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Year : 1998  |  Volume : 1  |  Issue : 1  |  Page : 56-66
Distortion product otoacoustic emissions in acute acoustic trauma

HNO-Universitätsklinik, Leipzig, Germany

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Acute acoustic traumas are caused by exposure to extremely high noise levels ranging from milliseconds to several hours' duration. In pure tone audiometry they range from the C5 dip to basomediocochlear sensorineural hearing loss. Their pathogenesis is assumed to consist of micromechanical-traumatic and biochemical-metabolic damage to the outer hair cells. In order to establish the changes to the DPOAE (distortion products of otoacoustic emissions), 17 patients were examined after sustaining acute acoustic trauma. The causes included firework explosions, anti-tank rocket launchers, vehicle tyre bursting, rock concerts, hand-gun shots, sub-machine gun fire, hand grenade explosion, exploding car battery. The pure tone audiogram, tympanogram, tinnitus maskability and DPOAE (both DP-gram and growth rate in various frequencies) were determined in all patients. If the event had occurred some time ago, measurements were taken only once; in acute cases measurements were repeated at different times. In nine patients with persistent hearing impairment, clear DPs were found in the unaffected frequencies but were completely absent in the affected frequency range. Four of these patients were unilaterally and two patients were bilaterally affected; three patients had a different (not noise-induced) hearing loss on the opposite side. In eight patients with regressive hearing loss, DPs were by contrast detectable throughout the entire frequency range, their amplitudes only rising slightly as hearing recovered. Of these eight patients, three were unilaterally and five bilaterally affected. DPOAE seem to indicate the likelihood of recovery of hearing threshold after an acute acoustic trauma. In cases with DPs completely absent in the affected frequency range, the prognosis seems to be much worse than in cases with present DPs in the frequency range of hearing.

Keywords: acute acoustic trauma, distortion-product otoacoustic emissions (DPOAE), sensorineural hearing loss

How to cite this article:
Oeken J. Distortion product otoacoustic emissions in acute acoustic trauma. Noise Health 1998;1:56-66

How to cite this URL:
Oeken J. Distortion product otoacoustic emissions in acute acoustic trauma. Noise Health [serial online] 1998 [cited 2023 Mar 25];1:56-66. Available from: https://www.noiseandhealth.org/text.asp?1998/1/1/56/31777

  Introduction Top

Both chronic and acute noise exposure lead to inner-ear damage, the scale of which depends on the duration and intensity of exposure. Acute acoustic trauma is a generic term for various types of noise-induced hearing loss caused by very short but extraordinarily intense noise impacts (such as explosions or individual gunshots), other causes include exposure to high noise levels for several hours (for instance attending loud rock concerts). That is why in the German-speaking countries a distinction is drawn between blast trauma syndrome (Knalltrauma), explosion trauma (Explosionstrauma) and acute noise trauma (akutes Larmtrauma) (Ruedi & Fuller, 1946; Lehnhardt, 1993; Ward, 1991), whereas in the Anglo-Saxon speaking countries no further differentiation is made. The various damage noxes involved are also discriminated accordingly: exposure to a volume exceeding 150 dB SPL for over 1.5 ms for instance leads to 'explosion trauma', whereas if the duration of the pressure peak is shorter than 1.5 ms, we speak of 'blast trauma' (Pilgram, 1994). Explosion trauma can also result in additional damage to the middle ear. By contrast, the term 'acute noise trauma' corresponds instead a temporary threshold shift (TTS), the cause of which is generally exposure to noise levels above 100 dB SPL for a number of hours (Lehnhardt, 1993). Sometimes it can also turn into a PTS (permanent threshold shift).

Hearing losses as shown by the PTA are relatively uniform. Less serious cases show a C5 dip; basocochlear sensorineural hearing losses are encountered in serious cases; and additionally the mid frequencies may be affected in very serious cases (Dieroff, 1994; Lehnhardt, 1993; Ward, 1991).

Audiometric tests comprise usually only pure tone audiogram (PTA) and tinnitus measurement by masking; other methods have not yet proved successful. Thus the question of whether spontaneous recovery from acute acoustic trauma is likely can only be indirectly concluded from the degree of hearing loss and the course of the threshold over the first 72 hours. According to Pilgramm (1985), spontaneous recovery is likely if 24 hours after initial measurement hearing impairment does not exceed 40 dB HL or hearing has improved by 20 dB.

