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…)
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…)
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…)
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
- Willey J. Effects of diving on brain. Alertdiveronline. http://www.alertdiver.com/Brain
- 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
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…)
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 maximum 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.
- 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.
- Morvan J-B, et al. Perilymphatic fistula after underwater diving: a series of 11 cases. Diving and Hyperbaric Medicine. 2016;46(2):72-75.
- Guenzani S, et al. Inner ear decompression sickness in nine trimix recreational divers. Diving and Hyperbaric Medicine. 2016;46(2):111-116.
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…)