Otogenic meningitis: causes, features of the course and treatment. Rhinogenic meningitis, arachnoiditis. Rhinogenic orbital complications

What is rhinogenic meningitis

What is rhinogenic meningitis

Develops at any age.

What causes rhinogenic meningitis

The causative agents of purulent meningitis are usually cocci (streptococci, staphylococci, diplococci), less often other microorganisms. Purulent meningitis often occurs with inflammation of the frontal and ethmoidal sinuses, sometimes complicates subdural and cerebral abscesses, and is difficult; lightning-fast form is possible.

Pathogenesis (what happens?) during rhinogenic meningitis

Primary (more often at acute diseases due to penetration into the subarachnoid space of a bacterial infection directly from the primary purulent focus in the nasal cavity or paranasal sinuses).

Secondary (against the background of other intracranial complications - subdural or brain abscess, sinus thrombosis, is more severe).

Serous (develops with the penetration of toxins). Serous meningitis is usually considered as a stage of a single pathological process, a transitional stage to purulent meningitis.

Symptoms of rhinogenic meningitis

The clinical course of rhinogenic meningitis does not differ from that of other secondary purulent meningitis.

The disease has an acute onset, constantly high fever, serious condition, mental disorder, general weakness, lethargy, pallor of the skin and a number of general symptoms are noted. This is a diffuse intense constant or paroxysmal headache with a predominance in the frontal region, aggravated by any movement of the head, accompanied by nausea and vomiting, as well as a slowing of the pulse under the influence of increased intracranial pressure on the medulla and the nucleus of the vagus nerve and changes in the fundus (congestion).

The position of the patient is forced on the side with legs pressed to the stomach and the head thrown back. Obscuration or loss of consciousness, delirium, monotonous cry, agitation or lethargy, increased response to sound, light and tactile effects are observed.

There is pain in the lower back and severe pain when pressing on the region of the spinous processes of the vertebrae due to irritation of the posterior roots of the spinal cord by purulent exudate. Meningeal symptoms are revealed: neck stiffness, Kernig and Brudzinsky symptoms, increased tendon reflexes, pathological pyramidal symptoms of Babinsky, Rossolimo, Oppenheim and Gordon, sometimes paresis and paralysis of individual cranial nerves, clonic and tonic convulsions.

Usually, all the attention of patients is paid to the manifestations of intracranial complications, so they rarely present complaints characteristic of diseases of the nasal cavity and paranasal sinuses. When a meningeal syndrome is detected in children, it is necessary to carefully examine the paranasal sinuses to exclude their disease as a cause of intracranial complications. Objectively revealed difficulty in nasal breathing, pain on palpation of the paranasal sinuses, swelling of the mucous membrane of the nasal concha, abundant mucopurulent discharge in the nasal passages.

Diagnosis of rhinogenic meningitis

The diagnosis is specified using the following methods.

X-ray of the paranasal sinuses allows you to clarify the violation of their pneumatization.

Examination of cerebrospinal fluid: cerebrospinal fluid in serous meningitis is transparent, flows out under high pressure; the increase in the number of cells is insignificant with a predominance of lymphocytes. With purulent meningitis, the cerebrospinal fluid is cloudy, opalescent, flows out quickly, under great pressure; increased protein content (Pandi's reaction); sharp cytosis from 10 to 1000 or more neutrophils per 1 µl, the amount of glucose and chlorides is reduced. AT severe cases bacterial growth is detected.

Differential diagnosis. Most often, rhinogenic meningitis is differentiated from tuberculous meningitis, which is characterized by:

slow start;
normal or subfebrile temperature;
paresis of the oculomotor nerve (ptosis, anisocoria), lack of reaction to light;
positive Mantoux reaction;
corresponding changes in the cerebrospinal fluid: flakes, mild xanthochromia, severe lymphocytosis, great content protein, the formation of a fibrin network after 5-6 hours, the fluid pressure is increased, the content of glucose and chlorides is reduced.

Which doctors should you contact if you have rhinogenic meningitis

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Otogenic and rhinogenic meningitis is an acute inflammation of the meninges, which is associated with a purulent process in the ear (otogenic meningitis), in the nose and its paranasal sinuses ah (rhinogenic meningitis). Among all otogenic intracranial complications, otogenic meningitis is, according to different authors, from 9.4 to 25.1‰.

Rhinogenic meningitis, as well as rhinogenic intracranial complications, is much less common, and in the literature there are only descriptions of individual observations of this disease. Rhinogenic intracranial complications are 12-15 times less common than otogenic ones. The causative agents of otogenic and rhinogenic meningitis are most often streptococci, pneumococci and other microorganisms, as well as adenoviruses and mycoplasmas.

An important role in the development of otogenic and rhinogenic meningitis is played by changes in the local and general resistance of the organism, its reactivity. The source of infection in otogenic meningitis is most often chronic purulent otitis media, especially epitympanitis, complicated by cholesteatoma, less often acute suppurative otitis media. The frequency of complications of chronic suppurative otitis media with meningitis, according to the literature, ranges from 0.5 to 3.6%.

Pathogenesis

Infection from the cavities of the middle ear into the cranial cavity can penetrate the contact, hematogenous and lymphogenous routes. With the contact spread of the process, the infection penetrates along the paths either anatomically already existing, or along the newly formed pathological process. In the first case, these are vascular connections, preformed anatomical messages in the form of holes and channels, labyrinthine windows, internal auditory meatus, aqueducts of the cochlea and vestibule, mastoid cells; in young children, there are open gaps at the junctions of the constituent parts of the temporal bone, which can remain open for a long time even in an adult.

The ways of spreading the infection in the second case are fistulas, which are formed as a result of caries of the walls of the middle ear. In chronic purulent otitis media, fistulas often form in the roof of the tympanic cavity and mastoid cave, as well as on the inner wall of the mastoid process. If the infection spreads through the inner ear, then such meningitis is called labyrinthogenic, if through the middle ear - tympanogenic.

The labyrinthine route of infection occurs in more than 50% of all otogenic meningitis. Otogenic meningitis can also be caused by other intracranial complications - subdural abscess, sinus thrombosis, abscess of the brain and cerebellum. Factors contributing to the penetration of infection into the cranial cavity are shaking of the head upon impact, falling, during surgical interventions using the “hammer” method on a sclerosed mastoid process, as well as weakening the body with infectious diseases.

Rhinogenic meningitis develops as a result of infection entering the subarachnoid space from the paranasal sinuses (often the frontal) or from the nasal cavity. The infection penetrates through the fistulas of the thin cerebral walls of the paranasal sinuses in chronic inflammation, through the veins of the mucous membrane of the ethmoidal labyrinth through existing anastomoses into the veins of the dura mater, and also through the sheaths of the olfactory nerve. It is possible to develop rhinogenic meningitis during surgical interventions in the nose and paranasal sinuses. This is most often observed during endonasal opening of the ethmoid labyrinth and frontal sinus and.

pathological anatomy

Pathological changes in otogenic and rhinogenic meningitis are characterized by the formation of inflammatory exudate in the subarachnoid space. By its nature, the exudate can be serous or purely purulent; depending on this, serous and purulent meningitis are distinguished. Exudate accumulations can be limited and localized mainly at the site of infection transition from the ear cavities to the cranial cavity, which is facilitated by the formation of adhesions between the pia mater in the chronic course of the disease. In this case, limited purulent meningitis is observed. If the inflammatory exudate spreads over large spaces, passing to the other hemisphere and the cerebellum, then diffuse purulent meningitis develops.

Clinical manifestations

Symptoms of otogenic and rhinogenic meningitis are varied and are due to the disease that caused them, the localization of the process, and the degree of increase in intracranial pressure. The main complaint of the patient is severe headaches of a diffuse or localized nature. Appears stiff neck, meningeal posture. There is a general hyperesthesia of the skin, photophobia, sensitivity to sounds is exacerbated. Clonic and tonic convulsions of the muscles of the limbs and face, as well as symptoms of damage to the cranial nerves (especially often oculomotor, facial, vagus, trigeminal) in the form of paralysis, paresis, sensitivity disorders and secretory disorders can be observed. With the localization of the pathological process in the posterior cranial fossa, breathing may slow down; sometimes Cheyne-Stokes breathing develops.

When the process spreads to the spinal cord, the functions are disturbed pelvic organs, pathological reflexes of Babinsky, Gordon, Rossolimo, Oppenheim appear, which may not always appear in full and not always be clearly expressed.

A particularly violent course with high fever, severe headaches, persistent vomiting, and unconsciousness is characteristic of purulent meningitis caused by hematogenous spread of the process in acute purulent otitis media.

