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Because of the ICD-10 disease coding system transition that occurred in the United States in 2015, coding and billing for services on behalf of patients who experience cochlear and/or vestibular toxicity may be daunting and misunderstood. Coding and billing for any audiology procedure can be compelling; choosing the appropriate codes for these specific patients is critical not only for payment for services rendered but also for the national and global implications, given their utilization is tracked for mortality and morbidity statistics and potential policies.

Objective:The aim of this study was to determine the incidence of inner ear involvement in various forms of acute otitis media (AOM) in ear, nose, and throat (ENT) practices in Germany.Methods:Patients who had been diagnosed with various forms of AOM in the years 2010 to 2017 were enrolled in the study from a nationwide, representative practice database (Disease Analyzer, IQVIA). In these patients, the incidence of simultaneous or subsequent inner ear disorders (IED) was determined within 7 days and within 12 months from the date of an AOM diagnosis.Results:A total of 286 186 patients with AOM were enrolled. The most frequent diagnoses were “nonsuppurative otitis media, unspecified” (47.6%) and “otitis media, unspecified” (39.0%). The diagnoses of hemorrhagic bullous myringitis (BM) or influenza-induced AOM were very rarely found in the database. The highest incidence of IED after 7 days and 12 months was found in “nonsuppurative otitis media, unspecified” (7.7% and 15.9%, respectively), followed by “otitis media, unspecified” (5.6% and 13.5%, respectively). The incidences of the most frequent IED “hearing loss, unspecified” and “sensorineural hearing loss, unspecified” increased proportionally with increasing patient age, while the rare diagnoses of “labyrinthitis” and “ototoxic hearing loss” were evenly distributed among the age groups.Conclusion:In ENT practices in Germany, both various forms of AOM, as well as simultaneous or subsequent IED, are mostly being coded in an unspecific way, while specific forms such as hemorrhagic BM, influenza-induced AOM, and labyrinthitis are coded very rarely. Older patients have a higher risk of IED in AOM. A visit due to AOM seems to be a regular occasion for the initial diagnosis of hearing impairment in the elderly individuals. The highest risk of IED was found in nonsuppurative AOM.

Drug-mediated ototoxicity, specifically cochleotoxicity, is a concern for patients receiving medications for the treatment of serious illness. A number of classification schemes exist, most of which are based on pure-tone audiometry, in order to assist non-audiological/non-otological specialists in the identification and monitoring of iatrogenic hearing loss. This review identifies the primary classification systems used in cochleototoxicity monitoring. By bringing together classifications published in discipline-specific literature, the paper aims to increase awareness of their relative strengths and limitations in the assessment and monitoring of ototoxic hearing loss and to indicate how future classification systems may improve upon the status-quo.Literature review.PubMed identified 4878 articles containing the search term ototox*.A systematic search identified 13 key classification systems. Cochleotoxicity classification systems can be divided into those which focus on hearing change from a baseline audiogram and those that focus on the functional impact of the hearing loss.Common weaknesses of these grading scales included a lack of sensitivity to small adverse changes in hearing thresholds, a lack of high-frequency audiometry (8 kHz), and lack of indication of which changes are likely to be clinically significant for communication and quality of life.

The aim of this study was to examine the pattern of changes in distortion product otoacoustic emissions (DPOAEs) in children with ototoxic hearing loss during chemotherapy. The participants included a control group of 15 normal hearing children (3-12 years) and an experimental group of 7 paediatric oncology patients (1-13 years). Participants were tested using pure tone audiometry (PTA), tympanometry, and DPOAEs (primaries 65/55 dB SPL). The results revealed no perfect match between PTA and DPOAE results with respect to frequency and pattern of decrease/increase of DPOAE amplitudes. Further analysis of DPOAEs in the experimental group revealed three main patterns of change: (1) Concurrent decreases in DPOAEs that matched pure tone threshold (PTT) changes at approximately the same frequencies; (2) DPOAE changes prior to PTT change, suggesting possible predictive power in DPOAE testing and (3) DPOAE and PTT changes not related in terms of test frequency and direction of change, noted in a patient with a high cumulative carboplatin dose.

