Computed tomography during endoscopic surgery. Discussing the technique of endoscopic sinus surgery proposed by scientists Stamberger and Meserklinger from the University of Graz, Professor H. Braun noted the need to adhere to the same principles of minimal trauma as those used in stapes surgery. Minimizing trauma during surgery can be achieved by identifying anatomical and topographic features using computed tomography. Access to the frontal sinus is through the recessus frontalis. Mucus flow from the sinus orifice can be blocked by the posterior and cranial infundibular cell (ager nazi cell), the uncinate process (processus uncinatus), and the anterior and cranial bulla. Having identified these structures using computed tomography, their removal can begin using endoscopic methods. The procedure, known as "uncapping the egg-conclusion," is performed using a 45-degree endoscope. Adherence to atraumatic principles, taking into account the anatomical features of each individual case, helps avoid iatrogenic complications, improve the postoperative course, and, most importantly, minimize the risk of restenosis of the frontal sinus ostium. Fungal rhinosinusitis. According to statistical studies conducted in the United States, chronic rhinosinusitis is the most common chronic disease, affecting 37 million Americans. The etiology of chronic rhinosinusitis is unknown; rather, it is believed to be multifactorial. Specialists at the Mayo Clinic in the United States, examining the nasal mucus discharge of patients with chronic rhinosinusitis, discovered fungal elements surrounded by eosinophils. The term "Mayo Clinic phenomenon" has even been coined. Having refined the mucus collection technique, other researchers, including those from the University of Graz, were able to make similar observations. For this purpose, an impression of the nasal mucosa is made using sterilized X-ray film, washed with saline solution into a sterile tube, and sent for mycological examination. Using Gomorrah staining or Oregon Green 488, fungi were detected in the mucus of 75% of patients (81% at the Mayo Clinic). Using hematoxylin and eosin staining, eosinophils were detected in the same mucus in 95% of patients (96% at the Mayo Clinic). The presence of fungi in the mucus was confirmed by microbiological methods. Since fungal elements are suspended in the mucus, the mucus was treated with mucolytics to precipitate them onto the nutrient medium in a Petri dish. After culturing the fungal culture, it was identified (various fungi were cultured, most frequently Alternaria). Histological examination of mucosal sections revealed inflammation and thickening of the mucosa, tissue imbibition by eosinophils, and polyps. Using a new method of fluorescent antibodies to detect fungi in nasal mucus, researchers at the University of Graz obtained surprising results: fungi were detected in 100% of patients with chronic rhinosinusitis. Furthermore, the nasal secretions of a group of healthy volunteers also contained fungal elements. The scientists concluded that everyone inhales fungal spores, and everyone's nasal mucus contains fungal elements, but not everyone reacts to their presence in the body; only some develop eosinophilic inflammation. The following pathogenesis is proposed: for some reason, eosinophils are activated by interleukin-5 and -13 (their concentrations in the blood of patients are elevated) and migrate from the vascular lumen into the tissue, penetrating the basement membrane supporting the columnar epithelial cells, passing between the cells, and entering the mucus. Here, eosinophils accumulate around the fungi, which, being large objects, cannot be phagocytized and degranulate, releasing the so-called basic protein. This substance not only aggressively attacks the fungi but also causes damage to the mucosal epithelium, thereby triggering an inflammatory response. Thus, the occurrence of inflammation, according to the hypothesis, depends on the "readiness" of eosinophils to respond to the generally harmless fungus. To confirm this theory, eosinophil activity was studied in vitro. Isolated eosinophils were placed in a medium containing the Alternaria fungus. Within an hour, eosinophils isolated from the blood of patients with chronic rhinosinusitis accumulated around the fungus and degranulated, a phenomenon not observed in healthy individuals. Should we assume that chronic rhinosinusitis