Lecture No. 8. Complications of purulent diseases of the middle and inner ear

Independent forms of purulent inflammation of the middle ear are acute purulent otitis media, mastoiditis, chronic purulent epitympanitis, mesotympanitis and purulent labyrinthitis. With their unfavorable course, abscesses can develop in neighboring anatomical regions, diffuse inflammation of the meninges (meningitis) and brain matter (encephalitis), as well as a septic state of the body.

Etiology

The microflora sown from the primary source of infection is mostly mixed and unstable.

Nevertheless, coccal flora most often prevails: staphylococci, streptococci, less often pneumococci and diplococci, even less often - Proteus and Pseudomonas aeruginosa. The occurrence of complications and the variant of the development of the inflammatory reaction depend on the virulence of the infection.

Pathogenesis

The pathogenesis of otogenic complications is complex and ambiguous. In addition to the virulence of the microflora, the state of the general resistance of the organism is of great importance. Ultimately, it is their ratio that determines the direction and severity of the inflammatory response.

The more virulent the flora, the more severe the inflammatory process is and the more difficult it is for the body to resist its spread.

Therefore, in acute purulent otitis media, otogenic intracranial complications may develop: meningitis, brain abscess, meningoencephalitis, and sepsis.

The structural features of the temporal bone and the structures of the middle and inner ear located in it also predetermine the possibility of developing complications. Among them, an abundance of folds and pockets of the mucous membrane of the attic and the cellular structure of the mastoid process are distinguished, ventilation and drainage of which are significantly hampered by inflammation.

Complications of acute purulent otitis media are mastoiditis and labyrinthitis. Labyrinthitis can also develop in chronic suppurative otitis media, progressively destroying the temporal bone.

The dura mater stands in the way of infection spreading into the cranial cavity, which, along with the blood-brain barrier, is a serious obstacle to the development of intracranial complications.

Nevertheless, inflammation, causing an increase in the permeability of the vascular walls, helps to overcome the infection and these barriers, the inflammatory process occurs between the hard and arachnoid membranes of the brain (subdural abscess or limited leptomeningitis), as well as in the cavity of the venous sinuses (sinus thrombosis).

Further spread of the infection leads to the formation of an abscess of the temporal lobe of the brain or cerebellum at a depth of up to 2-4 cm. The described process of the spread of infection is called "by continuation."

With the generalization of the process due to reduced resistance and altered reactivity of the body, intracranial complications may develop: purulent meningitis, meningoencephalitis or sepsis.

The septic condition in acute purulent otitis in children develops hematogenously when bacteria and their toxins enter the blood from the tympanic cavity. Contributing factors are the hyperreactivity of the child's body, the weakness of its protective immune reactions, as well as the difficulty in the outflow of pus from the tympanic cavity.

Chronic suppurative otitis media leads to sepsis through sinus thrombosis. The stages of the process are periphlebitis, endophlebitis, parietal thrombosis, complete thrombosis, infection and disintegration of a thrombus, septicemia and septicopyemia.

The ways of spreading infection in each of the purulent diseases of the ear are quite specific. Attention should be paid to the fact that the route of infection spread may not be limited to one mechanism (contact, hematogenous, lymphogenous, lymphomarinthogenic).

In acute purulent otitis media, the most common route of infection to the cranial cavity is through the roof of the tympanic cavity, predominantly hematogenous. In second place is the path to the labyrinth through the cochlear window and the annular ligament of the vestibule window.

Hematogenous spread of infection into the paracarotid plexus and from there to the cavernous sinus, as well as through the lower wall of the tympanic cavity into the bulb of the jugular vein, is possible.

With mastoiditis, pus, melting the bone, can break into the behind-the-ear region, through the top of the mastoid process under the muscles of the neck and through its front wall into the external auditory canal.

In addition, it is possible for the process to spread into the cranial cavity to the meninges, sigmoid sinus and cerebellum, and through the roof of the antrum to the temporal lobe of the brain.

In chronic purulent epitympanitis, in addition to intracranial complications, a fistula of the lateral semicircular canal may form, and labyrinthitis may occur.

Sometimes there are associated complications. They are most often sinus thrombosis and cerebellar abscess, as well as meningitis and brain abscess. In this case, it is appropriate to talk about the stages of the spread of infection into the cranial cavity.

The main condition conducive to the spread of infection beyond the structures of the middle and inner ear is the difficulty in the outflow of purulent discharge from the tympanic cavity and mastoid cells into the external auditory canal.

Clinic

In the first place among intracranial otogenic complications is meningitis, in the second - abscesses of the temporal lobe of the brain and cerebellum, in the third - sinus thrombosis. Sepsis develops less frequently.

Sinus thrombosis may not be complicated by a septic condition. The most common complication in childhood is diffuse meningoencephalitis.

