Rhinogenic meningitis. Complications of purulent meningitis
Develops at any age.
What provokes / Causes of Rhinogenic meningitis:
causative agents purulent meningitis 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 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, noted constantly high topics perature, 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 the 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 detected in children meningeal syndrome 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.
Study cerebrospinal fluid: cerebrospinal fluid with serous meningitis is transparent, flows under high blood 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.
Inflammatory diseases of the nose and paranasal sinuses can lead to various complications. The occurrence of intraocular and intracranial complications is due to several reasons.
Anatomical features: the orbit is surrounded on three sides by the walls of the paranasal sinuses; from below - maxillary, from the inside - ethmoid and wedge-shaped, from above - frontal.
Vascular connections: the veins of the nasal cavity through the angular and superior ophthalmic veins anastomose with the cavernous sinus and venous plexuses of the dura mater.
The lymphatic network of the nasal cavity communicates with the subarachnoid space of the brain.
The penetration of infection into the cavity of the orbit and skull can occur different ways: contact, hematogenous, perineural and lymphogenous. The most frequent of these is contact way. With regard to the frequency of the source of infection of intracranial complications, most researchers put cells in the first place. lattice labyrinth, then frontal, top-
jaw and finally sphenoid sinus. It should be noted that the symptoms of orbital complications often coincide, sometimes one form passes into another, which creates difficulties in differential diagnosis.
Patients with rhinogenic orbital and intracranial complications belong to a heavy contingent, which requires emergency specialized surgical care in a hospital, with the involvement of ophthalmologists and neurosurgeons.
2.7.1. Rhinogenic orbital complications
There are the following orbital complications:
Reactive edema of the eyelids and orbital tissues;
Orbital osteoperiostitis (purulent or non-purulent);
Abscess of the century;
Subperiosteal abscess;
Phlegmon of the orbit;
Retrobulbar abscess;
Thrombosis of the veins of the eye tissue.
Clinic. Local manifestations of orbital complications are characterized by reactive edema of the tissue of the orbit and eyelids, hyperemia of the conjunctiva, and in some cases its edema - chemosis (Fig. 2.38). The eyeball is displaced outward: exophthalmos, limitation of the mobility of the eyeball, pain during eye movements. Characterized by severe pain with pressure on the eyeball or on the edge of the orbit. Usually observed purulent discharge and nasal congestion. Decreased vision occurs quickly (blindness may occur within the next few hours), especially with a deep location of the focus of inflammation. In some cases, paresis of the muscles and nerves of the eye can be observed.
General disorders are characterized by an increase in body temperature up to 39-40 ° C, headache, general weakness sometimes vomiting.
At reactive edema of the eyelid and orbital tissue there is swelling of the eyelid, sometimes the displacement of the eyeball forward (exophthalmos), on palpation - its soreness. Reactive swelling of the soft tissues of the orbit can be caused by two factors: impaired collateral drainage, accumulation of secretions in the sinuses, and bacterial invasion into the tissues of the orbit with their subsequent purulent fusion.
Rice. 2.38. Rhinogenic orbital complication
Subperiosteal abscess in the area of upper wall of the maxillary sinus leads to an upward displacement of the eyeball, exophthalmos, edema of the lower eyelid, chemosis of the lower conjunctiva.
At eyelid abscess the eyeball is usually closed by an edematous, infiltrated and immobile eyelid. The latter is sharply painful on palpation, tense.
Retrobulbar abscess- purulent focus back departments fiber of the orbit, which can develop into phlegmon of the orbit- diffuse purulent process, accompanied by melting of the fiber of the orbit. The main symptom of the disease is painful exophthalmos with a sharp violation of mobility or complete immobility of the eyeball (ophthalmoplegia), diplopia, decreased vision and changes in the fundus. Distinguish preseptal and postseptal localization of the inflammatory process, depending on the location of the abscess - in front or behind the fascial septum of the orbit, which is important in determining the surgical approach to the focus of inflammation.
With thrombosis of the veins of the eye tissue, a severe general state patient, body temperature of the hectic type. Puffiness and infiltration of the eyelids are revealed first of one and then the other eye. There are dense bluish vascular bands around the eye. There is a great danger of involvement in the process of the cavernous sinus.
