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Author: admin | 22.12.2014 | Category: Ringing In The Ears Causes

Key words:aural rehabilitation, chemotherapy, cisplatin, COMP-VA, distortion-product otoacoustic emissions, DPOAE, hearing, OtoID, ototoxicity monitoring, sensitive range for ototoxicity. Prevention and rehabilitation of hearing loss and tinnitus are high priority initiatives in the Department of Veterans Affairs (VA). Within the inner ear, cisplatin primarily damages the cochlea, resulting in permanent, usually bilateral, high-frequency sensorineural hearing loss in approximately 60 percent of adults treated with the drug [9]. Currently, only a small fraction of Veterans undergoing chemotherapy with cisplatin are systematically monitored for signs of ototoxicity. Nearly 30 yr of prospective ototoxicity monitoring and research by the VA Rehabilitation Research and Development (RR&D) National Center for Rehabilitative Auditory Research (NCRAR) have shown that education and frequent communication with the monitoring audiologist improve the likelihood that oncologists will seek out and use information about ototoxic hearing changes for purposes of fine-tuning chemotherapy, when medically appropriate, to avoid disabling hearing loss. The purpose of this article is to report on a complete program of evidence-based ototoxicity monitoring protocols, the comprehensive ototoxicity monitoring program for VA (COMP-VA), developed at the NCRAR. COMP-VA is designed to be administered on the chemotherapy treatment unit just prior to treatment (chairside). The OtoID portable audiometer is comprised of a touch screen computer module, Sennheiser HDA200 circumaural headphones (Sennheiser Electronic Corp; Old Lyme, Connecticut) modified with ambient noise monitoring microphones and custom audiometric testing software.
The device has both manual (audiologist-directed testing) and automated (patient self-testing) modes. Ongoing development of the OtoID includes the secure exchange of information between the device and the VA’s computerized patient records system and telehealth capabilities.
Currently, most ototoxicity programs monitor in the conventional frequency range only, even though numerous studies show greater sensitivity is achieved by testing frequencies above 8,000 Hz [22]. We have recently confirmed that the risk for hearing shift from cisplatin is primarily related to the cumulative drug dose and, established in three separate data sets, that patients with better preexposure hearing have a greater risk of hearing change within the SRO at a given dose compared with patients with worse preexposure hearing [1–2,23]. In their respective clinical guidelines for ototoxicity monitoring, ASHA and the American Academy of Audiology (AAA) have proposed that both behavioral and nonbehavioral (objective) measures of auditory function be routinely used at the baseline evaluation because it is not clear which patients will become unable to provide reliable behavioral thresholds during treatment [20,26]. DPOAEs are objective measures able to identify cochlear changes associated with ototoxicity [29–30]. Another proposed DPOAE protocol involves the use of test-retest reference limits based on normal variability in serial DPOAE level plotted as a function of f2 frequency levels obtained in a nonexposed (to cisplatin) group of Veteran research participants. Even though many Veterans have preexisting hearing loss, most have DPOAEs that can be monitored for changes. Below, we describe ototoxicity in two patients seen as part of our research on ototoxicity monitoring at the Portland VAMC. This patient is a 63 yr-old male treated for squamous cell carcinoma of the right base of tongue (stage IVa) with lymph node involvement. This patient is a 58 yr-old male treated for squamous cell carcinoma of the right tonsil (stage IVa). Pretreatment ototoxicity risk assessment to demonstrate the anticipated hearing loss in the conventional frequency range as a result of the prescribed cisplatin dosing schedule.
Screening for early hearing changes to identify any ASHA-significant hearing shift within each patient’s individualized SRO, as measured directly using pure-tone threshold testing or estimated using DPOAE testing. Screening for outer hair cell dysfunction DPOAEs to identify early, potentially preclinical damage.
Screen failure follow-up testing to determine the extent that hearing changes include frequencies in the conventional audiometric frequency range as measured directly using pure-tone threshold testing or estimated using DPOAE testing.
Screening for tinnitus to determine whether the drug treatment is instigating or exacerbating tinnitus and the need for a tinnitus management referral.
