Acute purulent meningitis ICD code 10. Serous meningitis - symptoms in children, adults, treatment, consequences. G22* Parkinsonism in diseases classified elsewhere

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

Neurology, Pediatric Neurology, Pediatrics

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RSE on REM "Republican Center for Health Development"
Ministry of Health and social development Republic of Kazakhstan
dated May 26, 2015
Protocol No. 5

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

Date of development of the protocol: 2016

Protocol users: therapists, doctors general practice, infectious disease specialists, neurologists, resuscitators, clinical pharmacologists, expert doctors, emergency doctors/paramedics medical care.

Level of evidence scale:
The relationship between the strength of evidence and the type scientific research

A	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.
IN	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 low (+) risk of bias, the results of which can be generalized to relevant population.
WITH	Cohort or case-control study or controlled trial without randomization with no high risk bias (+), the results of which can be generalized to the relevant population or RCTs with very low or low risk of bias (++ or +), the results of which cannot be directly generalized to the relevant population.
D	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 and etc.),
· fungal (candidiasis, cryptococcosis, etc.),
· protozoal (for 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. In serous meningitis, lymphocytes predominate in the cerebrospinal fluid; in purulent meningitis, neutrophils predominate.

3. By pathogenesis Meningitis is divided into primary and secondary. Primary meningitis develops without a previous general infection or infectious disease 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 distinguished (for example, at the base of the brain - basal meningitis, on the convex surface of the cerebral hemisphere - convexital meningitis).

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

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

Diagnostics (outpatient clinic)

OUTPATIENT DIAGNOSTICS

Diagnostic criteria

Complaints :
· 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:
History - should be noted Special attention on the:
· determination of the connection between the onset and development of symptoms of the disease with signs of an infectious disease that have been transferred or present at the time of examination;
· collecting an epidemiological history, namely taking into account the seasonality of the disease, the geographic distribution of the pathogen, travel, the patient’s occupation, contact with infectious patients, animals and insects that carry infections;
· vaccination and immune status patient, including due chronic intoxications(drug addiction, alcoholism, substance abuse) and secondary immunodeficiency conditions.

Physical examination:

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

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

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

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

Focal neurological syndrome:
· damage to the skull - brain nerves;
presence of focal neurological symptoms, that is, associated with damage to a certain area of ​​the brain.

General infectious syndrome: increased body temperature, chills.

Laboratory research:
· Complete blood count - leukocytosis, possible anemia;
· General urine analysis - leukocyturia, bacteriuria, proteinuria, microhematuria (with severe course as a result of kidney damage).

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

Diagnostic algorithm:

Diagnostics (ambulance)

DIAGNOSTICS AT THE EMERGENCY CARE STAGE

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

Diagnostics (hospital)

DIAGNOSTICS AT THE INPATIENT LEVEL

Diagnostic criteria at the hospital level

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

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

Instrumental studies:
· CT/MRI of the brain without and with contrast - to exclude brain damage and detect cerebral edema;
· Radiography of the chest organs - to exclude lung pathology;
· Electrocardiographic study (12 leads) - to assess the activity of the heart);

Diagnostic algorithm

List of main diagnostic measures:
· General blood test 6 parameters;
· General clinical urine examination (general urine analysis);
· General clinical examination of cerebrospinal fluid;
· Determination of glucose in blood serum;
· General clinical examination of stool (coprogram);
· Determination of creatinine in blood serum;
· Determination of ALT in blood serum;

· Determination of ACaT in blood serum;
· Electrocardiographic study (12 leads);
· Radiography of the chest organs (1 projection);
· Computed tomography of the brain without and with contrast;

List of additional diagnostic measures:
· Staging the Wasserman reaction in blood serum;
· Counting platelets in the blood;
· Calculation of leukemia in blood;
· Bacteriological research blood for sterility (isolation of pure culture);
Determination of sensitivity to antimicrobials dedicated 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 for viruses herpes simplex types 1 and 2 (HSV-I, II) in blood serum;
· Bacteriological examination of cerebrospinal fluid for Neisseria meningitis;
· Bacteriological examination of transudate and exudate for sterility;
· Determination of Ig M to the early antigen of 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;
· Radiography paranasal sinuses nose (to exclude ENT pathology);
· Computed tomography of the pyramids of the temporal bones.

Differential diagnosis

Table 1. Differential diagnosis and rationale for additional research.

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.	CT scan brain, fundus examination, consultation with a therapist, infectious disease specialist.	· acute onset caused by physical and/or emotional stress against the background of high blood pressure; · presence of a previous vascular history; · history of headache paroxysms; · presence of signs of hemorrhage on CT scans; retinal vascular angiopathy, hyperemia; confirmation by therapist arterial hypertension;
Ischemic stroke	ischemic stroke debuts with the development of cerebral and meningeal syndromes with the subsequent development of focal symptoms	FAST algorithm, computed tomography	· predominance of focal neurological symptoms in meningeal syndrome;
Volumetric process brain (abscess, hemorrhage into a brain tumor)	The clinical picture of the volumetric process of the brain is characterized by the presence of a general cerebral syndrome and symptoms of focal brain damage, as well as a possible increase in body temperature and the presence of symptoms of intoxication.	computed tomography of the brain, fundus examination, consultation with a neurosurgeon, consultation with a therapist, infectious disease specialist.	· subacute development of cerebral syndrome, absence of infectious and epidemiological history; · CT scans show the presence of a brain space-occupying lesion; · on the fundus - signs intracranial hypertension, phenomena of stagnant disks optic nerves; · exclusion of an acute infectious disease by an infectious disease specialist; absence of a therapeutic disease that has a cause-and-effect relationship with the condition of this patient; · confirmation of the presence of a space-occupying brain tumor by a neurosurgeon;
Septic thrombosis of cerebral veins	septic thrombosis of the cerebral veins is characterized by the presence of meningeal, cerebral syndromes and symptoms of focal brain damage, as well as a possible increase in body temperature and the presence of symptoms of intoxication.	computed tomography of the brain with contrast, examination of the fundus, consultation with a neurosurgeon, infectious disease specialist, therapist.	· acute onset and development of cerebral and focal neurological symptoms against the background of general infectious syndrome/ intoxication; · correspondence of focal neurological symptoms to the localization of the venous sinus; · absence of signs of focal lesions of the brain substance on CT scans; · in the fundus - signs of intracranial hypertension; · exclusion of a space-occupying brain tumor by a neurosurgeon; · exclusion of an acute infectious disease by an infectious disease specialist; · confirmation of the presence of a septic condition by a therapist;
Intoxication	intoxication nervous system are characterized by the presence of a general cerebral syndrome, the phenomena of meningism and symptoms of focal brain damage, as well as the presence of symptoms of general intoxication.
Migraine	typical pattern in 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 vyy	caused by H. influenzae	staphylococcal	colibacterial	enteroviral	mumps		tuberculous
Premorbid background	Not changed	Pneumonia, sinusitis, otitis, transferred ARVI	Weakened children (rickets, malnutrition, frequent acute respiratory viral infections, pneumonia and otitis media)	Purulent lesions of the skin, bones, internal organs, sepsis.	Often perinatal pathology, sepsis	Not changed	Not changed		Primary tuberculosis focus
Onset of the disease	acute	In younger children it is subacute, in older children it is acute, violent	More often subacute	Subacute, less often violent	Subacute	Acute	Acute		Gradual, progressive
Height of body temperature, duration	High (39-40C), 3-7 days	High (39-40C), 7-25 days	First high (39-40C), then low-grade for up to 4-6 weeks	High (38-39C), less often subfebrile, wavy	Subfebrile, less often high, 15-40 days	Medium height(37.5-38.5C), 2-5 days	Medium altitude or high (37.5-39.5C), 3-7 days		Febrile, subfebrile
Meningeal syndrome	Sharply expressed from the first hours of illness	Pronounced, sometimes incomplete	Pronounced, sometimes incomplete	Moderately expressed	Weak or absent	Weakly expressed, dissociated, absent in 15-20%	Moderately expressed, dissociated,		On the 2nd week it is moderately pronounced, then steadily increasing
Main clinical syndrome		Intoxicating, encephalitic	Meningeal, intoxicating	Septic	Intoxication, hydrocephalic	Hypertensive	Hypertensive		Intoxicating
Symptoms of central nervous system damage	In the first days, disturbances of consciousness, convulsions. Hearing impairment, hemisyndrome, ataxia	Picture of meningoencephalitis: from the first days, impaired consciousness, focal convulsions, paralysis, damage to the cranial nerve. Hydrocephalus.	Sometimes cranial nerve lesions, paresis	Epileptiform seizures, cranial nerve lesions, paresis	Convulsions, strabismus, hemiparesis, hydrocephalus	Sometimes transient anisoreflexia, Easy damage ChMN	Sometimes damage to the facial and auditory nerves, ataxia, hyperkinesis		From the 2nd week, converging strabismus, convulsions, paralysis, stupor
Possible somatic disorders	Arthritis, myocarditis, with mixed forms-hemorrhagic rash	Pneumonia, otitis, sinusitis	Tracheitis, bronchitis, rhinitis, pemmonia, arthritis, conjunctivitis, buccal cellulitis, osteomyelitis	Purulent lesions of the skin, internal organs, sepsis	Enteritis, enterocolitis, sepsis	Herpangina, myalgia, exanthema, diarrhea	Mumps, pancreatitis, orchitis		Tuberculosis of internal organs, skin, lymph nodes
Flow	Acute, sanitation of cerebrospinal fluid for 8-12 days	In older children it is acute, in younger children it is often protracted, the cerebrospinal fluid is sanitized within 14-30 days	Wavy, sanitation of the cerebrospinal fluid on days 10-14, sometimes on days 30-60	Protracted, tendency to block the cerebrospinal fluid pathways, abscess formation	Protracted, wavy, sanitation of the 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 shift 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, moderate increased ESR		Moderate leukocytosis, lymphocytosis, moderately elevated ESR
Character 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 ingredients), used in the treatment

Aztreonam

Amikacin

Ampicillin

Amphotericin B

Acetylsalicylic acid(Acetylsalicylic acid)

Benzylpenicillin

Vancomycin

Gentamicin

Hydroxyethyl starch

Dexamethasone

Dextrose

Diazepam

Ibuprofen

Potassium chloride (Potassium chloride)

Calcium chloride

Ketoprofen

Clindamycin

Linezolid

Lornoxicam

Mannitol

Meloxicam

Meropenem

Metoclopramide

Metronidazole

Sodium hydrocarbonate

Sodium chloride

Oxacillin

Paracetamol

Prednisolone

Rifampicin

Sulfamethoxazole

Tobramycin

Trimethoprim

Fluconazole

Fosfomycin

Furosemide

Chloramphenicol

Chloropyramine

Cefepime

Cefotaxime

Ceftazidime

Ceftriaxone

Ciprofloxacin

Treatment (outpatient clinic)

OUTPATIENT TREATMENT

Treatment tactics: determined by the nature of the infection, extent of prevalence and severity 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 in Airways(turn on side).

