Meningitis. Serous meningitis Serous meningitis micb code 10

Meningitis - inflammatory disease meninges. Primary meningitis develops without previous diseases in other organs, due to the tropism of the infectious agent to the meninges of the brain.

Secondary meningitis develops against the background of a general or local infectious process, being one of the syndromes or a complication of the underlying disease. Depending on the nature of the exudate, serous and purulent meningitis are distinguished.

Purulent meningitis caused by bacteria and fungi: meningococcus (62% of cases), pneumococcus (19%), staphylococcus (7%), Pfeiffer's Haemophilus influenzae (6%), coli(4%), streptococcus (1%), Candida fungi (1%). In young children, especially newborns, staphylococcal meningitis is common as a manifestation of staphylococcal sepsis, which has a high lethality and is also caused by Escherichia coli. Possible infection intrauterine, during childbirth and in the postnatal period. The occurrence of purulent meningitis is promoted by hypoxemia, trauma, reduced immunity, chronic purulent foci.

Pathomorphology . The meninges are diffusely infiltrated, the serous-purulent infiltrate becomes purulent, turning into a dense fibro-purulent mass by the 4-8th day of the disease, mainly on the outer surface of the cerebral hemispheres, less on the base of the brain; possible germination of exudate, the formation of adhesions, sclerosis of the meninges. With ependymatitis and ventriculitis, obliteration of the cerebrospinal fluid sometimes occurs, and pyocephaly develops.

Epidemiology . It is transmitted by droplet directly from person to person. There is an increase in cases of the disease in the winter-spring period and against the background of influenza epidemics. Possibly a long term carrier.

Clinic : with a decrease in the reactivity of the body, meningococcal nasopharyngitis develops - a localized form of meningococcal infection. The generalized form - meningococcemia - is a consequence of the penetration of meningococcus into the subarachnoid space, where it, multiplying, causes an inflammatory process, mainly on the convexital surface of the brain.

Diagnosis meningococcal infection put on the basis of clinical (meningococcemia), epidemiological and laboratory data. If meningitis is suspected, a lumbar puncture must be done. The etiology of purulent meningitis is established by detecting meningococcus, pneumococcus or staphylococcus in the cerebrospinal fluid, as well as the nasopharynx. The latter can also be found in the blood, discharge from the ears, feces.

Pneumococcal meningitis. It is caused by pneumococcus, a Gram-positive diplococcus.

The primary focus may be the lungs, from where pneumococcus enters the subarachnoid space by the hematogenous route (in young children). The microorganism spreads by lymphogenous way if the paranasal sinuses are the primary focus.

Clinic . Pneumococcal meningitis also develops after an injury, especially a skull fracture, often accompanied by liquorrhea, which indicates the communication of the nasopharynx and subarachnoid space. The disease begins acutely. Meningeal signs are pronounced. Often there are convulsions, loss of consciousness, paresis and paralysis of the limbs, abducent nerves, facial nerve, bulbar paralysis. Greenish cerebrospinal fluid. It contains a large number of neutrophilic granulocytes and protein, the level of glucose is reduced.

Staphylococcal meningitis. It is a consequence of staphylococcal sepsis or subsepsis. It occurs more often in young children, starting from the first days of life. In the anamnesis of patients - umbilical sepsis, purulent otitis media, pustular skin diseases. With staphylococcal meningitis, the meningeal syndrome is not pronounced, but the general state patient: intoxication, chills, hectic body temperature. With late diagnosis and treatment, progressive hydrocephalus is observed. Staphylococcal meningitis at an older age is more pronounced. Cerebrospinal fluid of purulent chameningeal phenomena. Perhaps the development of hydrocephalus, epileptic syndrome. Cerebrospinal fluid is turbid or opalescent, mixed cytosis within 0.1-1 x 109/l. To establish the diagnosis, it is important to isolate the fungus from the cerebrospinal fluid. Residual-organic consequences are frequent.

Treatment of purulent M. should be intensive, complex and begin as early as possible, since the prognosis and frequency of residual effects largely depend on the timing of the start of treatment.

The basis of etiological treatment is antibacterial drugs, which are administered in massive doses intramuscularly, intravenously and in some cases even endolumbally. Their choice is determined by the sensitivity of the isolated microorganisms to them, but you can not wait more than 2-3 days. Since most purulent M. are caused by cocci, benzylpenicillin should be used as an urgent treatment at 200,000 - 300,000 IU / kg per day, in severe condition or a late start of treatment, 400,000 - 500,000 IU / kg at intervals of 4 hours, and with intravenous administration - every 2-3 hours. It is advisable for newborns to prescribe synthetic ampicillin or oxacillin sodium salt, gentamicin sulfate (6-8 mg / kg per day every 6 hours). These drugs remain leading in meningococcal, pneumococcal and streptococcal M. With staphylococcal M., before obtaining results on the sensitivity of microflora, it is better to use 2-3 antibiotics simultaneously (benzylpenicillin + semi-synthetic penicillins, chloramphenicol), combine them with antistaphylococcal plasma, toxoid. For meningitis caused by Escherichia coli, salmonella, or other gram-negative microorganisms, gentamicin or ampicillin, carbenicillin, amikacin, tobramycin, chloramphenicol succinate are prescribed. Polymyxin is also used. In sulfate intramuscularly (2-2.5 mg / kg per day after 6 hours). For meningitis caused by Pseudomonas aeruginosa, ampicillin or carbenicillin is indicated in combination with gentamicin sulfate or other aminoglycosides and polymyxin M sulfate. At M. on the basis of infection with Pfeiffer's Haemophilus influenzae, ampicillin or cephalosporins (kefzol, klaforan) are shown in combination with levomycetin, tetracycline, morphocycline. In M. fungal etiology, amphotericin B is prescribed, starting with 50-70 U / kg for children under 1 year old and 100-120 U / kg for older children intravenously 2 times a day and endolumbally, 1 U. During the week, the doses are gradually increased to 240-400 U/kg intravenously (up to 1000 U/kg in older children) and 15-20 U/kg endolumbally.

Serous meningitis(ICD-10-G02.0). Primary serous M. in most cases is caused by viruses (Koksaki and ECHO enteroviruses, mumps viruses, poliomyelitis, tick-borne encephalitis, lymphocytic choriomeningitis). Secondary serous meningitis can complicate typhoid fever, leptospirosis, syphilis and other infectious diseases as manifestations of a general non-specific reaction of the meninges.

Leading pathogenetic mechanism serous meningitis, which determines the severity of symptoms, is the acute development of hypertensive-hydrocephalic syndrome, which does not always correspond to the degree of cytological changes in the cerebrospinal fluid. Pleocytosis is represented by lymphocytes (in the early days there may be a few neutrophilic granulocytes) from 0.1 x 109/l to 1.5 x 109/l; the protein content is slightly increased, may be normal or even reduced due to dilution with abundantly secreted fluid.

Pathomorphology : swelling and hyperemia of the pia and arachnoid meninges, perivascular diffuse infiltration of lymphocytic and plasma cells, in some places small punctate hemorrhages. In the choroid plexus of the cerebral ventricles, the same changes. The ventricles are somewhat dilated.

Clinic serous meningitis is characterized by a combination of general infectious, hypertensive-hydrocephalic and meningeal symptoms varying degrees expressiveness. Latent forms (only with inflammatory changes in the cerebrospinal fluid) occur in 16.8% of cases (according to Yampolskaya). In manifest forms, hypertensive phenomena predominate in 12.3% of cases, a combination of hypertensive and meningeal symptoms in 59.3%, and encephalitic symptoms in 11.6%. Children of the first year of life are characterized by anxiety, a painful cry, bulging of a large fontanel, a symptom of the setting sun, tremor, convulsions. In older children - headache, vomiting, agitation, anxiety (sometimes a frozen protective posture). There may be congestion in the fundus. The pressure of the cerebrospinal fluid is increased to 300-400 mm of water.

The course of serous meningitis is often favorable. After 2-4 days, cerebral symptoms disappear. Sometimes a second rise in body temperature is possible, the appearance of cerebral and meningeal symptoms on the 5-7th day. The cerebrospinal fluid is sanitized by the end of the 3rd week.

Enteroviral meningitis most often caused by enteroviruses such as Coxsackie and ECHO - in whitefish and Brudzinsky lower. In young children, convulsions, stupor are possible, in older children - an excited state, delirium in severe cases of the disease, encephalitic reactions in an unfavorable premorbid state. The pressure of the cerebrospinal fluid is increased to 250-500 mm of water. Art., protein content 0.3-0.6 g / l. Cytosis from 0.1 x 109 / l to 1.5 x 109 / l, in young children is much higher, but normalizes faster.

The acute period lasts 5-7 days, the body temperature drops lytically on the 3rd-5th day, meningeal symptoms disappear by the 7th-10th day, from the 12th-14th day the residual cytosis is up to 0.1 x 109 / l, weakly positive globulin reactions. The appearance of symptoms of encephalitis along with a decrease in the signs of meningitis (increased tendon reflexes, spasticity in the extremities, clonus of the feet, intentional tremor, nystagmus, ataxia, psychosensory disorders) indicates mumps meningoencephalitis, but after 2 weeks they fade away, isolated neuritis persists up to 1 - 2 months, polyradiculoneuritis - up to 1-6 months, the outcome is usually favorable. The causes of mumps meningitis are established on the basis of epidemiological and clinical data, in doubtful cases using serological studies(an increase in antibody titer in paired blood sera by more than 4 times, a delay in the hemagglutination reaction and complement fixation).

Lymphocytic choriomeningitis(acute aseptic) - zoonotic viral infection. Infection occurs through inhaled dust or products contaminated with mouse excrement, less commonly through insect bites. The causative agent is not strictly neurotropic, so the disease manifests itself after 8-12 days ( incubation period) generalized intoxication process: hyperthermia, pathological changes in a number of organs (lungs, heart, salivary glands, testicles). Lymphocytic choriomeningitis occurs when a virus penetrates the blood-brain barrier, causing inflammatory changes in the choroid plexuses of the ventricles of the brain, pia mater, and in some cases the substance of the brain and spinal cord. With prolonged and chronic course diseases, obliteration of the subarachnoid spaces, gliosis and demyelination in the medulla are possible.

Clinic . The disease begins acutely, without prodromal phenomena with a picture of influenza, pneumonia, myocarditis. Chills are changing high temperature body. From the 1st day, meningeal phenomena, diffuse headache, nausea, and vomiting are noted. In severe cases of the disease, agitation, hallucinations, followed by loss of consciousness are observed. After 8-14 days from the onset of the disease, the body temperature drops to subfebrile during the body chiasm, legs and spreads anteriorly and posteriorly, to medulla oblongata. With belated treatment, it acquires a fibrinous character, especially in the region of the diencephalon and midbrain, where it is possible to melt the substance of the brain with the formation of caseous masses. Along the course of the vessels, especially the middle cerebral artery, there is a rash of miliary tubercles, endovasculitis is observed in the vessels of small and medium caliber, plexuses of the ventricles of the brain (choroiditis, ependymatitis, leading to periventriculitis). Possible blockade of the liquor pathways, in particular the cerebral aqueduct, adhesive process, hydrocephalic syndrome, the transition of the inflammatory process to the dura mater (leptopachimeningitis).

