Ann Otol 86: 1977
HEARING LOSS FROM ACUTE CARBON MONOXIDE INTOXICATION SHAN
R.
DAVID
J.
BAKER,
MD
LILLY, PHD
IOWA CITY, IOWA
SUMMARY - A case of fluctuating sensorineural hearing loss from acute carbon monoxide (CO) poisoning with presentation of a U-shaped audiogram is reported. Acute CO intoxication seems to involve vestibular function more frequently than auditory function. Hearing loss is uncommon, but when present, may often display a U-shaped audiometric curve. Decrease in hearing sensitivity probably results from hypoxia to the cochlea, VIII nerve and brain stem nuclei. Fluctuation in hearing sensitivity may be an early manifestation of acute CO exposure, and requires periodic audiometric examination until the hearing has stabilized.
Little has been written in the English literature concerning hearing loss from acute carbon monoxide (CO) intoxication. It is estimated that 12-14% of employed individuals have occupations in which there is likelihood of exposure to high levels of CO.l It is, therefore, important to be able to recognize and to diagnose the various neuro-otologic manifestations of CO poisoning. Carbon monoxide combines with hemoglobin to form carboxyhemoglobin (CORb) which is over 200 times more stable than oxyhemoglobin. The formation of CORb prevents oxygen from entering into combination with hemoglobin and consequently causes a deficiency of oxygen supply to vital organs. Neutralization of the oxygen carrying activity of the erythrocyte produces anoxia and accounts for the primary mechanism of CO poisoning. The central nervous system (CNS) is especially vulnerable to CO poisoning. Pathological changes caused by CO include demyelinization, hemorrhage, focal necrosis, and edema. Acute CO poisoning causes diffuse small hemorrhages in the brain stem and cerebrum while chronic poisoning often leads to demyelinization of the globus pallidus.P
A dose of CO that produces a CORb level of 60% usually is lethaJ.2 It generally is believed by clinicians that subjective symptoms rarely occur below CORb levels of 20%, while most acute signs of cardiac and CNS embarrassment occur at levels greater than 30%. Several investigators have indicated CNS impairment at CORb levels as low as 2-5%, or to low concentrations of CO in the air. 1 •3 ,4 Impairment of visual function has been documented when CORb concentrations reach 4-5%.1 Decreased capacity to discriminate the temporal lengths of tones, has been shown for patients exposed to low CO concentrations," and elevated auditory threshold has been demonstrated in humans subjected to CO concentrations of 0.02 mg/Iiter.! Some of the symptoms of acute CO poisoning that an otolaryngologist may be called on to evaluate include: aphasia, anosmia, facial and glossopharyngeal palsy, and disturbance of gustatorv function. Pharyngitis, ulcerations and bleeding from oral mucosa. and rhinitis also have been reported." Carbon monoxide induced lesions of the auditory and vestibular system cause tinnitus, hearing loss, nystagmus, and ataxia.
From the Department of Otolaryngology and Maxillofacial Surgery, ancI the Department of Speech Pathology and Audiology, University of Iowa, Iowa City, Iowa.
323
Downloaded from aor.sagepub.com at Harvard Libraries on June 30, 2015
324
BAKER-LILLY VESTlliULAR MANIFESTATIONS
Our review of the literature suggests that CO affects the vestibular system more often than clinically recognized. It also is apparent that vestibular function of the inner ear is involved more frequently than auditory function. Often the objective vestibular symptoms are marked with only minor subjective vertigo. One may see spontaneous and positional nystagmus, as well as hyperand hypoexcitability of the labyrinth to caloric stimulation. Nakashima" studied 14 patients after recovery of consciousness following CO intoxication and found no significant hearing loss. Seven of these patients, however, demonstrated spontaneous nystagmus on electronystagmography (ENG), and three patients showed positional nystagmus. Four patients demonstrated hyperexcitability to the ice water caloric test. In addition, Nakashima noted that several of the patients demonstrated pauses and dysrhythmic patterns on ENG with caloric stimulation. Twelve months after exposure to CO, spontaneous nystagmus remained unchanged in the seven patients who previously were affected and appeared as a new finding in two others. Nakashima concluded that these abnormalities seen on ENG were caused by central lesions. Monnier-Kuhn et al' evaluated 20 patients suffering from acute CO intoxication, 15 of which were in coma. None of these patients demonstrated loss of auditory function, vertigo, or equilibrial disturbances. Fourteen patients, however, demonstrated abnormal ENG. Ten patients showed hypofunction in caloric tests. Mounier-Kuhn and his colleagues found no correlation between the concentration of COHb and the intensity of the clinical sizns. but vestibular impairment appeared to be related directly to duration of exposure to CO. They concluded that the vestibular lesions produced by CO were more often peripheral than central, and most often presented a destructive ENG pattern. Earlier studies have supported these observations.s-" The findings of Mounier-Kuhn, how-
ever, have not been supported by other investigators who conclude that the major vestibular lesion seen with CO is centraPO-13 Kato B demonstrated spontaneous nystagmus with directional preponderance in animals subjected to CO intoxication. Postmortem examination revealed hemorrhages in the cerebellum. Butenburg-" found no evidence of degeneration of the peripheral vestibular system in test animals exposed to acute CO poisoning. Floberg-" showed that CO exposed cats with unilateral ligation of the common carotid artery developed reproducible vestibular symptoms of circus movement and nystagmus. Destruction of the labyrinth through surgery or by streptomycin did not change these symptoms, suggesting that the lesion accounting for circus movement was located central to the vestibular nuclei. AUDITORY MANIFESTATIONS
Chronic CO Intoxication. In general, chronic CO intoxication often results in a permanent, symmetrical, high-frequency hearing loss. Lumio-" reported an extensive study of 263 patients suffering from chronic CO poisoning. Audiometry disclosed hearing loss in 78.3% of the victims. A typical high-frequency bilaterally symmetrical, sensorineural hearing loss was seen in 67.7% of these patients, with the audiometric curve falling off steeply and progressively, starting at frequencies between 1000 and 2000 Hz. A pattern very much similar to that following noise exposure with a maximum hearing loss at 4000 Hz was seen in 2.7% of these patients. No patients were reported to have U-shaped audiograms. Follow-up examination revealed that hearing improved in only 26.7% and then only to a slight degree. Eighty cases of chronic CO poisoning studied by Zenk'? supported Lumino's findings of symmetrical high-frequency sensorineural loss. Acute CO Poisoning. It has been well-documented that hearing loss resulted from chronic CO poisoning, 1 " but it is much less frequent after acute CO intoxication. Presented is what we believe to be the first reported case of
Downloaded from aor.sagepub.com at Harvard Libraries on June 30, 2015
325
HEARING LOSS AND CARBON MONOXIDE 1 0 0
~2
0
i
(~--(
----
D-, \
...J
W
40
!:!! .0 ~ 60
m,,( '1'
-1--
28 APRIL 1975
,
-3 0
> ~
0
(1 MONTH POST CO
:~
INTOXICATION)
..
