Bacterial meningitis symptoms in adults clinical guidelines. Clinical guidelines for diagnosis and primary medical care for viral meningitis

AUTHORS:

Barantsevich E.R. Head of the Department of Neurology and Manual Medicine, First St. Petersburg State Medical University named after acad. I.P. Pavlova

Voznyuk I.A. - Deputy Director for Research, St. Petersburg Research Institute of St. I.I. Dzhanelidze, Professor of the Department of Nervous Diseases of the V.I. CM. Kirov.

Definition

Meningitis is an acute infectious disease with a primary lesion of the arachnoid and pia mater of the brain and spinal cord. With this disease, the development of situations that threaten the life of the patient (the occurrence of impaired consciousness, shock, convulsive syndrome) is possible.

CLASSIFICATION
In the classification, divisions are accepted according to etiology, type of course, nature of the inflammatory process, etc.

1. 
   According to the etiological principle, they are distinguished:

2. By the nature of the inflammatory process:

Purulent, predominantly bacterial.

Serous, predominantly viral meningitis.

3. By origin:

Primary meningitis (causative agents are tropic to the nervous tissue).

Secondary meningitis (before the development of meningitis, there were foci of infection in the body).

4. Downstream:

• 
  Fulminant (fulminant), often caused by meningococcus. A detailed clinical picture is formed in less than 24 hours.
• 
  Acute.
• 
  Subacute.
• 
  Chronic meningitis - symptoms persist for more than 4 weeks. The main causes are tuberculosis, syphilis, Lyme disease, candidiasis, toxoplasmosis, HIV infection, systemic connective tissue diseases.

ETIOLOGY AND PATHOGENESIS

Of primary importance in the pathogenesis of acute inflammatory processes is hematogenous or contact infection with bacteria, viruses, fungi, protozoa, mycoplasmas or chlamydia (bacteria that do not have a dense cell wall, but are limited by the plasma membrane) from lesions located in a variety of organs.

The source of meningitis, meningoencephalitis, epidural abscess, subdural empyema, brain abscess, septic thrombosis of the cerebral veins and sinuses of the dura mater can be chronic inflammatory diseases of the lungs, heart valves, pleura, kidneys and urinary tract, gallbladder, osteomyelitis of long tubular bones and pelvis, prostatitis in men and adnexitis in women, as well as thrombophlebitis of various localization, bedsores, wound surfaces. Especially often the cause of acute inflammatory diseases of the brain and its membranes are chronic purulent lesions of the paranasal sinuses, middle ear and mastoid process, as well as dental granulomas, pustular lesions of the facial skin (folliculitis) and osteomyelitis of the skull bones. In conditions of reduced immunological reactivity, bacteria from latent foci of infection or pathogens that enter the body from the outside become the cause of bacteremia (septicemia).

With exogenous infection with highly pathogenic bacteria (most often meningococci, pneumococci) or in cases where saprophytic pathogens become pathogenic, acute diseases of the brain and its membranes develop according to the mechanism of rapidly emerging bacteremia. The source of these pathological processes can also be pathogenic foci associated with infection of implanted foreign bodies (artificial pacemakers, artificial heart valves, alloplastic vascular prostheses). In addition to bacteria and viruses, infected microemboli can be introduced into the brain and meninges. Similarly, hematogenous infection of the meninges occurs with extracranial lesions caused by fungi and protozoa. It should be borne in mind the possibility of hematogenous bacterial infection not only through the arterial system, but also through the venous route - the development of ascending bacterial (purulent) thrombophlebitis of the veins of the face, intracranial veins and sinuses of the dura mater.

Most often bacterial meningitis are called meningococci, pneumococci, haemophilus influenzae,viral – coxsackie viruses,ECHO, mumps.

V pathogenesis meningitis are important factors such as:

General intoxication

Inflammation and swelling of the meninges

Hypersecretion of cerebrospinal fluid and violation of its resorption

Irritation of the meninges

Increased intracranial pressure

CLINICAL CHARACTERISTICS

Clinical picture of meningitis consists of general infectious, cerebral and meningeal symptoms.

To general infectious symptoms include feeling unwell, fever, myalgia, tachycardia, facial flushing, inflammatory changes in the blood, etc.

Meningeal and cerebral symptoms include headache, nausea, vomiting, confusion or depression of consciousness, generalized convulsive seizures. Headache, as a rule, is bursting in nature and is caused by irritation of the meninges due to the development of the inflammatory process and increased intracranial pressure (ICP). Vomiting is also the result of an acute increase in ICP. Due to an increase in ICP, patients may have Cushing's triad: bradycardia, increased systolic blood pressure, decreased breathing. In severe meningitis, convulsions and psychomotor agitation are observed, periodically replaced by lethargy, impaired consciousness. Possible mental disorders in the form of delusions and hallucinations.

Actually shell symptoms include manifestations of general hyperesthesia and signs of a reflex increase in the tone of the dorsal muscles when the meninges are irritated. If the patient is conscious, then he has intolerance to noise or hypersensitivity to it, loud conversation (hyperacusia). Headaches are aggravated by loud sounds and bright lights. Patients prefer to lie with their eyes closed. Almost all patients have stiff neck muscles and Kernig's symptom. Rigidity of the occipital muscles is detected when the patient's neck is passively flexed, when, due to a spasm of the extensor muscles, it is not possible to fully bring the chin to the sternum. Kernig's symptom is checked as follows: the leg of the patient lying on his back is passively flexed at an angle of 90º in the hip and knee joints (the first phase of the study), after which the examiner makes an attempt to straighten this leg in the knee joint (second phase). If a patient has meningeal syndrome, it is impossible to straighten his leg in the knee joint due to a reflex increase in the tone of the leg flexor muscles; in meningitis this symptom is equally positive on both sides.

Patients should also be checked for Brudzinski's symptoms. The upper symptom of Brudzinsky - when the patient's head is passively brought to the sternum, in the supine position, his legs are bent at the knee and hip joints. Average symptom of Brudzinski- the same bending of the legs when pressing on pubic articulation . Lower Brudzinski's symptom- with passive flexion of one leg of the patient in the knee and hip joints, the other leg is bent in the same way.

The severity of meningeal symptoms can vary significantly: meningeal syndrome is mild at an early stage of the disease, with fulminant forms, in children, elderly and immunocompromised patients.

The greatest alertness should be shown in terms of the possibility of a patient having purulent meningococcal meningitis, since this disease can be extremely difficult and requires serious anti-epidemic measures. Meningococcal infection is transmitted by airborne droplets and after entering the body, meningococcus vegetates for some time in the upper respiratory tract. The incubation period usually ranges from 2 to 10 days. The severity of the disease varies greatly, and it can manifest itself in various forms: bacterial carrier, nasopharyngitis, purulent meningitis and meningoencephalitis, meningococcemia. Purulent meningitis usually begins acutely (or fulminantly), the body temperature rises to 39-41º, there is a sharp headache, accompanied by vomiting that does not bring relief. Consciousness is initially preserved, but in the absence of adequate therapeutic measures, psychomotor agitation, confusion, delirium develop; with the progression of the disease, excitation is replaced by lethargy, turning into a coma. Severe forms of meningococcal infection can be complicated by pneumonia, pericarditis, myocarditis. A characteristic feature of the disease is the development of a hemorrhagic rash on the skin in the form of asterisks of various shapes and sizes, dense to the touch, protruding above the level of the skin. The rash is localized more often on the thighs, legs, in the buttocks. There may be petechiae on the conjunctiva, mucous membranes, soles, palms. In severe cases of generalized meningococcal infection, endotoxic bacterial shock may develop. In infectious-toxic shock, blood pressure decreases rapidly, the pulse is thready or not detected, cyanosis and a sharp blanching of the skin are noted. This condition is usually accompanied by impaired consciousness (somnolence, stupor, coma), anuria, acute adrenal insufficiency.

RENDERING EMERGENCY ASSISTANCE

AT THE PREHOSPITAL STAGE

At the prehospital stage - examination; detection and correction of severe respiratory and hemodynamic disorders; identification of the circumstances of the disease (epidemiological history); emergency hospitalization.

Caller tips:

• 
  It is necessary to measure the patient's body temperature.
• 
  In good light, the patient's body should be carefully examined for a rash.
• 
  At high temperatures, you can give the patient paracetamol as an antipyretic drug.
• 
  The patient should be given sufficient fluids.
• 
  Find the drugs that the patient is taking and prepare them for the arrival of the ambulance team.
• 
  Do not leave the patient unattended.

Diagnostics (D, 4)

Actions on a call

Mandatory questions to the patient or his environment

• 
  Has the patient had any recent contact with infectious patients (especially with meningitis)?
• 
  How long ago did the first symptoms of the disease appear? Which?
• 
  When and how much did the body temperature rise?
• 
  Does the headache bother you, especially if it gets worse? Is the headache accompanied by nausea and vomiting?
• 
  Does the patient have photophobia, hypersensitivity to noise, loud conversation?
• 
  Was there any loss of consciousness, convulsions?
• 
  Are there any skin rashes?
• 
  Does the patient have manifestations of chronic foci of infection in the head area (paranasal sinuses, ears, oral cavity)?
• 
  What drugs is the patient currently taking?

Examination and physical examination

Assessment of general condition and vital functions.

Assessment of mental status (whether delusions, hallucinations, psychomotor agitation are present) and the state of consciousness (clear consciousness, somnolence, stupor, coma).

Visual assessment of the skin in good light (hyperemia, pallor, the presence and location of a rash).

Pulse examination, measurement of respiratory rate, heart rate, blood pressure.

Measurement of body temperature.

Evaluation of meningeal symptoms (photophobia, stiff neck, Kernig's symptom, Brudzinsky's symptoms).

On examination - alertness regarding the presence or likelihood of life-threatening complications (toxic shock, dislocation syndrome).
Differential diagnosis of meningitis at the prehospital stage is not carried out; a lumbar puncture is necessary to clarify the nature of meningitis.

Reasonable suspicion of meningitis is an indication for urgent delivery to an infectious diseases hospital; the presence of signs of life-threatening complications (infectious toxic shock, dislocation syndrome) is a reason to call a specialized mobile ambulance team with subsequent delivery of the patient to a hospital in an infectious diseases hospital.

Treatment (D, 4)

Method of application and doses of drugs

With severe headache, you can use paracetamol 500 mg orally (it is recommended to drink plenty of liquid) - the maximum single dose of paracetamol is 1 g, daily - 4 g.

With convulsions - diazepam 10 mg intravenously per 10 ml of 0.9% sodium chloride solution (slowly - to prevent possible respiratory depression).