Patient and provider education about ototoxic-induced hearing and tinnitus, synergistic effects of ototoxins and noise overexposure, and rehabilitative solutions to hearing loss and tinnitus. The Table summarizes the COMP-VA clinical objectives pertinent to identifying and monitoring changes in hearing and outer hair cell function (objectives 1–4, listed above).
Description of proposed comprehensive ototoxicity monitoring program for Department of Veterans Affairs (COMP-VA) clinical objectives 1–4.
Regardless of age, cancer patients may experience a variety of common side effects caused by chemo and radiation therapies, such as nausea and hair loss. Antibiotics that might help reverse ototoxicity are also being studied, and there’s research being done to develop chemotherapy drugs that won’t cause hearing loss. Remember to ask your physician for a referral for a hearing evaluation and consultation if you notice dizziness, tinnitus, or hearing loss while undergoing chemotherapy treatment. By having someone else voice their view on what you may be missing, we can help pinpoint where we can help the most.
Due to each patient’s individual needs, we need to take time to truly understand their situation before making any recommendations. While hearing loss is most commonly caused by prolonged exposure to loud noises — also referred to as sensorineural hearing loss — a number of medical conditions can lead to hearing impairment as well. Current research is finding strong associations between hearing loss and cardiovascular disease, diabetes, smoking, obesity, and dementia. Poor blood flow is typically the result of circulatory system troubles and can restrict the flow of oxygen to the inner ear. Meningitis, a bacterial or fungal infection of the brain and spinal cord, can cause sudden hearing loss. Meniere’s disease, a disorder of the fluids in the inner ear, is one of the most common causes of hearing loss.
Cancers of the head, neck, or ear areas can affect the inner ear, but cancer treatments, such as chemotherapy and radiation, are also notorious for causing hearing loss.
If you or a loved one have had trouble hearing, call our office today to schedule an appointment with one of our hearing care experts. The structure shown here is that of cisplatin bound to the N7 atoms of two adjacent guanine nucleotides on the same strand, to which cisplatin is known to bind preferentially. Ohio State's Micah Berman, Expert on E-Cigarette Regulation, Available to Talk About the FDA's New Oversight. AbstractBackground : Cisplatin-induced ototoxicity shows high interindividual variability and is often accompanied by transient or permanent tinnitus. Materials and Methods : Fifty-seven patients scheduled for cisplatin-based chemotherapy were included in the study.
Results : The subjective hearing loss was found in seven patients, while six patients had tinnitus during the chemotherapy. Conclusion : As use of high-frequency audiometry is still limited in research work only, we need a strict protocol of adding high-frequency audiometry in the cisplatin-based chemotherapy regimen. IntroductionCisplatin contributed significantly in the early success of modern chemotherapy for solid tumors and today, cisplatin is a primary drug for testicular cancer, medulloblastoma, osteogenic sarcoma, cervix and ovarian cancers. During follow-up, seven patients complained of subjective hearing loss and six had tinnitus at the time of first follow-up but none had both complaints. DiscussionCisplatin induced ototoxicity compromises, [11] development of language, cognitive functions, learning ability, communication and quality of life in terms of isolation and depression. At least 4,000 Veterans, most with significant hearing loss, will receive cisplatin this year, with more than half sustaining permanent hearing shift and nearly 40% developing new tinnitus.
In the last decade, more than 33,000 Veterans nationally were treated with cisplatin chemotherapy at VA medical centers (VAMCs) (VA Informatics and Computing Infrastructure database, accessed 2012 May). This damage occurs in a relatively orderly manner of base (high frequency) to apex (low frequency) destruction [10] primarily of the outer hair cells, which are sensory receptor cells that provide for the large dynamic range and exacting frequency selectivity that characterizes human hearing. Too often, Veterans in treatment are asked to arrange for audiological testing once debilitating hearing loss is already apparent to the patient or treatment team.