/
~ ~.?
r0~~b.
:I: 70
I- f--- ~2 1/
.~V
~,
./ /
,./
90 24 MARCH 1975 (INITIAL AUDIOGRAM)
100
500
1000
2000
4000
...J
30 40
!:!! ~
60
I
'0 70
INTOXICATION)
~
f-------
t----
L1l
J
DECEMBER 1975
INTOXICATION I
t---- f-------
f---
f- f---
100
I
110
I
A.D. SOLlD CURVE A.S. BROKEN CURVE
~
'25
.r
-
( 8 MONTHS PoST CO
90
FREQUENCY (Hz)
~
~~ , I' \~- ..
I
-
I
1/
f" Xl ~' ,,
W
~
(1 MONTH POST CO
---,--:.-:::- " '
0
l - t----
8 000
,
d
+
28 APRIL 1975
J'
80
110
A
-
:I:
"f:::, ~/
80
(D
0
1
111
0
0
250
I 500
I
I 1000
2000
4000
6000
FREQUENCY (Hz)
Fig. 1. Composite audiograms. A) Lower curves represent initial pure-tone audiogram. A moderate, binaural sensorineural hearing loss is noted. Upper curves show subsequent improvement in audiometric results one month later. All bone-conduction symbols have been omitted. B) Audiometric symbols taken from Fig. lA represent patient's best pure-tone responses following CO intoxication. Bottom curves show reduction in hearing sensitivity for lower frequencies seven months later. Bone-conduction symbols have been omitted.
fluctuating bilateral sensorineural hearing loss following acute CO poisoning. A U-shaped audiometric curve manifests itself. CASE REPORT
Carhart tone-decay findings were within normal limits (not greater than 5 dB at any test frequency). A SISI score of 100% was obtained bilaterally for 1000 Hz at 20 dB sensation level. Discrimination scores were poor, showing 48% in the right ear and 64% in the left for recorded monosyllabic words (C.LD. Auditory Test, W-22) presented at 30 dB above the patient's speech reception threshold.
On March 15, 1976, a 16-year-old Caucasian female was admitted to the hospital for treatment of carbon monoxide poisoning after being found unconscious in a parked car. The ignition key was on, and the gasoline tank was empty. On arrival, the patient was decorticate to decerebrate with doll's eyes and bilateral upgoing toes. Her past history revealed no hearing loss or evidence of ear infections. She was transferred immediately to the Intensive Care Unit and treated with hypothermia, and intubated for controlled ventilation using high-flow oxygen. Thorazine'S>," heavy sedation, and intravenous steroids were administered.
One month later, the patient returned for selected audiometric studies. Pure tone audiometry showed an improvement of 25 to 48 dB in the right ear and 17 to 45 dB in the left ear. These findings are depicted in the upper curves of Figure LA, The audiometric pattern assumed a U-shaped configuration with maximum hearing loss at 2000 Hz. Bekesy audiometry showed Type I tracings for frequencies below 2000 Hz and Type II tracings for the higher test Irequencies.t?
Within three days, the patient showed dramatic improvement and was extubated. Neurologic examination at that time was unremarkable except for a moderate bilateral hearing loss. She continued to make an uneventful recovery and was seen by the department on March 24. An ENG was performed at this time and revealed no spontaneous or latent nystagmus. Ice water caloric test produced normal, symmetrical vestibular responses. Examination of the ears revealed clear, mobile tympanic membranes bilaterally. The patient's initial pure tone audiogram is shown as the lower curves in Figure LA. A bilateral sensorineural hearing loss was noted.
The patient returned in May for a third audiometric evaluation. Her audiogram showed an average reduction in hearing sensitivity of 10 dB for frequencies below 1000 Hz bilaterally. The U-shaped pattern, however, persisted, and the patient was aware of this increased loss. Bekesy tracings had changed from Type I to Type II at 1000 Hz. In view of this patient's fluctuating hearing loss, audiometric studies were repeated in June, July and December. Pure tone thresholds showed that her hearing loss had stabilized, keeping the U-shaped pattern. In Figure IB the audiometric symbols have been taken directly from the top curve of Figure lA and represent the
., Smith Kline & French Laboratories, Philadelphia, PA.
