Rhinogenic meningitis, arachnoiditis. Otogenic and rhinogenic meningitis. Treatment of purulent meningitis

Otogenic and rhinogenic meningitis

Otogenic and rhinogenic meningitis - acute inflammation 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 body, 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%.

Infection from the cavities of the middle ear into the cranial cavity can penetrate contact, hematogenous and lymphogenous ways. 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, labyrinth windows, internal ear canal, aqueducts of the cochlea and vestibule, mastoid cells; in children early age at the junctions constituent parts temporal bone there are open gaps that 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 suppurative otitis media, fistulas often form in the roof area. tympanic cavity and mastoid cave, as well as on inner wall mastoid process. If the infection spreads through 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 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 concussion of the head upon impact, fall, surgical interventions ah in the "hammer" way on the sclerosed mastoid process, as well as the weakening of the body by 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 with chronic inflammation through mucosal veins lattice labyrinth along existing anastomoses into the veins of the dura mater, as well as along the sheaths of the olfactory nerve. It is possible to develop rhinogenic meningitis with surgical interventions in the nose and paranasal sinuses. More often this is observed during endonasal opening of the ethmoid labyrinth and frontal sinus.

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. Accumulations of exudate 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 soft meninges at chronic course diseases. 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, the degree of increase 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. There may be clonic and tonic convulsions muscles of the limbs and face, as well as symptoms of damage cranial nerves(especially often oculomotor, facial, vagus, trigeminal) in the form of paralysis, paresis, sensitivity disorders and secretory disorders. When localized pathological process in the back cranial fossa possible slowing of breathing; sometimes Cheyne-Stokes breathing develops.

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

Particularly turbulent current high fever, severe headaches, persistent vomiting, 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 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 chronic purulent otitis media causes pain in the ear, otorrhea increases, fever and meningeal symptoms, then it must be assumed that otogenic meningitis. 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 characteristic of both the underlying disease and differential diagnosis becomes more difficult. The issue is resolved by the results of the study of cerebrospinal fluid, the presence of meningeal syndrome.

At differential diagnosis purulent otogenic and rhinogenic meningitis with meningococcal meningitis great importance has been found in the cerebrospinal fluid of meningococcus.

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 when serious condition sick; it can only be used sodium salt. 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.

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

Prevention

Prevention of otogenic and rhinogenic meningitis is timely diagnosis and proper treatment purulent diseases ear, nose and its paranasal sinuses.

Acute purulent meningitis

Meningitis is an acute infectious disease of the central nervous system With predominant lesion arachnoid and pia mater. With this disease, situations can develop that threaten the patient's life (impaired consciousness, shock, convulsive syndrome). The Yusupov hospital has all the conditions for treatment. Patients are placed in single isolated rooms with exhaust ventilation and air conditioning. The medical staff is attentive to the wishes of patients, provides care and dietary nutrition.

Examination of patients is carried out using the equipment of the world's leading manufacturers. Professors and doctors the highest category adhere to European and American recommendations, standards of rendering medical care patients with purulent-inflammatory diseases of the central nervous system. Neurologists individually approach the choice of antibiotic therapy for each patient.

Causes of purulent meningitis

Purulent meningitis develops when bacteria enter the body - meningococci, streptococci, listeria, Haemophilus influenzae and mycobacterium tuberculosis. Contribute to the development of the inflammatory process in the membranes of the brain and spinal cord hypothermia, decreased immunity, transferred infectious diseases. Purulent meningitis develops in patients with an open craniocerebral injury, after neurosurgical operations or inflammatory diseases of the middle ear, nasal sinuses. The source of infection may be on the mucous membranes of the nasopharynx, in carious teeth or tonsils affected by a chronic inflammatory process.

In conditions of reduced immunological reactivity, bacteria from the foci of infection or pathogens that have entered the body from the outside enter the bloodstream. When infected pathogenic bacteria from the external environment (meningococci, pneumococci) or in cases where saprophytic pathogens living in the patient's body become pathogenic, acute inflammatory diseases membranes of the brain develop according to the mechanism of rapidly emerging bacteremia. The source of these processes may be pathogenic foci associated with infection of implanted foreign bodies (artificial valves heart, alloplastic vascular prostheses, artificial drivers rhythm). Infected microemboli also enter the meninges. Bacteria can enter the meninges by the hematogenous route, not only through the arteries, but also through venous vessels. This is how ascending purulent thrombophlebitis of the veins of the face, intracranial veins and sinuses of the dura mater develops.