A constant symptom of otogenic or rhinogenic meningitis are changes in the cerebrospinal fluid: an increase in its pressure, sometimes up to 700-800 mm of water column; it is opalescent, sometimes cloudy. In the study of the cellular composition of the cerebrospinal fluid, pleocytosis is detected, mainly due to polynuclear cells. The protein content increases, sugar and chlorides decrease. In the blood, leukocytosis is detected (up to 20000-25000 in 1 μl), neutrophilia; ESR is accelerated. The temperature reaction, as a rule, is pronounced and constant. Symptoms of serous meningitis are much less pronounced, and the course of the disease is less severe.

Diagnostics

The diagnosis of otogenic and rhinogenic meningitis is based on the history, examination and examination of the cerebrospinal fluid. It is very important to establish a connection between purulent meningitis and an ear or nose disease. If, in chronic suppurative otitis media, pain in the ear appears, otorrhea increases, fever and meningeal symptoms appear, then the presence of otogenic meningitis should be assumed. It should also be assumed if the corresponding symptomatology appears with a disease of the nose and its paranasal sinuses or after surgical interventions on these organs. In acute purulent otitis media, pain in the ear, fever and otorrhea are also characteristic of the underlying disease, and the differential diagnosis becomes more difficult. The issue is resolved by the results of the study of cerebrospinal fluid, the presence of meningeal syndrome.

In the differential diagnosis of purulent otogenic and rhinogenic meningitis with meningococcal meningitis of great importance is the detection of meningococcus in the cerebrospinal fluid.

Treatment

Treatment of otogenic and rhinogenic meningitis should be complex - etiological, pathogenetic and symptomatic. The primary measure is the removal of the infectious focus, regardless of the severity of the patient's condition. The operation is performed against the background of the appointment antibiotic therapy; it is first necessary to determine the nature of the microflora and its sensitivity to antibiotics.

The method of administration of antibiotics, depending on the severity of the patient's condition, can be intramuscular, intravenous, intracarotid, endolumbar. Of the antibiotics, penicillin is more often used at a dose of 10 to 20 million units per day, less often sigmamycin, oleandomycin 1.0 g per day, etc. The introduction of penicillin by the endolumbar method is permissible in a serious condition of the patient; in this case, only its sodium salt can be used. The duration of the introduction of antibiotics depends on the nature of the course of the disease. Along with antibiotics, nystatin, sulfonamides are prescribed, detoxification, dehydration and symptomatic therapy is carried out.

Forecast

The prognosis for otogenic and rhinogenic meningitis before the introduction of sulfonamides and antibiotics into practice was severe, a lethal outcome was observed in 75-97% of cases. Subject to a comprehensive proper treatment lethality does not exceed 20%.

Develops at any age.

What provokes rhinogenic meningitis:

Pathogenesis (what happens?) during Rhinogenic meningitis:

Primary (usually in acute diseases due to penetration into the subarachnoid space of a bacterial infection directly from the primary purulent focus in the nasal cavity or paranasal sinuses).

Secondary (against the background of other intracranial complications - subdural or brain abscess, sinus thrombosis, is more severe).

Serous (develops with the penetration of toxins). Serous meningitis is usually considered as a stage of a single pathological process, a transitional stage to purulent meningitis.

Symptoms of rhinogenic meningitis:

The clinical course of rhinogenic meningitis does not differ from that of other secondary purulent meningitis.

The disease has an acute onset, constantly high fever, serious condition, mental disorder, general weakness, lethargy, pallor of the skin and a number of general symptoms are noted. This is a diffuse intense constant or paroxysmal headache with a predominance in the frontal region, aggravated by any movement of the head, accompanied by nausea and vomiting, as well as slowing of the pulse under the influence of increased intracranial pressure on the medulla oblongata and nuclei of the vagus nerve and changes in the fundus (congestion).

Diagnosis of rhinogenic meningitis:

The diagnosis is specified using the following methods.

X-ray of the paranasal sinuses allows you to clarify the violation of their pneumatization.

Differential diagnosis. Most often, rhinogenic meningitis is differentiated from tuberculous meningitis, which is characterized by:

slow start;
normal or subfebrile temperature;
paresis of the oculomotor nerve (ptosis, anisocoria), lack of reaction to light;
positive Mantoux reaction;
corresponding changes in the cerebrospinal fluid: flakes, mild xanthochromia, sharp lymphocytosis, high protein content, formation of a fibrin mesh after 5-6 hours, fluid pressure is increased, glucose and chloride levels are reduced.

A disease that can develop at any age. The causative agents of purulent meningitis usually include cocci (staphylococci, streptococci, diplococci), a little less often other microorganisms. Purulent meningitis often appears with inflammation of the ethmoid and frontal sinuses, sometimes complicating cerebral and subdural abscesses. The disease is severe; lightning-fast form cannot be ruled out. Forms of the disease:

primary (occurs most often in acute manifestations of the disease due to the penetration of a bacterial infection into the subarachnoid space directly from a purulent primary focus in the area of the nose or paranasal sinuses);
secondary (against the background of other intracranial complications - cerebral or subdural abscess, sinus thrombosis, is more severe);
purulent;
serous (formed in case of penetration of toxins).

Serous meningitis is usually considered as a stage of a single pathological process, a transitional stage to purulent meningitis.

treatment

As a rule, all the attention of the attending physician and patients is paid to the manifestations of intracranial complications, so they rarely complain about diseases of the nasal cavity and paranasal sinuses. If meningeal syndrome is detected in children, the paranasal sinuses should be carefully examined in order to exclude diseases resulting from intracranial complications. Objectively reveal difficulty in nasal breathing. There is pain on palpation of the paranasal sinuses, abundant mucopurulent discharge in the nasal passages, swelling of the mucous membrane of the nasal concha. The diagnosis is clarified using the following methods:

radiography of the paranasal sinuses (the factor of violation of their pneumatization is specified),
studies of cerebrospinal fluid (with serous meningitis, the cerebrospinal fluid is transparent, it flows out under high pressure; the number of cells with a predominance of lymphocytes increases, and in purulent meningitis, the cerebrospinal fluid is opalescent, cloudy, flows out quickly, under high pressure).

symptoms

The clinical course of the disease does not differ from that in other purulent secondary meningitis. The disease is characterized by:

acute start,
constantly high temperature
serious condition,
general weakness,
mental disorder,
lethargy,
pale skin, other general symptoms.

The patient is characterized by diffuse intense paroxysmal or constant headache, which prevails in the frontal zone, increases with any movement of the head. Nausea and vomiting appear, the pulse slows down under the influence of increased intracranial pressure on the medulla oblongata and nuclei of the vagus nerve, changes occur in the fundus (congestion). The position of the patient is forced on the side with legs pressed to the stomach and the head thrown back. There is also confusion or loss of consciousness, monotonous cry, delirium, lethargy, agitation, increased response to light, sound, tactile impact. They note pain in the lower back, severe pain when pressing on the zone of the spinous processes of the vertebrae due to irritation of the posterior roots of the spinal cord by purulent exudate. There are also meningeal symptoms:

Kernig's sign
Brudzinski's symptom
neck stiffness,
increased tendon reflexes
pathological pyramidal symptom of Rossolimo Babinsky, Gordon, Oppenheim,
paresis,
paralysis of individual cranial nerves,
tonic and clonic convulsions.

Rhinogenic purulent meningitisusually develops with acute or exacerbation of chronic purulent inflammation in the upper group of the paranasal sinuses(frontal, ethmoid, wedge-shaped) due to the fact that the infection can penetrate into the cranial cavity by contact and cause diffuse purulent inflammation of the meninges.

Numerous cases of purulent meningitis have been reported. with trauma to the sieve plate after intranasal surgery, with fractures of the base of the skull. In these cases, the infection spreads through fissures and along the perineural lymphatic pathways of the olfactory nerve fibers.

With rhinogenic purulent meningitis, increased production of cerebrospinal fluid occurs, resulting in increased intracranial pressure, which usually causes a diffuse headache. In addition, the inflammatory process to some extent extends to the brain and cranial nerves. Such an extensive lesion of the central nervous system causes the appearance of certain symptoms along with characteristic features meningitis.

With purulent meningitis, as a rule, register (see "Otogenic intracranial complications") stiff neck, Kernig's symptom, constant high body temperature. In severe cases of the disease, the upper and lower symptoms of Brudzinsky are usually detected. Diagnostic reliable sign is a change in the cerebrospinal fluid - an increase in the number of cells and protein content in it. During puncture, fluid flows out in frequent drops or a jet due to increased pressure. Biochemical and microscopic parameters are identical to those in otogenic purulent meningitis. However, the prognosis for rhinogenic inflammation is less favorable than for otogenic inflammation.

The treatment of the disease is urgent radical surgical intervention on the inflamed sinuses in order to eliminate the purulent focus. At the same time, massive anti-inflammatory and dehydration therapy, spinal punctures are carried out.

Riyaogeyayayy arachnoiditisis either the outcome of leptomeningitis with the development of scars and cysts of the arachnoid membrane, or the primary fibroplastic process in an organism sensitized by a purulent infection. Most often, arachnoiditis accompanies ethmoiditis, sphenoiditis, sinusitis, less often - frontal sinusitis.