Drug treatment:
· Symptomatic therapy :
Mild degree severity - outpatient therapy is not provided; treatment should begin during hospitalization.
Moderate and severe severity:

For 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 orally;
· 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 (over at least 3 minutes) 10 mg.
children from 1 to 18 years old, intramuscularly or intravenously slowly (over at least 3 minutes) 100 - 150 mcg/kg (max. 10 mg).

For infectious-toxic shock
Prednisolone 30 mg or dexamethasone 4 mg
adults prednisolone 10 - 15 mg/kg body weight, simultaneously possible
administration of up to 120 mg of prednisolone.
children prednisolone or dexamethasone 5 - 10 mg/kg (based on
prednisolone).

At 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 can be repeated after 30 - 60 minutes. To prevent seizures, a slow intravenous infusion can be used (maximum dose 3 mg/kg body weight over 24 hours);
Elderly: doses should not be more than half of the usually recommended doses;
For children 0.2 - 0.3 mg/kg body weight (or 1 mg per year) intravenously. The dose can be repeated if necessary after 30 - 60 minutes.

Detoxification therapy
· infusion of physiological sodium chloride solution 200 ml intravenously.

List of main medicines

Drugs	Single dose	Frequency of administration	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, from 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 (over at least 3 minutes) 100 - 150 mcg/kg (max. 10 mg).	WITH
prednisolone	30 mg	adults prednisolone 10 - 15 mg/kg body weight, simultaneously possible administration of up to 120 mg of prednisolone. children prednisolone or dexamethasone 5 - 10 mg/kg (based on prednisolone).	IN
diazepam	10 mg	Adults: intravenously or intramuscularly 0.15 - 0.25 mg/kg (usually 10-20 mg); the dose can be repeated after 30 - 60 minutes. To prevent seizures, a slow intravenous infusion can be used (maximum dose 3 mg/kg body weight over 24 hours); Elderly: Doses should not be more than half the usually recommended doses; Children 0.2 - 0.3 mg/kg body weight (or 1 mg per year) intravenously. The dose can be repeated if necessary after 30 - 60 minutes.	WITH

List of additional medicines

Algorithm of actions for 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 - intravenously (slowly) 0.2 - 0.5 mg every 2 - 5 minutes until maximum dose 5 mg, from 5 years and older 1 mg every 2 to 5 minutes up to a maximum dose of 10 mg; If necessary, treatment can be repeated after 2 - 4 hours.
Psychomotor agitation	Diazepam	10 - 20 mg - 2.0 once.	Children from 30 days to 5 years IV (slow) 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, 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: maximum daily dose - 0.5 mg of metoclopramide per 1 kg of body weight, therapeutic dose - 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 body weight, up to 120 mg of prednisolone can be administered at a time.	Prednisolone or dexamethasone 5 - 10 mg/kg (based on prednisolone).

Other treatments: no.

· consultation with an otorhinolaryngologist - to exclude pathologies of ENT organs;




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

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

Monitoring the patient's condition:
· assessment of life-supporting functions - breathing, hemodynamics;
· assessment of neurological status to identify and monitor the above-described cerebral, meningeal, and general infectious syndromes with notes from a doctor in accordance with the management rules medical documentation of this institution (PHC, medical centers and so on.).

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

Treatment (ambulance)

TREATMENT AT THE EMERGENCY STAGE

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

Treatment (inpatient)

INPATIENT TREATMENT

Treatment tactics: The choice of treatment tactics for meningitis will depend on its type and causative agent.
− Non-drug treatment:
Mode II, drinking plenty of fluids, installation of a nasogastric tube and tube feeding with a 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 on its side).

Treatment of purulent meningitis in children.

Hospitalization
All patients with purulent meningitis, regardless of clinical form and the severity of the disease are subject to mandatory hospitalization in a specialized infectious diseases department. On the first day of hospital stay, the child should lie on his side to prevent aspiration.
Children with signs of intracranial hypertension (ICH) and cerebral edema (CED) should be hospitalized in the intensive care unit or intensive care. If there are signs of ICH and/or AMG in a patient, the bed on which he is located should be with the head end raised by 30°. To prevent bedsores, it is necessary to turn the child over every 2 hours.
Monitoring of the child’s condition in the hospital is carried out nurse during the first period 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 during the first time of hospitalization, a spinal puncture was postponed, or the data from Gram staining of cerebrospinal fluid smears were uninformative.

Age of patients	Most likely pathogen	Recommended Antibiotic
From 0 to 4 weeks	Str.agalacticae E.s oli K. pneumoniae St. aureus L.monocytogenes	Ampicillin + cefotaxime ± gentamicin or amikacin
From 4 weeks to 3 months	H. influenza S. pneumoniae N. meningitidis	Ampicillin + 3rd generation cephalosporin (cefotaxime, ceftriaxone)
From 4 months to 18 years	N. meningitis s S. pneumoniae H. influenzae	3rd generation cephalosporin (cefotaxime, ceftriaxone) or benzylpenicillin
With head trauma, after neurosurgical operations, cerebrospinal bypass surgery, 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 If there is no evidence of sensitivity or suspected resistance to penicillin: Vancomycin + cefotaxime or ceftriaxone	Cefotaxime Ceftriaxone Chloramphenicol (chloramphenicol succinate) Cefepime Meropenem Linezolid
H. influenzae	Ceftriaxone Cefotaxime	Cefepime Meropenem Ampicillin
N. meningitidis	Benzylpenicillin Ceftriaxone Cefotaxime	Chloramphenicol (chloramphenicol succinate) Ampicillin
St. Аureus	Oxacillin	Vancomycin, Rifampicin Linezolid
St. epidermidis	Vancomycin + rifampicin	Linezolid
L. monocytogenes		Meropenem
Str. аgalacticae	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	Over 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 (chloramphenicol 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 a ratio of 1:5. Co - trimoxazole is the total - trimethoprim and sulfamethaxazole

Table - 7. Frequency 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 (chloramphenicol 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 antimicrobial therapy purulent meningitis in children

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

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

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

Adjuvant therapy

Indications for use dexamethasone
1. Meningitis in children aged 1 to 2 months. Dexamethasone is not prescribed to newborns with meningitis.
2. Children who have gram-negative bacilli detected in a cerebrospinal fluid smear.
3. Patients with high ICP.
4. Patients with AGM.
Dexamethasone is prescribed 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 antidiuretic hormone, impaired capillary permeability and the risk of developing ICH and/or OGM.

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

When blood pressure decreases and diuresis decreases, third generation hydroethyl starch (HES) preparations (130/0.4) at a dose of 10-20 ml/kg are indicated as a starting solution. When blood pressure stabilizes and diuresis resumes infusion therapy carried out with glucose-saline solutions.

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

Mannitol (10-20%) as a starting solution for increased ICP is used in case of threat or presence of acute hypertension, 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 (within 5-10 minutes), older children - 0.5-1.0 g/kg (within 15-30 minutes). Daily dose in children under 2 years of age it should not exceed 0.5-1.0 g/kg, in older children - 1-2 g/kg. Repeated administration of mannitol should be carried out no earlier than after 4 hours, but it is advisable 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 OGM.

4. Kidney failure.
5. Coma.
After the mannitol infusion 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, and after 2 hours - again at a dose of 0.5-1 mg/kg.
After mannitol is administered colloidal solutions(III generation HES preparations; 130/0.4) at a dose of 10-20 ml/kg. In children 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 potassium chloride solution - 20 - 40 mmol/l) and saline sodium chloride solution in a 1:1 ratio. In children 1 year of age this ratio is 3:1.

The rate of fluid administration for purulent meningitis with symptoms of ICH and OGM 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 pulmonary capillary wedge pressure (PCP) 8-16 mm Hg. Art.; mean arterial pressure (MAP) 65 mm Hg. Art. and more, central saturation venous blood more than 70%, stabilization of microcirculation.
b) control of isosmolarity and iso-oncoticity of plasma - hematocrit at the level of 35-40% in children under 6 months, 30-35% in children over 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
for purulent meningitis in children:
1. Impaired consciousness: complicated coma I and deeper degrees of suppression of consciousness (less than 8 points on the Glasgow scale), high ICH, threat of development of dislocation syndromes, repeated convulsions.
2. Increasing signs of respiratory distress syndrome (high cost of breathing, increasing psychomotor agitation, inhalation addiction high concentrations oxygen - partial pressure of oxygen (PaO2) 60 mm Hg. Art. or cyanosis with an oxygen concentration (FiO2) of 0.6, an increase in pulmonary shunting in excess of 15-20% - PaO2/FiO2<200).
3. Persistence of signs of ITS despite fluid infusion of 60-90 ml/kg body weight.

