[The adhesive process. Part II: Research on pathogenesis (author's transl)].
In adhesive middle ears the rate of recidives after operation is very high - irrespective of the tube function (part I). This may be caused by changed middle ear pressure and other pressure determinating factors like the tube function, the elasticity of the tympanic membrane, the volume of the middle ear space and gas diffusion. Registration of the tube function by pressure equalisation test as well as the direct, continous measurement of the middle ear pressure shows, that in 30-40% of the patients examined, a physiological tube function with normal pressure was found before and after tympanoplasty. In model studies we could demonstrate, that even in normal middle ear pressure tympanograms may be achieved, which are typical for adhesive processes, with a peak in the negative pressure area. The volumes of the middle ear spaces after tympanoplastics are larger (4,3 ml on an average) then preoperatively, but smaller than normal. Continuous registration of the middle ear pressure shows that in adhesive middle ears that development of negative pressure is diminished - compared with a collective of patients with normal elasticity of the tympanic membrane. This difference can only be explained by decreased elasticity of the membrane, found with adhesive processes and after tympanoplatics. Recidives after tympanoplastics in atelectatic ears may be caused by the development of negative pressure due to tube dysfunction. In cases of normal tube function (30-40% of the patients) and normal pressure, the rate of recidives is mostly caused by decreased elasticity of the tympanic membrane together with the smaller volume of the middle ear spaces.
D000158:Acoustic Impedance Tests; D002781:Cholesteatoma / Q000601:surgery; D002921:Cicatrix / Q000209:etiology; D006801:Humans; D008365:Manometry; D010033:Otitis Media / Q000601:surgery; D011183:Postoperative Complications / Q000209:etiology*; D000267:Tissue Adhesions; D014433:Tympanoplasty
Der Adhäsivprozess. Teil II: Untersuchungen zur Pathogenese.