The clinical picture consists of cerebral symptoms, focal signs and changes in the cerebrospinal fluid. The most characteristic clinic of arachnoiditis with optochiasmal syndrome. Headache in these cases is both diffuse and localized in the fronto-ophthalmic or occipital regions. It can be constant, dull, aggravated by exacerbations of arachnoiditis, but it can also have the character of neuralgia with irritation to the forehead and nose. Sometimes the headache is accompanied by nausea, vomiting usually does not occur, meningeal symptoms are very rare, expressed unsharply.

In the diagnosis, changes in visual fields, visual acuity and the condition of the fundus are important. At lumbar puncture almost always a high cerebrospinal fluid pressure is determined (up to 350-400 mm of water column at a rate of 100-180 mm of water column). The composition of the cerebrospinal fluid is either hydrocephalic (0.099 g/l) or moderately elevated protein (from 0.36-0.49 to 0.66 g/l). The number of cells is usually not increased.

The diagnosis of rhinogenic arachnoiditis is based on establishing an association between sinus disease and visual impairment. In differential diagnosis from a pituitary tumor, arachnoid endothelioma, radiographic changes in the area of the Turkish saddle, computed tomography and MRI data should be taken into account.

In the early diagnosis of rhinogenic arachnoiditis, the results of pneumo-, electro- and echoencephalography are important.

Treatment. Therapeutic tactics for rhinogenic arachnoiditis consists of surgical elimination of inflammation in the nasal cavity and paranasal sinuses and active drug anti-inflammatory and dehydration therapy. In some cases, treatment in a neurological or neurosurgical hospital is indicated.

Abscesses of the frontal lobe of the brain

The most common source of infection is the frontal sinus, less often the ethmoid labyrinth; the rest of the paranasal sinuses are of lesser importance. Abscess formation usually occurs with acute or exacerbation of chronic inflammation in the sinuses. The shape, location and size of the rhinogenic brain abscess are not constant, since the posterior wall of the frontal sinus - the main route of infection - varies in location, size and relation to frontal lobes.

local symptoms characterize mainly the features of the course of inflammation in the sinuses: swelling of the eyelids, more than the upper one, swelling and hyperemia of the conjunctiva, the presence of exophthalmos of varying severity with a displacement of the eyeball more often downwards and outwards. These symptoms are more pronounced in acute than in chronic frontal sinusitis, and are observed in the acute stage of brain abscess formation, significantly decreasing in the late stage, when general symptoms (moderate fever, slight blood changes) are the same for brain abscesses of all localizations (moderate leukocytosis, neutrophilia , increase in ESR). When an abscess encapsulates, there is a moderate increase in pressure in the cerebrospinal fluid; pleocytosis up to several hundred cells per cubic millimeter is often noted, with more neutrophils; protein content usually increases. A more pronounced pleocytosis, an increase in the content of sugar and chlorides in the cerebrospinal fluid, the appearance of microbes indicate the addition of meningitis.

Cerebral symptoms with frontal abscesses, in addition to headaches, they are mainly characterized by irritability, drowsiness, frequent mood swings with a transition from fun to sadness, and inappropriate behavior. In some cases, these symptoms can be explained by intracranial hypertension, but sometimes they can be regarded as focal symptoms of damage to the frontal lobe. The observed euphoria, inappropriate behavior, foolishness should also be attributed to focal symptoms. Nystagmus, olfactory disturbances, changes in statics and gait are never observed.

More conventional focal symptoms for frontal lobe abscesses are convulsions, paresis and visual disturbances. Convulsions are in the nature of focal, Jacksonian seizures, begin with the mimic muscles of the face of the opposite side and, with the progression of the disease, spread first to the upper, then to the lower limbs; in the advanced stage of the disease, general convulsive seizures with a focal onset are also possible. If a brain abscess is suspected, computed tomography is required.

Treatment of rhinogenic brain abscess only surgical providing for the rehabilitation of the source of inflammation, drainage of the abscess. In the postoperative period, massive antibiotic and dehydration therapy is indicated.

Thrombosis of the cavernous sinus

The disease is caused by the spread of infection, usually from the area of the nasolabial triangle (mainly for nasal furuncles) through veins that do not have a valve apparatus, directly into the cavernous sinus and its rapid generalization, the development of sepsis. A complication can also occur with purulent inflammation of the cells of the ethmoid labyrinth, maxillary, wedge-shaped, etc. due to the anatomical proximity of these formations.

The clinical picture of cavernous sinus thrombosis consists of general, cerebral, meningeal and local symptoms.

General symptoms consists in an increase in body temperature, pronounced signs of an infectious-septic process: seizures, accompanied by a significant increase in temperature and its decrease, combined with chills, profuse sweating and weakness. Sometimes the high body temperature is constant. There may be infectious metastases to the lungs and other organs. More frequent changes internal organs caused by impaired microcirculation.

In the blood, leukocytosis (segmented), elevated ESR, dysproteinemia with an increase in the relative content of a g, a 2 - and y-globulins. In cultures of blood taken at the height of body temperature, streptococci and staphylococci are more often found. Cerebral symptoms are associated with an increase in intracranial pressure and consist of headache, dilated veins and narrowing of the arteries of the fundus; meningeal symptoms - in pleocytosis and positive results of globulin reactions, mild stiff neck with negative symptoms Kernig and Brudzinsky (dissociated symptom complex). Local symptoms include exophthalmos, venous edema and redness, ptosis, chemosis, abducens, trochlear, oculomotor, and trigeminal neuritis.

important diagnostic method in addition to clinical data is computer research skulls.

Treatment. First of all, surgical sanitation of the focus of infection is performed (opening the abscess, sinus surgery, etc.). Conservative therapy consists mainly in stopping the blockade of microcirculation and thrombosis. Leading place divert therapy with heparin administered subcutaneously or intravenously. The dose of heparin is selected so that the blood becomes negative reactions for protamine, ethanol, naphthol and the presence fibrinolar complexes. Usually it does not exceed 30,000-40,000 IU per day. Replacement therapy of missing anticoagulants is important. For this purpose, fresh frozen plasma and fresh blood are administered. The use of low molecular weight dextrans (reopoliglyukin at a dose of 5-10 ml/kg) can reduce the aggregate properties of blood. For the prevention and treatment of blockade of microcirculation and thrombosis, drugs are used that have the ability to prevent platelet aggregation and activate the fibrinolytic activity of plasma (aspirin at a dose of 0.25-0.5 g 2-3 times a day, nicotinic acid 0.05-0.1 g 3 times a day or 3 ml of a 1% solution intramuscularly 1-2 times a day).

2. Features of acute otitis media in children.

Acute inflammation of the middle ear in newborns, in the thoracic and early childhood occurs much more often than in adults, and has a number of features. The peculiarity of the symptoms is determined by the characteristics of general and local immunity, the morphology of the mucous membrane of the middle ear and the structure of the temporal bone. In newborns, the tympanic cavity contains remnants of myxoid tissue, which is a breeding ground for the development of infection. During this period, the inflammatory process in the middle ear often occurs due to getting into tympanic cavity through the auditory tube of amniotic fluid during childbirth. At infants the mechanism of infection is the same, but not only the infection from the nose and nasopharynx, but also food masses during regurgitation can get into the middle ear. This is facilitated by the fact that in childhood the auditory tube is wide and short. Another mechanism for the occurrence of otitis media is also possible: the temporal bone in newborns and infants is richly vascularized, contains a large amount of bone marrow, and inflammation in the ear can be in the nature of osteomyelitis.

The causes of acute otitis media in children are often infectious diseases (measles, scarlet fever, influenza); the source of infection can be adenoids, in which viruses often vegetate, causing an inflammatory process in the middle ear. Mechanical closure of the mouth of the auditory tube with adenoid growths should also be taken into account when deciding on the cause of otitis media in a child.

clinical picture. In an infant, manifestations of acute otitis media may be mild. However, the behavior of a child whose ear hurts is significantly different from the behavior of an adult: he often cries out, refuses to take the breast because of painful swallowing, rubs his sore ear against his mother's hand. Starting from the year when the child himself can determine the localization of pain, the doctor quite easily establishes the focus of the disease. The main symptoms at this age are pain when pressing on the tragus (the ear canal bone has not yet formed), high body temperature (39.5-40 ° C). The behavior of a child with otitis media is almost always depressed, he sleeps a lot, the function of the gastrointestinal tract is disturbed, diarrhea, vomiting appear, the child becomes very thin. Keep in mind the possibility of meningeal symptoms accompanied by dimming of consciousness. This condition, unlike meningitis, is called meningism and does not develop due to inflammation of the meninges, but due to intoxication of the central nervous system. Meningism disappears as soon as perforation of the tympanic membrane and emptying of pus from the cavities of the middle ear occur.

Acute otitis media in children goes through the same stages as in adults. A feature of otitis media in childhood is that in them, more often than in adults, a cure occurs without perforation of the tympanic membrane, due to its greater resistance, high absorption capacity of the mucous membrane of the tympanic cavity and easier outflow through a wide and short auditory tube.