However, as the lesion caused by acute noise chiefly occurs in the outer hair cells and in the high frequency range, it ought to be possible to derive additional information on hearing loss by measuring frequency-specific distortion products of OAE (DPOAE) (Avan & Bonfils, 1993). So far only results about chronic occupational noise-induced hearing loss have been published, which show that DPOAE provide valuable information about the frequency areas, where the outer hair cells, and therefore the cochlear amplifier, do not work (Oeken & Miller, 1995; Sliwinska & Sulkowski, 1996; Plinkert & de Maddalena 1997). DPOAE measurement might also allow conclusions on the etiology (i.e. micromechanical-traumatic or biochemical-metabolic damage to the outer hair cells) and hence the chances of spontaneous recovery.

  Material and Methods Top


Between 1995 and 1998, 17 patients were examined after acute acoustic trauma. 16 patients were male, one female; their average age at the time of the event was 29 years (youngest 13 years, oldest 54 years); their average age upon examination was 32 years. Six patients suffering persistent hearing damage were examined a long time after the event; 11 patients were examined soon after intense noise exposure.


Each patient underwent otorhinolaryngological examination, pure tone audiometry, tinnitus measurement with masking and DPOAE measurement. Furthermore, tympanometry was used to rule out middle-ear damage to the affected organs.

A single measurement was taken in those patients who had experienced the event some time ago; those who had recently suffered intense noise exposure were measured three times (on the day of registration in the clinic, some days later, and about one or two months after the second measurement).

All patients who visited the clinic soon after the event underwent a therapy with vasoactive substances (i.v. infusion with pentoxifyllin). This is the same treatment which is used in cases of sudden deafness in Germany. The aim is to get a faster recovery. It is not known to have any direct interference with DPOAE.

DPOAE measurement

All measurements were taken using the system of the Institute of Laryngology and Otology, London (ILO 92). The 2f 1 -f 2 Distortion Product was studied using the following parameters (Hauser & Probst, 1991; Nielsen et al., 1993):

  • Ratio of the primary tone frequencies f 1 /f 2 = 1.22; stimulus level of the primary tones: L1 = 70 dB SPL, L 2 = 65 dB SPL; definition of the DP-gram: 4 measuring points per octave; averaging was used until the 'noise floor' did not change any longer
  • Measurement of the growth rate: ratio of the primary tone frequencies f 1 /f 2 = 1.22; volume of the primary tones falling in 5 dB increments starting with L 1 = 70 dB SPL, L 2 = 65 dB SPL; 'noise floor' is defined as two standard deviations above the mean noise level in the region of the DP frequency.
  • The frequency of f 2 was matched to the PTA (Kummer et al., 1995).

  Results Top

Persistent cases

In nine patients acute acoustic trauma had led to persistent hearing loss. Six patients were exposed to the noise impact more than a year ago, three patients were exposed only a few days previously. The latter were controlled for two months.

Four patients had a unilateral hearing loss and normacusis on the opposite ear, three were unilaterally affected with different hearing impairment on the opposite ear, and two had a bilateral hearing loss.

a) Unilateral hearing impairment with normacusis of the opposite ear

The four cases of unilateral hearing loss were caused by a lorry tyre bursting, a car tyre bursting, a car battery exploding [Figure - 1], and a firework explosion.

In all cases, different degrees of high-frequency loss were established by audiometry. In two cases normacusis prevailed up to 3 kHz, after which the threshold dropped to between 65 and 70 dB HL. In the other two cases, normacusis prevailed up to 1.5 kHz, while in the higher frequency range the threshold dropped to 50-60 dB HL. All patients suffered high-frequency tinnitus following the noise exposures.

In three patients clear DPs were ascertained in the DP-gram up to the frequency range in which persistent hearing loss started in the PTA. The amplitudes were in all cases well pronounced with a s/n-difference of 12-20 dB SPL. In one patient, DPs were detected throughout the entire frequency range despite persistent hearing loss. As was to be expected, clear DPs were detected across the whole frequency range in the unaffected ear (s/n-diff. 15-25 dB SPL).

