Acute inflammation of the middle ear

Acute otitis media is an acute inflammation of the mucous membrane of the middle ear, which occurs as a result of infection from the nasopharynx penetrating into the tympanic cavity through the auditory tube. Much less frequently, this disease occurs when infection spreads hematogenously from distant foci and in severe general infectious diseases during the period of rash.

Infection can also enter the tympanic cavity from the external auditory canal, but only if the integrity of the eardrum is compromised. The disease most often occurs in childhood and adolescence, equally often in males and females. As a rule, with acute inflammation of the middle ear, many cellular systems of the middle ear are involved in the pathological process, including the mastoid cave, which is why the disease is called otoantritis.

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What causes acute otitis media?

Most often, acute otitis media occurs with streptococcus infection (55-65%), pneumococcus is in second place (10-18%), staphylococcus infection occurs in 10-15% of cases. But in the vast majority of cases, the disease is due to the association of microorganisms. In some cases, the disease is initiated by influenza infection with subsequent addition of pyogenic. Sometimes, in acute otitis media, green streptococcus, diphtheria bacillus, Proteus, etc. are isolated. With mucous streptococcus and pneumococcus type III, the development of a special kind of acute otitis media is associated, characterized by persistence of the course and significant pathological changes in the structures of the middle ear, called mucous otitis.

The development of acute otitis media is facilitated by many risk factors and immediate causes. Among the latter, acute and chronic diseases of the upper respiratory tract (adenoiditis, tubootitis, rhinosinusitis, chronic tonsillitis, ozena) are in first place. Various volumetric processes in the nasopharynx (angiofibroma, choanal polyp, hyperplasia of the nasopharyngeal and tubal tonsils, etc.) can contribute to the development of acute otitis media. Surgical interventions in the nasopharynx, pharynx, in the nasal cavity and its paranasal sinuses, posterior nasal tamponade, catheterization of the auditory tube and even Politzer's ear blowing can also contribute to the development of the disease in question. Among the common infections most often complicated by acute otitis media, it is necessary to mention influenza, scarlet fever, measles, diphtheria, rubella, bronchopneumonia. Acute otitis media often occurs in the presence of dry perforation after washing the external auditory canal or bathing, taking a shower, accidental water getting into the eardrum.

The general condition of the body, decreased immunity, the presence of exudative diathesis in children, allergies, vitamin deficiency, diabetes, tuberculosis, syphilis, leukemia, etc. play an important role in the development of the disease. In the last decade, it has been established that the so-called ear allergy, which is an integral part of the systemic allergy of the body as a whole and the upper respiratory tract in particular, plays an important role in the development of acute otitis media. Often, frequently recurring acute otitis media is observed in children with allergies, suffering from obstructive bronchitis, exudative diathesis, allergic rhinosinusitis.

Among the local factors contributing to the development of acute otitis media, it is necessary to note a number of features of the histological structure of the mucous membrane of the middle ear and the anatomical structure of the bone tissue of the mastoid process. Thus, according to a number of studies, hyperplasia of the mucous membrane of the tympanic cavity and the remains of embryonic myxomatous tissue remaining under it are the substrate along which the infection easily spreads. This fact has been verified in children who most often develop acute otitis media, especially in infants, in whom myxomatous tissue is in excess under the mucous membrane of the middle ear. This fact also explains the frequent chronicization of acute inflammatory diseases of the middle ear. As for the structure of the mastoid process, most often and to a more pronounced degree, acute otitis media occurs with a pneumatic type of temporal bone structure.

A number of unfavorable conditions in the working environment also contribute to inflammatory diseases of the ear: changes in atmospheric pressure (divers, pilots, submariners, caisson workers), dampness, cold, fatigue, etc.

Pathological anatomy of acute otitis media

At the onset of the disease, the mucous membrane of the tympanic cavity is hyperemic, infiltrated, with the development of inflammation it thickens greatly and hemorrhages occur in it. At the same time, serous and purulent exudate accumulates in the tympanic cavity, protruding the eardrum. Later, at the height of clinical manifestations, foci of softening appear in the proper and mucous layers of the eardrum, and the epithelium of the skin layer is rejected. Due to the pressure of the exudate on the eardrum and its softening, it protrudes in various places, depending on the localization of the center of the inflammatory process.

