Antibiotics for meningococcal infection in children. Clinic of localized forms: meningococcal nasopharyngitis

Epidemiology

The source of infection is patients (especially at the beginning of the disease) and bacteria carriers. Way of transmission of infection: airborne. The contagiousness index is low. The incidence is 5-5.5 per 100 thousand of the population. Mostly young children get sick.

Etiology and pathogenesis

Meningococcus (Neisseria meningitidis), gram-negative diplococcus: unstable, quickly dies in the external environment.
In the pathogenesis of the development of hemorrhagic rash, disturbances in the processes of hemostasis are important, which lead to the development of DIC. Meningococci can cross the blood-brain barrier through the hematogenous route and enter the meninges, causing inflammation.

Principles of classification

In form: localized - nasopharyngitis, generalized - meningitis, meningoencephalitis, meningococcemia. By severity: mild, moderate and severe.

Clinic

The incubation period is from 1 to 7 days. The duration of periods of peak, reverse development, convalescence depends on the severity and clinical form of the disease. Meningococcal nasopharyngitis is rarely diagnosed if a positive result of meningococcal culture from the nasopharyngeal mucosa in contacts is established. Meningococcemia or meningococcal sepsis is a life-threatening form of the disease for a child. The average incidence is 1 per 1000 children infected with meningococcus. The main symptoms of this form are rapidly increasing severe intoxication and a characteristic urticarial, maculopapular hemorrhagic stellate rash. In the first hours of the disease, elements of the rash appear on the skin of the feet, legs, buttocks, then spread to the limbs, face and trunk. The rash is purple, cyanotic, round or star-shaped, the elements may merge. Extensive hemorrhages, at the site of which necrosis occurs, followed by their rejection and the formation of defects and scars that remain long time. With meningococcemia, joints (polyatritis), eyes (uveitis, iridocycline, panophthalmitis), heart (endo, myo-, pericarditis), liver (hepatolienal syndrome), kidneys (pyelitis, glomerulonephritis), adrenal glands (acute adrenal insufficiency) can be affected.
Meningococcal meningitis (meningoencephalitis) is characterized by an acute onset, a pronounced syndrome of general intoxication, headaches, repeated vomiting, meningeal symptoms - neck stiffness, Kernig's symptom, Lesage's, Brudzinsky's symptoms, pulsation and bulging of the large fontanel. Focal symptoms indicate the development of encephalitis, cerebral edema. In the general clinical analysis of blood: leukocytosis, neutrophilia with a shift to the left, aneosinophilia, increased ESR.

Diagnostics

Consultation of infectious disease specialist, neurologist. Sowing from the nasopharynx for meningococcus. Bacterioscopy of blood and cerebrospinal fluid for meningococcus. Mucus, blood and cerebrospinal fluid cultures for meningococcus. Serological diagnostics - RPGA, VIEF in dynamics.

Differential Diagnosis

Carried out with angina, acute pharyngitis, peritonsillar abscess, pseudotuberculosis, scarlet fever, tuberculous meningitis, adrenal insufficiency, etc.

Treatment and prevention

All patients with suspected meningococcal infection are subject to hospitalization in an infectious diseases hospital. Etiotropic therapy. Penicillin IV every 4 to 6 hours high doses ah or erythromycin, with meningitis "ceftriaxone (rocephin) or cefotaxime, chloramphenicol intravenously for 1 week. Children of the 1st year of life with meningitis are given a short course of dexazone: 0.6 mg per day (for 4 injections) for 2 days against the background of antibiotic therapy. Emergency care for acute adrenal insufficiency: intravenous injection of a 10% glucose solution, hydrocortisone 20-50 mg. After the appearance of a pulse, they switch to a drip of liquid (the daily dose of prednisolone is adjusted to 2.5-7 mg / kg, hydrocortisone to 10-15 mg / kg). The total duration of steroid therapy is 3-5 days.
Recovery Criteria: complete disappearance of clinical symptoms. Conducting a full course antibiotic therapy. Double negative cultures from the mucous membrane of the nasopharynx for meningococcus. Observation after recovery of a pediatrician and a neuropathologist according to clinical indications for at least 1 year. Anti-epidemic measures: isolation of the patient until complete clinical and bacteriological recovery. Quarantine on contacts is imposed for 10 days from the moment of separation from the patient. Contacts are monitored clinically with daily thermometry. All contacts with invasive forms of meninococcal infection (meningitis, meningococcemia) are prescribed chemoprophylaxis: 2 days of rifampicin or a single dose of ceftriaxone, ciprofloxacin. Sowing from the nasopharynx in contacts for meningococcus at least 2 times at intervals of 3-7 days, daily wet cleaning and ventilation of the premises.
Vaccination: meningococcal A, C, Y vaccines are administered to children at risk (asplenia, children under 2 years of age, primary immunodeficiency), during outbreaks of the disease.

RCHD (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical protocols MH RK - 2014

Meningococcal infection (A39)

Infectious diseases in children, Pediatrics

general information

Short description

RSE on REM "Republican Center for Health Development"

Ministry of Health and social development Republic of Kazakhstan

Meningococcal infection- an acute human infectious disease caused by meningococcus and characterized by a variety of clinical manifestations: from nasopharyngitis and healthy carriage to generalized forms in the form of purulent meningitis, meningoencephalitis and meningococcemia with damage to various organs and systems.

I. INTRODUCTION

Protocol name: Meningococcal infection in children

Protocol code:

Code (codes) according to ICD-10:

A39 - Meningococcal infection

A39.0 Meningococcal meningitis

A39.1 - Waterhouse-Friderichsen syndrome (meningococcal adrenal syndrome)

A39.2 - Acute meningococcemia

A39.3 Chronic meningococcemia

A39.4 Meningococcemia, unspecified

A39.5 ​​- Meningococcal heart disease

A39.8 - Other meningococcal infections

A39.9 Meningococcal infection, unspecified

Abbreviations used in the protocol:

In / in - intravenously

V / m - intramuscularly

GP - general practitioner

VR - recalcification time

GHB - gamma-hydroxybutyric acid

DIC - disseminated intravascular coagulation

DDU - preschool institution

IMCI - integrated management of childhood illnesses

ITSH - infectious-toxic shock

ELISA - enzyme immunoassay

CDC - advisory- diagnostic center
KOS - acid-base state
CT - CT scan
KShchR - acid-base balance
INR - international normalized ratio
MRI - magnetic resonance imaging
ENT - laryngo-otoringologist
HPF - general signs of danger
PT - prothrombin time
PHC - primary health care
PCR polymerase chain reaction
RNGA - reaction of indirect hemagglutination
RPHA - passive hemagglutination reaction
FFP - fresh frozen plasma
ESR - erythrocyte sedimentation rate
FAP - feldsher-obstetric station
CSF - cerebrospinal fluid
cranial nerves
TBI - traumatic brain injury
N. meningitidis

Protocol development date: 2014.

Protocol Users: pediatric infectious disease specialist, general practitioner, pediatrician, emergency physician, anesthesiologist-resuscitator, paramedic.

Classification

Clinical classification of meningococcal infection

According to clinical forms:

1. Typical:

A) localized forms: carriage; nasopharyngitis;
b) generalized forms: meningococcemia, meningitis, meningoencephalitis; mixed form (meningitis + meningococcemia);
in) rare forms Key words: endocarditis, arthritis, pneumonia, iridocyclitis.

2. Atypical:

A) subclinical form;
b) abortive form.

According to the severity of the process:

1. light;

2. moderate;

3. heavy.

According to the course of the disease:

1. acute;

2. lightning fast;

3. protracted;

4. chronic.

Classification of complications:

By the time of development of complications:
I. Early:

Infectious-toxic shock I, II, III degree;

swelling of the brain;

DIC;

Acute renal failure;

Cerebral hypotension;

subdural effusion;

Ependymatitis.

II. Later:

Impairment of the intellect;

Hypertension syndrome;

Hydrocephalus;

epileptic syndrome;

Paralysis and paresis;

Necrosis of the skin and subcutaneous tissue;

endocrine disorders ( diabetes insipidus, diencephalic obesity, hair loss, etc.);

Arthritis;

Hearing impairment.

Diagnostics

ΙΙ. METHODS, APPROACHES AND PROCEDURES FOR DIAGNOSIS AND TREATMENT

List of basic and additional diagnostic measures

Basic (mandatory) diagnostic examinations performed at the outpatient level in patients with meningococcal nasopharyngitis, meningococcal carriage and contact persons:

General blood analysis;

Additional diagnostic examinations performed at the outpatient level: not performed.

