Oxford Health Plans > Medical and Administrative Policies > Otoacoustic Emissions Testing
Title of Policy

Otoacoustic Emissions Testing

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Policy #: ENT 020.2 T1

Coverage Statement:

Policy is applicable to:

    Commercial plans

Note: Please refer to policy: Preventive Care for additional information regarding preventive health services.

Conditions of Coverage:
Benefit Type General benefits package
Referral Required
(Does not apply to non-gatekeeper products)
Yes - Office
No - Outpatient
Authorization (Precertification always required for inpatient admission) Yes - Outpatient
No - Office
Precertification with MD Review No
Site(s) of Service
(If not listed, MD Review required)
Office, Outpatient
Special Considerations

None

Description of Service/Assessment/Background Information:

Otoacoustic emissions (OAEs) are low-intensity sounds emitted by functioning outer hair cells of the cochlea. OAEs are measured by presenting a series of very brief clicks to the ear through a probe that is inserted in the outer third of the ear canal. The probe contains a loudspeaker that generates the clicks and a microphone for measuring the resulting OAEs that are produced in the cochlea and are then reflected back through the middle ear into the outer ear canal. OAE testing requires no behavioral or interactive feedback by the individual being tested.

OAEs are used as a screening test for hearing in newborns. Other potential applications of OAE testing include screening children or at-risk populations for hearing loss, and characterizing sensitivity and functional hearing loss and differentiating sensory from neural components in people with known hearing loss.

The two most common types of OAE measurements are 1) transient evoked otoacoustic emissions (TEOAEs) which are sounds emitted in response to acoustic stimuli of very short duration; usually clicks but can be tone-bursts, and 2) distortion product otoacoustic emissions (DPOAEs) which are sounds emitted in response to two simultaneous tones of different frequencies. TOAEs are used to screen infants, validate other tests, and assess cochlear function, and DPOAEs are used to assess cochlear damage, ototoxicity, and noise-induced damage. Spontaneous otoacoustic emissions (SOAEs) are sounds emitted without an acoustic stimulus (i.e., spontaneously). Sustained-frequency otoacoustic emissions (SFOAEs) are sounds emitted in response to a continuous tone. At present, SOAEs and SFOAEs are not used clinically.

The OAE test is an effective screening measure for middle-ear abnormalities and for moderate or severe degrees of hearing loss, because normal OAE responses are not obtained if hearing thresholds are approximately 30- to 40-dB hearing levels or higher. The OAE test does not further quantify hearing loss or hearing threshold level. The OAE test also does not assess the integrity of the neural transmission of sound from the eighth nerve to the brainstem and, therefore, will miss auditory neuropathy and other neuronal abnormalities. Individuals with such abnormalities will have normal OAE test results but abnormal auditory brainstem response (ABR) test results (Harlor, 2009).

Clinical Evidence:

Otoacoustic Emissions (OAEs) for Neonatal Hearing Screening
A study which involved 53,781 newborns provided a direct comparison of hearing impairment detection rates during periods of newborn hearing screening and no screening in the same hospitals (Wessex Universal Hearing Screening Trial, 1998). Those infants born during a period of screening underwent a two-stage screening test, with transient evoked otoacoustic emissions (TEOAE) at birth, followed by automated auditory brainstem response (AABR) before discharge if the first screen was failed. If the second screen was also failed, the babies were referred to an audiologist at 6 to 12 weeks of age. In this study, 4% of infants with hearing loss were missed during the screening period, while 27% were missed during the period of no screening. This study did not provide data on clinical outcomes such as speech and language development in screened versus unscreened children.

Another group of investigators compared clinical outcomes, including speech and language development, in 25 infants who were screened as part of the Colorado Universal Newborn Screening program with outcomes in 25 matched infants who were born in a hospital without a universal newborn hearing screening program (Yoshinaga-Itano et al., 2000). This study found that children who were identified as hearing impaired through the newborn hearing screening program had significantly better scores on tests of speech and language development than did children who were identified later.

Professional Societies and Guidelines
U.S. Preventive Services Task Force (USPSTF): The USPSTF recommends that newborn hearing screening programs include (USPSTF, 2008):
  • a 1- or 2-step validated protocol which includes otoacoustic emissions (OAEs) followed by auditory brainstem response (ABR) in those who failed the first test
  • quality-control programs in place to reduce avoidable false-positive test results
  • protocols to ensure that infants with positive screening-test results receive appropriate audiologic evaluation and follow-up after discharge
  • hearing screening before 1 month of age. Those infants who do not pass the newborn screening should undergo audiologic and medical evaluation before 3 months of age for confirmatory testing

The Joint Committee on Infant Hearing (JCIH): The JCIH, which includes organizations such as the American Academy of Pediatrics (AAP), the American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS), the American Academy of Audiology (AAA), and American Speech-Language-Hearing Association (ASHA), has a published position statement on principles and guidelines for early hearing detection and intervention programs. The JCIH endorses early detection of and intervention for infants with hearing loss. To maximize the outcome for infants who are deaf or hard of hearing, the hearing of all infants should be screened at no later than 1 month of age. Those who do not pass screening should have a comprehensive audiological evaluation at no later than 3 months of age. Infants with confirmed hearing loss should receive appropriate intervention at no later than 6 months of age from health care and education professionals with expertise in hearing loss and deafness in infants and young children. Separate protocols are recommended for NICU and well-infant nurseries. NICU infants admitted for more than five days are to have auditory brainstem response (ABR) included as part of their screening so that neural hearing loss will not be missed. For infants who do not pass automated ABR testing in the NICU, referral should be made directly to an audiologist for re-screening and, when indicated, comprehensive evaluation including ABR (JCIH, 2007).

American Academy of Pediatrics (AAP): In February 1999, the American Academy of Pediatrics endorsed the implementation of universal newborn hearing screening (AAP, 1999).

National Institutes of Health (NIH): An NIH Consensus Statement concluded that there is no ideal method for screening hearing (NIH, 1993). In the absence of an ideal screening program, the NIH recommends universal two-stage EOAE and ABR screening of all infants prior to hospital discharge, or within the first 3 months of life for infants born at an alternate birthing site. The NIH also states that universal hearing screening is superior to a hearing protocol that screens only neonates with high-risk indicators; a high-risk protocol identifies only 50% of hearing-impaired infants.

OAE Evaluation for Hearing Loss in Children
Chiong et al. (2007) evaluated evoked otoacoustic emission (OAE) and auditory brainstem response (ABR) results for hearing screening in infants. The objective of the study was to correlate hearing screening outcomes of a cohort of infants with developmental outcomes at 6 and 12 months. A total of 565 infants had both OAE testing and ABR. Overall in 1130 ears, OAE and ABR testing showed an observed agreement of 99%, agreement due to chance of 96%, and kappa agreement of 79% in diagnosing bilateral hearing losses. OAEs had a sensitivity of 86.4% and a specificity of 99.4%.

Between 1997 and 2003, a cohort of 421 infants was enrolled at birth from Minnesota Native American reservations and an urban clinic and followed to age 2 years. This study reports OAE hearing screening results related to otitis media and effusion (OME) diagnoses, as well as risk for recurrent hearing screening failure and OME in Native American infants and children. Infants were prospectively assessed at regular intervals with pneumatic otoscopy, distortion product otoacoustic emissions, and tympanometry by nurses who were trained in all procedures and validated on pneumatic otoscopy. In the newborn period, 23.5% of infants failed hearing screening in at least one ear. Hearing screening failures increased to 29.9% from 2 to 5 months of age. Technical fail results due to excessive noise occurred frequently in infants 6-24 months of age, making interpretation of true pass and fail rates questionable in older infants. OAE test result was associated with OM diagnosis, and this relationship strengthened with age, with the strongest association above 6 months of age. A high rate of hearing screening failures occurred among Native American infants in the first 5 months of age, and was significantly associated with a correspondingly high rate of otitis media. Only one infant out of 366 was identified with sensorineural hearing loss, thus essentially all of the hearing screening failures reflected either a middle ear origin or other temporary problems. OAE screening provided a valuable hearing screening measure in this population at high risk for recurrent otitis media, but due to excessive noise in infants 6 months and older, practical use of OAE screening is limited. Use of behavioral assessment is needed after 6 months of age, when high rates of OME persist in this population (Hunter et al. 2007).

Eiserman et al. (2008) screened underserved children 3 years or younger for hearing loss using otoacoustic emissions (OAE) technology and systematically document multi-step screening and diagnostic outcomes. A total of 4,519 children in four states were screened by trained lay screeners using portable OAE equipment set to deliver stimuli and measurement levels sensitive to mild hearing loss as low as 25 decibels (dB) hearing level. The screening and follow-up protocol specified that children not passing the multi-step OAE screening be evaluated by local physicians and hearing specialists. Of the 4,519 children screened as a part of the study, 257 (6%) ultimately required medical or audiological follow-up. One hundred and seven children were identified as having a hearing loss or disorder of the outer, middle or inner ear requiring treatment or monitoring. The investigators concluded that OAE screening, using a multi-step protocol, is a feasible and accurate practice for identifying a wide range of hearing-health conditions warranting monitoring and treatment among children 3 years or younger in early childhood care programs.

Silwa et al. (2011) compared test performance measures from audiometric and objective methods (OAEs and impedance audiometry). Hearing screening protocols were applied on a group of 190 children of about 12 years of age (6th grade of primary school). For a single application of a screening procedure, the best performance was observed in the automated four-tone audiometry, followed by the tympanometry and the TEOAE-based procedures. Screening performance was enhanced using a combination of automated and impedance audiometry. A four-tone audiometry test combined with tympanometry gives a sensitivity of 65%, and the PPV of 46%, which are reasonable values, acceptable for practical use. The use of a TEOAE protocol degrades the overall performance of screening. The investigators concluded that screening of school children is feasible with a combination of automated audiometry and tympanometry.

In a retrospective, cross-sectional study, evoked otoacoustic emissions (OAEs) and diagnostic auditory brainstem responses (ABRs) were determined in 379 high-risk children (mean age 41+/-47 months) referred for hearing screening. Of the 131 children whose parents gave their consent for concomitant OAE and ABR testing, agreements were observed between the two tests in terms of classifying the results as normal or abnormal of 78.9% in right and 78.6% in left ears. When the children were classified as either "with hearing loss-bilateral abnormal ABRs" or "at least one normal ABR", there was an observed agreement of 81%. OAEs had a sensitivity of 76.9% and a specificity of 90%. The investigators concluded that there is good concordance between OAE and ABR results among high-risk children referred for hearing screening (Llanes and Chiong 2004). This study is limited by lack of comparison to standard hearing tests.

