Histologic evaluation of the tissue seal and biologic response around cochlear implant electrodes in the human

Histopathologic study of the tissue seal and biologic response around cochlear implant electrodes in patients who had received a cochlear implant during life could provide clues concerning the pathogenesis of meningitis after cochlear implantation.

Bacterial meningitis has been reported as an infrequent complication of cochlear implantation using a variety of electrode designs. The cause of meningitis in cochlear implant recipients has not been firmly established. In an analogous surgical situation, namely stapedectomy, delayed meningitis could occur as a complication of ipsilateral acute suppurative otitis media in which there was open communication between the middle ear and perilymph.

Twenty-one temporal bones from 20 individuals who had undergone cochlear implantation during life were studied by light microscopy. All sections passing through the cochleostomy site and electrode track were examined to evaluate the tissue seal at the cochleostomy, the presence or absence of an extracochlear electrode sheath, and finally, to seek evidence of a cellular inflammatory response near the electrode. These data were compared with clinical data, including electrode system used, the number of years between implantation and death, type of tissue used at surgery, and the age and sex of the patients.

The 21 specimens included cases implanted with the Symbion Ineraid, Cochlear Corporation Nucleus 22-channel, Cochlear Corporation Nucleus 24-channel, a Cochlear Corporation Nucleus single channel, and Advanced Bionics Clarion C1 devices. At the cochleostomy site, and just within the cochlea, there was a robust fibrous and bony tissue response in all 21 ears and in most cases, there was a fibrous sheath surrounding the electrode in the middle ear. No recognizable open communication or potential communication between the middle ear and the inner ear was seen in any of the 21 ears. An inflammatory cellular response, including mononuclear leukocytes, histiocytes, and foreign body giant cells, were present in 12 of the 21 temporal bones (57%) and was most intense at the cochleostomy site. No statistically significant relationship was found between the presence or absence of inflammatory cells and the type of tissue graft used at surgery.

The histologic evidence presented in this study does not support open communication between the middle and the inner ear as part of the pathogenesis of bacterial meningitis as a late complication after cochlear implantation. Rather, the finding of a cellular inflammatory response in 12 of 21 temporal bones suggests that late hematogenous contamination and colonization of the implant is a much more likely pathogenic mechanism. This putative mechanism has implications for possible strategies to prevent meningitis after cochlear implantation.