The minimum list of examinations that must be carried out when referring to planned hospitalization: (only for planned hospitalization with nasopharyngitis and meningococcal disease):

General blood analysis;

Bacteriological examination of a swab from the nasopharynx for N. meningitidis.

The main (mandatory) diagnostic examinations carried out on stationary level (in case of emergency hospitalization):

General blood analysis;

General urine analysis;

Biochemical blood test (creatinine, urea, glucose, total protein and protein fractions, electrolytes: potassium, sodium, calcium, chlorine, ALT, AST, bilirubin);

Coagulogram (PV-PTI-INR, PV, APTT, RFMK, fibrinogen, TV, clotting time, bleeding time);

Spinal puncture: examination of cerebrospinal fluid for cytosis, determination of sugar, chlorides, protein;

Bacteriological examination of a swab from the nasopharynx for N. meningitidis

Bacteriological examination of cerebrospinal fluid;

Bacteriological examination of blood;

Blood on a "thick drop" for bacterioscopy;

Bacterioscopy of cerebrospinal fluid.

Additional diagnostic examinations carried out at the hospital level(in case of emergency hospitalization):

Determination of blood gases;

Bacteriological examination of exudate from petechiae;

X-ray of the chest organs;

MRI of the brain (in the absence of positive dynamics during treatment);

CT scan of the brain (in the absence of positive dynamics during treatment);

Diagnostic measures carried out at the stage of emergency emergency care:

Collection of complaints and anamnesis of the disease (including epidemiological anamnesis);

Physical examination.

Diagnostic criteria

Complaints and anamnesis:
Complaints:

Temperature rise;

headache, anxiety; painful shrill cry in infants;

Repeated vomiting that does not bring relief;

Rash on the body

convulsions;

Photophobia;

Nasal congestion;

Sore throat;

Anamnesis:

Acute onset of the disease;

Epidemiological history: contact with a patient with fever, rash and catarrhal phenomena, contact with a carrier of N. meningitidis.

Physical examination:

Paleness of the skin;

Rash with predominant localization on the buttocks, thighs, legs, hemorrhagic "star" with necrosis in the center at the onset of the disease; the presence of a hemorrhagic rash on the face indicates the severity of the disease and is an unfavorable prognostic sign;

In children under one year old - tension and bulging of a large fontanelle, a positive symptom of Lessage or "suspension";

Excitation, followed by lethargy;

Hyperesthesia, "brain scream";

Throwing back the head, the pose of the "pointing dog";

Neck stiffness;

Positive symptoms of Brudzinsky, Kernig;

Decreased abdominal reflexes;

Tachycardia, deafness of heart sounds, systolic murmur, decrease in blood pressure;

With the development of cerebral edema: a rapidly passing lesion of craniocerebral insufficiency - usually III, VI, VII and VIII pairs; positive symptom of Babinski (normally occurs in children under 1 month of age);

Hyperemia, edema and hyperplasia of the lymphoid follicles of the posterior pharyngeal wall, swelling of the lateral ridges, a small amount of mucus.

Laboratory research:
General blood analysis: neutrophilic leukocytosis with a stab shift to the left, increased ESR; possible anemia, thrombocytopenia.
General urine analysis: albuminuria, cylindruria, microhematuria (in severe generalized forms as a result of toxic damage to the kidneys).
CSF study:

Color - on the first day of illness, the cerebrospinal fluid may still be transparent or slightly opalescent, but by the end of the day it becomes cloudy, milky white or yellowish green (the norm is transparent);

Pressure - flows out in a jet or frequent drops, the pressure reaches 300-500 mm of water. Art. (norm - 100-150 mm water column);

Neutrophilic cytosis up to several thousand in 1 µl or more;

Increase in protein up to 1-4.5 g/l;

Decreased sugar;

Decrease in chlorides;

With the development of meningoencephalitis - high protein content.

Instrumental research:

X-ray of the respiratory organs: signs of pneumonia, pulmonary edema (with the development of nonspecific complications);

CT / MRI of the brain: cerebral edema, the presence of brain abscesses and volumetric process.

Indications for consultation of narrow specialists:

Consultation of a neurologist (for meningitis and meningoencephalitis);

Consultation of an ophthalmologist (for meningitis and meningoencephalitis);

Consultation of a surgeon (with meningococcemia - in case of development of necrosis);

Consultation of a neurosurgeon - if pathological changes are detected on CT / MRI of the brain;

Consultation of an otolaryngologist - with nasopharyngitis, differential diagnosis of meningitis.

Differential Diagnosis

Differential Diagnosis

Table 1)***Differential Diagnosis bacterial meningitis by etiology

Symptoms	meningococcal meningitis	Pneumococcal meningitis	Hib meningitis
Age	any, most often children under 2 years of age	any	1-15 years old
Epidemiological history	from the center or without features	without features
Premorbid background	nasopharyngitis or no features	pneumonia	pneumonia, ENT pathology, TBI
The onset of the disease	sharp, stormy	acute	acute or gradual
Complaints	sharp headache, repeated vomiting, fever up to 39-400C, chills	headache, repeated vomiting, fever up to 39-400C, chills	headache, fever, chills
Presence of exanthema	in combination with meningococcemia - hemorrhagic rash	with septicemia, a hemorrhagic rash (petechiae) is possible	not typical
meningeal symptoms	pronounced with an increase in the first hours of the disease	become pronounced from 2-3 days	become pronounced from 2-4 days
Damage to lymphoid tissue	-	-	-
Organ lesions	pneumonia, endocarditis, arthritis, iridocyclitis. With complications - hemorrhage and necrosis of the adrenal glands, cerebral edema, etc.	pneumonia, endocarditis	pneumonia, otitis, sinusitis, arthritis, conjunctivitis, epiglotitis
General blood analysis	hyperleukocytosis, shift of the formula to the left, increased ESR	severe leukocytosis with a shift to the left, increased ESR
Color, transparency of liquor	milky white, cloudy	green-gray, cloudy	white with a greenish tinge, cloudy
Pleocytosis (cell/µl)	incalculable, neutrophilic (up to 1000-15000)	neutrophilic up to 1000-2000
	0,66-16,0	3,0-16,0	1,0-16,0
Dissociation in CSF	mostly cellular protein	more often proteinaceous	not typical
Glucose content in cerebrospinal fluid	reduced moderately
	reduced moderately

Table 2)***Differential diagnosis of viral meningitis by etiology

Symptoms	Enteroviral meningitis	Mumps meningitis	tuberculous
Age	preschool and school age		any
Epidemiological background	summer autumn	winter spring	social factors or contact with a patient, history of pulmonary or extrapulmonary tuberculosis, HIV infection
The onset of the disease	acute		gradual, progressive
Clinic	headache, sharp, short, repeated vomiting, fever up to 38.5-390C, two-wave fever with intervals between waves of 1-5 days	at the height of the disease, after inflammation of the salivary glands, but sometimes before the development of parotitis, a severe headache, vomiting, hyperthermia appear	moderate headache, fever up to 37-39C
Organ manifestations of the disease	enteritis, exanthema, herpangina, myalgia, hepatolienal syndrome	damage to the salivary glands (mumps, submaxilitis, sublinguitis), orchitis, pancreatitis	specific damage to various organs, tuberculosis of the lymph nodes with hematogenous dissemination
meningeal syndrome	from the 1st-2nd day of illness, mild, short-term, absent in 20% of cases	positive meningeal symptoms	moderately pronounced, in dynamics with an increase
General blood analysis	normal, sometimes slight leukocytosis or leukopenia, neutrophilia, moderate increase in ESR		slight changes in leukogram parameters, moderate increase in ESR
Color, transparency of CSF	colorless, transparent		transparent, when standing for 72 hours, a delicate film of fibrin falls out
Pleocytosis (cell/µl)	initially mixed, then lymphocytic up to 400-800	lymphocytic up to 500	mixed up to 50-500
Protein content in liquor (g/l)	normal or reduced	normal or elevated to 1.0	1,0-10,0
Glucose content in cerebrospinal fluid	moderately elevated	normal or moderately elevated	significantly reduced
Chloride content (mmol/l)	moderately elevated	moderately elevated	significantly reduced

