Download Inner Ear Barotrauma in Scuba Divers

Inner Ear Barotrauma in Scuba Divers
A
Long-term Follow-up After Continued Diving
Joseph Parell, MD, Gary D. Becker,
G.
\s=b\ Divers who suffer inner ear barotrauma are usually
counseled to permanently avoid diving, reasoning that the
injured inner ear is at increased risk of further damage.
Twenty patients who suffered inner ear barotrauma while
diving, but continued to dive against medical advice, were
interim basis for 1 to 12 years. As difficulty
equalizing
during the barotraumatic event was a
universal finding, prior to resuming diving, all patients were
reinstructed on methods of maximizing eustachian tube
function. No further deterioration of cochleovestibular
function was noted. Based on these preliminary results, we
conclude that recommending no further diving after inner
ear barotrauma may be unnecessarily restrictive.
(Arch Otolaryngol Head Neck Surg. 1993;119:455-457)
assessed
on an
the
ears
commonly observed medical condition
ba (self-contained underwater breathing apparatus)
Thebreathhold
barotrauma that
(BH) divers middle
in scu¬
most
is
ear
results from the inability to equalize the ears during
descent. This condition usually resolves spontaneously
and without sequelae. Conversely, inner ear barotrauma
(IEBT) is much less common but potentially more serious
as the cochleovestibular (CV) symptoms, including tinni¬
tus, fullness in the ear, sensorineural hearing loss (SNHL),
and dizziness or vertigo, may be permanent and disabling.
Deep diving is not necessary, as both middle ear barotrau¬
ma and IEBT may occur in as little as 2.40 m (8 ft) of
water.1
Based on the uncorroborated theory that a previously
injured inner ear may be at increased risk of further inju¬
ry, the consensus of diving-trained physicians is to coun¬
sel patients with IEBT to permanently discontinue diving.
To establish guidelines concerning diving after IEBT
formulated on scientific principles rather than conjecture,
we followed and documented the otologie outcome of a
group of divers who sustained IEBT but, against medical
advice, continued to dive.
or
PATIENTS AND METHODS
For this article, our definition of IEBT is an injury to the inner
ear due to diving that causes a SNHL, with or without coexistent
CV symptoms. Twenty patients, including seven professional (US
Navy, commercial, or diving instructors) divers, sustained IEBT
while scuba or BH diving. All were examined at the time of ini-
Accepted
for
publication
October 30, 1992.
Bay Memorial Medical Center, Panama City, Fla (Dr Parell),
and the Department of Otolaryngology\p=m-\Headand Neck Surgery,
Kaiser-Permanente Medical Center, Panorama City, Calif (Dr Becker).
Reprint requests to 330 W 23rd St, Suite E, Panama City, FL 32405\x=req-\
4540 (Dr Parell).
From the
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MD
injury by us. This included an otologie history, statement of
difficulty equalizing the ears during the dive, documentation of
the dive profile (time-depth relationship), physical examination,
and serial air and bone conduction audiograms. Electronystagmograms were obtained on most patients undergoing middle ear
surgical exploration.
We counseled all patients with IEBT to discontinue diving
based on the hypothesis that the inner ear may be at increased risk
of further damage from diving. Those who refused this advice
constitute the patients in this series. Subsequent to their initial
IEBT, we taught them various methods of equalizing the ear. We
advocated initial equalization at the surface of the water, prefer¬
ably with the jaw thrust or yawning maneuver. Descent was ac¬
complished feet first, down an anchor line, equalizing continu¬
ously for at least the first 6.00 m (20 ft). If forceful Valsalva's
maneuver was required to equalize, the dive was aborted. Diving
with any amount of nasal or ear congestion was proscribed. All
divers stated they adhered closely to these instructions and none
admitted any further difficulty clearing their ears. The no decom¬
pression limits of the US Navy Dive Table or a personal submers¬
tial
ible dive computer was observed on all dives.
After the initial injury, diving resumed when the hearing level
stabilized, usually within a few weeks to several months. Each
patient's dive profile, stated difficulty in equalizing the ears,
changes in CV symptoms, and serial audiograms were obtained
on an interim basis.