In the place of the greatest change in the structure of the eardrum, its perforation occurs, most often slit-like, which "gives away" itself during otoscopy by the presence of a pulsating reflex. During recovery, the inflammatory phenomena in the mastoid process subside, hyperemia decreases, the exudate from the tympanic cavity is absorbed or partially evacuated through the auditory tube. The penetrating opening either closes with a scar or is transformed into a persistent perforation with a compacted connective tissue edge. A perforation surrounded by a part of the preserved eardrum is called rim perforation, a perforation directly bordering on the tympanic ring is called marginal. Bulging of the eardrum, perforation in its relaxed part indicate that the inflammatory process developed mainly in the supratympanic space (acute epitympanitis), a form of acute inflammation of the middle ear, most prone to a protracted clinical course and chronicity of the inflammatory process.

With significant development of granulations in the tympanic cavity and difficult evacuation of exudate and purulent contents from it, these tissues grow into connective tissue, resulting in the formation of scars (tympanosclerosis) and adhesions in the tympanic cavity. With such completion of the inflammatory process, the eardrum can be soldered to the medial wall of the tympanic cavity and completely lose mobility. The organization of exudate leads to immobilization of the auditory ossicles. Both of these significantly interfere with the air type of sound conduction.

Symptoms of acute otitis media

Symptoms of acute otitis media may differ in a number of ways depending on the age of the patient.

In newborns, this disease is extremely rare and occurs between the 3rd and 4th week after birth; it is caused either by the penetration of amniotic fluid during childbirth into the tympanic cavity through the auditory tube, or by a nasopharyngeal infection that penetrates in the first days after birth, for example, with mother's milk containing staphylococci.

The outcome is favorable. Recovery occurs either as a result of resorption of the inflammatory exudate of the mucous membrane, or by spontaneous drainage of the exudate from the tympanic cavity through the petrosquamous suture (sutura petrosquamosa), which is not consolidated at this age, into the retroauricular region with the formation of a subperiosteal abscess, the opening and drainage of which leads to recovery without any consequences.

In infants under 8 months, otitis occurs, which is extremely relevant for otopaediatrics, constituting one of the main pathological conditions at this age.

In adolescence, youth and adulthood, a typical clinical picture develops, which is described below with some features.

In old people, acute otitis media occurs less frequently and proceeds subacutely, the symptoms are less pronounced, the temperature reaction is moderate (38-38.5°C) with a relatively satisfactory general condition. A feature of the otoscopic picture is that as a result of sclerosis of the eardrum, which occurs in old and senile age, it is practically not hyperemic in acute otitis media or the hyperemia is of an insular nature in accordance with the "topography" of the sclerosis.

The clinical course of acute otitis media can be divided into three periods, covering an average of 2-4 weeks. The first period (from several hours to 6-8 days) is characterized by the initial symptoms of inflammation in the middle ear, its development, the formation of exudate, and pronounced general reactive phenomena. The second period (about 2 weeks) is perforation of the eardrum and purulent discharge from the ear, a gradual decrease in general reactive phenomena. The third period (7-10 days) is the recovery period, characterized by a decrease in discharge from the tympanic cavity, its thickening, the elimination of inflammatory phenomena in the tympanic cavity, normalization of the otoscopic picture and fusion of the perforation edges or, if the perforation was significant, the formation of a noticeable scar with subsequent calcification or persistent perforation. However, at present, due to changes in the virulence of the microbiota, the presence of highly effective antibiotics and significantly improved methods of general and local treatment, this periodization is rare. Thus, with timely and adequate treatment, inflammation can be limited to the first period, followed by recovery without any residual effects.

In the first period, the symptoms of the disease increase rapidly, and from the first hours, patients complain of pulsating pain in the ear, its congestion and general malaise. The pain in the ear quickly increases and radiates to the crown, temple, teeth. The pain is caused by inflammation of the nerve endings of the trigeminal nerve, abundantly innervating the eardrum and the mucous membrane of the tympanic cavity.

