And antiviral agents. If the disease becomes severe, resuscitation procedures may be required.

Can meningitis be cured or not? Obviously yes. Next, let's look at how to treat meningitis.

What to do if detected?

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 may 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 needs to be taken to the vascular center, where he will undergo a CT and MRI.

Which doctor treats meningitis? If no violations are detected, in this case, the victim will be sent to the hospital. When a patient has a fever, they should be referred to an infectious disease specialist. Under no circumstances should you leave him alone at home, since help in such situations must be provided immediately.

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

Important! Often, to treat such a disease, people turn to an infectious disease specialist, and if a child is affected, then to a pediatric infectious disease specialist.

Now you know who treats this disease.

Basic principles of treatment of meningitis

The main principle of treating meningitis 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 a timely manner, leads to death. The doctor may prescribe antibacterial drugs and broad-spectrum medications. This choice is due to the fact that the pathogen can be identified by collecting 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 prescription of steroids. Hormonal therapy will help the body cope with the infection and normalize the functioning of the pituitary gland. Diuretics are used in treatment because they relieve swelling. However, it is worth taking into account that all diuretics wash away calcium from the human body. A spinal tap not only alleviates the condition, but also reduces pressure on the brain.

How and with what to treat meningitis? There are several methods.

Medication method

The best cure for meningitis is antibiotics. Antibacterial agents are also prescribed along with them:

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

The following are prescribed among antipyretics:

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

Corticosteroid drugs include the following:

• 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 protected from loud sounds.

You can use these methods:

Diet

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

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

Exercise therapy

General strengthening exercises will help you recover faster and return to your normal rhythm of life. But you need to resort to exercise therapy only with the doctor’s permission - you don’t need to make decisions on your own.

Physiotherapy

Physiotherapy includes the following medications:

• Immunostimulating.
• Sedatives.
• Toning.
• Ion-correcting.
• Diuretics.
• Enzyme-stimulating.
• Hypocoagulating.
• Vasodilators.

When is surgery needed?

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

• A sharp increase in blood pressure and heart rate.
• Increased shortness of breath and pulmonary edema.
• Paralysis of the respiratory tract.

Is it possible to get rid of it at home?

Can it be treated at home? Meningitis can be treated at home only if it is at an early stage.

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

It is important to comply with the following conditions:

1. Monitor bed rest.
2. Darken the room in which the patient is located.
3. Nutrition should be balanced and drink plenty.

Recovery time

How long does it take to treat the disease? It depends on:

• Forms of the disease.
• General condition of the body.
• Time when treatment began.
• Individual sensitivity.

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

Possible complications and consequences

They can be represented like this:

• ITS or ICE. They develop as a result of the circulation of endotoxin in the blood. All this can lead to bleeding, impaired activity and death.
• Waterhouse-Friderichsen syndrome. It manifests itself as insufficiency 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.
• Swelling of the brain 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 separate materials on the site.

Duration of observation of contact patients?

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

Symptoms

All symptoms are conventionally divided into the following:

1. Intoxication syndrome.
2. Craniocerebral syndrome.
3. Meningeal syndrome.

The first is intoxication syndrome. It is caused due to septic lesions and the appearance of infection in the blood. Often sick people are very weak and get tired quickly. Body temperature rises to 38 degrees. Headache, cough, and brittle joints are very common.

The skin becomes cold and pale, and appetite is significantly reduced. In the first days, the immune system fights the infection, but after that it is impossible to do without the help of a professional doctor. Craniocerebral syndrome is the second.

It develops as a result of intoxication. Infectious agents quickly spread throughout the body and enter the blood. Here they attack cells. Toxins can cause blood to clot and form blood clots. In particular, the brain matter is affected.

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

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

The patient often vomits because the body may 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 impaired circulation of cerebrospinal fluid against the background of intracranial pressure. Fluid and swelling tissue irritate the receptors, the muscles contract, and the patient’s movements become abnormal. Meningeal syndrome can manifest itself as follows:

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AUTHORS:

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

Voznyuk I.A. – Deputy Director for Scientific Work at St. Petersburg Research Institute of SP named after. I.I. Dzhanelidze”, Professor of the Department of Nervous Diseases of the V.Med. CM. Kirov.