Diagnostics rhinogenic orbital complication is based on X-ray data, CT scan of the paranasal sinuses, external examination data, rhinoscopy, anamnesis. Perform if necessary diagnostic puncture sinuses, determination of acuity and visual fields. Differential diagnosis is carried out with erysipelas of the face, hematoma and emphysema of the eyelid, tumors of the orbit.
Treatment with rhinosinusogenic orbital complications only surgical, with simultaneous general anti-inflammatory therapy. Surgery should be emergency and is aimed at eliminating the primary purulent focus of inflammation in the paranasal sinuses. Radical surgery is performed on the affected sinus with complete removal pathologically altered tissues with the formation of a wide fistula with the nasal cavity. Radical surgery can be combined with endoscopic decompression of the orbital tissue.
The tactics of the surgeon varies depending on the nature of the lesion of the orbit. With abscesses of the tissue of the orbit, phlegmon, subperiosteal abscesses, the focus is opened with external incisions with the introduction of rubber drains into the tissues of the orbit. Positive effect gives decompression of the tissue of the orbit by the endonasal endoscopic method.
2.7.2. Rhinogenic purulent meningitis
Rhinogenic meningitis (meningitis rhinogena)- inflammation of the membranes of the brain, which develops as a result of the spread of a bacterial infection from the nasal cavity and paranasal sinuses. It is less common than with inflammation of the ear. Occurs during acute or exacerbation of chronic purulent inflammation in the upper group of paranasal sinuses: frontal, ethmoid, sphenoid. The infection most often penetrates into the anterior cranial fossa by contact and causes inflammation of the meninges. Purulent meningitis may occur with trauma to the sieve plate during intranasal operations, with fractures of the base of the skull.
Clinic and diagnostics. Purulent meningitis is characterized by an acute onset, high constant body temperature. An increase in intracranial pressure causes a diffuse headache, accompanied by nausea and vomiting. Besides, inflammatory process, extending to some extent to
the brain and cranial nerves, can cause seizures, psychomotor agitation, loss of consciousness and the appearance of pathological reflexes - Babinsky, Rossolimo, Oppenheim, Brudzinsky, etc.
Permanent signs of meningitis are symptoms of irritation of the meninges - 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 during spinal puncture flows out in frequent drops or a jet due to an increase in intracranial pressure due to sharp increase production of cerebrospinal fluid. Survey radiographs or computed tomography data reveal the primary purulent focus.
Treatment 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".
2.7.3. Extradural abscess
Extradural abscess (limited pachymeningitis) - accumulation of pus between the dura mater and bone, most often occurs as a result of the spread of infection by contact with the defeat of the frontal, ethmoid and less often sphenoid sinuses.
Clinic oligosymptomatic, usually accidentally discovered during surgery. Possible local headache, which increases in the projection of the abscess with percussion of the skull, as well as attacks of nausea and vomiting, difficulty in retracting the eyeball outward.
The general condition is characterized by fever, weakness, poor health, symptoms of damage to the paranasal sinuses.
The CT scan data of the SNP and the result of spinal puncture allow us to clarify the diagnosis.
Treatment surgical - a radical operation on the paranasal sinuses in order to eliminate the purulent focus, wide exposure of the meninges in the affected area and drainage of the abscess.
2.7.4. Rhinogenic brain abscess
Rhinogenic brain abscess - limited accumulation of pus in the brain, which occurs a second time in the presence of focal infection in the paranasal sinuses. The most common source of infection is the frontal sinus, less often the ethmoid labyrinth and maxillary sinus. The abscess is usually localized in the frontal lobe of the brain and is almost always located on the side of the affected sinus (Fig. 2.39).
In the clinic local and general symptoms can be distinguished.
local symptoms may be characterized by edema of the eyelids, edema and hyperemia of the conjunctiva, the presence of exophthalmos varying degrees severity with a shift of the eyeball more often downwards and outwards on the corresponding side.
General symptoms are characterized by signs infectious disease, meningeal symptoms, cerebral and focal (nested) symptoms.
In the development of an abscess, four stages can be conventionally distinguished.
AT initial stage there is a moderate increase in body temperature, headache, vomiting, general weakness.