Torular meningitis It is caused by cryptococcus, a widespread saprophyte that lives on the skin, mucous membranes of humans, and on plants. Penetrates into the child's body with food, through damaged skin, mucous membranes. Hematogenously transferred to the membranes of the brain, as the cerebrospinal fluid is an ideal environment for cryptococcus. Pathological changes: thickening of the meninges, serous-productive inflammation, accumulation of cryptococci around the vessels and in the ventricles of the brain.

Clinic . The disease develops acutely or subacutely. Body temperature rises, headache, meningeal symptoms appear. Cerebrospinal fluid is turbid or xanthochromic, initially clear, flows under high blood pressure, the protein content in it is increased. Reliable confirmation of the diagnosis is the detection of cryptococci in the cerebrospinal fluid. If untreated, the pressure of the cerebrospinal fluid increases, congestive optic discs appear, symptoms of damage to the base of the brain. The following forms are distinguished: meningitis without pronounced focal brain damage, basilar meningitis with lesions cranial nerves(auditory, visual, oculomotor and abducent), meningoencephalitis with phenomena of focal prolapse (paresis, ataxia), convulsions, dementia, pseudotumor, in which both cerebral and focal neurological symptoms are expressed. The course of the disease is often long, relapsing, progressive, often fatal.

Treatment : sulfanilamide preparations, tetracycline with nystatin, amphotericin B (intravenous drip every other day at the rate of 1 mg / kg in 100 ml of 5% glucose solution, 3-4 g per course of treatment). Symptomatic remedies, as in purulent meningitis.

Serous meningitis is manifested by inflammation of the lining of the brain, provoked by the action of pathogenic bacteria, fungi and viruses. The disease is considered characteristic for children 3-8 years old, the disease does not occur in adults. For serous meningitis, ICD-10 (International Classification of Diseases) assigns code A87.8.

Features of the pathology

Features of the disease are in the nature of its development. This form of meningitis develops rapidly, but without pronounced symptoms. Symptoms of this disease:

• nausea;
• vomit;
• headaches without exact localization;
• general malaise;
• increase in body temperature.

Meningeal complications in the serous form of the disease are not observed. Pathology does not provoke a violation of thinking, confusion and other symptoms characteristic of meningitis.

Establishing diagnosis

The reason for going to the doctor is the child's complaints of a headache, which is accompanied by vomiting, nausea and general malaise. The primary examination is carried out by a pediatric therapist, who then refers to a neurologist for a detailed examination.

After a bacteriological examination of the cerebrospinal fluid, a diagnosis is made and treatment is prescribed.

ICD-10 code

Serous meningitis is more often provoked by viruses. However, inflammation can begin due to a bacterial or fungal infection of the meninges. Due to the fact that serous meningitis can be caused by various pathogenic factors, it does not have an accurate classification according to ICD-10 and is categorized as "other viral meningitis".

The disease is listed under the code A87.8, where A87 is a classification of viral brain lesions, and the number 8 means viral inflammation of the brain, provoked by the action of other viruses not included in the classifier.

If the inflammation is caused by a bacterial lesion, it is classified as G00.8. This labeling describes purulent meningitis (class G00) provoked by other bacteria (this is indicated by the number 8 in the code).

Treatment of pathology

Treatment of the disease begins after determining the cause of the inflammatory process. If meningitis is provoked by the action of the virus, it is prescribed antiviral therapy. In case of a bacterial disease, antibiotics are used, and in case of a fungal infection, special antimycotics are used to combat a specific type of fungus.

In addition to treatment aimed at eliminating the cause of the disease, symptomatic therapy is used to improve the patient's well-being as soon as possible. Viral and bacterial damage to the brain can be accompanied by fever, so antipyretic drugs are additionally prescribed. For improvement cerebral circulation often used drugs of the nootropic group. Therapy is necessarily supplemented by the intake of vitamin complexes containing B vitamins in the composition.

With timely treatment, the pathology successfully passes without causing complications.

Serous meningitis

Serous meningitis is a disease that is infectious in nature and is provoked by the occurrence of viruses. The hard shells of the brain are affected. Pathology is dangerous to the life and health of the human body as a whole.

The primary character may begin due to the virus, and the secondary one arises as a result of other disorders.

The symptoms of pathology were described by Hippocrates. The case history of serous meningitis suggests that for a long time outbreaks of the virus have been recorded either in the United States or in African countries. There was no cure for this disease yet, and the sick tried to cure folk remedies, which did not bring results.

Children from 3 to 6 years old are especially susceptible to the disease, schoolchildren are less likely to suffer, sometimes viral meningitis is recorded in adults.

There are ways of infection:

• Air-drip. Transmitted by sneezing, coughing.
• Contact. If personal hygiene is not observed.
• Water. Infection can be obtained in the summer by swimming in a river/lake.

Serous inflammation tends to cause cerebral edema.

Depending on the cause of serous meningitis, the sources of the disease are divided into:

• caused by viruses, coxsackie, echo;
• bacterial. The causative agents are syphilis, tuberculosis.
• fungus, candida and others.

Pathology never appears suddenly, it always has a prodromal stage. A person begins to feel unwell, fever, lack of appetite. Along with these symptoms, it also occurs:

• Drowsiness;
• Loss of interest in surrounding events;
• Weakness of the body.
• In children, manifestations of cramps of the limbs are possible;
• Stomach ache;
• The sensitivity of the eyes, skin, hearing becomes high;
• AT oral cavity reddening of the tonsils, palate, pharynx may be detected;
• In young patients, and especially those who were born recently, meningitis can also manifest itself in inflammation of the heart muscle.

After a certain time, the symptoms do not leave the body, but rather increase. A patient with serous meningitis often suffers from pain in the temples and occiput, which are of a continuous nature. Elevated temperature does not decrease even with the help of tablets. There is nausea and frequent vomiting in a certain number of patients, serous meningitis can manifest itself in the form of constipation. Myalgia is pain in the muscles of the body.

There is no possibility to tilt the head as much as possible, bend the neck, since the muscles on the back of the head are in a tense state.

Important! Symptoms of serous meningitis are similar to the meningeal form of tick-borne encephalitis, this disease also has a seasonal manifestation, and, as a rule, occurs in children and adults in warm weather. summer period time.

The acute form of serous meningitis is a very dangerous pathology, and the consequences appear long years after the patient has already been cured. There is a pathogen in the body that can provoke a recurrence of serous meningitis.

Prevention and sanitary rules

• Prohibit children aged 3-6 from swimming in rivers and lakes;
• Do not drink tap water, only boiled water is allowed;
• Wash vegetables and fruits;
• Wash hands with soap after each visit to a public place;
• Lead an active lifestyle, have in your diet cereals, vegetables, fruits, fish, the whole list of healthy foods, along with this, actively engage in sports.

ICD code 10

By international classification diseases of the 10th revision, serous meningitis has codes:

• A87.0+ Enteroviral (G02.0*). Meningitis caused by Coxsackievirus, ECHO virus
• A87.1+ Adenovirus (G02.0*)
• A87.2 Lymphocytic choriomeningitis (lymphocytic meningoencephalitis)
• A87.8 Other viral meningitis
• A87.9 Unspecified

Diagnostics

To detect such a disease, serological diagnosis at the initial stage. It is able to detect antibodies in the body of a potential patient that induce the onset of the disease. Next, the patient is assigned a bacteriological blood test.

Accurate results are obtained by puncture of the cerebrospinal fluid, cerebrospinal fluid determines purulent and serous meningitis. MRI (magnetic resonance imaging), is prescribed to monitor the state of the brain as a whole, and to determine whether there are lesions. Specialists will issue referrals for blood tests.

Treatment of serous meningitis must begin, the sooner the better. When acute form the patient is admitted to the hospital. With any severity of the disease, antibiotic therapy will be prescribed. Types of antibiotics are selected individually.

If the child has symptoms of serous meningitis, it is necessary to immediately call ambulance, followed by hospitalization. Quarantine is announced for people who have been in contact with the patient.

The viral nature of the pathology is treated with antiviral drugs. In more serious forms, an injection into a vein is prescribed. saline solutions, antipyretic. Bacterial meningitis is eradicated with antibiotics combined with vitamins.

Complications

Inflammation does not often cause complications. However, despite the fact that the disease is benign, one should not forget that it can provoke an infectious process in the brain and spinal cord, and this will lead to bad consequences.

In children, due to complications, visual impairment, pain in the temples, dizziness, and pressure surges are observed.

Statistics show that most cases of serous meningitis ended well. The exceptions were precedents when the nervous system suffered along with myocarditis, such a phenomenon can be fatal. However, if diagnosed early this disease, there will be no consequences.

Proper treatment guarantees a patient of any age to get rid of the disease. The main thing is to timely diagnose serous meningitis, and begin to carefully deal with it. Do not take on your own medications and diagnose yourself and your child. We advise you to contact a doctor without delay, a specialist who will correctly and competently diagnose you and prescribe an effective treatment.

Non-pyogenic meningitis

Definition and background[edit]

Acute serous meningitis is caused by various viruses.

Etiology and pathogenesis[edit]

Most often (70-80% of all cases), the causative agents of serous meningitis are enteroviruses ECHO and mumps. Also known are acute lymphocytic choriomeningitis, influenza, parainfluenza, adenovirus, herpes-viral meningitis caused by tick-borne encephalitis virus, etc.

Clinical manifestations[edit]

AT clinical picture disease, meningeal symptoms and fever are more or less pronounced, which is often combined with a generalized lesion of other organs. With viral meningitis, a two-phase course of the disease is possible.

Non-pyogenic meningitis: Diagnosis[edit]

In the neurological status, along with meningeal phenomena, there may be signs of damage to the central and peripheral nervous system. In the cerebrospinal fluid, lymphocytes are found, often preceded by mixed pleocytosis with a predominance of neutrophils. With serous meningitis of viral etiology, an increased protein content is often determined in the cerebrospinal fluid. The causative agent of serous meningitis is detected by virological and serological testing (polymerase chain reaction, linked immunosorbent assay).

Differential diagnosis[edit]

Non-pyogenic meningitis: Treatment[edit]

Specific therapy for viral serous meningitis is aimed directly at the virion, which is in the stage of active reproduction and lacks a protective shell.

The principles of therapy for serous meningitis, aimed at preventing or limiting the formation of irreversible cerebral disorders, are as follows: protective regimen, the use of etiotropic drugs, reduction intracranial pressure, improvement of blood supply to the brain, normalization of brain metabolism.

Patients with meningitis should be on bed rest until the final recovery (until the CSF is completely normal), despite the normal body temperature and the disappearance of pathological symptoms. As a means of etiotropic therapy, recombinant interferons. In severe cases, with a threat to vital functions, intravenous immunoglobulins are prescribed.

It is advisable to use antibiotics for serous viral meningitis only with the development of bacterial complications. In the complex treatment of viral meningitis, a protective regimen is required for 3-5 weeks. If necessary, prescribe detoxification and symptomatic therapy. At intracranial hypertension(increased CSF pressure> 15 mm Hg) apply dehydration (furosemide, acetazolamide).