Diagnosis is based on the data of the general examination and the otoscopic picture. It should be borne in mind that in infants, the eardrum easily reddens after cleaning the ear and with any cry of the child. In older children, the otoscopic picture is similar to that in adults. A thicker, cloudy tympanic membrane in children does not always reflect the condition of the tympanic cavity, since the epidermis covering it lies in a thick layer, is easily rejected and hides hyperemia. With continued suppuration, differential diagnosis should be carried out between otitis media and otitis externa.

Treatment for acute otitis media in a child is the same as in an adult (except for ear catheterization). However, children in more early dates paracentesis is indicated, and immediately into the tympanic cavity through the incision, it is necessary to introduce an antibiotic solution and a suspension of hydrocortisone using the method of careful transmeatal injection (see above). At elevated body temperature, antibiotics are prescribed orally, and when high temperature- parenterally. When a perforation occurs in a child, more often than in an adult, granulations occur in the tympanic cavity, which can close the perforation and disrupt the outflow, so vasoconstrictor drops should be poured into the ear, for example, 0.1% adrenaline solution (3 drops 2 times a day) . After that, the ear is cleaned with a cotton wick and a 30% solution of sodium sulfacyl is poured in (5 drops 3 times a day). Dimexide (30%) has a good antimicrobial and anti-inflammatory effect, and against Pseudomonas aeruginosa and Proteus vulgaris - decametroxine (0.01%), both drugs are poured into the ear 10 drops 2-3 times a day. With a tendency to a protracted course of inflammation in the middle ear in a child, it is advisable to activate protective mechanisms by administering gamma globulin (in ampoules) 3 ml (or 1.5 ml) intramuscularly after 1 (or 2) days in the amount of three injections.

Prevention of diseases of the middle ear should be carried out from the day of birth, it consists of a set of measures, both general and individual, depending on the age, nutritional status, living conditions of the child, etc.

General measures: organization of a general hygienic regimen and nutrition, prevention of acute catarrhs of the upper respiratory tract and influenza infection (in particular, through anti-influenza vaccinations) - are the basis for the prevention of otitis in children and increase the resistance of the child's body. These activities also include hardening of the body, frequent walks in the open air, the child's stay in a bright, dry, well-ventilated, warm room, water procedures, proper diet, rich in vitamins and an age-appropriate diet. In children's institutions, UV irradiation of rooms and children, especially those suffering from rickets, should be widely used. The fight against rickets, diathesis is one of the important measures otitis media warnings.

The prevention of diseases of the nose and nasopharynx requires special attention, since they largely determine the occurrence of inflammatory changes in the middle ear in children.

One of the measures to prevent otitis is the observance of hygienic rules for feeding and caring for infants. Sick personnel should not be allowed near children. If the child is still ill with catarrh of the upper respiratory tract or influenza, one of the main tasks is to restore nasal breathing. To do this, before each feeding, it is necessary to pour 3 drops into each half of the nose of the child. % solution boric acid with adrenaline (1 drop of adrenaline per 1 ml of solution). Given that in infancy, secretion retention occurs more often in back departments nose, the child is given a more upright position during feeding, and during sleep it must often be turned from one side to the other. Under these conditions, the flow of mucus into the mouth of the auditory tube is prevented.

To prevent otitis media, the upper respiratory tract is sanitized in order to restore normal nasal breathing in a timely manner (removal of adenoid growths, elimination of inflammation of the nasal mucosa and nasopharynx, etc.). In the treatment of inflammatory diseases of the middle ear in a child, it is necessary to monitor the auditory function, since the timely detection of hearing loss and its early treatment allow you to get the best result.

3. Clinical anatomy of the outer and middle ear. Research methods (otoscopy, determination of the patency of the auditory tube).

Anatomy of the outer ear

The outer ear includes the auricle(auricula) and external auditory canal(meatus acusticus externus).

The auricle is located between the temporomandibular joint in front and the mastoid process behind; it distinguishes between a concave outer surface and a convex inner one facing the mastoid process. The skeleton of the shell is an elastic cartilage 0.5-1 mm thick, covered on both sides with perichondrium and skin.

On the concave surface, the skin is tightly fused with the perichondrium, and on the convex, where the subcutaneous connective tissue is more developed, it is folded. The cartilage of the auricle has complex structure due to the presence of elevations and depressions of various shapes. The auricle consists of a curl (helix), bordering the outer edge of the shell, and an antihelix (anthelix), located in the form of a roller medially from the curl. Between them is a longitudinal recess - a boat (scapha). Anterior to the entrance to the external auditory meatus is its protruding part - the tragus (tragus), and posteriorly is another protrusion - the antitragus (antitragus). Between them at the bottom there is a notch - incisura in-tertragica. On the concave surface of the auricle, there is a triangular fossa (fossa triangularis) at the top, and below there is a depression - the ear shell (concha auriculae), which in turn is divided into the shell shuttle (cymba con-chae) and the shell cavity (cavum canchae). From top to bottom, the auricle ends with a lobe, or lobule, of the ear (lobulus auriculae), which is devoid of cartilage and is formed only by fatty tissue covered with skin.

The auricle is attached with ligaments and muscles to the scales of the temporal bone, mastoid and zygomatic processes, and the muscles of the shell in humans are rudimentary. The auricle, forming a funnel-shaped narrowing, passes into the external auditory canal which is a tube bent along the length in adults, about 2.5 cm, not counting the tragus. The shape of its lumen approaches an ellipse with a diameter of up to 0.7-0.9 cm. The external auditory meatus ends at the tympanic membrane, which delimits the outer and middle ear.

The external auditory meatus consists of two sections: membranous-cartilaginous external and bone internal. The external section makes up two thirds of the entire length of the auditory meatus. At the same time, only its anterior and bottom wall, and the back and top are formed by dense fibrous connective tissue. The cartilaginous plate of the external auditory canal is interrupted by two transverse cuts of the cartilage of the auditory canal (incisura cartilaginis meatus acustici), or Santorini fissures, covered with fibrous tissue. The membranous-cartilaginous section is connected to the bone part of the external auditory canal through an elastic connective tissue in the form of a circle. This structure of the outer ear causes significant mobility of the ear canal, which facilitates not only examination of the ear, but also the performance of various surgical interventions. In the area of Santorini crevices due to the presence of loose fiber the auditory canal from below borders on the parotid gland, which causes the often observed transition of the inflammatory process from the outer ear to the parotid gland and vice versa.

The external auditory meatus in adults has an inclination from the tympanic membrane anteriorly and downwards, therefore, to examine the bone section and the tympanic membrane, the auricle (together with outer part ear canal) must be pulled upward and backward: in this case, the ear canal becomes straight. In children, when examining the ear, the shell should be pulled down and backwards.

In a newborn and a child in the first 6 months of life, the entrance to the external auditory canal looks like a gap, since the upper wall almost closely adjoins the lower one. In adults, there is a tendency to narrow the auditory canal from the entrance to it to the end of the cartilaginous part; in the bone part, the lumen expands somewhat, and then narrows again. The narrowest part of the external auditory meatus is located in the middle of the bone and is called the isthmus (isthmus).

Knowing the location of the narrowing of the external auditory canal allows you to avoid the possible pushing of a foreign body behind the isthmus when trying to remove it with an instrument. The anterior wall of the external auditory meatus delimits the joint of the lower jaw from the external ear, therefore, when an inflammatory process occurs in it, chewing movements cause severe pain. In some cases, there is an injury to the anterior wall when falling on the chin. The superior wall separates the outer ear from the middle cranial fossa therefore, blood or cerebrospinal fluid may leak from the ear when the base of the skull is fractured. The posterior wall of the outer ear, being the anterior wall of the mastoid process, is often involved in the inflammatory process in mastoiditis. At the base of this wall passes the facial nerve. The lower wall separates the parotid gland from the external ear.

In newborns, the temporal bone is not yet fully developed, so the bone part of the auditory canal is absent, there is only a bone ring to which the tympanic membrane is attached, and the walls of the passage almost close, leaving no lumen. The bone part of the ear canal is formed by the age of 4, and the diameter of the lumen, the shape and size of the external auditory canal change up to 12-15 years.

The external auditory meatus is covered with skin, which is a continuation of the skin of the auricle. In the membranous-cartilaginous part of the auditory canal, the thickness of the skin reaches 1–2 mm, it is abundantly supplied with hair, sebaceous and sulfuric glands. The latter are modified sebaceous glands. They give out a secret Brown color, which, together with the discharge of the sebaceous glands and the shed epithelium of the skin, forms earwax. Drying up, earwax usually falls out of the ear canal; this is facilitated by vibrations of the membranous-cartilaginous part of the auditory canal during movements of the lower jaw. In the bony part of the ear canal, the skin is thin (up to 0.1 mm). It has no glands or hair. Medially, it passes to the outer surface of the tympanic membrane, forming its outer layer.

