Getting Closer to A Complete Understanding of Decompression Sickness

Decompression sickness is a major risk for subjects exposed to a significant decrease of ambient pressure, like what occurs in underwater diving, tunneling, flying at high altitude or in space exploration. While we know that there is an association between post-decompression occurrences of gas bubbles in body tissues and DCS, we still do not know where the bubbles originate, why they do not occur in all divers on the same dive, and how they lead to DCS. An increasing number of studies are focusing on possible role of micro particles in DCS.


Microparticles are particles with diameters of 0.1

to 1 micrometer that various cells shed when exposed to noxious factors or various stimulations, and they play role in many biological processes and diseases. Microparticles are also elevated in divers after dive, and they seem to be related to bubbles. Some interventions that decrease number of post-dive bubbles, have been shown to diminish elevation of microparticles. It has also been shown that if animals not previously exposed to decompression receive microparticles from animal that were decompressed, they will develop symptoms of DCS. In blood samples from human divers who were admitted to recompression chambers for treatment of DCS, more microparticles were found than in a blood samples of the control group of divers who did not develop DCS.

A group of scientists led by Steven R. Thom of University of Maryland, previously University of Pennsylvania, did pioneering work in this area. They are identifying specific groups of microparticles involved, and biological processes through which they can contribute to occurrence or severity of DCS.

A group from Second Military Medical University in Shanghai led by Weighang Xu, recently published a series of articles describing their studies of how MPs may be related to DCS. Specifically, they studied a subgroup of endothelial microparticles (EMPs). The endothelium is a single cell layer that lines the inner surface of our blood and lymphatic vessels. There are more than a trillion endothelial cells in the body covering 3000 square meters area — they are involved in the control of vasomotor tonus, maintenance of structure and integrity of blood vessels, growth of new blood vessels, maintenance of blood fluidity, repair of tissue damage, regulation of blood clotting and prevention of hemorrhage, initiation and control of inflammation. It was shown previously that diving affects endothelial function and that it may be related to DCS.

In a series of in-vivo and in-vitro studies, Xu and his coworkers demonstrated how contact with bubbles changes endothelial cells and their function, described some of the mechanism and demonstrated how the adverse effects of bubbles may be prevented by various pre-treatments.

The progress of science is never smooth and straightforward and we cannot predict how long will it take to learn enough about bubbles, endothelium and DCS to be able to produce efficient prevention of DCS, but we know that science is making significant inroads into this matter and that we are every day closer to the ideals of precision medicine and individualized medical solutions.

Author: Petar J. Denoble

Yu X, Xu J, Huang G, Zhang K, Qing L, Liu W, et al. (2017) Bubble-Induced Endothelial Microparticles Promote Endothelial Dysfunction. PLoS ONE 12(1): e0168881. doi:10.1371/journal.pone.0168881.
Zhang, K. et al. Endothelia-Targeting Protection by Escin in Decompression Sickness
Rats. Sci. Rep. 7, 41288; doi: 10.1038/srep41288 (2017).
Yu  X,  Xu J,  Liu W,  Xu W. (2018): Bubbles Induce Endothelial Microparticle Formation via a Calcium-Dependent Pathway Involving Flippase Inactivation and Rho Kinase Activation. Cell Physiol Biochem 2018;46:965-974. DOI: 10.1159/000488825
Published online: April 17, 2018

Elite Breath Hold Divers and Short Term Memory

Author: Dr. Petar J. Denoble


The question about possible damages to the brain in breath-hold (BH) diving has been around for a long time. While the average people may hold their breath at rest (static apnea) for less than two minutes, trained BH divers easily double that time and elite BH divers can triple that to over six minutes. The top BH athletes regularly exceed 8 minutes and are close to ten. The world record in static apnea time without breathing oxygen in 2014 was set by Serbian Branko Petrovic at 11 minutes and 54 seconds. By now that record too has been exceeded. The superior performance of elite BH athletes could be attributed to their inherited biophysical characteristics, and some metabolic enhancement induced by training, but above all with the ability to postpone the break-through of apnea and sustain profound hypoxia. Inevitably, the longer the apnea lasts the worse hypoxia becomes, and it does affect the brain. The loss of motor control and consciousness during static BH competitions occurs at rates of 9.6% and 1.1% respectively. Negative acute effects of hypoxia on brain functions have been documented at high altitude in mountain climbers and in pilots. Studies of chronic effects of hypoxia in BH divers were less conclusive. Some previous psychometric studies did not find chronic effects that could be correlated to the years of practicing or to the number of negative neurological events. However, other studies using brain imaging and biochemical markers in elite BH divers have shown brain function abnormalities.

Recent study (1) involved 36 subjects divided in three groups: 12 Elite BH divers (EBHD), 12 novice BH divers (NBHD) and 12 participants without experience with BH diving (CTRL). The EBHD could perform static apnea longer freediver-free-diver_iStock-626817232_WEB.jpgthan 6 minutes (mean BH time 371 seconds) and practiced BH for at least two years. The NBHD could perform apnea longer than 3 minutes (mean BH time 245 seconds) and practiced BH for at less 5 months and less than one year. All subjects were subjected to a battery of psychometric tests. The EBHD group showed statistically lower performance on most tests, especially on tests measuring the short-term memory. The decrease in function was correlated to the length of static apnea. It was characterized as a mild short-term memory impairment not amounting to a pathological score except in one case. The diver with the pathological score was the one with the longest static apnea (436 seconds) and the longest diving career (19 years). There was no difference in psychometric performance between NBHD and CTRL.

The paper provides a review of previous testing and findings and it appears that positive findings of this study reflect the longer static BH times of EBHD group in comparison to BH divers studied previously. It appears that extreme apnea comes at price as it would be expected.

The conclusion of this study is that elite divers who practice for years are at risk of short-term memory impairment.





  1. Billaut FGueit PFaure SCostalat GLemaître F. Do elite breath-hold divers suffer from mild short-term memory impairments? Appl Physiol Nutr Metab.2018 Mar;43(3):247-251. doi: 10.1139/apnm-2017-0245. Epub 2017

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.


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. (more…)

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. (more…)

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. (more…)

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. (more…)

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. (more…)

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.


  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.

Endothelial cell dysfunction in diving

The EUBS annual scientific conference in Geneva, September 2016 presented several papers about endothelial dysfunction in diving. The endothelium is the layer of cells on the inner surface of blood vessels. It is very active in regulation of local blood flow, self-repair, prevention of blood coagulation and inflammatory response to various insults. An important mediator in activities of endothelium is nitric oxide (NO) which regulates also the constriction and dilatation of vessels. This has been found affected by diving due to hyperoxia which limits the availability of NO and thus reduces ability of vessels to dilate following temporary occlusion (flow-mediated dilatation; FMD). (more…)