Frequencies tested during audiometry were 250, 500, 1000,
2000,4000, and 8000 Hz. The severity of loss was characterized as
follows: 25 to 40 dB, mild; 40 to 55 dB, moderate; 55 to 70 dB,
moderately severe; 70 to 90 dB, severe; and greater than 90 dB,
profound. Audiograms were characterized as flat when all tested
frequencies (250 through 8000 Hz) were depressed, and high fre¬
quency when 4000 and 8000 Hz were involved. A discrete
frequency loss was considered present only if the frequency or
frequencies on either side were at least 10 dB better. Follow-up
audiograms were characterized as "no change" if they were
within 10 dB of the initial audiogram.
RESULTS
All patients were male. The mean, median, and age
ranges were 35 years, 35 years, and 21 to 50 years, respec¬
tively. Follow-up was from 1 to 12 years and the mean and
median durations were 62 months and 54 months, respec¬
tively. Thirteen patients dived recreationally and seven pa¬
tients (cases 1,4,5,8 through 10, and 19) dived profession¬
ally. The stated number of scuba tanks used during the du¬
ration of the follow-up represents the minimum number of
dives during which the ear was at risk of further CV damage
as multiple dives per tank of air may be accomplished.
When evaluated after the initial barotraumatic injury,
difficulty equalizing the ears during the dive was a
universal finding. A SNHL, present by definition in all pa¬
tients, was unilateral in all but one instance (case 11).
Hearing losses ranged from mild to profound. Partial to
Summary of Cases of Inner
Case
Initial
No./
Audiogram
Age, y
1/28
Moderate flat
2/31
Moderately
3/50
4/21
5/34
6/35
7/41
8/25
9/39
10/41
11/44
12/34
13/32
14/41
15/57
16/35
17/21
18/36
19/32
20/27
Follow-up
Audiogram
severe
Profound flat
Severe flat
Profound flat
Moderately
Moderately severe high
frequency
Moderate high frequency
severe
flat
Profound flat
Moderately severe high
frequency
Moderate bilateral high
frequency
Moderate severe high frequency
Mild high frequency
Profound flat
Mild 2 kHz
Moderate 2 kHz
Moderately
severe
change
change
Mild low frequency
No
flat
flat
Moderate severe low frequency
and 4 kHz
Moderate flat
Moderate 500 and 1 kHz
*CV indicates cochleovestibular; IEBT, inner ear
No
Normal
Normal
Normal
Ear Barotrauma*
Initial CV
Symptoms
Vertigo
Vertigo
Vertigo
Vertigo,
Vertigo,
No. of
Tanks Used
Since IEBT
Type of
60
400
F
72
60 BH
F
Length of
Follow-up, mo
IEBT
74
8
tinnitus
20
10
F
F
tinnitus
42
300
H
Tinnitus
12
60
H
No
Tinnitus
change
change
Vertigo
Moderate high frequency None
18
3 scuba 20 BH
H
No
99
>2000
H
38
>1000
H
Vertigo
99
>2000
frequency
change
No change
Profound high frequency
No change
Tinnitus
110
500
H
Tinnitus
Tinnitus
120
60
H
24
60
H
None
144
600
H
None
14
ICMT
Mild 2 kHz
Mild 1 kHz
Dizziness, tinnitus
80
8 scuba many BH
125 BH
Tinnitus
48
50 BH
ICMT
No
change
Mild bilateral
high
No
ICMT
Moderate 4 kHz
Mild 4 kHz
Dizziness
26
50
ICMT
Vertigo
64
>1000
ICMT
change
Tinnitus
145
No
60 scuba 100
H
ICMT
barotrauma; BH, breathhold dive; F, fistula; H, hemorrhage; and ICMT, intracochlear membrane
tear.
complete recovery occurred spontaneously in most pa¬
tients, usually within the first few weeks of injury. Com¬
plaints of vertigo (spinning sensation) or dizziness (a hal¬
lucination of movement other than spinning) resolved
within hours to weeks in all instances. Resolution of tinni¬
tus was variable. In cases 5,11,13, and 20 the tinnitus per¬
sisted. An electronystagmogram, including bithermal ca¬
loric responses and fistula testing (with positive and
negative pressure), was obtained in cases 1 through 3, and
10. The only abnormalities noted were a 6°/s spontaneous
left beating nystagmus with the eyes closed (case 10) and
a positive fistula test (case 3). Cases 1 through 4 underwent
surgical exploration for possible inner ear fistula. Recur¬
rent accumulation of fluid in the areas of the round or oval
windows on Valsalva's maneuver or reversed Trendelenberg's position was noted in all instances. All fistulas were
repaired using autologous tissue.