The DP-gram findings were largely confirmed by growth rate. In the frequency ranges in which DPs were clearly evident growth rates verifying the physiological nature of the DPs. In those frequencies in which the DP-gram showed no DPs no growth rate could be produced. In the special case with DPs despite a persisting hearing loss in the high frequency area the growth rate was very steep and more linear. The growth rate of the normal hearing contralateral ears was found to be typical in all frequencies.

b) Unilateral hearing impairment with differing impairment of the opposite ear

The causes were an anti-tank rocket launcher, sub-machine gunfire, and a pneumatic drill on metal. The opposite ear was affected in two cases by conductive hearing loss due to chronic middle-ear infection and in one case by deafness caused by previous sudden hearing loss. Audiometry established in the affected ear normacusis up to 1.5 kHz with subsequent threshold decline down to 100 dB HL at 3 kHz in the first case, normacusis up to 4 kHz with threshold decline down to 70 dB HL at 6 kHz in the second case, and normacusis up to 1.5 kHz with threshold decline down to 60-70 dB HL as of 2 kHz in the third case.

Tinnitus resulted in the affected ear in all three cases after intense noise exposure, which in one case (the patient with contralateral deafness due to acute hearing loss) was combined with broadband noise in the opposite ear.

In the DP-gram, DPs were clearly apparent in the damaged ear up to the frequency range at which persistent hearing loss started in the PTA. The amplitudes were well pronounced with s/n­differences from 10 to 25 dB SPL. DPs were naturally not found in the contralateral ears owing to previous illness.

The growth rate findings largely corresponded to those described under A), the difference being that the opposite ear could not be used for comparison.

c) Bilateral hearing impairment

The first case was caused by a hand grenade exploding in the immediate vicinity [Figure - 2], the second was caused by an anti-tank rocket launcher going off.

Audiometry established in the first case bilateral normacusis up to 3 kHz, after which the left ear suffered a hearing loss of up to 60 dB HL at 6 kHz. The second patient suffered asymmetrical hearing loss, comprising normacusis up to 3 kHz and then threshold drop to 50 and 90 dB HL on the right, and normacusis up to 1 kHz followed by steady threshold decline down to 80 dB HL at 6 kHz on the left.

Both patients suffered persisting tinnitus: in the first case bilaterally as a high-frequency tone and in the second case as a unilateral high-frequency hiss in the worse affected ear.

In the first case the DP-gram corresponded to the audiogram. DPs were apparent bilaterally up to f 2 =3 kHz, whereas in the higher frequency range there were no DPs. The amplitudes continuously dropped in the range of f 2 =1.5 to f 2 =3 kHz (s/n­ diff. from 17 dB to 6 dB SPL). In the second case, no DPs could be measured on the right despite repeated measurement, while on the left only low-amplitude DPs were detected in the range of f 2 =0.7 to f 2 =1.5 (s/n-diff. of 5 dB SPL). In the frequency ranges in which DPs were clearly detectable in the DP-gram, the growth rate exhibited typical characteristics, i.e. in the second case no growth rate could be measured on the right (despite normacusis up to 3 kHz).

Summary - DPOAE in persistent hearing loss after acute noise trauma

When the DPOAE of all 11 affected ears are taken into account we could find an expected result in 8 ears where we could measure clear DP-amplitudes (s/n-difference 10 until 25 dB SPL) in the unaffected and absent DPs in the noise-affected frequency area. Growth rates confirmed the findings of the DP-Gram, they showed the "non-linear" behaviour in frequencies of existing DPs. In three ears we found an atypical result, two ears showed no DPs at all in frequency areas of normacusis, one ear showed DPs over the whole frequency range though noise-induced hearing loss in the high frequencies.

Regressive cases

Eight persons were found to be suffering regressive hearing loss - three unilateral and five bilateral. All patients were examined repeatedly shortly after the event until the complete recovery of the hearing.

a) Unilateral hearing loss

The causes were two times an exploding fire cracker at New Year [Figure - 3] and a blank cartridge pistol firing.