Spend unloading lumbar puncture with slow removal of 5-8 ml of CSF. In severe cases (when meningitis or encephalitis is complicated by cerebral edema), mannitol is used.

It is mandatory for serous meningitis to use drugs that improve neurometabolism: nootropics in combination with vitamins. In the acute period it is possible intravenous administration ethylmethylhydroxypyridine succinate 0.2 ml/kg per day for children and 4-6 ml/day for adults.

In the presence of focal symptoms among neurometabolic agents, preference should be given to the central cholinomimetic choline alfoscerate (prescribed at a dose of 1 ml / 5 kg of body weight intravenously, 5-7 infusions, then orally at a dose of 50 mg / kg per day for up to 1 month).

Prevention[edit]

Anti-epidemic measures are carried out in accordance with the characteristics of the etiology and epidemiology of meningitis. In the event of acute lymphocytic choriomeningitis, the main attention is paid to the fight against rodents in residential and office premises, with meningitis of a different etiology - an increase in nonspecific resistance of the organism, as well as specific prevention.

Symptoms and treatment of serous meningitis

Serous meningitis in children and adults (ICD code - 10-G02.0) is acute inflammation membranes of the brain. The disease is seasonal and is usually diagnosed during the warm season. Children, regardless of age, who attend children's groups are most affected by it. With timely treatment, the disease quickly recedes, leaving no consequences. If the therapy was late or of poor quality, then the patient may have serious complications.

What is serous meningitis and how can you get it?

Serous meningitis is commonly referred to as an inflammatory lesion that develops rapidly in the meninges. Bacteria, viruses and fungi can provoke it. Most often, the cause is an enterovirus, which is very contagious and you can get it:

1. By contact, when eating unwashed vegetables and fruits, as well as water in which the pathogen may be present or neglecting the rules of personal hygiene.
2. Airborne. If the patient sneezes, coughs, or even just talks, the pathogen enters the air and can be transmitted to other people, settling on the mucous membrane of the respiratory tract.
3. Waterway. While swimming in a dirty pond, water may be swallowed, in which the pathogen will be located. At the same time, people with impaired immune systems are more at risk.

For more information about the pathology, see the video:

The disease poses the greatest threat to children under 1 year of age, when it can cause visual and hearing impairment and also lead to developmental delay.

Symptoms of the disease

The incubation period for serous meningitis is on average 2 to 4 days. After which, its symptoms are immediately pronounced:

• Fever is an obligatory symptom of serous meningitis. In most cases, the temperature can reach 40 degrees. After a few days, it decreases, but then it can rise again. In this case, they talk about the second wave of development of serous meningitis.
• Severe headache that occurs in the temporal region and then spreads to the entire surface of the head. In a patient, especially a child, this symptom may be aggravated by movement, bright light or noise. No drugs can reduce pain. The patient experiences some relief in a dark and quiet room.
• The child often has seizures. Babies become lethargic and moody, they usually have causeless crying.

• General weakness, muscle pain and other signs of intoxication are integral symptoms of the disease.
• Digestive disorders - nausea, vomiting, diarrhea.
• The child has pronounced symptoms of SARS - cough, runny nose, difficulty swallowing.

• Increased skin sensitivity.
• In infants, a protrusion of the fontanel is observed.
• Drowsiness and impaired consciousness.
• When the nerve endings are damaged, the patient develops neurological symptoms: strabismus, paresis or paralysis.

• In a child with serous meningitis, a strong tension of the cervical muscles occurs, their rigidity occurs - the inability to lower the chin down to the chest.
• Kerning's symptom, when the patient cannot fully straighten the legs bent at the knees.
• Brudzinsky's symptom - when the bent leg is extended, the second leg is reflexively flexed or when the head is bent, the legs are reflexively flexed.

Possible Complications

For adult patients, serous meningitis is practically not dangerous. But for children, especially the first years of life, the consequences of serous meningitis can be very serious. Most often, complications are observed with untimely or unqualified therapy, or in case of non-compliance with doctor's prescriptions. They can appear with a severe inflammatory process. Wherein:

1. Defeat occurs auditory nerve, hearing loss develops, coordination of movements is disturbed. In some cases, these changes are irreversible.
2. Visual functions are disturbed - strabismus occurs, visual acuity decreases. Over time, vision is restored.
3. Arthritis develops.
4. Pneumonia occurs.

1. Possible endocarditis.
2. The chance of having a stroke increases.
3. There are epileptic seizures.
4. An increase in intracranial pressure is diagnosed.
5. There is swelling of the lungs or brain, which leads to death.

If serous meningitis, especially in a child, was diagnosed in a short time and qualified treatment was immediately started, then there should not be serious violations.

Consequences of pathology

Subject to the prescribed treatment and rehabilitation of the patient, the consequences may appear only in half of them. As a rule, among such symptoms: headaches, weakness, muscle cramps and memory loss. If serous meningitis has led to complications, then hearing or vision loss is possible. But such consequences are extremely rare.

After recovery, the patient, especially the child, regardless of the etiology of the disease, needs special care. He can be assigned a recovery system, which consists in taking vitamin and mineral complexes, good nutrition, feasible physical activity, prolonged exposure to fresh air and special classes, the purpose of which is to restore normal thinking.

Diagnosis of the disease

The main diagnosis of serous meningitis is to perform a lumbar puncture, when CSF is taken from the spinal canal. Such an analysis allows you to identify the pathogen, exclude purulent meningitis and select the appropriate drug in a particular case. If a puncture cannot be done for certain medical reasons, mucus sampling from the nasopharynx may be performed.

Serous meningitis in adults and children is treated in a hospital setting. The main treatment is to reduce intracranial pressure, which will alleviate the patient's condition. good effect gives spinal puncture.

From medical preparations may be assigned:

• Antiviral ("Acyclovir"), antibacterial ("Ceftriaxone"), or antifungal ("Fluorocytosine") drugs, depending on what has become the causative agent of serous meningitis.
• Antipyretics.
• Dehydration preparations ("Diakarb").
• Immunoglobulins.
• Antiemetics.

For symptoms, causes, diagnosis, treatment and prevention of the disease, see our video (detailed video in Russian, with doctors' comments):

• Non-steroidal anti-inflammatory drugs.
• Analgesics.
• Sedatives.
• Antihistamines ("Dimedrol").
• Muscle relaxants that help reduce the frequency and severity of seizures.
• Detoxification drugs ("Polysorb").
• Glucocorticoids.
• Vitamin and mineral complexes.
• Oxygen therapy.

Prevention

The main prevention of serous meningitis is to prevent the pathogen from entering the human body. The following rules of prevention can be distinguished:

1. Ban on swimming in natural waters if it is polluted.
2. For drinking it is allowed to use only purified or boiled water.
3. All vegetables and fruits should be thoroughly washed before consumption. The rest of the products must be subjected to heat treatment.
4. Compliance with the rules of hygiene, which consists in washing hands with detergent before eating, after visiting the toilet and crowded places.
5. Compliance with the daily routine and good sleep (at least 10 hours for a child and 8 for an adult).

1. Leading an active lifestyle and hardening the body.
2. Ensuring proper nutrition and additional intake of multivitamins.
3. Limiting visits to crowded places during a seasonal outbreak of serous meningitis.
4. Regular washing of the child's toys and wet cleaning in the room where he is.
5. Do not allow the child to play at the computer or with gadgets for a long time, because this often leads the body into a stressful state, as a result of which the defenses of the immune system are reduced.

Due to the fact that serous meningitis can be secondary, it is necessary to promptly treat viral diseases: flu, chickenpox, mumps and measles. This will make it possible to prevent the occurrence in a child or adult inflammatory processes in the meninges.

Almost always, serous meningitis is successfully treated and has a positive trend. However, the result will depend on the stage at which the patient sought medical help, how correct the treatment was and what condition he is in. the immune system patient. If the lesion of the meninges was non-purulent, then there are no persistent complications in this case. Usually the disease is treated relatively quickly and does not lead to relapses.

If tuberculosis has become the root cause, then without special therapy, serous meningitis is fatal. Treatment in this case will be long, and the rehabilitation period will last at least 6 months. If the patient complies with all medical prescriptions, then such consequences as loss of hearing, vision or memory will pass over time.

Serous meningitis according to ICD

Serous meningitis(ICD-10-G02.0). Primary serous M. in most cases is caused by viruses (Coxsackie and ECHO enteroviruses, mumps viruses, poliomyelitis, tick-borne encephalitis, lymphocytic choriomeningitis). Secondary serous M. can complicate typhoid fever, leptospirosis, syphilis, and other infectious diseases as manifestations of a general nonspecific reaction of the meninges.

Leading pathogenetic mechanism of serous M., which determines the severity of symptoms, is the acute development of hypertensive-hydrocephalic syndrome, which does not always correspond to the degree of cytological changes in the cerebrospinal fluid. Pleocytosis is represented by lymphocytes (in the early days there may be a few neutrophilic granulocytes) from 0.1 x 109/l to 1.5 x 109/l; the protein content is slightly increased, may be normal or even reduced due to dilution with abundantly secreted fluid.

Pathomorphology: swelling and hyperemia of the pia and arachnoid meninges, perivascular diffuse infiltration of lymphocytic and plasma cells, in some places small punctate hemorrhages. In the choroid plexus of the cerebral ventricles, the same changes. The ventricles are somewhat dilated.

Clinic of serous M. is characterized by a combination of general infectious, hypertensive-hydrocephalic and meningeal symptoms of varying severity. Latent forms (only with inflammatory changes in the cerebrospinal fluid) occur in 16.8% of cases (according to Yampolskaya). In manifest forms, hypertensive phenomena predominate in 12.3% of cases, a combination of hypertensive and meningeal symptoms in 59.3%, and encephalitic symptoms in 11.6%. Children of the first year of life are characterized by anxiety, a painful cry, bulging of a large fontanel, a symptom of the setting sun, tremor, convulsions. In older children - headache, vomiting, agitation, anxiety (sometimes a frozen protective posture). There may be congestion in the fundus. The pressure of the cerebrospinal fluid is increased to 300-400 mm of water.

Serous course M. more often favorable. After 2-4 days, cerebral symptoms disappear. Sometimes a second rise in body temperature is possible, the appearance of cerebral and meningeal symptoms on the 5-7th day. The cerebrospinal fluid is sanitized by the end of the 3rd week.

In young children it is possible convulsions, stupor, in older children - an excited state, delirium in severe cases of the disease, encephalitic reactions in an unfavorable premorbid state. The pressure of the cerebrospinal fluid is increased to 250-500 mm of water. Art., protein content 0.3-0.6 g / l. Cytosis from 0.1 x 109 / l to 1.5 x 109 / l, in young children is much higher, but normalizes faster. The acute period lasts 5-7 days, the body temperature drops lytically on the 3rd-5th day, meningeal symptoms disappear by the 7th-10th day, from the 12th-14th day the residual cytosis is up to 0.1 x 109 / l, weakly positive globulin reactions. The appearance of symptoms of encephalitis along with a decrease in signs of meningitis (increased tendon reflexes, spasticity in the extremities, clonus of the feet, intentional tremor, nystagmus, ataxia, psychosensory disorders) indicates mumps meningoencephalitis, but after 2 weeks they fade away, isolated neuritis persists up to 1-2 months , polyradiculoneuritis - up to 1-6 months, the outcome is usually favorable. The etiology of mumps M. is established on the basis of epidemiological and clinical data, in doubtful cases with the help of serological studies (an increase in antibody titer in paired blood sera by more than 4 times, a delay in the hemagglutination reaction and complement fixation).