Table (3)***Differential diagnosis of meningococcemia

Symptoms	Meningococcal infection, meningococcemia	Measles	Scarlet fever	Pseudotuberculosis	allergic rash
1	2	3	4	5	6
The onset of the disease	acute, often violent, with an increase in body temperature, a violation of the general condition	catarrhal phenomena and intoxication, aggravated within 2-4 days	acute, fever, sore throat, vomiting	acute, with a gradual increase in symptoms, fever, abdominal pain	acute, rash and pruritus
Temperature response	rapid rise to high numbers in the first hours of the disease	up to 38-390С, two-wave (during the catarrhal period and during the period of rashes)	high up to 38-39С0 within 2-3 days	high, prolonged fever, may be undulating	-
Intoxication	pronounced	expressed within 5-7 days	pronounced	pronounced, prolonged	not typical
	upper respiratory catarrh	pronounced: barking cough, rhinitis, conjunctivitis	missing	missing	missing
Time of rash onset	1st day of illness, first hours of illness	On the 3rd-4th day of illness	1st-2nd day of illness	3-8th day of illness	1st day of illness
The order of the rashes	simultaneously	staging of rashes, starting from the face, within 3 days	simultaneously	simultaneously	simultaneously
Rash morphology	hemorrhagic, stellate irregular shape, necrosis in the center, single elements are possible	maculopapular, irregularly shaped, prone to fusion against an unchanged skin background	punctate, abundant on a hyperemic background of the skin	polymorphic (small-spotted, small-spotted) on an unchanged background of the skin	maculopapular, erythematous, urticarial
Rash size	from petechiae to extensive hemorrhages	medium size and large	shallow	shallow	large and medium size
Localization of the rash	buttocks, lower limbs, face, arms, torso	depending on the day of the rash (1st day - on the face, 2nd day - on the face and trunk, 3rd day - on the face, trunk and limbs)	all over the body (except for the nasolabial triangle), mainly on the flexion surfaces, symmetrical thickening in natural folds	on the flexion surfaces of the extremities, around the joints, like "socks", "gloves", "hood"	all over the body
Regression of the rash	necrosis and scars in the place of extensive hemorrhages	passes into pigmentation in the same order in which it appeared	disappears without a trace after 3-5 days	disappears without a trace	disappears after a few hours or days, sometimes with pigmentation
Peeling	missing	small bran-like	large-lamellar, at 2-3 weeks of illness	small pityriasis on the body and large-lamellar on the palms, feet on the 5th-6th day	missing
Changes in the oropharynx	hyperemia, hyperplasia of the lymphoid follicles of the posterior pharyngeal wall	diffuse hyperemia of the mucosa, Belsky-Filatov-Koplik spots, enanthema on the soft palate	limited hyperemia of the pharynx, the phenomenon of purulent tonsillitis, raspberry tongue	crimson tongue	missing
Changes in other organs and systems	may be associated with meningitis	conjunctivitis, laryngitis, pneumonia	missing	damage to the intestines, liver, spleen, joints	angioedema
General blood analysis	hyperleukocytosis, neutrophilia, increased ESR	leukopenia, neutropenia, with complications - increased ESR	leukocytosis, neutrophilia, accelerated ESR	high leukocytosis and neutrophilia, a significant increase in ESR	eosinophilia

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Treatment

Treatment goals:

Relief of intoxication;

Relief of meningeal syndrome and sanitation of cerebrospinal fluid;

Eradication (elimination) of the pathogen.

Treatment tactics

Non-drug treatment:
Bed rest (generalized forms).
The diet is a complete, easily digestible food.

Chloramphenicol - 40 mg / kg per day (tablets of 0.25 and 0.5 g);

Erythromycin - from 20 to 50 mg / kg per day (tablets of 0.1 and 0.25 gr.);

Amoxicillin - 45 mg / kg per day (tablets of 0.25 g, syrup of 5.0-125 mg).

Treatment of meningococcal meningitis
Antibacterial therapy(treatment course 7-10 days):
Options for antibiotic therapy regimens
Scheme 1: benzylpenicillin sodium salt - 300-500 thousand units / kg per day, administered every 3 or 4 hours, intramuscularly, intravenously;
Scheme 2: benzylpenicillin sodium salt - 300-500 thousand units / kg per day, administered every 3 or 4 hours, intramuscularly, intravenously; and / or ceftriaxone - 100 mg / kg per day (1-2 times a day) / m or / in,
Scheme 3: benzylpenicillin sodium salt - 300-500 thousand units / kg per day, (administered every 3 or 4 hours, intramuscularly, intravenously) in combination with cefotaxime - up to 200 mg / kg per day every 6 hours .
When indicating severe allergic reactions to cephalosporins and penicillins, prescribe chloramphenicol 100 mg/kg per day (iv).

Treatment of meningitis in combination with meningococcemia(without ITSH)
Antibacterial therapy(treatment course 7-10 days):
Chloramphenicol - 100 mg / kg per day IV for 1-2 days, followed by the appointment of benzylpenicillin sodium salt - 300-500 thousand U / kg per day, administered every 3 or 4 hours, intramuscularly, intravenously; (in the absence of the development of TSS) or according to the above schemes.

Criteria for antibiotic withdrawal:

clinical recovery;

Normalization of the parameters of the general blood test and sanitation of the cerebrospinal fluid (lymphocytic cytosis in 1 μl of less than 100 cells or total cytosis of less than 40 cells).

Detoxification therapy in dehydration mode
Infusion in / in is carried out in a volume of 30-40 ml / kg per day.
For this purpose, mannitol (15% solution) with furosemide, crystalloids (physiological saline, 10% dextrose solution) and colloids (dextran, hydroxyethyl starch solutions, gelafusin, meglumine sodium succinate) are used.

Pathogenetic therapy for the relief of intracranial hypertension:

Magnesium sulfate - 0.1-0.2 ml / kg of 20% solution in / m;

Acetazolamide - 10-15 mg / kg per day in combination with potassium and magnesium aspartate (according to the scheme).

Anticonvulsant therapy:

Phenobarbital at the rate of 1-3 mg / kg per day;

Diazepam - 5 mg / ml, solution - 0.1 ml / kg or 0.1 mg / kg / day.

Sodium oxybate - 20% solution - 50-150 mg / kg (single dose),

In the absence of effect - sodium thiopental - 5-10 mg / kg every 3 hours, daily dose up to 80 mg / kg;

Treatment of meningococcemia(without ITSH):

Criteria for antibiotic withdrawal:

clinical recovery;

Normalization of indicators of the general analysis of blood.

TSS treatment
For the treatment of patients with TSS in a hospital, it is necessary:
Continuous oxygenation by supplying humidified oxygen through a mask or nasal catheter;
Insertion of a catheter into bladder for a period until the patient is taken out of shock to determine hourly diuresis in order to correct the ongoing therapy.

Sequence of administration of drugs for TSS
Assess the patient's condition - hemodynamics (signs of shock in children under 5 years of age according to IMCI), respiration, level of consciousness, nature and growth of the rash.

Restore airway patency, give oxygen, if necessary - tracheal intubation and transfer to mechanical ventilation;

venous access. Start with central/peripheral venous catheterization.

Intensive infusion therapy successively 3 jet injections of 20 ml / kg (ratio of crystalloids and colloids 1: 1), if necessary, then more, based on the hemodynamic response to the infusion. If the child is severely malnourished, the volume of fluids and the rate of infusion should be different, so check to see if the child has severe violation nutrition.

Administer prednisolone at a dose of:

With TSS 1 degree - prednisolone 2-5 mg / kg / day, dexamethasone - 0.2-0.3 mg / kg / day, hydrocortisone - 12.5 mg / kg per day;

With TSS 2 degrees - prednisolone 10-15 mg / kg / day, dexamethasone - 0.5-1.0 mg / kg / day, hydrocortisone - 25 mg / kg per day;

With grade 3 TSS - prednisolone 20 mg / kg / day, dexamethasone - 1.0 mg / kg / day, hydrocortisone - 25-50 mg / kg per day;

Introduce an antibiotic - chloramphenicol at a dose of 25 mg / kg IV (single dose), per day - 100 mg / kg, every 6 hours;

Heparin therapy (every 6 hours):

ITSH 1 degree - 50-100 units / kg,
ITSH 2nd degree - 25-50 units / kg,
ITSH 3 degrees -10-15 units / kg

In the absence of the effect of hormonal therapy, start the introduction of first-order catecholamine - Dopamine with 5-10 mcg / kg / min under the control of blood pressure;

Correction metabolic acidosis: transfer to a ventilator;

In the absence of a hemodynamic response to dopamine (at a dose of 20 mcg / kg / min), start the introduction of Epinephrine / norepinephrine at a dose of 0.05-2 mcg / kg / min;

Re-introduction of hormones at the same dose - after 30 minutes with compensated THS, after 10 minutes with decompensated THS;

Protease inhibitors - aprotonin - from 500-1000 ATU / kg (single dose).