In the mechanism of development of meningitis, the following factors are important:

  • general intoxication of the body;
  • inflammation and swelling of the meninges;
  • excess production cerebrospinal fluid and violation of its reabsorption;
  • irritation of the meninges;
  • CSF hypertension (increased intracranial pressure).

Causes and consequences of purulent meningitis in children

In children, purulent meningitis mainly develops with meningococcal infection. The source of microorganisms is a sick person or a bacteriocarrier. Microorganisms are localized in the nasopharynx. The main route of transmission of infection is airborne. The entrance gates are the mucous membranes of the upper respiratory tract.

The incubation period for meningococcal purulent meningitis is from 3 to 20 days (usually 5 to 7 days). The disease begins acutely, with a sharp chill and fever up to 38 - 40 degrees. Before the onset of signs of meningitis, some patients experience symptoms of nasopharyngitis (nasal congestion, sore and sore throat, runny nose). There is general weakness, pain in the frontal-temporal and occipital regions, in eyeballs. Headache grows rapidly, becomes excruciating.

Children experience nausea, vomiting, which does not bring relief. Observed hypersensitivity to external stimuli, lethargy, lethargy, sleep disturbance. There are signs of inflammation of the meninges. In the first days of the disease, some children develop rashes in the form of stellate hemorrhages of irregular shape and various sizes. The rash is localized more often on the buttocks, lower and upper limbs, in the inguinal and axillary areas, rarely on the face.

inadequate and untimely therapy meningitis in children leads to unpredictable consequences. After purulent meningitis, patients often have regular headaches, hearing loss, and significant visual impairment. Sometimes there are epileptic seizures. In children after purulent meningitis, mental retardation may occur, the basic functions of the central nervous system may be disrupted.

Complications of purulent meningitis

Main clinical manifestations purulent meningitis are:

Muscle tone often decreases, depression of consciousness occurs. In the blood, there is a high erythrocyte sedimentation rate, neutrophilic leukocytosis. The cerebrospinal fluid is turbid, milky white or yellowish-greenish in color, flows under high blood pressure. A terrible complication of purulent meningitis is infectious-toxic shock. It manifests itself as a hemorrhagic rash with necrosis of skin areas, increased heart rate, and then a drop in blood pressure and coma. In the mechanism of shock development, meningoencephalitis syndrome is currently of great importance, and in hyperacute forms of the disease - rapid swelling and edema of the brain with subdural effusion.

Meningoencephalitis in purulent meningitis is manifested by symptoms of brain damage:

  • partial paralysis;
  • focal convulsions;
  • speech disorders.

Edema and swelling of the brain due to dislocation phenomena lead to the development of stem symptoms (respiratory and cardiovascular disorders). Subdural effusion is characterized by dislocation clinical symptoms. At the same time, meningeal symptoms decrease, and cerebral and focal symptoms increase. Congestive discs of the optic nerve appear on the fundus.

Treatment of purulent meningitis

Doctors of the Yusupov hospital begin antibiotic therapy for purulent meningitis as early as possible. The primary antibiotics that are used for inflammation of the meninges are benzylpenicillin preparations. They are administered intramuscularly at 3-6 million units every 4 hours. In an extremely serious condition of the patient, up to 30-40 million units of benzylpenicillin are prescribed per day. The drug is administered intravenously at 8-10 million units every 4 hours. As a second-line drug, chloramphenicol succinate is used, 1 gram 3 times a day. The antibiotic is administered intravenously.

Water-soluble sulfanilamide sulfalene meglumine is administered intravenously, sulfamonomethoxin is administered orally. Single intravenous administration 10 ml of an 18.5% solution of meglumine sulfalene provides a sufficient level of drug concentration in the cerebrospinal fluid for 3 days, and two grams for seven days. Sulfamonometoxin is administered orally on the first day of the disease, 2 g.