Initial audiometric measurement when the patients first reported to the clinic (i.e. a few days after the intense noise exposure) revealed in the first two cases normacusis up to 1.5 resp. 2 kHz followed by threshold decline down to 40 dB at 2 kHz, which decreased to 30 dB HL at 6 kHz in the first case and a threshold decline down to 50 dB at 4 kHz in the second case. The third case was characterised by a C5 dip of 35 dB HL.The three patients suffered from high­frequency tinnitus, which all described as a high whistle.

Clear DPs over the whole frequency range were detected bilaterally in the DP-gram during initial measurement. The amplitudes on the impaired side were reduced in comparison to the opposite ear. The reduction seems to be related to the hearing loss. In both cases with the hearing loss of 30 to 40 dB HL the averaged difference of the DP-amplitudes between both ears in the affected frequency area was 2.2 resp. 8 dB SPL, in the case with hearing loss of 60 dB HL the difference was 18 dB SPL. The growth rate was found to be typical in all frequencies.

Once normacusis was reached, the DP-gram indicated in the both cases with hearing loss of 30 to 40 dB HL a minor rise in DP amplitudes by 1.25 and 3 dB SPL (averaged in the affected frequency range). In the case of the 60 dB HL hearing loss the DP-amplitudes increased by 16,1 dB SPL.

The change in the growth rate was insignificant in the first two cases compared to initial measurement (point of dipping into the noise floor 5 dB SPL lower). In the third case there was a more obvious difference, the point of dipping into the noise floor was 15 dB SPL lower.

b) Bilateral hearing loss

The causes in two cases were attending a rock concert [Figure - 4] and in three cases a fire cracker exploding at New Year.

In four cases audiometry revealed a bilateral C5 dip of 30 to 40 dB HL in the frequencies of 3 and 4 kHz. In the fifth case normacusis prevailed up to 4 kHz, followed by a threshold decline of 20 dB at 6 kHz and 50 dB HL at 8 kHz. All patients suffered from high-frequency tinnitus.

Clear DPs were detectable in all cases throughout the entire frequency range. No difference between the two sides could be established due to the lack of a normally hearing reference ear caused by bilateral hearing impairment.

After reaching normacusis, a minor rise in the amplitudes was recorded on both sides (in the frequency area f2=3 to 4 kHz averaged increases of -0.33 to 7 dB SPL). In the growth rate, the point of dipping into the noise floor was found to be lower by about 15-20 dB in the principally affected frequencies of 3 and 4 kHz.

Summary - DPOAE in regressive hearing loss after acute noise trauma

Summarising all 13 affected ears the following features are common: DP-amplitudes are measurable over the whole frequency range. Only in three cases a comparison to a unaffected reference ear with normal hearing is possible. The averaged differences in the affected frequencies between the impaired and normal hearing ear were 2.2, 8 and 18 dB SPL. In 11 ears an increase of DP-amplitudes (averaged at the affected frequency area) could be demonstrated after hearing recovery (1.25, 1.43, 3.07, 3.2, 3.25, 5.5, 5.8, 7.12, 15.1 dB SPL). In two ears the amplitudes were nearly the same after recovery (-0.33, 0.15 dB SPL). Concerning the growth rate lower points of dipping into the noise floor could be measured. These were 3 times 5, 5 times 10, 4 times 15, once 20 dB SPL lower.

  Discussion Top

The pathogenesis of acute acoustic trauma is assumed to consist of mechanical-traumatic damage with micro-lacerations at the level of the basilar membrane and thus the direct destruction of sensory cells, as well as biochemical­metabolic damage with the oedematous swelling of the hair cells (Alexander & Githler, 1951; Beck, 1955; Dieroff & Beck, 1964; Spoendlin, 1958 & 1971; Gogniashwili, 1972; Engstrom & Ades, 1960). Being able to identify what inner­ear lesions are involved in individual cases would be of considerable practical interest as this is critical for prognosis of the regression or persistence of hearing impairment.