The blood supply to the external ear is carried out from the system of the external carotid artery (a.carotis externa); in front - from the superficial temporal artery (a.temporalis superficialis), behind - from the posterior ear (a.auricularis posterior) and occipital (a.occipitalis) arteries. The deeper sections of the external auditory canal receive blood from the deep ear artery (a.auricularis profunda - a branch of the internal maxillary artery - a.maxillaris interna). Venous outflow goes in two directions: anteriorly - into the posterior facial vein (v.facia-lis posterior), posteriorly - into the posterior ear (v.auricularis posterior).

Lymph outflow occurs in the direction of the nodes located in front of the tragus, on the mastoid process and under the lower wall of the external auditory canal. From here, the lymph flows into the deep lymph nodes of the neck (if inflammation occurs in the external auditory canal, these nodes increase and become sharply painful on palpation).

The innervation of the outer ear is carried out by sensitive branches of the ear-temporal (n.auriculotemporalis - the third branch of the trigeminal nerve - n.trigeminus) and the large ear (n.auricularis magnus - a branch of the cervical plexus) nerves, as well as the ear branch (r.auricularis) of the vagus nerve ( n.vagus). In this regard, in some people, mechanical irritation of the posterior and lower walls of the external auditory canal, innervated by the vagus nerve, causes a reflex cough. The motor nerve for the rudimentary muscles of the auricle is the posterior auricular nerve (n.auricularis posterior - a branch of p.facialis).

The tympanic membrane (membrana tympani, myrinx) is the outer wall of the tympanic cavity (Fig. 4.3) and delimits the outer ear from the middle ear. The membrane is an anatomical formation of irregular shape (an oval 10 mm high and 9 mm wide), very elastic, slightly elastic and very thin, up to 0.1 mm. In children, it has an almost round shape and is much thicker than in adults, due to the thickness of the skin and mucous membrane, i.e. outdoor and inner layers. The membrane is funnel-shaped retracted into the tympanic cavity. It consists of three layers: outer - skin (epidermal), which is a continuation of the skin of the external auditory canal, inner - mucous, which is a continuation of the mucous membrane of the tympanic cavity, and middle - connective tissue, represented by two layers of fibers: outer radial and inner circular. Radial fibers are more developed, circular. Most of radial fibers goes to the center of the membrane, where the place of greatest depression is located - the navel (umbo), however, some fibers reach only the handle of the malleus, attaching on the sides along its entire length. Circular fibers are less developed and there are no membranes in the center.

The tympanic membrane is enclosed in a groove of the tympanic ring (sulcus tympanicus), but there is no groove at the top: the notch is located in this place (incisura tympanica, s. Rivi ni), and the tympanic membrane is directly attached to the edge of the temporal bone scales. The upper-posterior part of the tympanic membrane is inclined outward to the long axis of the external auditory canal laterally, forming an obtuse angle with the upper wall of the auditory canal, and in the lower and anterior parts it is deflected inward and approaches the walls of the bone passage, forming with it sharp corner at 27 °, as a result of which a depression is formed - sinus tympanicus. The tympanic membrane in its different sections is unequally separated from the inner wall of the tympanic cavity: for example, in the center - by 1.5-2 mm, in the lower anterior section - by 4-5 mm, in the lower back - by 6 mm. The last department is preferable for performing paracentesis (an incision of the eardrum) in case of acute purulent inflammation of the middle ear. The handle of the malleus is tightly fused with the inner and middle layers of the tympanic membrane, the lower end of which, slightly below the middle of the tympanic membrane, forms a funnel-shaped depression - the navel (umbo). The handle of the malleus, continuing from the navel upwards and partly anteriorly, in the upper third of the membrane gives a short process visible from the outside (processus brevis), which, protruding outward, protrudes the membrane, as a result of which two folds are formed on it - anterior and posterior.

A small part of the membrane, located in the region of the tympanic (rivinium) notch (incisura tympanica) (above the short process and folds), does not have a middle (fibrous) layer - a loose, or sagging, part (pars flaccida, s.Shrap-nelli) in contrast from the rest - stretched (pars tensa). The size of the loose part depends on the size of the rivinus notch and the position of the short process of the malleus.

The tympanic membrane has a pearly gray color under artificial lighting, but it should be borne in mind that the light source has a significant effect on the appearance of the membrane, in particular forming the so-called light cone.

For practical purposes, the tympanic membrane is conditionally divided into four quadrants by two lines, one of which is drawn along the handle of the malleus to the lower edge of the membrane, and the other is perpendicular to it through the navel. In accordance with this division, the anteroposterior, posterior superior, anteroinferior, and posterior inferior quadrants are distinguished.

The blood supply to the tympanic membrane from the side of the outer ear is carried out by the deep ear artery (a.auricularis profunda - a branch of the maxillary artery - a.maxillaris) and from the side of the middle ear - the lower tympanic (a.tympanica inferior). The vessels of the outer and inner layers of the tympanic membrane anastomose with each other.

Vienna outer surface tympanic membrane empties into the outer jugular vein, and the inner surface - in the plexus located around the auditory tube, transverse sinus and veins of the dura mater.

Lymphatic drainage is carried out to the pre-, posterior and posterior cervical lymph nodes.

The innervation of the tympanic membrane is provided by the ear branch of the vagus nerve (r.auricularis n.vagus), the tympanic branches of the ear-temporal (n.auriculotemporalis) and glossopharyngeal (n.glossopharyngeus) nerves.

Middle ear anatomy

The middle ear (auris media) consists of several interconnected air cavities: the tympanic cavity (cavum tympani), the auditory tube (tuba auditiva), the entrance to the cave (aditus ad antrum), the cave (antrum) and the associated air cells of the mastoid process. (cellulae mastoidea). Through the auditory tube, the middle ear communicates with the nasopharynx; under normal conditions, this is the only communication of all cavities of the middle ear with the external environment.

drum cavity. The tympanic cavity can be compared to an irregularly shaped cube up to 1 cm 3 in volume. It distinguishes six walls: upper, lower, anterior, posterior, outer and inner.

The upper wall, or roof, of the tympanic cavity (tegmen tympani) is represented by a bone plate 1-6 mm thick. It separates the tympanic cavity from the middle cranial fossa. There are small openings in the roof through which vessels pass, carrying blood from the dura mater to the mucous membrane of the middle ear. Sometimes dehiscences form in the upper wall; in these cases, the mucous membrane of the tympanic cavity is directly adjacent to the dura mater.

In newborns and children of the first years of life, on the border between the pyramid and the scales of the temporal bone, there is an uncovered fissure (fissura petrosquamosa), which causes the occurrence of brain symptoms with acute inflammation of the middle ear. Subsequently, a suture (sutura petrosquamosa) is formed at this place and communication with the cranial cavity in this place is eliminated.

The lower (jugular) wall, or bottom of the tympanic cavity (paries jugularis), borders on the jugular fossa (fossa jugularis) lying under it, in which the bulb of the jugular vein (bulbus venae jugularis) is located. The more the fossa protrudes into the tympanic cavity, the thinner the bone wall. The inferior wall may be very thin or have dehiscences through which the bulb of the vein sometimes protrudes into the tympanic cavity. This makes it possible to injure the bulb of the jugular vein, accompanied by severe bleeding, during paracentesis or careless scraping of granulations from the bottom of the tympanic cavity.

The anterior wall, tubal or carotid (paries tubaria, s.caroticus), of the tympanic cavity is formed by a thin bone plate, outside of which is the internal carotid artery. There are two openings in the anterior wall, the upper one, narrow, leads to the semi-canal for the muscle that stretches the eardrum (semicanalis m.tensoris tympani), and the lower, wide one, to the tympanic mouth of the auditory tube (ostium tympanicum tybae auditivae). In addition, the anterior wall is permeated with thin tubules (ca-naliculi caroticotympanici), through which vessels and nerves pass into the tympanic cavity, in some cases it has dehiscence.

The posterior (mastoid) wall of the tympanic cavity (paries mastoideus) borders on the mastoid process. In the upper part of this wall there is a wide course (aditus ad antrum), communicating the epitympanic recess- attic with permanent mastoid cell- cave (antrum mastoideum). Below this passage is a bone protrusion - a pyramidal process, from which the stirrup muscle (m.stapedius) begins. On the outer surface of the pyramidal process is a tympanic opening (apertura tympanica canaliculi chordae), through which enters the tympanic cavity drum string(chorda tympani), extending from the facial nerve. In the thickness of the lower section of the posterior wall, the descending knee of the facial nerve canal passes.

The outer (membranous) wall of the tympanic cavity (paries membranaceus) is formed by the tympanic membrane and partially in the attic region. bone plate, which departs from the upper bone wall of the external auditory canal.