With pneumococcal meningitis, treatment is started with benzylpenicillin sodium salt. The antibiotic is administered intravenously, 5 million units every 4 hours. Patients are prescribed intramuscular injections ampicillin 3 grams every 3 hours or kanamycin sulfate 250 mg 2 times a day. Apply a combination of ampicillin and sulbactam (unazine) 2-3 grams every 6 hours. In children daily dose The drug is 150 mg per kilogram of body weight. As an alternative antibacterial drugs soluble chloramphenicol succinate, gentamicin sulfate, ceporin (cefamesin), ceftriaxone are used. All of these drugs are administered intravenously.

In staphylococcal meningitis, the first choice drugs include metacycline, benzylpenicillin sodium, oxacillin sodium, tseporin, a combination of ampicillin and sulbactam. Levomycetin succinate, ceporin, ceftriaxone, latamoxef and amikacin are used as second-line agents. Antibiotic therapy is canceled in case of:

  • a sharp improvement in the patient's condition;
  • reverse development of meningeal syndrome;
  • decrease in the concentration of cells in the cerebrospinal fluid to 100 in one microliter with a content of lymphocytes of at least 75%.

In parallel with antimicrobial treatment, the doctors of the Yusupov hospital carry out pathogenetic and symptomatic therapy aimed at combating intoxication, disorders of the cardiovascular and respiratory systems, cerebral edema. In case of infectious-toxic shock, levomycetin succinate is used. To eliminate hypovolemia (decrease in the volume of circulating blood), colloidal solutions are injected intravenously - polyglucin, reopoliglyukin, reogluman, 5% albumin. Simultaneously carry out infusion therapy 5% glucose solution, glucocorticoid hormones (dexamethasone) are administered. Polyionic mixtures and saluretics (furosemide) are used. To combat metabolic acidosis, under the control of blood osmolarity, 4% or 8.2% sodium bicarbonate solution or trisamine is injected intravenously. Cardiac agents are used - sulfocamphocaine, strophanthin, corglicon.

Rehabilitation of patients after meningitis

AT recovery period patients are engaged physical therapy in the rehabilitation clinic of the Yusupov hospital. Physiotherapists use treatments aimed at improving microcirculation and metabolism nervous tissue, restoration of normal circulation of cerebrospinal fluid. Improve metabolic processes and microcirculation in the nervous tissue following physiotherapy methods:

  • aerotherapy;
  • medicinal electrophoresis with drugs that improve metabolism, vasodilators;
  • transcerebral UHF-therapy;
  • thalassotherapy;
  • galvanization;
  • mud treatment.

Medicinal electrophoresis with drugs that have a neurostimulating effect, aerotherapy, massage, non-selective chromotherapy has a tonic effect. Excited patients are given sedative procedures: baths with iodine, bromine, pine needles, drug electrophoresis with sedatives, franklinization, carry out treatment according to the method of electrosleep. For stimulation immune system applied ultraviolet irradiation, radon baths, medicinal electrophoresis with drugs that increase immunity, magnetotherapy. To reduce cerebral edema and intracranial pressure, fresh, sodium chloride baths are prescribed, sessions of low-intensity decimeter therapy are performed.

If you suspect meningitis, call the Yusupov hospital at any time of the day, as patients are hospitalized daily and around the clock. Doctors spend adequate therapy to prevent undesirable consequences meningitis.

Rhinogenic meningitis

Rhinogenic purulent meningitis usually develops in acute or exacerbation of chronic purulent inflammation in the upper Group of the paranasal sinuses (frontal, ethmoid, sphenoid) due to the fact that the infection can penetrate into the cranial cavity on contact and cause purulent diffuse inflammation of the meninges.

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

At rhinogenic purulent meningitis there is increased production of cerebrospinal fluid, resulting in increased intracranial pressure, which usually causes diffuse headache. Besides, 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 temperature body. In severe cases of the disease, you are usually upper and lower symptoms Brudzinsky. Diagnostically reliable sign is a change in the cerebrospinal fluid - an increase in the number of cells and protein content in it. Fluid leaks out during puncture frequent drops or jet due to pressure increase. 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.

Treatment The disease consists in Urgent radical Nom 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.