Respiratory support should be carried out according to the principles of pulmonary protective ventilation:
1. Application of decelerating flow.
2. Selection of optimal positive end expiratory pressure (PEEP) - within 8-15 cm water column.
3. Tidal volume 6-8 ml/kg body weight, but not more than 12 ml/kg body weight.
4. Plateau pressure is no more than 32 cm water column.
5. Use of recruitment techniques and kinetic therapy in the absence of contraindications.
Treatment of children with purulent meningitis, which is accompanied by ITS, 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 (CED) should be hospitalized in the intensive care unit or intensive care unit.

Antibacterial therapy

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

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

Pathogen	First line remedies	Second line agents
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 (levomytin succinate) gentamicin	Ampicillin
C. albicans	Fluconazole	Fluconazole + amphoterecin 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 a reduction in pleocytosis by at least 1/3.
When the etiological cause of the disease is identified, the starting antibiotics can be replaced with others, in accordance with the sensitivity of the pathogen. However, if there are 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 effectiveness of initial antibiotic therapy within 48 - 72 hours or when the microorganism has a certain resistance to the prescribed antibiotic.
The criterion for discontinuing antibiotic therapy for purulent meningitis is sanitation of the cerebrospinal fluid. A control spinal puncture is carried out after stable normalization of body temperature, disappearance of meningeal syndrome, and normalization of a general blood count. Therapy is stopped if the number of cells in 1 μl of cerebrospinal fluid does not exceed 50.
If purulent meningitis recurs, reserve antibiotics are prescribed.

Adjuvant therapy
Indications for the use of dexamethasone for purulent meningitis in adults:
1. Patients with high ICP.
2. Patients with AGM.
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
When blood pressure decreases and diuresis decreases, third generation hydroethyl starch (HES) preparations (130/0.4) at a dose of 10 - 20 ml/kg are indicated as a starting solution. When blood pressure stabilizes and diuresis resumes, infusion therapy is carried out with glucose-saline solutions.
In case of hypovolemia, drip intravenous administration of isotonic solutions (sodium chloride, complex solution (potassium chloride, calcium chloride, sodium chloride) is necessary). To correct the acid-base state in order to combat acidosis, a 4 - 5% solution of sodium bicarbonate (up to 800 ml) is administered intravenously. For the purpose of deintoxication, plasma-substituting solutions are administered 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 AGM. With stable hemodynamics on the first day, it should be no more than half of the physiological requirement, provided there is normal diuresis and the absence of symptoms of dehydration. The volume of intravenous infusions per day is approximately 30 - 50 ml/kg body weight and should not exceed diuresis. The total volume of fluid (intravenous and orally) on the first day is prescribed based on physiological needs. Subject to positive dynamics, a one-time infusion for 6 to 8 hours is acceptable.

Dehydration therapy
If there are signs of increased ICP or BGM, infusion therapy is aimed at regulating volume and optimizing cerebral microcirculation by supporting isovolemia, isosmolarity and iso-oncoticity.
To reduce intracranial pressure, dehydration therapy is performed.
· The head end of the bed is raised at an angle of 30°C, the patient’s head is placed in a median position - this achieves a reduction in intracranial pressure by 5 - 10 mm Hg. Art.
· Reducing intracranial pressure in the first days of the disease can be achieved by limiting the volume of fluid administered to 75% of the physiological requirement, until the syndrome of inadequate secretion of antidiuretic hormone is excluded (can occur within 48 - 72 hours from the onset of the disease). Restrictions are gradually lifted as the condition improves and intracranial pressure decreases. Preference is given to an isotonic sodium chloride solution; all medications are also administered with it.
· You can use forced diuresis of the dehydration type. The starting solution is mannitol (20% solution) at a 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 body weight . There are different schemes of dehydration when intracranial pressure rises.

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

In the presence of subarachnoid hemorrhage or peripheral vascular spasm, the administration 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 be no less than the volume of fluid administered intravenously and not less than 75% of the total daily volume of fluid administered.

Monitoring of infusion therapy for severe forms of purulent meningitis:
1. Dynamics of symptoms from the central nervous system, control of pupil size.
2. Control of body temperature and seizures;
3. Monitoring hemodynamics, hourly diuresis (at least 0.5 ml/kg/h).
4. Monitoring the level of sodium, potassium, and, if possible, magnesium in the blood plasma, blood glucose levels, blood plasma osmolarity, blood acid-base balance.
5. Maintaining normovolemia, isosmolarity and iso-oncoticity of plasma:
Indications for tracheal intubation and initiation artificial lung ventilation (ALV) for purulent meningitis in adults:
1. Impaired consciousness: complicated coma I and deeper degrees of depression of consciousness, threat of 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 concentrations of oxygen - partial pressure of oxygen (PaO2) 60 mm Hg or cyanosis with oxygen concentration (FiO2) 0.6 , increase in pulmonary bypass beyond 15 - 20% - PaO2/FiO2<200).
3. Persistence of signs of ITS despite fluid infusion of 60 - 90 ml/kg body weight.
4. Left ventricular failure, threat of pulmonary edema.

List of medicines:

Drugs	Level of evidence
Benzylpenicillin	A
Oxacillin	A
Amikacin	A
Tobramycin	A
Ampicillin	A
Cefotaxime	A
Cefepime
Ceftriaxone	A
Ceftazidime	A
Vancomycin	A
Fosfomycin	IN
Meropenem	A
Linezolid	WITH
Clindamycin	IN
Ciprofloxacin	IN
Metronidazole	IN
Trimethoprim+sulfamethoxazole	WITH
Rifampicin	WITH
Aztreons	A
Amphoteracin B	WITH
Gentamicin	A
Tiloron	A
Flucanazole	IN
Dexamethosone	IN
Mannitol	IN
Furosemide	IN
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 consultation with specialists:
· consultation with an ophthalmologist - the need to visualize the fundus picture to exclude papilledema;
· consultation with an ENT doctor - to diagnose pathologies of ENT organs;
· consultation with a pulmonologist - to exclude pneumonia;
· consultation with an infectious disease specialist - to exclude the infectious nature of meningitis;
· consultation with a resuscitator - to determine indications for transfer to the ICU;
· consultation with a phthisiatrician - for differential diagnosis with tuberculous meningitis (according to indications);
· consultation with a neurosurgeon - for differential diagnosis with space-occupying processes in 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 with a pediatrician - to assess the somatic status of children.

Indications for transfer to the intensive care unit:

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

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

Indicators of treatment effectiveness:
Clinical criteria:
· stable normal temperature;
· relief of cerebral syndrome;
· relief of meningeal syndrome;
· relief of ITS symptoms.
Laboratory criteria:
· sanitation of the cerebrospinal fluid, cytosis of 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/p	Frequency of mandatory follow-up examinations by an infectious disease specialist (pediatrician)	Duration of observation	Indications and frequency of consultations with 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 case of chronic course - before transfer to the adult network.	· Neurologist · 1st year - every 1 month, then once every 3 months; 2-3 years - once every 6 months, 4-5 years - once a year. According to indications - more often. Orthopedic doctor, ophthalmologist - 1 month after discharge, then - according to indications

N p/p	List and frequency of laboratory, x-ray and other special studies	Therapeutic and preventive measures.	Clinical criteria for the effectiveness of clinical examination	The procedure for admitting sick people to work, preschool educational institutions, boarding schools, summer health 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) · Evoked brain 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, physical 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 chronic course; · absence of relapses, and in the chronic course of exacerbations of the disease; improvement (or complete recovery) motor deficit, cognitive deficit and other symptoms	Those who have recovered from the disease are admitted without additional laboratory examination for sporadic encephalitis. During epidemics and in cases of outbreaks developing in individual groups, the decision on examination is made by an infectious disease doctor

Dispensary observation of adults in the clinic at the place of residence: a person who has recovered from meningitis is registered at a dispensary, at a polyclinic with the supervision of a neurologist for a period of 2 years, examines the convalescent person once a month for 3 months after the disease, subsequently visits are once every 3 months for a year, and during 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 performed.

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

Information

Sources and literature

1. Minutes of meetings of the Expert Council of the RCHR of the Ministry of Health of the Republic of Kazakhstan, 2015
   1. 1. Skoromets A.A., Skoromets A.P., Skripchenko N.V., Kryukova I.A. Meningitis.// Neurology. National leadership, Moscow, 2009. 2. Lobzin B.S. Meningitis and arachnoiditis.- L.: Medicine, 1983.-192 p. 3. Kramarev S.A. Approaches to antibiotic therapy for purulent meningitis in children.// Daily 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. //Review of practical recommendations for the management of patients with bacterial meningitis of the Infectious Diseases Society of America 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. 2012 Jun; 79(6):393-400. 11. Clark T., Duffell E., Stuart J.M., Heyderman R.S. Lumbar puncture in the management of adults with suspected bacterial meningitis—a survey of practice. J Infect. May 2006; 52(5):315-9. 12. Schut E.S., de Gans J., van de Beek D. Community-acquired bacterial meningitis in adults. Pract Neurol. 2008 Feb;8(1):8-23. 13. Van de Beek D., de Gans J., Tunkel A.R., Wijdicks E.F. Community-acquired bacterial meningitis in adults. N Engl J Med. 2006 Jan 5; 354(1):44-53. 14. Flores-Cordero J.M., Amaya-Villar R., Rincón-Ferrari M.D., Leal-Noval S.R., Garnacho-Montero J., Llanos-Rodríguez A.C., Murillo-Cabezas F. Acute community-acquired bacterial meningitis in adults recognized to the intensive care unit: clinical manifestations, management and prognostic factors. Intensive Care Med. 2003 Nov; 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
OARIT	-	department of anesthesiology and resuscitation, intensive care
ADH	-	antidiuretic hormone
NSAIDs	-	nonsteroidal anti-inflammatory drugs
IPC	-	minimum inhibitory concentration
PV	-	prothrombin time
INR	-	international normalized ratio
CNS	-	central nervous system
ITS	-	infectious-toxic shock
BSF UD	- -	biosocial functions level of evidence