Definition

Meningitis is an acute infectious disease primarily affecting the arachnoid and soft membranes of the brain and spinal cord. With this disease, situations may develop that pose a threat to the patient’s life (the occurrence of disturbances of consciousness, shock, convulsive syndrome).

CLASSIFICATION
The classification is divided according to etiology, type of course, nature of the inflammatory process, etc.

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

2. According to the nature of the inflammatory process:

Purulent, predominantly bacterial.

Serous, predominantly viral meningitis.

3. By origin:

Primary meningitis (pathogens are tropic to 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.
• 
  Spicy.
• 
  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, gall bladder, osteomyelitis of long tubular bones and pelvis, prostatitis in men and adnexitis in women, as well as thrombophlebitis of various locations, bedsores, wound surfaces. Particularly common causes 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 entering 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 occurring 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. In a similar way, hematogenous infection of the meninges occurs with extracranial lesions caused by fungi and protozoa. One should keep 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 facial veins, intracranial veins and sinuses of the dura mater.

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

IN pathogenesis meningitis, the following factors are important:

General intoxication

Inflammation and swelling of the meninges

Hypersecretion of cerebrospinal fluid and impaired 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 a feeling of malaise, fever, myalgia, tachycardia, facial flushing, inflammatory changes in the blood, etc.

Meningeal and cerebral symptoms include headache, nausea, vomiting, confusion or depression, and generalized 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 also results from an acute increase in ICP. Due to increased ICP, patients may exhibit Cushing's triad: bradycardia, increased systolic blood pressure, decreased breathing. In severe cases of meningitis, convulsions and psychomotor agitation are observed, periodically followed by lethargy and disturbances of consciousness. Mental disorders in the form of delusions and hallucinations are possible.

The actual meningeal 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 exhibits intolerance to noise or increased sensitivity to it, loud conversation (hyperacusis). Headaches are aggravated by strong sounds and bright light. Patients prefer to lie with their eyes closed. Almost all patients have stiff neck muscles and Kernig's sign. Rigidity of the neck muscles is detected when the patient's neck is passively flexed, when due to spasm of the extensor muscles it is not possible to completely bring the chin to the sternum. The Kernig sign is checked as follows: the patient’s leg, lying on his back, is passively bent at an angle of 90º at the hip and knee joints (the first phase of the study), after which the examiner attempts to straighten this leg at the knee joint (the second phase). If a patient has meningeal syndrome, it is impossible to straighten his leg at the knee joint due to a reflex increase in the tone of the leg flexor muscles; with meningitis, this symptom is equally positive on both sides.

Patients should also be checked for Brudzinski's signs. The upper Brudzinski symptom is when the patient's head is passively brought to the sternum, in a supine position, his legs bend at the knee and hip joints. Average Brudzinski's symptom- the same bending of the legs when pressing on pubic symphysis . Lower Brudzinski's sign- when one leg of the patient is passively flexed at the knee and hip joints, the other leg is bent in a similar way.

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

The greatest caution should be exercised in terms of the possibility that the patient may have purulent meningococcal meningitis, since this disease can be extremely severe and requires serious anti-epidemic measures. Meningococcal infection is transmitted by airborne droplets and after entering the body, meningococcus grows in the upper respiratory tract for some time. The incubation period usually ranges from 2 to 10 days. The severity of the disease varies significantly, and it can manifest itself in various forms: bacterial carriage, nasopharyngitis, purulent meningitis and meningoencephalitis, meningococcemia. Purulent meningitis usually begins acutely (or fulminantly), body temperature rises to 39-41º, a sharp headache occurs, accompanied by vomiting that does not bring relief. Consciousness is initially preserved, but in the absence of adequate therapeutic measures, psychomotor agitation, confusion, and delirium develop; as the disease progresses, excitement gives way to lethargy, turning into coma. Severe forms of meningococcal infection can be complicated by pneumonia, pericarditis, and myocarditis. A characteristic feature of the disease is the development of a hemorrhagic rash on the skin in the form of stars of various shapes and sizes that are dense to the touch and protrude above the skin level. The rash is most often localized on the thighs, legs, and buttocks. Petechiae may occur on the conjunctiva, mucous membranes, soles, and palms. In severe cases of generalized meningococcal infection, endotoxic bacterial shock may develop. With infectious-toxic shock, blood pressure quickly decreases, the pulse is threadlike or undetectable, cyanosis and sharp pallor of the skin are noted. This condition is usually accompanied by disturbances of consciousness (somnolence, stupor, coma), anuria, and acute adrenal insufficiency.