Dille et al. (2007) compared transient evoked otoacoustic emissions (TEOAE) with distortion product otoacoustic emissions (DPOAE) to determine if they resulted in equivalent signal-to-noise ratios (SNRs) when used for hearing screening in a preschool population in a community setting. Thirty-three preschool children ages 4 months to 4 years, 4 months were tested using DPOAE and TEOAE. The frequencies 800-4000Hz were compared. The tympanometric gradient was obtained from a tympanogram done on each ear. A multivariate statistic was used to compare the emission SNR from both methods. The agreement between the pass/refer rates from the OAE screens and from the tympanometric gradient were compared. TEOAE and DPOAE SNRs were significantly different in the low frequency however, there were no significant differences found in the high frequencies. There were no significant pass/refer differences found between the methods at any frequency. When comparing the agreement between the OAE methods with the tympanometry, both methods produced nearly equivalent agreement with tympanometric gradient. However, the overall correspondence between OAE findings and tympanometry was not perfect. The investigators concluded that both methods are effective and especially equivalent in the high frequencies and can be recommended for use in a preschool population in the field. Tympanometric gradient disagreed with both OAE screening results about 25% of the time. The study also concluded that higher refer rates can be expected when young (younger than 3 years old) preschool children are included in the screen.

In a prospective trial, Krueger et al. (2002) compared the findings of 3 different hearing screening methods in second and third grade school-aged children. Three hundred children were screened by using 3 test modalities, pure-tone audiometry, distortion product otoacoustic emissions (DPOAE), and tympanometry. All of the tests were normal in 532 ears (89%), and all were abnormal in 12 ears (2%). Tympanometry yielded the most abnormalities (8.3%), and pure-tone testing demonstrated the fewest (3.3%), with a positive rate of 6.3% for DPOAE testing. False-positive rates were 1.2%, 4.2%, and 6.4% for pure tones, DPOAE, and tympanometry, respectively, when normal results on pure-tones or DPOAE were taken to represent true hearing. Based on the results of the study, the investigators continue to recommend pure-tone testing as an effective screening method, with follow-up by using otoacoustic emissions in those who fail the pure-tone test.

Five hundred eighty-three grade school children in four separate school populations were screened for hearing loss using the standard pure tone four-frequency protocol and transient evoked otoacoustic emissions. Students failing either test received a comprehensive audiogram by an audiologist that served as the "gold standard." Sensitivity and specificity of both tests were compared. The sensitivity and specificity of pure tone screening was 87% and 80%, respectively, compared with 65% and 91% for transient evoked otoacoustic emissions. The investigators concluded that pure tone screening is a statistically significant better screening test for detecting hearing loss in this population of grade school children (Sabo et al. 2000).

Lyons et al. (2004) examined the test performance of distortion product otoacoustic emissions (DPOAEs) when used as a screening tool in the school setting. A total of 1003 children (mean age 6.2 years) were tested with pure-tone screening, tympanometry, and DPOAE assessment. Optimal DPOAE test performance was determined in comparison with pure-tone screening results using clinical decision analysis. The results showed hit rates of 0.86, 0.89, and 0.90, and false alarm rates of 0.52, 0.19, and 0.22 for criterion signal-to-noise ratio (SNR) values of 4, 5, and 11 dB at 1.1, 1.9, and 3.8 kHz respectively. DPOAE test performance was compromised at 1.1 kHz. In view of the different test performance characteristics across the frequencies, the use of a fixed SNR as a pass criterion for all frequencies in DPOAE assessments is not recommended. When compared to pure tone plus tympanometry results, the DPOAEs showed deterioration in test performance, suggesting that the use of DPOAEs alone might miss children with subtle middle ear dysfunction. However, when the results of a test protocol, which incorporates both DPOAEs and tympanometry, were used in comparison with the gold standard of pure-tone screening plus tympanometry, test performance was enhanced. The investigators concluded that In view of its high performance, the use of a protocol that includes both DPOAEs and tympanometry holds promise as a useful tool in the hearing screening of schoolchildren, including difficult-to-test children.

In a cross-sectional, preliminary screening study, Georgalas et al. (2008) assessed the role of otoacoustic emissions in a screening program for middle-ear disorders and hearing loss in school-age children. One hundred and ninety-six children were evaluated using transient evoked otoacoustic emissions. Twenty per cent failed in both ears, while in 32 per cent otoacoustic emissions could not be produced in at least one ear. Younger children had higher rates of absent transient evoked otoacoustic emissions. The absence of otoacoustic emissions was highly correlated with tympanic membrane changes seen on otoscopy and the presence of a type B tympanogram. As a single screening modality, otoacoustic emissions had 100 per cent sensitivity in diagnosing hearing loss worse than 30 dB, and a 90 per cent sensitivity and 64 per cent specificity in diagnosing hearing loss worse than 25 dB, which did not improve by adding tympanometry to the screening protocol. According to the investigators, these results strongly suggest the potential usefulness of otoacoustic emission testing in screening school-age children for hearing loss. The validity of this study is limited by lack of a control group.

In a transversal-prospective study, Vasconcelos et al. (2008) evaluated 451 first grade school children. Otoscopic exams with the removal of wax and the TEOAE and DPEOAE exams were performed on all school children. Audiometry and acoustic impedance were performed on the children who presented alterations at any point during the TEOAE and/or DPEOAE exams. Regarding the TEOAE and DPEOAE triage, no significant statistic difference was found when comparing the results of the exams which failed only in the TEOAE and DOEOAE with audiometric exam data, nonetheless, when comparing this failure data to both of these exams there was a significant difference. The investigators concluded that both EOAE procedures responded well to the hearing triage in school children. The validity of this study is limited by lack of a control group.

Driscoll et al. (2001) investigated whether transient evoked otoacoustic emission (TEOE) testing provides a more accurate and effective alternative to a pure tone screening plus tympanometry protocol. Pure tone screening, tympanometry and TEOE data were collected from 940 subjects, with a mean age of 6.2 years. The TEOE failure rate for the group was 20.3%. The failure rate for pure tone screening was found to be 8.9%, whilst 18.6% of subjects failed a protocol consisting of combined pure tone screening and tympanometry results. In essence, findings from the comparison of overall TEOE pass/fail with overall pure tone screening pass/fail suggested that use of a modified Rhode Island Hearing Assessment Project criterion would result in a very high probability that a child with a pass result has normal hearing (true negative). However, the hit rate was only moderate. Selection of a signal-to-noise ratio (SNR) criterion set at > or =1 dB appeared to provide the best test performance measures for the range of SNR values investigated. Test performance measures generally declined when tympanometry results were included, with the exception of lower false alarm rates and higher positive predictive values. The exclusion of low frequency data from the TEOE SNR versus pure tone screening analysis resulted in improved performance measures. According to the investigators, the present study poses several implications for the clinical implementation of TEOE screening for entry level school children. TEOE pass/fail criteria will require revision. The findings of the current investigation offer support to the possible replacement of pure tone screening with TEOE testing for 6-year-old children. However, they do not suggest the replacement of the pure tone screening plus tympanometry battery.

Kirkim et al. (2005) evaluated pediatric patients with auditory neuropathy with regard to diagnostic criteria and audiological test results. Hearing assessment was made in five children with auditory neuropathy. The patients were tested with the use of acoustic immittance measures, transient evoked otoacoustic emissions (TEOAE), behavioral audiometry, and auditory brainstem responses (ABR). Transient otoacoustic emissions were recorded in all the patients in contrast to the lack of auditory evoked brainstem responses (i.e. there were no identifiable waves in all recordings). Another common feature was the absence of correlation between ABR, TEOAE, and behavioral test results. According to the investigators, otoacoustic emissions and the auditory brainstem responses, when used together, offer insight into pre-neural as well as neural function in the auditory system and thus, may form the necessary combination for the evaluation of hearing in children.

OAE Evaluation of Hearing Loss in Adults
Jupiter (2009) determined whether distortion product otoacoustic emissions (DPOAEs) could be used as a hearing screening tool with elderly individuals living independently and to compare the utility of different screening protocols: (a) 3 pure-tone screening protocols consisting of 30 dB HL at 1, 2, and 3 kHz; 40 dB HL at 1, 2, and 3 kHz; or 40 dB HL at 1 and 2 kHz; (b) the Hearing Handicap Inventory for the Elderly-Screening version (HHIE-S); (c) pure tones at 40 dB HL at 1 and 2 kHz plus the HHIE-S; and (d) DPOAEs. A total of 106 elderly individuals age 65-91 years were screened using the above protocols. Pass/fail results showed that most individuals failed at 30 dB HL, followed by DPOAEs, the 40-dB HL protocols, the HHIE-S alone, and the combined pure-tone/HHIE-S protocol. All screening results were associated except the HHIE-S and 30 dB HL and the HHIE-S and DPOAEs. A McNemar analysis revealed that the differences between the correlated pass/fail results were significant except for the HHIE-S and 40 dB at 1 and 2 kHz. The investigators concluded that DPOAEs can be used to screen the elderly, with the advantage that individuals do not have to voluntarily respond to the test. There is no evidence from this study that DPOAEs used in place of conventional hearing tests will improve patient management.

In a prospective study of adult 64 patients, Wang et al. (2002) evaluated the validity of hearing screening by means of the portable screening pure-tone audiometer and distortion-product otoacoustic emissions (DPOAE) measurement. The 64 study participants underwent hearing tests performed with screening pure-tone audiometer, DPOAE and conventional pure-tone audiometer. The results of conventional pure-tone audiometry were used for "gold standards" and the normal auditory function was defined as the threshold less than or equal to 20 dB. Compared with the "gold standards: For screening pure-tone audiometry, the kappa values at the 5 tested frequencies (0.5, 1, 2, 4, 8 kHz) ranged from 0.79 to 0.93 and the agreement with the gold standards was classified as "excellent." The sensitivity, specificity and test accuracy values ranged from 91.8-98.5%, 88.0-96.3% and 89.8-96.9%, respectively. For DPOAE measurement, the kappa values at the 3 tested frequencies (1, 2, 4 kHz) ranged from 0.62 to 0.78. The agreement was classified as "good" at 1, 4 kHz and "excellent" at 2 kHz. The sensitivity, specificity and test accuracy values ranged from 91.7-98.5%, 62.3-86.8% and 81.3-89.1%. The investigators recommend a hearing screening measured at 0.5, 1, 2, 4, 8 kHz with screening pure-tone audiometer in a simple-type soundproof chamber and performed by a screening assistant. The DPOAE measurement may be used as an auxiliary tool to provide more information for early identification and differential diagnosis of hearing loss in clinical applications. The impact of DPOAE measurement on patient management was not confirmed in this study.