The inner (labyrinthine, medial, promontory) wall of the tympanic cavity (paries labyrinthicus) is the outer wall of the labyrinth and separates it from the middle ear cavity. In the middle of this wall there is oval-shaped elevation- cape (promonto-rium), formed by the hatching of the main whorl of the cochlea. Behind and above the cape is vestibule window niche I ( oval window according to the old nomenclature; fenestra vestibuli), closed by the base of the stirrup (basis stapedis). The latter is attached to the edges of the window by means of an annular ligament (lig. annulare). In the direction backwards and downwards from the cape, there is 1 other niche, at the bottom of which there is a cochlea window (a round window according to the old nomenclature; fenestra cochleae), leading to cochlea I and closed by a secondary tympanic membrane (mem-I brana tympany secundaria), which consists of three layers: outer - mucous, middle - connective tissue and SCH internal - endothelial.

Above the window of the vestibule along the inner wall of the tympanic cavity in the direction from front to back passes horizontal knee of the bone canal of the facial nerve, which, having reached the protrusion of the horizontal semicircular canal on the inner wall of the antrum, turns vertically down - the descending knee - and goes to the base of the skull through the stylomastoid foramen (for. stylomastoideum). The facial nerve is located in the bone canal (canalis Fallopii). The horizontal segment of the canal of the facial nerve above the window of the vestibule protrudes into the tympanic cavity in the form of a bone roller (prominentia canalis facialis). Here it has a very thin wall, in which there are often dehiscences, which contributes to the spread of inflammation from the middle ear to the nerve and the occurrence of paralysis of the facial nerve. An otolaryngologist surgeon sometimes has to deal with various variants and anomalies in the location of the facial nerve, both in its tympanic and mastoid regions.

In the middle floor of the tympanic cavity, the chorda tympani departs from the facial nerve. It passes between the malleus and the incus through the entire tympanic cavity near the tympanic membrane and exits it through the stony-tympanic (glazer) fissure (fissura petrotym-panica, s.Glaseri), giving taste fibers to the tongue on its side, secretory fibers to salivary gland and fibers to the vascular plexuses.

The tympanic cavity is conditionally divided into three sections, or floors: upper- attic, or epitympanum(epitympanum), located above the upper edge of the stretched part of the tympanic membrane, the height of the attic ranges from 3 to 6 mm. The articulation of the malleus with the anvil enclosed in it divides the attic into external and internal sections. Bottom part the outer part of the attic is called the "superior recess of the tympanic membrane", or "Prussian space", posteriorly attic passes into antrum; average- the largest in size (mesotympanum), corresponds to the location of the stretched part of the eardrum; lower(hypotympanum) - a depression below the level of attachment of the tympanic membrane. The mucous membrane of the tympanic cavity is a continuation of the mucous membrane of the nasopharynx (through the auditory tube); it covers the walls of the tympanic cavity, auditory ossicles and their bundles, forming a series of folds and pockets. Tightly adhering to the bone walls, the mucous membrane is for them at the same time the periosteum (mucoperiostum). It is mainly covered squamous epithelium, with the exception of the mouth of the auditory tube, where there is a ciliated columnar epithelium. Glands are found in some places of the mucous membrane.

auditory ossicles - hammer(malleus), anvil(incus) and stirrup(stapes) - connected by joints, anatomically and functionally they represent a single chain (Fig. 4.6), which stretches from the tympanic membrane to the vestibule window. The handle of the malleus is woven into the fibrous layer of the tympanic membrane, the base of the stirrup is fixed in the niche of the vestibule window. The main mass of the auditory ossicles - the head and neck of the malleus, the body of the anvil - is located in the epitympanic space (see Fig. 4.5, b). The auditory ossicles are strengthened between themselves and with the walls of the tympanic cavity with the help of elastic ligaments, which ensures their free displacement during vibrations of the tympanic membrane.

AT malleus distinguish between the handle, neck and head. At the base of the handle is a short process that protrudes outwards from the eardrum. The mass of the malleus is about 30 mg.

Anvil consists of a body, a short process and a long process articulated with the stirrup. The mass of the anvil is about 27 mg.

AT stirrup distinguish between a head, two legs and a base. The annular ligament, with which the base of the stirrup is attached to the edge of the vestibule window, is sufficiently elastic and provides good oscillatory mobility of the stirrup. In the anterior section, this ligament is wider than in the posterior one; therefore, during the transmission of sound vibrations, the base of the stirrup is displaced mainly by its anterior pole. The stirrup is the smallest of the auditory ossicles; its mass is about 2.5 mg with a base area of 3-3.5 mm 2.

The muscular apparatus of the tympanic cavity is represented by two muscles: tensile eardrum(m.tensor tympani) and stirrup(m.stapedius). Both of these muscles, on the one hand, hold the auditory ossicles in a certain position, the most favorable for conducting sound, on the other hand, they protect the inner ear from excessive sound stimulation by reflex contraction. The muscle stretching the tympanic membrane is attached at one end in the region of the opening of the auditory tube, with the other - to the handle of the malleus near the neck. It is innervated by the mandibular branch of the trigeminal nerve through the ear ganglion; the stirrup muscle starts from the pyramidal protrusion and is attached to the neck of the stirrup; innervated by the stapedial nerve (n. stapedius) by a branch of the facial nerve.

The auditory (Eustachian) tube, as already noted, is a formation through which the tympanic cavity communicates with the external environment: it opens in the nasopharynx. The auditory tube consists of two parts: a short bone - "/5 canal (pars ossea) and a long cartilage - 2/5 (pars cartilaginea). Its average length in adults is 3.5 cm, in newborns - 2 cm.

At the point of transition of the cartilaginous part into the bone, an isthmus (isthmus) is formed - the narrowest place (diameter 1 - 1.5 mm); it is located approximately 24 mm from the pharyngeal opening of the tube. The lumen of the bony part of the auditory tube in the section is similar to a triangle, and in membranous-cartilaginous section of the wall of the tube are adjacent to each other.

The internal carotid artery passes medially to the bony part of the tube. It should be borne in mind that in the membranous-cartilaginous part, the lower and anterior walls of the tube are represented only by fibrous tissue. The pharyngeal opening of the auditory tube is 2 times wider than the tympanic one and is located 1-2.5 cm below it on the side wall of the nasopharynx at the level of the posterior end of the inferior turbinate.

The blood supply of the tympanic cavity is carried out from the pools of the external and partially internal carotid arteries: the anterior, tympanic artery, which departs from the maxillary; posterior auricular artery, arising from the stylomastoid artery and anastomosing with the middle meningeal artery. Branches depart from the internal carotid artery to the anterior parts of the tympanic cavity.

Venous outflow from the tympanic cavity occurs mainly through the veins of the same name.

Lymph outflow from the tympanic cavity follows along the mucous membrane of the auditory tube to the retropharyngeal lymph nodes.

The innervation of the tympanic cavity occurs due to the tympanic nerve (n.tympanicus) from the IX pair (n.glossopharyn-geus) of the cranial nerves. Having entered the tympanic cavity, the tympanic nerve and its branches anastomose on the inner wall with branches of the facial nerve, trigeminal and sympathetic plexuses of the internal carotid artery, forming a tympanic plexus on the cape(plexus tympanicus s. Jacobsoni).

Mastoid process (prosessus mastoideus). In a newborn, the mastoid part of the middle ear looks like a small elevation behind the upper posterior edge of the tympanic ring, containing only one cavity - the antrum (cave). Starting from the 2nd year, this eminence is extended downward due to the development of the muscles of the neck and occiput. The formation of the process ends mainly by the end of the 6th - the beginning of the 7th year of life.

The mastoid process of an adult resembles a cone, overturned by the tip - a ledge. The internal structure of the mastoid process is not the same and depends mainly on the formation of air cavities. This process occurs by replacing bone marrow tissue with ingrown epithelium. As the bone grows, the number of air cells increases. According to the nature of pneumatization, one should distinguish: 1) the pneumatic type of the structure of the mastoid process, when the number of air cells is large enough. They fill almost the entire process and sometimes even extend to the scales of the temporal bone, the pyramid, the bone part of the auditory tube, and the zygomatic process; 2) diploetic (spongy, spongy) type of structure. In this case, the number of air cells is small, they look like small cavities, limited by trabeculae, and are located mainly near the cave; 3) sclerotic (compact) type of structure: the mastoid process is formed by exceptionally dense bone tissue. If the pneumatic type of structure of the mastoid process is observed during the normal development of the child, then diploetic and sclerotic are sometimes the result of metabolic disorders or the result of general and local inflammatory diseases, etc. There is an opinion that some genetic or constitutional factors, as well as the resistance and organ-tissue reactivity associated with them, have a certain influence on the process of pneumatization of the mastoid process.

