Eur Arch Otorhinolaryngol (2009) 266:221–224 DOI 10.1007/s00405-008-0739-0

OTOLOGY

Sensorineural hearing loss in patients with chronic otitis media Sady Selaimen da Costa · Letícia Petersen Schmidt Rosito · Cristina Dornelles

Received: 13 November 2007 / Accepted: 30 May 2008 / Published online: 16 July 2008 © Springer-Verlag 2008

Abstract Chronic otitis media is generally associated with some degree of hearing loss, which is often the patient’s chief complaint. This hearing loss is usually conductive, resulting from tympanic membrane rupture and/or changes in the ossicular chain due to Wxation or erosion caused by the chronic inXammatory process. When cholesteatoma or granulation tissue is present in the middle ear cleft, the degree of ossicular destruction is even greater. An issue that has recently gained attention is additional sensorineural hearing loss due to chronic otitis media. While the conductive loss can be minimized through surgery, sensorineural hearing loss constitutes a permanent after eVect, attenuated only through the use of a hearing aid. However, a few groups have reported a decrease in sensorineural function in these patients as well. This survey study performed at a referral center evaluates the occurrence of sensorineural hearing loss in ambulatory patients with this disease. We reviewed the Wles of patients with unilateral chronic otitis media. One hundred and Wfty patients met the inclusion criteria: normal otoscopy and normal hearing in the contralateral ear. Main outcome measure: bone-conduction threshold averages were calculated for frequencies of 500, 1,000, 2,000, 3,000 and 4,000 Hz, with comparison between the normal ear and the ear with chronic otitis media. Thresholds were examined separately for each S. S. d. Costa · L. P. S. Rosito · C. Dornelles Department of Otolaryngology, Head & Neck Surgery, Universidade Federal do Rio Grande do Sul, Hospital de Clínicas, Porto Alegre, Brazil S. S. d. Costa (&) Serviço de Otorrinolaringologia, Hospital de Clínicas de Porto Alegre, Rua Ramiro Barcelos, 2350, Zona 19, sala 1922, Porto Alegre CEP 90003010, Brazil e-mail: [email protected]

frequency. The bone-conduction threshold averages for the normal side were lower than those for the ear with chronic otitis media. The threshold shift was statistically signiWcant for each frequency (P < 0.0001, Student’s t test). There were diVerences between the groups when analyzed for age (500 and 1,000 Hz) or the presence of cholesteatoma (1,000 Hz). This study shows that chronic otitis media is associated with a decrease in cochlear function. Keywords Sensorineural hearing loss · Chronic otitis media · Contralateral ear

Introduction Chronic otitis media (COM) is generally associated with some degree of hearing loss, which is often the patient’s chief complaint. This hearing loss is usually conductive, resulting from tympanic membrane rupture and/or changes in the ossicular chain due to Wxation or erosion caused by the chronic inXammatory process. When cholesteatoma or granulation tissue is present in the middle ear cleft (MEC), the degree of ossicular destruction is even greater. Surgical treatment usually results in improved hearing, principally if tympanoplasty, associated or not with ossicular chain reconstruction, is successful. An issue that has recently gained attention is additional sensorineural hearing loss due to COM. While the conductive loss can be minimized through surgery, sensorineural hearing loss constitutes a permanent after eVect, attenuated only through use of a hearing aid. Many studies suggest that chronic inXammatory processes in the MEC damage the inner ear [1, 2]. The actual clinical repercussions of these changes, as well as their pathogenesis, continue to be discussed [1].

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The objective of this study is to evaluate whether COM, with or without cholesteatoma, can cause sensorineural hearing loss by comparing the bone-conduction thresholds of aVected ears and their normal contralateral counterparts.

