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Doolette, David J. and Simon J. Mitchell. Biophysical they are likely to form. Early descriptions of IEDCS
basis for inner ear decompression sickness. J Appl Physiol after shallow dives often treated ear problems as being
94: 2145–2150, 2003. First published January 31, 2003; of secondary importance to the other central nervous
10.1152/japplphysiol.01090.2002.—Isolated inner ear decom- system manifestations of DCS that were almost invari-
pression sickness (DCS) is recognized in deep diving involv- ably present. However, the development of deeper div-
ing breathing of helium-oxygen mixtures, particularly when
ing techniques involving breathing of helium-oxygen
breathing gas is switched to a nitrogen-rich mixture during
decompression. The biophysical basis for this selective vul- gas mixtures has been associated with the occurrence
nerability of the inner ear to DCS has not been established. of “pure” or “isolated” IEDCS (7), especially when
A compartmental model of inert gas kinetics in the human switches to air or other nitrogen-rich breathing gas
http://www.jap.org 8750-7587/03 $5.00 Copyright © 2003 the American Physiological Society 2145
2146 INNER EAR DECOMPRESSION SICKNESS
CASE REPORT
METHODS
vascular (14). Additionally, inert gases diffused between the 0.025 (hend) and 0.058 cm (hper ⫹ hend) radius, respectively,
middle ear gas space and perilymph across the round window separated by the membranous labyrinth tissue, which has a
membrane, whereas the oval window membrane was consid- surface area of Avas on each face. The diffusion distance from
Vascular-endolymph 2
hend /DN2 48 DN2 ⫻ SN2 ⫻ Avas/hend 2.34 ⫻ 10⫺5
2
hend /DHe 16 DHe ⫻ SHe ⫻ Avas/hend 4.73 ⫻ 10⫺5
Vascular-perilymph 2
hper /DN2 84 DN2 ⫻ SN2 ⫻ Avas/hper 1.77 ⫻ 10⫺5
2
hper /DHe 28 DHe ⫻ SHe ⫻ Avas/hper 3.58 ⫻ 10⫺5
Middle ear-perilymph (hrw ⫻ Vie)/(DN2 ⫻ Arw) 3.83 ⫻ 105 DN2 ⫻ SN2 ⫻ Arw/hrw 1.07 ⫻ 10⫺8
(hrw ⫻ Vie)/(DHe ⫻ Arw) 1.26 ⫻ 105 DHe ⫻ SHe ⫻ Arw/hrw 2.17 ⫻ 10⫺8
Vascular perfusion Vvas/Q̇ 194 Q̇ ⫻ SN2 5.40 ⫻ 10⫺6
Inner ear perfusion Vie/Q̇ 761 Q̇ ⫻ SHe 3.6 ⫻ 10⫺6
zero vascular compartment oxygen tension, these data can be and the inspired oxygen tension because tissue oxygen
used to calculate approximate time constants ⫽ initial ten- tension is relatively independent of inspired oxygen
sion/(⫺initial slope) for diffusion of oxygen from the guinea partial pressures used in diving.
pig endolymph of 30 s and from the perilymph of 44 s; these The transient increase in gas tension after a substi-
are of the same order as the derived nitrogen time constants
in the present human model.
tution of nitrogen for helium in breathing gas results
from the difference in gas transfer between compart-
RESULTS ments (Table 2). The flow of nitrogen into the vascular
compartment via the arterial blood exceeds washout of
Simulations using the inner ear model. Figure 3 helium in venous effluent. The transfer of helium into
shows a simulation of the gas tensions in the inner ear the vascular compartment by diffusion from the peril-
model compartments during an isobaric gas switch ymph and endolymph exceeds the counterdiffusion of
reported to result in DCS (10). After a full-day resi- nitrogen in the opposite direction and temporarily ex-
dence at 37.4 atm abs breathing the chamber atmo- ceeds the washout of helium in the blood.