Lymphocytic choriomeningitis(acute aseptic), ICD-10-G02.8 - zoonotic viral infection. Infection occurs through inhaled dust or products contaminated with mouse excrement, less commonly through insect bites. The causative agent is not strictly neurotropic, therefore the disease manifests itself after 8-12 days (incubation period) by a generalized intoxication process: hyperthermia, pathological changes in a number of organs (lungs, heart, salivary glands, testicles). Lymphocytic choriomeningitis occurs when a virus penetrates the blood-brain barrier, causing inflammatory changes in the choroid plexuses of the ventricles of the brain, pia mater, and in some cases the substance of the brain and spinal cord. With a protracted and chronic course of the disease, obliteration of the subarachnoid spaces, gliosis and demyelination in the medulla are possible.

Clinic. The disease begins acutely, without prodromal phenomena with a picture of influenza, pneumonia, myocarditis. Chills are replaced by high body temperature. From the 1st day, meningeal phenomena, diffuse headache, nausea, and vomiting are noted. In severe cases of the disease, agitation, hallucinations, followed by loss of consciousness are observed. After 8-14 days from the onset of the disease, the body temperature drops to subfebrile.

RCHD (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical protocols MH RK - 2016

Neurology, Children's neurology, Pediatrics

general information

Short description

Recommended
Expert Council
RSE on REM "Republican Center for Health Development"
Ministry of Health and social development Republic of Kazakhstan
dated May 26, 2015
Protocol #5

Meningitis- inflammation of the membranes of the brain and spinal cord. Inflammation of the dura mater is referred to as "pachymeningitis", and inflammation of the pia and arachnoid membranes is referred to as "leptomeningitis". The most common inflammation of the meninges, the term "meningitis" is used. Its causative agents can be various pathogenic microorganisms: viruses, bacteria, protozoa.

Protocol development date: 2016

Protocol Users: therapists, doctors general practice, infectious disease specialists, neuropathologists, resuscitators, clinical pharmacologists, medical experts, doctors/ambulance paramedics medical care.

Level of evidence scale:
Correlation between strength of evidence and type of research

Classification

Classification :

1. By etiology:
bacterial (meningococcal, pneumococcal, staphylococcal, tuberculosis, etc.),
Viral (acute lymphocytic choriomeningitis caused by Coxsackie and ECHO enteroviruses, mumps, etc.),
fungal (candidiasis, cryptococcosis, etc.),
Protozoal (with toxoplasmosis, malaria) and other meningitis.

2. By the nature of the inflammatory process in the membranes and changes in the cerebrospinal fluid, serous and purulent meningitis are distinguished. With serous meningitis, lymphocytes predominate in the liquor, with purulent meningitis - neutrophils.

3. By pathogenesis meningitis is divided into primary and secondary. Primary meningitis develops without prior systemic infection or infectious disease any organ, and the secondary is a complication of an infectious disease (general and local).

4. By prevalence processes in the membranes of the brain, generalized and limited meningitis are isolated (for example, on the basis of the brain - basal meningitis, on the convex surface of the cerebral hemispheres - convexital meningitis).

5. Depending on the rate of onset and course of the disease:
· lightning fast;
acute;
subacute (sluggish);
chronic meningitis.

6. By severity allocate:
light;
· moderate;
heavy;
extremely severe form.

Diagnostics (outpatient clinic)

DIAGNOSTICS AT OUTPATIENT LEVEL

Diagnostic criteria

Complaints :
An increase in body temperature up to 38 C;
· headache;
· brokenness;
· dizziness;
· nausea and vomiting;
Weakness, decreased ability to work;
convulsions with loss of consciousness;
drowsiness.

Anamnesis:
Anamnesis - should be addressed Special attention on the:
determination of the relationship between the onset and development of symptoms of the disease with signs of an infectious disease transferred or present at the time of examination;
collection of an epidemiological history, namely, taking into account the seasonality of the disease, the geographical distribution of the pathogen, travel, the patient's occupation, contact with infectious patients, animals and insects - carriers of infections;
Immunization and immune status of the patient, including those caused by chronic intoxications (drug addiction, alcoholism, substance abuse) and secondary immunodeficiency states.

Physical examination:

General somatic examination with an emphasis on controlling the function of vital organs and systems (body temperature, respiratory rate, arterial pressure, frequency and rhythm of the pulse).

Neurological status: assessment of the level of consciousness (stupor, stupor, coma) using the 15-point Glasgow Coma Scale;

cerebral syndrome:
Determining the severity of cerebral syndrome (mild, moderate, severe);
dizziness, photophobia, vomiting, depression of consciousness, convulsions.

Meningeal Syndrome: the presence of meningeal signs (stiff neck, symptoms of Kernig, Brudzinsky, Bekhterev, Lessage, Bogolepov);

Focal neurological syndrome:
damage to the cranial nerves;
The presence of focal neurological symptoms, that is, associated with damage to a specific area of ​​​​the brain.

General infectious syndrome: fever, chills.

Laboratory research:
Complete blood count - leukocytosis, anemia is possible;
Urinalysis - leukocyturia, bacteriuria, proteinuria, microhematuria (in severe cases as a result of kidney damage).

Computed tomography of the brain - signs of cerebral edema, focal changes brain;
· Electrocardiography - indirect signs of myocarditis, endocarditis;
X-ray of organs chest- signs of pneumonia;

Diagnostic algorithm:

Diagnostics (ambulance)

DIAGNOSTICS AT THE STAGE OF EMERGENCY AID

Diagnostic measures: data evaluation - the level of consciousness, the nature and duration of the attack, control of blood pressure, respiratory rate, pulse, temperature.

Diagnostics (hospital)

DIAGNOSTICS AT THE STATIONARY LEVEL

Diagnostic criteria at the hospital level

Complaints and anamnesis:see ambulatory level.
Physical examination: see ambulatory level.

Laboratory research:
Complete blood count - to clarify inflammatory changes in the blood (possible leukocytosis of a neutrophilic nature with a stab shift, increase in ESR; possible anemia, thrombocytopenia);
Urinalysis - for the diagnosis of inflammatory changes (possible proteinuria, leukocyturia, hematuria in severe cases with kidney damage);
General analysis of cerebrospinal fluid - to determine the nature of inflammatory changes and their severity (level and nature of cytosis, transparency, protein level);
· Biochemical analysis blood - to clarify the indicators of toxins, electrolytes, liver tests, inflammatory markers (determination of glucose, urea, creatinine, alanine aminotransferase (ALaT), aspartate aminotransferase (ASaT), total bilirubin, potassium, sodium, calcium, C-reactive protein, total protein);

Instrumental research:
CT / MRI of the brain without and with contrast - to exclude damage to the medulla and detect cerebral edema;
X-ray survey of the chest - to exclude pathology of the lungs;
Electrocardiographic study (in 12 leads) - to assess the activity of the heart);

Diagnostic algorithm

List of main diagnostic measures:
· Complete blood count 6 parameters;
General clinical urinalysis (general urinalysis);
General clinical examination of cerebrospinal fluid;
Determination of glucose in blood serum;
· Examination of feces (coprogram) general clinical;
Determination of creatinine in blood serum;
Determination of ALAT in blood serum;

Determination of ASAT in blood serum;
· Electrocardiographic study (in 12 leads);
X-ray survey of the chest (1 projection);
Computed tomography of the brain without and with contrast;

List of additional diagnostic measures:
· Statement of the Wassermann reaction in the blood serum;
Counting platelets in the blood;
· Calculation of leukoformula in blood;
Bacteriological examination of blood for sterility (isolation of pure culture);
Determination of sensitivity to antimicrobials selected structures;
· Determination of "C" reactive protein (CRP) semi-quantitatively/qualitatively in blood serum;
Determination of total protein in blood serum;
Determination of total bilirubin in blood serum;
Determination of blood gases (pCO2, pO2, CO2);
Determination of potassium (K) in blood serum;
Determination of calcium (Ca) in blood serum;
Determination of sodium (Na) in blood serum;
Determination of blood clotting time;
· Determination of prothrombin time (PT) with subsequent calculation of prothrombin index (PTI) and international normalized ratio (INR) in blood plasma (PT-PTI-INR);
· Determination of Ig M to herpes simplex viruses 1 and 2 types (HSV-I, II) in blood serum;
· Bacteriological examination of cerebrospinal fluid for Neisseria meningitis;
· Bacteriological examination of transudate, exudate for sterility;
· Determination of Ig M to the early antigen of the Epstein-Barr virus (HSV-IV) in blood serum by immunochemiluminescence;
· Determination of Ig G to cytomegalovirus (HSV-V) in blood serum by immunochemiluminescence;
Determination of lactate (lactic acid) in blood serum
Determination of procalcitonin in blood serum
· Magnetic resonance imaging of the brain without and with contrast;
· Electroencephalography;
X-ray paranasal sinuses nose (to exclude ENT pathology);
Computed tomography of the pyramids of the temporal bones.

Differential Diagnosis

Table 1. Differential Diagnosis and rationale for additional research.

Table 2. Differential diagnosis of purulent and serous meningitis.

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Treatment

Drugs ( active ingredients) used in the treatment

Treatment (ambulatory)

TREATMENT AT OUTPATIENT LEVEL

Treatment tactics: is determined by the nature of the infection, the degree of prevalence and severity of the pathological process, the presence of complications and concomitant diseases.

Non-drug treatment:
Elevated position of the head in relation to the body;
prevention of aspiration of vomit Airways(turn to the side).

Medical treatment:
Symptomatic therapy :
Mild severity - outpatient therapy is not provided; treatment to begin at the stage of hospitalization.
Moderate and severe severity:

With hyperthermia(38 - 39 degrees C)
Paracetamol 0.2 and 0.5 g:
for adults 500 - 1000 mg orally;
for children aged 6 - 12 years - 250 - 500 mg, 1 - 5 years 120 - 250 mg, from 3 months to 1 year 60 - 120 mg, up to 3 months 10 mg / kg inside;
ibuprofen 0.2 g for adults and children over 12 years of age 300-400 mg orally.

When vomiting
metoclopramide 2.0 (10 mg):
adults intramuscularly or intravenously slowly (for at least 3 minutes) 10 mg.
children from 1 to 18 years, intramuscularly or intravenously slowly (over at least 3 minutes) 100 - 150 mcg / kg (max. 10 mg).

In toxic shock
prednisolone 30 mg or dexamethasone 4 mg
adults prednisolone 10 - 15 mg / kg body weight, one-time possible
administration of up to 120 mg of prednisolone.
children prednisolone or dexamethasone 5 - 10 mg / kg (based on
prednisone).

With an epileptic seizure and / or psychomotor agitation
diazepam 10 mg
Adults: intravenously or intramuscularly 0.15 - 0.25 mg / kg (usually 10 - 20 mg); the dose may be repeated after 30 to 60 minutes. For the prevention of seizures, a slow intravenous infusion can be carried out (maximum dose of 3 mg / kg of body weight for 24 hours);
Elderly: doses should not be more than half of the commonly recommended doses;
children 0.2 - 0.3 mg / kg body weight (or 1 mg per year) intravenously. The dose may be repeated if necessary after 30 to 60 minutes.