Downloaded from aor.sagepub.com at Harvard Libraries on June 30, 2015
.J2(i
BAKER-LILLY TIME ELAPSED SINCE CO INTOXICATION
BEKESY TRACINGS AT FOUR TEST FREQUENCIES
500 Hz (DATE)
1000 Hz
HL
BEKESY TYPE
(dB)
°rHllJ
1 MONTH
5,
(28 APR 75)
,
\,,{\,\,\:'
10~ BEKESY
::~ "
151!!fl!J
(25 JUN 75)
20
t\
,I
1\ :\
n f\:
\
25~
~
BEKESY TYPE
VV • ,
35 40
",iY/M 30
13 DEC 75)
35--BEKESY TYPE
55 • ,', \
es
- ::re ! "
\'
~!
'
'V"/V\'v'V
35 40
~
:YJJ:£ 60
TYPE n
TYPEII
\
3O
TYPElI (1)
••
65
70
TYPE II
'\ /' • !, ,~
8 MONTHS,
HL (dB)
'
45---
TYPE I
4000 Hz
HL
(dB)
TYPE 1(7)
3 MONTHS
/,
I
35'
TYPE I
TYPE
!
}. 2000 Hz
HL
(dB)
~
':
60 \/\,'\
l, I'' . ,"', /
. 65~¥.: 70
TYPE II
::~
75
TYPE
n
55~
! VY'VVVVV
60~
65
TYPEII 70
~
Fig. 2". Graphic summary of Bekesy audiometry for patient's right ear at one, three and eight months postea intoxication. Tracings show systematic migration of Type II (cochlear) pattern toward lower frequencies. patient's best pure-tone responses following CO intoxication. The bottom curve shows reduction in hearing sensitivity for lower frequencies seven months later. The magnitude and pattern of the tone decay remained unchanged. During the seven-month observation period, however, the Type II Bekesy pattern that originally was seen only at 2000 Hz and at 4000 Hz systematically migrated toward the lower frequencies (Fig. 2). By December, a Type II Bekesy tracing was observed for all test frequencies.
Hearing loss associated with acute CO poisoning is unpredictable. Meigs and Hughes" reported no hearing loss in 105 patients hospitalized for acute CO poisoning, although 83 had neurological abnormalities. Schullenberg-" studied 12 patients with hearing loss from acute CO poisoning. The majority of these patients showed asymmetrical sensorineural hearing loss that improved gradually with some damage persisting. Other investigators, however, have not documented asymmetric audiometric curves with acute CO poisoning.l''-" The U-shaped audiogram in our case report appeared to be a unique manifestation of hearing loss from CO poisoning. Further review of the literature, however, suggests that it is more frequent than one would expect by coincidence. Taniewski and Kugler''? SUf-
veyed 3000 audiograms and found only 19 If-shaped patterns not associated with CO intoxication. A bilateral, symmetrical, U-shaped audiometric curve, however, was observed for 31 of 35 patients suffering acute CO-induced hearing loss. As in our case, the most pronounced loss was observed near 2000 Hz. Speech discrimination was significantly poorer than pure-tone thresholds would suggest, and tone decay as measured by the method of Carhart was not demonstrated. When discrimination was tested after a lapse of time, it improved considerably, even when pure-tone thresholds did not. Special audiometric tests suggested the auditory injuries involved were retrocochlear. These patients, in general, demonstrated little improvement in pure-tone threshold, and no flattening of their U-shaped curve over a long period of time. For our patient, in contrast, the original audiometric configuration was flatter than those reported by Taniewski ancI Kugler. A characteristic U-shaped pattern did not emerge until one month after CO intoxication. DISCUSSIOX
There is little evidence to localize the specific site of injury in CO-induced hearing loss, but it is most likely a com-
Downloaded from aor.sagepub.com at Harvard Libraries on June 30, 2015
HEARING LOSS AND CARBON MONOXIDE
bination of cochlear, VIII nerve and central damage. Most case reports suggest a central location as the primary site of lesion, with damage to the cochlea less frequent in both acute and chronic CO intoxication. 1G•2 0 ,2 2 .23 Postmortem examination of CO victims has shown hemorrhage and cellular degeneration in the cochlear nuclei, vestibular nuclei, spiral ganglion, and in various parts of the cochlea itself.!" Hemorrhage and mucosal edema of the mastoid cells found in patients dying of CO poisoning explain the conductive components of CO-induced hearing loss when present." Animals exposed to CO have shown toxic degeneration of ganglion cells prevailing in the basal turn of the spiral ganglion and degeneration of the acoustic nerve.i? Kiittner'" subjected rabbits to repeated episodes of acute CO intoxication and found some congestion of the stria vascularis, but the inner and outer hair cells remained intact. The supporting cells, however, seem to show greater susceptibility to damage from CO, demonstrating vacuolization
:32'7
of their cytoplasm. This observation was supported by Lawrence and Wever.i" who also saw primarily damage to supporting cells while hair cell degeneration only occurred under more severe hypoxic conditions. The cochlear hair cells apparently are capable of withstanding relatively short hypoxic episodes better than the supporting cells. The hair cells may be equipped with greater lactate dehydrogenase for anaerobic metabolism than the more vulnerable supporting cells. Cochlear hair cells also seem to be more resistant to CO intoxication than the acoustic nerve itself. Intracellular edema of the nerve has been noted in animals exposed to CO.22 Other studies have shown irreversible depression of the VIII nerve action potential at a level of CO intoxication that causes only reversible depression of the cochlear microphonic (CM) .26 It is well-established that oxygen deprivation does not disturb the CM until the hypoxia is severe enough to cause respiratory and vascular collapse."
