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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.

 

Sources:
  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
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What’s Left to Learn about Bubbles?

IMG_8376_NOLOGO

 

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.

Chamber_Smooth_WEB

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.

 

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

Repeated DCS and the Efficacy of Counselling

Released this year, an interesting study on Belgian DCS cases looked at PFO presence, patency of present PFOs, and personality traits in divers who suffered cerebral DCS one or more times. Over the studies 20.5 year period (1993-2013) there were a total of 595 DCS cases treated in three major centers in Belgium. Among them 286 were identified as cerebral DCS and 209 had all necessary information for the analysis. Out of those 209 cases, 125 involved a patient experiencing a 1st episode of DCS, 70 involved 2nd episodes, and 14 involved patients experiencing a 3rd episode of DCS. There were no significant differences in age, body mass index or smoking habit between the subgroups. Divers with multiple episodes of DCS, however, dived deeper and more often than those with fewer episodes of DCS. All divers underwent PFO testing after each episode of DCS. When evaluated for PFO presence, the groups showed markedly different results. The group that had experienced only their 1st episode of DCS was found to have a PFO prevalence of 64%, while the groups with multiple episodes of DCS had a PFO prevalence of 100%. In addition, the amount of bubbles passing through the PFO increased in all divers with each subsequent episode of DCS.

PFO_HeartArt_Final

All divers with diagnosed PFOs received consultation about their risks and advice to dive more conservatively if they decide to continue diving. However, a number of them apparently did not follow the advice. Contrary to the advice, they dived deeper and more often than they had before their DCS episode. A small sample of divers were tested for risk taking traits and those with multiple episodes of DCS scored higher indicating that they are more inclined to risky behavior.

There are several lessons learned from this study. First, let’s keep in mind that Belgium is relatively small country with a large number of scuba divers and a relatively small number of centers that evaluate and treat divers. The percentage of cerebral DCS among all treated DCS cases appears quite high in comparison with some other regions, but that may be a result of dive environment which results in deeper diving. It is also possible that cerebral DCS is under diagnosed in some other regions. It appears that testing for PFO in divers with cerebral DCS in Belgium became the norm in the early 1990’s, something which is still not a case in the United States. Thanks to this practice, we stand to learn several important lessons about PFOs and DCS risk. First, a presence of PFO represents an increased risk of cerebral DCS. After a 1st episode of cerebral DCS divers should be advised that they may have PFO and if they want to continue diving, they should follow more conservative pattern of diving. Divers who do not follow this advice risk repeated episodes of DCS, with each subsequent episode being more severe and more likely to leave functional disability. This study also indicates that the size, or patency, of a PFO increases with age and the risks of subsequent DCS probably increases. Additionally, the work illustrates that the effectiveness of medical consultations for divers with PFOs depends largely on a diver’s psychological profile, and that psychological testing should become a part of physician consultation.

 

 

Reference:
Lafère P, Balestra C, Caers D and Germonpré P (2017) Patent Foramen Ovale (PFO), Personality Traits, and Iterative Decompression Sickness. Retrospective Analysis of 209 Cases. Front. Psychol. 8:1328. doi: 10.3389/fpsyg.2017.01328

Medicating Against DCS – Using Rosiglitazone to Prevent DCS Related Liver Injury

Decompression after diving often causes gas bubbles to occur in the systemic veins. Presumably, bubbles occur in tissues rich with fat, and one of the fattiest areas of the body is the mesentery, which holds together gastro-intestinal tract. Venous blood drains from this area into the portal vein of the liver, which directs it through capillary beds to process the nutrients it carries. If any gas bubbles occur in the mesentery, they would likewise be carried by venous blood into the portal vein.

Generally, the liver is not considered a target for decompression sickness, but there have been a few cases in which gas was accidentally found in the livers of divers. It was not, however, clear whether the gas preceded or appeared after decompression.

MedicinesStudies describing gas in the portal veins of animals has enabled researchers to develop a model that predictably reproduces portal vein embolization.3 The decompression stress in the model is severe enough to cause many bubbles all over the body, including the portal vein and liver tissue. Damaged capillary endothelium and liver cells release various markers and start an inflammatory cascade that can be measured. It is suspected that nitric oxide (NO) plays a major role in these processes and that the severity of DCS-caused injuries could be mitigated by controlling the NO.1

In a recent study, Peng and co-authors2 used this model to study mechanisms and possible prevention for decompression injury of the liver. They administered generic rosiglitazone to animals, which is supposed to reduce inflammatory effects mediated by NO. Indeed, the animals receiving this drug developed fewer symptoms of DCS, produced fewer markers of endothelial and liver injury, and had less inflammation. Researchers assigned most of the beneficial effects of rosiglitazone to protective effects on endothelium.

This study is a reminder that decompression sickness is a systemic disease. Endothelium protection may be a good strategy to mitigate the risk of DCS; however, the drug used in this study to protect animal livers from decompression injury may not necessarily be helpful in human subjects. Because rosiglitazone is an anti-diabetic drug that lowers blood sugar, healthy people should not use it. It can also cause a number of serious and adverse health effects in people with certain health conditions. We still do not have drugs that can be safely used to prevent DCS, but that may soon change, if the rate of current research is any indication at all.