List of protocol developers with qualification information:

FULL NAME.	Job title	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 neurologist of the Ministry of Health of the Republic of Kazakhstan, Chairman of the Association of Neurologists of the Republic of Kazakhstan.
Dairbaeva Leila Oralgazievna	Executive Director, NGO Kazakh National League against Epilepsy, assistant at the Department of Neurology, doctoral student at the Higher School of Public Health.
Elubaeva Altynay Mukashkyzy	Candidate of Medical Sciences, neuropathologist of the highest category, Astana Medical University JSC, Associate Professor of the Department of Neuropathology with a course in Psychiatry and Narcology, Director of the Center for Neurology and Epileptology LLP, the Association of Children's Neurologists of the Republic of Kazakhstan.
Kaishibaeva Gulnaz Smagulovna	candidate of medical sciences, Kazakh Medical University of Continuing Education JSC, head of the department of neurology, certificate of “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, neurologist 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 Association of Neurologists of the Republic of Kazakhstan.
Zhumagulova Kulparam Gabibulovna	Candidate of Medical Sciences, Kazakh Medical University of Continuing Education JSC, 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 Maternity and Childhood, neurologist - pediatric neurophysiologist, doctor of the highest category, member of the Association of Children's Neurologists of the Republic of Kazakhstan.
Lepesova Marzhan Makhmutovna	Doctor of Medical Sciences, Professor, Kazakh Medical University of Continuing Education JSC, Head of the Department of Child Neurology, President of the Association of Child Neurologists of the Republic of Kazakhstan, full member of the International, European, Asia-Ocean, Baltic Association of Child Neurologists.
Ibatova Syrdankyz Sultankhanovna	Candidate of Medical Sciences, JSC National Scientific Center for Neurosurgery, neurologist, member of the Association of Children's 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 Raikhan Yesenzhanovna	Candidate of Medical Sciences, Head of the Department of Pharmacology and Evidence-Based Medicine, State Medical University. Mr. Semey, member of the Association of Internal Medicine Doctors.

17. Indication of the absence of conflict of interest: No.

18. List of reviewers: Dushchanova 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 reviewing the protocol: Review of the protocol 3 years after its publication and from the date of its entry into force or if new methods with a level of evidence are available.

Attached files

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

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

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

Meningeal complications are not observed in the serous form of the disease. The pathology does not provoke impaired thinking, confusion and other symptoms characteristic of meningitis.

Establishing diagnosis

The reason for contacting a doctor is a child’s complaints of a headache, which is accompanied by vomiting, nausea and general malaise. The initial examination is carried out by a pediatrician, who then refers to a neurologist for a detailed examination.

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

ICD-10 code

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

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

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

Treatment of pathology

Treatment of the disease begins after determining the cause of the inflammatory process. If meningitis is caused by a virus, antiviral therapy is prescribed. For bacterial diseases, antibiotics are used, and for fungal infections, special antimycotics are used to combat a specific type of fungus.

In addition to treatment aimed at eliminating the cause of the disease, symptomatic therapy is used to improve the patient’s well-being as soon as possible. Viral and bacterial damage to the brain can be accompanied by an increase in temperature, so antipyretic medications are additionally prescribed. Nootropic medications are often used to improve cerebral circulation. Therapy must be supplemented by taking vitamin complexes containing B vitamins.

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

Serous meningitis is one of the serious diseases of the brain, characterized by inflammation of its membranes. Usually the cause is a viral infection or the proliferation of bacterial and fungal flora, but most of the recorded cases of this disease were caused by viruses. Most often it is recorded in children of primary school and preschool age.

It usually begins with symptoms characteristic of purulent inflammation of the meninges - nausea and vomiting, headache. The main difference between this form of the disease and all others is that inflammation develops sharply, but does not become a violent clinic. Rather, it occurs in a mild form, without disturbing the clarity of consciousness and passes without meningeal complications.

The diagnosis is established by clinical manifestations and data from bacteriological analysis of cerebrospinal fluid and PCR analysis.

Treatment is aimed at eliminating the pathogen and alleviating the general condition - prescribing painkillers, antipyretics, and antivirals. If, according to the treatment plan, the patient’s condition does not stabilize, additional antibacterial drugs belonging to broad-spectrum antibiotics are prescribed.

, , , , , , , , ,

ICD-10 code

A87.8 Other viral meningitis

Causes of serous meningitis

The causes of serous meningitis can be very diverse. Based on their form, they distinguish between primary and secondary. With primary inflammation, the painful condition is an independent process. With a secondary manifestation, it occurs as a complicated course of an existing disease of an infectious or bacterial nature.

Symptoms of serous meningitis

Symptoms of serous meningitis at an early stage are similar to a cold - fatigue, irritability, passivity appear, the temperature rises, and an unpleasant, raw sensation in the throat and nasopharynx. At the next stage, the temperature jump occurs - it rises to 40 degrees, the condition worsens, a severe headache appears, accompanied by dyspeptic disorders, muscle spasms, and delirium. Key manifestations of inflammation:

• positive reaction with Brudzinsky's test;
• "brain" vomiting;
• impaired muscle activity of the limbs, difficulty swallowing;
• significant hyperthermia - 38-40 degrees.

On days 5-7 from the onset of the disease, the symptoms may become weaker and the fever decreases. This period is the most dangerous, since if treatment is interrupted at the first sign of recovery, meningitis may develop again. A relapse is especially dangerous, as it can be accompanied by severe, persistent brain damage and pathologies of the nervous system. The nature of the pathogens can be confirmed using virological and serological examination of blood and cerebrospinal fluid.

The incubation period of serous meningitis lasts from the moment the pathogen enters the nasopharyngeal mucosa until the first signs of the disease appear. This can take a period of time from two to five days, but the timing largely depends on the nature of the pathogen and the resistance of the person’s immune system. In the prodromal stage, the disease is manifested by a decrease in general tone, headaches, a slight increase in temperature and the course is more similar to ARVI. In the incubation stage, a person is already a carrier of the pathogen and releases it into the environment, therefore, when the diagnosis is confirmed, it is necessary to isolate everyone who had contact with the patient as soon as possible.

But very often, serous inflammation of the brain begins acutely - with high fever, vomiting, and almost immediately characteristic symptoms of inflammation of the meninges appear:

• the appearance of stiffness in the neck muscles;
• positive reaction with the Kernig test;
• positive reaction with Brudzinski's test.

The prognosis is generally favorable, but in rare cases there are complications - visual impairment, hearing impairment, and persistent changes in the central nervous system. The first days after confirmation of the diagnosis, increased levels of lymphocytes are observed. A few days later - moderate lymphocytosis.

How is serous meningitis transmitted?

Inflammation of the meninges or meningitis develops rapidly. The main reason is representatives of the enterovirus group. You can easily become infected or become a carrier of the virus in the following situations:

• Contact infection. Bacteria and microorganisms enter the body with dirty food - fruits and vegetables with dirt particles, when drinking water that is not suitable for drinking, and when personal hygiene rules are neglected.
• Airborne infection. Infectious agents enter the mucous membranes of the nasopharynx upon contact with an already sick person or a carrier of the virus. Most often, pathogens are first released by patients into the environment, and then settle on the nasal and pharyngeal mucosa of a healthy person.
• Water route of infection. Possible when swimming in dirty waters, when the risk of ingesting contaminated water is high.

Serous inflammation of the lining of the brain is especially dangerous for children in the first year of life - during this period, exposure to infectious agents has such a detrimental effect on the children's brain and nervous system that it can cause mental retardation and partial impairment of visual and auditory functions.

Acute serous meningitis

It develops when enteroviruses enter the body, as well as viruses that cause mumps, lymphocytic choriomeningitis, herpes simplex type 2, and tick-borne encephalitis. With the viral etiology of this disease, a bacteriological examination of blood and spinal fluid will not give positive data; the manifestation of lymphocytic pleocytosis is diagnosed, the content is slightly higher than normal.

The clinical picture of the disease differs from the picture of the purulent form. The course of the disease is milder, manifested by headaches, pain when moving the eyes, spasms in the muscles of the arms and legs (especially flexors), positive Kernig and Brudzinski symptoms. In addition, the patient is bothered by vomiting and nausea, pain in the epigastric region, against the background of which physical exhaustion develops and photophobia develops. Persistent disturbances of consciousness, epileptic attacks, focal lesions of the brain and cranial nerves are also not recorded.

Acute serous meningitis does not cause severe complications and is easily treated, recovery occurs on the 5th-7th day of illness, but headaches and general malaise can last from several weeks to several months.

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Secondary serous meningitis

Meningoencephalitis occurs with concomitant viral conditions caused by mumps virus, herpes virus, etc. Most often, the cause of this process is mumps. It manifests itself like acute meningitis - the temperature rises, severe pain in the head, eyes water from the light, nausea, vomiting, pain in the stomach. The main role in diagnosing confirmation of damage to the meninges is played by a positive Kernig and Brudzinsky reaction, accompanied by stiffness of the neck muscles.

Serious changes are recorded only in moderate and severe forms of the disease, but in general, the secondary form of inflammation of the meninges goes away quite easily. More severe cases are characterized by a proliferative phenomenon not only of the salivary glands and meninges, but also by pancreatitis, inflammatory processes in the testicles. The course of the disease is accompanied by fever, basic brain symptoms, dyspeptic disorders, laryngitis, pharyngitis, and sometimes a runny nose. After 7-12 days, with a mild course, the general condition improves, but for another 1-2 months a person can be a carrier of the pathogen and pose a danger to others.