is a systemic disease rather than a local inflammatory process? Moreover, 73% of patients with bronchial asthma examined also had fungal elements surrounded by clusters of eosinophils in their bronchial mucus. Histological examination revealed eosinophilic inflammation, as in chronic rhinosinusitis. In recent years, the incidence of chronic rhinosinusitis has increased in parallel with the incidence of bronchial asthma. If such similarities in the pathogenesis of these diseases are observed, could they be the same disease with different clinical manifestations? Research in this area is ongoing by scientists at the University of Graz. Conservative treatment of acute and chronic otitis media. In acute otitis media, treatment is prescribed depending on whether it is perforated or non-perforated otitis. The main treatment measures include: - antibiotic therapy; - anti-inflammatory drugs; - painkillers; - vasoconstrictor drugs in the form of nasal drops; - digital massage of the pharyngeal opening of the auditory tube; - paracentesis; - myringotomy; - ear catheterization. Approaches to antibiotic therapy are controversial. Not all otolaryngologists prescribe antibiotics for acute otitis media. Comparative studies conducted in 1991 showed that the immediate results of treatment without antibiotics (placebo) are positive in 86% of cases, with the use of an antibiotic (Amoxicillin) - in 98%. Long-term treatment results were virtually identical in both groups of patients. However, it is recommended to prescribe antibiotics, since regular patient monitoring and timely prevention of complications are not always possible. Antibiotic therapy for acute otitis media shortens the duration of the illness and, in most cases, prevents the development of complications. Antibiotic selection should preferably be based on the antibiogram. For this purpose, a sample of middle ear exudate is analyzed, which can be easily obtained in cases of perforated otitis media or by paracentesis in cases of non-perforated otitis media. The sensitivity of the exudate's microflora to specific antibiotics is determined. As a rule, new-onset acute otitis media responds to treatment with Amoxicillin; in cases of relapse, Amoxiclav or Augmentin are recommended. If antibiotic treatment is ineffective within the first 2-3 days, it is discontinued and a different antibiotic is prescribed, to which the pathogenic microflora is sensitive. The duration of antibiotic therapy is 1-2 weeks. Ear drops are used in the comprehensive treatment of acute otitis media; in cases of non-perforated otitis media, they are used only for pain relief. In this case, antibiotic-containing drops are not recommended, as they do not penetrate the eardrum into the middle ear cavity. In cases of perforated otitis media, it is essential to thoroughly clean the ear canal and tympanic cavity before administering the drops. Otherwise, discharge from the ear canal will be forced into the middle ear and mastoid cells. Therefore, it is necessary to first remove the exudate and thoroughly dry the ear. Otofa and Normax ear drops, which contain a non-ototoxic antibiotic, are effective. Alcohol-containing drops are not recommended (unfortunately, many doctors recommend boric alcohol drops), as they increase pain and cause a burn of the mucous membrane of the middle ear. For acute catarrhal otitis media, digital massage of the pharyngeal orifice of the Eustachian tube for 4-5 seconds is a very effective method. This improves the patency of the Eustachian tube by removing mechanical obstructions in the orifice area, such as adhesions and scars, and by irritating the reflexogenic zone in the nasopharyngeal tube ridge. For non-perforated otitis media, paracentesis—piercing the eardrum—is recommended to remove exudate from the tympanic cavity and allow air to enter the middle ear. This reduces pain in the patient. The resulting exudate is tested for the sensitivity of the microorganisms it contains to antibiotics. If paracentesis is ineffective, myringotomy—incision of the eardrum—is performed. It is also indicated for complicated acute otitis media that is refractory to antibiotic therapy, for sluggish or recurrent cases, and in children under three years of age, especially newborns. Recurrent otitis media can be caused by adenoid vegetations, chronic rhinitis and sinusitis, and latent mastoiditis. Treatment involves shunting the eardrum