It has also become clear that audiology equipment and staffing limitations need to be overcome in order to consistently identify those patients who face the greatest risk for preventable hearing loss and to support those who need extra help and motivation to access VA’s comprehensive range of hearing loss and tinnitus rehabilitation services. COMP-VA was designed to achieve a range of customizable clinical objectives and to test all patients during treatment regardless of how sick they are or their ability to reliably take a hearing test using conventional methods. This eliminates the need for patients to make additional trips to the VA and the need for scheduled hearing evaluations in the audiology clinic. Sending HIPAA-compliant results from the OtoID built-in cell phone modem to a VA email address via secure text message is nearly complete. Standard air conduction testing in conventional and extended high frequencies is possible using the OtoID.
Significant hearing shifts during ototoxicity monitoring have been defined by the American Speech-Language-Hearing Association (ASHA) [20] as a 20 dB decrease at any one test frequency, a 10 dB decrease at any two adjacent test frequencies, or the loss of response at any three consecutively tested frequencies where responses were previously obtained. For example, one clinical study showed that if only conventional frequency testing (?8,000 Hz) were used, 36 percent of initial (early detection) changes would have gone undetected [4], potentially missing the opportunity to prevent changes in the more functionally critical conventional frequencies. Previous studies that examined extent of preexposure hearing as a potential risk factor for ototoxicity have conflicting results [24–25]. By our estimation, at least 30 percent of patients who receive chemotherapy do, in fact, become unable to respond reliably during testing [27–28]. DPOAEs depend on the physiological status of the outer hair cells, which are the initial site of ototoxic damage and, therefore, should be sensitive to hearing shifts [31].
Using a machine learning paradigm, we established that DPOAE shift metrics, obtained by comparing DPOAE baseline results to monitoring results, alone are sensitive predictors of hearing change in the SRO region, but when DPOAEs are combined in a multivariate model with cumulative drug dose and baseline hearing levels, sensitivity increases without causing unacceptably high false positive rates.
DPOAE level shifts obtained during ototoxicity monitoring that are greater than the decibel shift that marks the upper 90th percentile from the reference population identify a clinically significant DPOAE change [34].
For these individuals, chemotherapy treatments resulted in hearing shifts before the treatment was completed.
The case studies just presented illustrate how ototoxicity monitoring information can influence counseling, treatment decisions, and utilization of posttreatment audiological services for individual patients. The objectives are described in terms of the stakeholders requiring the data (who), the information being gathered (what), point in treatment to employ the test (when), basis for interpreting the results (how), and the evidence base supporting the test.
Table includes stakeholders in program (who), description of objective (what), implementation time (when), interpretation (how), and relevant citations (evidence base). But many people may be unaware that hearing loss is also a common side effect, and it can impact patients years after treatment. If you or someone you know is taking these drugs, we recommend you have a conversation regarding their effects on your hearing.
Cancer researchers are looking at agents that might prevent hearing loss but won’t inhibit the anti-tumor effects of the cancer treatment.
Frost earned her Doctor of Audiology degree in 2005 through the Arizona School for Health Sciences in Mesa, Arizona.
Fortunately, some of these medical conditions are reversible, allowing hearing to become fully restored. But many lesser-known conditions can impact your hearing health in potentially serious ways. Conditions affecting blood flow include sickle-cell anemia, diabetes, and heart conditions.
Hearing loss is also a side effect of treatment of tuberculosis — though it is possible that the medication used in treatment is what causes the impairment.
Its root is unknown, and the disease typically affects only one ear in individuals between ages 20 and 50.


Some serious genetic disorders, such as Waardenburg syndrome, cause the head and internal organs to develop differently, which may result in hearing loss that is difficult to correct through treatment or surgery. Once cisplatin is bound to DNA, several DNA repairing proteins are recruited to this region of the DNA.
Jude Children’s Research Hospital scientists have identified inherited genetic variations associated with hearing loss in young cancer patients treated with cisplatin, a drug widely used to treat adults with cancerNewswise — (MEMPHIS, TENN. Jude Children’s Research Hospital investigators have discovered inherited genetic variations that are associated with rapid hearing loss in young cancer patients treated with the drug cisplatin. It is not possible to identify the susceptible individuals before commencement of the treatment. All patients were divided into three groups depending on the dose of cisplatin infused in 3 weeks.