With the most severe and rapidly current forms of meningitis - with high fever, a sharp meningeal syndrome, severe depression of consciousness, a clear dissociation between tachycardia (100 or more in 1 min) and arterial hypotension (systolic pressure of 80 mm Hg and below) - t i.e. with signs of infectious-toxic shock - before being transported to a hospital, the patient must be injected intravenously with 3 ml of a 1% solution of diphenhydramine (or other antihistamines). The administration of corticosteroid hormones recommended in the recent past is contraindicated, since, according to recent data, they reduce the therapeutic activity of antibiotics.

PROVIDING EMERGENCY ASSISTANCE AT THE HOSPITAL STAGE IN THE INSPECTIVE EMERGENCY DEPARTMENT (STOSMP)

Diagnostics (D, 4)

A detailed clinical examination is carried out, a consultation with a neurologist is performed.

A lumbar puncture is performed, which allows differential diagnosis of purulent and serous meningitis. Urgent lumbar puncture for the study of cerebrospinal fluid is indicated for all patients with suspected meningitis. Contraindications are only the detection of congestive optic discs during ophthalmoscopy and the displacement of the "M-echo" during echoencephalography, which may indicate the presence of a brain abscess. In these rare cases, patients should be seen by a neurosurgeon.

CSF diagnostics of meningitis consists of the following methods of research:

1. 
   macroscopic assessment of the cerebrospinal fluid removed during lumbar puncture (pressure, transparency, color, loss of the fibrin mesh when the cerebrospinal fluid stands in the test tube);
2. 
   microscopic and biochemical studies (number of cells in 1 µl, their composition, bacterioscopy, protein content, sugar and chloride content);
3. 
   special methods of immunological express diagnostics (counter immunoelectrophoresis method, fluorescent antibody method).

In some cases, there are difficulties in the differential diagnosis of bacterial purulent meningitis from other acute lesions of the brain and its membranes - acute disorders of cerebral circulation; post-traumatic intracranial hematomas - epidural and subdural; post-traumatic intracranial hematomas, manifested after the "light gap"; brain abscess; acutely manifesting brain tumor. In cases where the severe condition of patients is accompanied by depression of consciousness, an expansion of the diagnostic search is required.

Differential Diagnosis

№ p.p.	diagnosis	differential sign
1	subarachnoid hemorrhage:	sudden onset, severe headache (“worst in life”), xanthochromia (yellowish coloration) of cerebrospinal fluid
2	brain injury	objective signs of injury (hematoma, cerebrospinal fluid leakage from the nose or ears)
3	viral encephalitis	mental status disorders (depression of consciousness, hallucinations, sensory aphasia and amnesia), focal symptoms (hemiparesis, cranial nerve damage), fever, meningeal symptoms, possibly combined with genital herpes, lymphocytic pleocytosis in CSF
4	brain abscess	headache, fever, focal neurological symptoms (hemiparesis, aphasia, hemianopsia), there may be meningeal symptoms, increased ESR, CT or MRI of the brain reveals characteristic changes, history of chronic sinusitis or recent dental intervention
5	neuroleptic malignant syndrome	high fever (may be over 40°C), muscle rigidity, involuntary movements, confusion associated with tranquilizers
6	bacterial endocarditis	fever, headache, confusion or depression of consciousness, epileptiform seizures, sudden focal neurological symptoms; cardiac symptoms (history of congenital or rheumatic heart disease, heart murmurs, valvular vegetations on echocardiography), increased ESR, leukocytosis, no changes in CSF, bacteremia
7	giant cell (temporal) arteritis	headache, visual disturbances, age over 50 years, thickening and tenderness of the temporal arteries, intermittent claudication of the chewing muscles (sharp pain or tension in the chewing muscles when eating or talking), weight loss, subfebrile condition

Treatment (D, 4)

Different antibiotics have different ability to penetrate the blood-brain barrier and create the necessary bacteriostatic concentration in the CSF. On this basis, instead of the antibiotics of the penicillin group, which were widely used in the recent past, it is now recommended to prescribe III–IV generation cephalosporins for initial empirical antibiotic therapy. They are considered the drugs of choice. However, in their absence, one should resort to the appointment of alternative drugs - penicillin in combination with amikacin or gentamicin, and in cases of sepsis - a combination of penicillin with oxacillin and gentamicin (table 1).
Table 1

Drugs of choice and alternative drugs for starting antibiotic therapy for purulent meningitis with an unidentified pathogen (according to D. R. Shtulman, O. S. Levin, 2000;
P. V. Melnichuk, D. R. Shtulman, 2001; Yu. V. Lobzin et al., 2003)

Drugs of choice		Alternative drugs
drugs; daily doses (pharmaceutical classes)	Multiplicity of introduction i/m or i/v (once a day)	drugs; daily doses (pharmaceutical classes)	Multiplicity of introduction i/m or i/v (once a day)
IV generation cephalosporins cefmetazole: 1–2 g cefpir: 2 g cefoxitim (mefoxime): 3 g 3rd generation cephalosporins cefotoxime (Claforan): 8–12 g ceftriaxone (rocerin): 2–4 g ceftazidime (fortum): 6 g cefuroxime: 6 g Meropenem (antibiotic beta-lactam): 6 g	2	Penicillins Ampicillin: 8–12 g Benzylpenicillin: 20–30 million units Oxacillin: 12–16 g Aminoglycoside antibiotics gentamicin: 12–16 g amikacin: 15 mg/kg; is administered intravenously in 200 ml of isotonic sodium chloride solution at a rate of 60 drops / min.

Emergency treatment of Waterhouse-Friderichsen syndrome(meningococcemia syndrome with symptoms of vasomotor collapse and shock).

In essence, it is an infectious-toxic shock. It occurs in 10-20% of patients with generalized meningococcal infection.

• 
  Dexamethasone, depending on the severity of the condition, may be administered intravenously at an initial dose of 15–20 mg, followed by 4–8 mg every 4 hours until the condition stabilizes.
• 
  elimination of hypovolemia - polyglucin or reopoliglyukin is prescribed - 400–500 ml intravenously for 30–40 minutes 2 times a day or 5% placental albumin - 100 ml of a 20% solution intravenously for 10–20 minutes 2 times a day day.
• 
  the appointment of vasopressors (adrenaline, norepinephrine, mezaton) in the collapse caused by acute adrenal insufficiency in the Waterhouse-Friderichsen syndrome does not work if there is hypovolemia and it cannot be stopped by the above methods
• 
  the use of cardiotonic drugs - strophanthin K - 0.5-1 ml of a 0.05% solution in 20 ml of a 40% glucose solution slowly in / in or corglicon (0.5-1 ml of a 0.06% solution in 20 ml of 40% glucose solution), or dopamine IV drip.
• 
  dopamine - the initial rate of administration of 2-10 drops of a 0.05% solution (1-5 mcg / kg) per 1 min - under constant hemodynamic control (blood pressure, pulse, ECG) to avoid tachycardia, arrhythmia and spasm of the kidney vessels.

With signs of an incipient dislocation syndrome:

• 
  the introduction of a 15% solution of mannitol 0.5-1.5 g/kg IV drip
• 
  transfer of the patient to the intensive care unit
• 
  observation by a neurologist, a neurosurgeon.

Appendix

Strength of recommendations (A- D), levels of evidence (1++, 1+, 1-, 2++, 2+, 2-, 3, 4) according to Scheme 1 and Scheme 2 are given when presenting the text of clinical recommendations (protocols).
Rating scheme for assessing the strength of recommendations (diagram 1)

Levels of Evidence	Description
1++	High quality meta-analyses, systematic reviews of randomized controlled trials (RCTs), or RCTs with very low risk of bias
1+	Well-conducted meta-analyses, systematic, or RCTs with low risk of bias
1-	Meta-analyses, systematic, or RCTs with a high risk of bias
2++	High-quality systematic reviews of case-control or cohort studies. High-quality reviews of case-control or cohort studies with very low risk of confounding effects or bias and moderate likelihood of causation
2+	Well-conducted case-control or cohort studies with moderate risk of confounding effects or bias and moderate likelihood of causation
2-	Case-control or cohort studies with a high risk of confounding effects or biases and an average likelihood of causation
3	Non-analytic studies (for example: case reports, case series)
4	Expert opinions

Power	Description
A	At least one meta-analysis, systematic review, or RCT rated 1++, directly applicable to the target population and demonstrating robustness of results, or body of evidence including results from studies rated 1+, directly applicable to the target population and demonstrating the overall stability of the results
V	A body of evidence that includes results from studies rated 2++ that are directly applicable to the target population and demonstrate overall robustness of results, or extrapolated evidence from studies rated 1++ or 1+
WITH	A body of evidence that includes results from studies rated 2+ that are directly applicable to the target population and demonstrate overall robustness of results, or extrapolated evidence from studies rated 2++
D	Level 3 or 4 evidence or extrapolated evidence from studies rated 2+

And antivirals. If the disease is severe, then resuscitation procedures may be required.

Can meningitis be cured or not? Obviously yes. Next, consider how to treat meningitis.

What to do when discovered?

The course of the disease is often rapid. If you notice one of the symptoms of purulent meningitis, then treatment should begin as soon as possible. The problem can become more global if a person loses consciousness. In this case, it will be very difficult to determine what he feels at the moment. The patient must be taken to the vascular center, where they will do a CT scan and MRI.

Which doctor treats meningitis? If violations are not detected, in this case, the victim will be sent to the hospital. When a patient has a fever, he should be sent to an infectious disease specialist. In no case should you leave him alone at home, since assistance in such situations must be provided immediately.

The appearance of a hemorrhagic rash is a very bad symptom. This suggests that the disease is severe, so the lesion can spread to all organs.

Important! Often, for the treatment of such a disease, they turn to an infectious disease doctor, and if a child has a lesion, then to a pediatric infectious disease specialist.

Now you know who treats this disease.

Basic principles of meningitis treatment

The main principle of meningitis treatment is timeliness. Treatment of the inflammatory process in the brain is carried out only in a hospital - in this case, the disease begins to develop very rapidly, which, if not treated in time, leads to death. The doctor may prescribe antibiotics and broad-spectrum medications. This choice is due to the fact that it is possible to establish the pathogen when taking cerebrospinal fluid.

Antibiotics are administered intravenously. The activity of antibacterial drugs is determined on an individual basis, but if the main signs have disappeared and the patient's temperature is at a normal level, then antibiotics will be administered for several days in order to consolidate the result.

The next direction is the appointment of steroids. Hormone therapy will help the body cope with the infection and bring the pituitary gland back to normal. Diuretics are used in the treatment, as they relieve swelling. However, it is worth taking into account that all diuretics wash out calcium from the human body. Spinal puncture not only relieves the condition, but also reduces pressure on the brain.

