pfo

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
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Bubble Production in Divers Who Have Had DCS

Venous gas embolism (VGE), or bubbles, in divers postdive indicates that their decompression was too fast, their bodies became supersaturated and free gas emerged from solution in tissues. The occurrence of free gas is considered a necessary condition for decompression sickness (DCS), which can happen even without VGE. However, the presence of VGE increases the number and types of possible harms to the body and thus the probability of DCS.

A number of studies indicate variability in proneness to DCS among divers; however, the question of whether divers who have suffered DCS produce bubbles more readily in general has not been answered yet. To answer this question, researchers would need to identify “bubblers” and “nonbubblers” and observe the outcomes of their dives over some period of time, which would require a lot of resources and time.
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PFO and Inner Ear DCS

Does the selective vulnerability of the inner ear to DCS help explain the disconnect between a prevalent risk factor and a rare disease?

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In his presentation at SPUMS 2014, Dr. Simon Mitchell has summarized the work he and Dr. David Doolette have done regarding the pathophysiology of inner ear decompression sickness (IEDCS) as well as some recent publications from other authors.

Mitchell addressed the reservations some experts have when it comes to the causal relationship of patent foramen ovale (PFO) and decompression sickness (DCS). Some experts say there is a disconnect; PFO must be present in many divers (one quarter), but DCS occurs only in few. Wilmshurst responds to this disconnect asserting that only divers with a large PFO are at risk and this is generally in line with the DCS statistics.

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PFO: Is It Time to Change the Course?

wooden pointerPresentations at SPUMS continue…

Peter Wilmshurst’s series of cases shows that 79% of all skin DCS have PFO, 10% lung disease and only remaining cases occur in divers with closed PFO due to severe dive exposure. Similar statistics were provided for inner ear DCS and neurological DCS. Other authors dispute association of PFO with spinal form of DCS  and say only cerebral DCS appears to be associated. Nevertheless, a large number of DCS cases could be avoided if the diver was aware of PFO and exercised caution.

How safe is the option of transcatheter closure?

Mark Turner, another cardiologist from the United Kingdom, provided a detailed presentation of the procedure, pitfalls and outcomes. The overall outcome: Successful with very low rate of adverse events.

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Review of PFO and Diving at SPUMS Meeting 2014

PFO_HeartArt_Final2At the 43rd Annual Scientific Meeting of South Pacific Underwater Medical Society going on May 18 – 25, 2014, a key theme is PFO and diving. The keynote speaker is Dr. Peter Wilmshurst, the cardiologist and diving physician who first described the association between PFO and decompression sickness in 1986. Here, he presented his findings in several hundred cases of DCS.  His insight into this problem is most valuable and we are looking forward to the publication of a synthesis of his findings.

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What is the practical significance of arterialization of gas bubbles after diving?

Decompression sickness (DCS) is a condition that may result from quick decompression, which may occur when diving or flying. One mechanism involved in DCS is the passage of venous gas emboli (VGE or “bubbles”) to the arterial side of circulation; this is known as arterialization.

Until recently, arterialization was considered a rare event except when there is a passage in the heart wall because of a patent foramen ovale, (PFO), atrial septal defect or ventricular septal defect. In people with normal hearts it was previously thought that when venous gas passed through the narrow pulmonary capillaries, the potential for VGE was eliminated. It is known that some pathways allow up to five percent of venous blood to bypass pulmonary capillary filters, but the caliber of these bypasses was considered too small to allow VGE to pass through. Occasionally, some bubbles would arterialize, but it was considered a rare event. Recently, however, several authors have reported postdive VGE arterialization, but the true incidence of this phenomenon was not known.

