Biophysical basis for inner ear decompression sickness

Abstract

Isolated inner ear decompression sickness (DCS) is recognized in deep diving involving breathing of helium-oxygen mixtures, particularly when breathing gas is switched to a nitrogen-rich mixture during decompression. The biophysical basis for this selective vulnerability of the inner ear to DCS has not been established. A compartmental model of inert gas kinetics in the human inner ear was constructed from anatomical and physiological parameters described in the literature and used to simulate inert gas tensions in the inner ear during deep dives and breathing-gas substitutions that have been reported to cause inner ear DCS. The model predicts considerable supersaturation, and therefore possible bubble formation, during the initial phase of a conventional decompression. Counterdiffusion of helium and nitrogen from the perilymph may produce supersaturation in the membranous labyrinth and endolymph after switching to a nitrogen-rich breathing mixture even without decompression. Conventional decompression algorithms may result in inadequate decompression for the inner ear for deep dives. Breathing-gas switches should be scheduled deep or shallow to avoid the period of maximum supersaturation resulting from decompression.

Cutis Marmorata skin decompression sickness is a manifestation of brainstem bubble embolization, not of local skin bubbles

“…PFO-related embolization most probably happens both in the carotid artery and vertebral artery territory, but, as evidenced by the clinical picture of other PFO related decompression sickness syndromes, the ''carotid artery" syndromes are far less frequent than syndromes arising from the vertebral artery territory (inner ear, cerebellar syndromes). This may be due to the fact that the territory of the vertebral artery is less capable of recruiting parallel circulation circuits than the carotid artery territory, or may simply reflect the fact that cerebral tissue is much more likely to be sufficiently desaturated so as not to provoke bubble stabilization or growthbrain tissue half-time is very short, estimated at 1.2-1.7 min [43].…”

Susceptibility of the Inner Ear Structure to Shunt-Related Decompression Sickness

“…In the inner ear it is the switch from a helium-rich atmosphere to nitrogen that was described as creating a transient supersaturation state. The model described by Doolette and Mitchell implicates transient supersaturation resulting from a counter-diffusion mechanism in which helium transfer from the perilymph to the other compartments temporarily exceeds the washout of helium in the venous blood ( 4 ). However, the gas counterdiffusion theory does not explain the occurrence of IEDCS after air dives without any gas switching or helium involvement, and there have been multiple studies published in the last decade describing isolated and combined symptoms of IEDCS after air diving ( 3 , 8 , 9 ).…”

Auditory Complaints in Scuba Divers: an Overview

“…Ear problems due to DCS are treated with secondary importance in comparison to those of the central nervous system [47]. It is not widely recognised that inner ear disorders resulting from decompression sickness are a serious hazard in diving, although they are present in 26% of all severe DCS cases [48,49].…”

“…When the concentration or solubility of a dissolved gas exceeds ambient pressure within the inner ear during ascent, this can develop into inner ear decompression sickness (IEDCS). Bubbles are known to form in the inner ear, although the exact location and circumstances where this occurs are unclear and usually only hypothesised [47]. Theories suggest formation within the micro-vessels and otic fluids or within the osteoclast cells of the inner ear bony lining, causing it to rupture due to pressure elevation, forcing it into the otic fluid spaces [10].…”

“…Either counter-diffusion through round and oval windows causing IEDCS at the interface of middle and inner ear, or gas osmosis transfer of the fluid between endolymph (perfused with blood) and perilymph (saturated with gas) could result in vestibular damage [10]. Doolette & Mitchell [47] used a physiological compartmental model to investigate the diffusion of gases across the membranous labyrinth. The model was able to demonstrate super-saturation in the early stages of decompression with a diffusion time through the membrane of 8.8 min, allowing considerable super-saturation and bubble formation.…”