The body temperature rises to 38-38.5°C, and in children sometimes to 40°C and higher. Significant leukocytosis, disappearance of eosinophils, and a sharply increased ESR are observed in the blood. These indicators largely reflect the severity of the disease, the virulence of the infection and the extent of its spread through the structures of the middle ear. A sharp increase in body temperature is not observed only in weakened individuals or if at the very beginning of the disease there was a perforation of the eardrum and, as a result, conditions were created for the outflow of pus from the tympanic cavity. If for some reason the perforation closes, the inflammatory process again worsens, the body temperature increases, ear pain and headache intensify. The later the perforation of the eardrum occurs with the increasing clinical picture, the more destructive are the consequences of acute inflammation of the middle ear. At the beginning of the acute process, a peculiar reactive "response" of the mastoid process is often observed, especially with its pneumatic type of structure. This is due to the fact that the mucous membrane of all cellular elements of the middle ear and especially the cave and cells of the mastoid process actually participate in the inflammatory process. Its participation in the inflammatory process is manifested by swelling and pain upon palpation in the area of the platform. Usually this reaction disappears after the perforation of the eardrum and the onset of discharge from the ear. In fact, the definition of "acute purulent inflammation of the middle ear" is valid only after the perforation of the eardrum and the appearance of purulent discharge from the ear.

In the pre-perforative period, vestibular irritation may also be observed, manifested by dizziness, nausea and vomiting. However, the main functional disorders are observed in the hearing organ. In this and the subsequent period, there is pronounced hearing loss: whispered speech is not perceived or is perceived only at the auricle, spoken speech - at the auricle or no further than 0.5 m. In part, such hearing loss depends on tinnitus, but mainly hearing loss is determined by a significant violation of the air conduction mechanism. In severe cases, with the occurrence of induced labyrinthine disease (toxic damage to the receptors of the cochlea), phenomena of perceptual hearing loss (increased thresholds of perception of high frequencies) may also be observed.

In the second period, after the perforation of the eardrum, the inflammation crosses the equator and in typical cases begins to subside. The pain subsides, the body temperature quickly decreases, the discharge from the ear, initially serous-bloody, becomes thick mucopurulent. A gradual decrease in leukocytosis, the appearance of eosinophils is observed, and at the end of the third period, the ESR approaches normal values. Discharge from the ear in the normal course of the disease continues for up to 7 days. In the third period, discharge from the ear gradually stops, the edges of the small perforation stick together, and after another 7-10 days, complete recovery and hearing restoration occurs.

A medium-sized perforation may close by scarring with subsequent impregnation of the scar with calcium salts or become persistent with callous edges, located in different quadrants of the tympanic membrane. In other cases, scars are formed that disfigure the structures of the tympanic cavity, soldering the tympanic cavity to the medial wall of the tympanic cavity and immobilizing the chain of auditory ossicles.

In some cases, certain deviations may be observed in the typical course of acute otitis media. For example, the pre-perforative period may last for several days as the inflammatory process increases; in this case, a high rise in body temperature to 39-40°C, a sharp increase in ear pain, nausea, vomiting, dizziness, and meningism in children are observed. The general condition deteriorates sharply. In the post-perforative period, despite the perforation of the eardrum and the release of pus, the patient's general condition does not improve, the body temperature does not decrease, and the ear pain does not subside, while the pastosity and soreness of the mastoid process persist. These phenomena may indicate purulent inflammation of the mucous membrane of the mastoid process cells, which significantly prolongs the recovery period. In some cases, the edematous mucous membrane prolapses through the perforation, the thickness of which increases tens of times at the height of the disease, or granulation tissue formed on the inner surface of the eardrum. These formations prevent the release of the contents of the tympanic cavity and prolong the clinical course of the inflammatory process and indicate its severity and the possibility of significant destruction of the structures of the tympanic cavity. It should also be borne in mind that if pus appears in the external auditory canal in large quantities immediately after cleaning the ear, this indicates inflammation of the cellular system of the mastoid process (mastoiditis).

In the past, especially during flu epidemics, hyperacute (otitis acutissima) and fulminant forms of acute otitis media were often observed, characterized by a sudden onset and rapid development of inflammation symptoms with severe general intoxication of the body, body temperature of 39-40°C and higher, irritation of the meninges, convulsions, sharp inflammatory changes in the blood, loss of consciousness, often ending in death. From the point of view of pathogenesis, it is assumed that against the background of a general immunodeficiency state, a highly virulent infection affects the entire tympano-mastoid-labyrinth system (panotitis), including the meninges. Nowadays, such forms of acute otitis media are encountered less and less often and only against the background of severe influenza infection or other diseases that impair immunity. It is also assumed that these forms occur in individuals who have previously suffered a TBI.