Our colleagues of University Split, Ljubkovic M., et al. studied VGE arterialization and published two papers. The first, “Determinants of arterial gas embolism after scuba diving” (http://jap.physiology.org/content/112/1/91.long), reports results of laboratory testing and postdive findings. They tested 34 subjects by injecting saline with air bubbles in an arm vein and used echocardiography to monitor for bubble passage to the left side of the heart. In 23 out of 34 subjects, the transpulmonary passage of bubbles was observed at rest or after mild exercise. Nine subjects with confirmed arterialization in lab conditions also experienced arterialization after a field dive. All nine had large amounts of VGE in their right heart (VGE grade of 4B or greater). In subjects with no arterialization in lab conditions, there was no arterialization postdive either despite five of them having VGE grade 4B.

Authors concluded that “Postdive VGE arterialization occurs in subjects that meet two criteria: 1) transpulmonary shunting of contrast bubbles at rest or at mild/moderate exercise and 2) VGE generation after a dive reaches the threshold grade.”

It is important to notice that none of the nine divers with echocardiographically detected arterialization had any symptoms or signs of DCS or cerebral arterial gas embolization (CAGE). There is also no clear evidence concerning long-term consequences of chronic embolization in divers without history of manifested DCS or CAGE. Read the Alert Diver article, “Effects of diving on the brain” to learn more.

The significance of these findings is dubious. In the first place, it is now clear that a certain level of arterialization occurs more often than previously assumed and proven. One of the reasons may be in increased resolution of new generations of echocardiography machines, which enables us to detect smaller VGE than before. Second, it is reasonable to assume that occurrence of DCS in cases of VGE arterialization depends on the size and quantity of VGE, but the threshold values are not known. Third, a loose relationship between the presence of PFO and DCS may be due to not accounting for transpulmonary bubble passage.

Thus, we are looking forward to results of a prospective study conducted by Germonpre, P. and colleagues, which relates to the presence of VGE in carotid artery (accounting for PFO and transpulmonary passage) to DCI.

Additional Readings:

PFO Research Foundation

“PFO and decompression illness in recreational divers”

“Effects of diving on the brain”

Post written by: Petar Denoble, MD, D.Sc.

When to refer a diver for PFO screening?

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Postdive occurrence of bubbles in divers venous blood (venous gas emboli or VGE) is quite common. VGE are usually filtered out of circulation by the pulmonary capillary filter. However, in the case of PFO, transpulmonary passage of venous blood or other rare causes of right-to-left shunt (RLS), VGE may pass to the arterial circulation and cause damage of vital tissues manifesting decompression illness (DCI). Note that DCI includes both decompression sickness and cerebral arterial gas embolism. Because of high prevalence of RLS, mainly as a result of PFO, and low incidence of DCI, there is a general agreement that screening for RLS should not be done routinely on all divers. While in some cases screening may be useful, there is no consensus about when the screening is justified. In a recent paper by Oliver Sykes and James E. Clark titled, “Patent foramen ovale and scuba diving: a practical guide for physicians on when to refer for screening,” the authors detail clear guidelines for physicians as well as their definitions of safe diving practices, provocative dive profiles and factors suggestive of PFO. Their recommendations are very useful. Do not miss this paper. It is available for free from the above link.

Their recommendations are summarized in Figure 8 of Sykes and Clark’s paper:

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Figure 1. Flow chart on when to refer for screening by a cardiologist with an interest in diving. Courtesy of London Hyperbaric Medicine.

The findings in DAN’s PFO study coincide with most of the recommendations above. Retrospectively established incidence of various DCI manifestations in divers with PFO participating in our study is shown in following table:

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Multiorgan DCI manifestations were a frequent finding and we suggest adding it to the indications for RLS screening. In this context, multiorgan means coincidental occurrence of symptoms from two or more of the following symptom groups: skin, neurological (brain, spinal cord, ocular or inner ear), pulmonary and constitutional.

Learn more: Read about the dive and DCS history in divers who tested positive for PFO and pursue closure. http://www.alertdiver.com/Study_Update_PFO

Post written by: Petar Denoble, MD, D.Sc.