sphere of 0.21 atm oxygen, balance helium, with no Examination of the flows and time constants in Ta-
change in ambient pressure, the subject began breath- ble 2 indicates that transfer of nitrogen and helium
ing 0.21 atm oxygen, 10 atm nitrogen, balance helium across the round window is negligible compared with
through a mask, during which severe nausea, vomit- the other transport processes. The time constant is
ing, and vertigo developed. The breathing-gas switch related to the flow by V ⫻ S/flow, and by definition 99%
results in a transient elevation of vascular compart- equilibration by this process alone occurs in 4.6 time
ment and endolymph gas tensions above ambient pres- constants. Whereas the round window is only 70 m
spread. It also illustrates the potential for isolated IEDCS may be associated with deep diving because a
IEDCS to occur in a seemingly random fashion during considerable gas burden must be acquired to cause
an otherwise uneventful deep technical dive that has symptoms. The model proposed here suggests an inner
gone according to plan. As we will discuss below, this ear half time (8.8 min) that allows considerable gas
case and others like it suggest that some decompres- uptake during a deep dive and considerable supersat-
sion algorithms for deep technical dives, particularly uration, and potentially bubble formation, in all inner
those incorporating switches to nitrogen-rich breath- ear compartments during the initial rapid phases of
ing gas, may need to be modified to avoid such events. decompression. Many decompression algorithms, in-
It certainly seems possible that isolated IEDCS will cluding the ZH-L16 (1) that forms the basis of many
become more common as technical diving grows in technical diving decompression algorithms including
popularity. the Proplanner used in the present case report, control
IEDCS is a poorly defined clinical entity and is dif- decompression according to the rule Pti ⬍ W ⫻ Pam ⫹
ficult to study epidemiologically. One of the principal Z, where Pti is the total inert gas tension in a compart-
difficulties is that several distinct pathological pro- ment and W and Z are constants. Although such rules
cesses may produce the same symptoms and there is no can be empirically derived without biophysical as-
gold standard test for distinguishing between them. In sumptions, they have also been interpreted as describ-
particular, there is frequent difficulty distinguishing ing a critical volume of released gas (bubbles) causing
between isolated IEDCS and inner ear barotrauma DCS (6). In this case, by mass balance of the amount of
(barotraumas are tissue damage caused by compres- inert gas in the compartment immediately before and
(23). It is on a similar premise that such breathing-gas ter Physiology V, edited by Lambertsen CJ. Bethesda, MD:
switches are used to accelerate decompression. FASEB, 1976.
3. Farmer JC, Thomas WG, Youngblood DG, and Bennett PB.
The present model suggests diffusion of middle ear Inner ear decompression sickness. Laryngoscope 86: 1315–1327,
gas across the round window is negligible, although pre- 1976.
viously proposed mechanisms implicated steady-state 4. Farmer JC Jr. Diving injuries to the inner ear. Ann Otol Rhinol
counterdiffusion of atmospheric helium and blood nitro- Laryngol Suppl 86: 1–20, 1977.
5. Goycoolea MV. Clinical aspects of round window membrane
gen across the round window and tympanic membranes permeability under normal and pathological conditions. Acta
(7, 10). This previous proposal appears to have been made Otolaryngol (Stockh) 121: 437–447, 2001.
by analogy with the production of dermal lesions and 6. Hennessy TR and Hempleman HV. An examination of the
continuous production of venous gas emboli by steady- critical released gas volume concept of decompression sickness.
state counterdiffusion across the skin in humans or ani- Proc R Soc Lond B Biol Sci 197: 229–313, 1977.
7. Hills BA. Decompression Sickness: The Biophysical Basis of
mals exposed to a helium atmosphere while breathing a Prevention and Treatment. Chichester, UK: Wiley, 1977.
different inert gas without decompression (10). 8. Igarashi M, Ohashi K, and Ishii M. Morphometric comparison
The present model of dissolved inert gas kinetics is of endolymphatic and perilymphatic spaces in human temporal
not a complete model of inner ear decompression; for bones. Acta Otolaryngol (Stockh) 101: 161–164, 1986.
9. Kennedy RS and Diachenko JA. Incidence of vestibular
instance, it does not explain the 50-min delay between symptomatology in 2,500 U. S. Navy diving accidents (1933–
predicted maximum supersaturation and onset of 1970). Aviat Space Environ Med 46: 432–435, 1975.
symptoms of IEDCS in the present case report. This 10. Lambertsen CJ and Idicula J. A new gas lesion syndrome in
delay may be related to the dynamics of bubble growth man, induced by “isobaric gas counterdiffusion.” J Appl Physiol
due to gas influx and expansion during decompression 39: 434–443, 1975.