and long-term courses of steroid anti-inflammatory medications. The criteria for recovery are: disappearance of general symptoms, normalization of body temperature, cessation of pain, restoration of hearing. In 40% of patients, signs of inflammation of the eardrum persist for a long time after clinical recovery. A long-term inflammatory infectious disease of the middle ear cavity - chronic otitis media is classified as non-purulent (secretory) and purulent, tuberculous otitis is distinguished separately. The primary tuberculous lesion is localized in the middle ear in the absence of foci in the lungs, Mycobacterium tuberculosis is found in the exudate, such otitis does not respond to treatment with traditional methods. According to M. Barton (2002), chronic otitis media is classified as follows: - consequences - scar formation in the tympanic cavity in combination with persistent dry perforation of the eardrum; - active mesotympanitis; - inactive mesotympanitis; - active epitympanitis; - inactive epitympanitis. Treatment of chronic otitis media, with the exception of mesotympanitis, is surgical. For long-term treatment (1-3 months) of mesotympanitis and in the preoperative period for other forms of chronic otitis media, Erespal is indicated. It reduces inactive inflammatory changes in the mucous membrane of the upper respiratory tract and restores mucociliary clearance. Otitis media is an inflammatory disease of the middle ear in which the atrophic eardrum shifts toward the medial wall of the tympanic cavity, the promontory, which is accompanied by a decrease in the volume of the middle ear cavity. Clinically, this is manifested by the formation of a retraction pocket (local retraction of the eardrum) due to invagination of the weakened area of ??the eardrum toward the tympanic cavity. Retraction of the eardrum can be partial (a specific area is retracted) or total (the entire eardrum is retracted). A retraction pocket is characterized by the depth of its penetration into the middle ear and its ability to self-clean. It can be localized in the pars flaccida or pars tensa, affecting both parts of the eardrum. When discussing the etiology of atelectatic otitis media, four main causes are identified. 1. Inflammatory processes in the upper respiratory tract. 2. Negative pressure in the middle ear cavities. The key factors in equalizing pressure are the auditory tube, which regulates gas exchange between the nasopharynx and middle ear, and the mucous membrane lining the middle ear cavities, ensuring gas exchange between the air in the tympanic cavity and the blood flowing through the mucous membrane vessels. Under normal atmospheric pressure and an intact mucous membrane, gas exchange through the auditory tube occurs at a volume of 1 ?L per opening of the tube (in total, the auditory tube opens up to 500-1000 times per day). During sudden changes in atmospheric pressure (diving into water, flying in an airplane, or during an explosion), the Eustachian tube acts as a protective valve, regulating the flow of air into the middle ear, thus ensuring optimal conditions for sound transmission to the inner ear. During slow, gradual pressure changes, the mucous membrane of the middle ear plays a primary role in regulation through gas exchange between the vessels and the air contained in the middle ear cavity (oxygen and nitrogen enter the bloodstream, while carbon dioxide and water are released). The intensity of gas exchange depends on the condition of the mucous membrane: its thickness, the degree of development of the vascular network, and the volume of blood flowing through the vessels. Inflammation disrupts normal gas exchange processes due to deterioration of both the Eustachian tube and the inflammatoryly altered mucous membrane of the middle ear. Negative pressure is created in the tympanic cavity, which directly predisposes to the formation of a retraction pocket. 3. Atrophy of the lamina propria of the eardrum. Biophysical theory explains the development of atrophy by a disruption of the elasticity of the collagen fibers of the lamina propria of the eardrum. Biochemical theory suggests that inflammation in these fibers results in the rupture of disulfide bonds. The eardrum loses elasticity, stretches, and thins. Weak points of the eardrum include the pars flaccida in the area of ??the notch in the bony ring (absent collagen fibers) and the posterior quadrants of the pars tensa (weak network of circular collagen fibers; in this area, the eardrum thickness is 60 µm, while in other areas it is 90 µm). 