PROVISION OF EMERGENCY MEDICAL CARE

AT THE PREHOSPITAL STAGE

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

Tips for the caller:

• 
  It is necessary to measure the patient's body temperature.
• 
  In good lighting, you should carefully examine the patient's body 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 medications that the patient is taking and prepare them for the arrival of the emergency medical team.
• 
  Do not leave the patient unattended.

Diagnostics (D, 4)

Actions on a call

Mandatory questions to ask the patient or his environment

• 
  Has the patient recently had contact with infectious patients (especially patients with meningitis)?
• 
  How long ago did the first symptoms of the disease appear? Which?
• 
  When and how much did your body temperature increase?
• 
  Do you have a headache, especially a growing one? Is the headache accompanied by nausea and vomiting?
• 
  Does the patient have photophobia, hypersensitivity to noise, loud conversation?
• 
  Was there any loss of consciousness or 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 medications 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 state of consciousness (clear consciousness, somnolence, stupor, coma).

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

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

Measuring body temperature.

Assessment of meningeal symptoms (photophobia, stiff neck, Kernig sign, Brudzinski sign).

Upon examination, alertness regarding the presence or likelihood of developing life-threatening complications (infectious-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 the hospital in an infectious diseases hospital.

Treatment (D, 4)

Method of administration and dosage of medicines

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

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

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

PROVISION OF EMERGENCY MEDICAL CARE AT THE HOSPITAL STAGE IN THE INPATIENT EMERGENCY DEPARTMENT (EMS)

Diagnostics (D, 4)

A detailed clinical examination is carried out, and a neurologist is consulted.

A lumbar puncture is performed, which allows for 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 examined by a neurosurgeon.

Liquor diagnostics of meningitis consists of the following research techniques:

1. 
   macroscopic assessment of the cerebrospinal fluid removed during lumbar puncture (pressure, transparency, color, prolapse of the fibrinous mesh when the cerebrospinal fluid stands in a 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, difficulties arise in the differential diagnosis of bacterial purulent meningitis from other acute lesions of the brain and its membranes - acute cerebrovascular accidents; post-traumatic intracranial hematomas - epidural and subdural; post-traumatic intracranial hematomas that appear after the “lucid interval”; brain abscess; acutely manifesting brain tumor. In cases where the serious condition of patients is accompanied by depression of consciousness, an expansion of the diagnostic search is required.

Differential diagnosis

№ p.p.	diagnosis	differential feature
1	subarachnoid hemorrhage:	sudden onset, severe headache (“the worst in life”), xanthochromia (yellowish color) of the cerebrospinal fluid
2	brain injury	objective signs of injury (hematoma, leakage of cerebrospinal fluid from the nose or ears)
3	viral encephalitis	mental status disorders (depression of consciousness, hallucinations, sensory aphasia and amnesia), focal symptoms (hemiparesis, damage to cranial nerves), fever, meningeal symptoms, possible combination with genital herpes, lymphocytic pleocytosis in the cerebrospinal fluid
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, a history of chronic sinusitis or recent dental intervention
5	neuroleptic malignant syndrome	high fever (may be more than 40 ° C), muscle rigidity, involuntary movements, confusion, associated with taking tranquilizers
6	bacterial endocarditis	fever, headache, confusion or depression of consciousness, epileptiform seizures, sudden onset of focal neurological symptoms; cardiac symptoms (history of congenital or rheumatic heart disease, cardiac murmurs, valvular vegetations on echocardiography), increased ESR, leukocytosis, no changes in the cerebrospinal fluid, bacteremia
7	giant cell (temporal) arteritis	headache, visual impairment, age over 50 years, hardening and tenderness of the temporal arteries, intermittent claudication of the masticatory muscles (sharp pain or tension in the masticatory muscles when eating or talking), weight loss, low-grade fever