  1. L’Abbate A, Kusmic C, Matteucci M, Pelosi G, Navari A, Pagliazzo A, Longobardi P, Bedini R. Gas embolization of the liver in a rat model of rapid decompression. Am J Physiol Regul Integr Comp Physiol 299: R673–R682, 2010.
  2. Peng B, Chen MM, Jiang ZL, Li X, Wang GH, Xu LH. Preventive effect of   rosiglitazone on liver injury in mouse model of decompression sickness. Diving and Hyperbaric Medicine 2017;47(1):17-23..

How is Eustachian Dysfunction related to Inner Ear Barotrauma

Diving and Hyperbaric Medicine Volume 46 No. 2 June 2016

Normal Eustachian tube (ET) function is important for fitness to dive. Eustachian tube dysfunction may result with ear injury during diving. The most common diving injury related to Eustachian tube dysfunction is middle ear barotrauma, and less common but more grave is inner ear barotrauma (IEBt). While middle ear barotrauma usually heals well, inner ear barotrauma may cause permanent damage if not recognized and treated on time and thus, the prevention of IEBt is very important. The Diving and Hyperbaric Medicine Volume 46 No. 2 June 2016 brings three articles addressing these issues.

Kitayima and co-authors studied Eustachian tube function in 16 divers who experienced IEBt and in 20 healthy divers without history of IEBt. They correlated the function of Eustachian tube to the incidence of IEBt. They measured the opening pressure for ET, the divelab20161013maximum volume of the air in the middle ear and the speed at which the equalization occurs. In the ideal conditions, the pressure differential needed to open the ET in either direction is 200 to 650 daPa which corresponds to a pressure gradient caused by depth change of 20 – 65 cm or 8-26 inches. The maximum volume of air in middle ear varies from 0.2 to 0.9 ml. The paper describes three main type of ET based on the equalization characteristics: patulous (open) ET, normal ET and stenotic (narrowed) ET. The patulous ET is open permanently or it takes pressure differential of less than 200 daPa to open it. Normal ET is collapsed but it takes less than 650 daPa to open it and it fills or empties instantaneously. The stenotic ET takes larger pressure (up to 1200 daPa/120 cm H2O measured) to open it or it fills and empties very slowly.

In healthy divers without a history of IEBt, one third had slow equalizing ET but the pressure differential required was within normal range. They avoided IEBt so far, probably by practicing slow ascent but they often experienced alternobaric vertigo. Among divers with IEBt, most had dysfunctional ET requiring either greater pressure differential to open it and/or it took longer time to equalize. However, some divers with IEBt had normal ET function at the time of measurement. Divers with IEBt and perilymph fistula had more severe ET dysfunction. Authors suspect that excessive pressure caused by forceful Valsalva may have been the cause of IEBt in some divers and especially in those with normal opening pressures but who became impatient with equalization and blew to strongly.

Morvan and co-authors presented a series of 11 cases of perilymphatic fistula due to IEBt in scuba divers. The perilymphatic fistula is most severe form of IEBt but it diagnosis is not always obvious. Dizziness, hearing impairment and tinnitus after scuba diving indicate likely injury of inner ear but the cause may be either decompression sickness or barotrauma. Delayed onset, fluctuation and progressive deterioration of deafness point toward perilymph fistula. In either case, occurrence of cochlea-vestibular symptoms after a dive is an emergency. Early evaluation should be focused on decompression sickness and need for hyperbaric oxygen treatment which may prevent permanent damage to inner ear. Effort must be made to exclude perilymph fistula before recompression treatment. However, that is not always possible and divers with a fistula sometimes get treated but there is no indication so far that it is deleterious if necessary precautions are taken. If there is no improvement on recompression or if there is worsening of symptoms, the treatment should be aborted and perilymph fistula considered.

Guenzani and co-authors reported case histories of nine cases of inner ear decompression sickness (IEDCS) in recreational technical divers who were identified through an online questionnaire. The most common leading symptom in IEDCS was vertigo, reflecting affliction of vestibular part of inner ear. The deafness which dominates in IEBt was seen in only three cases reported in this paper. IEDCS occurred in isolation (4 cases) and with other DCS manifestations (5 cases). The symptoms occur during ascent or soon after. IEDCS occurs more often than IEBt and due to growing participation in technical diving we may see it even more often in the future.

Presentation of these three papers in the same volume, seem like a good opportunity to re-fresh our knowledge about inner ear injuries in diving. Early recognition and prompt treatment are important to reduce the risk of permanent damage to hearing and orientation in space.

References

  1. Kitajima N, Sugita-Kitajima A, Kitajima S. Quantitative analysis of inner ear barotrauma using a Eustachian tube function analyzer. Diving Hyperb Med. 2016;46(2):76-81.
  2. Morvan J-B, et al. Perilymphatic fistula after underwater diving: a series of 11 cases. Diving and Hyperbaric Medicine. 2016;46(2):72-75.
  3. Guenzani S, et al. Inner ear decompression sickness in nine trimix recreational divers. Diving and Hyperbaric Medicine. 2016;46(2):111-116.