The hearing loss was sensorineural, dose dependent, symmetrical, bilateral and irreversible. Cisplatin is a cell cycle-nonspecific cytotoxic drug and has a toxic profile that is different from other important cytotoxic drugs.
No patient had distant metastasis, and hence none underwent cranial radiation for treatment. The tinnitus was present in one subject of Group 1 (50-year-old male) and group 3 (34-year-old male), while group 2 had 4 patients (mean age 50 years). Eight patients had significant hearing loss at Fisher′s scale and this loss was observed in 11 of 12 patients at 4 and 6 KHz. In all three groups, hearing loss was sensorineural, irreversible and symmetrical, and there was no sex predilection. Predicting cisplatin ototoxicity in children: The influence of age and the cumulative dose. Ototoxicity of high-dose cisplatin by bolus administration in patients with advanced cancers and normal hearing. Evoked otoacoustic emissions--an approach for monitoring cisplatin induced ototoxicity in children. Ototoxicity in children receiving platinum chemotherapy: Underestimating a commonly occurring toxicity that may influence academic and social development.
Platinum compound-related ototoxicity in children: Long-term follow-up reveals continuous worsening of hearing loss. Left-right asymmetry in hearing loss following cisplatin therapy in children--the left ear is slightly but significantly more affected.
Ototoxicity of cis-diamminedichloroplatinum (II): influence of dose, schedule and mode of administration. The role of hyperbaric oxygen therapy (hot) as an otoprotection agent against cisplatin ototoxicity. Ototoxicity in a randomized phase III trial of intra-arterial compared with intravenous cisplatin chemoradiation in patients with locally advanced head and neck cancer.
Early changes in auditory function as a result of platinum chemotherapy: use of extended high-frequency audiometry and evoked distortion product otoacoustic emissions. Detection of late ototoxic side effect of cisplatin by distortion otoacoustic emission (DPOAE). With improved survivability following cancer treatment, Veterans treated with cisplatin are approached with the dual goals of effective treatment and preserved quality of life. Cisplatin is an antineoplastic agent used for the treatment of a variety of adult cancers, including bladder, testicular, gynecologic, head and neck, and lung. Damage also occurs to the marginal cells of the stria vascularis [11–14], which provides the electrochemical drive for the outer hair cells and spiral ganglion cells of the auditory nerve. This testing must then be coordinated with a patient’s already overburdened treatment schedule and into audiology clinic time slots that are routinely scheduled months in advance.
Further, the VA’s existing mechanisms for tracking patients throughout the system need to be exploited in order to ensure patients receive the audiological services they may need at various stages of cancer treatment and survivorship. This program includes an individualized pretreatment prediction model that identifies the likelihood of hearing shift from cisplatin and supports both manual and automated hearing testing with a newly developed portable audiometer capable of performing the recommended procedures on the chemotherapy unit during treatment.
To accomplish this, researchers at the NCRAR designed and engineered a portable ototoxicity identification device, the OtoID, that can provide reliable and accurate hearing thresholds on the hospital ward during treatment [17]. The automated mode prompts the user when headphone placement is incorrect and employs catch trials to achieve bias-free threshold estimates.
Automated testing combined with telehealth capabilities provides major advantages of the OtoID over current modes of ototoxicity monitoring.
However, the sensitive range for ototoxicity (SRO) technique [19] is also supported by COMP-VA. ASHA’s criteria for a significant hearing shift when used with the SRO result in a reliable test [5,18]. Further, use of the SRO screening protocol together with tests to rule out ear disease or obstruction (otoscopy, tympanometry) reduces testing time substantially in comparison to the full diagnostic evaluation that is commonly done, which includes otoscopy, tympanometry, air and bone conduction, and speech testing. Differences across studies can be understood in terms of the differences in testing methodology, specifically the different test frequency ranges used. Using data from our recently completed ototoxicity research project at NCRAR, 50 of the 118 (41%) study subjects treated with cisplatin became untestable at some point in their treatment due to fatigue, illness, disease progression, or unwillingness to go to a sound suite for testing [2]. DPOAEs are elicited using two tones that are close in frequency and presented simultaneously. Because there is no commonly accepted gold standard of outer hair cell damage in humans, test accuracy can never be completely known for this method. Importantly, in a separate trial investigating DPOAE test performance for detecting ototoxicity, only 10 percent of ears had to be excluded for a lack of DPOAEs at baseline [2].