It is well established that ototoxic antibiotics and acoustic trauma can damage cochlear hair cells and cause hearing loss. Previous studies using transcanal LLLT (Low level laser therapy) showed that LLLT can promote recovery of hearing thresholds and cochlear hair cells. However, its mechanism has not been studied. Aim: The aim of this study is to investigate the mechanism of hearing recovery from gentamicin induced ototoxic hearing loss by LLLT. Methods: HEI- OC1 (House ear institute organ of Corti) cells were cultured for 18 hours and ototoxicity was induced by gentamicin (GM) treatment to the cells. Cultured cells were divided into 6 groups, No treatment control, LLLT only, GM 6.6 mM and GM 13.1 mM, GM 6.6 mM+LLLT and GM 13.1 mM+LLLT cells. LD laser 808 nm, 15 mW, was irradiated to the cultured cells for 15 min, at 4 hours after GM treatment to the cells. ATP was assayed using the ATP assay Kit. ROS was measured using confocal microscope after application of H2DCFDA dye. Results: ATP was decreased in GM 13.1 mM cells and increased in LLLT only cells and GM 13.1 mM+LLLT cells compared to control and 13.1 mM cells. ROS was increased in GM 6.6 mM and GM 13.1 mM cells, and decreased in GM 6.6 mM+LLLT and GM 13.1 mM+LLLT cells compared to GM 6.6 and 13.1 mM cells immediately after laser irradiation. Conclusion: This study demonstrated that LLLT on GM treated HEI-OC1 cells increased ATP and decreased ROS that may contribute to the recovery of hearing.

The first molecular defect for nonsyndromic hearing loss was identified in 1993, and was a mitochondrial mutation. Since then a number of inherited mitochondrial DNA (mtDNA) mutations have been implicated in hearing loss, and acquired mtDNA mutations have been proposed as one of the causes of the hearing loss associated with aging, presbyacusis. These molecular findings have raised as many questions as they have answered, however, since the pathophysiology between the mutations and the clinical phenotype remains poorly understood. This mini-review will, after a short background review of mitochondrial genetics, (1) outline the different mtDNA mutations associated with inherited syndromic, nonsyndromic, and ototoxic hearing loss, (2) summarize the data on acquired mtDNA mutations and their possible association with presbyacusis, (3) describe the biochemical consequences of the inherited mtDNA mutations, (4) suggest the clinical implications of the identification of these mutations, and (5) discuss the penetrance and tissue specificity of the hearing associated mtDNA mutations.

tice and research.Through understanding the underlying mechanisms of ototoxic hearing loss, we have the very real possibility of developing new drugs in the near future that either do not have ototoxicity as a side effect or work specifically to prevent ototoxicity as a side effect of other drugs. The mechanisms of ototoxic damage and protection can be complex but some general concepts apply. In virtually all scientific journals and even in the popular press, we read about “oxidative damage” and “oxidative stress” as a factor in many degenerative processes. Although oxidative processes are part of normal metabolic activity, they also play a major role in many disease processes and in aging. Oxidative damage is also a common factor in cisplatin-induced, aminoglycoside-induced, and noise-induced hearing loss. Therefore audiologists and others working in hearing loss prevention should have a working knowledge of oxidative mechanisms. The following is a list of terms and concepts that may be helpful in reading the articles on ototoxicity in this issue of JAAA.

A 61-year-old artist in Israel had been painting for 30 years in his home studio. He had been healthy until he reached the age of 59.5 years, at which time he began complaining of weakness and paresthesia in both hands and legs. He also complained that he had difficulty concentrating, and his memory was impaired. His work was unusual in that he painted large posters (i.e., 2 x 3 m) with different mixtures of organic solvents, including toluene, xylene, benzene, methyl ethyl ketone, toluene diisocyanate, acetone, and thinner. He did not use any protective gloves and did not wear a mask. He was evaluated with several methods and was diagnosed as having peripheral and central neuropathy, including ototoxic hearing loss as a result of long exposures to organic solvents. The authors were unable to find any similar case report in the literature.

In summary, the clinician has a variety of protocols available for monitoring ototoxicity. Depending on the patient's risk factors and ability to be tested, the protocol for a given patient may vary. A flow chart reflecting some of the possible decisions and options is presented in Figure 1. Certainly, as we learn more about ototoxicity and the advantages and disadvantages of the various test methods, further refinements of patient and test selection will ensue. Ototoxicity is a rapidly expanding and interesting area. Hopefully, the care of patients receiving ototoxic medications will continue to improve and will ultimately prevent, or at least ameliorate, ototoxic hearing loss.