Engdahl et al. (2005) evaluated the risk for decreased OAEs associated with occupational and leisure noise, head injuries and recurrent ear infections. The predictive power of the environmental factors on different OAE values is compared with the prediction of conventional pure-tone hearing thresholds (PTTs). The analyses are based on data from 5072 adult subjects comprising a sub-sample of the 51975 subjects from the Nord-Trøndelag Hearing Loss Study. The subjects participated in a general health screening, including an examination of pure-tone audiometry, transient OAEs and distortion-product OAEs, and completed a questionnaire regarding history of noise exposure and ear disease. The predictions of OAEs and PTTs were analyzed using regression analysis for various sex and age groups. The fraction of the variance explained by exposure was generally moderate (0-4%, varying with age, sex, and type of measurement). Males showed moderate effects of work noise, impulse noise and ear infection, while ear infection was the only significant predictor in females. There were no effects of music noise and head injuries. According to the investigators, the effect of exposure on OAEs that remained after controlling for PTTs was small and similar to the effect of exposure on PTTs that remained after controlling for OAEs. There is no evidence from this study that OAEs used in place of conventional hearing tests will improve patient management.

Wagner et al. (2008) evaluated the test-retest repeatability for distortion product otoacoustic emissions (DPOAE). Measurements of DPOAE were performed in triplicate in 40 subjects. The investigators concluded that although the measurements were conducted under practical conditions resembling the clinical setting, repeatability was generally good. The widely used minimum SNR of 6 dB seems to be a recommendable criterion when considering both practicability and measurement quality under clinical conditions. The current findings underline the suitability of DPOAE as a monitoring tool of cochlear status over time. These findings require confirmation in a larger study.

Ellison et al. (2005) assessed how well stimulus-frequency otoacoustic emissions (SFOAEs) identify hearing loss, classify hearing loss as mild or moderate-severe, and correlate with pure-tone thresholds in a population of adults with normal middle ear function. Based on the study results, the investigators concluded that although SFOAEs were significantly correlated with hearing threshold, they do not appear to have clinical utility in predicting a specific behavioral threshold. Information on middle ear status as assessed by acoustic transfer function measures offered minimal improvement in SFOAE predictions of auditory status in a population of normal and impaired ears with normal middle ear function.

Bertoli et al. (1997) investigated the clinical value of measuring transient evoked otoacoustic emissions (TEOAEs) in the routine audiological evaluation of older people reasoning that a finding of hearing loss in the presence of TEOAEs could indicate a form of presbycusis with a primary central component. Click-evoked otoacoustic emissions (CEOAEs) were measured in 201 subjects without middle ear problems aged 60 years and older (range 60 to 97 years) who volunteered for the study because of complaints concerning their hearing. Audiological procedures included a pure-tone audiogram, modified Speech Perception in Noise test, and the Hearing Handicap Inventory for the Elderly. Results from ears with a pure-tone average (PTA) at 0.5, 1, and 2 kHz of < or = 30 dB HL were further analyzed with respect to the presence or absence of CEOAEs. In addition, tone burst evoked otoacoustic emissions (TbOAEs) were tested in ears with responses to click stimuli. CEOAEs were not detectable in ears with a PTA > 30 dB HL. The prevalence of CEOAEs in ears with a PTA < or = 30 dB HL was 60%. Response levels decreased as hearing thresholds became poorer, but there was no apparent influence on TEOAE level due to age alone. The audiological measures from ears with and without CEOAEs and with PTAs < or = 30 dB HL were similar with the exception of small between group differences at lower frequencies. According to the investigators, the lower overall amplitudes of TEOAEs and the lower prevalence of 60% in comparison to results from younger subjects with normal hearing imply that cochlear changes do occur with aging. However, the preservation or loss of TEOAEs does not separate subjects with presbycusis into distinct audiological categories or handicaps. Tone burst results suggest that frequency processing within the cochlea is not affected by age alone. The investigators concluded that TEOAEs add no relevant information in the routine clinical evaluation of elderly persons with hearing problems.

Well-designed trials with larger sample sizes are needed to demonstrate that OAE testing used as a method for hearing screening in adults has an impact on clinical outcomes such as increasing communication skills in these patients.

OAE Testing in Individuals Who Cannot Cooperate With Other Methods of Hearing Testing
In a prospective, clinical, observational study, Hamill et al. (2003) assessed hearing impairment in adults admitted to a university surgical intensive care unit in order to identify patients at risk for impaired receptive communication. Patients included in the study were 442 adult patients admitted to the surgical intensive care unit for trauma, a critical illness, or postoperative monitoring. As part of a continuing quality improvement protocol, adults admitted to the surgical intensive care unit were screened for hearing loss. Screening included otoscopy, tympanometry, and distortion product otoacoustic emissions. Almost two thirds of patients studied failed the screening protocol. The investigators concluded that screening with otoscopy, tympanometry, and DPOAE is an efficient and sensitive way to identify patients at risk for impaired auditory acuity. The validity of this study is limited by lack of a control group.

Tas et al. (2007) evaluated hearing in autistic children by using transient evoked otoacoustic emission (TEOAE) and auditory brainstem response (ABR). Tests were performed on 30 children with autism and 15 typically developing children, following otomicroscopy and tympanometry. The children with autism were sedated before the tests. Positive emissions and normal hearing level at ABR were obtained in both ears of all children in the control group and of 25 children with autism. TEOAE and ABR results varied in the remaining five children with autism. The mean III-V interpeak latencies (IPLs) in both ears of children with autism were longer than those in the control group. According to the investigators, hearing loss may be more common in children with autism than in typically developing children.

Tharpe et al. (2006) described the auditory characteristics of children with autism relative to those of typically developing children and described the test-retest reliability of behavioral auditory test measures with this population of children with autism. Audiometric data were obtained from 22 children diagnosed with autism and 22 of their typically developing peers. The audiologic test battery consisted of behavioral measures (i.e., visual reinforcement audiometry, tangible reinforcement operant conditioning audiometry, and conditioned play audiometry) and physiological measures (auditory brain stem response audiometry, distortion product otoacoustic emissions, and acoustic reflexes). Children with autism had physiologic test results equivalent to their typically developing counterparts. That is, no differences in auditory brain stem response audiometry, distortion product otoacoustic emissions, or acoustic reflex results were noted between the children with autism and typically developing children. However, behavioral measures revealed that about half of the children diagnosed with autism presented pure-tone averages outside of normal limits (i.e., >20 dB HL), although their response thresholds to speech were within normal limits. All behavioral test results were within normal limits (i.e., </=20 dB HL) for the typically developing children. In addition, test-retest variability was typically 15 dB or greater for children with autism as compared with variability of 10 dB or less for most of the typically developing children. The investigators concluded that children with autism demonstrated essentially equivalent results on a battery of physiological auditory tests as those obtained from typically developing children. However, on average, behavioral responses of children with autism were elevated and less reliable relative to those of typically developing children. Furthermore, approximately half of the children with autism demonstrated behavioral pure-tone averages outside of the normal hearing range (i.e., >20 dB HL) despite having normal to near-normal hearing sensitivity as determined by other audiometric measures.

During the German Special Olympics Summer Games 2006, 552 athletes with intellectual disabilities (ID) had their hearing screened according to the international protocol of Healthy Hearing, Special Olympics. This screening protocol includes otoscopy, measurement of distortion product otoacoustic emissions, and, if necessary, tympanometry and pure tone audiometry (PTA) screening at 2 and 4 kHz. Additionally, 195 athletes underwent a full diagnostic PTA. The results of the screening and diagnostic PTA were compared. Of the 524 athletes who completed the screening protocol, 76% passed and 24% failed it. Ear wax was removed in 48% of all athletes. 42% of the athletes were recommended to consult an otolaryngologist or an acoustician. Of the 99 athletes whose screening-based suspicion of a hearing loss was confirmed with diagnostic PTA, 74 had an undetected hearing loss. The correlation (Cramer's V) between screening and diagnostic PTA was .98. The sensitivity of the screening was 100% and the specificity 98%. The investigators concluded that the screening reliably detects hearing disorders among persons with ID. The prevalence of hearing impairment in this population is considerably higher than in the general population, and the proportion of undetected hearing impairments is large, even among people with only mild and moderate ID, as examined in this study. Therefore, a screening is highly recommended for persons with ID (Hild, 2008). The screening protocol includes otoscopy, measurement of distortion product otoacoustic emissions, tympanometry, and pure tone audiometry (PTA) screening.

Hassmann et al. (1998) investigated the features of hearing impairment in subjects with Down syndrome. Forty-seven children and 14 adults with Down syndrome were included in the study. Depending on age, intellectual level and middle ear status the following examinations were performed: pure-tone 'play audiometry', tympanometry, acoustic reflex, auditory brain response (ABR) and distortion products otoacoustic emissions (DPOAE). The results were compared with age matched control groups. Tympanometry of B and C type was detected in 56% of ears. The amplitude of DPOAE was lower in children with Down syndrome than in the control group. This difference was more expressed in adults with Down syndrome. Pure-tone audiometry was carried out in all patients except one. The pure-tone average hearing loss was 32.3 dB HL in this group. Two patients had normal hearing, at PTA 15 dB HL, considered as within the normal range and four had normal hearing at PTA 25 dB HL, also considered as within the normal range. Severe hearing loss was reported in one case - PTA 56 and 82 dB HL. According to the investigators, DPOAE examination results in subjects with Down syndrome without conductive hearing loss indicate early age related inner ear impairment.

OAE Testing for Other Conditions

Ototoxcity
Hotz et al. (2000) investigated the action of midazolam and its active metabolite alpha-hydroxy-midazolam on different parts of the auditory pathway in six healthy volunteers in a randomized, double-blind, three-way cross-over study. Acoustically evoked short (SLP) and middle (MLP) latency potentials, transitory evoked otoacoustic emissions (TEOAE), and EEG power spectra were analyzed after short i. v. injections of placebo, or 0.15 mg kg-1 midazolam, or alpha-hydroxy-midazolam, respectively. SLP showed a significant transient increase of Jewett wave V 10 min after injection for midazolam and alpha-hydroxy-midazolam while the latency of wave I was unchanged. Both benzodiazepines induced a marked and long-lasting MLP amplitude decrease for 240 min with slow recovery over the following 360 min. No changes of TEOAE were observed. In agreement with earlier reports, increases in EEG beta activity and decreases in alpha activity were observed after administration of either drug. The investigators concluded that systemically administered benzodiazepines modulate the auditory pathway above the level of the cochlea. While SLP changes were closely associated with sedation and high plasma benzodiazepine concentrations, MLP effects persisted for hours after sedation even at low benzodiazepine plasma levels. Evoked potentials may therefore be more sensitive than EEG as a tool to monitor benzodiazepine effects. Further research is needed to confirm this conclusion.