Otogenic diffuse purulent meningitis, or leptomeningitis, is an inflammation of the pia and arachnoid membranes of the brain with the formation of purulent exudate and increased intracranial pressure. As a result of inflammation of the membranes and increased pressure of the cerebrospinal fluid, the inflammatory reaction spreads to the substance of the brain. encephalitis occurs.

The general condition of the patient is severe. There is clouding of consciousness, delirium. The patient lies on his back or on his side with his head thrown back.

The position lying on your side with your head thrown back and legs bent is called the "pose of a pointing dog." Extension of the head and flexion of the limbs are caused by irritation of the meninges.

Body temperature is constantly elevated to 39-40 ° C or more. Pulse quickened.

The patient is concerned about severe headache, nausea and vomiting of central origin, associated with increased intracranial pressure. The headache is aggravated by the action of light, sound or touching the patient.

The diagnosis is confirmed by meningeal symptoms - neck stiffness, Kernig's symptom, upper and lower Brudzinsky's symptoms, caused by irritation of the posterior roots of the spinal cord.

The development of encephalitis is diagnosed when the pyramidal symptoms of Babinsky, Rossolimo, Gordon, Oppenheim appear, indicating damage to the motor centers of the cerebral cortex and anterior horns of the spinal cord.

In severe cases, the cranial nerves are affected; the function of the abducens nerve is the first to suffer. Neutrophilic leukocytosis over 20 x 10 is observed in peripheral blood⁹/l - 25 x 10⁹/l, increased ESR.

Purulent meningitis is confirmed by pathological changes in the cerebrospinal fluid. An increase in its pressure is noted (normally it is 150-200 mm of water column, and the cerebrospinal fluid flows out of the needle at a rate of 60 drops per minute). The liquid becomes cloudy, the content of cellular elements increases to tens of thousands per 1 µl (pleocytosis).

The protein content increases (norm 150-450 mg / l), the amount of sugar and chlorides decreases (sugar norm 2,5-4,2 mmol / l, chlorides - 118-132 mmol / l). When sowing the cerebrospinal fluid, the growth of microorganisms is detected.

Otogenic meningitis, unlike epidemic cerebrospinal meningitis, develops slowly. Sometimes there are fulminant forms of meningitis in acute suppurative otitis media in children.

Otogenic abscesses of the temporal lobe of the brain and cerebellum occur in the immediate vicinity of the focus of infection. These abscesses are primary in contrast to deep and contralateral secondary abscesses in sepsis.

In the temporal lobe of the brain, the abscess is more often round in shape, and in the cerebellum it is slit-like.

Smooth-walled abscesses with a well-defined capsule proceed most favorably. However, the capsule is often absent and the abscess is surrounded by inflamed and softened brain matter.

Allocate the initial, latent and explicit stages of abscess development.

The initial stage is characterized by mild brain symptoms: headache, weakness, nausea and vomiting, subfebrile body temperature.

Its duration is 1-2 weeks. Further, within 2-6 weeks of development of the latent stage, no obvious symptoms of brain damage are observed, but the patient's state of health is more often changed.

The mood worsens, apathy develops, general weakness, increased fatigue are noted. The apparent stage lasts an average of 2 weeks.

Symptoms in the explicit stage can be divided into four groups: general infectious, cerebral, conductive and focal. The first group includes general weakness, lack of appetite, stool retention, weight loss.

Body temperature is usually normal or subfebrile, ESR is increased, leukocytosis is moderate without significant changes in the leukocyte blood count.

There may be an occasional irregular increase in body temperature.

Cerebral symptoms are characterized by increased intracranial pressure. Headache, vomiting without previous nausea, neck stiffness, Kernig's symptom are characteristic. Unlike meningitis, there is bradycardia due to pressure on the medulla oblongata.

Focal neurological symptoms are of the greatest diagnostic value.

Damage to the temporal lobe of the brain (left - in right-handers and right - in left-handers) is characterized by sensory and amnestic aphasia.

With sensory aphasia and intact hearing, the patient does not understand what is being said to him. His speech becomes a meaningless set of words.

This is due to damage to the center of Wernicke in the middle and posterior sections of the superior temporal gyrus. The patient also cannot read (alexia) and write (agraphia).

Amnestic aphasia is manifested by the fact that the patient describes their purpose instead of the name of objects, which is associated with visual-auditory dissociation as a result of damage to the lower and posterior parts of the temporal and parietal lobes.

Cerebellar abscess is characterized by impaired limb tone, ataxia, spontaneous nystagmus, and cerebellar symptoms.

With brain abscesses, moderate neutrophilic leukocytosis is noted with a shift of the leukocyte formula to the left, an increase in ESR up to 20 mm/h and above.

