УДК 616-08:616.21
Usmonov S.H.
Narbayev Z.K. department of otorhinolaryngology Andijan State Medical Institute
IMPROVING THE EFFECTIVENESS OF MODERN ENDOSCOPIC
METHODS IN THE TREATMENT OF ACUTE TUBOOTITIS
Resume: The article is devoted to acute tubootitis, which began with the information that this inflammatory lesion of the middle ear and auditory tube causes catarrhal otitis, the disease is also called eustachiitis, tubotimpanitis and salpingootitis.
This article again provides the following information: tubootitis is an inflammatory lesion of the middle ear and auditory tube that causes catarrhal otitis. The disease also has names: eustachiitis, tubotimpanitis, salpingootitis. Tubotitis is fraught with serious complications - the development of exudative, viscous, purulent otitis media, conductive hearing loss and absolute hearing loss. In the early stages of the disease, it is important to begin professional and individually selected treatment. Therefore, at the first signs of inflammation of the middle ear, contact an otolaryngologist.
Key words: acute tubotitis, efficacy, endoscopy, surgery.
Relevance. Pathology of the middle ear is an urgent problem of modern otorhinolaryngology. Inflammatory and non-inflammatory diseases of the middle ear often lead to severe, life-threatening complications, and are often the cause of hearing loss and an increase in the number of people suffering from hearing loss. In the structure of modern hearing loss according to D.I. Tarasov et al. (2018), M.E. Zagoryanskaya et al. (2013), I.V. Bravagina (2014), conductive hearing loss accounts for up to 18.7% of cases.
One of the leading etiopathogenetic factors leading to pathology of the middle ear, and, in particular, conductive hearing loss, is the dysfunction of the auditory tube [3,6]
Currently, quite deep knowledge has been accumulated concerning the etiology, pathogenesis, clinic and treatment of acute and chronic tubootitis, but some issues remain unclear. The functioning of the auditory tube in norm and pathology has not been fully studied [2,5]
Among the wide variety of causes of tubootitis, a significant place is given to the pathology of the nasal cavity and paranasal sinuses [1,4]. However, it has not been established that mechanical obstruction of the nasal cavity or inflammatory changes in the nasal cavity, paranasal sinuses or nasopharynx contribute more to the development of auditory tube dysfunction[3]. The
question of the relationship between the degree of violation of the patency of the cavity and the degree of tubar dysfunction also remains unclear.
A generally accepted position when considering issues related to tubootites is the statement that due to the dysfunction of the auditory tube, low pressure develops in the cavities of the middle ear[2]. However, in some conditions: valvular dysfunction of the auditory tube, changes in gas exchange in the middle ear, with the pumping effect of the auditory tube, positive pressure develops in the middle ear. The possibility of developing positive intra-drum pressure in tubotites is currently recognized by some researchers[7]
In 1998, I.A. Anikin et al. The pumping effect of the auditory tube (NEST) was first recorded and described in patients with chronic perforated otitis media, characterized by a pulsating increase in air pressure in the tympanic cavity at rest (in the absence of swallowing and chewing movements, straining). Subsequently, M.I. Anikin (2003, 2004) discovered the pumping effect of the auditory tube in patients with nonperforative otitis media and associated it with vasomotor and inflammatory changes in the auditory tube[6].
Currently, there are no clear ideas about the change in the clinical picture of tubotitis with positive intra-drum pressure, the causes of its development and adequate treatment.
All this dictates the need for further study of the etiology, patterns of development and clinical treatment of tubootites.
The purpose of the study. The purpose of treatment of tubootitis is to restore the normal patency of the auditory tube. First of all, attention is paid to the elimination of the cause of the disease (to stop: overcooling, blowing your nose hard, rinsing your nose and blowing with a damp nose) and measures to restore the normal functioning of the nasopharynx.
Material and methods of research. To solve the problem, we conducted scientific tests on a total of 65 patients with acute tubootitis.
The results of the study. In order to reduce the swelling of the mucous membranes in 65 patients who underwent examination, referring to the discussion of the results of our study, the patient was prescribed vasoconstrictive nasal drops (naphthysin, sanorin, nazivin, tizin); we recommended antihistamines (suprastin, fensarol, tavegil, setrin).
We noticed that medicinal antimicrobial nasal drops (dioxidin, isofra, polydex, Miramistin, protargol) well suppressed the activity of microbial flora in the group of our main patients who underwent examination.
Rapid reduction and restoration of edema of the mucous membranes of the ENT organs, general warming of the body (hot baths for hands and feet, warm clothes, hot drinking in small sips) and local thermal procedures (alcohol ear drops, turunds with alcohol solutions, vodka and ointment compresses behind the ears, warming of the maxillary and frontal sinuses over warm steam, physiotherapy - UHF). Warming up is carried out in the absence of purulent inflammation and fever.
After the disappearance of acute phenomena in the nose and nasopharynx, the auditory tubes are cleaned, as well as pneumatic massage of the eardrums, which helps to remove the transudate from the tympanic cavity.
With a sufficiently selected treatment, acute tubatitis, as a rule, passes within a few days.
Widely used in the treatment of tubotitis with a pronounced or prolonged process of subsidence is the catheterization of the Eustachian tube, which consists in the introduction of the drug into the middle ear cavity using a catheter. This procedure is very complicated, and if it is performed incorrectly, injury to the mouth of the Eustachian tube and deterioration of the patient's condition may occur.
If conservative therapy is ineffective, eustachiitis is treated surgically. Surgical treatment includes the installation of an ear catheter (shunts). This ensures the release of fluid from the tympanic cavity. Such interventions are listed in GBU. A. Successfully implemented in the conditions of the law-rules of the "OKB im. Semashko".
If tubatitis is not treated and the cause of its occurrence is not eliminated, it often turns into catarrhal or purulent otitis, since this is the stage before otitis.
A dangerous complication of chronic tubootitis is the development of a viscous form of otitis media. As a result of repeated episodes of inflammation, scars and adhesions form in the middle ear cavity. Connective tissue grows and impairs the mobility of auditory elements. Persistent hearing loss develops.
Prevention of the development of tubootitis is an explanatory work on the consequences of hypothermia among the population and timely treatment of exacerbation of chronic diseases and pathological conditions of ENT organs under the supervision of an ENT doctor.Conclusion. Thus, the viruses that cause tubotitis form their interrelations in the etiology and pathogenesis of dis and ESO, which explains the negative effects of their antibacterial therapy. Viruses contribute to reducing the accumulation of antibiotics in the tissues of the mucous membrane of the middle ear, the lowest concentration of which is observed in viral infection, slightly higher — in mixed bacterial and viral, higher — only in bacterial infection.
Conclusion. The main negative role in terms of the impact of viruses on the endothelium and the development of its dysfunction is to stimulate the synthesis of histamine and inflammatory cytokines. Histamine promotes vasodilation, the occurrence of endothelial dysfunction, the expansion of interendothelial spaces and an increase in the permeability of the vascular bed. In addition, viruses lead to delayed (secondary) bacterial infection, first through the dysfunction of neutrophils, endothelium, and then to the development of DST.
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