Among patients receiving cisplatin for the treatment of cancer, Reavis et al. (2011) sought to (1) identify the combination of DPOAE metrics and ototoxicity risk factors that best classified ears with and without ototoxic-induced hearing changes; and (2) evaluate the test performance achieved by the composite measure as well as by DPOAEs alone. The odds of experiencing hearing changes at a given patient visit were determined using data collected prospectively from 24 veterans receiving cisplatin. Pure-tone thresholds were examined within an octave of each subject's high-frequency hearing limit. DPOAE were collected as a set of four response growth (input/output) functions. Logistic regression modeled the risk of hearing change using several DPOAE metrics, drug treatment factors, and other patient factors as independent variables. An optimal discriminant function was derived by reducing the model so that only statistically significant variables were included. Receiver operating characteristic curve analysis was used to evaluate test performance. At higher cisplatin doses, ears with better hearing at baseline were more likely to exhibit ototoxic hearing changes than those with poorer hearing. The investigators concluded that DPOAEs alone and especially in combination with pre-exposure hearing and cisplatin dose provide an indication of whether or not hearing has changed as a result of cisplatin administration. These results need to be validated in a separate sample.

Yilmaz et al. (2009) investigated cisplatin ototoxicity by using the transient evoked otoacoustic emission (TEOAE) test and the pure tone audiometer. Twenty adult lung cancer patients and 20 control group patients were included in the study. The investigators compared the hearing of the patients who received 100 mg/m(2) 4-cycle cisplatin for lung cancer, with pure tone audiometer and transient evoked otoacoustic emission test in 1,000, 2,000 and 4,000 Hz. A 55% hearing decrease with pure tone audiometer was found in patients that are receiving 100 mg/m(2) 4-cycle cisplatin for lung cancer. An established emission amplitude decrease with TEOAE test was found in 85% of the patients. When the patients' pure tone audiometer in 1,000, 2,000 and 4,000 Hz and TEOAE amplitude changes were compared, there were no statistically significant results, but when the patients' TEOAE amplitude changes in 1,000, 2,000 and 4,000 Hz was compared with the control group, statistically significant results were found. The investigators concluded that the study results demonstrate that cisplatin ototoxicity could be find out with TEOAE test before it is seen with pure tone audiometer. These findings require confirmation in a larger study.

Delehaye et al. (2008) compared the efficacy of otoacoustic emissions (distortion-product otoacoustic emissions) with that of pure-tone audiometry as method of audiological monitoring in 60 patients undergoing Deferoxamine therapy. Distortion-product otoacoustic emissions were obtained as DP-grams. Threshold changes from baseline were found to be statistically significant from 4 to 8kHz in 68.4% of the subjects. Distortion-product otoacoustic emissions demonstrated a significant threshold shift and a decreased amplitude in the frequencies >3kHz. Furthermore, DP-gram amplitude also reduced significantly at 3kHz without any similar change in pure-tone audiometry. According to the investigators, ototoxicity screening tool DP-gram was extremely sensitive and superior to pure-tone audiometry. Their use is recommended for regular monitoring of cochlear function, aiming in prevention of permanent damage. This study is limited by its small sample size.

Biro et al. (2006) studied the characteristics and risk factors of the long-term ototoxic effect of cisplatin in testicular cancer patients by measuring distortion product otoacoustic emissions (DPOAEs). A total of 223 patients who received cisplatin were assessed by DPOAE. The control group consisted of 40 testicular cancer patients who did not undergo chemotherapy. Symptomatic ototoxicity was observed in 20% of the patients. In patients receiving <or=300 mg/m2 cisplatin, no amplitude changes were detected. Beyond this dose, hearing impairment proved to be dose dependent. In patients receiving >or=400 mg/m2, DPOAE could detect significant hearing impairment at lower frequencies that are important for speech perception. At 400 mg/m2, significant amplitude change was detected at 3,000 Hz; at 500-600 mg/m2, significant amplitude change was detected at 1,500, 2,000 and 3,000 Hz, and at 700 mg/m2 significant amplitude change was detected at 3,000 Hz. The investigators concluded that DPOAE is a fast, noninvasive and reliable method in detecting late ototoxicity in testicular cancer patients. The limitation of this study is that there is no comparison to standard hearing tests.

Reavis et al. (2008) analyzed 53 patients receiving ototoxic medications and showing significant hearing changes in at least one ear. The investigators concluded that DPOAEs are a useful screening tool for ototoxicity in adults with pre-exposure hearing loss, but are less sensitive compared with a behavioral test method that targets thresholds near the upper limit of a subject's audible frequency range.

Stavoulaki et al. (2002) investigated whether transient-evoked and distortion-product (DP) otoacoustic emissions (OAEs) are more sensitive than pure-tone audiometry (PTA) in revealing gentamicin-induced ototoxicity in children with cystic fibrosis (CF) in a prospective case-control study. The study group consisted of a consecutive sample of 12 audiologically normal children with CF and a history of gentamicin exposure (CF-gentamicin group). The control groups consisted of 8 age-matched children with CF and 11 age-matched healthy volunteers. The investigators found that otoacoustic emissions measurement (especially of DP OAEs) proved more sensitive than PTA in revealing minor cochlear dysfunction after gentamicin exposure. They should be used for monitoring patients receiving ototoxic factors such as aminoglycosides. This study is limited by its small sample size.

Arora et al. (2009) conducted a prospective, randomized and observational study to evaluate the effects of different doses of cisplatin on hearing in 57 patients. All patients were divided into three groups depending on the dose of cisplatin infused in 3 weeks. Subjective hearing loss was found in seven patients, while six patients had tinnitus during the chemotherapy. The hearing loss was sensorineural, dose dependent, symmetrical, bilateral and irreversible. Higher frequencies were first to be affected in cisplatin chemotherapy. According to the investigators, high-frequency audiometry should be used to evaluate hearing loss in patients undergoing cisplatin-based chemotherapy.

Well-designed trials with larger sample sizes are needed to demonstrate that OAE testing is as effective as standard hearing tests or has an impact on clinical outcomes such as increasing speech, language, and communication skills in patients with a risk of developing ototoxicity.

Early Identification of Noise-Induced Hearing Loss
Fetoni et al. (2009) evaluated whether distortion product otoacoustic emissions (DPOAEs) can discriminate normal subjects with a risk of damage induced by sound exposure, the effectiveness of OAEs in monitoring the protective effects of Coenzyme Q10 terclatrate (QTer), and the role of blood parameters in monitoring preventive therapies. Twenty volunteers were randomized to two groups: the first (n=10) was treated with Q-Ter (200 mg orally once daily) for 7 days before noise exposure and the second group was treated with placebo using the same schedule. All participants were exposed to white noise of 90 dB HL for 15 minutes. DPOAEs and pure-tone audiometry (PTA) were measured before and 1 h, 16 h, and 7 and 21 days after exposure. Inflammatory and oxidative stress parameters were measured before and 2 and 24 h after exposure. In the placebo group, DPOAE amplitudes were reduced 1 and 16 h after exposure compared with the baseline values. In the Q-Ter group, DPOAEs did not show any significant difference between baseline and post-exposure. PTA threshold values in the Q-Ter and placebo groups did not differ before and after exposure. No significantly different levels of the inflammatory markers were observed in the Q-Ter and placebo groups at the different time points. The investigators concluded that this pilot study confirms that DPOAEs represent a sensitive test for monitoring the effects of noise in preclinical conditions and pharmacological treatment. Further research is needed to confirm this conclusion.

Korres et al. (2009) evaluated noise-induced hearing loss in a group of industrial workers, using distortion product otoacoustic emissions (DPOAEs) in conjunction with standard pure tone audiometry (PTA). A total of 105 subjects were included in the study. PTA, tympanometry, and DPOAEs were performed. Statistically significant lower DPOAE levels were found in the noise-exposed group as compared to the control group. Based on the results of the study, the investigators concluded that DPOAEs and PTA are both sensitive methods in detecting noise-induced hearing loss, with DPOAEs tending to be more sensitive at lower frequencies. These findings require confirmation in a larger study.

In a longitudinal study with 338 volunteers, audiometric thresholds and otoacoustic emissions were measured before and after 6 months of noise exposure on an aircraft carrier. The investigators found significant changes in group audiometric thresholds along with changes in OAEs, but there was little consistency between changes in thresholds and OAEs in individual ears. The study failed to show that OAEs were more sensitive than audiometric thresholds (Lapsley Miller 2006).

In a prospective controlled trial, Shupak et al. (2007) evaluated changes in transient evoked and distortion product otoacoustic emissions (TEOAEs, DPOAEs) as they relate to pure-tone audiometry thresholds during the first 2 years of occupational noise exposure. Pure-tone audiometry thresholds, TEOAE and DPOAE amplitudes, and contralateral medial olivocochlear reflex strength were repeatedly evaluated during 2 years and compared between and within a cohort of 135 ship engine room recruits and a control group of 100 subjects with no noise exposure. Based on the results of the study, the investigators concluded that although TEOAEs changes after 1 year showed high sensitivity in predicting NIHL after 2 years of exposure, they cannot be recommended as an efficient screening tool due to high false-positive rates.

Helleman et al. (2010) assessed the hearing status of workers (n=233) in a printing office twice within seventeen months by pure-tone audiometry and otoacoustic emissions (OAEs). One of the questions was how a quality criterion of OAE measurements based on a minimum signal-to-noise-ratio (SNR) would affect the applicability on the entire population. Secondly, effects of noise exposure were investigated in overall changes in audiogram and OAE measurements. For TEOAEs (transient evoked OAEs) in the frequency band of 4 kHz, only 55% of the data points meet the SNR-inclusion criterion. For DPOAEs (distortion product OAEs) around 6 kHz approximately 80% of the data points satisfy the criterion. On group level, OAEs show a decline in a larger frequency region than the audiogram, suggesting an increased sensitivity of OAEs compared to audiometry. According to the investigators, OAEs have a limited applicability for monitoring the hearing status of this entire population.