REFERE~CES
I. Coburn RF: Biological effects of carbon monoxide. Ann NY Acad Sci 174:1-430, 1970 2. Bour H, Ledingham 1M: Carbon monoxide poisoning. Prog Brain Res 24: 1-203, 1967 3. Beard RR, Wertheim GA: Behavioral impairment associated with small doses of carbon monoxide. Am J Public Health 57: 2012-2022, 1967 4. Chapek AV: The effect of small doses of carbon monoxide upon the acoustic and vestibular analyzers. Vestn Otorinolaringol I: 99, 1966 5. Meigs JW, Hughes JPW: Acute carbon monoxide poisoning an analysis of one hundred five cases. Arch Ind Hyg Occup Med 6:344-356, 1952 6. Nakashima M: Vestibular function of patients with acute carbon monoxide poisoning. Otol Fukuoka (Jibi To Rinsho ) 13(1): 101-109, 1967 7. Mounier-Kuhn P, Roche L, Morgen A, et al : Vestibular involvement immediately following acute carbon monoxide poisoning. J Fr Otorhinolaryngol 17 :512-515, 1968 8. Alt F: Neuritis of the eighth nerve from carbon monoxide intoxication. Arch Klin Exp Ohren Nasen Kehlkopfheilkd 96: 183-185, 1915
9. Huttin E: Injury to hearing from gas intoxication. Z Ohren Heilkunde 77: 60-65, 1918 10. Radmark K: The otoneurologic findings of generator gas intoxication. Acta Otolaryngol (Stockh) 31 :454-465, 1943 11. Koumrouyan H: Cochleo-vestibular lesions in acute carbon monoxide intoxication. Pract Otorhinolaryngol (Basel) 11:307-321, 1949 12. Floberg LE: Vestibular symptoms in carbon monoxide poisoning after unilateral ligation of the common carotid artery: an experimental study in cats. Acta Otolaryngol [SuPPII (Stockh) 106: 1-55, 1953 13. Rutenburg D\I: Changes in the hearing apparatus from CO intoxication. Arch Klin Exp Ohren Nasen Kehlkopfheilkd 124: 3-26, ]930 14. Kato N: Microchemical investigation of the central nervous system of the rabbit after pendular nystagmus induction by CO intoxication. Zentralbl Has Nasen Ohrenh 13:862, 1929 15. Lumio JS: Otoneurological studies of chronic carbon monoxide poisoning in Finland. Acta Otolaryngol [Suppl ] (Stockh) 71: 1-107, 1948
Downloaded from aor.sagepub.com at Harvard Libraries on June 30, 2015
.'328
BAKER-LILLY
16. Zenk H: The effects of occupational CO poisoning on the sense of smell, hearing and equilibrium. Z Laryngol Rhinol Otol 44:821, 828, 1965 17. Jerger J: Bbkbsy audiometry in analysis of auditory disorders. J Speech Hear Res .'3: 275-287, 1960 18. Schullenberg W: Damage of the inner ear through acute carbon monoxide poisoning. Z Laryngol Rhinol Otol.'32:339-353, 1953 19. Morris TMO: Deafness following acute carbon monoxide poisoning. J Laryngol Otol 8.3:1219-1225,1969 20. Taniewski J, Kugler R: U-shapes in the audiometric curves in CO poisoning. Monatsschr Ohrenheilkd Laryngorhinol 98:298-301 1964 ' 21. Coto I, Miyoshi T, Ooya Y: Deafness and peripheral neuropathy following carbon monoxide intoxication. Folia Psychiat Neurol Jap 26:35-38, 1972 22. Kiittner K: On the pathomorphology of changes in the peripheral organ of hearing during repeated experimental carbon monox-
ide intoxication. Z Laryngol Rhinol Otol 47; 779-785, 1968 23. Sakashita K, Ogawa K, Takane H: Auditory disturbances seen in 14 cases of various types of industrial poisoning. Audiol jap 14:492-503, 1971 24. Polaskova V: Changes in the cavity of the middle ear in the drowned. Soudni Lek 13:27-31, 1968 25. Lawrence M, Wever EG: Effects of oxygen deprivation upon the structure of the organ of Corti. Arch Otolaryngol 55:.'31-37, 1952 26. Friegang B, Seidel P, Flach M: The question of the effect of carbon monoxide on the microphonic and action potentials in the guinea pig cochlea. Arch Klin Exp Ohren Nasen u Kehlkopheilkd 190:24-35, 1968 27. Tonndorf J, Hyde RW, Brogan FA: Combined effect of sound and oxygen deprivation upon cochlear microphonics in guinea pigs. Ann Otol Rhinol Laryngol 64:392-405, 1955
REPRINTS-Shan R. Baker, MD, Department of Otolaryngology and Maxillofacial Surgery, University of Iowa, Iowa City, IA 52242.
OTOLARYNGIC PATHOLOGY TRAINING PROGRAM A training program on otolaryngic pathology, presented by the Armed Forces Institute of Pathology (AFIP) in conjunction with the Committee on Otolaryngic Pathology, AAOO, is currently being offered at the Department of Otolaryngic Pathology, AFIP. The course covers both temporal bone pathology as well as surgical pathology of the head and neck area. Requirements are flexible but preference is given to residents and practitioners in Otolaryngology and Pathology, both military and civilian, who wish to expand their knowledge of ENT pathology. The course, for which there is no charge, is designed to be given quarterly, beginning in January, April, July and October; however, consideration will be given to those seeking shorter training periods. Requests for course applications should be directed to: The Director, Armed Forces Institute of Pathology, ATTN: AFIP-EDZ, Washington, DC 20306.