With stabilization of blood pressure - furosemide 1% - 1-3 mg / kg / day;

In the presence of concomitant cerebral edema - mannitol 15% - 1-1.5 g / kg;

Transfusion of FFP, erythrocyte mass.

Transfusion of FFP 10-20 ml / kg, erythrocyte mass, if indicated, in accordance with the order of the Minister of Health of the Republic of Kazakhstan dated 06.11.2009 No. 666.

Treatment of cerebral edema
Treatment of cerebral edema is reduced to the elimination of cerebral hypoxia, normalization of the metabolism of brain tissue and osmoregulatory systems of the brain.

General medical measures with cerebral edema:
1. Ensure adequate lung ventilation and gas exchange. This is achieved either by various methods of oxygen therapy, or by transferring the patient to mechanical ventilation with the addition of non-toxic oxygen concentrations (30-40%) to the respiratory mixture. It is advisable to maintain PaO2 at the level of 100-120 mm Hg. with moderate hypocapnia (PaCO2 - 25-30 mm Hg), i.e. carry out IVL in the mode of moderate hyperventilation.

2. Ensuring vascular access

3. Dehydration therapy:

10% sodium chloride solution - 10 ml/kg for 1 hour

25% magnesium sulfate solution - 0.2-0.8 ml / kg

Osmodiuretics - daily dose of mannitol solution (10, 15 and 20%):

For children infancy- 5-15 g

Younger age - 15-30 g

Older age - 30-75 g.

diuretic effect expressed very well, but depends on the rate of infusion, so the estimated dose of the drug should be administered in 10-20 minutes. The daily dose (0.5-1.5 g dry matter/kg) should be divided into 2-3 injections.

You should pay attention!
Contraindications to the appointment of mannitol are:

Acute tubular necrosis

BCC deficit

Severe cardiac decompensation.

Saluretics - furosemide at doses of 1-3 (in severe cases up to 10) mg / kg several times a day to supplement the effect of mannitol (introduced 30-40 minutes after the end of the mannitol infusion)

Corticosteroids - dexamethasone is prescribed according to the following scheme: an initial dose of 2 mg / kg, after 2 hours -1 mg / kg, then every 6 hours during the day - 2 mg / kg; then 1 mg/kg/day for a week.

4. Barbiturates. 10% sodium thiopental solution intramuscularly at 10 mg/kg every 3 hours. Daily dose up to 80 mg/kg. You should pay attention! You can not use barbiturates with arterial hypotension and not replenished BCC.

5. Antihypoxants- sodium oxybate 20% solution at a dose of 50-70 mg/kg (single dose).

6. With severe peripheral vasoconstriction- dopamine at a dose of 5-10 mcg / kg / min

7. Infusion therapy It is aimed at normalizing indicators of central and peripheral hemodynamics, correcting indicators of water and electrolyte balance, acid-base status, prevention and relief of DIC.

8. Limiting water load up to 2/3 daily requirement

table Physiological needs for fluids depending on the age of the child

Age	Water requirement, ml/kg/day
1 day	60-80
2 days	80-100
3 days	100-120
4-7 days	120-150
2-4 weeks	130-160
3 months	140-160
6 months	130-155
9 months	125-145
1 year	120-135
2 years	115-125
4 years	100-110
6 years	90-100
10 years	70-85
14 years old	50-60
18 years	40-60

9. Calculation of the child's daily fluid requirement: physiological need + fluid deficiency + pathological fluid loss

10. Calculation of fluid deficit:
dehydration 1 tbsp.:
up to 1 year - 5% of body weight (50 ml / kg / day)
> 1 year - 3% of body weight (40 ml/kg/mut)

Dehydration stage 2:
up to 1 year - 10% of body weight (75 ml / kg / day)
>1 year - 6% of body weight (60 ml/kg/day)

Dehydration 3 tbsp.:
up to 1 year - 15% of body weight (100 ml / kg / day)
>1 year - 10% of body weight (80 ml/kg/day)

11. Calculation of fluid pathological losses:

Losses to fever - 10 ml / kg / day for every degree Celsius over 37;

Losses due to tachypnea - 10 ml / kg / day for every 10 respiratory movements over the age norm;

Losses with vomiting - 10 ml/kg/day;

Losses with diarrhea - 20-30 ml / kg / day.

Medical treatment provided on an outpatient basis

List of essential medicines:
chloramphenicol tab 250 mg, 500 mg
erythromycin enteric coated tablets 250mg
amoxicillin tablets tablets 250 mg

Ibuprofen - oral suspension in vials 100mg/5ml 100g

List of additional medicines:

Medical treatment provided at the inpatient level

List of essential medicines:
chloramphenicol - tablets 250 mg, 500 mg;
erythromycin - enteric-coated tablets 250 mg;
amoxicillin - tablets 250 mg;
benzylpenicillin sodium salt - powder for solution for intravenous and intramuscular administration in a vial 1000000 units;
ceftriaxone - powder for solution for injection for intramuscular and intravenous administration in a 1g vial
cefotaxime - powder for solution for injection for intramuscular and intravenous administration in a 1g vial
Chloramphenicol Powder for solution for intravenous and intramuscular administration, in the form of chloramphenicol sodium succinate - 0.5 g, 1.0 g.
Prednisolone solution for injections in ampoules 30mg/ml 1ml
Dexamethasone solution for injections in ampoules 4mg/ml 1ml
Hydrocortisone-hydrocortisone microcrystalline suspension for injection in 5 ml vials
Ringer - solution for infusions 200 ml, 400 ppm
Reopoliglyukin - solution for infusions 200 ml
Gelofusin fat emulsion
Sterofundin fat emulsion
Meglumine sodium succinate solution for infusion 1.5% in bottles of 100, 200 and 400 ml or in polymer containers of 250 and 500 ml

Albumin - solution for infusions 20% 100 ml
Fresh frozen plasma for infusions
Erythrocyte mass - solution for intravenous administration
Sodium chloride solution for infusion in vials 0.9% 200ml
Glucose solution for infusion in vials 5%,10% 200ml
Calcium gluconate solution for injection in ampoules 10% 5ml, tablets 0.5g
Heparin solution for injections in vials 5000IU/ml 5ml
Adrenaline solution for injections in ampoules 0.18% 1 ml
Norepinephrine - solution for intravenous administration
Aprotinin - powder for solution for injection in vials 100000 AtrE
Mannitol solution for injections 15% 200ml
Acetaminophen capsules, effervescent powder for oral solution [for children], solution for infusion, oral solution [for children], syrup, rectal suppositories, rectal suppositories [for children], oral suspension, suspension
Ibuprofen oral suspension in vials 100mg/5ml 100g
Benzodiazepine - powder for the preparation of a solution for intravenous and intramuscular administration in a bottle of 1000000 units

Phenobarbital-: 100 mg tablets.
Diazepam - solution for injections in ampoules 10mg/2ml 2ml
Magnesium sulfate - solution for injection in ampoules 25% 5ml
Furosemide - solution for injection in ampoules 1% 2ml
Dopamine solution for injection in ampoules 4% 5ml
Diacarb tablets 250mg
Asparkam tablets 250mg
Diazepam - solution for intravenous and intramuscular administration, solution for injection
Sodium oxybate injection in ampoules 20% 5ml

List of additional medicines:
Metamizole sodium - solution for injection in ampoules 50% 2ml
Drotoverin - solution for injections in ampoules 40mg/2ml 2ml
Diphenhydromine - solution for injections in ampoules 1% 1ml
Papaverine hydrochloride - solution for injection in ampoules 2% 2ml
Dibazol - ampoule of 1, 2 and 5 ml of 0.5 or 1% solution
Droperidol injection 0.25%
Sodium thiopental - powder for solution for intravenous administration in vials 1g

Other types of treatment: not carried out.