Audiometric thresholds and otoacoustic emissions (OAEs) were measured in 285 U.S. Marine Corps recruits before and three weeks after exposure to impulse-noise sources from weapons' fire and simulated artillery, and in 32 non-noise-exposed controls. A subgroup of 60 noise-exposed volunteers with complete data sets for both ears showed significant decreases in OAE amplitude but no change in audiometric thresholds. According to the investigators, the analysis showed an increased sensitivity of OAEs in comparison to audiometric threshold. The investigators also concluded that low-level OAEs indicate an increased risk of future hearing loss by as much as ninefold (Marshall et al. 2009). Although promising, the results of this study cannot be generalized to a larger population because all study participants were young men and the study duration of 13 weeks was too short for aging to have any measurable impact.

Jansen et al. (2009) assessed the hearing status of 241 musicians of professional symphony orchestras to determine if OAEs have an added value in the diagnosis of noise induced hearing loss (NIHL) in musicians. The musicians were subjected to an extensive audiological test battery, which contained testing of audiometric thresholds, loudness perception, diplacusis, tinnitus, speech perception in noise, and otoacoustic emissions. Most musicians could be categorized as normal hearing, but their audiograms show notches at 6 kHz, a frequency that is associated with NIHL. Musicians often complained about tinnitus and hyperacusis, while diplacusis was generally not reported as a problem. Based on the study results, the investigators concluded that otoacoustic emissions were more intense with better pure-tone thresholds, but due to large individual differences it can still not be used as an objective test for early detection of NIHL.

Sudden Hearing Loss
Otoacoustic emissions (OAE) and pure tone audiogram (PTA) were examined in 25 patients suffering from sudden hearing loss from the 1st day to up to 505 days following the drop of hearing to test the hypothesis whether the OAEs are capable of delivering predictive information about the recovery process. Transitory evoked otoacoustic emissions (TEOAE) and distortion product otoacoustic emissions (DPOAE) were measured under constant stimulus and recording conditions in three to nine sessions. The relation between OAE level and actual pure tone threshold was subject to a regression analysis. The correlation between both parameters is small but significant According to the investigators, the reliability of an individual prediction based on the OAE level combined with the threshold after sudden hearing loss and the consequences for the physiologic mechanisms underlying the sudden hearing loss remain to be proved in further investigations (Hoth, 2005).

Canale (2005) assessed whether OAEs could be considered as a reliable prognostic test in low frequency sudden hearing loss (LFSHL). The study group consisted of 20 patients presenting with a unilateral LFSHL. Each patient was submitted to spontaneous otoacoustic emissions (SOAEs), transient otoacoustic emissions (TEOAEs) and distortion products (DPOAEs) recording and then treated with glycerol administrated intravenously in 3-h intervals for 4 days. Pure tone audiometry (PTA) threshold was evaluated again 1 hour after the last administration of glycerol. The relationship between the pretherapy presence or absence of SOAEs, TEOAEs and DPOAEs and PTA modification was not significant at the exact Fisher's test. The investigators concluded that even if the results of the study supports the use of OAEs as an indicator of the inner ear functional state, they cannot be utilized as a prognostic test in LFSHL in relation to the efficacy of osmotic therapy. Among the other parameters evaluated, only the precocity of therapy seems to be related to prognosis in LFSHL.

Other Indications Such as Tinnitus and Acoustic Trauma
Santaolalla et al. (2007) investigated otoacoustic emissions (OAEs) in 44 patients with tinnitus using Spontaneous Otoacoustic Emissions (SOAEs) and Transitory Evoked Otoacoustic Emissions (TEOAEs). A correlation was determined between the OAEs results and the results obtained using hearing thresholds. Statistically significant differences at 500, 1000, 2000, 4000 and 8000 Hz frequencies were not found at mean hearing thresholds between the sample of ears with tinnitus and the sample of ears without tinnitus. Based on the results of the study, the investigators concluded that there is no significant relation between tinnitus and OAEs registration.

Kim et al. (2011) defined the clinical and audiological features of normal-hearing tinnitus patients with spontaneous otoacoustic emissions, and evaluated the role of spontaneous otoacoustic emissions in tinnitus generation. Thirty-two patients with spontaneous otoacoustic emissions were compared with 29 patients without spontaneous otoacoustic emissions, regarding clinical and audiological aspects. The study group had significantly quieter tinnitus, and higher transient evoked and distortion product otoacoustic emission responses, compared with the control group. According to the investigators, normal-hearing tinnitus patients with spontaneous otoacoustic emissions have different clinical and audiological characteristics, compared with those without spontaneous otoacoustic emissions. Appropriate evaluation and treatment should be considered at an early stage in these patients. These findings require confirmation in a larger study.

Nottet et al (2006) evaluated the possible predictive value of hearing thresholds and otoacoustic emissions during the first 24 hours after acoustic trauma. A group of 24 young military subjects without any otologic problem before the acoustic trauma were examined at three time intervals after an accidental acoustic trauma caused by the discharge of a firearm: 24 hours, 72 hours, and 15 days. Pure tone audiometry was performed from 1 to 8 kHz per half octave. Transiently evoked otoacoustic emissions were recorded in the nonlinear mode at 80 dB pSPL, and distortion product otoacoustic emissions were recorded from 1 to 6 kHz, using a distortion product-gram type procedure, at 65/55 dB SPL, with f2/f1 = 1.22. Two groups of subjects were defined: group 1 (n = 8) represented subjects with short-lasting tinnitus (less than72 hours) and group 2 (n = 16) subjects with long-lasting tinnitus (greater than 72 hours). Hearing thresholds did not differ significantly between these two groups 24 hours after the acoustic trauma. However, otoacoustic emissions showed significantly lower amplitudes 24 hours after the acoustic trauma in subjects showing a longer lasting tinnitus. The investigators concluded that otoacoustic emissions appear to be a better predictor of the persistence of tinnitus than hearing thresholds alone 24 hours after an acute acoustic trauma. These findings require confirmation in a larger study.

Otoacoustic emissions (OAEs) testing has also been used for other indications such as evaluating pseudohypacusis (Balatsouras, 2003), facioscapulohumeral muscular dystrophy (Balatsouras, 2007), diagnosing endolymphatic hydrops (Rotter, 2008), and evaluating vestibular schwannoma (Ferri, 2009). The evidence is insufficient to determine the usefulness of OAE testing to diagnose or manage these conditions.

Professional Societies and Guidelines
American Academy of Pediatrics (AAP): In a clinical report for hearing assessment in infants and children, the AAP states that ABR and OAEs are tests of auditory pathway structural integrity but are not true tests of hearing. Even if ABR or OAE test results are normal, hearing cannot be definitively considered normal until a child is mature enough for a reliable behavioral audiogram to be obtained. Behavioral pure-tone audiometry remains the standard for hearing evaluation. According to the AAP, a failed infant hearing screening or a failed screening in an older child should always be confirmed by further testing. Audiologists may repeat the audiometric tests in a sound booth and using a variety of other tests. ABR can also be used for definitive testing of the auditory system. Diagnostic ABR is often the definitive test used by audiologists in children and infants who are unable to cooperate with other methods of hearing testing. A diagnostic ABR is usually performed under sedation or general anesthesia in children aged approximately 3 to 6 months and older. Diagnostic ABR provides information that is accurate enough to allow for therapeutic intervention. According to the AAP, the OAE test also does not assess the integrity of the neural transmission of sound from the eighth nerve to the brainstem and, therefore, will miss auditory neuropathy and other neuronal abnormalities. Infants with such abnormalities will have normal OAE test results but abnormal auditory brainstem response (ABR) test results. A failed OAE test only implies that a hearing loss of more than 30 to 40 dB may exist or that the middle-ear status is abnormal (Harlor, 2009).

In a policy statement for the pediatrician's role in the diagnosis and management of autistic spectrum disorder in children, the AAP states that any child who has language delays should be referred for an audiologic and a comprehensive speech and language evaluation. If the child is uncooperative, diagnostic otoacoustic emissions or sedated brainstem auditory evoked responses should be obtained (AAP, 2001).

The Joint Committee on Infant Hearing (JCIH): The JCIH which includes organizations such as the American Academy of Pediatrics (AAP), the American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS), the American Academy of Audiology (AAA), and American Speech-Language-Hearing Association (ASHA), has a published position statement on principles and guidelines for early hearing detection and intervention programs. According to the JCIH, all infants, regardless of newborn hearing-screening outcome, should receive ongoing monitoring for development of age-appropriate auditory behaviors and communication skills. Any infant who demonstrates delayed auditory and/or communication skills development, even if he or she passed newborn hearing screening, should receive an audiological evaluation to rule out hearing loss. The JCIH recommends that subsequent audiologic assessments for infants and children from birth to 36 months of age should include OAE testing. The JCIH indicates that infants with hearing loss related to neural conduction disorders or auditory neuropathy/auditory dyssynchrony may not be detected through the use of otoacoustic emission [OAE] testing alone. Because these disorders typically occur in children who require NICU care, the JCIH recommends screening this group with the technology capable of detecting auditory neuropathy/dyssynchrony: automated ABR measurement (JCIH, 2007).

American Academy of Neurology (AAN): In a practice parameter for the evaluation of the child with global developmental delay, the AAN recommends that audiometric assessment for children with global developmental delay can include behavioral audiometry or brainstem auditory evoked response testing when feasible (Level C; class III evidence). The AAN also states that early evidence from screening studies suggests that transient evoked otoacoustic emissions should offer an alternative when audiometry is not feasible (Level A; class I & II evidence). Level A rating requires at least one convincing class I study or at least two consistent, convincing class II studies. According to the AAN, global developmental delay is a subset of developmental disabilities defined as significant delay in two or more of the following developmental domains: gross/fine motor, speech/language, cognition, social/personal, and activities of daily living. The term global developmental delay is usually reserved for younger children (i.e., typically less than 5 years of age) (Shevell, 2003).

American Speech-Language-Hearing Association (ASHA): In the Audiologic screening section of the Preferred Practice Patterns for the Profession of Audiology, ASHA indicates that OA may be used to monitor for toxicity before, during, and after administration of or exposure to agents known to be toxic (e.g., aminoglycosides, chemotherapy agents, and heavy metals) (ASHA, 2006). In a Guideline for Audiologic Screening, the ASHA indicates that evoked otoacoustic emissions (OAE) are suggested as an alternative procedure for infants and children (through age 2) when behavioral audiologic methods are ineffective (ASHA, 1997).