Downloaded from aor.sagepub.com at Harvard Libraries on June 30, 2015
HEARING LOSS FROM ACUTE CARBON MONOXIDE INTOXICATION SHAN
R.
DAVID
J.
BAKER,
MD
LILLY, PHD
IOWA CITY, IOWA
SUMMARY - A case of fluctuating sensorineural hearing loss from acute carbon monoxide (CO) poisoning with presentation of a U-shaped audiogram is reported. Acute CO intoxication seems to involve vestibular function more frequently than auditory function. Hearing loss is uncommon, but when present, may often display a U-shaped audiometric curve. Decrease in hearing sensitivity probably results from hypoxia to the cochlea, VIII nerve and brain stem nuclei. Fluctuation in hearing sensitivity may be an early manifestation of acute CO exposure, and requires periodic audiometric examination until the hearing has stabilized.
Little has been written in the English literature concerning hearing loss from acute carbon monoxide (CO) intoxication. It is estimated that 12-14% of employed individuals have occupations in which there is likelihood of exposure to high levels of CO.l It is, therefore, important to be able to recognize and to diagnose the various neuro-otologic manifestations of CO poisoning. Carbon monoxide combines with hemoglobin to form carboxyhemoglobin (CORb) which is over 200 times more stable than oxyhemoglobin. The formation of CORb prevents oxygen from entering into combination with hemoglobin and consequently causes a deficiency of oxygen supply to vital organs. Neutralization of the oxygen carrying activity of the erythrocyte produces anoxia and accounts for the primary mechanism of CO poisoning. The central nervous system (CNS) is especially vulnerable to CO poisoning. Pathological changes caused by CO include demyelinization, hemorrhage, focal necrosis, and edema. Acute CO poisoning causes diffuse small hemorrhages in the brain stem and cerebrum while chronic poisoning often leads to demyelinization of the globus pallidus.P
A dose of CO that produces a CORb level of 60% usually is lethaJ.2 It generally is believed by clinicians that subjective symptoms rarely occur below CORb levels of 20%, while most acute signs of cardiac and CNS embarrassment occur at levels greater than 30%. Several investigators have indicated CNS impairment at CORb levels as low as 2-5%, or to low concentrations of CO in the air. 1 •3 ,4 Impairment of visual function has been documented when CORb concentrations reach 4-5%.1 Decreased capacity to discriminate the temporal lengths of tones, has been shown for patients exposed to low CO concentrations," and elevated auditory threshold has been demonstrated in humans subjected to CO concentrations of 0.02 mg/Iiter.! Some of the symptoms of acute CO poisoning that an otolaryngologist may be called on to evaluate include: aphasia, anosmia, facial and glossopharyngeal palsy, and disturbance of gustatorv function. Pharyngitis, ulcerations and bleeding from oral mucosa. and rhinitis also have been reported." Carbon monoxide induced lesions of the auditory and vestibular system cause tinnitus, hearing loss, nystagmus, and ataxia.
From the Department of Otolaryngology and Maxillofacial Surgery, ancI the Department of Speech Pathology and Audiology, University of Iowa, Iowa City, Iowa.
323
Downloaded from aor.sagepub.com at Harvard Libraries on June 30, 2015
324
BAKER-LILLY VESTlliULAR MANIFESTATIONS
Our review of the literature suggests that CO affects the vestibular system more often than clinically recognized. It also is apparent that vestibular function of the inner ear is involved more frequently than auditory function. Often the objective vestibular symptoms are marked with only minor subjective vertigo. One may see spontaneous and positional nystagmus, as well as hyperand hypoexcitability of the labyrinth to caloric stimulation. Nakashima" studied 14 patients after recovery of consciousness following CO intoxication and found no significant hearing loss. Seven of these patients, however, demonstrated spontaneous nystagmus on electronystagmography (ENG), and three patients showed positional nystagmus. Four patients demonstrated hyperexcitability to the ice water caloric test. In addition, Nakashima noted that several of the patients demonstrated pauses and dysrhythmic patterns on ENG with caloric stimulation. Twelve months after exposure to CO, spontaneous nystagmus remained unchanged in the seven patients who previously were affected and appeared as a new finding in two others. Nakashima concluded that these abnormalities seen on ENG were caused by central lesions. Monnier-Kuhn et al' evaluated 20 patients suffering from acute CO intoxication, 15 of which were in coma. None of these patients demonstrated loss of auditory function, vertigo, or equilibrial disturbances. Fourteen patients, however, demonstrated abnormal ENG. Ten patients showed hypofunction in caloric tests. Mounier-Kuhn and his colleagues found no correlation between the concentration of COHb and the intensity of the clinical sizns. but vestibular impairment appeared to be related directly to duration of exposure to CO. They concluded that the vestibular lesions produced by CO were more often peripheral than central, and most often presented a destructive ENG pattern. Earlier studies have supported these observations.s-" The findings of Mounier-Kuhn, how-
ever, have not been supported by other investigators who conclude that the major vestibular lesion seen with CO is centraPO-13 Kato B demonstrated spontaneous nystagmus with directional preponderance in animals subjected to CO intoxication. Postmortem examination revealed hemorrhages in the cerebellum. Butenburg-" found no evidence of degeneration of the peripheral vestibular system in test animals exposed to acute CO poisoning. Floberg-" showed that CO exposed cats with unilateral ligation of the common carotid artery developed reproducible vestibular symptoms of circus movement and nystagmus. Destruction of the labyrinth through surgery or by streptomycin did not change these symptoms, suggesting that the lesion accounting for circus movement was located central to the vestibular nuclei. AUDITORY MANIFESTATIONS
Chronic CO Intoxication. In general, chronic CO intoxication often results in a permanent, symmetrical, high-frequency hearing loss. Lumio-" reported an extensive study of 263 patients suffering from chronic CO poisoning. Audiometry disclosed hearing loss in 78.3% of the victims. A typical high-frequency bilaterally symmetrical, sensorineural hearing loss was seen in 67.7% of these patients, with the audiometric curve falling off steeply and progressively, starting at frequencies between 1000 and 2000 Hz. A pattern very much similar to that following noise exposure with a maximum hearing loss at 4000 Hz was seen in 2.7% of these patients. No patients were reported to have U-shaped audiograms. Follow-up examination revealed that hearing improved in only 26.7% and then only to a slight degree. Eighty cases of chronic CO poisoning studied by Zenk'? supported Lumino's findings of symmetrical high-frequency sensorineural loss. Acute CO Poisoning. It has been well-documented that hearing loss resulted from chronic CO poisoning, 1 " but it is much less frequent after acute CO intoxication. Presented is what we believe to be the first reported case of
Downloaded from aor.sagepub.com at Harvard Libraries on June 30, 2015
325
HEARING LOSS AND CARBON MONOXIDE 1 0 0
~2
0
i
(~--(
----
D-, \
...J
W
40
!:!! .0 ~ 60
m,,( '1'
-1--
28 APRIL 1975
,
-3 0
> ~
0
(1 MONTH POST CO
:~
INTOXICATION)
..