Measuring DPOAE could provide the solution. Although the measurement of DPOAE upon chronic noise-induced hearing loss has already been successfully used (Oeken & Miiller, 1995; Sliwinska & Sulkowski, 1996; Plinkert & de Maddalena, 1997), there has so far been a lack of publications on DPOAE measurement after acute acoustic trauma. Despite an insufficient number for statistical evaluation, our measurements demonstrated that with nearly all persisting hearing impairment, the DPOAE had also disappeared in the frequency range of hearing loss. This indicated that the cochlear amplifier in this basilar membrane segment was no longer functioning, which in turn was probably attributable to the destruction of outer hair cells. The disappearance of DPOAE was found in both the DP-gram and the growth rate. Solely in cases in which the hearing loss is only fully pronounced in the 6 kHz range is the frequency specificity of DPOAE probably insufficient, with DPs being present despite persistent hearing impairment.

Nevertheless, it can in principle be stated that the complete absence of DPOAE constitutes an unfavourable prognosis factor. Of special interest is not so much the correlation between the degree of hearing loss and the absence of DPOAE but rather ascertaining the breakdown of the function of the cochlear amplifier itself.

By contrast, DPs are detectable throughout the entire frequency range in all regressive cases; there are no segments in which DPOAE are completely absent. During the process of recovery, DP amplitudes only increase slightly, to an extent which is inversely proportional to the hearing loss. This can be verified in both the DP-gram and the growth rate. Interestingly enough, this corresponds to the DPOAE changes after TTS found by Oeken & Menz (1996), which were produced by 20 minutes of white noise at 90 dB SPL in 102 ears belonging to people with unimpaired hearing. Here too, a significant but quantitatively minor drop in the DP amplitudes was found after statistical analysis. The cochlear amplifier appears to be still functioning and persistent hearing impairment is unlikely.

However, further investigations are necessary to find out whether existence of DPOAE can really provide an information about the prognosis of a hearing recovery independently of the degree of the hearing loss.

To resume, it can be stated that DPOAE measurement can be used to a further differentiation of noise-induced damage to the inner ear. Whereas in chronic acoustic trauma emphasis is placed on detecting cochlear lesion (especially in medical opinion), measuring the DPOAE upon acute acoustic trauma could be relevant to prognosis - something which is of considerable importance for both therapy decisions and patient advice.

  Conclusions Top

  1. DPOAE measurement can provide further information about the function of outer hair cells in cases of acute acoustic trauma.
  2. Cases in which clear DPs are measurable despite hearing loss are more likely to be blessed by spontaneous recovery. Cases in which no DPs can be detected in the affected frequencies will more probably lead to persistent hearing loss.
  3. Measurement of the DP-gram alone is sufficient; the growth rate provides no additional information.

  Acknowledgements Top

This work was kindly supported by the "Hauptverband der gewerblichen Berufsgenossenschaften" ("Confederation of Commercial Professional Associations").

This paper was presented at the 3rd European Conference on Protection Against Noise (PAN), 12-15 March 1998, Stockholm Sweden organised and supported by the European Commission BIOMED 2 concerted action PAN (Contract BMH 4-CT96-0110).[22]