The anatomical structure of the mastoid process is such that all its air cells, regardless of their distribution and location, communicate with each other and with the cave, which, through aditus ad antrum, communicates with the epitympanic space of the tympanic cavity. The cave is the only congenital air cavity; its development does not depend on the type of structure of the mastoid process. In infants, unlike adults, it is much larger in volume and is located quite close to the outer surface. In adults, the cave lies at a depth of 2-2.5 cm from the outer surface of the mastoid process. The dimensions of the mastoid process in adults range from 9-15 mm in length, 5-8 mm in width and 4-18 mm in height. In a newborn, the dimensions of the cave are the same. From the dura mater middle cranial fossa the cave is separated by a bone plate (tegmen antri), when destroyed by a purulent process, inflammation can pass to the meninges.

Solid meninges posterior cranial fossa separated from the mastoid cavity by the Trautmann triangle, which is located posterior to the facial nerve to the sigmoid sinus. The mucous membrane lining the cave and air cells is a continuation of the mucous membrane of the tympanic cavity.

On the inner back surface (from the side of the cranial cavity) of the mastoid process there is a recess in the form of a gutter. In it lies sigmoid venous sinus(sinus sig-moideus), through which the outflow of venous blood from the brain to the jugular vein system is carried out. The dura mater of the posterior cranial fossa is delimited from the cellular system of the mastoid process by means of a thin but rather dense bone plate (lamina vitrea). In some cases, purulent inflammation of the cells can lead to the destruction of this plate and the penetration of infection into the venous sinus. Sometimes a mastoid injury can break the integrity of the sinus wall and lead to life-threatening bleeding. Near the cells of the mastoid process is the mastoid part of the facial nerve. This neighborhood sometimes explains paralysis and paresis of the facial nerve in acute and chronic inflammation of the middle ear.

Outside, the mastoid process has a compact bone-cortical layer, the surface of which is rough, especially in the lower section, where the sternocleidomastoid muscle (m.sternocleidomastoideus) is attached. On the inner side of the apex of the process there is a deep groove (incisura mastoidea), where the digastric muscle (m.digastricus) is attached. Through this furrow, pus sometimes breaks out of the cells of the process under cervical muscles. Within the outer surface of the mastoid process is a smooth a triangular-shaped platform, called the Shipo triangle. In the anterior upper corner of this triangle there is a fossa in the form of a platform (planum mastoidea) and a comb (spina suprameatum), which correspond to the outer wall of the antrum. In this area, bone trepanation is performed in search of a cave with mastoiditis in adults and anthritis in children.

The blood supply to the mastoid region is carried out from the posterior auricular artery (a.auricularis posterior - a branch of the external carotid artery - a.carotis externa). Venous outflow occurs in the vein of the same name, which flows into the external jugular vein (v.jugularis externa).

The innervation of the mastoid region is provided by sensory nerves from the superior cervical plexus, the large ear (n.auricularis magnus) and the small occipital (p.os-cipitalis minor). The motor nerve for the rudimentary behind the ear muscle (m.auricularis posterior) is the branch of the facial nerve of the same name.

Ear examination methods

External examination and palpation of the ear. Preparation for inspection is carried out in the same way as above. Inspection begins with a healthy ear: they examine the auricle, the external opening of the auditory canal, the behind-the-ear region, the area in front of the auditory canal. Normally, the auricle and tragus are painless on palpation. To examine the external opening of the right auditory canal, it is necessary to pull the auricle backwards and upwards, holding the curl of the auricle with fingers I and II of the left hand. For inspection on the left, the auricle must also be pulled back with the right hand (Fig. 5.12). To examine the behind-the-ear region, the right auricle is pulled forward with the right hand. Pay attention to the fold behind the ear (the place where the auricle is attached to the mastoid process): normally, it is well contoured. Then, with the first finger of the left hand, the mastoid process is palpated at three points: in the projection of the antrum, sigmoid sinus, and the apex of the mastoid process. On palpation of the left mastoid process, the auricle is pulled with the left hand, and the palpation is carried out with the first finger of the right hand; The second finger of the left hand palpates the regional lymph nodes of the right ear anterior and posterior to the external auditory canal, the second finger of the right hand - similarly the lymph nodes of the left ear. Normally, lymph nodes are not palpable; With the finger of the right hand, they press on the tragus: normally, its palpation is painless.

Otoscopy. With the left hand, the right auricle is pulled backwards and upwards in adults, backwards and downwards in children; I and II fingers of the right hand introduce the ear funnel into the cartilaginous section of the external auditory canal. When examining the left ear, the auricle is pulled back with the right hand, and the funnel is inserted with the fingers of the left hand. The funnel is selected so that its diameter corresponds to the transverse diameter of the external auditory canal. The ear funnel should not be inserted into the bony part of the ear canal, as this causes pain. The long axis of the funnel must coincide with the axis of the bone section of the ear canal, otherwise the funnel will rest against its wall. Light movements of the outer end of the funnel are made in order to sequentially examine all parts of the tympanic membrane. From side effects observed with the introduction of the funnel, especially with pressure on the posterior-inferior wall, there may be a cough resulting from irritation of the endings of the branches of the vagus nerve.

The ear canal is cleaned dry or by rinsing. For dry cleaning, a small piece of cotton wool is wound on a threaded ear probe in the form of a brush so that the tip of the probe is closed. The cotton wool on the probe is slightly moistened in vaseline oil, injected during otoscopy into the external auditory canal and the earwax contained in it is removed.

When flushing, warm water of body temperature is drawn into Janet's syringe (so as not to cause irritation of the vestibular apparatus), a kidney-shaped tray is placed under the patient's ear, the tip of the syringe is inserted into the initial part of the ear canal and a stream of fluid is directed along its posterior wall. After rinsing, the remaining water must be removed using cotton wool wrapped around the probe. If a dry perforation is suspected, ear rinsing is contraindicated due to the risk of developing inflammation in the middle ear.

The external auditory meatus, having a length of 2.5 cm, is covered with skin, there are hairs in its membranous-cartilaginous part; it may contain a secretion of the sulfur glands (earwax).

The tympanic membrane is gray in color, with a pearly tint. It has identification points: a handle and a short process of the malleus, anterior and posterior folds, a light cone (reflex), umbo (navel). The tympanic membrane consists of two parts: tense and relaxed. On the surface of the tympanic membrane, four quadrants are conditionally distinguished, which are obtained by mentally drawing two perpendicular lines: one passes along the handle of the malleus, the other is perpendicular to it through the center of the navel. The resulting quadrants are called anterior and posterior superior, anterior and posterior inferior.

Determination of the patency of the auditory tubes. To study the patency of the auditory tubes, it is necessary to have a special elastic (rubber) tube with ear inserts at both ends (otoscope), a rubber pear with an olive at the end (Politzer balloon), a set of ear catheters of various sizes (from No. 1 to No. 6).

The study is based on blowing the auditory tube and listening to the noise of the air passing through it. Consistently apply 4 methods of blowing (determining the degree of patency) of the auditory tube. Depending on the possibility of blowing in one way or another, I, II, III or IV degree of pipe patency is established. When performing the study, one end of the otoscope is placed in the external auditory canal of the subject, the second - the doctor, who listens through the otoscope to the noise that occurs when air passes through the auditory tube.

Toynbee method. The patency of the auditory tubes is determined at the moment of swallowing, with the mouth and nose closed (normally, a push in the ears is felt).

Valsalva method. The subject is asked to take a deep breath, and then to produce enhanced expiration (inflation) with the mouth and nose tightly closed. Under the pressure of the exhaled air, the auditory tubes open, and the air enters the tympanic cavity with force, which is accompanied by a slight crackle that the subject feels, and the doctor listens to the characteristic noise through the otoscope. With a disease of the mucous membrane of the auditory tubes, the Valsalva experiment fails.

Politzer method. The olive of the ear balloon is inserted into the vestibule of the nose on the right and held with the II finger of the left hand, and with the I finger the left wing of the nose is pressed against the nasal septum. One olive of the otoscope is inserted into the external auditory canal of the subject, and the other - into the doctor's ear and the patient is asked to pronounce the words "steamboat" or "one, two, three." At the moment of pronouncing a vowel sound, the balloon is squeezed with four fingers of the right hand (I finger serves as a support). At the moment of blowing, when a vowel is pronounced, the soft palate deviates posteriorly and separates the nasopharynx; air enters the closed cavity of the nasopharynx and evenly presses on all walls; part of the air with force passes into the mouth of the auditory tubes, which is determined by the characteristic sound in the otoscope. Similarly, blowing is carried out along the Politzer and through the left half of the nose.

Ticket number 12

1. Chronic rhinitis. Ozen.

Chronic runny nose (chronic rhinitis)

The main forms of chronic rhinitis (rhinitis chronica)- catarrhal, hypertrophic and atrophic - are nonspecific dystrophic process mucous membrane and, in some cases, the bony walls of the nasal cavity. The disease is common.