Latent (latent) period- all symptoms are mild, the patient's condition improves, the temperature drops, the condition
Rice. 2.39. Computed tomogram. Rhinogenic abscess in the frontal lobe of the brain (posterior wall defect frontal sinus, subperiosteal abscess in the anterior wall of the frontal sinus)
remains relatively satisfactory. If the focus is encapsulated, then the condition is normalized for a long time.
AT explicit stage along with signs infection: weakness, fever, loss of appetite, etc., cerebral symptoms may increase - headache, localized in the frontal region, vomiting, drowsiness; meningeal symptoms - stiff neck, Kernig's symptom, symptoms of Brudzinsky, Bekhterev, etc. Characteristic focal symptoms lesions of the frontal lobe: mental disorder, disturbance of statics and gait, pathological reflexes - grasping and sucking. Mental disorder is expressed in a decrease in intelligence and memory. There is euphoria, inadequacy of behavior, foolishness, voracity.
Convulsions, paresis and visual disturbances are also characteristic of focal symptoms of frontal lobe abscess. Convulsions are in the nature of Jacksonian seizures, begin with facial muscles opposite side and spread first to the top, then to lower limbs. Sometimes speech disorders can also be observed.
When spread inflammatory response outside the frontal lobe, dislocation symptoms occur - sensory and motor disorders on the side opposite to the abscess.
terminal stage abscess is characterized by gross violations of the functions of the body, due to both general intoxication, and the phenomena of cerebral edema.
Diagnostics consists of characteristic complaints, clinical and neurological symptoms. When primary signs disease, CT or MRI is indicated, which will give accurate data regarding the presence and localization of a volumetric process in the skull. A spinal puncture is shown, in which protein-cell dissociation is detected, the fluid flows out under pressure. However, it is necessary to remember about the possibility of transtentorial or temporal herniation of the brain and to minimize CSF sampling.
Treatment rhinogenic abscess of the brain is emergency surgical elimination of purulent process in the paranasal sinuses. If the source of the abscess is the frontal sinus, surgical debridement is combined with decompression trepanation cerebral (posterior) wall of the sinus. After exposure of the dura mater, attention is paid to its color, thickness, presence of fibroids.
pink raids, granulations. Puncture of the dura mater is performed after treatment with iodine with a special thick needle with a blunt end to a depth of 3-4 cm. When a brain abscess is detected, the wound is expanded along the needle and a rubber strip is inserted into the abscess cavity.
Surgical intervention must be combined with massive anti-inflammatory, antibacterial, detoxification and dehydration therapy in the intensive care unit.
2.7.5. Thrombosis of the cavernous sinus
Thrombosis of the cavernous (cavernous) sinus - thrombus formation up to complete occlusion sinus lumen, accompanied by inflammation of its vascular wall.
The disease may be due to the spread of infection from the region of the nasolabial triangle (with nasal furuncles) or with purulent inflammation of the paranasal sinuses.
Clinical picture thrombosis of the cavernous sinus consists of general infectious, cerebral, meningeal and local symptoms.
General symptoms characterized by a severe general septic condition, accompanied by a high remitting rise in temperature, combined with chills, profuse sweating and weakness.
Cerebral symptoms associated with increased intracranial pressure and is expressed in headache, nausea, vomiting.
Meningeal symptoms characterized by stiff neck muscles negative symptoms Kernig and Brudzinsky (dissociated symptom complex).
From local features there are bilateral swelling of the eyelids and conjunctiva, chemosis of the conjunctiva, exophthalmos and ptosis of the eyeballs, paralysis eye muscles. Through the thin skin of the eyelids, in the forehead and the root of the nose, dilated veins protrude. When examining the fundus, stagnation, swelling of the nipple are visible optic nerve, sharply dilated veins, hemorrhages on the retina.
Diagnostics thrombosis of the cavernous sinus is carried out on the basis of general clinical data, the results of spinal puncture, CT scan of the SNP and x-ray examination of the paranasal sinuses.
Treatment consists in emergency sanitation of the purulent focus in the paranasal sinuses and the use of a massive antibiotic therapy in combination with anticoagulants.
important place in conservative therapy assigned to anticoagulant therapy according to the appropriate scheme.