Treatment (D, 4)

Different antibiotics have different abilities to penetrate the blood-brain barrier and create the required bacteriostatic concentration in the CSF. On this basis, instead of the penicillin antibiotics that were widely used in the recent past, it is currently recommended to prescribe III-IV generation cephalosporins for initial empirical antibacterial therapy. They are considered the drugs of choice. However, in their absence, one should resort to the prescription 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 initial antibacterial therapy of purulent meningitis with an unknown 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 (pharma classes)	Frequency of administration IM or IV (once a day)	Drugs; daily doses (pharma classes)	Frequency of administration IM or IV (once a day)
IV generation cephalosporins cefmetazole: 1–2 g cefpir: 2 g cefoxitim (mefoxime): 3 g III generation cephalosporins cefotoxime (claforan): 8–12 g ceftriaxone (rocerin): 2–4 g ceftazidime (Fortum): 6 g cefuroxime: 6 g Meropenem (beta-lactam antibiotic): 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).

Essentially 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, can 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 rheopolyglucin is prescribed - 400–500 ml IV drip over 30–40 min 2 times a day or 5% placental albumin - 100 ml of 20% solution IV drip over 10–20 min 2 times a day day.
• 
  the prescription of vasopressors (adrenaline, norepinephrine, mesaton) for collapse caused by acute adrenal insufficiency in Waterhouse-Friderichsen syndrome does not have an effect if there is hypovolemia and it cannot be relieved by the above methods
• 
  use of cardiotonic drugs - strophanthin K - 0.5–1 ml of 0.05% solution in 20 ml of 40% glucose solution slowly intravenously or corglicon (0.5–1 ml of 0.06% solution in 20 ml of 40% glucose solution), or dopamine intravenously.
• 
  dopamine - initial rate of administration of 2-10 drops of a 0.05% solution (1-5 mcg/kg) per 1 minute - under constant hemodynamic monitoring (blood pressure, pulse, ECG) to avoid tachycardia, arrhythmia and renal vasospasm.

With signs of incipient dislocation syndrome:

• 
  administration of a 15% solution of mannitol at 0.5-1.5 g/kg intravenously by drip
• 
  transfer of the patient to the intensive care unit
• 
  supervision by a neurologist, neurosurgeon.

Application

Strength of recommendation (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 (Scheme 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 ones, 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 probability of causality
2+	Well-conducted case-control or cohort studies with moderate risk of confounding effects or bias and moderate probability of causality
2-	Case-control or cohort studies with a high risk of confounding effects or bias and a moderate probability of causality
3	Non-analytical studies (for example: case reports, case series)
4	Expert opinions

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

PROTOCOL

diagnosis and treatment of serous meningitis

Code MKH-10

G 02.0 Meningitis in viral diseases

Meningitis (caused by a virus):

Enteroviral (A 87.0 +)

Mumps (B 26.1+)

Herpes simplex (B 00.3 +)

Chickenpox (01.0+)

Herpes zoster (B 02.1+)

Adenoviral (A 87.1 +)

Corey (05.1+)

Rubella (B 06.0 +)

Infectious mononucleosis (B 27.-+)

G 03.0 Non-pyogenic meningitis (non-bacterial)

DIAGNOSTIC CRITERIA

Clinical:

General infectious syndrome:

its clinical manifestations mainly depend on the nature and properties of the pathogens

increase in body temperature to 38-39.5°C

severe headache, dizziness

• adynamia

Meningeal syndrome:

in 10-15% of patients may be absent in the presence of inflammatory changes in the cerebrospinal fluid

dissociation of the meningeal symptom complex is often detected, some symptoms may be absent

meningeal symptoms - rigidity of the neck muscles and the upper Brudzinski sign. Visual and tactile hyperesthesia is often observed

hydrocephalic-hypertensive syndrome - headache, repeated, sometimes repeated vomiting, which is not associated with food intake

Additional clinical criteria:

With enteroviral meningitis: catarrhal phenomena in the oropharynx, herpangina, pain in skeletal muscles (pleurodynia); exanthema of a polymorphic nature; diarrhea syndrome; spring-summer seasonality.