In a 2004 Guideline for the Audiologic Assessment of Children from Birth to 5 Years of Age, the ASHA specified the following assessment protocols for children (ASHA, 2004):
  • Assessment Protocol for Children Who Are Chronologically/Developmentally Birth Through 4 Months of Age (Age Adjusted for Prematurity): At these very young ages, or for children with severe developmental delays or multiple health conditions, the suggested methods for comprehensive assessment rely primarily on physiologic measures of auditory function: ABR [and/or auditory steady-state response (ASSR)] using frequency-specific stimuli are used to estimate the audiogram; ABR using click stimuli is used to assess VIIIth nerve integrity. OAEs and acoustic immittance measures are used to supplement and corroborate the evoked-potential findings. The results of these physiologic measures should always be considered in combination with case history, parent/caregiver report, and behavioral observation of the infant's responses to a variety of auditory stimuli. The behavioral observation is intended for corroboration of parent/caregiver report of the child's auditory behavior rather than for threshold estimation.

  • Assessment Protocols for Children Who Are Chronologically/Developmentally 5 through 24 Months of Age (Age Adjusted for Prematurity): OAEs and auditory brainstem response (ABRs). When behavioral audiometric tests are judged to be unreliable, ear-specific thresholds cannot be obtained, or when results are inconclusive regarding type, degree, or configuration of hearing levels, (evoked) EOAEs and/or ABR testing should be completed. In addition, if the neurological integrity of the auditory system through the level of the brainstem is in question, ABR testing should be conducted.

  • Assessment Protocol for Children Who Are Chronologically/Developmentally 25 to 60 Months of Age (Adjusted for Prematurity): OAE and ABR are recommended when the validity or adequacy (ear-specific information) of behavioral test results is limited or if the neurologic integrity of the auditory pathways to the level of the brainstem is in question. When ear-specific information cannot be obtained, EOAE testing should be completed for each ear. If EOAE (TEOAE or DPOAE) responses are not present at expected levels across the frequency range, ABR testing should be conducted.

U.S. Food and Drug Administration (FDA)
There are a number of diagnostic auditory brainstem response (ABR), automated ABR, transient evoked otoacoustic emissions (EOAE), and distortion EOAE devices currently approved for marketing by the FDA. These devices are designated by the FDA as Class II medical devices suitable for infant and adult hearing assessment.

See the following Web site for more information: http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfPMN/pmn.cfm. Accessed April 2011. Use product codes GWJ (evoked response auditory stimulator) or EWO [(audiometer); otoacoustic emission test]. Note that not all of these clearances are for otoacoustic emission testing.

Note that devices in product category EWO (audiometer) are 510(k) exempt devices. Although manufacturers may voluntarily submit product information via the 510(k) process, it is not a requirement. All manufacturers are, however, required to register their establishment and submit a "Device Listing" form.

Policy and Rationale:
Oxford will provide coverage for otoacoustic emissions (OAEs) testing as outlined in the Treatment/Application Guidelines section of this policy.

Treatment/Application Guidelines:

Neonatal hearing screening using otoacoustic emissions (OAEs) is medically necessary for infants who are 90 days or younger.

Otoacoustic emissions (OAEs) testing is medically necessary for the evaluation of hearing loss in the following:
  • infants and children up to 3 years of age
  • children and adults who are or who are unable to cooperate with other methods of hearing testing (e.g. individuals with autism or stroke)
Auditory screening or diagnostic testing using otoacoustic emissions (OAEs) is not medically necessary for all other patient populations and conditions including ototoxic hearing changes in individuals treated with ototoxic medications.

There is inadequate evidence that hearing screening with OAEs is superior to screening audiometry in improving health outcomes such as timely facilitation of speech, language, and communication skills in older children or adults. There is also inadequate evidence to indicate that the use of diagnostic otoacoustic emissions (OAEs) testing is superior to screening audiometry in improving health outcomes such as timely facilitation of speech, language, and communication skills in patients with other conditions such as ototoxic hearing changes in individuals treated with ototoxic medications, noise-induced hearing loss, sudden hearing loss, tinnitus, and other suspected hearing loss.

Payment Guidelines:

CPT® Code Description
92558 Evoked otoacoustic emissions, screening (qualitative measurement of distortion product or transient evoked otoacoustic emissions), automated analysis (Effective 1/1/2012)
92587 Distortion product evoked otoacoustic emissions; limited evaluation (to confirm the presence or absence of hearing disorder, 3-6 frequencies) or transient evoked otoacoustic emissions, with interpretation and report
92588 Distortion product evoked otoacoustic emissions; comprehensive diagnostic evaluation (quantitative analysis of outer hair cell function by cochlear mapping, minimum of 12 frequencies), with interpretation and report
CPT® is a registered trademark of the American Medical Association.

ICD-9 Code Description
045.0 Acute paralytic poliomyelitis specified as bulbar
045.00 Acute paralytic poliomyelitis specified as bulbar, unspecified poliovirus
045.01 Acute paralytic poliomyelitis specified as bulbar, poliovirus type I
045.02 Acute paralytic poliomyelitis specified as bulbar, poliovirus type II
045.03 Acute paralytic poliomyelitis specified as bulbar, poliovirus type II
045.10 Acute poliomyelitis with other paralysis, unspecified poliovirus
045.11 Acute poliomyelitis with other paralysis, poliovirus type I
045.12 Acute poliomyelitis with other paralysis, poliovirus type II
045.13 Acute poliomyelitis with other paralysis, poliovirus type III
045.9 Acute unspecified poliomyelitis
045.90 Acute unspecified poliomyelitis, unspecified poliovirus
045.91 Acute unspecified poliomyelitis, poliovirus type I
045.92 Acute unspecified poliomyelitis, poliovirus type II
045.93 Acute unspecified poliomyelitis, poliovirus type III
138 Late effects of acute poliomyelitis
290.0 Senile dementia, uncomplicated
290.10 Presenile dementia, uncomplicated
290.11 Presenile dementia with delirium
290.12 Presenile dementia with delusional features
290.13 Presenile dementia with depressive features
290.20 Senile dementia with delusional features
290.21 Senile dementia with depressive features
290.3 Senile dementia with delirium
290.40 Vascular dementia, uncomplicated
290.41 Vascular dementia with delirium
290.42 Vascular dementia with delusions
290.43 Vascular dementia with depressed mood
299.00 Autistic disorder, current or active state
299.01 Autistic disorder, residual state
299.10 Childhood disintegrative disorder, current or active state
299.11 Childhood disintegrative disorder, residual state
299.80 Other specified pervasive developmental disorders, current or active state
299.81 Other specified pervasive developmental disorders, residual state
299.90 Unspecified pervasive developmental disorder, current or active state
299.91 Unspecified pervasive developmental disorder, residual state
306.0 Musculoskeletal malfunction arising from mental factors
310.9 Unspecified nonpsychotic mental disorder following organic brain damage
314.00 Attention deficit disorder of childhood without mention of hyperactivity
314.01 Attention deficit disorder of childhood with hyperactivity
314.1 Hyperkinesis of childhood with developmental delay
314.2 Hyperkinetic conduct disorder of childhood
315.2 Other specific developmental learning difficulties
315.4 Developmental coordination disorder
317 Mild mental retardation
318.0 Moderate mental retardation
318.1 Severe mental retardation
318.2 Profound mental retardation
319 Unspecified mental retardation
331.0 Alzheimer's disease
332.0 Paralysis agitans
333.0 Other degenerative diseases of the basal ganglia
333.71 Athetoid cerebral palsy
337.09 Other idiopathic peripheral autonomic neuropathy
343.0 Diplegic infantile cerebral palsy
343.1 Hemiplegic infantile cerebral palsy
343.2 Quadriplegic infantile cerebral palsy
343.3 Monoplegic infantile cerebral palsy
343.4 Infantile hemiplegia
343.8 Other specified infantile cerebral palsy
343.9 Unspecified infantile cerebral palsy
344.89 Other specified paralytic syndrome
344.9 Unspecified paralysis
348.1 Anoxic brain damage
352.6 Multiple cranial nerve palsies
356.8 Other specified idiopathic peripheral neuropathy
359.3 Periodic paralysis
436 Acute, but ill-defined, cerebrovascular disease
437.0 Cerebral atherosclerosis
437.1 Other generalized ischemic cerebrovascular disease
437.8 Other ill-defined cerebrovascular disease
438 Late effects of cerebrovascular disease
758.0 Down's syndrome
781.4 Transient paralysis of limb
806.00 Closed fracture of C1-C4 level with unspecified spinal cord injury
806.01 Closed fracture of C1-C4 level with complete lesion of cord
806.02 Closed fracture of C1-C4 level with anterior cord syndrome
806.03 Closed fracture of C1-C4 level with central cord syndrome
806.04 Closed fracture of C1-C4 level with other specified spinal cord injury
806.05 Closed fracture of C5-C7 level with unspecified spinal cord injury
806.06 Closed fracture of C5-C7 level with complete lesion of cord
806.07 Closed fracture of C5-C7 level with anterior cord syndrome
806.08 Closed fracture of C5-C7 level with central cord syndrome
806.09 Closed fracture of C5-C7 level with other specified spinal cord injury
806.10 Open fracture of C1-C4 level with unspecified spinal cord injury
806.11 Open fracture of C1-C4 level with complete lesion of cord
806.12 Open fracture of C1-C4 level with anterior cord syndrome
806.13 Open fracture of C1-C4 level with central cord syndrome
806.14 Open fracture of C1-C4 level with other specified spinal cord injury
806.15 Open fracture of C5-C7 level with unspecified spinal cord injury
806.16 Open fracture of C5-C7 level with complete lesion of cord
806.17 Open fracture of C5-C7 level with anterior cord syndrome
806.18 Open fracture of C5-C7 level with central cord syndrome
806.19 Open fracture of C5-C7 level with other specified spinal cord injury
806.20 Closed fracture of T1-T6 level with unspecified spinal cord injury
806.21 Closed fracture of T1-T6 level with complete lesion of cord
806.22 Closed fracture of T1-T6 level with anterior cord syndrome
806.23 Closed fracture of T1-T6 level with central cord syndrome
806.24 Closed fracture of T1-T6 level with other specified spinal cord injury
806.25 Closed fracture of T7-T12 level with unspecified spinal cord injury
806.26 Closed fracture of T7-T12 level with complete lesion of cord
806.27 Closed fracture of T7-T12 level with anterior cord syndrome
806.28 Closed fracture of T7-T12 level with central cord syndrome
806.29 Closed fracture of T7-T12 level with other specified spinal cord injury
806.30 Open fracture of T1-T6 level with unspecified spinal cord injury
806.31 Open fracture of T1-T6 level with complete lesion of cord
806.32 Open fracture of T1-T6 level with anterior cord syndrome
806.33 Open fracture of T1-T6 level with central cord syndrome
806.34 Open fracture of T1-T6 level with other specified spinal cord injury
806.35 Open fracture of T7-T12 level with unspecified spinal cord injury
806.36 Open fracture of T7-T12 level with complete lesion of cord
806.37 Open fracture of T7-T12 level with anterior cord syndrome
806.38 Open fracture of T7-T12 level with central cord syndrome
806.39 Open fracture of T7-T12 level with other specified spinal cord injury
806.4 Closed fracture of lumbar spine with spinal cord injury
806.5 Open fracture of lumbar spine with spinal cord injury
806.60 Closed fracture of sacrum and coccyx with unspecified spinal cord injury
806.61 Closed fracture of sacrum and coccyx with complete cauda equina lesion
806.62 Closed fracture of sacrum and coccyx with other cauda equina injury
806.69 Closed fracture of sacrum and coccyx with other spinal cord injury
806.7 Open fracture of sacrum and coccyx with spinal cord injury
806.70 Sacrum and coccyx, open; With unspecified spinal cord injury
806.71 Sacrum and coccyx, open; With complete cauda equina lesion
806.72 Sacrum and coccyx, open; With other cauda equina injury
806.79 Sacrum and coccyx, open; With other spinal cord injury
997.02 Iatrogenic cerebrovascular infarction or hemorrhage
V12.54 Personal history of transient ischemic attack [TIA], and cerebral infarction without residual deficits