2.7.6. Sepsis - rhinogenic, tonsillogenic, otogenic
Sepsis - a pathological symptom complex due to the constant or periodic entry of microorganisms into the blood from the focus of purulent inflammation.
Rhinogenic sepsis is relatively rare, characterized by the fact that primary focus purulent inflammation is located in the nose and paranasal sinuses. The occurrence of rhinogenic sepsis is usually preceded by thrombophlebitis of the cavernous sinus or thrombosis of the veins of the eye tissue. With purulent processes in the palatine tonsils and paratonsillar space, cases of tonsillogenic sepsis are possible; otogenic sepsis, which occurs more often than others, is associated, as a rule, with thrombophlebitis of the sigmoid and petrosal sinuses.
AT clinical picture severe general and multiple organ disorders predominate, local inflammatory symptoms expressed clearly.
There are two forms of sepsis: septicemic and septicopyemic, however, they can also be considered as stages of a single process. According to the duration of the process, there are acute sepsis- up to 6 weeks and chronic sepsis - more than 6 weeks.
The septicemic form of sepsis is not accompanied by the formation of metastatic foci of purulent infection, but it can more or less quickly turn into a septicopyemic form, characterized by the formation of metastatic foci of purulent infection.
Patients are characterized by a severe general condition, high fever, usually of the hectic type, tremendous chills, headache, weakness, loss of appetite. The drop in temperature is accompanied profuse sweating. The pulse rate usually changes according to body temperature. There may be changes in the psycho-emotional status to gross cerebral disorders (coma). Subsequently, inflammatory changes from the side internal organs: kidneys, endocardium, liver, intestines, spleen.
Local changes are characterized by swelling, hyperemia and infiltration of the eyelids and paraorbital region of one or both eyes with the formation of dense vascular cords. Exophthalmos ( eyeball shifted forward), the mobility of the eye is sharply limited, painful. Visual impairment up to blindness can occur quickly.
Diagnostics. Suspicion of sepsis occurs when the duration of fever is more than 5 days and the appearance of unmotivated rises in body temperature to febrile values, followed by a fall to subfebrile. Laboratory blood tests are characterized by leukocytosis or leukopenia, stab shift to the left, thrombocytopenia. Positive results bacteriological research blood - detection of hemoculture. For getting reliable result 3-fold blood sampling in a volume of 20-30 ml is required at intervals of 1 hour during the rise in temperature, if possible, before the start of antibiotic therapy.
Treatment. Required intensive therapy, including urgent surgical sanitation of the causative focus and etiopathogenetic drug exposure. Until the results of bacteriological examination are obtained, empirical antibiotic therapy is carried out at the maximum dosage. The introduction of tobramycin 3-5 mg/kg per day intravenously in combination with an antibiotic of the cephalosporin group, metronidazole, is effective. Antibiotics are prescribed for 2 weeks, despite the normalization of temperature. Detoxification therapy - intravenous administration large amounts of fluid in combination with diuretics (forced diuresis method). It must be borne in mind that the amount of fluid administered should not exceed the amount of urine excreted. Effective simultaneous short course of corticosteroid therapy (5-7 days), given the immunosuppressive effect of glucocorticoids. Symptomatic therapy, relief of heart failure, vasodilators, analgesics are carried out.
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 extensive damage to the central nervous system and 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, upper and lower symptoms Brudzinsky. Diagnostic 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.
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 the sensitized purulent infection body. 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.
When diagnosing importance have a change in visual fields, visual acuity and the condition of the fundus. 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, radiological changes in the area of the Turkish saddle should be taken into account, data computed tomography and MRI.
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 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.
When diagnosing, changes in visual fields, visual acuity and the condition of the fundus are important. 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 the differential diagnosis from a pituitary tumor, arachnoid endotheliomas, radiographic changes in the area of the sella turcica, computed tomography and MRI data should be taken into account.
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.
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 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 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 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 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 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 the veins of the mucous membrane of the ethmoid labyrinth along the 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. 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 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, 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. There may be 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. 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, 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 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.
In the differential diagnosis of purulent otogenic and rhinogenic meningitis with meningococcal meningitis great importance has been found in the cerebrospinal fluid of meningococcus.
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 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.
Forecast
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%.