How and how to treat meningitis? There are several methods.

Medical method

The best cure for meningitis is antibiotics. Together with them, antibacterial agents are also prescribed:

• Amikacin (270 rubles).
• Levomycetin succinate (58 p.).
• Meronem (510 rubles).
• Tarivid (300 rubles).
• Abaktal (300 rubles).
• Maximim (395 rubles).
• Oframax (175 rubles).

Among the antipyretics, the following are prescribed:

• Aspinat (85 rubles).
• Maxigan (210 rubles).
• Paracetamol (35 p.).

Corticosteroid drugs include:

• Daxin
• Medrol

All tablet prices are approximate. They may vary depending on the region and area.

Taking herbs and fruits

Advice! Before using any of the recipes, it is important to consult a specialist. In the process of taking alternative medicine, a person is provided with complete peace of mind and is protected from loud sounds.

You can use these methods:

Diet

The doctor should tell you that you need to follow a special diet for such a disease. It will be supported by vitamin balance, metabolism, protein and salt-water balance. Prohibited products include the following:

• Horseradish and mustard.
• beans.
• Hot sauces.
• Buckwheat, barley.
• Whole milk.
• Sweet dough.

exercise therapy

General strengthening exercises will help you recover faster and return to your usual rhythm of life. But you need to resort to exercise therapy only with the permission of the doctor - you do not need to make decisions on your own.

Physiotherapy

Physiotherapy includes taking such means:

• Immunostimulating.
• Sedative.
• Tonic.
• Ion-correcting.
• Diuretic.
• Enzyme stimulating.
• Hypocoagulants.
• Vasodilator.

When is an operation needed?

Surgery is needed if meningitis is severe. Indications for surgical intervention are as follows:

• Sudden increase in blood pressure and heart rate.
• Increased dyspnea and pulmonary edema.
• Respiratory paralysis.

Is it possible to get rid of at home?

Can it be treated at home? You can treat meningitis at home only if it is at an early stage.

Also at home, you can restore the health of the patient, providing him with proper care and peace. During this period, a person is given antibiotics, and folk remedies are also used.

It is important to comply with the following conditions:

1. Follow bed rest.
2. Darken the room in which the patient is located.
3. Nutrition should be balanced, and drinking plentiful.

Terms of recovery

How long does it take to treat an illness? It depends on:

• Forms of the disease.
• General condition of the body.
• The time the treatment started.
• individual susceptibility.

REFERENCE! The duration of treatment depends on the form - if it is severe, then more time will be needed to recover.

Possible complications and consequences

They can be represented like this:

• ITSH or DVS. They develop as a result of circulating endotoxin in the blood. All this can lead to bleeding, impaired activity and even death.
• Waterhouse-Frideriksen syndrome. It manifests itself as an insufficiency of the function of the adrenal glands, which produce a number of hormones. All this is accompanied by a decrease in blood pressure.
• Myocardial infarction. This complication occurs in older people.
• Cerebral edema due to intoxication and subsequent wedging of the brain into the spinal canal.
• Deafness as a result of toxic nerve damage.

Read more about the complications and consequences of meningitis in the separate materials of the site.

Timing of follow-up for contact patients?

The observation period for contacts is 10 days. During this time, the patient fully recovers.

Symptoms

All symptoms are conditionally divided into the following:

1. Syndrome of intoxication.
2. Craniocerebral Syndrome.
3. meningeal syndrome.

The first is the syndrome of intoxication. It is caused due to septic lesions and the appearance of infection in the blood. Often sick people are very weak, they get tired quickly. Body temperature rises to 38 degrees. Very often there is a headache, cough, fragility of the joints.

The skin becomes cold and pale, and the appetite is significantly reduced. In the early days, the immune system fights the infection, but after that, you can’t do without the help of a professional doctor. The craniocerebral syndrome is the second.

It develops as a result of intoxication. Infectious agents quickly spread throughout the body and are introduced into the blood. Here they attack cells. Toxins can lead to blood clotting and blood clots. In particular, the medulla is affected.

ATTENTION! Blockage of blood vessels leads to the fact that the metabolism is disturbed, and fluid accumulates in the intercellular space and brain tissues.

Due to edema, different parts of the brain are affected. The center of thermoregulation is affected, and this leads to an increase in body temperature.

Often, the patient is observed vomiting, because the body can not tolerate the smell and taste of food. Progressive cerebral edema increases intracranial pressure. This leads to impaired consciousness and psychomotor agitation. The third syndrome is meningeal.

It is caused by a violation of the circulation of cerebrospinal fluid against the background of intracranial pressure. Fluid and edematous tissue irritates the receptors, the muscles contract, and the patient's movements become abnormal. Meningeal syndrome can manifest itself in this way:

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General approaches to diagnostics.
Diagnosis of meningococcal infection is made by collecting anamnesis, detailed clarification of complaints, clinical examination, additional (laboratory and instrumental) examination methods and is aimed at determining the clinical form, severity of the condition, identifying complications and indications for treatment, as well as identifying factors in the anamnesis that prevent immediate initiation of treatment or requiring correction of treatment. These factors can be:
the presence of intolerance to drugs and materials used at this stage of treatment;
inadequate psycho-emotional state of the patient before treatment;
a life-threatening acute condition/disease or an exacerbation of a chronic disease requiring the involvement of a specialist in the profile of the condition/disease for prescribing treatment;
refusal of treatment.
2.1 Complaints and anamnesis.
MI can occur in various forms with a combination of certain syndromes.
(Appendix D2). The threat is represented by generalized forms, due to the high risk of life-threatening complications (Appendix D3-D6, D9).
For the timely detection of children at risk for the development of GMI, it is recommended, when collecting an anamnesis, to clarify the fact of possible contact with patients with meningococcal infection (carriers of meningococcus).

A comment. Possible contacts in the family, in the close environment of the sick person, facts of stay or close contact with people who visited regions in regions with a high incidence of MI (countries of the "meningitis belt" of Subequatorial Africa; Saudi Arabia) are specified. .
It is recommended to focus on complaints indicating a high risk of developing GMI, which include:
persistent febrile fever;
headache,.
photophobia,.
hyperesthesia.
vomiting (profuse regurgitation in children under 1 year old).
dizziness,.
rapid breathing.
cardiopalmus,.
drowsiness,.
unmotivated excitement.
refusal to eat.
reduced fluid intake (more than 50% of normal intake within 24 hours - for children under 1 year old),.
monotonous / shrill cry (for children under one year old),.
change in color and temperature of the skin.
leg pain.
rash,.
decreased diuresis.
Level of persuasiveness of recommendations B (level of evidence - 2+).
A comment. GMI is characterized by a sharp rise in temperature to high numbers (38.5-40 ° C and above); a 2-hump character of the temperature curve is often noted - on the first rise in temperature, a short-term effect on the antipyretics used is noted, with a second rise (after 2-6 hours) - the introduction of antipyretics has no effect. A similar nature of the temperature curve is observed not only with HMI, but also with other severe infections occurring with sepsis syndrome, with viral and bacterial neuroinfections (encephalitis, meningitis).
The presence of hyperesthesia in young children m. B. Suspected with the so-called “mother's hands” symptom: when the mother complains that the child begins to worry sharply when trying to take him in her arms.
In the structure of the general infectious syndrome, complaints of diffuse and local muscle and joint pains are often noted, however, it is complaints of intense pain in the legs and abdomen (in the absence of manifestations of an intestinal infection and the presence of surgical pathology) that refer to the symptoms of the so-called "red flags" with clinical diagnosis of sepsis, m. B. Signs of developing septic shock. .
In the presence of a rash, it is recommended to specify the time of appearance of the first elements, their nature, localization, dynamics of changes. The presence of a hemorrhagic rash is pathognomonic for GMI, however, in most cases, the appearance of hemorrhagic elements is preceded by a roseolous or roseolous-papular rash (so-called Rash-rash), the elements of which can be located on different parts of the body and are often regarded as allergic manifestations. The appearance of a widespread hemorrhagic rash without a previous rash within a few hours of the onset of the disease, as a rule, indicates the extreme severity of the disease. .
It is necessary to clarify the features of diuresis: the time of the last urination (in infants - the last change of diapers). Decrease / absence of diuresis (more than 6 hours in children of the 1st year of life, more than 8 hours in patients older than a year) may be signs of the development of septic shock. .

2.2 Physical examination.

An objective physical examination is recommended to actively identify signs of HMI and associated complications. The presence of GMI should be assumed when identifying:
hemorrhagic rash that does not disappear with pressure.
hyper/hypothermia.
increasing the capillary filling time by 2 seconds,.
changes in the color of the skin (marbling, acrocyanosis, diffuse cyanosis).
hypothermia of the distal extremities.
changes in the level of consciousness.
meningeal symptoms.
hyperesthesia.
tachypnea/dyspnea.
tachycardia.
decrease in blood pressure.
decrease in diuresis.
an increase in the Algover shock index (normal: heart rate / blood pressure systolic = 0.54).
Strength of recommendation C (level of evidence -3).
A comment. In the debut of GMI, excitation can be observed, followed by depression from somnolence to deep coma. The degree of impairment of consciousness is assessed on the Glasgow coma scale, where 15 points corresponds to clear consciousness, a level of 3 points or less corresponds to transcendental coma (Appendix D10).
A certain help in assessing the severity of the patient's condition is the presence / absence of clinical signs of a systemic inflammatory response (SIVR) with the determination of the level of blood pressure, frequency and quality of the pulse, respiration. Identification of 2 or more signs of SIRS is associated with a high risk of severe bacterial (not only meningococcal) infection. Threshold diagnostic values ​​of SSVR depending on age are presented in Appendix D4. .
The presence of pathological types of respiration is detected in the extreme severity of the course of HMI in cases of the development of a dislocation syndrome against the background of BT or in the terminal stage of the disease complicated by refractory septic shock.
The most typical hemorrhagic rash in the form of irregularly shaped elements, dense to the touch, protruding above the level of the skin. The number of elements of the rash is very different - from single to covering the entire surface of the body. Most often, the rash is localized on the buttocks, back of the thighs and legs; less often - on the face and sclera, and usually in severe forms of the disease. Roseolous and roseolous-papular elements of the previous rach-rash (observed in 50-80% of cases of GMI) quickly disappear, leaving no traces within 1-2 days from the moment of appearance. Signs of impaired microcirculation are pallor, cyanosis, marble pattern of the skin, hypothermia of the distal extremities. .
In the first hours from the onset of the disease, meningeal symptoms can be negative even with mixed forms and isolated MM, the maximum severity of meningeal symptoms is observed on days 2-3. Infants are characterized by dissociation of meningeal symptoms; for the first year of life, the most informative symptoms are persistent bulging and increased pulsation of the large fontanel and stiff neck. .