There are also forms of acute otitis media with a latent or subacute hypergic course, which are characterized by a gradual onset, a significantly weakened general reaction, subfebrile body temperature, minor inflammatory changes in the blood and unexpressed local changes in the eardrum and tympanic cavity. These forms most often occur in infants with still undeveloped immunobiological protective reactions or in old people in whom these reactions have faded. Sometimes hypergic forms of acute otitis media occur as a consequence of infection with special types of microorganisms or irrational treatment with sulfonamides and antibiotics. These forms of acute otitis media tend to become chronic, have the property of creeping spread to the entire cellular system of the temporal bone with damage to the endosteum, bone tissue and spread to the cranial cavity, causing damage to the membranes of the brain.

The localization, size and shape of perforations are of certain importance for determining the clinical picture, the direction of development of the inflammatory process and its consequences. Thus, perforations occurring in the anterior-inferior or posterior-inferior quadrants indicate in most cases a favorable clinical course of acute inflammation of the middle ear. Even if the perforation becomes permanent and the disease has passed into the stage of chronic inflammation, the latter affects only the mucous membrane, and discharge is sometimes caused only by chronic inflammation of the otitis media.

Localization of perforation in the relaxed part of the tympanic membrane with an isolated inflammatory process localized in the epitympanic space indicates an unfavorable ("malignant") form of otitis. With such localization of perforation, two topographic forms of acute epitympanitis are considered - with localization in the posterosuperior part of the epitympanic space and with localization in the anterosuperior part of this space. The presence of the malleus articulation, ligaments, BA, pathologically formed adhesions in this area delays the evacuation of pathological contents and contributes to the chronicity of the inflammatory process.

Each of the above forms of inflammation localization in the epitympanic space has its own clinical features. Thus, when the process is localized in the posterior-superior part of the epitympanic space, hyperemia and protrusion of the eardrum are observed only in its upper-posterior part, while the normal color and shape of the rest of the eardrum are preserved for several days. This localization of the perforation of the eardrum indicates the seriousness of the inflammatory process, the possibility of its transition to a chronic form and the occurrence of intracranial complications.

In case of inflammation localized in the anterior-superior part of the epitympanic space, the eardrum becomes hyperemic and significantly protrudes with exudate, creating the impression of a false polyp. Perforation of the eardrum occurs late, and no pronounced subjective symptoms arise. At the same time, the limited space causes the direct spread of the inflammatory process to the neck of the malleus, its ligaments and joint located here, which is also fraught with various complications.

Some features of the clinical course of acute otitis media also depend on the microbiota. Thus, the predominance of Staphylococcus aureus gives the purulent discharge a bluish-golden hue, containing an abundance of fibrin. Complications in the presence of this microorganism are relatively rare, but when they occur, they primarily affect the sigmoid sinus.

Special attention should be paid to otitis caused by mucous pneumococcus and streptococcus, which are called "mucous otitis". According to the Vienna otology school, this form of acute inflammation of the middle ear most often occurs in adult men and the elderly. The onset of the disease is sluggish with erased symptoms, signs of inflammation of the BPe and pain syndrome are not expressed, perforation of the eardrum occurs early, but quickly becomes clogged with viscous mucopurulent discharge. Because of this, paracentesis of the eardrum is ineffective, moreover, inflammation of the eardrum worsens, it thickens, becomes hyperemic and acquires a fleshy appearance. Hearing loss in this type of otitis is more significant than in its other forms. Mild but constant pain in the ear and the corresponding half of the head, poorly amenable to analgesics, exhausts the patient. Deep palpation of the mastoid process causes pain, which indicates the involvement of its cells in the inflammatory process. The general condition suffers little: subfebrile body temperature with minor intermittent increases in it, to which the patient does not attach much importance. Indifference to the environment, apathy, insomnia, a feeling of fatigue are characteristic signs of the general condition in this form of acute inflammation of the middle ear. Mucous otitis caused by mucous pneumococcus slowly progresses over weeks and months without interruption, spreading into the deep bone sections of the mastoid region. This type of microorganism has an increased tropism to bone tissue, so its destructive action does not encounter any special barriers and can spread beyond the temporal bone, reaching the cranial cavity.