One patient opted to change medication; the other patient’s disease necessitated that he continue with the planned regimen. An audiometric baseline evaluation was completed, at which time he presented with normal hearing through 4,000 Hz sloping to a moderate loss of hearing at 6,000 and 8,000 Hz in both ears.
At the audiometric baseline evaluation, he presented with normal hearing through 2,500 Hz sloping to a moderately-severe hearing loss at 8,000 Hz with a high-frequency limit of hearing of 10,000 Hz in both ears. Tinnitus screening and educational clinical objectives (objectives 5 and 6, respectively) are not included in the table. Toxicities from chemotherapy and radiation can cause damage in the inner ear structures that leads to hearing loss. Things like high blood pressure, hypercoagulability, and polycythemia can also cause bloodrelated hearing loss. Both hearing loss and tinnitus are common side effects of Lyme disease (carried by ticks), as well as some STDs, like syphilis. Other issues known to affect hearing include hypothyroidism (an underactive thyroid), kidney disease medications, Paget’s disease, and autoimmune inner ear disease, which results in sudden onset hearing loss and must be treated as a medical emergency. Other conditions, like otosclerosis, affect the bones in the middle ear that conduct sound to the cochlea; some of these conditions are correctable with surgery. Though it is very effective, it has several serious side-effects, including renal toxicity, neurotoxicity and hearing loss, among others.
These become irreversibly bound to the DNA distorting its structure and preventing effective repair of the DNA and ultimately resulting in cell death. We conducted a prospective, randomized and observational study in a tertiary care centre and evaluated the effects of different doses of cisplatin on hearing. High doses of cisplatin cause nephrotoxicity, gastrointestinal toxicity, neurotoxicity and ototoxicity. During radiation for the head and neck cancers, ipsilateral temporal bone and ear of patients were protected by beam-modification devices (shielding block made up of lead) so as to avoid any affect of radiation on hearing.
This article describes COMP-VA, a comprehensive ototoxicity monitoring program developed for VA patients receiving cisplatin. If trends continue, more than 4,000 Veterans will receive cisplatin this year, with more than 50 percent sustaining a permanent hearing shift and 39 percent developing new tinnitus [1–3].
A main mechanism of cisplatin ototoxicity is associated with the production of free radicals [15]. Further, these appointments include lengthy diagnostic testing when a narrowly focused hearing screening done at each cisplatin-treatment visit would seem to be a better approach. Also included are two objective test methods for identifying outer hair cell changes and predicting audiogram changes using distortion-product otoacoustic emissions (DPOAEs).
The automated test mode saves audiological professional time by having the patient conduct the behavioral hearing screening portion of the monitor visit. The SRO technique is proposed as the behavioral hearing test method of choice for ototoxicity monitoring, as long as the Veteran is able to provide reliable hearing results despite the exhaustion caused by chemotherapy treatment. The SRO technique is also sensitive (94% detection) regardless of whether the SRO falls above 8,000 Hz [19,21] or below 8,000 Hz [4]. Extensive audiometric evaluations, typically done in the audiology clinic, are best saved until the patient has finished treatment and, perhaps, is ready to pursue hearing aid amplification. Hearing tests lose sensitivity for subjects with good preexposure hearing when testing does not include frequencies near the high frequency hearing limit.
Responses are influenced by hearing loss at the DPOAE frequency (2f1-f2), the eliciting frequencies (f1 and f2, where f1 < f2), and comparatively higher frequencies coded by more basal cochlear regions [29,32–33]. Providing objective techniques for identifying shifts in behavioral pure-tone thresholds when a patient is unable to provide reliable hearing test results, due to extreme illness or fatigue characteristic of chemotherapeutic treatment, is a very important and often overlooked programmatic component. However, a false positive rate of DPOAE change can be estimated for a tester or group of testers using group variability from a nonexposed control group.