Materials and methods Six hundred and Wfty patients from the Chronic Otitis Media Outpatient Clinic of the Hospital de Clínicas in Porto Alegre, Brazil were evaluated. Inclusion criteria were: (1) presence of chronic, unilateral otitis media, deWned as inXammation of the MEC lasting more than 3 months, with or without associated cholesteatoma and/or tympanic perforation; (2) normal contralateral otoscopy; and (3) contralateral audiometry with tonal threshold ·20 dB at 25 dB all frequencies, with no air-bone gap. Otomicroscopy was performed on all patients included in the study. In addition to being evaluated by the same observer, these results were Wlmed and digitalized. For each patient, COM was classiWed according to the presence of cholesteatoma. There was considered pediatric group patients with age below 18 years. To evaluate sensorineural hearing loss associated with COM, bone-conduction thresholds of the aVected and control ears were determined for frequencies 500, 1,000, 2,000, 3,000 and 4,000 Hz. When necessary, we used the technique suggested by Katz [3], and Musiek and Rintelmann [4] to mask air and bone thresholds. To calculate the eVective masking noise to a speciWc frequency, we took the bone threshold value of the testing ear added to the interaural attenuation value of this very frequency, less 5 dB HL (to avoid overmasking of the testing ear). The masking noise, which was calibrated to eVective level, was applied on the contralateral ear using supraural earphone. Audiometry was performed by four diVerent staV audiologists with similar training and experience in this area.

Table 1 Description of sample hearing loss

COM Chronic otitis media ear, CLE contralateral ear

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Variable

Mean

COM 500

6.63

9.06

COM 1000

6.88

COM 2000

8.81

COM 3000 COM 4000

Statistical analysis was conducted using SPSS 10.0. The Mann–Whitney test was used to compare diVerences between pediatric and adult patient groups for COM, with and without cholesteatoma. The Wilcoxon test was used to evaluate diVerences between bone-conduction thresholds for each patient’s aVected and normal ears. Two-tailed analysis was applied for all of these tests, with P values ·0.05 considered signiWcant.

Results Of the 650 patients evaluated, 150 met the inclusion criteria. Ages varied between 3 and 55 years, with an average age of 22 § 13 years, and 52% of them were females. Cholesteatoma was identiWed in 31% of the aVected ears. We described the data in Table 1. As the data of hearing loss did not present normal distribution, the given variables are presented by their median and interquartile range. By the same fact, all the statistical analysis was carried out with nonparametric tests. When the paired bone-conduction threshold averages for the aVected and normal ears were compared frequency-byfrequency, we found higher thresholds in the aVected ear. These diVerences were statistically signiWcant for every tested frequency (Table 2). The averages of the diVerences between bone conduction (DBC) for the aVected ear and the normal ear were compared for the pediatric group and adult group as shown in Table 3. There was a signiWcant diVerence between the two groups (with higher thresholds in the pediatric group) only for the frequencies of 500–1,000 Hz (Table 3). Finally, we tried to verify the impact of the presence of a cholesteatoma in the bone conduction. For such we compared the hearing thresholds of ears with COM with or without cholesteatoma. At the frequencies studied, the presence of cholesteatoma in the aVected ear determined a

Standard deviation

Median

Interquartile range

Minimum

Maximum

5

0–10

0

50

9.01

10

5–15

0

50

8.28

10

5–15

0

40

12.44

9.41

15

5–20

0

40

12.56

10.49

15

5–20

0

50

CLE 500

5.44

5.69

5

0–10

0

20

CLE 1000

4.69

4.80

5

0–10

0

15

CLE 2000

5.25

4.96

5

0–10

0

20

CLE 3000

6.00

4.73

5

0–10

0

20

CLE 4000

5.69

5.20

5

0–10

0

20

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Table 2 Paired bone-conduction threshold averages for the aVected and normal ears were compared for the frequencies Bone conduction frequency

500 Hz

1,000 Hz

2,000 Hz

3,000 Hz

Ear with COM

5 (0–10)

10 (5–15)

10 (5–15)

15 (5–20)

4,000 Hz 15 (5–20)

Contralateral ear

5 (0–10)

5 (0–10)

5 (0–10)

5 (0–10)

5 (0–10)

P value

0.001

<0.0001

<0.0001

<0.0001

<0.0001

Wilcoxon test, median (interquartile range)

Table 3 Averages of the diVerences between bone conduction (DBC) for the COM ear and the normal ear were compared for the pediatric group and adult group DBC

500 Hz

1,000 Hz

2,000 Hz

3,000 Hz

4,000 Hz

Pediatric group (n = 80)