4. Dysfunction of the stratified squamous epithelium of the eardrum. Normally, the outer surface of the eardrum is cleared by centrifugal movement of the epithelium from the center to the periphery and its desquamation. Centripetal growth (from the periphery to the center) ensures healing of the tympanic membrane perforation. Disruption of these processes contributes to the development of a retraction pocket. Local predisposing factors—individual structural features of the temporal bone formed during organogenesis—also affect middle ear function. There are conservative and surgical treatments for retraction pockets. The question of surgical intervention is controversial. With atelectatic otitis media, hearing function is typically intact for a long time, but it takes a long time for a cholesteatoma to form or for hearing loss to develop due to destruction of the auditory ossicles. In these cases, complex surgical intervention is necessary. Therefore, it is important to begin treatment in the early stages of retraction pocket formation. Bernard Ars identifies three main treatment approaches. 1. Treatment of inflammatory processes in the upper respiratory tract, which is especially important in pediatric practice: anti-inflammatory drugs, antibiotics, antihistamines, and vaccine therapy are prescribed; adenoidectomy, paranasal sinus surgery, and treatment of gastroesophageal reflux are performed when indicated. 2. Normalization of impaired middle ear pressure regulation—restoration of the function of the auditory tube, the mucous membrane of the tympanic cavity, and the mastoid cells. Obstructive or dynamic disorders of the auditory tube may occur. Drug therapy is used to eliminate inflammation and swelling of the mucous membrane of the auditory tube, laser catheterization of the posterior wall of the auditory tube and the vault of the nasopharynx in case of mechanical obstruction, and kinesiotherapy and logotherapy for dysfunction of the auditory tube muscles and impaired opening processes. Restoration of the mucous membrane of the middle ear cavity is carried out using medications (local and systemic) or surgical treatment methods: granulation tissue and polyps are removed from the tympanic cavity, communication between the tympanic cavity and the antrum of the mastoid process is restored (anthro- and aditotomy with preservation of the posterior wall of the auditory canal), posterior tympanotomy, drainage of the mastoid process. 3. Bernard Ars distinguishes three stages of retraction pocket development. Stage I - R. P. Safe (stable). The risk of cholesteatoma formation is minimal. Hearing is normal. Conservative treatment is effective. Stage II - R. P. Uncertain (unstable). Hypotrophy of the eardrum, high risk of cholesteatoma formation. Hearing function is preserved. Stage III - R. P. Unstable (unstable). Erosion of the frame of the bony ring, fusion of the pocket with the wall of the tympanic cavity. Карман не способен к самоочищению, есть признаки воспаления, полипы в области ретракционного кармана. В 70% случаев ретракционный карман локализуется в pars tensa. При І стадии проводят консервативное лечение, при ІІ стадии — иссечение кармана и шунтирование барабанной перепонки, в ІІІ стадии зачастую заменяют барабанную перепонку аллотрансплантатом. В 30% случаев ретракционные карманы располагаются в pars flaccida: при І и ІІ стадии развития поддаются консервативному лечению, а при ІІІ стадии проводят тимпанопластику, иногда в сочетании с мастоидэктомией. Основные принципы тимпанопластики. Первые операции на ухе были санирующего характера и преследовали цель устранить гноетечение, а также ликвидировать угрозу внутричерепных осложнений у больных хроническим гнойным отитом. Однако хирургическое вмешательство не гарантировало достижения поставленных задач: гноетечение сохранялось в 40-70% случаев после операции, очень редко, но возникали внутричерепные осложнения. После плановой санирующей операции высок риск развития и таких осложнений, как стойкое головокружение и шум в ухе, ухудшение слуха вплоть до полной глухоты. Осложнения возможны из-за небрежного отношения во время операции к элементам среднего уха, в особенности к стремечку, что связано с квалификацией хирурга. Очень важно также правильное послеоперационное