2.3 Laboratory diagnostics.

All patients with suspected MI are recommended to have a clinical blood test with a leukocyte count.
Recommendation strength level C (level of evidence - 3).
Comments. The detection of leukopenia or leukocytosis in the leukocyte formula, which are beyond the age reference values ​​according to the table (Appendix D4), may indicate the presence of a systemic inflammatory reaction characteristic of HMI.
All patients with suspected HMI are recommended to study a general urine test; blood biochemical parameters: urea, creatinine, alanine aminotransferase (ALaT), aspartate aminotransferase (ASaT), blood electrolytes (potassium, sodium), bilirubin, total protein, acid-base balance, lactate levels.

Comments. Changes in the biochemical parameters of blood and urine make it possible to diagnose a specific organ dysfunction, assess the degree of damage and the effectiveness of the therapy. .
It is recommended to determine the CRP and the level of procalcitonin in the blood of all patients with suspected HMI.
Level of persuasiveness of recommendations B (level of evidence - 2++).
Comments. Detection in the blood of an increase in C-reactive protein2 standard deviations from the norm and procalcitonin 2 ng/ml indicates the presence of a systemic inflammatory reaction characteristic of HMI. Evaluation of indicators in dynamics allows you to evaluate the effectiveness of ongoing antibiotic therapy. .
It is recommended to study the parameters of hemostasis in all patients with suspected HMI with the determination of the duration of bleeding, blood clotting time, coagulograms.
Level of persuasiveness of recommendations C (level of evidence - 3).
Comments. For the diagnosis of DIC. The parameters of hemostasis change according to the stages of DIC, the study of the hemostasis system is necessary to assess the effectiveness of the therapy and its correction. .
etiological diagnosis.
Regardless of the form of the disease, bacteriological examination of nasopharyngeal mucus for meningococcus is recommended for all patients with suspected MI.

A comment. Inoculation of meningococcus from the mucous membranes of the nasopharynx allows verifying the etiological diagnosis of nasopharyngitis and establishing the carriage of N. Meningitidis For generalized forms of GMI, in the absence of detection of N. Meningitidis in sterile fluids (blood / cerebrospinal fluid / synovial fluid) cannot be the basis for establishing an etiological diagnosis, however, it is important a factor for the choice of ABT, which should contribute both to the treatment of a systemic disease and the eradication of meningococcus from the mucous membranes of the nasopharynx.
All patients with suspected GMI are recommended bacteriological examination (culture) of blood.

Comments. Isolation and identification of a culture of meningococcus from sterile media of the body (blood, cerebrospinal fluid) is the "gold standard" for the etiological verification of the disease. Blood sampling should be carried out as quickly as possible from the moment the patient enters the hospital until the start of ABT. A blood test is especially important in situations where there are contraindications for CSP. The absence of growth of the pathogen does not exclude meningococcal etiology of the disease, especially when antibiotic therapy is started at the prehospital stage. .
A clinical examination of cerebrospinal fluid is recommended for all patients with suspected mixed HMI or MM.
Level of persuasiveness of recommendations C (level of evidence - 3).
Comments. Cerebrospinal puncture is possible only if there are no contraindications (Appendix D11). Considering the absence of specific meningeal manifestations in young children, CSP is indicated for all patients of the first year of life with HMI. Qualitative characteristics of CSF are assessed (color, transparency), pleocytosis is examined with the determination of the cellular composition, biochemical indicators of protein, glucose, sodium, chloride levels). MM is characterized by the presence of neutrophilic pleocytosis, an increase in protein levels, and a decrease in glucose levels. In the first hours of the disease and during SMP in the later stages, pleocytosis m. B. Mixed, a decrease in glucose levels with an increase in lactate testifies in favor of the bacterial nature of menenitis during differential diagnosis and viral neuroinfections. .
All patients with suspected mixed HMI or MM are recommended to undergo bacteriological examination (culture) of cerebrospinal fluid.
Strength of recommendation A (level of evidence -1+).
Comments. The study of CSF is possible only in the absence of contraindications (Appendix G11) Isolation of other pathogens from the blood and CSF by the cultural method helps to make a differential diagnosis, verify the etiology of the disease and adjust antimicrobial therapy.
Blood smear microscopy (thick spot) with Gram stain is recommended for patients with suspected GMI.
Level of persuasiveness of recommendations C (level of evidence - 3).
Comments. Detection of characteristic Gram-negative diplococci in a smear serves as a guideline and may warrant the initiation of specific therapy, but the diagnosis of MI is not based on microscopy alone.
For express diagnostics of GMI, it is recommended to carry out the latex agglutination test (RAL) in blood serum and CSF to determine the antigens of the main causative agents of bacterial neuroinfections.
Recommendation strength level C (level of evidence - 3).
Comments. The test systems used in practice for RAL in the diagnosis of bacterial neuroinfections make it possible to detect antigens of meningococci A, B, C, Y / W135, pneumococci, Haemophilus influenzae. The detection of AH of bacterial pathogens in sterile fluids in the presence of a clinical picture of GMI or BGM makes it possible to verify the etiology of the disease with a high degree of probability. False-positive and false-negative results are possible, therefore, in addition to RAL, it is necessary to take into account the results of cultural and molecular methods. In cases of discrepancy between the RAL data and the results of PCR or cultures, preference is given to the latter to verify the etiological diagnosis. .
It is recommended to conduct molecular research methods to identify the causative agent of GMI.
Level of persuasiveness of recommendations B (level of evidence -2+).
Comments. Amplification of nucleic acids of causative agents of bacterial neuroinfection is carried out by using the polymerase chain reaction method. Detection of DNA fragments of meningococcus by PCR in sterile fluids (blood, cerebrospinal fluid, synovial fluid) is sufficient to establish the etiology of the disease. Used in practice, commercial test systems allow you to simultaneously conduct a study for the presence of pneumococcal, hemophilic and meningococcal infections, which allows for differential diagnosis with diseases that have a similar clinical picture, and to choose the optimal antibiotic therapy. .
Criteria for laboratory confirmation of the diagnosis.
It is recommended that a reliable diagnosis of MI be considered cases of typical clinical manifestations of a localized or generalized form of MI in combination with the isolation of a meningococcal culture during bacteriological culture from sterile fluids (blood, cerebrospinal fluid, synovial fluid), or when DNA (PCR) or antigen (RAL) of meningococcus is detected in the blood or CSF.
Level of persuasiveness of recommendations B (level of evidence -2+).
A comment. Inoculation of meningococcus from nasopharyngeal mucus is taken into account for the diagnosis of localized forms of MI (carriage, nasopharyngitis), but is not the basis for the etiological confirmation of the diagnosis of GMI in case of negative results of cultures, RAL, PCR CSF and blood. .
It is recommended to consider cases of the disease with clinical and laboratory manifestations characteristic of GMI with negative results of bacteriological examination as a probable diagnosis of GMI.
Level of persuasiveness of recommendations C (level of evidence - 3).

RCHD (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical Protocols of the Ministry of Health of the Republic of Kazakhstan - 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 of the 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: general practitioners, general practitioners, infectious disease specialists, neuropathologists, resuscitators, clinical pharmacologists, medical experts, doctors/ambulance paramedics.

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

A	High-quality meta-analysis, systematic review of RCTs, or large RCTs with a very low probability (++) of bias, the results of which can be generalized to an appropriate population.
V	High-quality (++) systematic review of cohort or case-control studies or High-quality (++) cohort or case-control studies with very low risk of bias or RCTs with not high (+) risk of bias, the results of which can be extended to the appropriate population.
WITH	Cohort or case-control or controlled trial without randomization with low risk of bias (+) whose results can be generalized to the appropriate population or RCTs with very low or low risk of bias (++ or +) whose results are not can be directly extended to the relevant population.
D	Description of a case series or uncontrolled study or expert opinion.

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 a previous general infection or infectious disease of any organ, and secondary is a complication of an infectious disease (general and local).

4. By prevalence process 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 severity;
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 - you should pay special attention to:
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, blood pressure, pulse rate and rhythm).

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 certain 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 in the brain;
· Electrocardiography - indirect signs of myocarditis, endocarditis;
X-ray of the 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 (leukocytosis of a neutrophilic nature with a stab shift is possible, an increase in ESR; anemia, thrombocytopenia are possible);
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 blood test - 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 squirrel);

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 antimicrobial preparations of isolated 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 of the paranasal sinuses (to exclude ENT pathology);
Computed tomography of the pyramids of the temporal bones.

Differential Diagnosis

Table 1. Differential diagnosis and rationale for additional studies.

Diagnosis	Rationale for differential diagnosis	Surveys	Diagnosis Exclusion Criteria
Hemorrhagic stroke	hemorrhagic stroke debuts with the development of cerebral and meningeal syndromes and may also be accompanied by a rise in body temperature.	computed tomography of the brain, examination of the fundus, consultation of a general practitioner, infectious disease specialist.	acute onset due to physical and / or emotional overstrain against the background of high blood pressure; the presence of a previous vascular history; a history of paroxysms of headache; The presence of signs of hemorrhage on CT scans; Angiopathy of retinal vessels, hyperemia; Confirmation by the therapist of arterial hypertension;
Ischemic stroke	ischemic stroke debuts with the development of cerebral and meningeal syndromes, followed by the development of focal symptoms	FAST algorithm, computed tomography	Predominance of focal neurological symptoms in meningeal syndrome;
Volumetric process of the brain (abscess, hemorrhage in a brain tumor)	the clinical picture of the volumetric process of the brain is characterized by the presence of a cerebral syndrome and symptoms of focal brain damage, as well as an increase in body temperature and the presence of symptoms of intoxication.	computed tomography of the brain, examination of the fundus, consultation of a neurosurgeon, consultation of a general practitioner, infectious disease specialist.	subacute development of cerebral syndrome, absence of infectious and epidemiological history; On CT scans, the presence of a volumetric formation of the brain; On the fundus - signs of intracranial hypertension, the phenomenon of congestive optic discs; exclusion of an acute infectious disease by an infectious disease specialist; the absence of a therapeutic disease that has a causal relationship with the condition of the patient; Confirmation of the presence of a volumetric formation of the brain by a neurosurgeon;
Septic cerebral vein thrombosis	septic cerebral vein thrombosis is characterized by the presence of meningeal, cerebral syndromes and symptoms of focal brain damage, as well as an increase in body temperature and the presence of symptoms of intoxication.	computed tomography of the brain with contrast, examination of the fundus, consultation of a neurosurgeon, infectious disease specialist, therapist.	acute onset and development of cerebral and focal neurological symptoms against the background of a general infectious syndrome / intoxication; Correspondence of focal neurological symptoms with the localization of the venous sinus; absence of signs of focal lesions of the substance of the brain on CT scans; On the fundus - signs of intracranial hypertension; exclusion of volumetric formation of the brain by a neurosurgeon; exclusion of an acute infectious disease by an infectious disease specialist; confirmation of the presence of a septic condition by the therapist;
Intoxication	Intoxication of the nervous system is characterized by the presence of a cerebral syndrome, meningism phenomena and symptoms of focal brain damage, as well as the presence of symptoms of general intoxication.
Migraine	typical pattern in the clinical picture pronounced cerebral syndrome	CT scan	absence of somatic disorders, general infectious and meningeal syndromes.