Viral serous meningitis

It is considered one of the most common uncomplicated forms of this disease. Caused by coxsackie viruses, mumps, herpes simplex, measles, enteroviruses and sometimes adenoviruses. The onset of the disease is acute, beginning with a sharp increase in temperature, painful sensations in the throat, sometimes a runny nose, dyspeptic disorders, and muscle spasms. In severe cases - clouding of consciousness and diagnosing stupor, coma. Signs of meningeal syndrome appear on the second day - rigidity of the neck muscles, Kernig syndrome, Brudzinski syndrome, increased blood pressure, very severe headaches, cerebral vomiting, pain in the abdomen. The analysis of spinal fluid shows a pronounced form of cytosis and many lymphocytes.

The prognosis for almost all adults with viral non-purulent inflammation of the meninges is favorable - complete recovery occurs in 10-14 days. In just a few cases of the disease, survivors suffer from headaches, hearing and vision disorders, poor coordination and exhaustion. Children in the first year of life may develop persistent developmental dysfunctions - minor mental retardation, lethargy, decreased hearing and vision.

Enteroviral serous meningitis

This is a type of meningitis caused by the Coxsackie and ECHO viruses. It can be either a single recorded case of infection or it can be in the nature of an epidemic. Most often, children become infected with it in the summer and spring, and the epidemic spreads especially quickly in communities - in kindergartens, schools, and camps. You can become infected from a sick person or child, as well as from a healthy carrier; this type of inflammation of the meninges spreads mainly through airborne droplets or when hygiene rules are not followed.

After the viral agent enters the body, within a day or three the first signs appear - redness and swelling of the pharynx, enlarged lymph nodes, abdominal pain and diffuse pain, and a rise in temperature. The disease moves to the next stage when the pathogen penetrates directly into the blood and, spreading through the bloodstream, concentrates in the nervous system, which leads to an inflammatory process in the lining of the brain. At this stage, meningeal syndrome becomes pronounced.

The course of the disease in general dynamics rarely entails severe complications. On the second or third day, the brain syndrome disappears, but on days 7-9 of illness, the clinical symptoms of serous inflammation may return and the temperature may also rise. In children under one year of age, the process is sometimes accompanied by the formation of inflammatory foci of the meningeal membranes of the spinal cord and persistent damage to the central nervous system.

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Serous meningitis in adults

It proceeds quite easily and does not cause serious complications. Its causes are viral agents, bacteria and fungi; primary inflammation of the meninges is caused by the Coxsackie virus, Echo enterovirus. Secondary cases are caused by the virus that causes polio, mumps, and measles.

In adulthood, viral inflammation occurs in an uncomplicated form, but this does not mean that this form does not require treatment. The onset is similar to a cold - headache, swollen throat, muscle pain and dyspeptic symptoms, meningeal syndrome and, in severe cases, convulsions. By the end of the first week of illness, the temperature is fixed at a normal level, muscle spasms and headaches are not disturbing. This stage requires special observation, since the likelihood of relapse increases, and the first signs of pathologies of the central nervous system and intracranial nerves may appear.

The most effective way to identify the pathogen is a serological and bacteriological analysis of blood and spinal fluid, PCR. After this, specific antibacterial and antiviral treatment is prescribed in combination with antipyretic, antiemetic, analgesic and sedative drugs.

Serous meningitis in adults is treatable, and the earlier it is started, the lower the risk of the disease returning and developing complications.

Serous meningitis in children

It is more severe than in adults and, if not treated promptly, can lead to serious complications. The incubation period lasts about 2-4 days; those who attend events with large concentrations of children of different ages - school and preschool institutions, clubs, various sections, camps - get sick more often. The root cause of the disease are viruses that cause measles, mumps, herpes, various enteroviruses, etc. At first, inflammation of the lining of the brain is similar to other forms of meningitis - it also suffers from severe headaches, dyspeptic disorders, and cerebral syndrome manifests itself. The main difference between the viral form and others is the sudden, acute onset of the disease, with relatively clear consciousness.

The diagnosis is confirmed by PCR and analysis of spinal cerebrospinal fluid. After determining the nature of the pathogen, a treatment plan is prescribed - for a viral etiology, a course of antiviral drugs is prescribed, if other pathogens are identified, antibiotics and antifungal drugs are prescribed. In addition to eliminating the cause of inflammation of the meninges, therapeutic measures are aimed at alleviating the general condition - for this, antipyretic, analgesic, antiemetic, and sedative medications are prescribed.

Serous meningitis in children ends quite quickly and without complications, but is dangerous for babies in the first year of life.

Complications of serous meningitis

Complications of serous meningitis for an adult pose minimal danger, but for children in the first year of life they are especially dangerous. Most often, the consequences of inflammation of the meninges make themselves felt when the course is aggravated, due to unqualified drug therapy or non-compliance with medical prescriptions.

Disorders that occur during severe inflammatory pathology of the meninges:

• Impaired functioning of the auditory nerve - hearing loss, dysfunction of motor coordination.
• Weakening of visual function - decreased acuity, strabismus, uncontrolled movements of the eyeballs.
• Decreased vision and motor activity of the eye muscles are completely restored, but persistent hearing impairment is mostly irreversible. The consequences of meningeal pathology suffered in childhood later manifest themselves in intellectual delay and hearing loss.
• Development of arthritis, endocarditis, pneumonia.
• Threat of strokes (due to obstruction of cerebral vessels).
• Epileptic seizures, high intracranial pressure.
• Development of cerebral and pulmonary edema, leading to death.

If you seek qualified medical help in a timely manner, severe systemic changes can be avoided and there will be no relapses during treatment.

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Consequences of serous meningitis

The consequences of serous meningitis, subject to treatment and proper rehabilitation after recovery, are expressed only in half of all cases of the disease. Basically, they manifest themselves in general malaise, headaches, decreased memory and memorization speed, and sometimes involuntary muscle spasms appear. In complex forms, the consequences will be more serious, including partial or complete loss of the ability to see and hear. Such violations are observed only in isolated cases and with timely organized drug therapy this can be easily avoided.

If the disease proceeded as a complicated course of another disease, then the person who had been ill will be more concerned about the problems that were associated with the root cause. Regardless of what form a person is ill with (primary or secondary), treatment measures should begin immediately. Basically, antibacterial, antifungal and antiviral drugs are used for this, as well as a complex of drugs for symptomatic therapy and alleviation of the general condition.

After suffering a pathological condition, a person requires special care and gradual recovery - this is a vitamin nutrition program, moderate physical activity and activities aimed at the gradual restoration of memory and thinking.

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Diagnosis of serous meningitis

Diagnosis is carried out in two directions - differential and etiological. For etiological differentiation, they resort to the serological method - RSC, and the neutralization reaction also plays an important role in isolating the pathogen.

As for the distinctive diagnosis, its conclusion depends on clinical data, epidemiological summary and virological conclusion. When diagnosing, pay attention to other types of disease (tuberculosis and inflammation of the meninges caused by influenza, mumps, polio, Coxsackie, ECHO, herpes). Due attention is given to confirming meningeal syndrome:

1. Rigidity of the neck muscles (the person cannot touch the chin to the chest).
2. Positive Kernig test (with the leg bent at 90 degrees at the hip and knee joint, a person cannot straighten it at the knee due to hypertonicity of the flexors).
3. Positive result of the Brudzinski test.

Consists of three stages:

• A person cannot press his head to his chest - his legs are pulled towards his stomach.
• If you press on the area of ​​the pubic fusion, the legs bend at the knees and hip joints.
• When checking the Kernig symptom on one leg, the second involuntarily bends at the joints simultaneously with the first.

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Liqueur for serous meningitis

Liqueur in serous meningitis has an important diagnostic value, since the nature of its components and the results of bacteriological culture can make a conclusion about the causative agent of the disease. Cerebrospinal fluid is produced by the ventricles of the brain; normally its daily volume is no more than 1150 ml. To take a sample of biomaterial (CSF) for diagnosis, a special manipulation is performed - lumbar puncture. The first milliliters obtained are usually not collected because they contain blood. The analysis requires several milliliters of CSF collected in two test tubes - for general and bacteriological examination.

If there are no signs of inflammation in the collected sample, then the diagnosis is not confirmed. With non-purulent inflammation, leukocytosis is observed in the punctate; the protein is usually slightly elevated or normal. In severe forms of pathology, neutrophilic pleocytosis is recorded and the content of protein fractions is significantly higher than acceptable values; when punctured, the sample flows out not drop by drop, but under pressure.

Liquor not only helps to accurately differentiate from other forms of this disease, but also to identify the pathogen, severity, and select antibacterial and antifungal drugs for therapy.

Differential diagnosis of serous meningitis

Differential diagnosis of serous meningitis is aimed at a more detailed study of the patient’s medical history, current symptoms and serological conclusion. Despite the fact that the meningeal complex is characteristic of all types of inflammation of the meninges, in some of its forms significant differences are observed. With a viral etiology, general meningeal manifestations may be mild or absent altogether - moderate headache, nausea, pain and cramping in the abdomen. Lymphocytic choriomeningitis is characterized by violent symptoms - severe headaches, repeated cerebral vomiting, a feeling of squeezing in the head, pressure on the eardrums, pronounced spasm of the neck muscles, a pronounced Kernig and Brudzinsky sign; during a lumbar puncture, cerebrospinal fluid flows out under pressure.

The pathological process caused by the polio virus is accompanied by signs characteristic of this disease - Lasegue, Amossa, etc. During EMS, cerebrospinal fluid flows out under slight pressure. Often the disease is accompanied by nystagmus (due to damage to the medulla oblongata).

The tuberculous form, unlike the serous one, develops slowly and occurs in people suffering from chronic tuberculosis. The temperature rises gradually, the general condition is sluggish and depressed. Spinal puncture contains a lot of protein, the presence of Koch's bacillus is determined, and the collected material is covered with a specific film over time.

