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  • AutorenbildMichael Mutter

Inner ear decompression syndrome - more common than thought

- and with a usual suspect as risk factor.

Lake Marmorera. Courtesy Patrick Oswald, Tauchschule H2O

Inner Ear Decompression Syndrome (IEDCS) is characterized by vestibular symptoms such as dizziness, nausea, disturbances in balance and coordination of movement, but also by hearing loss and tinnitus (ringing in the ear). If it occurs during a dive, it can be potentially catastrophic because of loss of orientation and severe vomiting. It was considered rare. However, recent registry data show that it is much more common than thought.

IEDCS is more common than thought and does not only affect technical divers.

Classically, IEDCS has been considered associated with deep dives using heliox or trimix, but it is increasingly observed after air dives, albeit at the deeper end of the recreational diving range. IEDCS symptoms, like all manifestations of DCS, occur after the end of a dive, typically within 30 minutes. Rarely, IEDCS manifests before surfacing during decompression after deep dives. During deep dives, the occurrence of IEDCS has been associated with breathing gas changes from helium-containing mixtures to air or nitrox.

The genesis of IEDCS is complex.

Various pathomechanisms are discussed, such as the formation of bubbles from supersaturated gas in the inner ear itself, whereby this supersaturation is caused by decompression or by isobaric counterdiffusion after the change from helium- to nitrogen-rich breathing gas mixtures and is favored by the different nature of the compartments within the inner ear (endolymph, perilymph, vascular compartment). However, recent data also suggest an association with right-to-left shunts, such as large PFOs (patent foramen ovale).

As previously discussed in this blog, an arterial gas embolus begins to shrink once it enters the arterial blood. If the way to an end organ (in this case, the inner ear) is far enough, there is sufficient time for it to shrink enough to do no more damage. If it does not shrink enough, it reaches a compartment in the inner ear that is highly supersaturated with inert gas. This supersaturation causes the bubble to grow again in the inner ear, favoring an IEDCS. The slower elimination of inert gas and the longer-lasting supersaturation in the inner ear than in the brain offer an explanation for the selective vulnerability of the inner ear compared to the brain when both are exposed to bubbles.

A patent foramen ovale is a risk factor for IEDCS.

The risk for this process increases the higher the inert gas pressure in the gas bubble and the shorter the transit time in the arterial blood, i.e. the deeper the dive was and the shorter the way from the venous blood to the inner ear. The shortest path is via a PFO, as has also been pointed out in this blog. Thus, deep divers with a PFO are at greatest risk for IEDCS, and a PFO must be interpreted as an independent risk factor for IEDCS.

A consistent decompression strategy given sufficient time and adherence to the principles of "low bubble diving" as recommended by SUHMS is - as always - essential to avoid this potentially deleterious syndrome.

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