The initial barotraumatic injury was due to scuba diving
in all instances except case 2, which resulted from BH div¬
ing in a swimming pool. After the initial barotraumatic in¬
jury, cases 2 and 17 exclusively, and cases 7,15, and 20 fre¬
quently, engaged in BH rather than scuba diving. Most of
these dives were within 9.00 m (30 ft). Deep diving is not
a factor in barotraumatic injuries. The greatest volume
change in air-containing (eg, middle ear) spaces and,
hence, the greatest potential for difficulty in equalizing the
ears, is within 9.90 m (33 ft) of the surface.
We speculated that patients with a fistula or severe-toprofound hearing loss would be at greatest risk of further
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hearing and vestibular dysfunction. However, during the
follow-up period, no diver experienced a further deterio¬
ration of hearing, recurrence of vestibular symptoms, or
deterioration (or recurrence) of tinnitus.
COMMENT
the first to audiometrically docu¬
ment IEBT as a result of diving. He speculated that the in¬
jury resulted from labyrinthine damage from the pressure
wave generated in the inner ear during forceful autoinfla¬
tion of the eustachian tube. Simmons3 postulated that co¬
chlear membrane breaks result in sudden hearing loss and
Goodhill4 described possible abnormal inner ear fluid dy¬
namics as a cause of window fistulas, both resulting from
sudden and intense inner ear pressure changes. Scuba
divers were represented in both authors' series. Pullen,5 in
1972, was the first to document an inner ear (round win¬
dow) fistula resulting from scuba diving. Many additional
clinical reports of IEBT and fistulas have since been
reported. Histologie documentation of inner ear hemor¬
rhage and cochlear membrane tear after barotraumatic in¬
jury (drowning while scuba diving and flying, respective¬
ly) has been reported.6-7 Pareli et al collected 20 temporal
bones from patients who died while scuba diving (G.J.P.
and G.B. and P. Antonelli, MD, and M. M. Paparella, MD,
Macfie2 in 1964
was
unpublished data, 1992).
Intracochlear hemorrhage was
noted in several instances but membrane tears were not
observed (G.J.P. and G.B. and P. Antonelli, MD, and M. M.
Paparella, MD, unpublished data, 1992). Nevertheless,
based
on
literature
reports
as
well
as
observations of
our
speculate that IEBT may be caused by three
mechanisms, acting separately or in combination: inner ear
hemorrhage, intracochlear membrane tear, or fistula of the
round or oval window.8 The Table categorizes patients ac¬
cording to this classification.
Most hearing losses due to diving-induced IEBT as re¬
ported in the literature are severe and diffuse (flat) or high
frequency. Butler and Thalmann,9 however, described a
Navy diver who noted unilateral tinnitus after a dive. He
continued to dive during the next few days until the tin¬
nitus became much worse and a hearing loss was noted. A
flat 65- to 70-dB SNHL with a poor speech discrimination
score (SDS) was demonstrated. He discontinued diving
and within several weeks the hearing levels and SDS
patients,
we
returned to normal except for an isolated 1000-Hz loss of
20 dB. After the hearing stabilized, the patient continued
to dive without further hearing loss. We speculate that this
diver had a cochlear hemorrhage causing the flat SNHL
that normalized when the hemorrhage resolved, as well as
an intracochlear membrane tear resulting in a persistent
SNHL at the site of the tear. Our patients with intracochle¬
ar membrane tear differ in that they temporarily discon¬
tinued diving immediately after the precipitating event.
Three patients presented initially with discrete frequency
SNHL and the remainder had multiple frequencies in¬
volved initially that became a discrete frequency loss on
follow-up audiogram. All patients maintained normal
SDS. All hearing levels improved and stabilized after sev¬
eral weeks of convalescence.