Table 2. Differential diagnosis of purulent and serous meningitis.

Main features	Purulent meningitis					Serous meningitis
	meningococcal	pneumococcus out	caused by H.influenzae	staphylococcal	colibacterial	enteroviral	mumps		tuberculous
Premorbid background	Not changed	Pneumonia, sinusitis, otitis, transferred SARS	Weakened children (rickets, malnutrition, frequent SARS, pneumonia and otitis media)	Purulent lesions of the skin, bones, internal organs, sepsis.	Often perinatal pathology, sepsis	Not changed	Not changed		Primary tuberculosis focus
The onset of the disease	sharpest	In younger children, subacute, in older children, acute, stormy	More often subacute	Subacute, rarely violent	Subacute	Acute	Acute		gradual, progressive
Body temperature height, duration	High (39-40C), 3-7 days	High (39-40C), 7-25 days	First high (39-40C), then subfebrile up to 4-6 weeks	High (38-39C), less often subfebrile, undulating	Subfebrile, rarely high, 15-40 days	Medium height (37.5-38.5C), 2-5 days	Medium height or high (37.5-39.5C), 3-7 days		Febrile, subfebrile
meningeal syndrome	Sharply expressed from the first hours of illness	Expressed, sometimes incomplete	Expressed, sometimes incomplete	Moderately pronounced	Weak or absent	Mild, dissociated, absent in 15-20%	Moderately expressed, dissociated,		On the 2nd week, moderately pronounced, then steadily increasing
Major clinical syndrome		Intoxication, encephalitic	Meningeal, intoxication	Septic	Intoxication, hydrocephalic	Hypertensive	Hypertensive		intoxication
Symptoms of CNS damage	In the early days of impaired consciousness, convulsions. Hearing impairment, hemisyndrome, ataxia	A picture of meningoencephalitis: from the first days, impaired consciousness, focal convulsions, paralysis, craniocerebral injury. Hydrocephalus.	Sometimes lesions of craniocerebral insufficiency, paresis	Epileptiform seizures, craniocerebral lesions, paresis	Seizures, strabismus, hemiparesis, hydrocephalus	Sometimes transient anisoreflexia Mild CFM	Sometimes damage to the facial and auditory nerve, ataxia, hyperkinesis		From the 2nd week convergent strabismus, convulsions, paralysis, stupor
Possible somatic disorders	Arthritis, myocarditis, with mixed forms - hemorrhagic rash	Pneumonia, otitis media, sinusitis	Tracheitis, bronchitis, rhinitis, pneumonia, arthritis, conjunctivitis, buccal cellulitis, osteomyelitis	Purulent foci of the skin, internal organs, sepsis	Enteritis, enterocolitis, sepsis	Herpetic sore throat, myalgia, exanthema, diarrhea	Parotitis, pancreatitis, orchitis		Tuberculosis of internal organs, skin, lymph nodes
Flow	Acute, sanitation of cerebrospinal fluid for 8-12 days	In older children, acute, in younger children - often protracted, sanitation of cerebrospinal fluid for 14-30 days	Undulating, sanitation of cerebrospinal fluid for 10-14 days, sometimes for 30-60 days	Prolonged, tendency to block the cerebrospinal fluid, abscess formation	Protracted, undulating, sanitation of cerebrospinal fluid on the 20-60th day	Acute, sanitation of cerebrospinal fluid for 7-14 days	Acute, sanitation of cerebrospinal fluid for 15-21 days		Acute, with treatment - subacute, recurrent
blood picture		Leukocytosis, neutrophilia with a shift of the leukocyte formula to the left, increased ESR	Anemia, leukocytosis, neutrophilia, increased ESR	Leukocytosis, neutrophilia, increased ESR	High leukocytosis, (20-40*109) neutrophilia, high ESR		Normal, sometimes slight leukocytosis or leukopenia, moderately elevated ESR		Moderate leukocytosis, lymphocytosis, moderately elevated ESR
The nature of the liquor:
Transparency	Cloudy, whitish	Cloudy, greenish	Cloudy, greenish	Cloudy, yellowish	Cloudy, greenish	Transparent		Transparent	Transparent, xanthochromic, a delicate film falls out when standing
Cytosis, *109 /l	Neutrophilic, 0.1-1.0	Neutrophilic, 0.01-10.0	Neutrophilic, 0.2-13.0	Neutrophilic, 1.2-1.5	Neutrophilic, 0.1-1.0	First mixed, then lymphocytic, 0.02-1.0		First mixed, then lymphocytic, 0.1-0.5, rarely 2.0 and higher	Lymphocytic, mixed, 0.2-0.1
Protein content, g/l	0,6-4,0	0,9-8,0	0,3-1,5	0,6-8,0	0,5-20	0,066-0,33		0,33-1,0	1,0-9,0

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Treatment

Drugs (active substances) used in the treatment

Aztreonam

Amikacin (Amikacin)

Ampicillin (Ampicillin)

Amphotericin B (Amphotericin B)

Acetylsalicylic acid (Acetylsalicylic acid)

Benzylpenicillin (Benzylpenicillin)

Vancomycin (Vancomycin)

Gentamicin (Gentamicin)

Hydroxyethyl starch (Hydroxyethyl starch)

Dexamethasone (Dexamethasone)

Dextrose (Dextrose)

Diazepam (Diazepam)

Ibuprofen (Ibuprofen)

Potassium chloride (Potassium chloride)

Calcium chloride (Calcium chloride)

Ketoprofen (Ketoprofen)

Clindamycin (Clindamycin)

Linezolid (Linezolid)

Lornoxicam (Lornoxicam)

Mannitol (Mannitol)

Meloxicam (Meloxicam)

Meropenem (Meropenem)

Metoclopramide (Metoclopramide)

Metronidazole (Metronidazole)

Sodium bicarbonate (Sodium hydrocarbonate)

Sodium chloride (Sodium chloride)

Oxacillin (Oxacillin)

Paracetamol (Paracetamol)

Prednisolone (Prednisolone)

Rifampicin (Rifampicin)

Sulfamethoxazole (Sulphamethoxazole)

Tobramycin (Tobramycin)

Trimethoprim (Trimethoprim)

Fluconazole (Fluconazole)

Fosfomycin (Fosfomycin)

Furosemide (Furosemide)

Chloramphenicol (Chloramphenicol)

Chloropyramine (Chloropyramine)

Cefepime (Cefepime)

Cefotaxime (Cefotaxime)

Ceftazidime (Ceftazidime)

Ceftriaxone (Ceftriaxone)

Ciprofloxacin (Ciprofloxacin)

Treatment (ambulatory)

TREATMENT AT OUTPATIENT LEVEL

Treatment tactics: It 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 into the respiratory tract (turning 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 Essential Medicines

Preparations	single dose	Multiplicity of introduction	UD
paracetamol	0.2 and 0.5 g each	for adults 500 - 1000 mg; for children aged 6-12 years 250-500 mg, 1-5 years 120-250 mg, 3 months to 1 year 60-120 mg, up to 3 months 10 mg/kg orally	A
metoclopramide	2.0 (10 mg)	adults: intramuscularly or intravenously slowly (over at least 3 minutes) 10 mg. children 1 - 18 years old, intramuscularly or intravenously slowly (for at least 3 minutes) 100 - 150 mcg / kg (max. 10 mg).	WITH
prednisolone	30 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).	V
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 usually 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.	WITH

List of additional medicines

Algorithm of actions in emergency situations:

Table - 3. Algorithm of actions in emergency situations

Syndrome	A drug	Dose and frequency for adults	Dose and frequency for children
Convulsive	Diazepam	10 - 20 mg 2.0 once.	Children from 30 days to 5 years - IV (slowly) 0.2 - 0.5 mg every 2 - 5 minutes up to a maximum dose of 5 mg, from 5 years and older 1 mg every 2 - 5 minutes up to a maximum dose of 10 mg ; if necessary, the treatment can be repeated after 2-4 hours.
psychomotor agitation	Diazepam	10 - 20 mg - 2.0 once.	Children 30 days to 5 years IV (slow) 0.2-0.5 mg every 2-5 minutes up to a maximum dose of 5 mg, 5 years and older 1 mg every 2-5 minutes up to a maximum dose of 10 mg ; if necessary, the treatment can be repeated after 2-4 hours.
dyspeptic	Metoclopramide 5.27 mg	Adults and teenagers over 14 years of age: 3 - 4 times a day, 10 mg of metoclopramide (1 ampoule) intravenously or intramuscularly.	Children 3-14 years old: the maximum daily dose is 0.5 mg of metoclopramide per 1 kg of body weight, the therapeutic dose is 0.1 mg of metoclopramide per 1 kg of body weight.
cephalgic	Ketoprofen Lornoxicam	100 mg, 2 times a day
hyperthermia	Paracetamol Acetylsalicylic acid	500-1000 mg orally	Contraindicated in children under 15 years of age
Infectious-toxic shock	Prednisolone / Dexamethasone	Doses - prednisolone 10 - 15 mg / kg of body weight, simultaneous administration of up to 120 mg of prednisolone is possible.	Prednisolone or dexamethasone 5-10 mg/kg (based on prednisolone).

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 of premorbid background - somatic disorders (otitis media, sinusitis, pneumonia, sepsis, etc.);
Sanitation of chronic foci of infection.

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

maintaining life-supporting functions stable with the transfer of the patient to the stage of emergency care for transportation 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 fluids, placing a 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 the clinical form and 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 hospitalized in the intensive care unit or intensive care unit. 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.

