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Middle ear pressure maintenance: 1) a concert played by many instruments. 2) Pathology as compensation.

Presenting Author: Udi Cinamon

Published online by Cambridge University Press:  03 June 2016

Udi Cinamon
Udi Cinamon*
Affiliation:
Wolfson Medical Center
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Abstract

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Type
Abstracts
Information
The Journal of Laryngology & Otology , Volume 130 , Supplement S3: Abstracts for the 10th International Conference on Cholesteatoma , May 2016 , pp. S59
Copyright
Copyright © JLO (1984) Limited 2016 

Learning Objectives: Middle ear pressure maintenance: 1) a concert played by many instruments. 2) Pathology as compensation.

It is crucial that the pressure in the middle ear (ME) will be kept circa to ambient pressure. As a physiological system that needs to confront constant intrinsic and extrinsic changes (e.g., cardiovascular system, respiratory system, etc.) the ME requires to possess special capabilities to maintain a physiological steady state. This ME pressure homeostasis is a concert played by several mechanisms, i.e., pressure regulators meant to neutralize or minimize pressure changes. Adjusting the amount of gas, its flow and diffusion, as well as the volume of the middle ear cleft, temperature all mechanism that follow the law of gases [PV = nRT]:

Volume: Size matters, the mastoid and the tympanic membrane (TM) being a “pressure buffers”.

Surface matters: The “radiator” effect of the ME cleft regarding gas exchange, temperature, moisture (number of molecules, Temperature). The Eustachian tube (ET) being a conduit possessing a pumping effect. Nerves and pressure receptors may control ventilation by opening the ET. When one or more of these mechanisms fails a “disorder” may kick-in. Therefore, developing a chronic ME insufficiency is accepted as the patho-physiological setting for developing chronic ME disease, clinically presented as otitis media with effusion, atelectasis of the TM or associated with developing cholesteatoma.

These chronic changes can be addressed as compensatory mechanisms (e.g., heart hypertrophy to keep-up with perfusion having a failing heart). Edema of the mucosa, engorgement of vessels and transudate will diminish the volume and influence gaseous content in the ME elevating pressure. TM atelectasis changes the ME volume being a pressure buffer.

Failure to confront a prompt and significant pressure change, a situation in which the ME pressure needs to be elevated instantly, will be presented as barotrauma. The consequence would be transudate, hemorrhage, and TM perforation all means “trying” to compensate.