Rhinogenic arachnoiditis is either the outcome of leptomeningitis with the development of scars and cysts of the arachnoid membrane, or the primary fibro-plastic process in the sensitized purulent infection body. Most often, arachnoiditis accompanies ethmoiditis, sphenoiditis, sinusitis, less often - frontal sinusitis.

Rhinogenic meningitis, arachnoiditis

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

There are numerous cases of purulent meningitis with injury to the sieve plate after intranasal surgery, with fractures of the base of the skull.

In these cases, the infection spreads through the 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 the characteristic signs of 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. A diagnostically 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 consists in an 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.

Rhinogenic arachnoiditis is either the outcome of leptomeningitis with the development of scars and cysts of the arachnoid membrane, or a 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 headache accompanied by nausea, vomiting usually does not occur, meningeal symptoms are very rare, expressed unsharply.

D i a g n o s t i k e importance have a change in visual fields, visual acuity and the condition of the fundus. With lumbar puncture, high CSF pressure is almost always 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, radiological changes in the area of ​​the Turkish saddle should be taken into account, data computed tomography and MRI.

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

Treatment. Therapeutic tactics for rhinogenic arachnoiditis consists of the 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.

Rhinogenic purulent meningitis

Rhinogenic meningitis (rhinogenic meningitis) is an inflammation of the meninges of the brain that develops as a result of the spread bacterial infection from the nasal cavity and paranasal sinuses. It is less common than with inflammation of the ear.

Clinic and diagnostics. Purulent meningitis is characterized by ‘to tr and from the beginning, high constant temperature body. An increase in intracranial pressure causes a diffuse headache accompanied by nausea and vomiting. In addition, the inflammatory process, to some extent spreading to the brain and cranial nerves, can cause seizures, psychomotor agitation, loss of consciousness and the appearance of pathological reflexes - Babinsky, Rossolimo, Oppengsim, Brudzinsky, etc.

Permanent signs of meningitis are symptoms of ra! - meninges dragee - stiff neck, Kernig's symptom.

diagnostically reliable and constant sign meningitis is a change in cerebrospinal fluid - an increase in the number of cells and protein content in it. Liquor with spinal cord! puncture follows frequent drops or a jet due to an increase in intracranial pressure due to a sharp increase in the production of cerebrospinal fluid. Survey radiographs or computed tomography data reveal the primary purulent focus.

The treatment of the disease consists in an urgent extended radical operation on the paranasal sinuses concerned with exposure of the meninges in order to eliminate the purulent focus. At the same time, massive anti-inflammatory, dehydration therapy, spinal punctures are carried out.

More complete material on meningitis is presented in the section "Otogenic meningitis".

  • 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 skin and row common symptoms. 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 medulla and kernels 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 soreness with pressure on the region of the spinous processes of the vertebrae due to irritation purulent exudate posterior roots of the spinal cord. 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

Diagnosis is confirmed with 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 oculomotor nerve(ptosis, anisocoria), lack of reaction to light;
  • positive reaction Mantu;
  • 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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Develops at any age.

What provokes 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 (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).

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. In 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, sharp lymphocytosis, high protein content, formation of a fibrin mesh after 5-6 hours, fluid pressure is increased, glucose and chloride levels are reduced.

Develops at any age.

What provokes / Causes of 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 (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).

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. In 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, sharp lymphocytosis, high protein content, formation of a fibrin mesh after 5-6 hours, fluid pressure is increased, glucose and chloride levels are reduced.

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 paranasal sinuses (rhinogenic meningitis). Among all otogenic intracranial complications, otogenic meningitis, according to different authors, ranges from 9.4 to 25.1‰.

Rhinogenic meningitis, as well as rhinogenic intracranial complications, is much less common, and the literature contains only descriptions of individual cases 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 body, its reactivity. The source of infection in otogenic meningitis is most often chronic purulent otitis media, especially epitympanitis, complicated by cholesteatoma, less often acute purulent 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. More often this is observed during endonasal opening of the ethmoid labyrinth and frontal sinus.

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 of the pelvic organs are disrupted, 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, the detection of meningococcus in the cerebrospinal fluid is of great importance.

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 of 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. With proper complex treatment, mortality does not exceed 20%.

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