Differential diagnosis is mainly based on virological and immunological examination of CSF and blood. This provides the most accurate information about the nature of the pathogen.

Treatment of serous meningitis

Treatment of serous meningitis requires special attention. Depending on what tactics will be taken in the first days of the disease, the further prognosis of medical prescriptions depends. Drug therapy for non-purulent inflammation of the meninges is carried out in a hospital - this way the person receives the necessary care and can observe all changes in well-being and carry out the necessary diagnostic manipulations.

Prescription largely depends on the severity of pathological changes, the nature of the pathogen and the general condition of the patient. According to the study of CSF and PCR, specific therapy is prescribed - for the viral form, these are antiviral drugs (Acyclovir, etc.), for the bacterial form, broad-spectrum antibiotics or specific antibacterial drugs (Ceftriaxone, Meropenem, Ftivazid, Chloridine, etc.), and also antifungal (Amphotericin B, Fluorocytosine), if the identified pathogen belongs to the group of fungi. Measures are also being taken to improve the general condition - detoxification medications (Polysorb, Hemodez), painkillers, antipyretics, antiemetics. In some cases, when the course of the disease is accompanied by high blood pressure, diuretics and sedatives are prescribed. After complete recovery, a course of rehabilitation is carried out, including exercise therapy, myostimulation, electrophoresis, and psychorehabilitation is also required.

Treatment can be carried out at home, but only if the disease is mild, and the patient’s well-being and compliance with the principles of medication prescriptions are monitored by an infectious disease specialist.

Treatment of serous meningitis in children requires special attention and a responsible attitude towards compliance with all medical prescriptions. In childhood, this disease is often accompanied by complications; it is especially dangerous for babies in the first year of life, when the consequences are persistent and can cause mental retardation, hearing loss, and poor vision.

Most of the recorded cases of non-purulent inflammation of the meninges are caused by viruses, so antibacterial therapy does not give the desired result. Acyclovir, Arpetol, Interferon are prescribed. If the child’s condition is severe and the body is weakened, immunoglobulins are administered intravenously. In case of significant hypertension, diuretics are additionally prescribed - Furosemide, Lasix. In severe forms, when the disease is accompanied by severe intoxication, glucose, Ringer's solution, Hemodez are injected intravenously - this promotes the adsorption and elimination of toxins. For severe headaches and high blood pressure, a spinal tap is performed. The rest of the treatment measures are symptomatic - antiemetics, painkillers, antipyretics, and vitamins are recommended.

Treatment, subject to the doctor's instructions, ends with recovery after 7-10 days and is not accompanied by long-term complications.

Prevention of serous meningitis

Prevention of serous meningitis is aimed at preventing the causative agent of this disease from entering the body. General preventative rules should include:

• Measures prohibiting swimming in polluted water bodies in the summer and autumn.
• Drink only boiled, purified or bottled water from certified wells.
• Careful preparation of products for cooking, proper heat treatment, washing hands before eating and after visiting crowded places.
• Maintaining a daily routine, maintaining an active lifestyle, quality nutrition according to the body’s expenses. Additional use of vitamin complexes.
• During a seasonal outbreak, avoid attending mass performances and limit your circle of contacts.
• Carry out regular wet cleaning of the premises and treatment of the child’s toys.

In addition, the serous form of inflammation of the meninges can be secondary, which means that it is necessary to promptly treat chickenpox, measles, mumps, and influenza. This will help eliminate the risk of inflammation of the membranes of the brain and spinal cord, both in adults and in children. You should not neglect preventive rules, because it is easier to prevent infection than to treat it and recover from complications associated with it.

Prognosis of serous meningitis

The prognosis of serous meningitis has a positive trend, but the final result largely depends on the state of the patient’s immune system and the timing of seeking medical help. Non-purulent changes in the membranes of the brain most often do not cause persistent complications, are quickly treated and do not relapse on days 3-7 of the disease. But if the root cause of tissue degeneration is tuberculosis, without specific drug treatment the disease is fatal. Treatment of the serous form of tuberculous meningitis is protracted and requires inpatient treatment and care for six months. But if the instructions are followed, residual pathologies such as weakening of memory, vision and hearing disappear.

In childhood, especially in babies under one year of age, a non-purulent form of inflammation of the meninges can cause serious complications - epileptic seizures, visual impairment, hearing impairment, developmental delays, low learning ability.

In rare cases, after an illness, adults develop persistent memory disorders, decreased concentration and coordination, and regularly experience severe pain in the frontal and temporal parts. The disorders persist from several weeks to six months, after which, with proper rehabilitation, complete recovery occurs.

It is important to know!

When identifying clinical manifestations of meningeal syndrome in a patient, the first priority is to establish the nature of the disease that caused it. It is imperative to exclude traumatic, inflammatory and other brain diseases accompanied by volumetric effects.

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

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

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

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

Epidemiology . Transmitted by droplets directly from person to person. There is an increase in cases of the disease in the winter-spring period and against the background of influenza epidemics. Long-term carriage is possible.

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

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

Pneumococcal meningitis. Caused by pneumococcus - a gram-positive diplococcus.

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

Clinic . Pneumococcal meningitis also develops after injury, especially a skull fracture, often accompanied by liquorrhea, which indicates communication between the nasopharynx and the subarachnoid space. The disease begins acutely. Meningeal signs are clearly expressed. Convulsions, loss of consciousness, paresis and paralysis of the limbs, abducens nerves, facial nerve, and bulbar palsy are often observed. Cerebrospinal fluid is greenish in color. It contains a large number of neutrophilic granulocytes and protein, and glucose levels are reduced.

Staphylococcal meningitis. It is a consequence of staphylococcal sepsis or subsepsis. It occurs more often in young children, starting from the first days of life. The patients' medical history included umbilical sepsis, purulent otitis media, and pustular skin diseases. With staphylococcal meningitis, the meningeal syndrome is mildly expressed, but the general condition of the patient is significantly impaired: intoxication, chills, hectic body temperature. With late diagnosis and treatment, progressive hydrocephalus is observed. Staphylococcal meningitis manifests itself more clearly in older people. Cerebrospinal fluid purulent chameningeal phenomena. The development of hydrocephalus and epileptic syndrome is possible. The cerebrospinal fluid is turbid or opalescent, mixed cytosis in the range of 0.1-1 x 109/l. To make a diagnosis, it is important to isolate the fungus from the cerebrospinal fluid. Residual organic consequences are common.

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

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

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

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

Pathomorphology : swelling and hyperemia of the soft and arachnoid meninges, perivascular diffuse infiltration of lymphocytes and plasma cells, in places small-point hemorrhages. There are similar changes in the choroid plexuses of the cerebral ventricles. The ventricles are somewhat dilated.

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

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

Enteroviral meningitis most often caused by enteroviruses such as Coxsackie and ECHO - in whitefish and Brudzinsky Lower. In young children, convulsions and stupor are possible, in older children - an excited state, delirium in severe cases of the disease, encephalitic reactions in unfavorable premorbid conditions. The cerebrospinal fluid pressure is increased to 250-500 mmH2O. Art., protein content 0.3-0.6 g/l. Cytosis is from 0.1 x 109/l to 1.5 x 109/l; in young children it is much higher, but normalizes faster.

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

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

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

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

Clinic . The disease develops acutely or subacutely. Body temperature rises, headache and meningeal symptoms appear. The cerebrospinal fluid is turbid or xanthochromic, initially transparent, flows out under increased pressure, and its protein content is increased. Reliable confirmation of the diagnosis is the detection of cryptococci in the cerebrospinal fluid. In the absence of treatment, the pressure of the cerebrospinal fluid increases, congestive optic discs appear, and symptoms of damage to the base of the brain appear. The following forms are distinguished: meningitis without pronounced focal brain damage, basilar meningitis with damage to the cranial nerves (auditory, optic, oculomotor and abducens), meningoencephalitis with symptoms of focal prolapses (paresis, ataxia), convulsions, dementia, pseudotumor, in which they are expressed as cerebral, and focal neurological symptoms. The course of the disease is often long-term, recurrent, progressive, and often fatal.

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

Class VI. Diseases of the nervous system (G00-G47)

This class contains the following blocks:
G00-G09 Inflammatory diseases of the central nervous system
G10-G13 Systemic atrophies affecting primarily the central nervous system
G20-G26 Extrapyramidal and other movement disorders
G30-G32 Other degenerative diseases of the central nervous system
G35-G37 Demyelinating diseases of the central nervous system
G40-G47 Episodic and paroxysmal disorders

INFLAMMATORY DISEASES OF THE CENTRAL NERVOUS SYSTEM (G00-G09)

G00 Bacterial meningitis, not elsewhere classified

Included: arachnoiditis)
leptomeningitis)
meningitis) bacterial
pachymeningitis)
Excluded: bacterial:
meningoencephalitis ( G04.2)
meningomyelitis ( G04.2)

G00.0 Influenza meningitis. Meningitis caused by Haemophilus influenzae
G00.1 Pneumococcal meningitis
G00.2 Streptococcal meningitis
G00.3 Staphylococcal meningitis
G00.8 Meningitis caused by other bacteria
Meningitis caused by:
Friedlander wand
Escherichia coli
Klebsiella
G00.9 Bacterial meningitis, unspecified
Meningitis:
purulent NOS
pyogenic NOS
pyogenic NOS

G01* Meningitis in bacterial diseases classified elsewhere

Meningitis (with):
anthrax ( A22.8+)
gonococcal ( A54.8+)
leptospirosis ( A27. -+)
listeriosis ( A32.1+)
Lyme disease ( A69.2+)
meningococcal ( A39.0+)
neurosyphilis ( A52.1+)
salmonellosis ( A02.2+)
syphilis:
congenital ( A50.4+)
secondary ( A51.4+)
tuberculosis ( A17.0+)
typhoid fever ( A01.0+)
Excluded: meningoencephalitis and meningomyelitis due to bacterial
diseases classified elsewhere ( G05.0*)