The predominance of enterococci in the microbiota during acute inflammation of the middle ear often causes severe forms of otitis, fraught with serious complications.

Fusospirochetal association causes severe ulcerative-necrotic otitis with significant destruction in the tympanic cavity and inflammation outlet in the external auditory canal. Purulent discharge has a bloody appearance and a putrid nauseating smell.

Symptoms of acute otitis media in newborns and infants are somewhat different from those in adults. Most often, the disease proceeds unnoticed by others, until discharge from the ear appears. In some cases, the child is restless, wakes up at night, cries, turns his head, rubs the sore ear on the pillow, reaches for the ear, refuses the breast, since sucking and swallowing intensifies the pain in the ear due to increased pressure in the middle ear. Usually, the cause of acute otitis media in infants is acute or chronic nasopharyngitis. With a pronounced clinical picture of acute otitis media, it can be accompanied by meningism - a clinical syndrome that develops due to irritation of the membranes of the brain and manifests itself as headache, stiffness of the occipital muscles, Kernig and Brudzinsky symptoms, dizziness and vomiting. In this case, the child experiences an increase in body temperature, pale skin, dyspeptic symptoms, and swelling of the soft tissues of the retroauricular region.

Often, in infants, inflammation of the mucous membrane of the mastoid process (at this age, the mastoid process and its cellular system have not yet developed) develops either as a complication of acute otitis media or independently against the background of toxic dyspepsia, dysentery or some childhood infection.

Diagnosis of acute otitis media

In most cases, diagnostics is not difficult and the diagnosis is established in accordance with the symptoms and clinical picture described above: acute onset against the background of a cold (acute rhinitis, sinusitis, nasopharyngitis, etc.), ear pain, congestion in it and hearing loss, typical otoscopic picture of the eardrum, presence of perforation and pulsating reflex, pain during deep palpation of the mastoid process area (projection of the mastoid cave), general signs of an inflammatory process (increased body temperature, weakness, malaise, headache, inflammatory phenomena in the cellular composition of the blood, increased ESR).

X-ray examination in standard projections or CT is of great importance in establishing the localization and prevalence of the inflammatory process and possible complications.

Differential diagnostics are carried out with respect to myringitis (inflammation of the eardrum as a complication of acute external otitis), with acute catarrhal otitis media, external otitis media and furuncle of the external auditory canal, herpetic inflammation and exacerbation of chronic purulent otitis media.

With meringitis, there are no general signs of an inflammatory process and hearing remains at a practically normal level. With external diffuse otitis and furuncle of the external auditory canal - sharp pain when pressing on the tragus and during chewing, the pain is localized in the area of the external auditory canal, while with acute inflammation of the middle ear - in the depth of the ear, radiating to the crown and temporo-occipital region. With inflammatory processes in the external auditory canal, there is no pain with deep palpation of the mastoid process, discharge from the ear is purely purulent, while with acute inflammation of the middle ear they are characterized as mucopurulent, viscous. With acute inflammation of the external auditory canal, hearing loss is observed only with complete closure of its lumen, while with acute inflammation of the middle ear, hearing loss is a constant symptom. In case of herpetic lesion of the eardrum, vesicular eruptions are determined on it, when they rupture, bloody discharge appears from the external auditory canal. The pain is localized in the external auditory canal, and is of a burning, constant nature. As the viral infection spreads, temporary paralysis of the facial nerve, dizziness, and hearing loss of a perceptual type may be observed. Herpetic vesicles are located not only on the eardrum, but also on the skin of the external auditory canal and auricle in the so-called Ramsay Hunt zone, innervated by the sensory fibers of the PUN. Eruptions can also be observed simultaneously on the mucous membrane of the soft palate and pharynx, which is an important differential diagnostic sign.

Of particular importance is the differentiation between acute inflammation of the middle ear and exacerbation of chronic purulent otitis media, since the latter can often proceed unnoticed by the patient, and in the case of dry perforation and satisfactory hearing, be completely unknown to the patient. The distinctive signs of exacerbation of chronic purulent otitis media are described below.

