Otoacoustic emissions--an approach for monitoring aminoglycoside induced ototoxicity in children.

OBJECTIVES

The early detection of hearing impairment caused by ototoxic drugs, such as aminoglycosides, has been the aim of research world-wide. Histopathological studies have shown that the outer hair cells are the most susceptible cochlear components to injury from ototoxic drugs like aminoglycosides. Otoacoustic emissions reflect the functional status of the outer hair cells and constitute the only non-invasive means of objective cochlear investigation. The aim of this study was to evaluate the potential of otoacoustic emissions in early identification of aminoglycoside-induced cochlear dysfunction. In addition, a comparison with pure-tone audiometry or auditory brainstem responses was performed in order to determine if this test might provide a more reliable method of monitoring early ototoxic insults to the cochlea.

METHODS

Twenty four children receiving gentamicin (4 mg/kg once daily) for 6-29 days were included in the study. Eleven children received gentamicin for up to 7 days (group A), while 13 underwent longer-term therapy lasting 8-29 days (group B). Hearing was serially monitored using transient evoked otoacoustic emissions and pure-tone audiometry (0.25-12 kHz) or auditory brainstem responses for younger or uncooperative children. Transient evoked otoacoustic emissions data were analysed in terms of emission amplitude and response reproducibility as a function of frequency.

RESULTS

All patients yielded a normal baseline audiometric assessment upon hospital admission. For group A patients no significant changes in hearing levels were observed either by pure-tone audiometry (P = 0.2), auditory brainstem responses (P = 0.3) or transient evoked otoacoustic emissions (mean response: P = 0.06, reproducibility by frequency: P > 0.05). For group B patients no significant changes in hearing levels measured by pure-tone audiometry (P = 0.1) or auditory brainstem responses (P = 0.4) were observed. Transient evoked otoacoustic emissions however revealed a statistically significant decrease in the mean response level (P = 0.017) and in the reproducibility over the whole frequency spectrum (1 kHz: P = 0.0057, 2 kHz: P = 0.0247, 3 kHz: P = 0.0134, 4 kHz: P = 0.0049, 5 kHz: P = 0.0019).

CONCLUSIONS

The findings suggest that transient evoked otoacoustic emissions are an extremely sensitive measure of the early effects of aminoglycoside-induced injury to the peripheral auditory system. Therefore, their use is recommended for regular monitoring of cochlear function, in the presence of potentially toxic factors, aiming at prevention of permanent damage.