With adenoviral meningitis: catarrhal phenomena in the form of nasal congestion, runny nose, cough, changes in the oropharynx, eye damage (conjunctivitis, scleritis); lymphadenopathy, mesadenitis, diarrhea.

With mumps meningitis: enlargement of the parotid salivary glands (submandibular, mental) now or several days ago; hyperemic, swollen duct of the salivary gland on the buccal mucosa (Murson's symptom); abdominal pain, pancreatitis; lack of vaccination against mumps.

Paraclinical studies

General blood test - moderate leukopenia, sometimes slight lymphocytosis, shift of the formula to the left, normal ESR.

Analysis of cerebrospinal fluid - pleocytosis within several tens to hundreds of lymphocytes, protein content is normal or slightly increased (0.4-1 g/l), glucose level is normal, with the exception of tuberculous meningitis, in which a decrease in glucose content is a pathognomonic sign.

PCR of cerebrospinal fluid and blood - the presence of nucleic acid of the pathogen.

Virological studies of blood, cerebrospinal fluid - isolation of the pathogen from blood, cerebrospinal fluid by infecting laboratory animals or tissue cultures.

Bacteriological cultures of cerebrospinal fluid, blood, mucus from the nasopharynx, by inoculation on selective nutrient media - to isolate the pathogen.

Serological methods of RNGA, RSK, RN in order to identify specific antibodies and increase their titer by 4 or more times; RIF, ELISA for determining viral antigen.

Etiotropic therapy. For meningitis caused by the herpes simplex virus, chickenpox, and herpes zoster, acyclovir or its derivatives are prescribed in a single dose of 10-15 mg/kg 3 times a day, intravenously for 5-7 days.

Mode. Strict pastel regime until the general condition improves, body temperature decreases, and cerebrospinal fluid levels improve, on average for 7-10 days. After this - semi-bed rest for 5-7 days, followed by free rest.

Nutrition. For children of the first year after stabilization of hemodynamics - expressed milk or adapted milk formulas with a decrease in the amount of food on the first day to 1/2-1/3 of the age norm, followed by an increase to normal over 2-3 days. If swallowing is impaired, feeding through a tube.

For older children - a diet with the consumption of steamed food 5-6 times a day, fractionally, in small portions - table No. 5 according to Pevzner.

The drinking regime meets the daily fluid requirement, taking into account solutions administered intravenously - juices, fruit drinks, mineral water.

Pathogenetic therapy.

Dehydration (in the presence of hypertensive-hydrocephalic syndrome): magnesium sulfate solution 25% intramuscularly; furosemide 1% intravenously or intramuscularly 1-3 mg/kg, acetazolamide orally.

Detoxification. With moderate severity, you can get by with enteral fluid intake in the amount of physiological daily requirement.

In severe cases, the volume of intravenous infusion on the first day should not exceed 1/2 FP (physiological need). The total daily fluid volume is 2/3 of the FP, provided there is normal diuresis and no dehydration. From the second day, maintain a zero water balance, ensure diuresis in an amount of no less than 2/3 of the total volume of fluid received.

General approaches to diagnosis.
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 treatment adjustment. Such factors may be:
the presence of intolerance to medications and materials used at this stage of treatment;
inadequate psycho-emotional state of the patient before treatment;
a life-threatening acute condition/disease or exacerbation of a chronic disease, requiring the involvement of a specialist in the profile of the condition/disease to prescribe treatment;
refusal of treatment.
2.1 Complaints and anamnesis.
MI can occur in various forms with a combination of certain syndromes.
(Appendix G2). Generalized forms pose a threat, due to the high risk of developing life-threatening complications (Appendix G3-G6, G9).
For the timely identification of children at risk of developing GMI, it is recommended to clarify the fact of possible contact with patients with meningococcal infection (carriers of meningococcus) when collecting anamnesis.