Surgical intervention

The presence of deep necrosis in meningococcemia: necrectomy.
The presence of abscesses and empyema of the brain: craniotomy to remove the abscess

Preventive actions:

Isolation of patients;

Frequent ventilation of the room where the patient is located;

Wet cleaning indoors;

In kindergarten, incl. in orphanages, orphanages, schools, boarding schools where a case of meningococcal infection is registered, quarantine is established for 10 days from the moment of isolation of the last patient. During this period, the admission of new and temporarily absent children, as well as the transfer of children and staff from one group to another, is prohibited;

All persons who communicated with the patient should be subject to medical supervision with daily clinical examination and thermometry, a single bacteriological examination;

Bacteriological examinations of contacts in kindergartens, incl. closed type are carried out at least 2 times with an interval of 3-7 days;

Persons who have communicated with patients and have catarrhal phenomena in the nasopharynx are preventive treatment erythromycin in age dosages for 5 days without isolation from the team.

Further management:

Persons who have had a meningococcal infection are admitted to schools, preschool institutions, sanatoriums, educational institutions after a single negative bacteriological examination conducted 5 days after discharge from the hospital or recovery of the patient with nasopharyngitis at home;

Clinical examination of patients who have had a generalized form of meningococcal infection (meningitis, meningoencephalitis) is carried out for 2 years: examination by a neurologist during the first year of observation 1 time per quarter, then 1 time in 6 months.

Drugs (active substances) used in the treatment

Human albumin (Albumin human)

Amoxicillin (Amoxicillin)

Aprotinin (Aprotinin)

Acetazolamide (Acetazolamide)

Acetazolamide (Acetazolamide)

Bendazol (Bendazol)

Benzylpenicillin (Benzylpenicillin)

Heparin sodium (Heparin sodium)

Hydrocortisone (Hydrocortisone)

Hydroxyethyl starch (Hydroxyethyl starch)

Dexamethasone (Dexamethasone)

Dextran (Dextran)

Dextrose (Dextrose)

Diazepam (Diazepam)

Diphenhydramine (Diphenhydramine)

Dopamine (Dopamine)

Droperidol (Droperidol)

Drotaverine (Drotaverinum)

Ibuprofen (Ibuprofen)

Potassium chloride (Potassium chloride)

Potassium, magnesium aspartate (Potassium, magnesium aspartate)

Calcium gluconate (Calcium gluconate)

Calcium chloride (Calcium chloride)

Magnesium sulfate (Magnesium sulfate)

Mannitol (Mannitol)

Meglumine (Meglumine)

Metamizole sodium (Metamizole)

Sodium hydroxybutyrate (Sodium hydroxybutyrate)

Sodium chloride (Sodium chloride)

Norepinephrine (Norepinephrine)

Papaverine (Papaverine)

Paracetamol (Paracetamol)

Plasma, fresh frozen

Prednisolone (Prednisolone)

Sterofundin isotonic (Sterofundin Isotonic)

Succinylated gelatin (Succinylated gelatin)

Thiopental-sodium (Thiopental sodium)

Phenobarbital (Phenobarbital)

Furosemide (Furosemide)

Chloramphenicol (Chloramphenicol)

Cefotaxime (Cefotaxime)

Ceftriaxone (Ceftriaxone)

Epinephrine (Epinephrine)

Erythromycin (Erythromycin)

erythrocyte mass

Hospitalization

Indications for hospitalization

Indications for emergency hospitalization:

Presence of HPF (for children under 5 years of age according to IMCI);

Generalized forms of meningococcal infection.

Patients with nasopharyngitis with severe symptoms of intoxication;

Indications for planned hospitalization:

Carriers of N. meningitidis according to epidemiological indications (children from boarding schools, orphanages, orphanages and families with unfavorable social and living conditions).

Information

Sources and literature

1. Minutes of the meetings of the Expert Council of the RCHD MHSD RK, 2014
   1. 1) "Bacterial Meningitis and Meningococcal Septicemia: Management bacterial meningitis and meningococcal septicemia in children and young people under 16 in primary and secondary care”. KR 2010 2) Provision of inpatient care for children. WHO guidelines for the management of the most common diseases in primary hospitals adapted to the conditions of the Republic of Kazakhstan. pp. 1-36, 133-170 3) Zinchenko A.P. Acute neuroinfections in children. Guide for doctors. - L: "Medicine", 1986. 320s. 4) Uchaikin V.F. "Guidelines for infectious diseases in children" - M: GEOTAR-MED, 2002 509–527 p. 5) Order of the First Deputy Chairman of the Agency of the Republic of Kazakhstan for Health Affairs dated 12.06.2001 No. No. 566 “On measures to improve epidemiological surveillance, prevention and diagnosis of meningococcal infection 6) Izvekova, I. Ya. Meningococcal infection: tutorial/ I. Ya. Izvekova, V. P. Arbekova. - Novosibirsk: Sibmedizdat NGMA, 2005. - 168 p.: ill. (Code 616.831.9-002 I-33) 7) Meningococcal infection in children / NV Skripchenko [et al.] // Epidemiology and infectious diseases. - 2005. - N 5. - C. 20-27. 8) Pediatric anesthesiology and resuscitation. Mikhelson V.A., Grebennikov V.A. 480 pages. Year of publication: 2001. 9) National Collaborating Center for Women's and Children's Health. Bacterial meningitis and meningococcal septicaemia. Management of bacterial meningitis and meningococcal septicaemia in children and young people younger than 16 years in primary and secondary care. London (UK): National Institute for Health and Clinical Excellence (NICE); Jun. 2010 10) 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.

Information

III. ORGANIZATIONAL ASPECTS OF PROTOCOL IMPLEMENTATION

List of protocol developers with qualification data:

1) Kuttykozhanova G.G. - Doctor of Medical Sciences, Professor, Head of the Department of Children's Infectious Diseases of KAZ NMU named after S.D. Asfendiyarov.

2) Efendiev I.M. ogly - Candidate of Medical Sciences, Associate Professor, Head of the Department of Children's Infectious Diseases and Phthisiology, Semey State Medical University.

3) Baesheva D. A. - Doctor of Medical Sciences, Head of the Department of Children's Infectious Diseases of JSC "Astana Medical University".

4) Bakybaev D.E. - doctor - clinical pharmacologist of JSC "National Center for Neurosurgery".

Indication of no conflict of interest: none.

Reviewer:
Kosherova Bakhyt Nurgalievna - Doctor of Medical Sciences, Professor of the Republican State Enterprise on the REM "Karaganda State medical University» Vice-Rector for Clinical Work and Continuous Professional Development, Professor of the Department of Infectious Diseases, Chief Freelance Infectionist of the Ministry of Health and Social Development of the Republic of Kazakhstan

Acceptance of proposals(with completed justification form) goes until March 29, 2019: [email protected] , [email protected] , [email protected]

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Meningococcal infection is one of the most severe acute infectious diseases with various clinical manifestations of localized or generalized forms of the infectious process.

The danger of infection lies in the fact that it can have a very rapid, lightning-fast development of the most severe forms with a high risk of death and a possible impact on the neuropsychic subsequent development of the child.

Only humans get this infection. Susceptibility to meningococcus is low. The most common infection among children: up to 80% of all patients. Children of any age are susceptible to the disease, quite often the infection affects children in the first year of life.

Cause of the disease

The disease caused by meningococcus can be severe.

The disease is caused by various strains (varieties) of meningococcus. The source of infection of the child may be a sick person or a "healthy" carrier of meningococcus. The number of such carriers in meningococcal infection is very large: for one case of a generalized form of the disease, there are from 2 to 4 thousand healthy carriers of this microbe.

Carriers are usually adults, although they do not know about it, and children mainly get sick.

The causative agent lives in the nasopharynx and is released into the external environment when sneezing, talking. The danger increases when inflammation occurs in the nasopharynx. Fortunately, meningococcus is very unstable in environmental conditions: it survives no more than half an hour.

Infection occurs by airborne droplets with very close (at a distance of up to 50 cm) and prolonged contact. The infection has a pronounced winter-spring seasonality with a peak incidence from February to April.

Periodic increases in the incidence rate are recorded after about 10 years, which is associated with a change in the strain of the pathogen and the lack of immunity to it. There are both isolated cases of morbidity in children, and massive ones in the form of outbreaks and epidemics. In the period between epidemics, young children get sick more, and more older children during the epidemic.

Meningococcus is sensitive to antibiotics, sulfa drugs.

When the pathogen enters the mucous membrane of the nasopharynx, it most often does not cause inflammation: this is how a “healthy” carriage is formed. But sometimes inflammatory changes occur in the nasopharynx, a localized form of the disease develops: meningococcal nasopharyngitis.