In differential diagnostics of common acute otitis media, it is necessary to keep in mind the so-called allergic otitis media, which has become increasingly common in recent years. It is characterized by the absence of a temperature reaction and hyperemia of the eardrum, allergic edema of the mucous membrane of the auditory tube and tympanic cavity. The eardrum is pale, edematous, its contours are blurred. The tympanic cavity and the cells of the mastoid process contain viscous mucus saturated with a large number of eosinophils. This form of otitis is characterized by a sluggish, long course and occurs in people suffering from general allergies, bronchial asthma, allergic rhinosinusopathy; it is difficult to treat and only after a decrease in the severity of the general allergic background and allergic manifestations in other organs.

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Treatment of acute inflammation of the middle ear

Treatment is aimed at reducing pain, accelerating the resorption of the inflammatory infiltrate in the cavities of the middle ear, draining it by improving the patency of the auditory tube or by creating an artificial perforation of the eardrum by paracentesis, as well as restoring hearing function and preventing tympanic and intracranial complications. The nature of treatment depends on the stage of the inflammatory process and is divided into general and local.

The patient is prescribed complete rest and bed rest, hospitalized if indicated. In the pre-perforative period, broad-spectrum antibiotics are prescribed; if ear discharge occurs, the sensitivity of the microbiota to antibiotics is determined and the appropriate drug is prescribed. According to indications, thymalin immunoprotectors are prescribed to stimulate immunity. In case of high body temperature and pain, modern analgesics, antipyretics and anti-inflammatory drugs are prescribed - derivatives of salicylic acid and other compounds. The diet is light, easily digestible, rich in vitamins. Warming compresses, heating pads, sollux, UHF currents, laser irradiation of the mastoid process area are used locally. If heat intensifies the pain, cold is prescribed to the retroauricular area using a special bladder with a cutout for the auricle. A short-term (20-30 min) disinfectant and analgesic effect is provided by 96% ethyl alcohol in the form of warm drops in the ear. Ya.S. Temkin recommends in the pre-perforation period to put warm 5% carbol-glycerin drops into the ear, 8-10 drops 2-3 times a day. These drops increase the elasticity of the eardrum and thereby relieve tension in it from the pressure from the exudate inside. To enhance the analgesic effect, cocaine hydrochloride, dicaine or some other analgesic for application anesthesia are added. After perforation occurs, the introduction of carbol-glycerin drops is stopped, since when combined with water, the carbolic acid bound by glycerin passes into the water and can cause a burn of the skin of the external auditory canal.

Paracentesis of the tympanic membrane. If the treatment used during the pre-perforation period (provided that it is adequate) does not bring any effect within 24 hours, and the tympanic membrane is sharply hyperemic, bulges into the external auditory canal, and the general condition of the patient continues to deteriorate, then paracentesis should be used - artificial perforation of the tympanic membrane (first used in 1800 by A. Cooper to improve hearing in case of obstruction of the auditory tube; in 1862 it was introduced into practice by the outstanding German otologist H. Schwartze to remove inflammatory exudate from the tympanic cavity). This procedure accelerates recovery, prevents otogenic complications and damage to the sound-conducting system of the tympanic cavity and helps to preserve hearing. Therefore, with increasing severity of the disease, one should not take a wait-and-see attitude, since after a successful paracentesis, there are practically no traces left on the eardrum, and after spontaneous perforation, which in itself can be of significant size, coarse scars remain on the eardrum, affecting the function of the eardrum.

In infants, paracentesis should also not be delayed if there are appropriate indications, but it is more difficult to establish indications for them. Firstly, the eardrum in small children with acute otitis media sometimes changes little, while the tympanic cavity contains pus and inflammatory exudate; secondly, when the child cries, physiological hyperemia of the eardrum occurs; thirdly, the eardrum can be covered by desquamating epidermis; and finally, fourthly, acute otitis media in a child suffering from general toxicosis can proceed sluggishly without pronounced local changes. As noted by Ya.S. Temkin (1961), under such circumstances, poor symptoms and the impossibility of checking the state of the child's hearing function, the question of paracentesis is very difficult to resolve, especially if there are other data to explain the increase in body temperature and other signs of a general disease.