/
~ ~.?
r0~~b.
:I: 70
I- f--- ~2 1/
.~V
~,
./ /
,./
90 24 MARCH 1975 (INITIAL AUDIOGRAM)
100
500
1000
2000
4000
...J
30 40
!:!! ~
60
I
'0 70
INTOXICATION)
~
f-------
t----
L1l
J
DECEMBER 1975
INTOXICATION I
t---- f-------
f---
f- f---
100
I
110
I
A.D. SOLlD CURVE A.S. BROKEN CURVE
~
'25
.r
-
( 8 MONTHS PoST CO
90
FREQUENCY (Hz)
~
~~ , I' \~- ..
I
-
I
1/
f" Xl ~' ,,
W
~
(1 MONTH POST CO
---,--:.-:::- " '
0
l - t----
8 000
,
d
+
28 APRIL 1975
J'
80
110
A
-
:I:
"f:::, ~/
80
(D
0
1
111
0
0
250
I 500
I
I 1000
2000
4000
6000
FREQUENCY (Hz)
Fig. 1. Composite audiograms. A) Lower curves represent initial pure-tone audiogram. A moderate, binaural sensorineural hearing loss is noted. Upper curves show subsequent improvement in audiometric results one month later. All bone-conduction symbols have been omitted. B) Audiometric symbols taken from Fig. lA represent patient's best pure-tone responses following CO intoxication. Bottom curves show reduction in hearing sensitivity for lower frequencies seven months later. Bone-conduction symbols have been omitted.
fluctuating bilateral sensorineural hearing loss following acute CO poisoning. A U-shaped audiometric curve manifests itself. CASE REPORT
Carhart tone-decay findings were within normal limits (not greater than 5 dB at any test frequency). A SISI score of 100% was obtained bilaterally for 1000 Hz at 20 dB sensation level. Discrimination scores were poor, showing 48% in the right ear and 64% in the left for recorded monosyllabic words (C.LD. Auditory Test, W-22) presented at 30 dB above the patient's speech reception threshold.
On March 15, 1976, a 16-year-old Caucasian female was admitted to the hospital for treatment of carbon monoxide poisoning after being found unconscious in a parked car. The ignition key was on, and the gasoline tank was empty. On arrival, the patient was decorticate to decerebrate with doll's eyes and bilateral upgoing toes. Her past history revealed no hearing loss or evidence of ear infections. She was transferred immediately to the Intensive Care Unit and treated with hypothermia, and intubated for controlled ventilation using high-flow oxygen. Thorazine'S>," heavy sedation, and intravenous steroids were administered.
One month later, the patient returned for selected audiometric studies. Pure tone audiometry showed an improvement of 25 to 48 dB in the right ear and 17 to 45 dB in the left ear. These findings are depicted in the upper curves of Figure LA, The audiometric pattern assumed a U-shaped configuration with maximum hearing loss at 2000 Hz. Bekesy audiometry showed Type I tracings for frequencies below 2000 Hz and Type II tracings for the higher test Irequencies.t?
Within three days, the patient showed dramatic improvement and was extubated. Neurologic examination at that time was unremarkable except for a moderate bilateral hearing loss. She continued to make an uneventful recovery and was seen by the department on March 24. An ENG was performed at this time and revealed no spontaneous or latent nystagmus. Ice water caloric test produced normal, symmetrical vestibular responses. Examination of the ears revealed clear, mobile tympanic membranes bilaterally. The patient's initial pure tone audiogram is shown as the lower curves in Figure LA. A bilateral sensorineural hearing loss was noted.
The patient returned in May for a third audiometric evaluation. Her audiogram showed an average reduction in hearing sensitivity of 10 dB for frequencies below 1000 Hz bilaterally. The U-shaped pattern, however, persisted, and the patient was aware of this increased loss. Bekesy tracings had changed from Type I to Type II at 1000 Hz. In view of this patient's fluctuating hearing loss, audiometric studies were repeated in June, July and December. Pure tone thresholds showed that her hearing loss had stabilized, keeping the U-shaped pattern. In Figure IB the audiometric symbols have been taken directly from the top curve of Figure lA and represent the
., Smith Kline & French Laboratories, Philadelphia, PA.