CSF flows out under pressure, transparent, with a low protein content and mild pleocytosis (up to 100-200 cells per 1 µl). With a breakthrough of pus into the subarachnoid space, secondary meningitis develops with a corresponding picture of cerebrospinal fluid.

The dislocation of brain structures is confirmed by echoencephalography.

The exact localization of the abscess is established by means of computed tomography or magnetic resonance imaging.

In the absence of the possibility of performing the latter, cerebral angiography and pneumoencephalography, as well as radioisotope scintigraphy, can be performed.

otogenic sepsis. Generalization of infection in acute otitis occurs often primary hematogenous, and in chronic otitis media - most often after thrombophlebitis of the sigmoid sinus. Less commonly, the bulb of the jugular vein, transverse, superior and inferior petrosal sinuses are affected. The infection and disintegration of a blood clot leads to the penetration of a purulent infection into the bloodstream. Sinus thrombosis does not always lead to sepsis.

Even in the case of infection, its organization is possible. With sinusogenic sepsis, the prognosis in the vast majority of cases is favorable.

Mortality is 2-4%. There are three clinical forms of otogenic sepsis: septicemia, septicopyemia and bacterial shock.

With the primary hematogenous nature of sepsis on the basis of acute purulent otitis in children, the septic reaction develops rapidly, but it is relatively easily reversible.

This form of sepsis is characterized predominantly by septicemia and toxemia.

With a pronounced decrease in resistance and a change in reactivity, fulminant forms of sepsis can be observed. Their prognosis is unfavorable.

The characteristic symptom of sepsis is hectic remitting fever accompanied by chills followed by profuse sweating.

There may be several such sharp rises and falls in temperature during the day, so body temperature is measured every 4 hours.

In children, the temperature is often elevated constantly.

Pallor of the skin with an earthy tint is noted. Yellowness of the skin and icterus of the sclera develop as a result of disseminated intravascular coagulation (DIC) and hepatosplenomegaly.

Blood changes consist in severe neutrophilic leukocytosis with a shift of the leukocyte formula to the left, toxic granularity of neutrophils, an increase in ESR, increasing hypochromic anemia, hypoalbuminemia and hypoproteinemia.

Treatment

Treatment of otogenic complications involves the urgent elimination of a purulent focus in the ear and brain, as well as intensive drug therapy.

An otolaryngologist performs paracentesis of the tympanic membrane in case of acute purulent otitis media, mastoid surgery in case of mastoiditis and radical surgery in case of chronic purulent otitis media and labyrinthitis. Mastoid and radical ear surgeries are performed with exposure of the dura mater of the middle and posterior cranial fossae, as well as the sigmoid sinus.

The condition of the dura mater is assessed (presence or absence of an inflammatory reaction, extradural abscess). If a subdural abscess or abscess of the temporal lobe of the brain and cerebellum is suspected, the brain substance is punctured to a depth of 4 cm. The sigmoid sinus is also punctured to diagnose thrombosis.

An abscess of the brain tissue is most often opened along the needle, and drains are introduced into the wound.

Sanitation can also be carried out in a closed way through punctures and washing the abscess cavity with antiseptic solutions. If there is an abscess capsule, it is removed with the capsule.

When a thrombus is detected in the sigmoid sinus, its wall is dissected longitudinally and most of the thrombus is removed. When thrombosis spreads to the internal jugular vein, it is ligated at the level of the middle third of the neck.

Intensive care involves the introduction of large doses of antibiotics.

After receiving the result of a bacteriological examination of discharge from the ear, brain abscess, blood, cerebrospinal fluid, antibiotics are used in accordance with the sensitivity of the microflora to them.

Other areas of intensive care are dehydration and detoxification with diuretics, solutions of various blood substitutes (rheopolyglucin, rheogluman, mannitol, etc.), glucocorticoids.

Glucose, ascorbic acid, B vitamins, antihistamines and symptomatic agents can be administered intravenously and intramuscularly.

In case of thrombosis of the sigmoid sinus, under the control of the level of prothrombin and the time of blood clotting, anticoagulants are prescribed (heparin, 10 - 000 IU per day).

With otogenic sepsis, blood transfusions, transfusions of fresh frozen plasma, extracorporeal ultraviolet irradiation of blood, plasmapheresis, and hemosorption are indicated.

Patients with suspected otogenic intracranial complications need urgent hospitalization, and if the diagnosis is confirmed, they are subject to urgent surgical treatment.

Timely diagnosis, paracentesis of the tympanic membrane in acute purulent otitis media, as well as dispensary observation of patients with chronic purulent otitis media and early sanitation of the ear are effective measures to prevent otogenic complications.

Authors: Drozdov A.A., Drozdova M.V.

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