Age of patients	Most likely pathogen	Recommended Antibiotic
0 to 4 weeks	Str. agalacticae E.c oli K. pneumoniae St. aureus L.monocytogenes	Ampicillin + cefotaxime ± gentamicin or amikacin
4 weeks to 3 months	H. influenzae S. pneumoniae N. meningitidis	Ampicillin + 3rd generation cephalosporin (cefotaxime, ceftriaxone)
From 4 months to 18 years	N. meningitidі s S.pneumoniae H. influenzae	3rd generation cephalosporin (cefotaxime, ceftriaxone) or benzylpenicillin
With head trauma, after neurosurgical operations, cerebrospinal shunting, nosocomial, otogenic meningitis	St. a ureus Str. R neumoniae Enterococcus Pseudomonas aeruginosa	Vancomycin + ceftazidime

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

Pathogen	1st line antibiotic	Reserve antibiotic
Str.pneumoniae*	When isolating penicillin-sensitive strains: Benzylpenicillin; Ampicillin In the absence of data on sensitivity or suspected resistance to penicillin: Vancomycin + cefotaxime or ceftriaxone	Cefotaxime Ceftriaxone Chloramphenicol (levomycetin succinate) cefepime Meropenem Linezolid
H. influenzae	Ceftriaxone Cefotaxime	cefepime Meropenem Ampicillin
N. meningitides	Benzylpenicillin Ceftriaxone Cefotaxime	Chloramphenicol (levomycetin succinate) Ampicillin
St. aureus	Oxacillin	Vancomycin, Rifampicin Linezolid
St. epidermidis	Vancomycin + Rifampicin	Linezolid
L. monocytogenes		Meropenem
Str. agalacticae	Ampicillin or benzylpenicillin + amikacin	Ceftriaxone Cefotaxime Vancomycin
Enterobacteriaceae (Salmonella, Proteus, Klebsiella	ceftriaxone or cefotaxime + amikacin	Ampicillin Meropenem [Sulfamethoxazole, Trimethoprim]
Pseudomonas aeruginosa, Acinetobacter spp.	Ceftazidime or cefepime + gentamicin or amikacin	Ciprofloxacin + gentamicin or amikacin
candida albicans	Fluconazole	Amphotericin B
Enterococcus (faecalis, faecium)	Ampicillin + gentamicin or amikacin	Vancomycin + gentamicin or amikacin Linezolid

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

A drug	Daily doses per kg of body weight depending on the age of the child
	0 - 7 days	8 - 28 days	Older than 1 month
Benzylpenicillin	100 thousand units	200 thousand units	250 - 300 thousand units
Ampicillin	100 - 150 mg	150 - 200 mg	200 - 300 mg
Oxacillin	40 - 80 mg	40 - 80 mg	120 - 160 mg
Cefotaxime	100 - 150 mg	150 - 200 mg	200 mg
Ceftriaxone	-	-	100 mg
Ceftazidime	50 mg	50-100 mg	100 mg
cefepime	-	-	150 mg
Amikacin	15 - 20 mg	20 - 30 mg	20 - 30 mg
Gentamicin	5 mg	7.5 mg	7.5 mg
Chloramphenicol (levomycetin succinate)	50 mg	50 mg	100 mg
Vancomycin	20 mg	30 mg	50 - 60 mg
Meropenem	-	120 mg	120 mg
Netilmicin	6 mg	7.5 - 9 mg	7.5 mg
Fluconazole	10 - 12 mg	10 - 12 mg	10 - 12 mg
Amphotericin B	Initial dose 0.25 - 0.5 mg maintenance dose 0.125 - 0.25 mg	Initial dose 0.25 - 0.5 mg maintenance dose 0.125 - 0.25 mg	1 mg
Linezolid	-	-	30 mg
Rifampicin	10 mg	10 mg	20 mg
Ciprofloxacin	-	10 mg	15-20 mg
[Sulfamethoxazole, Trimethoprim]	-	-	30 mg**

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

Table - 7. Multiplicity of antibiotic administration per day

A drug	newborns	Children over 1 month of age
Benzylpenicillin	2 - 4	6
Ampicillin	4	6
Cefotaxime	4	4 - 6
Ceftriaxone	-	2
Ceftazidime	2	2-3
cefepime	-	3
Amikacin	2	3
Gentamicin	2	3
Chloramphenicol (levomycetin succinate)	2	4
Vancomycin	2-3	2-3
Meropenem	3	3
Netilmicin	2	3
Fluconazole	1	1
Amphotericin B	1	1
Linezolid	3	3
Rifampicin	2	2
Ciprofloxacin	2	3 - 4
[Sulfamethoxazole, Trimethoprim]	-	2 - 4

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

Pathogen	Recommended duration of antibiotic therapy in days
N. meningitides	7
H. influenzae	10
Str. pneumoniae	10 - 14
Str. agalacticae	14
L.monocytogenes	21
Enterobacteriaceae	21
St. aureus, St. epidermidis Enterococcus	28
Pseudomonas aeruginosa	28

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. 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 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 threat or 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 OHM.

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 oxygen concentrations - oxygen partial pressure (PaO2) 60 mm Hg or cyanosis at an oxygen concentration (FiO2) 0.6, an increase in lung shunting 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

Hospitalization

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.

Pathogen	First line remedies	Second line drugs
Gram-positive bacteria
St. pneumonia
penicillin sensitive (MIC≤ 0.1 µg/ml)	Benzylpenicillin	Cefotaxime or ceftriaxone
penicillin intermediate (MIC=0.1-1.0 µg/ml)	Cefotaxime or ceftriaxone
penicillin resistant (MIC≥ 0.5 µg/ml)	Cefotaxime or ceftriaxone	Cefepime or meropenem, rifampicin
cephaloresistant (MIC ≥ 0.5 µg/ml)	Cefotaxime or ceftriaxone + vancomycin	Meropenem, rifampicin
Listera monocytogenes	Ampicillin + gentamicin	Vancomycin + gentamicin
S. agalactiae	Benzylpenicillin + gentamicin	Ampicillin + gentamicin
Gram-negative bacteria
N.meningitis
- penicillin sensitive (MIC≤ 0.1 µg/ml)	Benzylpenicillin	Cefotaxime or ceftriaxone
penicillin intermediate (MIC=0.1-1.0 µg/ml)	Benzylpenicillin	Cefotaxime, ceftriaxone, vancomycin
β-Lactamase positive	Vancomycin
H.influenzae
ampicillin-sensitive	Ampicillin	Cefotaxime, ceftriaxone, chloramphenicol
ampicillin-resistant	Cefotaxime or ceftriaxone	Chloramphenicol
Enterobacteriaceae	Cefotaxime or ceftriaxone	cefepime, meropenem
P.aeruginosa	Ceftadizim + gentamicin	cefepime, meropenem
Salmonella spp.	Chloramphenicol (Levomycitin Succinate) Gentamicin	Ampicillin
C.albicans	Fluconazole	Fluconazole + amphotericin B

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 HMO, 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:

Preparations	Level of Evidence
Benzylpenicillin	A
Oxacillin	A
Amikacin	A
Tobramycin	A
Ampicillin	A
Cefotaxime	A
cefepime
Ceftriaxone	A
Ceftazidime	A
Vancomycin	A
Fosfomycin	V
Meropenem	A
Linezolid	WITH
Clindamycin	V
Ciprofloxacin	V
Metronidazole	V
Trimethoprim + sulfamethoxazole	WITH
Rifampicin	WITH
Aztreonam	A
Amphoteracin B	WITH
Gentamicin	A
Tiloron	A
Flucanazole	V
Dexamethosone	V
Mannitol	V
Furosemide	V
Diazepam	WITH
Chloramphenicol	WITH
Paracetamol	A
Ibuprofen	A
sodium chloride	WITH
metoclopramide	WITH
Meloxicam	WITH
Chloropyramine	WITH

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

N p/n	Frequency of mandatory follow-up examinations by an infectious disease specialist (pediatrician)	Observation duration	Indications and frequency of consultations of medical specialists
1	2	3	4
1	・After discharge from the hospital. Further - according to indications.	3-5 years depending on the severity and persistence of neurological symptoms. In chronic course - before transfer to an adult network.	・Neurologist 1st year - after 1 month, then 1 time in 3 months; 2-3-years - 1 time in 6 months, 4-5 years - 1 time per year. According to indications - more often. Orthopedist, ophthalmologist - 1 month after discharge, then - according to indications

N p/n	List and frequency of laboratory, radiological and other special studies	Therapeutic and preventive measures.	Clinical criteria for the effectiveness of clinical examination	The procedure for admission of those who have been ill to work, to preschool educational institutions, boarding schools, summer recreational and closed institutions.
1	2	3	4	5
	MRI of the brain and / or spinal cord 1.5-2 months after the acute period (if there are changes in the acute period) · Brain evoked potentials - after 3 months, 12 months. further - according to indications. ENMG (only for myelitis and encephalomyelitis) - on the 60th day, after 12 months, then - according to indications. EEG, duplex scanning - after 3 months, 12 months, then - according to indications.	Courses of drug therapy 2-4 times a year, depending on the severity of the disease. · Courses of physiotherapy, massage, exercise therapy 2-4 times a year, depending on the severity of the disease. Spa treatment at least once a year (but not earlier than 3 months after the acute period).	absence of a chronic course; absence of relapses, and in the chronic course of exacerbations of the disease; improvement (or full recovery) motor deficits, cognitive deficits and other symptoms	Those who have been ill are allowed without additional laboratory examination in case of sporadic encephalitis. In case of epidemics and in cases of outbreaks in individual groups, the decision on the examination is made by the infectious disease specialist.