Downloaded from aor.sagepub.com at Harvard Libraries on June 30, 2015
.J2(i
BAKER-LILLY TIME ELAPSED SINCE CO INTOXICATION
BEKESY TRACINGS AT FOUR TEST FREQUENCIES
500 Hz (DATE)
1000 Hz
HL
BEKESY TYPE
(dB)
°rHllJ
1 MONTH
5,
(28 APR 75)
,
\,,{\,\,\:'
10~ BEKESY
::~ "
151!!fl!J
(25 JUN 75)
20
t\
,I
1\ :\
n f\:
\
25~
~
BEKESY TYPE
VV • ,
35 40
",iY/M 30
13 DEC 75)
35--BEKESY TYPE
55 • ,', \
es
- ::re ! "
\'
~!
'
'V"/V\'v'V
35 40
~
:YJJ:£ 60
TYPE n
TYPEII
\
3O
TYPElI (1)
••
65
70
TYPE II
'\ /' • !, ,~
8 MONTHS,
HL (dB)
'
45---
TYPE I
4000 Hz
HL
(dB)
TYPE 1(7)
3 MONTHS
/,
I
35'
TYPE I
TYPE
!
}. 2000 Hz
HL
(dB)
~
':
60 \/\,'\
l, I'' . ,"', /
. 65~¥.: 70
TYPE II
::~
75
TYPE
n
55~
! VY'VVVVV
60~
65
TYPEII 70
~
Fig. 2". Graphic summary of Bekesy audiometry for patient's right ear at one, three and eight months postea intoxication. Tracings show systematic migration of Type II (cochlear) pattern toward lower frequencies. patient's best pure-tone responses following CO intoxication. The bottom curve shows reduction in hearing sensitivity for lower frequencies seven months later. The magnitude and pattern of the tone decay remained unchanged. During the seven-month observation period, however, the Type II Bekesy pattern that originally was seen only at 2000 Hz and at 4000 Hz systematically migrated toward the lower frequencies (Fig. 2). By December, a Type II Bekesy tracing was observed for all test frequencies.
Hearing loss associated with acute CO poisoning is unpredictable. Meigs and Hughes" reported no hearing loss in 105 patients hospitalized for acute CO poisoning, although 83 had neurological abnormalities. Schullenberg-" studied 12 patients with hearing loss from acute CO poisoning. The majority of these patients showed asymmetrical sensorineural hearing loss that improved gradually with some damage persisting. Other investigators, however, have not documented asymmetric audiometric curves with acute CO poisoning.l''-" The U-shaped audiogram in our case report appeared to be a unique manifestation of hearing loss from CO poisoning. Further review of the literature, however, suggests that it is more frequent than one would expect by coincidence. Taniewski and Kugler''? SUf-
veyed 3000 audiograms and found only 19 If-shaped patterns not associated with CO intoxication. A bilateral, symmetrical, U-shaped audiometric curve, however, was observed for 31 of 35 patients suffering acute CO-induced hearing loss. As in our case, the most pronounced loss was observed near 2000 Hz. Speech discrimination was significantly poorer than pure-tone thresholds would suggest, and tone decay as measured by the method of Carhart was not demonstrated. When discrimination was tested after a lapse of time, it improved considerably, even when pure-tone thresholds did not. Special audiometric tests suggested the auditory injuries involved were retrocochlear. These patients, in general, demonstrated little improvement in pure-tone threshold, and no flattening of their U-shaped curve over a long period of time. For our patient, in contrast, the original audiometric configuration was flatter than those reported by Taniewski ancI Kugler. A characteristic U-shaped pattern did not emerge until one month after CO intoxication. DISCUSSIOX
There is little evidence to localize the specific site of injury in CO-induced hearing loss, but it is most likely a com-
Downloaded from aor.sagepub.com at Harvard Libraries on June 30, 2015
HEARING LOSS AND CARBON MONOXIDE
bination of cochlear, VIII nerve and central damage. Most case reports suggest a central location as the primary site of lesion, with damage to the cochlea less frequent in both acute and chronic CO intoxication. 1G•2 0 ,2 2 .23 Postmortem examination of CO victims has shown hemorrhage and cellular degeneration in the cochlear nuclei, vestibular nuclei, spiral ganglion, and in various parts of the cochlea itself.!" Hemorrhage and mucosal edema of the mastoid cells found in patients dying of CO poisoning explain the conductive components of CO-induced hearing loss when present." Animals exposed to CO have shown toxic degeneration of ganglion cells prevailing in the basal turn of the spiral ganglion and degeneration of the acoustic nerve.i? Kiittner'" subjected rabbits to repeated episodes of acute CO intoxication and found some congestion of the stria vascularis, but the inner and outer hair cells remained intact. The supporting cells, however, seem to show greater susceptibility to damage from CO, demonstrating vacuolization
:32'7
of their cytoplasm. This observation was supported by Lawrence and Wever.i" who also saw primarily damage to supporting cells while hair cell degeneration only occurred under more severe hypoxic conditions. The cochlear hair cells apparently are capable of withstanding relatively short hypoxic episodes better than the supporting cells. The hair cells may be equipped with greater lactate dehydrogenase for anaerobic metabolism than the more vulnerable supporting cells. Cochlear hair cells also seem to be more resistant to CO intoxication than the acoustic nerve itself. Intracellular edema of the nerve has been noted in animals exposed to CO.22 Other studies have shown irreversible depression of the VIII nerve action potential at a level of CO intoxication that causes only reversible depression of the cochlear microphonic (CM) .26 It is well-established that oxygen deprivation does not disturb the CM until the hypoxia is severe enough to cause respiratory and vascular collapse."
