptoms, some hospitals offer stroke telemedical consultations to enhance diagnosis of and establish early eligibility for thrombolytic medication. By using video connections, they establish a correct diagnosis in 96% of cases, as compared with only 83% of cases in which symptoms are only reported by phone.