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 JM, Amaya-Villar R., Rincón-Ferrari MD, Leal-Noval SR, Garnacho-Montero J., Llanos-Rodríguez AC, 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

VCHG	-	intracranial hypertension
OGM	-	cerebral edema
EEG	-	electroencephalography
SARIT	-	department of anesthesiology and resuscitation, intensive care
ADG	-	antidiuretic hormone
NSAIDs	-	non-steroidal anti-inflammatory drugs
IPC	-	minimum inhibitory concentration
PV	-	prothrombin time
INR	-	international normalized ratio
CNS	-	central nervous system
ITSH	-	infectious-toxic shock
BSF UD	- -	biosocial functions level of evidence

List of protocol developers with qualification data:

FULL NAME.	Position	Signature
Zhusupova Alma Seidualievna	doctor of medical sciences, professor, neuropathologist of the highest category, JSC "Astana Medical University" head of the department of neuropathology with a course of psychiatry and narcology, chief freelance neuropathologist of the Ministry of Health and Social Development of the Republic of Kazakhstan, chairman of the ALE "Association of Neurologists of the Republic of Kazakhstan".
Dairbayeva Leyla Oralgazievna	executive director, NGO of the Kazakh National League against epilepsy, assistant of the department of neurology, doctoral student of the Higher School of Public Health.
Elubaeva Altynai Mukashkyzy	Candidate of Medical Sciences, neuropathologist of the highest category, JSC "Astana Medical University" Associate Professor of the Department of Neuropathology with a course of psychiatry and narcology, director of "Center for Neurology and Epileptology" LLP, "Association of Pediatric Neurologists of the Republic of Kazakhstan".
Kaishibaeva Gulnaz Smagulovna	Candidate of Medical Sciences, JSC "Kazakh Medical University of Continuing Education", Head of the Department of Neurology, certificate "adult neurologist", member of the World Association of Neurologists, member of the Association of Neurologists of the Republic of Kazakhstan, member of the League of Neurologists of the Republic of Kazakhstan.
Zharkinbekova Nazira Asanovna	candidate of medical sciences, neuropathologist of the highest category South Kazakhstan Regional Clinical Hospital, head of the neurological department.
Dzhumakhaeva Aliya Serikovna	Candidate of Medical Sciences, Head of the Neurological Department of City Hospital No. 2 of Astana, neuropathologist of the highest category, member of the ALE "Association of Neurologists of the Republic of Kazakhstan".
Zhumagulova Kulparam Gabibulovna	Candidate of Medical Sciences, JSC "Kazakh Medical University of Continuing Education", Associate Professor of the Department of Neurology, member of the "World Association of Neurologists", member of the "Association of Neurologists of the Republic of Kazakhstan", member of the League of Neurologists of the Republic of Kazakhstan.
Kenzhegulova Raushan Bazargalievna	Candidate of Medical Sciences, JSC "National Scientific Center for Motherhood and Childhood", neurologist - pediatric neurophysiologist, doctor of the highest category, member of the "Association of Pediatric Neurologists of the Republic of Kazakhstan".
Lepesova Marzhan Makhmutovna	Doctor of Medical Sciences, Professor, JSC "Kazakh Medical University of Continuing Education", Head of the Department of Pediatric Neurology, President of the Association of Pediatric Neurologists of the Republic of Kazakhstan, full member of the International, European, Asian-Ocean, Baltic Association of Pediatric Neurologists.
Ibatova Syrdankyz Sultankhanovna	Candidate of Medical Sciences, National Scientific Center of Neurosurgery JSC, neurologist, member of the Association of Pediatric Neurologists of the Republic of Kazakhstan, member of the Association of Neurophysiologists of the Republic of Kazakhstan, member of the Association of Neurosurgeons of the Republic of Kazakhstan.
Tuleutaeva Raykhan Yesenzhanovna	Candidate of Medical Sciences, Head of the Department of Pharmacology and Evidence-Based Medicine, State Medical University. Mr. Semey, a member of the "Association of Physicians of Therapeutic Profile".

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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All-Russian public organization

Association of General Practitioners (Family Doctors) of the Russian Federation
PROJECT

DIAGNOSIS AND PRIMARY CARE

FOR VIRAL MENINGITIS

(MENINGOENCEPHALITIS)

IN GENERAL MEDICAL PRACTICE

2015

Chairman: Denisov Igor Nikolaevich - Doctor of Medical Sciences, Academician of the Russian Academy of Medical Sciences, Professor

Working group members:

Zaika Galina Efimovna– Candidate of Medical Sciences, Associate Professor, Head of the Department of General Medical Practice (Family Doctor) of the Novokuznetsk State Institute for Postgraduate Medical Education of the Ministry of Health of Russia, [email protected]

Postnikova Ekaterina Ivanovna – Candidate of Medical Sciences, Associate Professor of the Department of General Medical Practice (Family Doctor) of the Novokuznetsk State Institute for Postgraduate Medical Education of the Ministry of Health of Russia, kafedraovpngiuv@ rambler. en

Drobinina Natalya Yurievna – assistant of the department of general medical practice (family doctor) of the Novokuznetsk State Institute for Postgraduate Medical Education of the Ministry of Health of Russia

Tarasko Andrey Dmitrievich – Doctor of Medical Sciences, Professor, Professor of the Department of General Medical Practice (Family Doctor) SBEE DPO "Novokuznetsk State Institute for Postgraduate Medical Education" of the Ministry of Health of Russia,

Expert Council:

MD, prof. Abdullaev A.A. (Makhachkala); PhD, prof. Agafonov B.V. (Moscow); Aniskova I.V. (Murmansk); Doctor of Medical Sciences, Prof. Artemyeva E.G. (Cheboksary); MD, prof. Bayda A.P. (Stavropol); MD, prof. Bolotnova T.V. (Tyumen); MD prof. Budnevsky A.V. (Voronezh); MD, prof. Burlachuk V.T. (Voronezh); MD, prof. Grigorovich M.S. (Kirov); MD, prof. Drobinina N.Yu. (Novokuznetsk); Candidate of Medical Sciences, Assoc. Zaika G.E. (Novokuznetsk); Ph.D. Zaugolnikova T.V. (Moscow); MD, prof. Zolotarev Yu.V. (Moscow); MD, prof. Kalev O.F. (Chelyabinsk); MD, prof. Karapetyan T.A. (Petrozavodsk); MD, prof. Kolbasnikov S.V. (Tver); MD, prof. Kuznetsova O.Yu. (Saint Petersburg); MD, prof. Kupaev V.I. (Samara); MD, prof. Lesnyak O.M. (Yekaterinburg); PhD Malenkova V.Yu. (Cheboksary); MD, prof. Nechaeva G.I. (Omsk); MD, prof. Popov V.V. (Arkhangelsk); Reutsky A.A. (Kaliningrad); MD, prof. Sigitov O.N. (Kazan); MD, prof. Sineglazova A.V. (Chelyabinsk); MD, prof. Khovaeva Ya.B. (Permian); MD, prof. Shavkuta G.V. (Rostov-on-Don); PhD Shevtsova N.N. (Moscow).

Content

1. 
   Methodology
2. 
   Definition
3. 
   Codes about ICD-10
4. 
   Epidemiology
5. 
   Etiology
6. 
   Classification
7. 
   Principles of diagnosis of the disease in adults and children
8. 
   Criteria for early diagnosis on an outpatient basis
9. 
   Indications for hospitalization
10. 
    Principles of treatment of viral meningitis
11. 
    Assistance at the stage of primary health care
12. 
    Management of patients after hospital treatment
13. 
    Prevention
14. 
    Forecast
15. 
    Bibliography
16. 
    Applications

List of abbreviations

HSV - herpes simplex virus

HSV-1 - herpes simplex virus type 1

HSV-2 - herpes simplex virus type 2

EBV - Epstein-Barr virus

TBE - tick-borne encephalitis

ME-meningoencephalitis

CMV - cytomegalovirus

1. 
   Methodological background

Methods used to formulate evidence:

expert consensus.

Rating systems for assessing the classification (quality) of evidence and the level (strength) of recommendations:
Table 2(a) Evidence classification scheme for diagnostic measurements. (b) Evidence classification scheme for rating recommendations for diagnostic measurements

(a) ClassI A prospective study in a wide range of individuals with a suspected condition using well-standardized case-finding where the test was applied with blind evaluation and run by evaluation of appropriate diagnostic precision tests

ClassII A prospective study of a narrow range of individuals with suspected conditions using retrospective studies of good design of a wide range of individuals with established conditions (good standard) versus a wide range of controls where tests are blinded and driven by appropriate diagnostic rigorous tests.

ClassIII Evidence provided by a retrospective study where either individuals with established conditions or controls were narrow-spectrum and where tests are blinded

ClassIV Any design where tests were not used in blinded evaluation OR evidence provided only by expert opinion or descriptive case series (no controls)

(b) Level A rating (set as helpful/predictive or predictive not useful) requires at least one Class I conclusive study or at least two Class II conclusive studies matched

Level B rating (set as likely helpful/predictive or not helpful/predictive) requires at least one conclusive Class II study or preponderance of evidence from Class III studies

Level C rating (set as possibly helpful/predictive or not helpful/predictive) require at least two evidence-based Class III studies

Table 1(a) Evidence Classification Scheme for Therapeutic Intervention. (b) Evidence classification scheme for rating recommendations for therapeutic intervention

(a) ClassI Adequately strong prospective randomized controlled clinical trial with masked outcome assessment in representative populations. The following is required:

(a) Hidden randomization

(b) Primary outcome(s) clearly defined(s)

(c) Exclusions/inclusions are clearly defined

(d) Adequate calculation of dropouts and overlaps with numbers low enough to have minimal potential for error

(e) appropriate baseline characteristics are presented and generally equivalent across the treatment group, or there is an appropriate statistical adjustment to differentiate

ClassII Prospective cohort studies of selected groups with implicit outcome measures that meet Randomized Controlled Trials labeled a-e above in a representative population missing one criterion from a-e

ClassIII All other controlled trials (including well-defined controls with common history) in a representative population where outcome measures are independent of patient treatment

ClassIV Evidence from uncontrolled studies, case series, case reports, or expert opinion

(b) Level A rating (set as effective, ineffective or harmful) requires at least one evidence from a Class I study or at least two consensus evidence from a Class II study

Level B rating (probably effective, ineffective, harmful) requires at least one evidence from a Class II study or overwhelming evidence from Class III studies

Level C(possibly effective, ineffective or harmful) rating requires at least two evidence from a class III study

Good practice indicators ( Good practice points – GPPs)

2. Definition

Viral meningitis is an acute inflammatory process of the meninges. Most viral meningitis can occur in the form of meningoencephalitis (with simultaneous inflammation in the brain parenchyma) or meningoencephalomyelitis. The structure of the nervous system causes the associated inflammation of the meninges involved in encephalitis, and therefore symptoms that reflect meningitis invariably accompany encephalitis. Moreover, in the relevant world medical literature (reviews, guidelines, textbooks), the term viral meningoencephalitis (ME) is often used to refer to a viral infectious process for both the brain and spinal cord, and the meninges. Due to the viral nature, any of the listed forms is diffuse.

