Department of Otorhinolaryngology Faculty for Postgraduate Education First Moscow State Medical University. IM Sechenov. (Head of Department Professor, MD, Honorary Doctor of Russia Shadyev HJ)
Adverse types of acute Evstahiit (tubootitis), leading three months later to chronicity with subsequent conductive hearing loss, in the form Tubo-tympanosclerosis or cholesteatoma the attic disease, were identified during the carrying out pathophysiological analysis of acute catarrhal inflammation of the middle ear, is presented in textbooks: Acute otitis media (2008) and Chronic otitis media (2007).
1. Pathophysiology features of acute catarrhal inflammation of the middle ear
Feature of acute catarrhal inflammation of the middle ear is the development of acute Evstahiit (tubootitis), which is accompanied increasing vacuum in cavities due to violations of the patency of the Eustachian tube.
This occurs as a result of swelling of catarrhal inflammation of the mucous membrane of the middle ear, leading to narrowing of the lumen of the Eustachian tube, which complicates the flow of air in the middle ear and leads to the development in him of the vacuum of swelling, which further narrows the lumen of the Eustachian tube, which creates a "vacuum vicious circle" of the inflammatory process, which does not allow over the stage of catarrhal inflammation, while the incoming transudate (serous otitis media) fills the middle ear, destroying this "vacuum vicious circle".
However sluggish or overly active increasing vacuum condition in the middle ear leads to the formation of unfavorable variants of acute catarrhal stage of inflammation, leading to chronic inflammation after three months.
2.The sluggish increase in vacuum condition in the middle ear
In acute tubootitis sluggish increase vacuum state of catarrhal inflammation ends without the stage of transudative of fluid in the middle ear, and after three months it becomes chronic Evstahiit.
And then the stage of exudation takes place in the same flaccid state – no active exudation and, finally, ends with a productive inflammation with opening of the Eustachian tube.
However, due to the sluggish turnover inflammatory process, in secluded places of the middle ear, in the mucosa and beneath the mucous layer, are stored the portions of the vacuum-exudative infiltrate, which is replaced by connective tissue, with development of fibrous, of cartilaginous and bony processes that form the foci of tympanosclerosis.
Such pockets of tympanosclerosis, settling in the joints of the ossicular chain and the annular ligament of the stapes plasty pasture, which leads to conductive hearing loss.
Because pathogenetic basis for the development of this form of tympanosclerosis is a vacuum condition in the middle ear caused by Eustachian tube blockage, to reflect the pathogenesis in the clinical name of this form of tympanosclerosis, is most suitable to name it as Tubo-tympanosclerosis.
This pathophysiological analysis of chronic Evstahiit reveals the early formation of tympanosclerosis, which repeatedly mention oto-surgeons - O. K. Patakina (1998) and others, emphasizing that tympanosclerosis may develop already at the stage of catarrhal inflammation.
Because clinical manifestations of chronic Evstahiit three months differ little from acute Evstahiit, and at the end produktivnogo inflammation they abruptly change as shown in the form of Tubo-tympanosclerosis, there is a need to consider separately Primary chronic evstahiit (three months) and Secondary chronic evstahiit (at the conclusion of the productive stage of inflammation).
The craze of vasoconstrictive drops in a nose are the most frequent cause of this sluggish current of chronic Evstahiit
Our experience of more than 1,000 stapedoplasty about otosclerosis showed that about 80 % of otosclerosis is not detected, and was detected theTubo-tympanosclerosis.
3.Active increasing vacuum condition in the middle ear
With the active buildup of a vacuum condition in the middle ear, due to the complete blockade of the Eustachian tube, negative pressure increases so quickly that the eardrum is sooner than the time to develop stage the transudation.
A ruptured eardrum occurs in epitympanic part where it is significantly weaker due to the lack of a fibrous layer, and the time of the perforation occurs to a patient is almost unnoticed because it is not accompanied by pain and hearing loss.
And the fading feeling of fullness in the ear creates in the patient a false impression of complete well-being not necessary to be observed at an ENT specialist.
Eliminating the negative pressure in the middle ear destroys the "vacuum vicious circle" of the inflammatory process that contributes to the successful completion of the catarrhal stage of inflammation (without stage transudate) and successful completion of exudative and productive stage and then, with restoration of patency of the auditory tube, which is subjectively perceived as a recovery.
However, the presence of perforations in epitympanum creates its own problems, since, when the vacuum retraction of the epidermis edges of the perforation are immersed in mucous pockets formed by folds of the mucous membrane in epitympanic area.
Such an immersion of migratory epidermis in epitympanum more likely to occur in the recess at the neck of the Malleus, which is the upper pocket of the tympanic membrane (membrane tympani recessus superior), which is connected to the top part of the lateral recessus epitympanicus located outside the head of the Malleus and incus, and the bottom, with a back pocket of the tympanic membrane. Not coincidentally, this site in epitympanum has long received the name Prussakov space, because the eardrum perforation in this area was considered as an indication for the presence of cholesteatoma.
Perforation in epitympanum may be localized over the rear pocket of the tympanic membrane - recessus membranae tympani posterior, open downward between the rear part of the pars flaccida and the fold of mucous membrane covering the posterior plica mallearis, with the rear part of the chordae tympani.