Etiology and pathogenesis. The occurrence of chronic rhinitis is usually associated with dyscirculatory and trophic disorders in the mucous membrane of the nasal cavity, which can be caused by such factors as frequent acute inflammation in the nasal cavity (including with various infections), irritating environmental influences (most often dust , gas), dryness or humidity of the air, fluctuations in its temperature, etc. A significant role in the etiology of chronic rhinitis can be played by general diseases - cardiovascular, kidney, dysmenorrhea, frequent coprostasis, alcoholism, as well as local processes - narrowing or obstruction of the choanae by adenoids, purulent discharge during sinusitis, etc. Hereditary prerequisites may be important in the etiology of the disease , malformations and defects of the nose. In some cases, chronic rhinitis is a symptom of another disease, such as chronic purulent sinusitis.(sinusitis, frontal sinusitis, ethmoiditis), foreign body in the nose and others, which is important to consider in the diagnosis and treatment.

The impact of dust on the nasal mucosa can be different. Mineral and metal dust has hard pointed particles that injure the mucous membrane; flour, chalk, cotton, wool and other dust consists of soft particles, which, although they do not injure the mucous membrane, but, covering its surface, lead to the death of the cilia of the ciliated epithelium and can cause its metaplasia, disrupt the outflow from the mucous glands and goblet cells. Accumulations of dust in the nasal passages can cement and form nasal stones (rhinoliths).

Vapors and gases of various substances have a chemical effect on the nasal mucosa, first causing its acute and then chronic inflammation. Some occupational hazards have an irritating, toxic effect: vapors of mercury, iodine, formalin, nitric, sulfuric, hydrochloric acids, etc., radiation exposure.

Thus, the combined effect of some exogenous and endogenous factors for different periods of time can cause the appearance of one form or another of chronic rhinitis. Prevention of this disease includes sanitation of the paranasal sinuses and nasopharynx, treatment of common diseases, improvement of working conditions, implementation of measures personal protection in the presence of harmful effects in production, hardening of the body. For the purpose of early detection of the disease, a preventive examination by an otorhinolaryngologist is carried out.

clinical picture. Chronic catarrhal rhinitis(rhinitis cataralis chronica). The main symptoms of chronic rhinitis in its catarrhal form - difficulty in nasal breathing and discharge from the nose (rhinorrhea) - are moderately expressed. Significant disruption of breathing through the nose usually occurs periodically, often in the cold, but the congestion of one half of the nose is more constant. When lying on the side, congestion is more pronounced in that half of the nose, which is lower, which is explained by the filling of the cavernous vessels of the underlying shells with blood, the tone of which is weakened in chronic rhinitis. Mucous discharge from the nose; usually it is not much, but with an exacerbation of the process, it becomes purulent and plentiful. With rhinoscopy, pastosity and swelling of the mucous membrane are determined, often with a cyanotic tint, and a slight thickening of it, mainly in the region of the lower shell and the anterior end of the middle shell; while the walls of the nasal cavity are usually covered with mucus. Olfactory disturbance (hyposmia) is more often temporary, usually associated with an increase in the amount of mucus; rare complete prolapse sense of smell (anosmia).

Morphological changes in catarrhal rhinitis are mainly localized in the superficial layers of the mucous membrane. The ciliated epithelium to some extent loses cilia, which can be restored when the condition improves. In some places, the epithelial cover is broken or infiltrated with round cell elements, the subepithelial layer is often edematous. The vessels of the mucous membrane of the turbinates are dilated, their walls can be thinned.

To distinguish a simple catarrhal form of rhinitis from a hypertrophic one, a test with anemia is performed - the thickened mucous membrane is lubricated with a vasoconstrictor (0.1% solution of adrenaline, etc.); while a significant decrease in swelling of the mucous membrane indicates the absence of true hypertrophy. If the contraction of the mucous membrane is expressed slightly or it has not decreased at all, this indicates the hypertrophic nature of its swelling. It is necessary to monitor the condition of the paranasal sinuses in order to exclude the secondary (symptomatic) nature of rhinitis.

Chronic hypertrophic rhinitis(rhinitis chronica hipertrophica). Main features hypertrophic form of the common cold are constant difficulty in nasal breathing, mucous and mucopurulent discharge, growth and thickening of the nasal mucosa, mainly of the entire lower concha and to a lesser extent the average, i.e. in places of localization of cavernous tissue. However, hypertrophy can also occur in other parts of the nose, in particular on the vomer at its posterior edge, in the anterior third of the nasal septum. The surface of hypertrophic areas can be smooth, bumpy, and coarse-grained in the area of the posterior or anterior ends of the shell. The mucous membrane is usually hyperemic, plethoric, slightly cyanotic or purple-cyanotic, gray-red, covered with mucus. If the mucopurulent discharge is localized under the middle shell, inflammation of the maxillary, ethmoid or frontal sinuses should be excluded; if it is in the olfactory gap, then, perhaps, the process is involved sphenoid sinus or posterior squamous cells. The posterior ends of the inferior shells are usually thickened, often compressing the pharyngeal mouths of the auditory tubes, thereby causing eustachitis (otosalpingitis). A sharp thickening of the anterior sections of the inferior concha can compress the opening of the lacrimal canal, which causes lacrimation, inflammation of the lacrimal sac and conjunctivitis. The hypertrophied lower shell often presses on nasal septum, which can reflexively cause headaches, nervous disorders.

Decreased sense of smell at first has the character respiratory hypo- or anosmia, however, gradually, due to the atrophy of the olfactory receptors, essential (irreversible) anosmia sets in, and the taste also somewhat decreases in parallel. Nasal congestion causes a change in the timbre of the voice - appears closed nasality(rhinolalia clausa). The morphological picture in this form of the common cold is characterized by hypertrophy of the mucous membrane, glands, and in rare cases bone tissue nasal conchas; the epithelial layer is loosened, cilia are absent in places. The function of the ciliary apparatus can be impaired to varying degrees.

In some patients, polypous degeneration of the mucous membrane is fixed, more often in the region of the middle shell; congestive edema may also occur in the region of the posterior ends of the inferior turbinates. The formation of polyps and swelling contributes to the allergization of the body. Localization of polyps in upper divisions the nasal cavity may not affect respiratory function until the polyps descend into the respiratory region of the nose, while the olfactory function in these cases is often impaired immediately. Polypous and edematous thickening has wide base, polypous hypertrophy can gradually transform into nasal polyps. To clarify the diagnosis in these cases, they feel with a bellied probe after preliminary anemization of the turbinates. Using this technique, you can also determine the presence of bone hypertrophy of the lower or middle shell, which sometimes occurs in the hypertrophic form. The most convincing and complete data can be obtained by endoscopy using an operating microscope or using endonasal microendoscopes.

Atrophic rhinitis(rhinitis atrophica). A simple chronic atrophic process of the nasal mucosa can be diffuse and limited. Often there is a slightly pronounced atrophy of the mucous membrane, mainly the respiratory region of the nose, such a process in practice is sometimes called subatrophic rhinitis. The occurrence of an atrophic process in the nose is usually associated with long-term action dust, gases, steam, etc. Mineral dust (silicate, cement), tobacco, etc. has a particularly strong influence. Often, atrophic rhinitis develops after surgery, for example, extensive conchotomy, or after a nose injury. Sometimes the cause of diseases can be associated with constitutional and hereditary factors.

In childhood, the atrophic process is sometimes the result of infectious diseases such as measles, influenza, diphtheria, scarlet fever.

Diagnostics. Frequent symptoms include a scanty, viscous mucus or mucopurulent discharge that usually sticks to the mucous membrane and dries up, resulting in crusting. Periodic obstruction of nasal breathing is associated with the accumulation of crusts in the common nasal passage, most often in its anterior section. Patients complain of dryness in the nose and throat, a decrease in one degree or another of smell. Crusts in the nose often cause itching and difficulty breathing, so the patient tries to remove them with a finger, which leads to damage to the mucous membrane, usually in the anterior part of the nasal septum, the introduction of microbes here and the formation of ulcers and even perforation. In connection with the rejection of the crusts, small bleeding often occurs, usually from the Kisselbach zone.

The histological picture is characterized by thinning of the own tissue of the nasal mucosa, a decrease in the number of glands and their hypoplasia. The multi-row cylindrical epithelium also becomes thinner, its cilia are absent in many places. There is metaplasia of the columnar epithelium into a flat one. With anterior and posterior rhinoscopy, depending on the severity of atrophy, more or less enlarged nasal passages are visible, reduced in shell volume, covered with a pale, dry, thinned mucous membrane, on which there are crusts or viscous mucus in places. Usually with anterior rhinoscopy after removal of the crusts, you can see back wall nasopharynx.

In differential diagnosis, one should keep in mind the possibility of localization of the tuberculous process in the area of the nasal septum, in which a granulating ulcer and perforation is formed, capturing only the cartilaginous part, as well as a syphilitic process in the bone part on the border with the cartilage.

Treatment. In various forms of chronic rhinitis, it includes:

Elimination of possible endo- and exogenous factors that cause and maintain a runny nose;

drug therapy in relation to each form of rhinitis;

Surgical intervention according to indications;

Physiotherapy and climate therapy.