ICD - preventing Inner Ear DCS

[Dr Simon Mitchell]

The second type of IEDCS is the shallow dive version. These are the common ones that occur at 20 and 30m dives. I am not aware of an explanation for these as yet, and no apparent supersaturation conditions exist to trigger it.

Hello Ross,

The explanation is well established, and we have discussed this before. ~80% of "shallow" IEDCS victims have a large PFO in comparison of <5% of people in the general diving population [1]. This strongly implicates the passage of VGE across the PFO early after surfacing in causation of this problem. The supersaturation conditions required for these VGE to grow and create problems when they arrive in the inner ear circulation do exist; they have been modeled and published [2].

1. Mitchell SJ, Doolette DJ. Pathophysiology of inner ear decompression sickness: potential role of the persistent patent foramen ovale. Diving Hyperb Med. 2015;45:105-110.

2. Mitchell SJ, Doolette DJ. Selective vulnerability of the inner ear to decompression sickness in divers with right to left shunt: the role of tissue gas supersaturation. J Appl Physiol. 2009;106:298-301.

Simon's description misses one key aspect of the deep IBCD/IEDCS issue. The cause has two parts - part a/ is a big gas switch causing a strong He off gas gradient (per Simon's post), and part b/ is the continued ascent which creates excessive the supersaturation in the inner ear fluids.

I clearly stated the importance of the pre-existing inner ear supersaturation in this process, and also mentioned that the ascent means that these switches are never truly isobaric.

Simon M

 

[Dr Simon Mitchell]

Mitchell and Doolette use a water solubility approach, Stephen Burton used a lipid solubility approach. I cannot argue about those choices.

Hi Miyaru,

The inner ear is the only tissue thought to be injured by IBCD processes and its composition is understood. As you know, we have published a physiological model of the inner ear based on its known anatomy and tissue composition. I don't know how Steve Burton would justify his choices / predictions, but I would be skeptical about their physiological provenance.

In answer to your question about a depth threshold beyond which IBCD becomes relevant, there is no hard answer. But it is clear (as Ross implied) that the risk of IBCD-related inner ear DCS is higher in deeper dives. This is consistent with our finding that pre-existing supersaturation seems to be critically important in gas-switch / IBCD-related inner ear DCS (deeper dives would likely produce more inner ear supersaturation around the time the initial gas switches are often contemplated).

Simon M