0 (0–5)

5 (0–10)

5 (0–8.5)

5 (0–10)

5 (5–20)

Adult group (n = 70)

0 (0–5)

0 (0–5)

0 (0–7.5)

5 (0–12)

5 (0–10)

P value

0.013

0.020

0.211

0.556

0.978

Mann–Whitney test, median (interquartile range)

Table 4 Comparison of bone conduction between the presence of cholesteatoma in the aVected ear and COM/control pairs without cholesteatoma DBC

500 Hz

1,000 Hz

2,000 Hz

3,000 Hz

COM with cholesteatoma (n = 47)

0 (0–5)

0 (0–6)

0 (0–6)

5 (0–15)

4,000 Hz 7.5 (0–15)

COM without cholesteatoma (n = 103)

0 (0–5)

5 (0–5)

0 (0–10)

5 (0–10)

5 (0–10)

P value

0.044

0.424

0.353

0.059

0.053

Mann–Withney test, median (interquartile range)

statistically signiWcant diVerence in DBC when compared with COM/control pairs without cholesteatoma only for 500 Hz, as shown in Table 4.

Discussion There was a statistically signiWcant diVerence between the average bone-conduction thresholds of ears with COM and their controls for all frequencies. For 1,000 to 2,000 Hz, the diVerence was approximately 5 dB, increasing to about 10 dB for frequencies of 3,000–4,000 Hz. These results are consistent with those found by Noordzij et al. [1] who, in a similar study of 69 patients, found signiWcant diVerences at higher frequencies. MacAndie and O’Reilly [5] found diVerences between bone-conduction thresholds at all the frequencies studied and they also observed that this diVerence increased as sound frequency progressed. Papp et al. [2] also found greater diVerences at 4,000 Hz than at 500, 1,000 and 2,000 Hz. Despite being statistically signiWcant, however, this diVerence may not be clinically relevant, since changes of 5–10 dB on tonal audiometry do not represent an important hearing loss, nor does it imply any change in treatment plan, such as indicating use of a hearing aid. The presence of a cholesteatoma in the ear with COM is associated with greater morbidity and inner ear changes,

principally in relation to the integrity of the ossicular chain, as was found in other studies [1, 5], but it seems to cause additional diVerences in conduction thresholds only for 500 Hz when compared to COM ears without cholesteatoma. When patient age is taken into consideration, there was statistical diVerence found between the groups, only in 500 and 1,000 Hz. Theoretically, adult patients would have a longer period of disease progression and suppuration, and therefore more middle ear damage, which is often diYcult to determine through patient history. Other studies have been unable to relate disease duration with sensorineural hearing loss [1]. Although there is currently no consensus on the pathogenesis of sensorineural hearing loss due to COM, repeated Wndings of increased damage at higher frequencies lead us to believe that the passage of toxins through the round window membrane is the most probable hypothesis. Lundman et al. [6] demonstrated that Pseudomonas aeruginosa exotoxin A is capable of crossing the round window in chinchillas, causing irreversible hair cell loss, especially in the basal turn of the spiral organ. Cureoglu et al. [7] demonstrated cochlear damage in patients with COM. They found statistically signiWcant loss of both outer and inner hair cells in the basal turn of the cochlea and a decrease in the areas of stria vascularis and spiral ligament in temporal bones with COM when compared to normal contralateral ears. The increased permeability of the round window due

