OBJECTIVE: This study was designed to quantitatively assess the contribution of various factors to the conductive hearing loss in otitis media. BACKGROUND: In the conductive hearing loss seen in cases of serous otitis media, various volumes of fluid of different viscosities along with subatmospheric (negative) pressure are found in the middle ear. METHODS: To evaluate the contribution of each of these factors to hearing loss, various volumes of saline, whole blood, or glycerol were applied to the open middle ear cavity of guinea pigs for short periods of time and auditory function was evaluated by recording the threshold of auditory nerve-brainstem evoked responses. In some of the saline experiments, the bulla cavity was also sealed, allowing a subatmospheric (negative) pressure to develop in the cavity as water was osmotically absorbed because of the gradient in colloid osmotic pressure between saline and blood in the vessels lining the middle ear cavity. In other experiments, a thoracic drainage system was connected to the middle ear cavity to induce desired negative middle ear pressures. RESULTS: The degree of hearing loss increased as larger volumes of fluid were introduced into the middle ear, reaching a maximum of 15 to 16 dB. There was no difference in the degree of hearing loss induced by saline or by fluids with viscosities up to 1,000 times greater than that of water (glycerol). A subatmospheric pressure in the middle ear contributed only a small additional (1-2 dB) threshold elevation. CONCLUSION: The major factor contributing to hearing loss in serous otitis media is the volume of fluid in the middle ear, irrespective of its viscosity. The contribution of negative middle ear pressure is much smaller.
OBJECTIVE: This study was designed to quantitatively assess the contribution of various factors to the conductive hearing loss in otitis media. BACKGROUND: In the conductive hearing loss seen in cases of serous otitis media, various volumes of fluid of different viscosities along with subatmospheric (negative) pressure are found in the middle ear. METHODS: To evaluate the contribution of each of these factors to hearing loss, various volumes of saline, whole blood, or glycerol were applied to the open middle ear cavity of guinea pigs for short periods of time and auditory function was evaluated by recording the threshold of auditory nerve-brainstem evoked responses. In some of the saline experiments, the bulla cavity was also sealed, allowing a subatmospheric (negative) pressure to develop in the cavity as water was osmotically absorbed because of the gradient in colloid osmotic pressure between saline and blood in the vessels lining the middle ear cavity. In other experiments, a thoracic drainage system was connected to the middle ear cavity to induce desired negative middle ear pressures. RESULTS: The degree of hearing loss increased as larger volumes of fluid were introduced into the middle ear, reaching a maximum of 15 to 16 dB. There was no difference in the degree of hearing loss induced by saline or by fluids with viscosities up to 1,000 times greater than that of water (glycerol). A subatmospheric pressure in the middle ear contributed only a small additional (1-2 dB) threshold elevation. CONCLUSION: The major factor contributing to hearing loss in serous otitis media is the volume of fluid in the middle ear, irrespective of its viscosity. The contribution of negative middle ear pressure is much smaller.
Authors: Jennifer L Thornton; Keely M Chevallier; Kanthaiah Koka; Sandra A Gabbard; Daniel J Tollin; Daniel Tollin Journal: J Assoc Res Otolaryngol Date: 2013-04-25