ведение для восстановления слуха у таких больных. Операции, направленные на улучшение слуха, начали проводить в конце ХІХ — начале ХХ века: попытки закрыть дефекты барабанной перепонки, сопоставление сохранившихся слуховых косточек в единую цепь и даже стапедэктомия. Попытки не были продолжены по причине неудач, отсутствия на то время антибактериальных средств, специальных оптических приборов и, наконец, опыта и выработанной тактики. В 50-х годах прошлого века Horst Wullstein и Fritz Zollner систематизировали все сообщения о функциональных реконструктивных операциях на среднем ухе и предложили пять типов тимпанопластики. Сегодня тимпанопластика включает целый ряд оперативных вмешательств, направленных на восстановление слуховой функции: — закрытие дефектов барабанной перепонки; — тотальная реконструкция барабанной перепонки; — транспозиция сохранившихся слуховых косточек и использование их в качестве колумелл; — использование аллотрансплантатов и протезов из пластмасс для восстановления цепи слуховых косточек; — реконструкция костных стенок барабанной полости; — формирование просвета барабанной полости с помощью тефлоновых прокладок. Особенно эффективно использование аллотрансплантатов барабанной перепонки или барабанной перепонки и слуховых косточек. Для предупреждения сращения трансплантата с медиальной стенкой барабанной полости применяются пластиковые прокладки (тефлон, силикон, сипрамид, силастик). При выполнении тимпанопластики важна этапность проведения операции. Если имеется перфорация барабанной перепонки в сочетании с фиксированным стремечком, хирург не имеет права мобилизовать пластинку стремечка, так как создаются предпосылки для попадания инфекционного агента во внутреннее ухо, что может привести к полной глухоте (ятрогенная глухота). Поэтому операцию осуществляют в два этапа. На первом этапе с помощью тефлоновых прокладок формируется воздухоносная тимпанальная полость, и хирург оценивает состояние слизистой оболочки. Если слизистая оболочка патологически не изменена, на втором этапе хирург имеет право открыть преддверие и заменить фиксированную пластинку стремечка на тканевой трансплантат. При сохранившемся стремечке или его пластинке между ним (его пластинкой) и барабанной перепонкой устанавливается колумелла. Иногда тимпалопластику проводят в три этапа. После формирования стерильной воздухоносной полости хирург может принять решение не проводить колумеллизацию сразу, а добиться образования в овальном окне подвижной мембраны. Дело в том, что после закрытия овального окна тканевым трансплантатом во время второго этапа очень трудно угадать необходимую длину протеза: можно либо не довести его до уровня рамы овального окна (протез не будет проводить звук), либо внедрить его в преддверие (это приведет к постоянному головокружению у больного). Поэтому во время второго этапа удаляют пластинку стремечка, окно закрывают сгустком крови, барабанную полость закрывают. За несколько месяцев на месте сгустка крови образуется подвижная мембрана, на которой очень легко установить колумеллу и нет риска, что она провалится в преддверие или окажется короткой. Операция проводится в три этапа и в том случае, если слизистая оболочка изменена, утолщена и контуры окон не видны. Колумеллизация, как третий этап, осуществляется спустя несколько месяцев, после того как состояние слизистой оболочки нормализуется. Важными условиями для получения положительных результатов проведенной операции являются: сохраненная функция звуковоспринимающего аппарата (улитки), сохраненная функция слуховой трубы. Для успешного функционирования трансплантата слуховая труба должна быть проходима. Расширение костной части слуховой трубы осуществляется при помощи металлических бужей. Конечно, есть риск последующего рубцевания вследствие травматизации слизистой оболочки слуховой трубы. Чтобы при регенерации слизистой оболочки не образовывались рубцы, буж имеет в сечении не круглую форму, а эллипсовидную. Травмируется только часть слизистой оболочки, а другие участки, не соприкасавшиеся с поверхностью бужа, сохраняются и за их счет происходит регенерация. Перед проведением тимпанопластики больному необходимо объяснить суть оперативного вмешательства, особенно это касается операций на единственно слышащем ухе или на лучше слышащем ухе. При оформлении истории болезни нельзя писать «больному показана тимпанопластика», можно только рекомендовать эту операцию и проводить ее лишь с согласия больного.