  References Top

1.Alexander, E. and Githier, J. (1951) Histological examination of cochlear structure following exposure to jet engine noise. J. Comp. Physiol. 44, 513  Back to cited text no. 1    
2.Avan, P. and Bonfils, P. (1993) Frequency specificity of human distortion product otoacoustic emissions. Audiology 32, 12-26  Back to cited text no. 2    
3.Beck, C. (1955) Kernveranderungen der Haarzellen nach Beschallung. Arch. Klin.-Exp. Ohr.-, Nas.- u. Kehlk.-Heilk. 167, 262-269  Back to cited text no. 3    
4.Dieroff, H.G. (1994) Larmschwerhorigkeit. Fischer Jena Stuttgart, pp 187-189  Back to cited text no. 4    
5.Dieroff, H.G. and Beck, C. (1964) Experimentell­mikroskopische Studie zur Frage der Lokalisation von bleibenden Horschaden nach Industrieiarmbeiastung mit tonalen Gerauschanteilen. Arch. Ohr-. Nas.- u. Kehik.­Heilk. 184, 33  Back to cited text no. 5    
6.Engstrom, H. and Ades, W. (1960) Effect of high intensity noise on inner ear sensory epithelia. Acta Oto-laryng (Stockh.) Suppl. 158, 219-224  Back to cited text no. 6    
7.Gogniashwili, O.S. (1972) Electron microscopic investigation of the organ of Corti after noise trauma. Bull. of the Academy of Sciences of the Georgian SSR 68, 1  Back to cited text no. 7    
8.Hauser, R. and Probst, R. (1991) The influence of systematic primary tone level variation L2-L1 on the acoustic distortion product emission 2f1-f2 in normal hearing ears. J. Acoust. Soc. Am. 89, 280-286  Back to cited text no. 8    
9.Kummer, P., Janssen, T., Arnold, W. (1995) Suppression tuning characteristics of the 2f1-f2 distortion-product otoacoustic emission in humans. J.Acoust.Soc.Am. 98(1):197-210  Back to cited text no. 9    
10.Lehnhardt, E. and Koch, T. (1993) Akustisches Trauma In: Oto-Rhino-Laryngologie in Klinik und Praxis. Naumann, H.H., Helms, J., Herberhold C. and Kastenbauer, E. (eds.). Bd. 1. Thieme Stuttgart, pp 757-767  Back to cited text no. 10    
11.Nielsen, L.H., Popeika, G.R., Rasmussen, A.N. and Osterhammel, P.A. (1993) Clinical significance of probe­tone frequency ratio on distortion product otoacoustic emissions. Scand Audiol 22, 159-164  Back to cited text no. 11    
12.Oeken, J. and Menz, D. (1996) Amplitudenveranderungen von Distorsionsprodukten otoakustischer Emissionen nach akuter Larmeinwirkung. Laryngo-Rhino-Otol. 75, 265-269  Back to cited text no. 12    
13.Oeken, J. and Miiller, H. (1995) DPOAE bei chronischer Larmschwerhorigkeit - Vorschlag zur Begutachtung. Laryngo-Rhino-Otol. 74, 473-480  Back to cited text no. 13    
14.Pilgram, M. and Schumann, K. (1985) Hyperbaric oxygen therapy for acute acoustic trauma. Arch. Otorhinolaryngol. 241, 247-257  Back to cited text no. 14    
15.Pilgram, M. (1994) Akutes akustisches Trauma durch SchuBbelastung. In Larmschwerhorigkeit. Dieroff, H.G. (ed.). Fischer Jena Stuttgart, pp 142-157  Back to cited text no. 15    
16.Plinkert, P.K. and de Maddalena, H. (1996) Die Ableitung otoakustischer Emissionen bei der Begutachtung der chronischen Larmschwerhorigkeit. HNO 44, 313-318  Back to cited text no. 16    
17.Riiedi, L. and Furrer, W. (1946) Das akustische Trauma. Pract. Otorhinolaryngol. 8, 177-372  Back to cited text no. 17    
18.Riiedi, L. and Furrer, W. (1946) Physics and physiology of acoustic trauma. J.Acoust.Soc.Amer. 18, 409-412 Sliwinska-Kowalska, M. and Sulkowski, W. (1995) Otoacoustic emissions in assessment of occupational noise-induced hearing loss. Proceedings European Conference on Audiology, Noordwijkerhout 335-338  Back to cited text no. 18    
19.Spoendlin, H. (1958) Submikroskopische Veranderungen am Corti'schen Organ des Meerschweinchens nach akustischer Belastung. Pract. Oto-rhino-laryng. (Basel) 20, 197  Back to cited text no. 19    
20.Spoendlin, H. (1971) Primary structural changes in the organ of Corti after acoustic overstimulation. Acta Oto­laryngol. 71, 166-176  Back to cited text no. 20    
21.Spoendlin, H. (1971) Degeneration behaviour of the cochlear nerve. Arch. Klin.-Exp. Ohr.-, Nas.- u. Kehlk.­Heilk. 200, 275-291  Back to cited text no. 21    
22.Ward, W.D. (1991) Noise-Induced Hearing Damage. In Otolaryngology Vol. 2. Paparella, M.M., Shumrick, D.A., Gluckmann, J.L. and Meyerhoff, W.L. (eds.) Saunders­Company, Philadelphia, London, Toronto, Montreal, Sydney, Tokyo, pp 1639-1652  Back to cited text no. 22    

Correspondence Address:
Jens Oeken
HNO-Universitätsklinik, Liebigstr. 18a, D- 04103 Leipzig
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Source of Support: None, Conflict of Interest: None

PMID: 12689368

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  [Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4]