Technique of the operation. The procedure is very painful, so before it is carried out, it is necessary to provide for the use of local anesthesia. For this purpose, a few minutes before the operation, drops of the following composition are introduced into the external auditory canal:

• Carbohydrates 0.5
• Mentholi2.0
• Cocaine hydroxide 2.0
• Spiriti aethylici rectificati 10.0

This procedure cannot achieve complete anesthesia, so they try to perform the operation quickly. Instead of application anesthesia, infiltration anesthesia can be performed by a behind-the-ear injection, injecting a 2% solution of novocaine in small portions, passing the needle along the surface of the posterior bone wall to the tympanic ring. This procedure requires the skill of an otolaryngologist. If performed correctly, complete anesthesia occurs. The use of "short" general anesthesia is also acceptable. In children under 2 years of age, paracentesis is performed without any anesthesia.

Paracentesis is performed only under visual control with the patient in a sitting or lying position with his head firmly fixed. Before the operation, the skin of the external auditory canal is treated with ethyl alcohol. Special spear-shaped paracentesis needles are used, the ends of which are similar to a double-edged scalpel; such a needle not only pierces the eardrum, but also cuts it. As a rule, the eardrum is punctured in its posterior quadrants, which are located at a greater distance from the inner wall of the tympanic cavity than the anterior quadrants, or in the place of the greatest protrusion of the eardrum. They try to make the puncture simultaneously through the entire thickness of the eardrum, starting from the lower-posterior quadrant and continuing the incision to the upper-posterior quadrant. Through the resulting linear incision, purulent-bloody fluid is immediately released under pressure. It should be borne in mind that when the mucous membrane of the middle ear, including the one covering the eardrum, is inflamed, it can thicken ten times or more, so paracentesis may be incomplete. You should not try to reach the cavity, since the incision itself will accelerate the spontaneous perforation of the eardrum and the effect of incomplete paracentesis will still be achieved.

After paracentesis, a dry sterile turunda is inserted into the external auditory canal and loosely fixed at the entrance to the canal with a wad of cotton wool. The external auditory canal is cleaned several times a day, treated with boric alcohol or furacilin. Unforced rinsing of the external auditory canal with antiseptic solutions is allowed, followed by drying it with sterile dry cotton wool, after which medicinal substances are introduced by tilting the head towards the healthy ear. Light "pumping" in the middle ear is allowed in the presence of perforation of drops used for treatment, for example, a mixture of an antibiotic solution with hydrocortisone, by pressing the tragus in the external auditory canal or using a Politzer balloon with an auricular olive. In the post-perforation period, catheterization of the auditory tube with the introduction of a mixture of a solution of the appropriate antibiotic and hydrocortisone into the tympanic cavity is also allowed. The use of the latter prevents the formation of coarse scars and ankylosis of the joints of the auditory ossicles. In the established phase of suppuration, the method of "dry" bandaging with sterile dressing material is used. For this, a dry turunda is brought to the perforation or incision of the eardrum and its end is brought out into the scaphoid fossa, then a dry cotton-gauze bandage is applied to the ear, which is changed 3 times a day. The patient is recommended, if possible, to lie with the diseased ear to a pillow to improve the outflow of purulent contents from the tympanic cavity. Otolaryngological treatment from the very beginning should be accompanied by procedures aimed at sanitation of the nasopharynx and auditory tube. For this, various types of nasal instillations, irrigation of the nasopharynx with antiseptics, vasoconstrictors in aerosol form are carried out. Medicinal substances should be introduced into the tympanic cavity through a catheter with caution and only after paracentesis or spontaneous perforation of the tympanic membrane, otherwise increased pressure is created in the tympanic cavity, as a result of which the infection can spread beyond the middle ear through the dehiscences, perineural and perivasal spaces. After closure of the perforation or paracentesis incision and cessation of discharge from the ear for 5-7 days, Politzer or any other ear inflation should not be performed without special need, since increased pressure in the tympanic cavity can lead to divergence of the perforation edges and a delay in the healing process. Inflation of the auditory tube may be recommended if there is retraction of the tympanic membrane and stiffness in the joints of the auditory ossicles, manifested by hearing loss. In this condition, pneumatic massage of the tympanic membrane is also indicated, starting with low-intensity pulsating pressure in the external auditory canal.