G02.0* Meningitis in viral diseases classified elsewhere
Meningitis (caused by a virus):
adenoviral ( A87.1+)
enteroviral ( A87.0+)
herpes simplex ( B00.3+)
infectious mononucleosis ( B27. -+)
measles ( B05.1+)
mumps ( B26.1+)
rubella ( B06.0+)
chickenpox ( B01.0+)
herpes zoster ( B02.1+)
G02.1* Meningitis due to mycoses
Meningitis (with):
candida ( B37.5+)
coccidioidomycosis ( B38.4+)
cryptococcal ( B45.1+)
G02.8* Meningitis in other specified infectious and parasitic diseases classified elsewhere
Meningitis caused by:
African trypanosomiasis ( B56. -+)
Chagas disease ( B57.4+)

G03 Meningitis due to other and unspecified causes

Included: arachnoiditis)
leptomeningitis) due to other and unspecified
meningitis) causes
pachymeningitis)
Excluded: meningoencephalitis ( G04. -)
meningomyelitis ( G04. -)

G03.0 Non-pyogenic meningitis. Nonbacterial meningitis
G03.1 Chronic meningitis
G03.2 Benign recurrent meningitis [Mollaret]
G03.8 Meningitis caused by other specified pathogens
G03.9 Meningitis, unspecified. Arachnoiditis (spinal) NOS

G04 Encephalitis, myelitis and encephalomyelitis

Includes: acute ascending myelitis
meningoencephalitis
meningomyelitis
Excluded: benign myalgic encephalitis ( G93.3)
encephalopathy:
NOS ( G93.4)
alcoholic origin ( G31.2)
toxic ( G92)
multiple sclerosis ( G35)
myelitis:
acute transverse ( G37.3)
subacute necrotizing ( G37.4)

G04.0 Acute disseminated encephalitis
Encephalitis)
Encephalomyelitis) post-immunization
If necessary, identify the vaccine
G04.1 Tropical spastic paraplegia
G04.2 Bacterial meningoencephalitis and meningomyelitis, not elsewhere classified
G04.8 Other encephalitis, myelitis and encephalomyelitis. Postinfectious encephalitis and encephalomyelitis NOS
G04.9 Encephalitis, myelitis or encephalomyelitis, unspecified. Ventriculitis (cerebral) NOS

G05* Encephalitis, myelitis and encephalomyelitis in diseases classified elsewhere

Includes: meningoencephalitis and meningomyelitis in diseases
classified elsewhere

If it is necessary to identify the infectious agent, use an additional code ( B95-B97).

G06.0 Intracranial abscess and granuloma
Abscess (embolic):
brain [any part]
cerebellar
cerebral
otogenic
Intracranial abscess or granuloma:
epidural
extradural
subdural
G06.1 Intravertebral abscess and granuloma. Abscess (embolic) of the spinal cord [any part]
Intravertebral abscess or granuloma:
epidural
extradural
subdural
G06.2 Extradural and subdural abscess, unspecified

G07* Intracranial and intravertebral abscess and granuloma in diseases classified elsewhere

Brain abscess:
amoebic ( A06.6+)
gonococcal ( A54.8+)
tuberculous ( A17.8+)
Granuloma of the brain in schistosomiasis ( B65. -+)
Tuberculoma:
brain ( A17.8+)
meninges ( A17.1+)

G08 Intracranial and intravertebral phlebitis and thrombophlebitis

Septic(s):
embolism)
endoflibit)
phlebitis) intracranial or intravertebral
thrombophlebitis) venous sinuses and veins
thrombosis)
Excluded: intracranial phlebitis and thrombophlebitis:
complicating:
abortion, ectopic or molar pregnancy ( O00 -O07 , O08.7 )
pregnancy, childbirth or the postpartum period ( O22.5, O87.3)
non-purulent origin ( I67.6); non-purulent intravertebral phlebitis and thrombophlebitis ( G95.1)

G09 Consequences of inflammatory diseases of the central nervous system

NoteThis category should be used to indicate
conditions primarily classified under headings

G00-G08(excluding those marked with *) as the cause of consequences that are themselves attributed to
Other headings The concept of “consequences” includes conditions specified as such or as late manifestations or consequences that exist for a year or more after the onset of the condition that caused them. When using this rubric, it is necessary to be guided by the appropriate recommendations and rules for coding morbidity and mortality, given in volume 2.

SYSTEMIC ATROPHY AFFECTING PRIMARILY THE CENTRAL NERVOUS SYSTEM (G10-G13)

G10 Huntington's disease

Huntington's chorea

G11 Hereditary ataxia

Excluded: hereditary and idiopathic neuropathy ( G60. -)
cerebral palsy ( G80. -)
metabolic disorders ( E70-E90)

G11.0 Congenital non-progressive ataxia
G11.1 Early cerebellar ataxia
Note: Usually begins in people under 20 years of age
Early cerebellar ataxia with:
essential tremor
myoclonus [Hunt's ataxia]
with preserved tendon reflexes
Friedreich's ataxia (autosomal recessive)
X-linked recessive spinocerebellar ataxia
G11.2 Tardive cerebellar ataxia
Note: Usually begins in people over 20 years of age
G11.3 Cerebellar ataxia with impaired DNA repair. Telangiectatic ataxia [Louis-Bar syndrome]
Excludes: Cockayne syndrome ( Q87.1)
xeroderma pigmentosa ( Q82.1)
G11.4 Hereditary spastic paraplegia
G11.8 Other hereditary ataxia
G11.9 Hereditary ataxia, unspecified
Hereditary cerebellar:
ataxia NOS
degeneration
disease
syndrome

G12 Spinal muscular atrophy and related syndromes

G12.0 Pediatric spinal muscular atrophy, type I [Werdnig-Hoffmann]
G12.1 Other hereditary spinal muscular atrophies. Progressive bulbar palsy in children [Fazio-Londe]
Spinal muscular atrophy:
adult uniform
child form, type II
distal
juvenile form, type III [Kugelberg-Welander]
scapuloperoneal form
G12.2 Motor neuron disease. Familial motor neuron disease
Lateral sclerosis:
amyotrophic
primary
Progressive:
bulbar palsy
spinal muscular atrophy
G12.8 Other spinal muscular atrophies and related syndromes
G12.9 Spinal muscular atrophy, unspecified

G13* Systemic atrophies affecting primarily the central nervous system in diseases classified elsewhere

G13.0* Paraneoplastic neuromyopathy and neuropathy
Carcinomatous neuromyopathy ( C00-S97+)
Neuropathy of the sensory organs in the tumor process [Denia-Brown] ( C00-D48+)
G13.1* Other systemic atrophies, affecting primarily the central nervous system, in tumor diseases. Paraneoplastic limbic encephalopathy ( C00-D48+)
G13.2* Systemic atrophy due to myxedema, affecting primarily the central nervous system ( E00.1+, E03. -+)
G13.8* Systemic atrophy, affecting primarily the central nervous system, in other diseases classified elsewhere

EXTRAPYRAMIDAL AND OTHER MOTOR DISORDERS (G20-G26)

G20 Parkinson's disease

Hemiparkinsonism
Shaking paralysis
Parkinsonism, or Parkinson's disease:
NOS
idiopathic
primary

G21 Secondary parkinsonism

G21.0 Neuroleptic malignant syndrome. If necessary, identify the drug
use an additional code for external causes (class XX).
G21.1 Other forms of drug-induced secondary parkinsonism.
G21.2 Secondary parkinsonism caused by other external factors
If it is necessary to identify an external factor, use an additional code of external causes (class XX).
G21.3 Postencephalitic parkinsonism
G21.8 Other forms of secondary parkinsonism
G21.9 Secondary parkinsonism, unspecified

G22* Parkinsonism in diseases classified elsewhere

Syphilitic parkinsonism ( A52.1+)

G23 Other degenerative diseases of the basal ganglia

Excludes: multisystem degeneration ( G90.3)

G23.0 Hallervorden-Spatz disease. Pigmented pallidal degeneration
G23.1 Progressive supranuclear ophthalmoplegia [Steele-Richardson-Olszewski]
G23.2 Striatonigral degeneration
G23.8 Other specified degenerative diseases of the basal ganglia. Calcification of the basal ganglia
G23.9 Degenerative basal ganglia disease, unspecified

G24 Dystonia

Included: dyskinesia
Excludes: athetoid cerebral palsy ( G80.3)

G24.0 Drug-induced dystonia. If necessary, identify the drug
use an additional code for external causes (class XX).
G24.1 Idiopathic familial dystonia. Idiopathic dystonia NOS
G24.2 Idiopathic nonfamilial dystonia
G24.3 Spasmodic torticollis
Excludes: torticollis NOS ( M43.6)
G24.4 Idiopathic orofacial dystonia. Orofacial dyskinesia
G24.5 Blepharospasm
G24.8 Other dystonias
G24.9 Dystonia, unspecified. Dyskinesia NOS

G25 Other extrapyramidal and movement disorders

G25.0 Essential tremor. Familial tremor
Excludes: tremor NOS ( R25.1)
G25.1 Drug-induced tremor
If it is necessary to identify the drug, use an additional code for external causes (class XX).
G25.2 Other specified forms of tremor. Intention tremor
G25.3 Myoclonus. Drug-induced myoclonus. If it is necessary to identify the drug, use an additional code for external causes (class XX).
Excluded: facial myokymia ( G51.4)
myoclonic epilepsy ( G40. -)
G25.4 Drug-induced chorea
If it is necessary to identify the drug, use an additional code for external causes (class XX).
G25.5 Other types of chorea. Chorea NOS
Excludes: chorea NOS with cardiac involvement ( I02.0)
Huntington's chorea ( G10)
rheumatic chorea ( I02. -)
Sydenchen's chorea ( I02. -)
G25.6 Drug-induced and other organic tics
If it is necessary to identify the drug, use an additional code for external causes (class XX).
Excludes: de la Tourette syndrome ( F95.2)
tick NOS ( F95.9)
G25.8 Other specified extrapyramidal and movement disorders
Restless legs syndrome. Shackled person syndrome
G25.9 Extrapyramidal and movement disorder, unspecified