3. Codes according to ICD-10

A87 Viral meningitis

A87.0 Enteroviral meningitis (G02.0)

A87.1 Adenovirus meningitis (G02.0)

A87.2 Lymphocytic choriomeningitis

A87.8 Other viral meningitis

A87.9 Viral meningitis, unspecified

In addition to enteroviral and adenoviral meningitis, G02.0 includes a range of viral meningitis - "Meningitis in viral diseases classified elsewhere". This group of meningitis is very large; some of them, the most significant in wide practice, are given below:

G00.0 Influenza meningitis

A80 Acute poliomyelitis

A.84 Tick-borne encephalitis

B00.3 Herpesvirus meningitis (B00.4 Herpesvirus encephalitis)

B02.1 Herpes zoster meningitis (B02.0 Herpes zoster encephalitis)

B05.1 Measles meningitis (B05.0 Measles virus encephalitis)

B26.1 Mumps meningitis (B26.2 Mumps virus encephalitis)

However, with rare exceptions (primary viral meningitis is lymphocytic choriomeningitis), in most of these diseases, damage to the central nervous system can occur both in the form of meningitis and in the form of meningoencephalitis (and encephalitis, which is not discussed in these clinical guidelines). That is, the given coding of viral meningitis is suitable only for a specified syndrome of damage to the central nervous system. In the presence of a combined lesion, both codes should be indicated as the final diagnosis: both for meningitis and for encephalitis (the latter is given in brackets in the list above).

In addition, during the initial examination of the patient, followed by a referral to a hospital if meningitis is suspected, it is not always possible to distinguish meningitis from meningoencephalitis.

1. 
   Etiology

Viral meningitis (meningoencephalitis) is a disease with a pronounced polyetiology. At the same time, in the group of pathogens there are viruses for which meningitis is most typical, for example:

• 
  Enteroviruses
• 
  Adenoviruses
• 
  Virus of the arenavirus family (Arenaviridae) that causes lymphocytic choriomeningitis

In addition, a large number of viruses cause not only meningitis, but also encephalitis, as well as meningoencephalitis. However, these neuroinfections often occur as meningitis rather than encephalitis. The main pathogens with the properties listed above, common in the Russian Federation are:

• 
  Polio viruses
• 
  Far Eastern (taiga) encephalitis virus
• 
  Herpes simplex viruses
• 
  Shingles virus (herpes zoster virus)
• 
  Human herpes virus type 6
• 
  Epstein-Barr virus
• 
  Cytomegalovirus
• 
  mumps virus
• 
  measles virus
• 
  rubella virus
• 
  flu virus
• 
  Hemorrhagic fever viruses
• 
  West Nile virus
• 
  JC virus* that causes PML (PML - progressive multifocal leukoencephalopathy).

*JC virus is a member of the polyomavirus family, formerly considered an opportunistic virus that infects HIV-infected people in the AIDS stage, but has now been shown to affect individuals with other forms of immunosuppression and also, apparently, occasionally, immunocompetent individuals. Recently, subacute developing PML has been reported following treatment with monoclonal antibodies (rituximab, natalizumab, and efalizumab). The virus has a large number of types, one of them - JC-M causes meningitis, difficult to distinguish from other viral meningitis.

1. 
   Epidemiology

Susceptibility

Herpes simplex virus type I (HSV-1), varicella-zoster virus (VZV), Epstein-Barr virus (EBV), cytomegalovirus, mumps, measles, rubella, adenoviruses, enteroviruses, West Nile virus cause most cases of viral ME in both immunocompetent and immunocompromised patients. Recently, the susceptibility of immunocompetent individuals to the JC virus, which was previously considered exclusively the causative agent of one of the opportunistic infections in HIV-infected patients in the stage of severe immunodeficiency, has been proven.

Transmission routes .

As sources or carriers of infection in viral meningitis (meningoencephalitis) are persons suffering from acute infectious diseases (influenza, other acute respiratory diseases, measles, rubella, chicken pox), carriers of persistent viruses, various insects, wild and domestic animals, including including house mice, etc.

A large number of pathogens that cause viral meningitis (ME) and a variety of sources and vectors of infection determine the variety of pathogen transmission routes. Airborne transmission predominates (primarily for meningitis, which complicates childhood airborne infections and respiratory viral infections, including influenza), but waterborne, alimentary, and transmissible transmission routes are not uncommon.

1. 
   Classification

Classification of viral meningitis (or meningoencephalitis), as such, does not exist. Given the numerous classifications of meningitis, it should only be mentioned that viral meningitis belongs to the category of serous. However, the phrases “viral meningitis” and “serous meningitis” are not synonymous, since, for example, tuberculous meningitis (primary bacterial meningitis) is serous in the nature of CSF changes, and there is a group of serous meningitis (ME) that accompanies (or complicates) a number of diseases bacterial nature (for example, typhus, anicteric leptospirosis, diseases from the group of yersiniosis, etc.). A more correct synonym for "viral meningitis" may be "aseptic meningitis" - a term indicating the infectious, but not bacterial nature of the disease.

Of all the classifications proposed for meningitis, for viral meningitis it is most appropriate to use a classification according to the severity of the disease:

1. 
   Light form
2. 
   Medium
3. 
   heavy

However, at the primary, outpatient stage of the diagnosis of viral meningitis (meningoencephalitis), it is not advisable to finally differentiate the disease according to severity. At the same time, the severity of the disease, established during inpatient treatment, should be taken into account at the stage of rehabilitation treatment after the patient is discharged from the hospital.
7. Principles of diagnosis of the disease in adults and children

The diagnosis of viral meningoencephalitis should be established based on the patient's complaint, medical history, clinical examination, subsequent lumbar puncture, CSF protein and glucose testing, cytosis, and identification of the pathogen by an increase in polymerase chain reaction ( recommendation level A) and serological reaction ( recommendation level B). Difficulties occasionally encountered in establishing the diagnosis of meningoencephalitis and encephalitis can be alleviated by neuroimaging, preferably MRI, ( recommendation level B). Diagnostic lumbar puncture may follow neuroimaging when available immediately, but if it cannot be done immediately, lumbar puncture may be delayed only in unusual circumstances where there is a contraindication for lumbar puncture, and MRI can confirm contraindications and recognize their character. Brain biopsy should be reserved only for unusual, exceptionally severe, diagnostically difficult cases.

7.1. Clinical manifestations, significant conditions and personal information

The diagnosis of viral meningitis (meningoencephalitis or encephalitis) (hereinafter, as a nosological specification - meningoencephalitis - ME) is suspected in the context of a febrile illness accompanied by intense headache. If the disease occurs with simultaneous or isolated damage to the substance of the brain (viral meningoencephalitis or viral encephalitis), it is accompanied by so-called general cerebral symptoms: varying degrees of impaired consciousness and signs of cerebral dysfunction (for example, cognitive and behavioral disorders, focal neurological symptoms and convulsions) . After ME is suspected, the clinical approach should be a thorough history taking and a thorough general and neurological examination.

Anamnesis

History is essential for the evaluation of patients with suspected viral ME. If an adult patient is unconscious (agitated or disoriented) or ME is suspected in a neonate, infant, or child, it is important to obtain substantial information from accompanying persons (parents, caregivers, relatives, etc.). The clinician evaluating the patient's environment should take into account the importance of geographic residence (may be relevant for identifying possible pathogens that are endemic or prevalent in certain geographic regions), recent travel. Seasonal spread may be important for other pathogens such as enteroviruses, tick-borne encephalitis virus, and for making a differential diagnosis (eg, with leptopyrosis meningitis, meningoencephalitis caused by bacteria of the genus Yersinia), a vaccine history to rule out varicella, mumps, measles, and rubella ME. Contact with animals, farmed and wild for certain occupations, sometimes indicates a specific cause, since animals serve as a reservoir for arbovirus infections, insect bites or a history of animal bites can be a possible cause of tick-borne encephalitis, West Nile fever, or rabies. Information about contact with patients suffering from any anthroponotic viral diseases that may be accompanied by ME is important.

The characteristic features of the disease before the appearance of neurological signs can help in assessing the etiology, for example, a two-phase course is typical for enterovirus infection, tick-borne encephalitis, for lymphocytic choriomeningitis; tendency to bleeding - for hemorrhagic fevers), the presence of characteristic rashes - for measles, rubella, chickenpox ME. The age of the patient is of great importance for etiology in terms of epidemiological prerequisites: while, for example, adults are more prone to tick-borne (taiga) encephalitis, children and adolescents who have not been vaccinated or who have lost post-vaccination immunity are more prone to ME in childhood infections; for young children, infants and, especially, newborns, ME is typical, caused by viruses of the herpes family: herpes simplex virus, cytomegalovirus and Epstein-Barr virus.

General study

A viral infection of the nervous system is almost always part of a generalized systemic infectious disease. Thus, other organs may be involved before or simultaneously with CNS manifestations, and appropriate information must be obtained from both the history and physical examination. The presence of a general infectious syndrome is mandatory: high fever (often - hyperthermia), malaise, headache; chills, pain in muscles and joints, etc. are possible. Skin rashes often accompany viral infections, parotitis can be associated with the mumps virus, gastrointestinal symptoms - with enterovirus disease. Signs from the upper respiratory tract may accompany infection with influenza virus, measles and rubella virus, herpesvirus-1 encephalitis, less often other viral meningitis (lymphocytic choriomeningitis, meningitis caused by West Nile fever virus, etc.).

Neurological examination

Neurological signs of meningitis include:

• 
  signs of irritation of the meninges (on an outpatient basis, it is sufficient to identify stiff neck, Kernig's symptom, upper, middle and lower Brudzinsky symptoms);
• 
  general cerebral symptoms: sleep and mood disturbances, irritability or lethargy and adynamia, initial or pronounced signs of impaired consciousness, up to a coma.
• 
  signs of increased intracranial pressure: a sharp headache, repeated vomiting and pain in the eyeballs (especially common in lymphocytic choriomeningitis due to damage to the vascular plexuses of the brain and severe CSF hyperproduction).
• 
  focal symptoms of CNS damage: signs of involvement of cranial nerves, especially defiantly damage to the oculomotor and facial nerves; violations of coordination tests, asymmetry of muscle tone, tendon and periosteal reflexes, paresis, etc.
• 
  behavioral, cognitive disorders (in older children, adolescents and adults), reflect impaired brain function.

Focal and behavioral disturbances can be either signs of meningoencephalitis or severe meningitis, in which case they are usually transient. However, in the primary study, such differentiation is difficult. In meningitis, seizures are more common in infants and/or may have the character of febrile seizures. Additional features may include autonomic and hypothalamic disorders, diabetes insipidus, and syndrome of inappropriate secretion of antidiuretic hormone.

The above symptoms and signs (including their dynamic assessment) are only relevant for the diagnosis and differentiation of meningitis and meningoencephalitis, but are an unreliable diagnostic tool for identifying the causative virus. Likewise, the severity and dynamics of the clinical signs of meningitis (ME) depend on the host organism and other factors, such as, for example, immune status. The very young and the very old have the most extensive and serious signs of the disease, usually in the form of meningoencephalitis or encephalitis. The diseases also have a worse prognosis and more serious consequences compared with adolescents and adults of young and adulthood. But the age of the patient can only serve as a limited guide to pathogen identification.