How to prevent acute otitis media?

Preventive measures are especially important for children, since they are the ones who experience frequent relapses of acute otitis media and chronic inflammation, often leading to severe hearing loss and related speech development deficiencies. They include measures to sanitize the upper respiratory tract, strengthen the immune system, prevent colds, restore nasal breathing, hardening, eliminate harmful household habits, and minimize the effects of harmful professional factors (humidity, cooling, barometric pressure changes, etc.). As noted by V. T. Palchun and N. A. Preobrazhensky (1978), rational treatment (non-surgical or surgical) of purulent sinusitis is of great importance for the prevention of acute otitis media. In childhood, acute otitis media is often caused by chronic adenoiditis and hypertrophy of the pharyngeal tonsils, which contribute to the development of inflammation of the mucous membrane of the auditory tube, its obstruction and penetration of infection into the middle ear. Complications of acute otitis media. The proximity of the tympanic cavity and temporal bone cells to the cranial cavity under certain conditions of development of the inflammatory process in the middle ear (immunodeficiency, diabetes, blood disease, pronounced virulence and penetrance of pathogenic microorganisms), a number of anatomical features (excessive pneumatization of the temporal bone, dehiscence, features of the vascular course, etc.) can contribute to the development of a number of intracranial complications, as well as the spread of infection within the temporal bone. The former are described in the section on complications in chronic purulent otitis media; In this section we will focus on acute mastoiditis and inflammation of the petrous pyramid of the temporal bone, as well as some forms of atypical mastoiditis.

Prognosis of acute otitis media

The most common outcome of acute otitis media is complete morphological and functional recovery, even spontaneous, without any significant therapeutic or surgical measures. In other cases, even with intensive treatment, the clinical picture can be severe with various complications or with the transition of the inflammatory process to a chronic form. Such an outcome is possible with a sharp depletion of the body due to a severe previous disease, with diabetes, weakened immunity, during periods of flu epidemics, etc. Often, perforation of the eardrum leaves behind scars of varying sizes, which in the subsequent period are saturated with calcium salts and acquire a yellowish or white color. Cessation of discharge from the ear, increased pain, increased body temperature and resumption of other signs of acute otitis media indicate a delay in the tympanic cavity and the cellular system of the middle ear of pus and exudate and may indicate the onset of some complication. A sharp rise in body temperature, constant headaches, hyperleukocytosis, a significant increase in ESR, severe weakness, apathy, indifference to the environment and to one's own condition with good drainage of the tympanic cavity indicate severe intoxication of the body and the possibility of an intracranial complication. This condition, which has arisen against the background of positive dynamics of acute otitis media and continues to worsen, is a direct indication for surgical treatment with a wide opening of the entire cellular system of the temporal bone, while the direction of elimination of tissues affected by the purulent process indicates their pathological change per continuitatem. In the absence of complications that have already arisen and developed (mastoiditis, apicitis, sinus thrombosis, meningitis, abscess of the temporal lobe of the brain, etc.), early surgical intervention in such a clinical picture prevents, like paracentesis of the eardrum, the destruction of the sound conduction system and, with careful attention to its elements, allows preserving hearing. In the event of intracranial complications, which include thrombophlebitis of the sigmoid and transverse venous sinuses, the prognosis for life is cautious and is determined by the timeliness of the appropriate surgical intervention, the effectiveness of subsequent treatment and the general condition of the body.

The prognosis for hearing function is determined by the degree of alteration of the tympanic membrane and the ossicular chain. Small marginal perforations in the lower parts of the tympanic membrane and rim perforations without disrupting the sound-conducting capacity of the ossicular chain practically do not change the hearing function. Perforations located in the relaxed part and inflammatory ankylosis of the malleus-anvil joint cause conductive hearing loss of varying degrees. Extensive cicatricial changes (tympanosclerosis) sharply worsen hearing function, and if vestibular disorders and high-frequency tonal tinnitus (intoxication of cochlear receptors) were noted during the peak period, then in the recovery period, conductive hearing loss is often accompanied by perceptive hearing loss that progresses over the years.