References:

  1. American Academy of Pediatrics. Newborn and Infant hearing loss: Detection and Intervention (RE9846). Pediatrics. 1999;103:527-530.

  2. American Academy of Pediatrics. The Pediatrician's Role in the Diagnosis and Management of Autistic Spectrum Disorder in Children 2001 Available at: http://aappolicy.aappublications.org/cgi/reprint/pediatrics;107/5/1221.pdf. Accessed April 2011.

  3. American Speech-Language-Hearing Association. (2006). Preferred Practice Patterns for the Profession of Audiology. Available from www.asha.org/policy. Accessed April 2011

  4. American Speech-Language-Hearing Association. (1997). Guidelines for Audiologic Screening Available at: www.asha.org/policy. Accessed April 2011.

  5. American Speech-Language-Hearing Association. (2004). Guidelines for the Audiologic Assessment of Children from Birth to 5 Years of Age Available at: http://www.asha.org/docs/html/GL2004-00002.html. Accessed April 2011.

  6. Amiridavan, M, Nemati, S, Hashemi, SM, Jamshidi, M, Saberi, A, and, AM. Otoacoustic emissions and auditory brainstem responses in patiens with sudden sensorineural hearing loss. Do otoacoustic emissions have prognostic value? Journal of Research in Medical Sciences. 2006;11(4):263-269.

  7. Arora R, Thakur JS, Azad RK, Mohindroo NK, Sharma DR, Seam RK. Cisplatin-based chemotherapy: Add high-frequency audiometry in the regimen. Indian J Cancer. 2009 Oct-Dec;46(4):311-7.

  8. Attias J, Bresloff I, Reshef I, Horowitz G, Furman V. Evaluating noise induced hearing loss with distortion product otoacoustic emissions. Br J Audiol. 1998 Feb;32(1):39-46.

  9. Balatsouras DG, Kaberos A, Korres S, et al. Detection of pseudohypacusis: a prospective, randomized study of the use of otoacoustic emissions. Ear Hear. 2003 Dec;24(6):518-827.

  10. Balatsouras DG, Korres S, Manta P, et al. Cochlear function in facioscapulohumeral muscular dystrophy. Otol Neurotol. 2007 Jan;28(1):7-10.

  11. Berg, AL, Papri, H, Ferdous, S, Khan, NZ, Durkin, MS. Screening methods for childhood hearing impairment in rural Bangladesh. Int J Pediatr Otorhinolaryngol 2006;70(1):107-114.

  12. Bertoli S, Probst R. The role of transient-evoked otoacoustic emission testing in the evaluation of elderly persons. Ear Hear. 1997 Aug;18(4):286-93.

  13. Biro K, Noszek L, Prekopp P, et al. Characteristics and risk factors of cisplatin-induced ototoxicity in testicular cancer patients detected by distortion product otoacoustic emission. Oncology. 2006;70(3):177-84.

  14. Canale A, Lacilla M, Giordano C, et al. The prognostic value of the otoacoustic emission test in low frequency sudden hearing loss. Eur Arch Otorhinolaryngol. 2005 Mar;262(3):208-12.

  15. Chiong C, Ostrea E Jr, Reyes A, et al. Correlation of hearing screening with developmental outcomes in infants over a 2-year period. Acta Otolaryngol. 2007 Apr;127(4):384-8.

  16. Delehaye E, Capobianco S, Bertetto IB, et al. Distortion-product otoacoustic emission: early detection in deferoxamine induced ototoxicity. Auris Nasus Larynx. 2008 Jun;35(2):198-202.

  17. Dhooge I, Dhooge C, Geukens S, et al. Distortion product otoacoustic emissions: an objective technique for the screening of hearing loss in children treated with platin derivatives. Int J Audiol. 2006 Jun;45(6):337-43.

  18. Dille, M, Glattke, TJ, and Earl, BR. Comparison of transient evoked otoacoustic emissions and distortion product otoacoustic emissions when screening hearing in preschool children in a community setting. Int J Pediatr Otorhinolaryngol. 2007;71(11):1789-1795.

  19. Driscoll C, Kei J, McPherson B. Outcomes of transient evoked otoacoustic emission testing in 6-year-old school children: a comparison with pure tone screening and tympanometry. Int J Pediatr Otorhinolaryngol. 2001 Jan;57(1):67-76. PubMed PMID: 11165644.

  20. ECRI Institute. Hotline Response. Hearing Screening for Infants. May 2006.

  21. ECRI Institute. Hotline Response. Otoacoustic Emission Testing for Screening and Diagnosing Hearing Loss in Children, Adolescents, and Adults. April 2010.

  22. Eiserman, WD, Hartel, DM, Shisler, L, et al. Using otoacoustic emissions to screen for hearing loss in early childhood care settings. Int J Pediatr Otorhinolaryngol. 2008;72(4):475-482.

  23. Ellison, JC, Keefe, DH. Audiometric predictions using stimulus-frequency otoacoustic emissions and middle ear measurements. Ear Hear. 2005;26(5):487-503.

  24. Engdahl, B, Tambs, K, Borchgrevink, HM, et al. Otoacoustic emissions in the general adult population of Nord-Trondelag, Norway: III. Relationships with pure-tone hearing thresholds. Int J Audiol. 2005;44(1):15-23.

  25. Engdahl B, Woxen O, Arnesen AR, et al. Transient evoked otoacoustic emissions as screening for hearing losses at the school for military training. Scand Audiol. 1996;25(1):71-8.

  26. Ferri GG, Modugno GC, Calbucci F, et al. Hearing loss in vestibular schwannomas: analysis of cochlear function by means of distortion-product otoacoustic emissions. Auris Nasus Larynx. 2009 Dec;36(6):644-8.

  27. Fetoni AR, Garzaro M, Ralli M, et al. The monitoring role of otoacoustic emissions and oxidative stress markers in the protective effects of antioxidant administration in noise-exposed subjects: a pilot study. Med Sci Monit. 2009 Nov;15(11):PR1-8.

  28. François M, Laccourreye L, Huy ET, et al. Hearing impairment in infants after meningitis: detection by transient evoked otoacoustic emissions. J Pediatr. 1997 May;130(5):712-7.

  29. Georgalas, C, Xenellis, J, Davilis, D, et al. Screening for hearing loss and middle-ear effusion in school-age children, using transient evoked otoacoustic emissions: a feasibility study. J Laryngol Otol. 2008;122(12):1299-1304.

  30. Grenner J, Tideholm B, Hinriksdóttir I, et al. Hearing thresholds in four-year-old children with weak or no transient-evoked otoacoustic emissions. Scand Audiol. 1997;26(2):107-11.

  31. Hamill-Ruth RJ, Ruth RA. Evaluation of audiologic impairment in critically ill patients: results of a screening protocol. Crit Care Med. 2003 Sep;31(9):2271-7.

  32. Harlor AD Jr, Bower C; Committee on Practice and Ambulatory Medicine; Section on Otolaryngology-Head and Neck Surgery. Hearing assessment in infants and children: recommendations beyond neonatal screening. Pediatrics. 2009 Oct;124(4):1252-63.

  33. Hassmann E, Skotnicka B, Midro AT, et al. Distortion products otoacoustic emissions in diagnosis of hearing loss in Down syndrome. Int J Pediatr Otorhinolaryngol. 1998 Oct 15;45(3):199-206.

  34. Hatzopoulos, S, Ciorba, A, Petruccelli, J, et al. Estimation of pure-tone thresholds in adults using extrapolated distortion product otoacoustic emission input/output-functions and auditory steady state responses. Int J Audiol. 2009;48(9):625-631.

  35. Hayes Directory. Neonatal hearing screening. July 25, 2005. Last update August 2009. Archived August 2010.

  36. Helleman HW, Jansen EJ, Dreschler WA. Otoacoustic emissions in a hearing conservation program: general applicability in longitudinal monitoring and the relation to changes in pure-tone thresholds. Int J Audiol. 2010 Jun;49(6):410-9.

  37. Hild U, Hey C, Baumann U, et al High prevalence of hearing disorders at the Special Olympics indicate need to screen persons with intellectual disability. J Intellect Disabil Res. 2008 Jun;52(Pt 6):520-8.

  38. Hoth S. On a possible prognostic value of otoacoustic emissions: a study on patients with sudden hearing loss. Eur Arch Otorhinolaryngol. 2005 Mar;262(3):217-24.

  39. Hotz MA, Ritz R, Linder L, et al. Auditory and electroencephalographic effects of midazolam and alpha-hydroxy-midazolam in healthy subjects. Br J Clin Pharmacol. 2000 Jan;49(1):72-9.

  40. Hunter, LL, Davey, CS, Kohtz, A et al. Hearing screening and middle ear measures in American Indian infants and toddlers. Int J Pediatr Otorhinolaryngol. 2007;71(9):1429-1438.