REFERE~CES
I. Coburn RF: Biological effects of carbon monoxide. Ann NY Acad Sci 174:1-430, 1970 2. Bour H, Ledingham 1M: Carbon monoxide poisoning. Prog Brain Res 24: 1-203, 1967 3. Beard RR, Wertheim GA: Behavioral impairment associated with small doses of carbon monoxide. Am J Public Health 57: 2012-2022, 1967 4. Chapek AV: The effect of small doses of carbon monoxide upon the acoustic and vestibular analyzers. Vestn Otorinolaringol I: 99, 1966 5. Meigs JW, Hughes JPW: Acute carbon monoxide poisoning an analysis of one hundred five cases. Arch Ind Hyg Occup Med 6:344-356, 1952 6. Nakashima M: Vestibular function of patients with acute carbon monoxide poisoning. Otol Fukuoka (Jibi To Rinsho ) 13(1): 101-109, 1967 7. Mounier-Kuhn P, Roche L, Morgen A, et al : Vestibular involvement immediately following acute carbon monoxide poisoning. J Fr Otorhinolaryngol 17 :512-515, 1968 8. Alt F: Neuritis of the eighth nerve from carbon monoxide intoxication. Arch Klin Exp Ohren Nasen Kehlkopfheilkd 96: 183-185, 1915
9. Huttin E: Injury to hearing from gas intoxication. Z Ohren Heilkunde 77: 60-65, 1918 10. Radmark K: The otoneurologic findings of generator gas intoxication. Acta Otolaryngol (Stockh) 31 :454-465, 1943 11. Koumrouyan H: Cochleo-vestibular lesions in acute carbon monoxide intoxication. Pract Otorhinolaryngol (Basel) 11:307-321, 1949 12. Floberg LE: Vestibular symptoms in carbon monoxide poisoning after unilateral ligation of the common carotid artery: an experimental study in cats. Acta Otolaryngol [SuPPII (Stockh) 106: 1-55, 1953 13. Rutenburg D\I: Changes in the hearing apparatus from CO intoxication. Arch Klin Exp Ohren Nasen Kehlkopfheilkd 124: 3-26, ]930 14. Kato N: Microchemical investigation of the central nervous system of the rabbit after pendular nystagmus induction by CO intoxication. Zentralbl Has Nasen Ohrenh 13:862, 1929 15. Lumio JS: Otoneurological studies of chronic carbon monoxide poisoning in Finland. Acta Otolaryngol [Suppl ] (Stockh) 71: 1-107, 1948
Downloaded from aor.sagepub.com at Harvard Libraries on June 30, 2015
.'328
BAKER-LILLY
16. Zenk H: The effects of occupational CO poisoning on the sense of smell, hearing and equilibrium. Z Laryngol Rhinol Otol 44:821, 828, 1965 17. Jerger J: Bbkbsy audiometry in analysis of auditory disorders. J Speech Hear Res .'3: 275-287, 1960 18. Schullenberg W: Damage of the inner ear through acute carbon monoxide poisoning. Z Laryngol Rhinol Otol.'32:339-353, 1953 19. Morris TMO: Deafness following acute carbon monoxide poisoning. J Laryngol Otol 8.3:1219-1225,1969 20. Taniewski J, Kugler R: U-shapes in the audiometric curves in CO poisoning. Monatsschr Ohrenheilkd Laryngorhinol 98:298-301 1964 ' 21. Coto I, Miyoshi T, Ooya Y: Deafness and peripheral neuropathy following carbon monoxide intoxication. Folia Psychiat Neurol Jap 26:35-38, 1972 22. Kiittner K: On the pathomorphology of changes in the peripheral organ of hearing during repeated experimental carbon monox-
ide intoxication. Z Laryngol Rhinol Otol 47; 779-785, 1968 23. Sakashita K, Ogawa K, Takane H: Auditory disturbances seen in 14 cases of various types of industrial poisoning. Audiol jap 14:492-503, 1971 24. Polaskova V: Changes in the cavity of the middle ear in the drowned. Soudni Lek 13:27-31, 1968 25. Lawrence M, Wever EG: Effects of oxygen deprivation upon the structure of the organ of Corti. Arch Otolaryngol 55:.'31-37, 1952 26. Friegang B, Seidel P, Flach M: The question of the effect of carbon monoxide on the microphonic and action potentials in the guinea pig cochlea. Arch Klin Exp Ohren Nasen u Kehlkopheilkd 190:24-35, 1968 27. Tonndorf J, Hyde RW, Brogan FA: Combined effect of sound and oxygen deprivation upon cochlear microphonics in guinea pigs. Ann Otol Rhinol Laryngol 64:392-405, 1955
REPRINTS-Shan R. Baker, MD, Department of Otolaryngology and Maxillofacial Surgery, University of Iowa, Iowa City, IA 52242.
OTOLARYNGIC PATHOLOGY TRAINING PROGRAM A training program on otolaryngic pathology, presented by the Armed Forces Institute of Pathology (AFIP) in conjunction with the Committee on Otolaryngic Pathology, AAOO, is currently being offered at the Department of Otolaryngic Pathology, AFIP. The course covers both temporal bone pathology as well as surgical pathology of the head and neck area. Requirements are flexible but preference is given to residents and practitioners in Otolaryngology and Pathology, both military and civilian, who wish to expand their knowledge of ENT pathology. The course, for which there is no charge, is designed to be given quarterly, beginning in January, April, July and October; however, consideration will be given to those seeking shorter training periods. Requests for course applications should be directed to: The Director, Armed Forces Institute of Pathology, ATTN: AFIP-EDZ, Washington, DC 20306.
Downloaded from aor.sagepub.com at Harvard Libraries on June 30, 2015
