Dive Pacific Iss 171 Oct- Nov 2019

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DIVEMEDICINE The fascinating problem of inner ear decompression sickness By Professor Simon Mitchell, University of Auckland In this incident a diver was evacuated for recompression, but flew home sooner than DAN advised and, unfortunately, the symptoms returned and persisted for some time. Could this have been avoided if the diver had delayed his flight home? Decompression sickness (DCS) is the well-known diving disorder caused by bubbles formed from inert gas (usually nitrogen) that we have breathed and absorbed during a dive. Everyone who has done an entry level dive course knows the story. We absorb nitrogen into blood and tissues from the air we breathe during a dive. The deeper we go the more nitrogen we can absorb, and the longer we stay at depth the more nitrogen is taken up. Most dives are performed according to time and depth guidelines that allow us to make a direct ascent to the surface at the end of the dive (so-called “no-decompression diving”) but if we exceed certain depth and time limits then we have to ascend more slowly and make “decompression stops” to allow time for nitrogen or other inert gases we may breathe to be eliminated from the body. What dive tables and computers attempt to do in prescribing no-decompression time limits, or in prescribing a pattern of decompression stops during ascent, is to prevent the pressure of dissolved gas in our bodies from exceeding the surrounding pressure (a condition known as supersaturation) by more than is considered safe. Supersaturation of dissolved gas in our bodies is the primary driver for bubbles to form, so by controlling supersaturation we control bubble formation and lower the risk of DCS – that’s the theory anyway! Nothing is simple about DCS. Bubbles can form in tissue themselves, or in the blood (typically the venous blood because it drains from the tissues where all the nitrogen has accumulated). Organs can be affected Many organs can be affected, producing confusing patterns of symptoms of varying severity. Some symptoms are caused by those bubbles that form in tissues, and others are thought more likely related to bubbles that have formed in the blood. Some organs can be affected by both. The inner ear is a tiny organ that lies in the bone deep to the ear. It is responsible for processing the neural signals of hearing and balance. It is easy to understand how something going wrong with it can produce very unpleasant and potentially disabling symptoms, like intractable vertigo, nausea, vomiting and deafness. Why now? Why write about it now? Well, I was reminded of the issue this month in processing the next issue of Diving and Hyperbaric Medicine to be published at the end of September. In It there is an article by a group from Malta describing their DCS caseload since the late 80s. Around 1990 about 5% of their DCS cases had inner ear symptoms but by 2017 this had risen to 50%, an extraordinary increase [1]. Our DCS case numbers are low across the board in New Zealand, …The inner ear is tiny, but it contains several relatively large pools of fluid that can absorb and eliminate gas from the blood – but only through the sensitive neural tissues. These pools of fluid have no blood supply of their own… but we too are seeing more inner ear cases. The obvious question is why? And the answer is that it probably reflects the nature of the diving going on. Basically, with the increasing popularity of technical diving and rebreather use we are going deeper. Going deeper To understand why depth can be a particular issue for inner ear DCS we need to consider its fascinating pathophysiology. Here it can get a little complicated. The inner ear is one of those organs we believe can be injured by bubbles forming in the organ itself, and also by bubbles reaching it in the blood. Let’s start with bubbles forming in the inner ear itself. That seems like a fairly simple concept. If the inner ear tissue became excessively supersaturated with inert gas then bubbles could form, disrupt the inner ear function, and cause symptoms. This has often been seen during decompressions from very deep dives (I’m thinking typically more than 100m). 54 Dive New Zealand | Dive Pacific
Fig. 1 Advantageous counter-diffusion after a helium to nitrogen switch during decompression. This situation would likely apply in all tissues except the inner ear. Fig. 2 Disadvantageous counter-diffusion in the inner ear after a helium to nitrogen switch during decompression. The fluid pools are represented by the darker blue panel. Terrifying instance I had one particularly terrifying experience with a buddy suffering this problem during a decompression from a 120m dive when we still had two hours of decompression to go. He was so dizzy he could not open his eyes and spent those hours coming off the rebreather to vomit on open circuit scuba, and going back on the rebreather again. It was a remarkable feat of diving skill and endurance that we were able to complete the decompression. The puzzling thing is that, as in this case, it is often only the inner ear affected by the problem. Why only the inner ear? Why aren’t other organs affected at the same time? Unique risk factor… The answer is that the inner ear has a unique risk factor for developing excess supersaturation during decompression from deep dives: it is the one and only organ in the body vulnerable to isobaric counter-diffusion problems (there’s a term you can drop into a diving medicine conversation!). In deep diving helium is typically blended with oxygen and nitrogen as ‘trimix’ and used for its non-narcotic, low density properties. In decompressing from deep dives it has been common practice to switch from helium breathing to nitrogen breathing (air or nitrox) during the decompression. In theory, this should result in faster reduction of tissue inert gas because the helium being a light molecule will diffuse from tissue to blood faster than nitrogen will diffuse from blood to tissue. The principle is illustrated in Figure 1 which shows a theoretical tissue with a blood vessel passing by just after a switch from …normal scuba air divers are also vulnerable to inner ear DCS, particularly if they venture down around the 25-30m depth much… breathing primarily helium to primarily nitrogen. The helium diffuses rapidly into the blood (large arrow) because there is little helium there after the gas switch to nitrogen breathing, and nitrogen diffuses into the tissue but more slowly (smaller arrow) than the helium diffuses out. The net effect is a faster reduction of inert gas pressure in the tissue and this process of the two gases diffusing in opposite directions is called isobaric counter-diffusion. Figure 1. Advantageous counter-diffusion after a helium to nitrogen switch during decompression. This situation would likely apply in all tissues except the inner ear. …because of unique anatomy Unfortunately this does not quite work for the inner ear because of some unique anatomy. The inner ear is tiny, but it contains several relatively large pools of fluid that can absorb and eliminate gas from the blood – but only through the sensitive neural tissues. These pools of fluid have no blood supply of their own. If this fluid has absorbed a lot of helium during the dive, and it only loses it slowly through the tissue space, then a switch to nitrogen will have the opposite effect to that described above. Yes, helium moves from the tissue into the blood faster than the nitrogen diffuses from the blood into the tissue, but the helium pressure in the tissue is constantly topped up by helium moving into the tissue from the adjacent pools of fluid, and so the helium pressure in the tissue does not fall. The net effect is that the diffusion of nitrogen into the tissue will transiently increase the dissolved gas pressure in the inner ear, thus www.dive-pacific.com 55
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Dive Pacific Iss 171 Oct- Nov 2019

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