A comment. Possible contacts in the family, in the close circle of the sick person, facts of stay or close contact with persons who visited regions with a high incidence of MI (countries of the “meningitis belt” of Subequatorial Africa; Saudi Arabia) are clarified. .
It is recommended to focus attention on complaints indicating a high risk of developing GMI, which include:
persistent febrile fever;
headache,.
photophobia,.
hyperesthesia.
vomiting (excessive regurgitation in children under 1 year old).
dizziness,.
rapid breathing.
cardiopalmus,.
drowsiness,.
unmotivated excitement.
refusal to eat.
reduction in fluid consumption (more than 50% of normal consumption within 24 hours - for children under 1 year),.
monotonous/high-pitched scream (for children under one year old).
changes in skin color and temperature.
leg pain.
rash,.
decreased diuresis.
Recommendation strength level B (evidence level 2+).
A comment. GMI is characterized by a sharp rise in temperature to high numbers (38.5-40 ° C and above); a two-humped nature of the temperature curve is often noted - on the first rise in temperature there is a short-term effect on the antipyrrhetics used, with a repeated rise (after 2-6 hours) - the introduction of antipyretics has no effect. A similar nature of the temperature curve is observed not only with GMI, 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 in the so-called “mother’s hands” symptom: when the mother complains that the child begins to become very anxious when trying to pick him up.
In the structure of the general infectious syndrome, complaints of diffuse and local muscle and joint pain are often noted, however, it is complaints of intense pain in the legs and abdomen (in the absence of manifestations of intestinal infection and the presence of surgical pathology) that are considered to be the so-called “red flag” symptoms of clinical diagnosis of sepsis, m. B. Signs of developing septic shock. .
If a rash is present, it is recommended to clarify the time of appearance of the first elements, their nature, location, and dynamics of changes. Pathognomonic for GMI is the presence of a hemorrhagic rash, 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 in various parts of the body and are often regarded as allergic manifestations. The appearance of a widespread hemorrhagic rash without a previous rash rash a few hours after the onset of the disease, as a rule, indicates an extreme severity of the disease. .
It is necessary to clarify the features of diuresis: the time of the last urination (in infants - the last diaper change). A decrease/absence of diuresis (more than 6 hours in children 1 year of life, more than 8 hours in patients older than 1 year) may be signs of the development of septic shock. .

2.2 Physical examination.

During an objective physical examination, it is recommended to actively identify signs of GMI 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 refill time by 2 seconds.
changes in skin color (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.
decreased diuresis.
an increase in the Algover shock index (norm: heart rate/BP systolic = 0.54).
Strength of recommendation: C (level of evidence – 3).
A comment. At the onset of GMI, excitement may be observed, followed by depression from somnolence to deep coma. The degree of impairment of consciousness is assessed using the Glasgow Coma Scale, where 15 points corresponds to clear consciousness, a level of 3 points or less corresponds to extreme coma (Appendix D10).
Some help in assessing the severity of the patient’s condition is the presence/absence of clinical signs of a systemic inflammatory response (SIRR) with determination of the level of blood pressure, frequency and quality of pulse, and respiration. Detection of 2 or more signs of SIRS is associated with a high risk of severe bacterial (not only meningococcal) infection. Threshold diagnostic values ​​for SIRS depending on age are presented in Appendix D4. .
The presence of pathological types of breathing is detected with extreme severity of the course of GMI in cases of development of dislocation syndrome against the background of GMI or in the terminal stage of the disease complicated by refractory septic shock.
The most typical hemorrhagic rash is in the form of irregularly shaped elements, dense to the touch, protruding above the skin level. The number of rash elements varies greatly - from single ones 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 facial areas 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 microcirculation disorders are pallor, cyanosis, marbled skin pattern, hypothermia of the distal extremities. .
In the first hours from the onset of the disease, meningeal symptoms can be negative, even in 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 undergo a clinical blood test with a study of the leukocyte formula.
Strength of recommendation: C (level of evidence: 3).
Comments. Detection of leukopenia or leukocytosis in the leukocyte formula that exceeds the age-related reference values ​​according to the table (Appendix D4) may indicate the presence of a systemic inflammatory reaction characteristic of GMI.
All patients with suspected GMI are recommended to undergo a general urinalysis; biochemical blood parameters: urea, creatinine, alanine aminotransferase (ALaT), aspartate aminotransferase (ASaT), study of blood electrolytes (potassium, sodium), bilirubin, total protein, acid-basic acid indicators, lactate level.