Much less often (in 5% of sick children), the microbe enters the bloodstream and spreads to various organs. This is how meningococcal sepsis (meningococcemia) develops.

Severe toxic syndrome occurs as a result of the destruction of meningococci (under the action of produced antibodies or antibiotics) and the release of a significant amount of endotoxin. This can cause the development of infectious-toxic shock.

In addition to the internal organs (lungs, joints, adrenal glands, retina, heart), meningococcus can also affect the central nervous system: the membranes and substance of the brain and spinal cord. In these cases, purulent (or meningoencephalitis) develops. In severe cases, pus covers the brain in the form of a cap.

After the disease and even as a result of the carriage of meningococcus, a strong immunity is developed.

Symptoms

The incubation period can last from 2 to 10 days, it is usually short: 2-3 days.

Distinguish between localized and generalized clinical forms of meningococcal infection.

Localized:

• asymptomatic meningococcal carriage;
• meningococcal nasopharyngitis.

Generalized:

• meningococcemia (meningococcal sepsis);
• meningitis (inflammation of the meninges);
• meningoencephalitis (inflammation of both membranes and brain matter);
• mixed form (a combination of meningococcemia and meningitis).

Rare forms include: caused by meningococcus, iridocyclitis,.

Asymptomatic meningococcal carriage - the most common form of the disease (develops in 99.5% of all infected). More commonly seen in adults. The condition does not show any signs, and the person is unaware of his infection.

Meningococcal nasopharyngitis develops in 80% of patients with meningococcal infection. It manifests itself with symptoms common to the inflammatory process in the nasopharynx: acute onset, sore throat, nasal congestion, dry cough,. The temperature may rise in the range of 37.5 ° C. The general condition and well-being of the child suffer little.

On examination, redness in the pharynx and swelling of the mucosa, sometimes redness of the conjunctiva, scanty mucopurulent discharge from the nose are revealed. More often the condition is regarded as a manifestation. The correct diagnosis is made only in the focus of infection when examining contact persons.

The duration of the disease is from 2 to 7 days; ends with recovery. But often (about 30% of cases) this form precedes the subsequent development of a generalized form of infection.

Meningococcemia develops sharply, suddenly. Its manifestations are growing very quickly. Parents can specify the exact time of onset of the illness, not just the date. The temperature rises sharply with chills (up to 40 ° C), which is difficult to reduce with antipyretics. There is recurrent vomiting and severe headache, thirst.

But the main and most characteristic sign of meningococcal sepsis is a rash. It manifests itself already in the first day of the disease, less often on the second. The earlier a rash appears from the onset of the disease process, the more severe the course and prognosis of the disease.

More often it is localized on the thighs, legs, lower abdomen, buttocks. The rash spreads quickly, literally "growing before our eyes." The appearance of rashes on the face indicates the severity of the process. This is an unfavorable prognostic sign.

The size of the rash can be different: from small punctate hemorrhages to large irregular (“star-shaped”) elements of purple-bluish color. The rash is a hemorrhage into the skin, it does not disappear with pressure, it is located on a pale background of the skin. Spotted rashes last 3-4 days, become pigmented and disappear.

In the center of large elements of the rash, tissue necrosis (necrosis) may develop after a couple of days. The necrotic surface is covered with a crust, after its discharge, ulcers form, which scar very slowly (up to 3 weeks or more).

Necrosis can also occur on the tip of the nose, phalanges of the fingers, auricles with the development of dry gangrene.

Clinical symptoms in meningococcemia can grow very rapidly, especially with a fulminant variant of the course of the disease. Hemorrhage in the conjunctiva or sclera of the eyes may appear even earlier than a skin rash. Other manifestations of hemorrhagic syndrome may also occur: (nasal, gastric, renal) and hemorrhages in various organs.

Due to impaired blood supply and due to toxicosis, with meningococcemia, children have symptoms of kidney damage, of cardio-vascular system, lungs, eyes, liver, joints. All children appear, reduced.

When the kidneys are involved in the process, changes appear in the urine (protein, erythrocytes and leukocytes). The defeat of the joints is characterized by the occurrence of pain in large joints and their swelling, limitation of range of motion.

In the case of hemorrhage in the adrenal glands, acute adrenal insufficiency develops due to hormone deficiency, which can cause death. Such a complication, like an acute one, is possible with a fulminant form of meningococcemia (hyperacute sepsis).

Clinically, adrenal insufficiency is manifested by a sharp drop in blood pressure, vomiting, the appearance of cyanotic spots on the skin against the background of severe pallor, frequent weak pulse, severe shortness of breath and subsequent respiratory rhythm disturbance, temperature drop below normal. In the absence of qualified assistance, death can occur even in a few hours.

Extremely rare chronic form meningococcemia with periodic relapses. It can last for several months.

If the meninges are involved in the pathological process, then the child's condition deteriorates sharply.

Purulent meningococcal meningitis also characterized by an acute onset. A sharp diffuse headache appears, small children react to it with the appearance of anxiety, piercing crying. The temperature with chills can rise to 40 ° C and does not decrease after the child takes antipyretic drugs.

The headache intensifies in response to any stimulus: loud sound, light, even touch: in young children this manifests itself as a symptom of "repulsion of mother's hands." Increased headache is noted at the slightest movement, when turning the head.

There is no appetite. Repeatedly repeated vomiting does not bring relief. It has nothing to do with eating. It may also appear, especially at an early age. The child is pale, lethargic, the pulse is quickened, the blood pressure is reduced.

Muscle tone is increased. The child's posture in bed is characteristic: lying on his side, "curled up", with his legs drawn to his stomach and his head thrown back.

In small children, there is bulging, tension and pulsation of the large one. Sometimes there is a divergence of the seams between the bones of the skull. When dehydrated small child due to vomiting and loose stools, the fontanel sinks.

Babies may experience reflex and lack of urination.

Sometimes children have motor restlessness, but there may also be lethargy, drowsiness and lethargy. In small children, you can notice.

When the process spreads to the substance of the brain, it develops meningoencephalitis, which is manifested by symptoms such as impaired consciousness, mental disorders, motor excitation and .

On examination, the doctor reveals focal symptoms: paresis (or paralysis), pathological changes in the cranial nerves (oculomotor disorders, hearing and vision loss). In severe cases, when cerebral edema occurs, swallowing, speech, cardiac activity and respiration may be impaired.

At mixed form both clinical manifestations of meningitis and symptoms of meningococcemia may predominate.

In the course of the generalized form of the disease, rare forms can also develop: damage to the joints, heart, retina and lungs. But if meningococcus enters the lungs with air immediately, then meningococcal pneumonia can develop primarily.

Diagnostics

During the examination, the doctor assesses the condition of the large fontanel in young children and checks for meningeal symptoms.

To diagnose meningococcal infection, the following methods are used:

• a survey of parents and a child (if possible by age): allows you to find out the presence of contact with sick people, clarify complaints, the dynamics of the development of the disease and the sequence of symptoms;
• examination of the child by a doctor: assessment of the severity of the condition and identification of a number of clinical signs of the disease (temperature, skin color, rash, meningeal symptoms, the condition of a large fontanel in young children, convulsions, etc.);

In the case of generalized forms of the disease, the diagnosis can already be made on the basis of clinical manifestations. Methods used to confirm the diagnosis laboratory diagnostics (it is carried out already in a hospital after an emergency hospitalization of the child):

• clinical examination of blood and urine: in the blood with meningococcal infection, an increased total number of leukocytes, an increase in the number of stab and segmented leukocytes, the absence of eosinophils and accelerated ESR are noted; urinalysis allows you to evaluate the work of the kidneys;
• clinical examination (bacterioscopy) of a thick drop of blood and cerebrospinal fluid sediment to detect meningococci;
• bacteriological method: culture of mucus from the nasopharynx, culture of cerebrospinal fluid, culture of blood to isolate meningococcus and determine its sensitivity to antibiotics;
• a biochemical blood test (coagulogram, liver and kidney complex) allows you to assess the severity of the child's condition;
• a serological blood test (paired sera taken at an interval of 7 days) can detect antibodies to meningococcus and an increase in their titer; diagnostic is a 4-fold increase in titer;

Additional examination methods:

• consultations of a neurologist, ENT doctor and oculist (examination of the fundus);
• in some cases, echoencephalography is performed ( ultrasound procedure of the brain for diagnosing complications of the disease), computed tomography;
• according to indications, an ECG can be prescribed,.

Treatment

At the slightest suspicion of meningococcal infection, an urgent hospitalization of the child is carried out.