Detoxification therapy
Infusion of saline sodium chloride solution 200 ml intravenously.

List of main medicines

List of additional medicines

Algorithm of actions in emergency situations:

Table - 3. Algorithm of actions in emergency situations

Other treatments: no.

consultation of an otorhinolaryngologist - to exclude the pathology of the ENT organs;




consultation of a pediatrician - to assess the somatic status of children;
consultation with an ophthalmologist - examination of the fundus;
consultation of a neurosurgeon - to decide on surgical treatment.

Preventive actions:
Measures of primary and secondary prevention are:
· timely treatment premorbid background - somatic disorders (otitis, sinusitis, pneumonia, sepsis, etc.);
Sanitation of chronic foci of infection.

Patient monitoring:
assessment of life-supporting functions - respiration, hemodynamics;
· grade neurological status to identify and monitor the above-described cerebral, meningeal, general infectious syndromes with records by a doctor in accordance with the rules of conduct medical records this institution (PHC, medical centers etc.).

maintaining life-supporting functions stable with the transfer of the patient to the ambulance stage emergency care for transport to the hospital.

Treatment (ambulance)

TREATMENT AT THE EMERGENCY STAGE

Non-drug treatment: lay the patient on his side, prevent aspiration of vomit, protect the head from impact during an attack, unfasten the collar, access to fresh air, oxygen supply.
Medical treatment: see ambulatory level.

Treatment (hospital)

TREATMENT AT THE STATIONARY LEVEL

Treatment tactics: The choice of tactics for the treatment of meningitis will depend on its type and pathogen.
− Non-drug treatment:
Mode II, drinking plenty of water, setting nasogastric tube and tube feeding at risk of aspiration and depression of consciousness;
Elevated position of the head in relation to the body;
Prevention of aspiration of vomit into the respiratory tract (turning to the side).

Treatment of purulent meningitis in children.

Hospitalization
All patients with purulent meningitis, regardless of clinical form and the severity of the disease, are subject to mandatory hospitalization in a specialized infectious diseases department. The child on the first day of hospitalization should lie on his side to prevent aspiration.
Children with signs of intracranial hypertension (ICH) and cerebral edema (CSE) should be admitted to the intensive care unit or intensive care. If there are signs of ICH and / or OMO in a patient, the bed on which he is located should be with a raised head end by 30 °. In order to prevent bedsores, it is necessary to turn the child every 2 hours.
The monitoring of the child's condition in the hospital is carried out by a nurse at the first time of hospitalization every 3 hours, then every 6 hours. The doctor assesses the child's condition 2 times a day, more if necessary.

Antibacterial therapy

for meningitis, it is used in cases where the etiology of meningitis could not be established at the first time of hospitalization, the lumbar puncture was postponed, or the Gram staining of CSF smears is uninformative.

Etiotropic therapy of purulent meningitis, taking into account the isolated pathogen

Table - 6. Doses of antibiotics for purulent meningitis in children*

* All drugs are administered intravenously
**Dose in the ratio 1:5

Table - 7. Multiplicity of antibiotic administration per day

Table - 8. Duration of antimicrobial therapy for purulent meningitis in children

After 24-48 hours from the start of therapy, a control lumbar puncture is performed to monitor the effectiveness of the therapy started. The criterion for its effectiveness is the reduction of pleocytosis by at least 1/3.

Reserve antibiotics are used in the absence of the effectiveness of initial antibiotic therapy within 48-72 hours or with a certain resistance of the microorganism to the prescribed antibiotic.
The criterion for the abolition of antibiotic therapy for purulent meningitis is the sanitation of the cerebrospinal fluid. Control spinal puncture is performed after stable normalization of body temperature, disappearance of meningeal syndrome, normalization general analysis blood. Therapy is stopped if the number of cells in 1 µl of CSF does not exceed 50 due to lymphocytes.

Complementary Therapy

Indications for appointment dexamethasone
1. Meningitis in children aged 1 to 2 months. Dexamethasone is not prescribed for newborns with meningitis.
2. Children who have gram-negative bacilli in a CSF smear.
3. Patients with high ICP.
4. Patients with BT.
Dexamethasone is given at a dose of 0.15 mg/kg every 6 hours for 2-4 days. The drug is administered 15-20 minutes before the first dose of antibiotic or 1 hour after.

Infusion therapy
Infusion therapy for purulent meningitis requires some caution due to the tendency to hypervolemia, which is associated with the syndrome of inadequate production of antidiuretic hormone, impaired capillary permeability and the risk of developing ICH and / or AHM.

As starting solutions for purulent meningitis, a 5-10% glucose solution (with potassium chloride solution - 20-40 mmol / l) and saline sodium chloride solution in a ratio of 1: 1 are recommended. In children of 1 year of age, this ratio is 3:1.

With a decrease in blood pressure, a decrease in diuresis, hydroethyl starch (HES) of the III generation (130/0.4) at a dose of 10-20 ml/kg is indicated as a starting solution. With the stabilization of blood pressure, the resumption of diuresis, infusion therapy is carried out with glucose-salt solutions.

The volume of intravenous infusions on the first day is limited due to the threat of developing ICH and BT. With stable hemodynamics on the first day, it should be no more than half of the physiological need, provided that diuresis is normal and there are no symptoms of dehydration. The volume of intravenous infusions per day is approximately 30-50 ml / kg of body weight and should not exceed diuresis. The total volume of fluid (intravenous and through the mouth) on the first day is prescribed based on the physiological need. Subject to positive dynamics, a single infusion is acceptable for 6-8 hours.

Mannitol (10-20%) as a starting solution in case of increased intracranial pressure is used in case of a threat or the presence of BT, coma or convulsions, plasma hypoosmolarity less than 260 mOsmol/l. Mannitol is administered as a bolus, if necessary, 2-4 times a day. Children under 2 years old - in a single dose of 0.25-0.5 g / kg (for 5-10 minutes), older children - 0.5-1.0 g / kg (for 15-30 minutes). The daily dose in children under 2 years of age should not exceed 0.5-1.0 g / kg, older children - 1-2 g / kg. Re-introduction of mannitol should be carried out no earlier than after 4 hours, but it is desirable to avoid this due to its ability to accumulate in the interstitial space of the brain, which can lead to a reverse osmotic gradient and an increase in BT.

4. Renal failure.
5. Coma.
After the infusion of mannitol and 2 hours after it, furosemide is prescribed at a dose of 1-3 mg/kg. Also, after the end of this infusion, dexamethasone is administered at a dose of 1-2 mg/kg, after 2 hours - again at a dose of 0.5-1 mg/kg.
After mannitol, colloidal solutions are administered (preparations of HES of the IIIrd generation; 130/0.4) at a dose of 10-20 ml/kg. In children of 1 year of age - 5% albumin solution at a dose of 10-20 ml / kg.

Standard maintenance infusion is carried out with 5 - 10% glucose solution (with a solution of potassium chloride - 20 - 40 mmol / l) and saline sodium chloride in a ratio of 1: 1. In children of 1 year of age, this ratio is 3:1.

The rate of fluid administration in purulent meningitis with ICH and OMO phenomena is 10–15 ml/year in children of the first 2 years of life, and 60–80 ml/year in older children, with the exception of mannitol.

a) control of normovolemia - central venous pressure (CVP) 8-12 mm Hg. Art. or wedge pressure in the pulmonary capillaries (DZLK) 8-16 mm Hg. Art.; mean arterial pressure (SAT) 65 mm Hg. Art. and more, the saturation of the central venous blood is more than 70%, the stabilization of microcirculation.
b) control of plasma isoosmolarity and iso-oncoticity - hematocrit at the level of 35-40% in children under 6 months, 30-35% in children older than 6 months, plasma sodium level - 145-150 mmol / l, blood albumin level - 48-52 g / l, Plasma osmolarity - up to 310-320 mosmol / kg, normoglycemia, normokalemia.

Respiratory support
with purulent meningitis in children:
1. Impairment of consciousness: complicated coma I and deeper degrees of oppression of consciousness (less than 8 points on the Glasgow scale), high ICH, the threat of developing dislocation syndromes, repeated convulsions.
2. Increasing signs of respiratory distress syndrome (high cost of breathing, increasing psychomotor agitation, dependence on inhalation of high concentrations of oxygen - partial pressure oxygen (PaO2) 60 mm Hg. Art. or cyanosis at an oxygen concentration (FiO2) of 0.6, an increase in pulmonary bypass over 15-20% - PaO2 / FiO2<200).
3. Preservation of signs of TSS despite the infusion of fluid with a volume of 60-90 ml/kg of body weight.

Respiratory support should be carried out according to the principles of lung-protective ventilation:
1. Applying a decelerating flow.
2. Selection of the optimal positive end-expiratory pressure (PEEP) - within 8-15 cm of water.
3. Tidal volume 6-8 ml/kg body weight, but not more than 12 ml/kg body weight.
4. Plateau pressure is not more than 32 cm w.c.
5. The use of recruitment techniques and kinetic therapy in the absence of contraindications.
Treatment of children with purulent meningitis, which is accompanied by TSS, is carried out as for meningococcemia.

Treatment of purulent meningitis in adults

All patients with purulent meningitis, regardless of the clinical form and severity of the disease, are subject to mandatory hospitalization.
Patients with cerebral edema (CSE) should be hospitalized in the intensive care unit or intensive care unit.

Antibacterial therapy

Empiric antibiotic therapy for meningitis, it is used in cases where the etiology of meningitis could not be established during the first time of hospitalization, the spinal puncture was postponed.

Etiotropic therapy of purulent meningitis, taking into account the isolated pathogen
When examining a culture isolated from CSF, antibiotic therapy is prescribed taking into account the specificity of the pathogen, its sensitivity or resistance to antibiotics.

MIC - minimum inhibitory concentration.

Monitoring the effectiveness of antibiotic therapy

After 48 - 72 hours from the start of therapy, a control lumbar puncture is performed to monitor the effectiveness of the therapy started. The criterion for its effectiveness is the reduction of pleocytosis by at least 1/3.
When the etiological cause of the disease is identified, starting antibiotics can be replaced with others, in accordance with the sensitivity of the pathogen. However, in the presence of pronounced positive dynamics, namely, a decrease in intoxication syndrome, normalization of body temperature, disappearance of meningeal symptoms, a significant decrease in pleocytosis, a decrease in leukocytosis, a neutrophil shift in the blood count, it is advisable to continue it.

Reserve antibiotics are used in the absence of the effectiveness of initial antibiotic therapy for 48-72 hours or with a certain resistance of the microorganism to the prescribed antibiotic.
The criterion for the abolition of antibiotic therapy for purulent meningitis is the sanitation of the cerebrospinal fluid. A control spinal puncture is performed after a stable normalization of body temperature, the disappearance of meningeal syndrome, and normalization of the general blood test. Therapy is stopped if the number of cells in 1 µl of CSF does not exceed 50.
With a recurrence of purulent meningitis, reserve antibiotics are prescribed.