G26* Extrapyramidal and movement disorders in diseases classified elsewhere

OTHER DEGENERATIVE DISEASES OF THE NERVOUS SYSTEM (G30-G32)

G30 Alzheimer's disease

Includes: senile and presenile forms
Excluded: senile:
brain degeneration NEC ( G31.1)
dementia NOS ( F03)
senility NOS ( R54)

G30.0 Early Alzheimer's disease
Note The onset of the disease usually occurs in people under 65 years of age
G30.1 Late Alzheimer's disease
Note The onset of the disease usually occurs in people over 65 years of age
G30.8 Other forms of Alzheimer's disease
G30.9 Alzheimer's disease, unspecified

G31 Other degenerative diseases of the nervous system, not elsewhere classified

Excluded: Reye's syndrome ( G93.7)

G31.0 Limited brain atrophy. Pick's disease. Progressive isolated aphasia
G31.1 Senile degeneration of the brain, not elsewhere classified
Excludes: Alzheimer's disease ( G30. -)
senility NOS ( R54)
G31.2 Nervous system degeneration caused by alcohol
Alcoholic:
cerebellar:
ataxia
degeneration
cerebral degeneration
encephalopathy
Alcohol-induced autonomic nervous system disorder
G31.8 Other specified degenerative diseases of the nervous system. Gray matter degeneration [Alpers disease]
Subacute necrotizing encephalopathy [Leigh's disease]
G31.9 Degenerative disease of the nervous system, unspecified

G32* Other degenerative disorders of the nervous system in diseases classified elsewhere

G32.0* Subacute combined degeneration of the spinal cord in diseases classified elsewhere
Subacute combined degeneration of the spinal cord due to vitamin deficiency AT 12 (E53.8+)
G32.8* Other specified degenerative disorders of the nervous system in diseases classified elsewhere

DEMYELINATING DISEASES OF THE CENTRAL NERVOUS SYSTEM (G35-G37)

G35 Multiple sclerosis

Multiple sclerosis:
NOS
brain stem
spinal cord
disseminated
generalized

G36 Other form of acute disseminated demyelination

Excluded: post-infectious encephalitis and encephalomyelitis NOS ( G04.8)

G36.0 Neuromyelitis optica [Devic's disease]. Demyelination in optic neuritis
Excluded: optic neuritis NOS ( H46)
G36.1 Acute and subacute hemorrhagic leukoencephalitis [Harst disease]
G36.8 Another specified form of acute disseminated demyelination
G36.9 Acute disseminated demyelination, unspecified

G37 Other demyelinating diseases of the central nervous system

G37.0 Diffuse sclerosis. Periaxial encephalitis, Schilder's disease
Excluded: adrenoleukodystrophy [Addison-Schilder] ( E71.3)
G37.1 Central demyelination of the corpus callosum
G37.2 Central pontine myelinolysis
G37.3 Acute transverse myelitis in demyelinating disease of the central nervous system
Acute transverse myelitis NOS
Excluded: multiple sclerosis ( G35)
Neuromyelitis optica [Devic's disease] ( G36.0)
G37.4 Subacute necrotizing myelitis
G37.5 Concentric sclerosis [Balo]
G37.8 Other specified demyelinating diseases of the central nervous system
G37.9 Demyelinating disease of the central nervous system, unspecified

EPISODICA AND PAROXYSMAL DISORDERS (G40-G47)

G40 Epilepsy

Excluded: Landau-Kleffner syndrome ( F80.3)
seizure NOS ( R56.8)
status epilepticus ( G41. -)
Todd's paralysis ( G83.8)

G40.0 Localized (focal) (partial) idiopathic epilepsy and epileptic syndromes with seizures with focal onset. Benign childhood epilepsy with EEG peaks in the central temporal region
Childhood epilepsy with paroxysmal activity and EEG in the occipital region
G40.1 Localized (focal) (partial) symptomatic epilepsy and epileptic syndromes with simple partial seizures. Seizures without changes in consciousness. Simple partial seizures, developing into secondary
generalized seizures
G40.2 Localized (focal) (partial) symptomatic epilepsy and epileptic syndromes with complex partial seizures. Seizures with changes in consciousness, often with epileptic automatism
Complex partial seizures progressing to secondary generalized seizures
G40.3 Generalized idiopathic epilepsy and epileptic syndromes
Benign(s):
myoclonic epilepsy of early childhood
neonatal seizures (familial)
Childhood epileptic absence seizures [pycnolepsy]. Epilepsy with grand mal seizures on awakening
Juvenile:
absence epilepsy
myoclonic epilepsy [impulsive petit mal]
Nonspecific epileptic seizures:
atonic
clonic
myoclonic
tonic
tonic-clonic
G40.4 Other types of generalized epilepsy and epileptic syndromes
Epilepsy with:
myoclonic absence seizures
myoclonic-astatic seizures

Baby spasms. Lennox-Gastaut syndrome. Salaam's tick. Symptomatic early myoclonic encephalopathy
West syndrome
G40.5 Special epileptic syndromes. Epilepsy partial continuous [Kozhevnikova]
Epileptic seizures associated with:
drinking alcohol
use of medicines
hormonal changes
sleep deprivation
exposure to stress factors
If it is necessary to identify the drug, use an additional code for external causes (class XX).
G40.6 Grand mal seizures, unspecified (with or without minor seizures)
G40.7 Minor seizures, unspecified, without grand mal seizures
G40.8 Other specified forms of epilepsy. Epilepsy and epileptic syndromes not defined as focal or generalized
G40.9 Epilepsy, unspecified
Epileptic:
convulsions NOS
seizures NOS
seizures NOS

G41 Status epilepticus

G41.0 Status epilepticus grand mal (convulsive seizures). Tonic-clonic status epilepticus
Excluded: partial continuous epilepsy [Kozhevnikova] ( G40.5)
G41.1 Zpileptic status petit mal (minor seizures). Status epilepticus absence seizures
G41.2 Complex partial status epilepticus
G41.8 Other specified status epilepticus
G41.9 Status epilepticus, unspecified

G43 Migraine

Excludes: headache NOS ( R51)

G43.0 Migraine without aura [simple migraine]
G43.1 Migraine with aura [classical migraine]
Migraine:
headache-free aura
basilar
equivalents
familial hemiplegic
hemiplegic
With:
aura in acute onset
long lasting aura
typical aura
G43.2 Migrainous status
G43.3 Complicated migraine
G43.8 Another migraine. Ophthalmoplegic migraine. Retinal migraine
G43.9 Migraine, unspecified

G44 Other headache syndromes

Excluded: atypical facial pain ( G50.1)
headache NOS ( R51)
trigeminal neuralgia ( G50.0)

G44.0 Histamine headache syndrome. Chronic paroxysmal hemicrania.

Histamine headache:
chronic
episodic
G44.1 Vascular headache, not elsewhere classified. Vascular headache NOS
G44.2 Tension type headache. Chronic tension headache
Episodic tension headache. Tension headache NOS
G44.3 Chronic post-traumatic headache
G44.4 Drug-induced headache, not elsewhere classified
If it is necessary to identify the drug, use an additional code for external causes (class XX).
G44.8 Other specified headache syndrome

G45 Transient transient cerebral ischemic attacks [attacks] and related syndromes

Excludes: neonatal cerebral ischemia ( P91.0)

G45.0 Vertebrobasilar arterial system syndrome
G45.1 Carotid artery syndrome (hemispheric)
G45.2 Multiple and bilateral cerebral artery syndromes
G45.3 Transient blindness
G45.4 Transient global amnesia
Excludes: amnesia NOS ( R41.3)
G45.8 Other transient cerebral ischemic attacks and associated syndromes
G45.9 Transient cerebral ischemic attack, unspecified. Cerebral artery spasm
Transient cerebral ischemia NOS

G46* Vascular brain syndromes in cerebrovascular diseases ( I60-I67+)

G46.0* Middle cerebral artery syndrome ( I66.0+)
G46.1* Anterior cerebral artery syndrome ( I66.1+)
G46.2* Posterior cerebral artery syndrome ( I66.2+)
G46.3* Brainstem stroke syndrome ( I60-I67+)
Syndrome:
Benedicta
Claude
Fauville
Millard-Jublay
Wallenberg
Weber
G46.4* Cerebellar stroke syndrome ( I60-I67+)
G46.5* Pure motor lacunar syndrome ( I60-I67+)
G46.6* Pure sensory lacunar syndrome ( I60-I67+)
G46.7* Other lacunar syndromes ( I60-I67+)
G46.8* Other vascular syndromes of the brain in cerebrovascular diseases ( I60-I67+)

G47 Sleep disorders

Excluded: nightmares ( F51.5)
sleep disorders of non-organic etiology ( F51. -)
night terrors ( F51.4)
sleepwalking ( F51.3)

G47.0 Disturbances in falling asleep and maintaining sleep [insomnia]
G47.1 Disturbances in the form of increased sleepiness [hypersomnia]
G47.2 Disturbances in sleep-wake cycles. Delayed sleep phase syndrome. Disturbance of the sleep-wake cycle
G47.3 Sleep apnea
Sleep apnea:
central
obstructive
Excludes: Pickwickian syndrome ( E66.2)
sleep apnea in newborns ( P28.3)
G47.4 Narcolepsy and cataplexy
G47.8 Other sleep disorders. Kleine-Levin syndrome
G47.9 Sleep disorder, unspecified