Comments. Changes in biochemical parameters of blood and urine make it possible to diagnose specific organ dysfunction, assess the extent of damage and the effectiveness of therapy. .
It is recommended to determine CRP and procalcitonin levels in the blood in all patients with suspected GMI.
Recommendation strength level B (evidence level 2++).
Comments. The detection in the blood of an increase in C-reactive protein 2 standard deviations from the norm and procalcitonin 2 ng/ml indicates the presence of a systemic inflammatory reaction characteristic of GMI. Evaluating indicators over time allows one to evaluate the effectiveness of ongoing antibacterial therapy. .
A study of hemostasis indicators is recommended for all patients with suspected GMI, determining the duration of bleeding, blood clotting time, and coagulograms.
Strength of recommendation: C (level of evidence: 3).
Comments. For the diagnosis of DIC syndrome. Hemostasis parameters change according to the stages of DIC; examination 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, a bacteriological examination of nasopharyngeal mucus for meningococcus is recommended for all patients with suspected MI.

A comment. Culture of meningococcus from the mucous membranes of the nasopharynx allows one to verify the etiological diagnosis of nasopharyngitis and establish 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, but is important factor for choosing ABT, which should contribute to both the treatment of systemic disease and the eradication of meningococcus from the mucous membranes of the nasopharynx.
All patients with suspected GMI are recommended to undergo bacteriological examination (culture) of blood.

Comments. Isolation and identification of meningococcal culture from sterile body media (blood, cerebrospinal fluid) serves as the “gold standard” for etiological verification of the disease. Blood samples should be collected as quickly as possible from the moment the patient is admitted to the hospital before the start of ABT. Blood testing is especially important in situations where there are contraindications to DSP. The absence of growth of the pathogen does not exclude the meningococcal etiology of the disease, especially when antibacterial therapy is started at the prehospital stage. .
A clinical examination of cerebrospinal fluid is recommended for all patients with suspected mixed forms of GMI or MM.
Strength of recommendation: C (level of evidence: 3).
Comments. Cerebrospinal puncture is possible only in the absence of contraindications (Appendix D11). Considering the absence of specific meningeal manifestations in young children, CSP is indicated for all patients in the first year of life with GMI. The qualitative characteristics of the CSF (color, transparency) are assessed, pleocytosis is examined with the determination of cellular composition, biochemical indicators of the levels of protein, glucose, sodium, chlorides). MM is characterized by the presence of neutrophilic pleocytosis, increased protein levels, decreased glucose levels. In the first hours of the disease and during emergency medical treatment in the later stages, pleocytosis m. B. Mixed, a decrease in glucose levels with an increase in lactate indicates the bacterial nature of menenitis when carrying out differential diagnosis and viral neuroinfections. .
All patients with suspected mixed forms of GMI or MM are recommended to undergo bacteriological examination (culture) of the cerebrospinal fluid.
Strength of recommendation level A (level of evidence –1+).
Comments. Examination of CSF is possible only in the absence of contraindications (Appendix G11). Isolation of other pathogens from the blood and CSF by culture helps to make a differential diagnosis, verify the etiology of the disease and adjust antimicrobial therapy.
Microscopy of blood smears (“thick spot”) with Gram staining is recommended for patients with suspected GMI.
Strength of recommendation: C (level of evidence: 3).
Comments. The detection of characteristic Gram-negative diplococci in a smear serves as an indicative assessment and may be the basis for initiating specific therapy, however, based on microscopy alone, the diagnosis of MI is not valid.
For the express diagnosis of GMI, it is recommended to carry out a latex agglutination test (RAL) in blood serum and CSF to determine the antigens of the main causative agents of bacterial neuroinfections.
Strength of recommendation: C (level of evidence: 3).
Comments. Test systems for RAL used in practice in the diagnosis of bacterial neuroinfections make it possible to detect antigens of meningococci A, B, C, Y/W135, pneumococci, and Haemophilus influenzae. Detection of antigens of bacterial pathogens in sterile liquids 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 RAL data and PCR or culture results, preference is given to the latter to verify the etiological diagnosis. .
It is recommended to carry out molecular research methods to identify the causative agent of GMI.
Strength of recommendation level B (level of evidence –2+).
Comments. Amplification of nucleic acids of bacterial neuroinfection pathogens is carried out using the polymerase chain reaction method. Detection of meningococcal DNA fragments by PCR in sterile fluids (blood, cerebrospinal fluid, synovial fluid) is sufficient to determine the etiology of the disease. The commercial test systems used in practice allow simultaneous testing for the presence of pneumococci, Haemophilus influenzae and meningococcal infections, which allows differential diagnosis with diseases that have a similar clinical picture and selection of optimal antibacterial therapy. .
Criteria for laboratory confirmation of diagnosis.
It is recommended to consider 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 upon detection of DNA (PCR) or antigen (RAL) of meningococcus in the blood as a reliable diagnosis of MI. or CSF.
Strength of recommendation level B (level of evidence –2+).
A comment. Culture 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 etiological confirmation of the diagnosis of GMI if the results of culture, RAL, PCR of CSF and blood are negative. .
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.
Strength of recommendation: C (level of evidence: 3).