Complementary Therapy
Indications for the appointment of dexamethasone for purulent meningitis in adults:
1. Patients with high ICP.
2. Patients with BT.
Dexamethasone is prescribed at a dose of 4-8 mg every 6 hours for 4 days. The drug is administered 15-20 minutes before the first dose of antibiotic or 1 hour after.

Infusion therapy
With a decrease in blood pressure, a decrease in diuresis, hydroethyl starch preparations (HES) of the III generation (130/0.4) at a dose of 10 - 20 ml / kg are indicated as a starting solution. With the stabilization of blood pressure, the resumption of diuresis, infusion therapy is carried out with glucose-salt solutions.
In case of hypovolemia, drip intravenous administration of isotonic solutions (sodium chloride, a complex solution (potassium chloride, calcium chloride, sodium chloride) is necessary. To correct the acid-base state in order to combat acidosis, 4-5% sodium bicarbonate solution (up to 800 ml) is administered intravenously In order to detoxify, plasma-substituting solutions are injected intravenously, which bind toxins circulating in the blood.
The volume of intravenous infusions on the first day is limited due to the threat of developing ICH and BT. With stable hemodynamics on the first day, it should be no more than half of the physiological need, provided that diuresis is normal and there are no symptoms of dehydration. The volume of intravenous infusions per day is approximately 30 - 50 ml / kg of body weight and should not exceed diuresis. The total volume of fluid (intravenous and through the mouth) on the first day is prescribed based on the physiological need. Subject to positive dynamics, a single infusion is acceptable for 6-8 hours.

Dehydration therapy
If there are signs of increased intracranial pressure or BT, infusion therapy is aimed at regulating the volume and optimizing cerebral microcirculation by supporting isovolemia, isoosmolarity, and isooncoticity.
To reduce intracranial pressure, dehydration therapy is performed.
· Raise the head end of the bed at an angle of 30C, the patient's head is given a median position - this achieves a decrease in intracranial pressure by 5 - 10 mm Hg. Art.
Reduction of intracranial pressure in the first days of the disease can be achieved by limiting the volume of fluid administered to 75% of the physiological need, until the syndrome of inadequate secretion of antidiuretic hormone is excluded (may occur within 48-72 hours from the onset of the disease). Restrictions are gradually canceled as the condition improves and intracranial pressure decreases. Preference is given to an isotonic solution of sodium chloride, all drugs are also administered on it.
You can apply forced diuresis of the dehydration type. The starting solution is mannitol (20% solution) at the rate of 0.25 - 1.0 g / kg, it is administered intravenously for 10 - 30 minutes, then after 60 - 90 minutes it is recommended to administer furosemide at a dose of 1 - 2 mg / kg of body weight . There are different patterns of dehydration when intracranial pressure rises.

Contraindications to the introduction of mannitol:
1. The level of sodium in the blood plasma is more than 155 mmol / l.
2. Plasma osmolarity is greater than 320 mOsmol/kg.
3. Heart failure.
4. Renal failure.
After the infusion of mannitol and 2 hours after it, furosemide is administered at a dose of 1–3 mg/kg.
Colloidal solutions are used as starting solutions for ICH, OMT in combination with hypovolemia, arterial hypotension.
The volume of infusions on the first day with purulent meningitis from ICH or BT should not exceed 50% of the physiological need, provided that diuresis is preserved, geodynamics is stable and it is evenly distributed throughout the day. The total volume of fluid is 75% of the physiological need.

In the presence of subarachnoid hemorrhage, spasm of peripheral vessels, the introduction of colloidal solutions is contraindicated. Of the crystalloid solutions, only physiological sodium chloride solution is administered.
From the second day, the goal of infusion therapy is to maintain a zero water balance, in which the amount of urine excreted should not be less than the intravenously administered volume of fluid and not less than 75% of the total daily volume of fluid administered.

Monitoring of infusion therapy in severe forms of purulent meningitis:
1. Dynamics of symptoms from the side of the central nervous system, control of the size of the pupils.
2. Control of body temperature and seizures;
3. Control of hemodynamics, hourly diuresis (not less than 0.5 ml/kg/h).
4. Control of the level of sodium, potassium, if possible - magnesium in the blood plasma, blood glucose levels, blood plasma osmolarity, acid-base balance of the blood.
5. Maintenance of normovolemia, isosmolarity and iso-oncoticity of plasma:
Indications for tracheal intubation and initiation artificial lung ventilation (ALV) with purulent meningitis in adults:
1. Violation of consciousness: complicated coma I and deeper degrees of depression of consciousness, the threat of the development of dislocation syndromes, repeated convulsions.
2. Increasing signs of respiratory failure, respiratory distress syndrome (high cost of breathing, increasing psychomotor agitation, dependence on inhalation of high oxygen concentrations - oxygen partial pressure (PaO2) 60 mm Hg or cyanosis at oxygen concentration (FiO2) 0.6 , increase in pulmonary bypass over 15 - 20% - PaO2/FiO2<200).
3. Preservation of signs of TSS despite the infusion of fluid volume of 60 - 90 ml/kg of body weight.
4. Insufficiency of the left ventricle, the threat of pulmonary edema.

List of medicines:

Surgical intervention: no.
- Other types of treatment: not provided.

Indications for expert advice:
consultation of an ophthalmologist - the need to visualize the picture of the fundus to exclude edema of the optic nerve head;
consultation of an ENT doctor - for diagnosing the pathology of ENT organs;
Consultation with a pulmonologist - to rule out pneumonia;
consultation of an infectious disease specialist - to exclude the infectious nature of meningitis;
consultation of a resuscitator - to determine the indications for transfer to the ICU;
· consultation of a phthisiatrician - for differential diagnosis with tuberculous meningitis (according to indications);
consultation of a neurosurgeon - for differential diagnosis with volumetric processes of the brain (abscess, epiduritis, tumor, etc.), the presence of signs of occlusion;
consultation with a cardiologist - in the presence of clinical and electrocardiographic signs of severe heart damage (endocarditis, myocarditis, pericarditis);
consultation of a pediatrician - to assess the somatic status of children.

Indications for transfer to the intensive care unit and resuscitation:

Indications for transfer to the intensive care unit and resuscitation in children:
Disturbance of consciousness: stunning, stupor, coma I and deeper degrees of oppression of consciousness (less than 8 points on the Glasgow scale), high ICH, the threat of developing dislocation syndromes, repeated convulsions;
An increase in signs of respiratory distress syndrome (high cost of breathing, increasing psychomotor agitation, dependence on inhalation of high oxygen concentrations - partial pressure of oxygen (PaO2) 60 mm Hg or cyanosis at an oxygen concentration (FiO2) of 0.6, an increase in pulmonary bypass over 15-20% - PaO2/FiO2<200);
Preservation of signs of ITS (infectious-toxic shock) despite the infusion of fluid with a volume of 60-90 ml / kg of body weight;

Indications for transfer to the intensive care unit and resuscitation in adults:
Disturbance of consciousness: stunning, stupor, coma;
Respiratory failure
signs of infectious-toxic shock with symptoms of acute adrenal insufficiency;
left ventricular failure, the threat of pulmonary edema.

Treatment effectiveness indicators:
Clinical Criteria:
persistent normal temperature;
relief of cerebral syndrome;
relief of meningeal syndrome;
relief of symptoms of ITS.
Laboratory Criteria:
Sanitation of cerebrospinal fluid, cytosis less than 50 cells in 1 µl.

Further management:

Dispensary observation of children in the clinic at the place of residence

Table - 12. Dispensary observation of children

Dispensary observation of adults in the clinic at the place of residence: who has been ill with meningitis is registered at the dispensary, on the basis of a polyclinic with the supervision of a neuropathologist for a period of 2 years, examines the convalescent once a month for 3 months after the transfer of the disease, subsequently visits are 1 time in 3 months during the year, and over the next - 1 once every 6 months. The duration of dispensary observation can be 2 years or more.

medical rehabilitation

It is carried out in accordance with the Standard for organizing the provision of medical rehabilitation to the population of the Republic of Kazakhstan, approved by order of the Minister of Health of the Republic of Kazakhstan dated December 27, 2013 No. 759.

Hospitalization

Indications for planned hospitalization: not carried out.

Indications for emergency hospitalization:
acute development of meningitis;
An increase in cerebral and meningeal symptoms in patients (signs of edema-swelling of the brain, dislocation of brain structures, impaired consciousness, a series of epileptic seizures, status epilepticus).

Information

Sources and literature

1. Minutes of the meetings of the Expert Council of the RCHD MHSD RK, 2015
   1. 1. Skoromets A.A., Skoromets A.P., Skripchenko N.V., Kryukova I.A. Meningitis.// Neurology. National leadership, Moscow, 2009 2. Lobzin B.C. Meningitis and arachnoiditis.- L.: Medicine, 1983.-192 p. 3. Kramarev S.A. Approaches to antibiotic therapy of purulent meningitis in children.// Current infections. 2000, pp. 84-89. 4. Berlit.P., Neurology // Moscow, 2010 p. 335 5. Karpov I.A., Ivanov A.S., Yurkevich I.V., Kishkurno E.P., Kachanko E.F. //Infectious Diseases Society of America Guidelines for Management of Patients with Bacterial Meningitis Review 6. Fitch M.T., van de Beek D. Emergency diagnosis and treatment of adult meningitis. Lancet Infect Dis 2007; 7(3): 191-200. 7. Chaudhuri A, Martinez-Martin P, Kennedy PG, Andrew Seaton R, Portegies P, Bojar M, Steiner I, EFNS Task Force. EFNS guideline on the management of community-acquired bacterial meningitis: report of an EFNS Task Force on acute bacterial meningitis in older children and adults. Eur J Neurol. 2008 Jul;15(7):649-59. 8. Deisenhammer F., Bartos A., Egg R., Gilhus N. E., Giovannoni G., Rauer S., Sellebjerg F. Guidelines on routine cerebrospinal fluid analysis. Report from an EFNS task force. Eur J Neurol. 2006 Sep; 13(9):913-22. 9. Brouwer M.C., McIntyre P., Prasad K., van de Beek D. Corticosteroids for acute bacterial meningitis. Cochrane Acute Respiratory Infections Group/ Cochrane Database of Systematic Reviews/ Published: 12 September 2015/ 10. Bhimraj A. Acute community-acquired bacterial meningitis in adults: an evidence-based review. Cleve Clin J Med. Jun 2012; 79(6):393-400. 11. Clark T., Duffell E., Stuart J.M., Heyderman R.S. Lumbar puncture in the management of adults with suspected bacterial meningitis--a survey of practice. J Infect. May 2006; 52(5):315-9. 12. Schut E.S., de Gans J., van de Beek D. Community-acquired bacterial meningitis in adults. Pract Neurol. 2008 Feb;8(1):8-23. 13. Van de Beek D., de Gans J., Tunkel A.R., Wijdicks E.F. Community-acquired bacterial meningitis in adults. N Engl J Med. 2006 Jan 5; 354(1):44-53. 14. Flores-Cordero J.M., Amaya-Villar R., Rincón-Ferrari M.D., Leal-Noval S.R., Garnacho-Montero J., Llanos-Rodríguez A.C., Murillo-Cabezas F. Acute community-acquired bacterial meningitis in adults admitted to the intensive care unit: clinical manifestations, management and prognostic factors. Intensive Care Med. Nov 2003; 29(11):1967-73. 15. Aronin S.I., Peduzzi P., Quagliarello V.J. Community-acquired bacterial meningitis: risk stratification for adverse clinical outcome and effect of antibiotic timing. Ann Intern Med. 1998 Dec 1; 129(11):862-9. 16. Klein M., Pfister H.W., Leib S.L., Koedel U. Therapy of community-acquired acute bacterial meningitis: the clock is running. Expert Opin Pharmacother. 2009 Nov;10(16): 2609-23.