  41. Jansen EJ, Helleman HW, Dreschler WA, et al. Noise induced hearing loss and other hearing complaints among musicians of symphony orchestras. Int Arch Occup Environ Health. 2009 Jan;82(2):153-64.

  42. Job A, Raynal M, Kossowski M, et al. Otoacoustic detection of risk of early hearing loss in ears with normal audiograms: a 3-year follow-up study. Hear Res. 2009 May;251(1-2):10-6.

  43. Joint Committee on Infant Hearing (JCIH) American Academy of Audiology/American Academy of Pediatrics/ (AAP)/ American Speech-Language-Hearing Association/Directors of Speech and Hearing Programs in State Health and Welfare Agencies: Year 2007 Position Statement Principles and Guidelines for Early Hearing Detection and Intervention Programs published online October 1, 2007 in Pediatrics Vol. 120 No. 4 October 2007, pp. 898-921 (doi:10.1542/peds.2007-2333).

  44. Jupiter T. Screening for hearing loss in the elderly using distortion product otoacoustic emissions, pure tones, and a self-assessment tool. Am J Audiol. 2009 Dec;18(2):99-107.

  45. Kim DK, Park SN, Park KH, et al. Clinical characteristics and audiological significance of spontaneous otoacoustic emissions in tinnitus patients with normal hearing. J Laryngol Otol. 2011 Mar;125(3):246-50.

  46. Kim DO, Paparello J, Jung MD,et al. Distortion product otoacoustic emission test of sensorineural hearing loss: performance regarding sensitivity, specificity and receiver operating characteristics. Acta Otolaryngol. 1996 Jan;116(1):3-11.

  47. Kirkim G, Serbetçioglu MB, Ceryan K. Auditory neuropathy in children: diagnostic criteria and audiological test results. Kulak Burun Bogaz Ihtis Derg. 2005;15(1-2):1-8.

  48. Korres GS, Balatsouras DG, Tzagaroulakis A, et al. Distortion product otoacoustic emissions in an industrial setting. Noise Health. 2009 Apr-Jun;11(43):103-10.

  49. Krueger WW, Ferguson L. A comparison of screening methods in school-aged children. Otolaryngol Head Neck Surg. 2002 Dec;127(6):516-9.

  50. Lapsley Miller JA, Marshall L, Heller LM, et al. Low-level otoacoustic emissions may predict susceptibility to noise-induced hearing loss. J Acoust Soc Am. 2006 Jul;120(1):280-96.

  51. Llanes EG, Chiong CM. Evoked otoacoustic emissions and auditory brainstem responses: concordance in hearing screening among high-risk children. Acta Otolaryngol. 2004 May;124(4):387-90.

  52. Lucertini M, Moleti A, Sisto R. On the detection of early cochlear damage by otoacoustic emission analysis. J Acoust Soc Am. 2002 Feb;111(2):972-8.

  53. Lyons A, Kei J, Driscoll C. Distortion product otoacoustic emissions in children at school entry: a comparison with pure-tone screening and tympanometry results. J Am Acad Audiol. 2004 Nov-Dec;15(10):702-15.

  54. Marshall L, Lapsley Miller JA, et al. Detecting incipient inner-ear damage from impulse noise with otoacoustic emissions. J Acoust Soc Am. 2009 Feb;125(2):995-1013.

  55. National Institutes of Health (NIH) [website]. Early Identification of Hearing Impairment in Infants and Young Children. NIH Consensus Statement Online 1993 Mar 1-3;11(1):1-24. Available at: http://consensus.nih.gov/1993/1993HearingInfantsChildren092html.htm. Accessed April 2011.

  56. Nozza RJ, Sabo DL, Mandel EM. A role for otoacoustic emissions in screening for hearing impairment and middle ear disorders in school-age children. Ear Hear. 1997 Jun;18(3):227-39.

  57. Nottet JB, Moulin A, Brossard N, et al. Otoacoustic emissions and persistent tinnitus after acute acoustic trauma. Laryngoscope. 2006 Jun;116(6):970-5.

  58. Pavlovcinová G, Jakubíková J, Trnovec T, et al. A normative study of otoacoustic emissions, ear asymmetry, and gender effect in healthy schoolchildren in Slovakia. Int J Pediatr Otorhinolaryngol. 2010 Feb;74(2):173-7.

  59. Reavis KM, McMillan G, Austin D, et al. Distortion-product otoacoustic emission test performance for ototoxicity monitoring. Ear Hear. 2011 Feb;32(1):61-74.

  60. Reavis KM, Phillips DS, Fausti SA, et al. Factors affecting sensitivity of distortion-product otoacoustic emissions to ototoxic hearing loss. Ear Hear. 2008 Dec;29(6):875-93.

  61. Ress BD, Sridhar KS, Balkany TJ, et al. Effects of cis-platinum chemotherapy on otoacoustic emissions: the development of an objective screening protocol. Third place--Resident Clinical Science Award 1998. Otolaryngol Head Neck Surg. 1999 Dec;121(6):693-701.

  62. Richardson MP, Williamson TJ, Lenton SW, et al. Otoacoustic emissions as a screening test for hearing impairment in children. Arch Dis Child. 1995 Apr;72(4):294-7.

  63. Richardson MP, Williamson TJ, Reid A, et al. Otoacoustic emissions as a screening test for hearing impairment in children recovering from acute bacterial meningitis. Pediatrics. 1998 Dec;102(6):1364-8.

  64. Rotter, A, Weikert, S, Hensel, J, et al. Low-frequency distortion product otoacoustic emission test compared to ECoG in diagnosing endolymphatic hydrops. Eur Arch Otorhinolaryngol. 2008;265(6):643-649.

  65. Sabo MP, Winston R, Macias JD. Comparison of pure tone and transient otoacoustic emissions screening in a grade school population. Am J Otol. 2000 Jan;21(1):88-91.

  66. Santaolalla Montoya F, Ibargüen AM, del Rey AS, et al. Evaluation of cochlear function in patients with tinnitus using spontaneous and transitory evoked otoacoustic emissions. J Otolaryngol. 2007 Oct;36(5):296-302.

  67. Shevell M, et al. Quality Standards Subcommittee of the American Academy of Neurology and the Practice Committee of the Child Neurology Society. Practice parameter: evaluation of the child with global developmental delay: report of the Quality Standards Subcommittee of the American Academy of Neurology and The Practice Committee of the Child Neurology Society. Neurology 2003 Feb 11;60(3):367-80. Reaffirmed October 15, 2005. Available at: http://www.neurology.org/cgi/reprint/60/3/367.pdf. Accessed April 2011.

  68. Shupak A, Tal D, Sharoni Z, et al. Otoacoustic emissions in early noise-induced hearing loss. Otol Neurotol. 2007 Sep;28(6):745-52.

  69. Sideris I, Glattke TJ. A comparison of two methods of hearing screening in the preschool population. J Commun Disord. 2006 Nov-Dec;39(6):391-401.

  70. Sliwa L, Hatzopoulos S, Kochanek K, et al. A comparison of audiometric and objective methods in hearing screening of school children. A preliminary study. Int J Pediatr Otorhinolaryngol. 2011 Apr;75(4):483-8.

  71. Stavroulaki P, Apostolopoulos N, Segas J, et al. Evoked otoacoustic emissions--an approach for monitoring cisplatin induced ototoxicity in children. Int J Pediatr Otorhinolaryngol. 2001 May 31;59(1):47-57.

  72. Stavroulaki P, Vossinakis IC, Dinopoulou D, et al. Otoacoustic emissions for monitoring aminoglycoside-induced ototoxicity in children with cystic fibrosis. Arch Otolaryngol Head Neck Surg. 2002 Feb;128(2):150-5.

  73. Tas A, Yagiz R, Tas M, et al. Evaluation of hearing in children with autism by using TEOAE and ABR. Autism. 2007 Jan;11(1):73-9.

  74. Tharpe AM, Bess FH, Sladen DP, et al. Auditory characteristics of children with autism. Ear Hear. 2006 Aug;27(4):430-41.

  75. Uchida Y, Ando F, Nakata S, et al. Distortion product otoacoustic emissions and tympanometric measurements in an adult population-based study. Auris Nasus Larynx. 2006 Dec;33(4):397-401.

  76. Uchida Y, Ando F, Shimokata H, et al. The effects of aging on distortion-product otoacoustic emissions in adults with normal hearing. Ear Hear. 2008 Apr;29(2):176-84.

  77. US Preventive Services Task Force. Universal screening for hearing loss in newborns: US Preventive Services Task Force recommendation statement. Pediatrics. 2008 Jul;122(1):143-8. See the following Web site for more information: http://www.ahrq.gov/clinic/pocketgd1011/pocketgd1011.pdf Accessed April 2011.

  78. Vasconcelos, RM, Serra, LS, and Aragao, VM. Transient evoked otoacustic emissions and distortion product in school children. Braz J Otorhinolaryngol. 2008;74(4):503-507.

  79. Vatovec J, Velickovic Perat M, Smid L, et al. Otoacoustic emissions and auditory assessment in infants at risk for early brain damage. Int J Pediatr Otorhinolaryngol. 2001 Apr 27;58(2):139-45.

  80. Wagner W, Heppelmann G, Vonthein R, et al. Test-retest repeatability of distortion product otoacoustic emissions. Ear Hear. 2008 Jun;29(3):378-91.

  81. Wang YF, Wang SS, Tai CC, et al. Hearing screening with portable screening pure-tone audiometer and distortion-product otoacoustic emissions. Zhonghua Yi Xue Za Zhi (Taipei). 2002 Jun;65(6):285-92.

  82. Wessex Universal Hearing Screening Trial Group. Controlled trial of universal neonatal screening for early identification of permanent childhood hearing impairment. Lancet. 1998;352(9145):1957-1964.

  83. Yílmaz S, Oktem F, Karaman E. Detection of cisplatin-induced ototoxicity with transient evoked otoacoustic emission test before pure tone audiometer. Eur Arch Otorhinolaryngol. 2009 Nov 28.

  84. Yin L, Bottrell C, Clarke N, et al. Otoacoustic emissions: a valid, efficient first-line hearing screen for preschool children. J Sch Health. 2009 Apr;79(4):147-52.

  85. Yoshinaga-Itano C, Coulter D, Thomson V. The Colorado Newborn Hearing Screening Project: effects on speech and language development for children with hearing loss. J Perinatol. 2000;20(8 pt 2):S132-S137.

Effective Date: December 1, 2011