Experience has shown that DPOAE measures are maximally sensitive to ototoxicity if they are within one octave of the behaviorally tested SRO [3]. Associated audiometric data for the patient described in case study 1 are presented in the “Clinical Objectives for COMP-VA” section. His high frequency limit of hearing was 12,500 and 11,200 Hz in the right and left ears, respectively. We envision that these clinical objectives would be tailored to the needs and preferences of the audiologists, oncology teams, and individual patients. Acoustic neuromas and tumors that grow on the auditory nerve can cause hearing loss or tinnitus, and they may put pressure on the brain, leading to other conditions.
Ototoxicity is one of the dose-limiting side effects of cisplatin because it increases with increase in the dose.
Of 9 patients, 6 had significant hearing loss at 8 and 12 KHz, while only 4 of 7 patients showed significant hearing loss at 16 KHz.
Cisplatin blocks transduction channels within the outer hair cells of the cochlea and causes progressive destruction of outer hair cells, inner hair cells and supporting cells within the organ of Corti. The program includes an individualized pretreatment prediction model that identifies the likelihood of hearing shift given cisplatin dose and patient factors. Importantly, in our experience, the average age of Veterans entering treatment is 60 yr and most report a history of significant noise exposure [4–5], which accounts for the high rate of preexisting hearing loss in this population.


Overabundance of these unstable molecules overloads intracellular antioxidant enzymes and leads to a cascade of damaging oxidative reactions and upregulation of programmed cell death.
The primary goal of COMP-VA is early detection of ototoxicity in order to optimize both audiological outcomes and therapeutic management of patients receiving cisplatin chemotherapy. Additionally, the OtoID measures the ambient room noise at earphone level before each tone presentation.
Once the patient completes self-testing and the results are received in the audiology clinic, the audiologist can then travel to the treatment unit, complete additional tests (otoscopy and tympanometry, screen-fail follow-up testing if necessary), and discuss results with the patient and the oncology team, ensuring that fully informed and timely treatment decisions can be made.
The SRO technique was designed to identify hearing shifts within an individualized range of relatively high frequencies so that treatment changes can be considered, if deemed necessary, to prevent hearing loss from spreading to the frequencies considered most important for understanding speech (those up to 4,000 Hz). The theorized basis for this high sensitivity is that the high frequency-coded base is the most physiologically vulnerable area within the cochlea to cisplatin-related damage, and this damage progresses from base to apex. Although current ASHA and AAA guidelines urge that DPOAE testing be included programmatically, little guidance is currently given as to how to interpret the findings.
In practice, we have found that there are many instances in which drug-induced pure-tone threshold shifts are restricted to a DPOAE frequency range that did not have a valid response at the baseline test session. The research appears in the current online issue of the scientific journal Nature Genetics.Cisplatin is one of the most widely used anti-cancer drugs and is a mainstay of treatment for children and adults with many types of brain and other solid tumors. It supports both manual and automated hearing testing with a newly developed portable audiometer capable of performing the recommended procedures on the chemotherapy unit during treatment. Depleting the natural defense system of cells leaves them especially susceptible to further ototoxic damage with each additional treatment. This goal is to be accomplished using a team-based approach made possible in large part by delivering COMP-VA services chairside on the oncology treatment unit.
If the ambient noise exceeds ANSI S3.1–1999 maximum permissible ambient noise levels (MPANLs), the tone is not presented and the patient is instructed to either wait until the room is quiet or move to a quieter location. In such cases, we have found that DPOAEs obtained at comparatively lower f2 frequencies are still useful for predicting hearing shifts, either because DPOAEs are sensitive to preclinical damage or are influenced by threshold shifts at comparatively higher frequencies than the eliciting primaries [2]. Following his first dose of cisplatin (cumulative dose = 200 mg), he became neutropenic, which resulted in a 2 wk delay in his cisplatin treatment. But in some patients the drug causes debilitating side effects, including severe hearing loss. Cisplatin-induced ototoxicity is often accompanied by transient or permanent tinnitus [4],[5] and shows high interindividual variability. All included patients underwent a detailed history, clinical examination, hearing (tuning fork tests and pure tone audiometry) and vestibular functions assessment (bithermal caloric, positioning and positional tests), blood (complete hemogram, liver and renal function tests) and urine analysis. Cisplatin ototoxicity is also associated with the generation of reactive oxygen species, depletion of intracellular glutathione and interference with antioxidant enzymes within the cochlea.