Information

Abbreviations used in the protocol

List of protocol developers with qualification data:

17. Indication of no conflict of interest: no.

18. List of reviewers: Dushanova Gulsim Abdurakhmanovna - Doctor of Medical Sciences, Professor, Head of the Department of Neurology, Psychiatry and Psychology of the South Kazakhstan State Pharmaceutical Academy.

19. Indication of the conditions for revising the protocol: Revision of the protocol 3 years after its publication and from the date of its entry into force or in the presence of new methods with a level of evidence.

Attached files

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Note. This disease can cause lobar (sometimes parenchymal-subarachnoid) hemorrhages and diffuse lesions of the white matter (leukoareosis) of the brain in elderly and senile patients.

168.1* Cerebral arteritis in OFD. Same as ICD-10

Cerebral arteritis:

listeriosis (A32.8+)

syphilitic (A52.0+)

tuberculous (A18.8+)

168.2* Cerebral arteritis in OFD. Same as in ICD-10

other diseases classified elsewhere

Cerebral arteritis in systemic lupus erythematosus (M32.1+)

Note. In addition to the subnomination of systemic lupus erythematosus mentioned in the subheading, angiitis with cerebral vascular lesions can develop in the following diseases: thromboangiitis obliterans [Buerger's disease] (173.1+), periarteritis nodosa (M30.0+), polyarteritis with lung damage [Churg-Strauss ] (allergic granulomatous angiitis) (M30.1+), mucocutaneous lymphonodular syndrome [Kawasaki] (M30.3), hypersensitivity angiitis [Goodpasture's syndrome] (M31.0+), Wegener's granulomatosis (M31.3+), aortic arch syndrome [Takayasu] (M31.4+), giant cell arteritis with polymyalgia rheumatica (M31.5+), other giant cell arteritis (M31.6+), other specified necrotizing vasculopathies (hypocomplementemic vasculitis) (M31.8+), necrotizing vasculopathy, unspecified (M31.9+), Behcet's disease (M35.2+), systemic connective tissue lesions, unspecified (collagenosis NOS) (M35.9+), etc.

168.8* Other vascular lesions of the OFD. See brain note in diseases classified elsewhere.

Note. This subheading may be coded for: muscular and connective tissue dysplasia of arteries(177.3+), etc.

6. Vascular diseases of the spinal cord (spinovascular diseases)

Vascular diseases of the spinal cord most often manifest themselves acutely and are associated with an acute violation of the spinal circulation, which is also referred to as a spinal stroke. Like cerebral stroke, spinal stroke can be either ischemic (spinal cord infarction) or hemorrhagic (hematomyelia).

Chronic progressive vascular myelopathy occurs extremely rarely, usually against the background of severe atherosclerotic lesions of the aorta and its main branches. An arteriovenous malformation of the spinal cord may also be the cause of progressive myelopathy (Q28.2).

In the ICD-10, vascular diseases of the spinal cord are coded

in G95.1 Vascular myelopathy.

Chapter 1. Vascular diseases of the brain and spinal cord

Note. spinal cord infarction usually the result of atherosclerosis or dissecting aneurysm of the aorta, cardiogenic embolism, a complication of surgery on the heart or aorta, and only very rarely - a consequence of damage to the spinal cord's own arteries. Sometimes spinal infarction is associated with vasculitis, neurosyphilis, compression of the spinal vessels by a tumor, or other space-occupying formation. With systemic arterial hypotension, especially in patients with atherosclerosis of the aorta and its main branches, parts of the spinal cord located on the border of the vascular pools and most sensitive to ischemia may be affected, which is manifested by the development of paresis, sometimes of a mixed type, without impaired sensitivity and resembles a picture of lateral amyotrophic sclerosis.

Hematomyelia is a hemorrhage in the substance of the spinal cord, which may be associated with trauma, vascular malformation, vasculitis, coagulopathy, spinal cord tumor. Hematomyelia is manifested by an acute transverse lesion of the spinal cord with the development of a pronounced pain syndrome and sometimes with a breakthrough of blood into the subarachnoid space. The diagnosis is confirmed by CT and MRI.

Aseptic (non-pyogenic) phlebitis of the veins of the spinal cord may develop in diseases (or conditions) accompanied by increased blood clotting

diseases of the central nervous system

1. Meningitis

1.1. Bacterial meningitis

1.3. Meningitis due to other and unspecified causes

2. Encephalitis and myelitis

3. Intracranial and intravertebral abscesses, granulomas

and phlebitis

4. Neurological manifestations HIV infections

5. Syphilis of the nervous system (neurosyphilis)

6. Tuberculosis of the nervous system

7. Slow infections C N C

1. Meningitis

Meningitis is a generic name for inflammation of the membranes of the brain and spinal cord. There are pachymeningitis - inflammation of the dura mater, leptomeningitis - inflammation of the soft and arachnoid membranes, arachnoiditis - inflammation of the arachnoid *. In practice, the term "meningitis" most often means leptomeningitis.

* In ICD-10, arachnoiditis is coded under G96.1 (“Disorders of the meninges, not elsewhere classified”).

Meningitis is classified according to etiology (bacterial, viral, fungal, mycoplasmal, rickettsial), the nature of the inflammatory process (purulent, serous), course (acute, subacute, chronic), origin (primary and secondary, i.e. arising against the background of another diseases: otitis media, sinusitis, H M T, etc.).

The clinical picture of meningitis consists of three groups of symptoms: general infectious (fever, malaise, tachycardia, myalgia), cerebral (intense headache, nausea, vomiting, confusion or depression of consciousness up to coma) and meningeal syndrome.

1.1. Bacterial meningitis

The classic form of bacterial meningitis is acute purulent meningitis, but bacterial meningitis can also be serous and subacute or chronic (eg, tuberculous or syphilitic meningitis).

In bacterial meningitis, in addition to general cerebral and meningeal symptoms, focal neurological symptoms are often encountered due to the involvement of the cranial (especially oculomotor) and spinal nerves, less often the very substance of the brain. In the presence of signs of inflammatory damage to the membranes and substance of the brain, the term is traditionally used "meningoencephalitis"(if the spinal cord is involved - "meningomyelitis"). However, it should be borne in mind that the cause of damage to the brain substance in a significant number of cases of bacterial meningitis is not the transfer of infection from the membranes to the substance of the brain, but thrombosis or inflammation of the vessels at the base of the skull (internal carotid artery, middle cerebral artery), which lead to ischemia and the development of a heart attack. brain (usually in the first 5 days of illness). Brain dysfunction is also associated with intracranial hypertension due to edema or the development of hydrocephalus, and hypoxia. In this regard, the use of the term "meningoencephalitis" in cases where meningitis occurs with focal and cerebral symptoms is not always correct. Nevertheless, the use of the term "meningoencephalitis" is allowed as a preliminary diagnosis, however, it is desirable to clarify the nature of the brain lesion using CT or MRI.

Handbook for the formulation of the diagnosis of diseases of the nervous system

On the basis of clinical data, three degrees of severity of acute meningitis can be conditionally distinguished:

1) mild degree (mild course) - there are no pronounced cerebral symptoms, consciousness remains clear, there are no focal symptoms;

2) medium degree (moderate course) - the presence of stunning and minimal or moderate neurological deficit, for example, due to damage to the cranial nerves;

3) severe degree (severe course) - pronounced cerebral symptoms with depression of consciousness to the level of stupor or coma, epileptic seizures, severe neurological deficit, for example, hemiparesis.

When formulating a detailed diagnosis of bacterial meningitis, the following should be indicated:

1) type of course (acute, subacute, chronic);

2) origin (primary, secondary);

3) the nature of the inflammatory process (purulent, serous);

4) the nature of the pathogen (after it has been determined by bacteriological methods);

5) severity;

6) period (acute, convalescence, remote);

7) complications (intracranial hypertension, hydrocephalus, epileptic seizures, cerebrovascular accidents, subdural effusion, cranial nerve lesions, septic shock, endocarditis, purulent arthritis, respiratory adult distress syndrome, pneumonia, deep vein thrombosis of the lower leg and pulmonary embolism, etc.).

In the ICD-10, bacterial meningitis is coded under G00 (“Bacterial meningitis, not elsewhere classified”) and G01*.

Note. The subheading encodes purulent meningitis caused by Haemophilus influenzae Afanasiev-Pfeiffer. Most cases of this disease occur in children under 6 years of age, but occasionally this disease also occurs at an older age, usually against the background of sinusitis, epiglottitis, pneumonia, otitis media, TBI, diabetes mellitus, alcoholism, splenectomy, hypogammaglobulinemia, AIDS

G00.1 Pneumococcal meningitis CRF. Same as in ICD-10

PRFD. Acute secondary purulent pneumococcal meningitis against the background of bilateral purulent sinusitis and septicopyemia; severe course; sopor; acute period

Note. Pneumococcal meningitis is the most common variant of meningitis in people over 30 years of age. It often develops as a result of the spread of infection from distant foci (with pneumonia, otitis media, mastoiditis, sinusitis, endocarditis) and is especially severe in patients with reduced immunity (with alcoholism, diabetes mellitus, multiple myeloma, hypogammaglobulinemia, liver cirrhosis, after splenectomy against the background of corticosteroid therapy, hemodialysis). Pneumococcus pneumoniae is a common causative agent of post-traumatic meningitis in patients with a fracture of the base of the skull and liquorrhea. Pneumococcal meningitis is usually severe, often causing depression of consciousness, focal symptoms and epileptic seizures, often fatal; may recur

G00.2 Streptococcal meningitis CRF. Same as in ICD-10

PRFD. Acute purulent secondary streptococcal meningitis against the background of septic endocarditis,

Handbook for the formulation of the diagnosis of diseases of the nervous system

severe course with the development of cerebral edema; moderate coma; acute period

Note. Group B streptococci most often cause meningitis in newborns and parturient women, as well as in patients with bacterial endocarditis and in immunocompromised individuals due to diabetes mellitus, renal and hepatic insufficiency, AIDS, alcoholism, etc. When formulating a diagnosis, indicate localization of the primary purulent focus or predisposing disease

G00.3 Staphylococcal meningitis CRF. Same as in ICD-10

PRFD. Acute purulent secondary staphylococcal meningitis against the background of purulent otitis media, severe course with intracranial hypertension, deep stunning, repeated generalized convulsive seizures; acute period

Note. Staphylococcus aureus is most often the causative agent of secondary purulent meningitis in patients with bacterial endocarditis, traumatic brain injury, and in individuals undergoing neurosurgical intervention. Staphylococcal meningitis may be a complication of suppurating bedsores, pneumonia, or due to infection of the ventriculoperitoneal shunt. When formulating a diagnosis, the localization of the primary purulent focus or septic disease should be indicated.