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to chronic inXammation may also permit the passage of various inXammatory mediators, such as histamine, which links to acetylcholine receptors, thereby diminishing the eVectiveness of eVerent innervation [8]. A methodological critique that can be made of several studies [1, 5], including ours, is the failure to exclude patients using topical antibiotics, principally aminoglycosides, in the aVected ear. These medications are commonly used during episodes of otorrhea. The most common (and least expensive) compounds include neomycin and polymyxin B. The ototoxicity of topical antibiotics in patients with COM is the subject of debate, although animal studies indicate that it exist [9, 10]. Lundy and Graham [11], in their survey of 2,235 American ENT physicians, found that of the 84.1% that use topical antibiotics when treating draining perforation, and of the 93.7% that use this treatment for otorrhea after grommet insertion, only 3.4% reported having ever seen evidence of irreversible cochlear damage. Linder et al. [12] related two cases of sensorineural deafness after use of topical antibiotics for COM without cholesteatoma during the past 40 years at Zurich Hospital. These patients used antibiotic eardrops continuously for more than two weeks, even after resolution of otorrhea. In 1978, Kellerhals [13] estimated that, based on 15 known cases of hearing loss attributed to ototoxic eardrops during 6 years, deafness would occur in one out of every 3,000 patients prescribed topical antibiotics after membrane perforation. The diVerence between results of animal studies and observations in human patients can be attributed to species-speciWc diVerences in the size, thickness and localization of the round window [14]. In addition, the thickening of the mucous membrane in the middle ear due to chronic inXammation, as well as the presence of secretion, may help to reduce the drug’s absorption through the oval and round windows [15–17].

Conclusion The diVerences found between the bone-conduction threshold in ears with COM and their contralateral controls permits us to infer that chronic inXammation in the auditory

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cleft leads to cochlear damage resulting in sensorineural hearing loss. Although statistically signiWcant, this diVerence may be not clinically relevant and should be appreciated on an individual basis.

References 1. Noordzij JP, Dodson E, Ruth RA, Arts HÁ, Lambert P (1995) Chronic otitis media and sensorineural hearing loss: is there a clinically signiWcant relation? Am J Otol 4:420–423 2. Papp Z, Rezes S, Jòkay I, Sziklai I (2003) Sensorineural hearing loss in chronic otitis media. Otol Neurotol 24:141–144 3. Goldstein BA, Newman CW (1999) Mascaramento clínico: tomando decisões. In: Katz J (ed) Tratado de audiologia clínica, 4th edn. Manole, São Paulo, pp 109–131 4. Musiek FE, Rintelmann WF (2001) Perspectivas atuais em avalição auditiva. Manole, São Paulo 5. MacAndie C, O’Reilly B (1999) Sensorineural hearing loss in chronic otitis media. Clin Otolaryngol 24(3):220–222 6. Lundman L, Santi PA, Morizo T, Hadara T, Junhn SK, BaggerSjoback D (1992) Inner ear damage and passage through the round window membrane of Pseudomonas aeruginosa exotoxin A in a chinchilla model. Ann Otol Rhinol Laryngol 101:437–444 7. Cureoglu S, Schchern P, Paparella M, Lindgren R (2004) Cochlear changes in chronic otitis media. Laryngoscope 114(4):622–626 8. Engel F, Beatz R, Hellner J et al (1995) Breakdown of round window membrane permeability barrier evoked by streptolysin O: possible etiologic role in development of sensorineural hearing loss in acute otitis media. Infect Immunol 63:1305–1310 9. Pickett B, Shinn J, Smith M (1997) Ear drop ototoxicity: reality or myth? Am J Otol 18:782–791 10. Jinn T, Kim P, Russel P et al (2001) Determination of ototoxicity of common otic drops using isolated cochlear outer hair cells. Laryngoscope 11:2105–2108 11. Lundy L, Graham M (1993) Ototoxicity and ototopical medications: a survey of otolaryngologists. Am J Otol 14(2):141–146 12. Linder T, Zwicky S, Brandle P (1995) Ototoxicity of ear drops: a clinical perspective. Am J Otol 16(5):653–657 13. Kellerhals B (1978) Horschaden durch ototoxische Ohrtropfen. HNO 26:49–52 14. Goycoolea MV, Muchow D, Schachern P (1988) Experimental studies on round window structure: function and permeability. Laryngoscope 98(Suppl 44):1–20 15. Sahni RS, Paparella MM, Schachern PA, Goycoolea MV, Le CT (1987) Thickness of human round window membrane in diVerent forms of otitis media. Arch Otolaryngol Head Neck Surg 113:630–634 16. Schchern PA, Paparella MM, Duval AJII, Choo YB (1984) The human round window. Arch Otolaryngol 110:15–21 17. Juhn SK, Harnaguchi Y, Goycoolea M (1988) Review of round window permeability. Acta Otolaryngol Suppl 457:43–48