Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4466_Библиотеки_им_академика_М_И_Перельмана

In the early stages of bacterial meningitis, SNHL typically develops and pro­gresses within 48h [36–38]. Histopathologic studies in animals with Hib meningitis indicate that labyrinthitis is a probable cause of SNHL [36, 39]. The pathophysiol­ogy of labyrinthitis associated with bacterial meningitis was investigated by histo­pathologically examining the inner ears of 114 rats with Hib meningitis [36]. Except for the endolymphatic space, cochlear nerve bers, and middle ear, the perilym­phatic spaces of the cochlea and semicircular canals were inamed. The inamma­tion reached a peak 48h after inoculation. Immunouorescent staining of cochleae demonstrated the presence of bacteria in the inamed areas and the endolymphatic space and organ of Corti. In a histopathology study of 41 human temporal bones after death from acute bacterial meningitis, 20 (41%) temporal bones had suppura­tive labyrinthitis, and the cochlea was affected [40]. While the cochlear aqueduct was the sole pathway for spreading infection in the rabbit, in humans, the modiolus and the aqueduct were potential pathways suggested. It is mainly accepted that the transmission of infection from the subarachnoid space to the labyrinth is the cause of HL, and both the cochlear aqueduct and the cochlear nerve in the modiolus are the potential pathways of the infection extension [41]. Inammatory cell inltra­tion, serobrinous exudate formation, and granulation cells also indicate cochlear pathology [41–43]. Vascular events such as septic emboli and thrombotic occlusion of the cochlear artery and vein result in cochlear hypoxia, ischemia, and neural damage [44]. Inammatory products such as nitric oxide and superoxide induce cytotoxic injury on the cochlea by destroying the blood–labyrinth barrier [9].