At home, it is possible to treat carriers of meningococcus and meningococcal nasopharyngitis (in the absence of other children in the family at preschool age).

For the treatment of nasopharyngitis of meningococcal etiology, the following is prescribed:

• antibiotics (Tetracycline, Erythromycin, Levomycetin) orally at an age-appropriate dosage;
• gargling with a 3% solution of baking soda, a solution of furacilin;
• irrigation of the pharynx with Ectericide.

Treatment of generalized forms includes:

• antibacterial therapy;
• detoxification therapy;
• symptomatic treatment.

In order to influence meningococcus, Penicillin and Levomycetin-succinate are prescribed. And the choice of antibiotic, and its dosage, and the duration of the course depend on the clinical form of the disease, the severity, age and body weight of the child and his other individual characteristics.

In the treatment of meningitis and meningoencephalitis, high doses of antibiotics are used to overcome the blood-brain barrier and create a sufficient concentration of the antibiotic in the brain substance. Preferably, Penicillin is prescribed.

With meningococcemia, even at the prehospital stage (in the clinic or by the staff of the ambulance), Prednisolone and Levomycetin-succinate are administered, and not Penicillin, which has a detrimental effect on meningococcus. When the microbe dies, endotoxin is released in large quantities, and an infectious-toxic shock may develop. And Levomycetin just will not allow the reproduction of the pathogen.

Hormonal drugs (Prednisolone, Hydrocortisone) are used in cases severe course infections in order to suppress the violent reaction of the immune system to the penetration of the pathogen and to maintain blood pressure at the proper level.

In case of developed infectious-toxic shock, treatment is carried out in the intensive care unit.

The following are used as detoxification agents: 10% glucose solution, plasma and plasma substitutes, Ringer's solution, Reopoliglyukin, etc. Plasmapheresis and ultraviolet blood irradiation can be used.

Symptomatic therapy includes the appointment of anticonvulsants (Sibazon, Relanium, Sodium oxybutyrate), cardiac agents (Korglikon, Kordiamin), diuretics (Lasix), vitamins (C, group B), heparin under the control of the blood coagulation system.

To reduce cerebral hypoxia, oxygen therapy and cerebral hypothermia are used (an ice pack is applied to the head).

If breathing is disturbed, the child is connected to an artificial respiration apparatus.

Prognosis and outcomes of the disease

IN recovery period weakness and increased intracranial pressure may be noted, which disappear after a few months.

A more severe prognosis in children under one year old. In rare cases, they can develop severe consequences in the form of hydrocephalus, epilepsy.

Complications of meningococcal infection are divided into specific and nonspecific. Specific (develop at an early stage of the disease):

• infectious-toxic shock;
• acute cerebral edema;
• bleeding and hemorrhage;
• acute adrenal insufficiency;
• acute heart failure;
• and etc.

Non-specific (due to other bacterial flora):

• pneumonia;
• and etc.

Specific complications are manifestations of the pathological process itself. Any of them can cause the death of a child.

After the disease, residual effects and complications may be detected.

Functional residuals:

• asthenic syndrome, the manifestation of which at an early age is emotional instability and motor hyperactivity, disinhibition, and at an older age - reduced memory and fatigue;
• during adolescent puberty.

Organic complications:

• hydrocephalus (increased amount of fluid in the cranial cavity);
• increased intracranial pressure;
• child's lag in psychomotor development;
• hearing loss or loss;
• epileptiform (convulsive) syndrome;
• paresis with movement disorders.

Dispensary observation of children

Convalescent children are subject to medical supervision after the infection. To resolve the issue of admission to a children's institution, the child is examined 2-4 weeks after discharge from the hospital.

Subsequently, quarterly examinations by a pediatrician and a neurologist are carried out in the first year and 2 times a year in the second. According to indications, consultations of other specialists (oculist, psychoneurologist, audiologist) are appointed.

During dispensary observation can be carried out and additional methods examinations (echoencephalography, electroencephalography, rheoencephalography, etc.). If residual effects are detected, it is recommended to provide the child with a sparing regimen, proper rest and prolonged sleep age-appropriate diet. Treatment is carried out according to the appointment of specialists.

As prescribed by a neurologist, courses of treatment with nootropics (Piracetam, Aminalon, Nootropil) can be carried out. With organic lesions of the central nervous system, aloe, lidase (improve the resorption of inflammation), Diacarb (to reduce intracranial pressure), Actovegin and Cerebrolysin (with delayed psychomotor development) can be prescribed.

With motor disorders, physiotherapy exercises, physiotherapy (electrical stimulation, electrophoresis, acupuncture, etc.) are widely used.

Prevention

• early detection and hospitalization of patients;
• measures in the focus of infection: identification of carriers of meningococcus and their treatment, 10-day observation of those in contact with the patient and their 2-fold examination (nasopharyngeal swab), admission of contact children to Kindergarten only after a negative test result;
• discharge of a sick child from the hospital only after a 2-fold negative bacteriological analysis of mucus from the nasopharynx (performed 3 days after the course of treatment with an interval of 1 or 2 days);
• limiting contact of infants with adults and older children;
• during the outbreak of the disease, the exclusion of holding mass events with overcrowding of children;
• treatment of chronic foci of infection;
• vaccination (with the Meningo A + C vaccine): schoolchildren (when more than 2 cases of meningococcal infection are registered at school) and children before traveling to a region unfavorable in terms of the incidence of this infection. The use of the vaccine in children is possible from 1.5 years; immunity is formed by the 10th day and is maintained for 3-5 years.

Summary for parents

Meningococcal disease is a serious illness, especially for young children. The danger of this infection is not only in acute period(due to the development of complications and a threat to life), but also after recovery (serious consequences may remain for life).

Considering the likelihood of a very rapid development of the disease, one should not delay the time of going to the doctor with any disease of the child. Only correct and timely treatment can save a child.

It must be remembered that a lumbar puncture (which parents are so afraid of) is a necessary diagnostic procedure which will help the doctor prescribe the right treatment.

Which doctor to contact

If a child has symptoms of inflammation of the nasopharynx, you should usually contact your pediatrician. With a rapid rise in temperature, deterioration of the child's condition, severe headache, and especially the appearance skin rash an ambulance should be called immediately. Treatment is carried out in an infectious disease hospital. The child is examined by a neurologist, ophthalmologist, ENT doctor, if necessary, a cardiologist and other specialists.

In the structure of infectious morbidity, one of the life-threatening and unpredictable in terms of lightning speed is meningococcal infection (MI).

The urgency of the problem lies in the fact that among invasive infections, meningococcal infection requires special approach to the organization of diagnostics and the provision of emergency and emergency medical care due to the fact that its generalized forms, most common in childhood, with late treatment give a high percentage of mortality.

Since 1962, there has been a significant increase in the incidence of MI in a number of countries in Europe and Asia, Canada and the United States, and since 1968, in our country, the situation in the Russian Federation has been characterized as a "sluggish epidemic."

The data of the analysis of the global situation in 2005 indicate that in the countries of the "meningitis belt" of sub-Saharan Africa, where meningococcus serogroup A predominates, the incidence rate of MI in the population as a whole ranges from 100-800 per 100 thousand population, with mortality - up to 14 %. In other countries and continents, where the dominant serogroups are mainly serogroups B and C, the average incidence ranges from 1-3 per 100,000 population. Up to 76% of MI cases in Saudi Arabia are due to the predominant W135 serogroup. On the European continent, the highest incidence rate - 5-6.6 per 100 thousand of the population was recorded in Iceland and Ireland, where serogroup B predominates, and in the countries of Oceania (New Zealand) the incidence rate of MI during this period was 14.5 per 100 thousand .population. IN last years in 40 regions of the Russian Federation as a whole, there was a decrease in the incidence of this infection. However, since 1999, in 6 large regions, there has been a significant increase in that by 22-40%: in the Astrakhan, Perm, Chelyabinsk, Kemerovo, Novosibirsk, Omsk regions with the highest level in the Khabarovsk Territory - up to 8.2 per 100 thousand population . Meningococcus serogroup A prevails in the general serogroup characteristics across the country. In the Khabarovsk Territory, the duration of the last epidemic is largely due to the change of meningococcus serogroup A to serotypes B and C. Accounting for these indicators is important due to the increasing increase in migration flows of the population in our country and in the world due to tourism , searching for employment, pilgrimage to Mecca, etc. All this cannot but have significant epidemiological significance in relation to the spread of infection.