Meningitis is an inflammation of the lining of the brain or spinal cord. It is assumed that this disease was known to Hippocrates and Avicenna, but until the end of the 19th century, the etiology remained a mystery. In 1887, the bacteriologist A. Weikselbaum proved the bacterial nature of the infection. Later, in the middle of the 20th century, a possible viral, fungal and protozoal onset of the disease was also established.

With serous meningitis in the cerebrospinal fluid, there is a predominance of lymphocytic cells, and with purulent meningitis - neutrophils.

An exception is enteroviral meningitis, in which neutrophils predominate in the cerebrospinal fluid in the first week.

Serous meningitis is predominantly caused by viruses.

Serous meningitis is more common in children than in adults.

According to ICD 10, enteroviral meningitis belongs to code A 87.0, and serous meningitis according to ICD 10 is in the viral subgroup - under code A 87. 9.

Epidemiology

Children under 7 years of age are at risk, adults rarely get sick. The disease is characterized by seasonality with a maximum prevalence from February to April. However, the increase in the number of infected occurs already in November.

Such a dependence on the time of year is due to favorable weather conditions (high humidity levels and sudden temperature changes), as well as weakened immunity and beriberi. With a wide distribution, it reaches the scale of epidemics with a frequency of 10-15 years.

The first mass outbreak of meningitis in Russia dates back to 1940. For every 10,000 inhabitants, there were 5 patients. Presumably, the disease has become so widespread due to the rapid migration of people. The next outbreak occurred in the early 70s, however, a reliable cause was established only in 1997. Scientists have found that the cause was a new strain of meningococcus that appeared in China. Residents of the USSR did not develop strong immunity to this strain.

Meningitis occurs in all countries on the planet, however, the highest prevalence is typical for third world countries. The prevalence rate is 40-50 times higher than in Europe.

According to official statistics in Western countries, 3 people are affected by the bacterial form per 100,000 people, and 11 by the viral form. In South America, the number of cases reaches 46 people, in Africa the figure reaches critical values ​​- up to 500 patients per 100,000 people.

Causes (etiology)

The vast majority of the cause of meningitis of the soft membranes of the brain are viruses:

• human herpesvirus type 4;
• cytomegaloviruses;
• adenoviruses;
• influenza virus;
• measles viruses;
• rubella virus;
• chickenpox virus;
• paramyxoviruses.

The incubation period for serous meningitis depends on the pathogen.

In isolated cases, the serous type of the disease is diagnosed as a complication of a bacterial infection (syphilis or tuberculosis). It is extremely rare that the fungal nature of the disease is detected.

How is serous meningitis transmitted?

Ways of transmission - airborne (sneezing, coughing), contact-household (contact with skin or objects) and water (in summer through swimming in open water). The source of infection is a sick person or carrier of the virus.

Also known is a non-infectious (aseptic) form of the disease that accompanies oncological pathologies.

Pathogenesis

There are 2 ways of penetration of the pathogen to the soft membranes of the brain:

• hematogenous - a pathogen from the area near the underlying inflammatory focus penetrates into the bloodstream and reaches the soft membranes.
• lymphogenous - the virus spreads with the flow of lymph.
• contact is realized due to the migration of viruses from the ENT organs located in close proximity to the brain.

When pathogens reach the soft membranes of the brain, they actively reproduce and form a focus of inflammation. Until the introduction of effective treatment, patients with meningitis died at this stage, mortality rates were close to 90%.

Signs of infection in children

The first signs of serous meningitis in children are similar to those of other infectious diseases. These include:

• a sharp increase in body temperature, often to critical values ​​\u200b\u200b(40 ° C);
• prolonged acute pain in the head;
• recurring vomiting fountain;
• photophobia;
• the appearance of meningeal signs;
• numbness of the neck muscles, it is difficult for the child to tilt and turn his head;
• indigestion, decrease or complete loss of appetite;
• children very often have prolonged diarrhea;
• in the case of contact penetration of the virus into the brain, a sharp change in the behavior of the child is noted: excessive activity or passivity, hallucinations are not excluded.

Important: you should immediately consult a doctor at the first signs of a manifestation of viral meningitis in a child.

Timely diagnosis and an adequately designed course of therapy will avoid serious consequences and complications.

Symptoms of serous meningitis in children

Minor signs of the disease may appear on the first day after infection with the virus, while the infection itself is in a latent phase. The typical clinical picture is observed 7-12 days after infection.. The main symptoms of serous viral meningitis in a child include:

• subfebrile fever, chills;
• excessive sensitivity to external factors (light, sound);
• confusion, loss of orientation in time and space. Serous meningitis in children in severe form can lead to a coma;
• refusal of food;
• vomiting fountain;
• violation of the chair;
• convulsive symptoms;
• on palpation, there is an increase and soreness of the lymph nodes, which indicates the penetration of the virus into the lymphatic system;
• Kernig's symptom is specific for serous meningitis. In this case, the patient cannot independently unbend the legs in the knee joint as a result of excessive tension of the hip muscles;

• the lower symptom of Brudzinsky, which is characterized by involuntary movement of the lower extremities as a result of tilting the head;
• ankylosing spondylitis - a spasm of the facial muscles that occurs in response to a mechanical effect on the facial arch;
• Pulatov's symptom - pain syndrome even with light tapping on the parietal and occipital region;
• Mendel's symptom is manifested in pain when pressed in the area of ​​​​the external auditory canal;
• in newborn children, Lesage's symptom is diagnosed - pulsation and an increase in the membrane over the fontanel. When lifting the child under the armpits, the head involuntarily tips back, and the legs are reflexively drawn up to the stomach.

Symptoms of serous meningitis in adults

The disease is more susceptible to young men from 20 to 30 years. Pregnant women are included in the risk group, since at this time the natural defenses of the body are significantly reduced.

Signs of the viral form of serous meningitis in adults are similar to those in children: the general condition worsens, weakness, pain in the head and neck, fever, impaired consciousness and confusion of orientation.

In adult patients with high immunity, the disease can proceed in a sluggish form, while all symptoms are mild and their relief occurs soon after the start of therapy. The outcome is a complete recovery, without consequences.

In addition to the above symptoms characteristic of children, adults may experience atypical manifestations of viral meningitis:

• there is a sharp deterioration in vision, the development of strabismus is possible;
• hearing loss;
• cough, runny nose, sore throat, difficulty swallowing;
• pain syndrome in the abdominal region;
• convulsive contractions of the limbs;
• epileptic seizures without movement disorders;
• heart palpitations and high blood pressure;
• behavioral changes - aggressiveness, delirium and irritability.

Only the attending physician can correctly diagnose serous meningitis in children and adults. It is important to go to the hospital as soon as possible at the first signs of the disease in order to select and implement a course of therapy as soon as possible. Such tactics will avoid complications and consequences of the disease, the most severe of which is a fatal outcome.

Primary diagnosis

The first stage of diagnosis consists of a triad of specific syndromes:

• meningeal complex of symptoms similar in etiology and pathogenesis. The complex consists of clinical manifestations affecting the membranes of the brain and the organ as a whole. There are cases of critically severe headache, in which patients fell into an unconscious state. Often - patients scream and groan in pain, clasp their heads in their hands.

Diagnosis of shell (meningeal) symptoms consists of a neurological examination of the patient, with testing the reaction to light, sound and mechanical stress. With serous meningitis, each of these tests gives the patient a sharp pain.

• general syndrome of intoxication of the human body;
• pathological changes occurring in the cerebrospinal fluid. This symptom is given a leading place in the diagnosis.

Even with the manifestation of the two previous symptoms, in the absence of inflammatory processes in the cerebrospinal fluid, the diagnosis of meningitis is not made.

Specific Methods

If it is difficult to make an accurate diagnosis in medicine, additional diagnostic methods are used. A bacteriological study of exudate of the nasal passages and cerebrospinal fluid is carried out.

In order to identify bacterial cells (Neisseria meningitidis) and microscopic fungi in the biomaterial, the fixed preparation is Gram-stained and microscoped. A pure culture is obtained by culturing the biomaterial on blood agar media. Then the pathogen is identified by biochemical and antigenic properties.

This technique is used exclusively for the diagnosis of a bacterial infection (with purulent meningitis), since the cultivation of viruses on nutrient media is impossible. Therefore, for their isolation, serological diagnostics (enzymatic immunoassay) is used - the identification of the titer of specific antibodies. A 1.5-fold increase in titer is diagnostically significant.

The polymerase chain reaction method is considered the "gold standard". In this case, specific sections of the nucleic acid (DNA or RNA) of the pathogen are identified. The advantages of the technique are short terms, the highest sensitivity, a guarantee of results and reliability even at the stage of antibiotic therapy.

Treatment of serous meningitis

The first signs of the disease can appear as early as a day after contact with a sick person. Therefore, if you suspect a possible infection, you should immediately consult a doctor. It is strictly forbidden to independently select a treatment regimen. According to statistics: 95% of cases in which alternative therapy methods are used end in the death of the patient.

When the diagnosis is confirmed, the patient is hospitalized in a special department of the infectious diseases hospital. In severe forms of the disease, the patient is placed in intensive care until stable relief of symptoms. The patient must be under round-the-clock medical supervision. personnel, as a sharp deterioration in the condition is possible.

Etiotropic therapy

Methods of etiotropic therapy are aimed at the destruction of the pathogen and its complete removal from the human body. The bacterial form of meningitis requires mandatory antibiotic therapy. If it is impossible to isolate and identify strains (difficult-to-cultivate forms, lack of time for bac. research), the antibiotic is selected empirically.

At the same time, preference is given to antibacterial drugs with a wide range of effects, in order to cover all possible variants of pathogens. Required injection of the drug.

With the viral nature of the infection, preparations based on interferon and glucocorticosteroids are used. The selection of medications is carried out taking into account the species of the viral infection.

With a herpes infection, anti-herpetic drugs are prescribed.

Be sure to prescribe diuretics that increase the excretion of urine and fluid from the body.

Symptomatic treatment is carried out: antipyretic and analgesic drugs, anticonvulsant therapy, diuretics (with cerebral edema), etc. When selecting a regimen for the treatment of serous meningitis in young children, the minimum age for each drug must be taken into account.

Consequences of serous meningitis in children

With the timely provision of qualified medical care, the prognosis of serous meningitis is favorable. The outcome of the disease is complete recovery after a week of treatment. However, pain in the head can persist for several weeks.

Possible options for complications with a delay in diagnosis and therapy:

• hearing loss;
• epilepsy;
• hydrocephalus;
• mental retardation in younger patients.

Self-medication or drawing up an illiterate therapy regimen leads to death.

Measures to prevent serous meningitis by contact

It is recommended to limit contact with a sick person, communication only using gauze bandages or respirators; obligatory thorough washing of hands after communication; avoid traveling to countries with a high incidence rate and swimming in water bodies in their territory.

Vaccination

Currently, vaccines have been developed against some pathogens of serous meningitis (measles, rubella, etc.).

There are also vaccines against the main pathogens of purulent meningitis.