Four of our patients (cases 1 through 4) had surgically
confirmed inner ear fistulas. Patient 1 was a Navy diver
who completed an uneventful helium-oxygen dive fol¬
lowed by decompression according to the tables. About 15
minutes later he made multiple BH dives while instructing
students. During this time, hearing loss, nausea, and ver¬
tigo prompted recompression for possible decompression
sickness. Symptoms did not improve. After 1 week of bed
rest, the hearing did not improve and surgical exploration
confirmed a fistula. Authorities in diving medicine believe
that recompression of a patient with an inner ear fistula is
contraindicated as this may worsen the hearing. In this case
there was no change in hearing after recompression. The
patient continues to dive without recurrence of CV symp¬
toms. Patient 2 had a BH diving-related inner ear fistula
repaired (by another surgeon) in 1983. Preoperatively the
audiogram demonstrated a flat 55-dB SNHL with 52% SDS
which, after surgery, improved to a flat 30-dB SNHL with
100% SDS. He continued to BH dive until 1986 when, after
a period of 2 months of no diving, rapidly progressive de¬
terioration of hearing in the operated-on ear prompted an
exploratory tympanotomy by one of us (G.J.P.). A fat graft
was observed significantly lateral to the round window
with normal mucosa interposed between the graft and
round window membrane. The graft was removed, the
overhang of the round window niche was removed with
a drill, the mucosa was deepithelialized, and a temporalis
fascia graft was placed. After this second operation, the
audiogram remained flat at 55 dB but the SDS improved
from 56% to 88%. The patient has since made multiple BH
dives without further problems. Patients 3 and 4, unlike the
first two patients, had significant improvement in hearing
levels and SDS after surgery.
In 10 patients we speculated cochlear hemorrhage as the
cause of the IEBT. There were two distinct subgroups,
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however. In six instances, (cases 7, 8, and 10 throughl3),
the hearing loss was limited to high (4000 and 8000 Hz)
frequencies, the SDS was excellent, and the hearing levels
never improved. Besides hearing loss, the presenting
symptom in two of these patients was vertigo (which may
have been the alternobaric variety, ie, due to unequal
pressures in the middle ears) and in four patients it was
tinnitus. The other subgroup comprised four patients who
presented with a much more pronounced, usually flat
hearing loss with poor SDS. Within 7 to 19 days, the hear¬
ing levels and SDS had returned to normal, except for a
residual high-frequency loss in some cases (see Table).
Coexistence of other CV symptoms at the time of IEBT was
variable. Perhaps this subgroup had fistulas that resolved
spontaneously, and this supports the belief of waiting a
few weeks before considering exploratory tympanotomy.
A typical example is patient 5, a 34-year-old scuba instruc¬
tor who was making multiple bounce (rapid descent and
a class. He
ascent) dives to 9.00 m (30 ft) while
noted fullness and pressure in the right ear that increased
in severity over the next 2 days, despite no further diving.
He then made one dive to 42.00 m (140 ft) for 8 minutes
during which the right ear "closed up" and tinnitus was
noted without dizziness. An audiogram revealed a pro¬
found SNHL with no SDS. He discontinued diving and 11
days later the hearing levels and SDS were normal. He re¬
sumed diving as an instructor and has had no further
teaching
hearing problems.
CONCLUSION
We believe our data are preliminary and require confir¬
mation before definitive recommendations can be made.
However, current recommendations regarding diving after
IEBT may be unnecessarily restrictive. As difficulty equal¬
izing the ears is a universal precipitating cause of IEBT, all
divers with an abnormally functioning eustachian tube
should not dive until this is corrected, and they should be
reinstructed on the various methods of equalizing the mid¬
dle ear. The dive should be aborted if difficulty equalizing
the ears is encountered. If this is accomplished, the diver may
return to diving probably without incurring an inordinate
risk of further CV dysfunction in the previously injured ear.
After the manuscript was accepted for
pa¬
tient 9 returned in December 1992 with a severe SN hear¬
ing loss in his opposite ear following six dives to 24 m (80
ft) in one day. Each dive was about 40 mintues in duration.
He was given a course of oral corticosteroids. One month
later, the hearing in this ear had returned completely to the
preinjury level.
publication,
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5. Pullen FW. Round window membrane rupture, a cause of sudden deafness. Trans Am Acad Ophthalmol Otolaryngol. 1972;76:1444-1450.
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rupture. Arch Otolaryngol. 1981;107:598-600.
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