Objectives: (1) To determine the ototoxicity detection rate (sensitivity) for distortion-product otoacoustic emissions (DPOAEs) testing in adults who received ototoxic medications and experienced pure-tone threshold changes during the course of treatment; (2) to determine the extent to which DPOAE sensitivity to ototoxicity depends on the type of drug administered (platinum or antibiotic), magnitude of ototoxic threshold shifts, pre-exposure pure-tone threshold, and DPOAE data; and (3) to build a model to predict DPOAE sensitivity. Design: DPOAE and audiometric data were obtained as part of a prospective Veterans Affairs study investigating methods of ototoxicity monitoring. Data were analyzed from 90 ears of 53 subjects receiving ototoxic medications and showing significant hearing changes in at least one ear. Pure-tone threshold data were obtained at frequencies from 0.5 to 20 kHz, using 1/6-octave precision near the upper frequency limit of hearing. DPOAE data are reported for f2’s from 0.8 to 8.0 kHz in 1/6-octave increments using primary levels (L1/L2) of 65/59 dB SPL and a primary frequency ratio (f2/f1) of 1.2. Test results were evaluated at various times during drug treatment to determine whether DPOAE level changes were associated with behavioral hearing changes. Univariate and multivariate analysis techniques were used to determine factors that affected DPOAE sensitivity to ototoxic damage. Results: Of the 90 ears examined, 82 (91%) had DPOAEs that could be monitored for changes. Sixty-four of these 82 ears (78%) had DPOAEs that were reduced or absent following drug treatment. DPOAE sensitivity to ototoxicity was unrelated to the type of ototoxic drug administered. Rather, DPOAE sensitivity depended on the magnitude of postexposure hearing changes and on variables related to pre-exposure audiogram and DPOAE measurements. Behavioral hearing changes not detected by DPOAEs were small on average (

Ototoxic hearing loss is usually detected earliest through monitoring of the highest audible frequencies in individuals administered ototoxic medications. Conducting ototoxicity monitoring may require testing patients in the hospital room. This study evaluated the use of insert earphones for obtaining reliable threshold responses at bedside. Twenty adult subjects were tested during two different sessions in the sound booth and on the ward. Thresholds were obtained for frequencies from 5 to 16 kHz and at 2 kHz with the use of the KOSS Pro/4X Plus earphones and Etymotic ER-4B MicroPro insert earphones. Results indicate that ER-4B insert earphones are as reliable as KOSS earphones for testing on the ward for high-frequency ototoxicity monitoring.

The primary cause of hearing loss includes damage to cochlear hair cells. Low-level laser therapy (LLLT) has become a popular treatment for damaged nervous systems. Based on the idea that cochlea hair cells and neural cells are from same developmental origin, the effect of LLLT on hearing loss in animal models is evaluated. Hearing loss animal models were established, and the animals were irradiated by 830-nm diode laser once a day for 10 days. Power density of the laser treatment was 900 mW/cm(2), and the fluence was 162 to 194 J. The tympanic membrane was evaluated after LLLT. Thresholds of auditory brainstem responses were evaluated before treatment, after gentamicin, and after 10 days of LLLT. Quantitative scanning electron microscopic (SEM) observations were done by counting remaining hair cells. Tympanic membranes were intact at the end of the experiment. No adverse tissue reaction was found. On SEM images, LLLT significantly increased the number of hair cells in middle and basal turns. Hearing was significantly improved by laser irradiation. After LLLT treatment, both the hearing threshold and hair-cell count significantly improved.

Several species undergo age-dependent changes in susceptibility to noise-induced and drug-induced hearing loss. In this experiment 18-day-old mice were given 200 mg/kg kanamycin plus varying doses of bumetanide (20, 30 or 40 mg/kg). Thresholds of the scalp-recorded compound action potential of the auditory nerve indicated that diuretic doses of 30 and 40 mg/kg produced significant loss of hearing sensitivity. Thirty-eight-day-old mice were then treated with 200 mg/kg kanamycin plus 40 mg/kg bumetanide and demonstrated no loss of hearing sensitivity. These results confirm the existence of age-dependent changes in susceptibility to ototoxic hearing loss in mice. Furthermore, the treatment, consisting of two injections on the same day, offers promise as a means of defining the critical period of susceptibility in greater detail than has been possible with aminoglycosides alone.