It also includes objective methods for identifying outer hair cell changes and predicting audiogram changes using distortion-product otoacoustic emissions. Furthermore, health-related quality of life concerns are important to oncologists because improved treatments and early diagnoses have increased long-term cancer survivability.
The resultant peripheral hearing loss from this cell damage has been shown to be dose dependent in both animals [11] and humans [16]. Three weeks after his first dose (cumulative dose = 190 mg) and just before his second dose, a monitor evaluation revealed an ASHA-significant hearing change (average +10 dB shift) at 10,000 to 12,500 Hz in the right ear with normal otoscopy and tympanometry.
Before the second dose of cisplatin, the audiologist detected ASHA-significant hearing changes from 3,000 to 10,000 Hz in the right ear and 3,000 to 8,000 Hz in the left ear in the presence of normal otoscopy and tympanometry. Inside the cell, one of the chloride ions is replaced by a molecule of water allowing the compound to bind to a nitrogen atom on a DNA nucleotide. In this study, hearing assessment was done before starting cisplatin therapy and at one and three months after cisplatin infusion. We describe this program of evidence-based ototoxicity monitoring protocols using a case example to give the reader an understanding of how this program would be applied, along with a plan for future work to accomplish the final stages of program development. The approach of VA is to provide cancer management that is patient centered and directed toward improving the quality of life following treatment. The largest hearing shift was at 3,000 Hz (+30 dB average shift in the left and right ears) with lesser changes (+10 to +15 dB shifts) seen in the higher frequencies (?4,000 Hz). This is followed by the second chloride ion being replaced by a water molecule as well, resulting in the platinum binding to another nucleotide. Identification of susceptible individuals before commencement of the treatment is not possible; however, early ototoxic effects can be detected by high-frequency audiometry [7] and otoacoustic emission. A “screen failure” follow-up audiogram indicated the hearing shift was confined to the ultra-high frequencies in one ear. The patient reported using a power drill on concrete without hearing protection following his first dose of cisplatin, despite being counseled by the audiologist to avoid noise overexposure. Oncology was notified of these early unilateral hearing changes outside the speech frequency range and their decision was to continue with the second cisplatin dose.
Because of concern that the noise exposure exacerbated the cisplatin effects, the patient was counseled again and provided new hearing protection. Materials and MethodsThis study was conducted in the Departments of Otolaryngology- Head and Neck Surgery, and Radiation-Oncology (Regional Cancer Centre). Three weeks after his second dose and just before infusion with his third dose (cumulative dose = 380 mg), ASHA-significant hearing change in the right ear expanded to include the 4,000 to 12,500 Hz frequency range (average +25 dB shift) with no response to tones above 10,000 Hz. The oncology team was notified of the hearing changes but counseled the patient to proceed with cisplatin treatment to give him the best radiation therapy support. There was a concomitant +25 dB average shift in hearing in the left ear from 4,000 to 11,200 Hz, and middle ear function remained normal bilaterally.
Few studies [14],[15] involving follow-up to two years had also found irreversible hearing loss by cisplatin.
We found no correlation between age and hearing loss or between baseline hearing level and cisplatin-induced hearing loss.
The 2 wk delay in day 22 of treatment complicated by the recent hospital admission resulted in the discontinuation of day 43 treatment. At this point, the oncology nurse practitioner and audiologist together counseled the patient regarding the potential for further hearing changes if he continued treatment with cisplatin versus the option of changing to a less toxic chemotherapy drug, but with an undetermined effect on treatment efficacy. A postexposure follow-up examination was conducted 1 mo following the second dose of cisplatin.
Group 2 comprised 35 patients (21 male and 14 female) of whom 23 had various head and neck cancer (excluding larynx) and the remaining 12 were suffering from carcinoma of the cervix.
The audiologist explained options for aural rehabilitation, including the use of hearing aids.