Dovgalyuk I.F., Starshinova A.A., Korneva N.V.,Moscow, 2015

Tuberculous meningitis is a tuberculous inflammation of the meninges, characterized by multiple rashes of miliary tubercles on the soft meninges and the appearance of serous-fibrinous exudate in the subarachnoid space.

Primary tuberculous meningitis - occurs in the absence of visible tuberculous changes in the lungs or other organs - “isolated” primary meningitis. Secondary tuberculous meningitis - occurs in children as a hematogenous generalization with damage to the meninges against the background of active pulmonary or extrapulmonary tuberculosis.

Tuberculosis of the meninges (TBMT) or tuberculous meningitis (TBM) is the most severe localization of tuberculosis. Among diseases accompanied by the development of meningeal syndrome, tuberculous meningitis accounts for only 1-3% (G. Thwaites et al, 2009). Among extrapulmonary forms, tuberculous meningitis accounts for only 2-3%.

In recent years, 18-20 cases of tuberculosis of the central nervous system and meninges have been registered in the Russian Federation (Tuberculosis in the Russian Federation 2011), which is a rare pathology. Late diagnosis of TBM, and therefore untimely initiation of treatment (later than the 10th day of illness) affects the results of treatment, reduces the chances of a favorable outcome and leads to death.

The prevalence of TBM is a generally recognized marker of tuberculosis distress in a territory. In various regions of the Russian Federation, the prevalence of TBM is from 0.07 to 0.15 per 100,000 population. In the context of the HIV epidemic, the incidence of TBM tends to increase.

The development of tuberculous meningitis follows general patterns that are inherent in tuberculous inflammation in any organ. The disease usually begins with nonspecific inflammation, which later (after 10 days) becomes specific. The exudative phase of inflammation develops, and then the alterative-productive phase with the formation of caseosis.

The central place in the inflammatory process is occupied by damage to cerebral vessels, mainly veins, small and medium-sized arteries. Large arteries are rarely affected. Most often, the middle cerebral artery is involved in the inflammatory process, which leads to necrosis of the subcortical ganglia and internal capsule of the brain. Around the vessels, voluminous cellular couplings of lymphoid and epithelioid cells are formed - periarteritis and endarteritis with proliferation of subendothelial tissue, concentrically narrowing the lumen of the vessel.

Changes in the vessels of the pia mater and the brain substance, such as endoperivasculitis, can cause necrosis of the vessel walls, thrombosis and hemorrhage, which entails a disruption of the blood supply to a certain area of ​​the brain substance - softening of the substance.

The tubercles, especially in treated processes, are rarely visible macroscopically. Their sizes vary - from poppy seed to tuberculoma. Most often they are localized along the Sylvian fissures, in the choroid plexuses, at the base of the brain; large foci and multiple miliary ones - in the substance of the brain. Edema and swelling of the brain and dilatation of the ventricles are observed.

Localization of specific lesions in tuberculous meningitis in the soft meninges of the base of the brain from the optic chiasm to the medulla oblongata. The process can spread to the lateral surfaces of the cerebral hemispheres, especially along the Sylvian fissures, in which case basilar-convexital meningitis develops.