Ototoxicity and hearing loss
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Aetiology of acquired hearing loss
Many drugs are known to cause hearing loss. The most ototoxic drugs in paediatric oncology are the platinum agents, particularly cisplatin and to a lesser extent carboplatin. Cisplatin ototoxicity may be potentiated by other treatments notably prior radiotherapy and supportive care drugs such as aminoglycosides and the loop diuretics (frusemide).
The main site of damage is the outer hair cells but damage may occur to the inner hair cells, type I cells in the spiral ganglion, the stria vascularis and cochlea nerve. Damage sufficient to destroy hair cells is irreversible. The severity of cisplatin induced ototoxicity is related to the dose and mode of delivery. Ototoxicity occurs more frequently with increased dose of cisplatin, and with prior irradiation. Carboplatin can be ototoxic on its own; it also potentiates cisplatin-induced ototoxicity when used in combination. Mannitol decreases cisplatin ototoxicity.
Up to 77% of children treated with cisplatin will have some measurable hearing loss and between 18-36% of patients will have severe loss.
Drugs responsible for ototoxicity
- Cisplatin. High frequency loss occurs at cumulative doses of 270-450 mg/m2. Peripheral neuropathy occurs at cumulative doses of 300-600 mg/m2.
- Aminoglycosides (gentamicin is the most ototoxic)
- Loop diuretics
Prevention of ototoxicty
Protocols frequently specify when further testing should take place prior to administration of additional doses of platinum agents. There may be a protocol available for use of an agent which is being trialled for hearing protection in the context of platinum ototoxicity (eg amifostine or sodium thiosulphate). Check with the oncologist if this applies.Avoid, if possible, the use of aminoglycosides in patients who have had platinum agents - follow the antibiotic protocol for the management of febrile neutropenia.
Methods of hearing assessment
Pure tone audiometry
Cisplatin hearing loss begins in the high tone 8 kHz range and progresses down the frequencies into the audible range. Most children over 3 years of age can be tested. It is recommended that the order of testing be reversed in the preschool age to ensure that the high frequencies are tested before the child's concentration is lost. Obtain a pre-treatment audiogram when clinically feasible.
High frequency audiometry
Extended high frequency audiometry is not readily available but testing the 9-20 kHz range could identify hearing loss before speech frequencies are affected.
Auditory brain stem response
ABR is the standard method of assessment of hearing in the very young. It may require sedation or anaesthesia. ABR uses a click frequency correlating with hearing at around 2-4 kHz range.
Oto-acoustic emissions are the best objective screening test in
infants as they are thought to reflect outer hair cell activity.
Two types of emissions are clinically useful - EOAEs (evoked) and
DPOAEs (distortion product).
EOAEs are produced in response to broad band sound and are normally present when the hearing threshold is 25 dB or better, but give no information of hearing threshold when absent. This method is quicker than the ABR in a sleeping cooperative child. EOAEs over the 0.6-6 kHz range are reduced following cisplatin therapy.
DPOAEs can be demonstrated when there is mild/moderate sensorineural hearing loss and are frequency specific.
Check with the audiology service which of the acoustic emission tests are available for the monitoring of infants.
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- Date last published: 25 November 2016
- Document type: Clinical Guideline
- Services responsible: National Child Cancer Network
- Owner: Stephen Laughton
- Review frequency: 2 years
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