At that time, ASHA-significant hearing changes were noted from 2,000 to 10,000 Hz in the right ear and 2,000 to 8,000 Hz in the left ear compared with baseline measurements in the presence of normal otoscopy and tympanometry. The maximum increase in the hearing threshold after cisplatin administration was 45 dB at 8 KHz in both ears of a 43-year-old patient.
This patient-centered care approach involving both oncology and audiology resulted in the patient having the knowledge to make an informed decision regarding his care.
Results indicated hearing loss had progressed following the second cycle to include hearing changes at 2,000 Hz in both ears averaging +48 dB shifts. He chose to preserve his hearing, and the oncologist changed his chemotherapy drug to carboplatin, a chemotherapy drug associated with less toxicity, for his last dose. The patient underwent imaging 3 mo following his last treatment, which indicated the cancer that had spread to the lymph nodes was no longer present, and endoscopy revealed the base of tongue primary cancer had regressed completely. The patient now reported increased difficulty understanding speech, especially women and children, but denied other otologic complaints including aural fullness and changes in baseline tinnitus. Audiological follow-up with the patient was remarkable for otalgia, a retracted tympanic membrane, and worsening hearing loss in the right ear. A repeat audiological examination was conducted again 2 mo following cessation of cisplatin treatment (approximately 6 wk following cessation of radiation therapy) and confirmed continued hearing changes through 2,000 Hz. Following treatment, he presents with a fairly flat moderately severe to severe hearing loss beginning at 2,000 Hz.
He was referred to otolaryngology, where a pressure equalization tube was placed in the right ear due to eustachian tube dysfunction secondary to radiation therapy. He feels that his hearing has significantly deteriorated since treatment and has been fit with bilateral hearing aids. In Group 2, cisplatin caused a maximum increase of 40 dB in the hearing threshold at 12 KHz in the hearing threshold of right ear in a 19-year-old patient. In the left ear, uniform increase of about 30 dB was observed in hearing threshold at all frequencies in all age groups. Few authors [20],[21] have found relationship between free circulating cisplatin in plasma with time. They found that cisplatin infusion during afternoon and evening results in low plasma levels of free cisplatin, and hence cisplatin administrated during the early evening hours results in fewer side effects including ototoxicity. Measurement of correlation between time and plasma concentration was beyond the scope of this study. We found no correlation of tinnitus with the dose of cisplatin or age, which was comparable to the study by Moroso et al . The risk of permanent hearing damage from platinum chemotherapy is stimulating the development of otoprotectants for coadministration with platinum to reduce hearing damage without affecting the antitumor activity of the platinum agent. There are numerous otoprotectant agents under research, which include aspirin, antioxidants, [24] intratympanic dexamethasone [25] and hyperbaric oxygen therapy, [26] Ginkgo biloba extract, [27] diethyldithiocarbamate, [28] lipoic acid, [29] adenosine agonist, [30] vitamin E [31] and sodium thiosulfate. Although, the importance of high-frequency audiometry in cisplatin chemotherapy was established about 25 years earlier, [33] but in majority of the centers including our department, it is used only during research work. However, lack of infrastructure, non-availability of high-frequency audiometer and audiologist is a major problem in these centers, especially in our country. To conclude, we all know that cancer patients are living in physical and mental agony and cisplatin-induced ototoxicity further enhances this morbidity. Audiological monitoring is an essential part of the management of adults and children receiving platinum-based chemotherapy.
Although few authors [12],[34],[35] found distortion product otoacoustic emission as a better method of detecting cisplatin-induced early ototoxicity but high-frequency pure-tone audiometry is the first choice due to its high sensitivity. High-frequency monitoring alerts the physician of early ototoxic effects, who has opportunity to change a patient′s course of treatment.
Therefore, high-frequency audiometry should be included in the cisplatin-based chemotherapy regimen. Increase in the dose of cisplatin lead to increase in ototoxicity that warrants further research to find therapeutic efficacy of low-dose cisplatin or a better substitute of cisplatin. Otoprotective drugs are still at experimental level but may be beneficial in cisplatin ototoxicity.AcknowledgmentDr RS Minhas provided general help in this research work.



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