For pediatricians in Russia, the problem of MI is especially importance, since the incidence rate among children has always exceeded that in adults by several times, reaching 8-11 per 100 thousand of the population of children under 14 years of age. More than 50% of the total number of cases are children under 5 years of age. It is among the child population that a high frequency of development of generalized forms of MI is characteristic. To a large extent, the risk of developing a fatal outcome in MI depends on the age of the child: the younger, the higher the likelihood of an adverse outcome. Up to 75% of the number of deaths due to MI are children under 2 years of age, while the proportion of children in the first year of life reaches 40%. The experience of the leading clinics of the country indicates that MI in recent years is characterized by clinical and epidemiological features of the course of the disease in children. Analysis of the features of the disease in the light of new ideas about the mechanisms of development of fulminant forms and complications in MI made it possible to substantiate schemes for more rational therapy based on etiopathogenetic aspects.

MI is a typical anthroponosis. Pathogen - Neisseria meningitidis, a gram-negative diplococcus, has the shape of a coffee bean and is located intra- and extracellularly. It produces exo- and endotoxin, which are very unstable in the external environment. At low temperatures, they die after 1-2 hours, when treated with UV radiation or disinfectants - after a few minutes. The optimum temperature for growth is +37 °C. There are more than 13 serotypes of meningococcus, with type-specific immunity. According to capsular polysaccharides, A, B, C, D43, 44 are distinguished; X, Y, Z, 29E, W-135. According to antigens in membrane proteins, more than 20 serotypes and subtypes are distinguished. By immunotypes of lipopolysaccharide - more than 11 immunotypes. For example, in the east of the Russian Federation, the appearance of W135:2a:P1,2,3 strains caused the course of MI with high rates lethality.

The ability of meningococci to form L-forms has been proven, which can probably cause protracted variants of meningitis.

The source of infection is meningococcal carriers, patients with nasopharyngitis and generalized forms of infection. The route of transmission is airborne, contact-household. The entrance gate of infection is the mucous membrane of the upper respiratory tract. MI is characterized by periodicity with intervals between individual rises from 4 to 12-15 years. An increase in the incidence during these periods is recorded mainly among the urban population due to crowding in transport and premises during the cold season. The most conclusive relationship between the frequency of MI and epidemic rises in acute respiratory viral infections and influenza with a peak in the winter-spring period of the year. Children and young people get sick mainly, more often from closed groups. The risk group for the development of predominantly septic, hypertoxic forms of MI are young children (up to 3 years). A genetic predisposition to meningococcal disease and its recurrence has been established in individuals with HLA B12, B16 antigens, deficiency of complement factors C2-C8, properdin, IgG2 and IgM (Samuels M., 1997).

Population resistance to MI, according to some researchers, is associated with the HLA-A1 locus of the histocompatibility antigen.

A feature of the clinical forms of MI in recent years, compared with previous years, is a decrease in the frequency of mixed forms and meningococcemia without manifestations of meningitis against the background of an increase in the frequency of meningitis, which is probably the cause of diagnostic errors. This is evidenced by the data of the Research Institute of Children's Infections (NIIDI St. Petersburg, St. Petersburg) and the Morozov Children's Clinical Hospital - MDKB, Moscow. In NIIDI St. Petersburg, with meningitis of meningococcal etiology, ARVI was initially diagnosed in 83.2% of cases. According to the MDKB, from 2002-2004. the diagnosis of meningitis was made only in 5 cases out of 31, while ARVI, acute appendicitis, meningococcemia without meningitis of unknown etiology, capillary toxicosis, closed craniocerebral injury, thrombocytopenic purpura, acute glomerulonephritis, pneumonia, etc. were diagnosed.

A feature of recent years is the registration of cases during the year with approximately equal frequency without a clear seasonality of MI.

In the pathogenesis of MI, 3 factors play a leading role: the pathogen, its endotoxin, and the allergenic substance. At the site of the entrance gate, inflammatory changes often do not occur, but at the same time, meningococcus vegetates without causing harm, in the form of meningococcal carriage. Only in 10-15% of cases, with a decrease in the body's resistance, it is possible to develop an inflammatory process in the nasopharynx in the form of meningococcal nasopharyngitis. If meningococci overcome local protective barriers, they spread through the lymphatic pathways into the blood. Meningococci in the form of bacterial emboli are introduced into various organs and tissues. When the blood-brain barrier is crossed, purulent meningitis or meningoencephalitis. In this case, the pathogen can penetrate into the membranes of the brain, bypassing hematogenous spread, through the ethmoid bone along the lymphatic tracts and sheaths of nerve fibers. This option is possible in cases of a defect in the ethmoid bone or traumatic brain injury. Hyperacute meningococcal sepsis develops as a result of massive bacteremia and endotoxinemia. With the mass decay of meningococci, the released endotoxin affects the vascular endothelium and blood cell membranes, leading to a microcirculation disorder. As a result of generalized damage to the vascular endothelium, defects are closed by platelets, the aggregation of which leads to the release of thromboxane and inhibition of prostacyclin synthesis. The rheological properties of blood are disturbed with aggregation of formed elements on which fibrin is fixed. In addition, the effect of lipid A endotoxin on macrophage monocytes is important, which, when activated, release TNF-α, the primary mediator of toxic effects in toxic shock. In addition to it, nitric oxide, prostaglandins, complement factors, histamine, leukotrienes, platelet activating factor and interleukins 1, 2, 6, 8 play an enormous role during septic shock. An excess amount of biologically active substances is released: catecholamines, serotonin, histamine, systems Hageman factor, kallikrein-kinin, coagulation and subsequently fibrinolytic. Prothrombin, kallikrein, etc. are powerfully ejected from the liver, which ultimately leads to hypercoagulability with the formation of a large number of bacterial thrombi (emboli) in small vessels - thrombohemorrhagic syndrome with bacterial embolism. Utilization of factors of the coagulation system leads to consumption coagulopathy - hypocoagulation, which results in massive hemorrhages in tissues and various organs. Excessive activation of the plasmin system by kallikrein leads to uncontrolled bleeding (a symptom of "bloody tears"). The change from hyper- to hypocoagulation in hyperacute meningococcal sepsis can occur in a matter of hours. Under the influence of kallikrein, bradykinin is excessively formed, while the vessels expand systemically and blood pressure (BP) drops; the renin-angiotensin system is activated compensatory, which leads to the formation of the most powerful vasopressor of the body - angiotensin-2, which, together with catecholamines, leads to spasm of small arteries, centralization of blood circulation, and impaired microcirculation. In addition to the direct action of endotoxin, cytokines, metabolic acidosis, and a decrease in coronary blood flow, one of the causes of myocardial dysfunction in toxic shock is myocardial inhibitory factor (MUF), upon reaching a critical level of which, left ventricular dilatation and a maximum decrease in ejection fraction (FI) occur.

Thus, septic shock in MI has simultaneously signs of hypovolemic (lack of blood volume), distributive (violation of vascular tone) and cardiogenic (insufficiency of cardiac output) shock.

There is a stage in its development.

Stage I - the phase of "warm normotonia" - the initial manifestations of shock are accompanied by a hyperdynamic circulation regime in combination with vasodilation peripheral vessels when, under the influence of endotoxin, cardiac output increases, including the accumulation of cytokines, the vascular tone sharply decreases. Relative hypovolemia develops, in response to which hypercatecholemia develops, leading to vasoconstriction.

II stage of shock - the phase of "warm hypotension" - due to vascular spasm, hypoxia and acidosis, in which cardiac output decreases and relative hypovolemia increases.

III stage of shock - the phase of "cold hypotension" - accompanied by the need for vascular autoregulation to maintain the performance of the heart at a sufficient level at the cost of peripheral vasoconstriction, leading to a syndrome of small ejection, hypoperfusion and arterial hypotension.

IV stage of shock - decompensation, blood pressure does not respond to an increase in circulating blood volume (CBV), tissue perfusion is inadequate.

Clinical manifestations of meningococcal infection are represented by a variety of clinical forms - from localized (nasopharyngitis and meningococcal carriage) to generalized, among which fulminant, extremely severe often lead to lethal outcome during few hours.

It is difficult to diagnose meningococcal nasopharyngitis on the basis of the clinical picture, without indicating the corresponding epidemiological history. Up to 80% of all forms of MI are meningococcal nasopharyngitis. IN clinical picture diseases, the most typical symptoms are nasal congestion, sore throat, hyperemia and swelling of the posterior pharyngeal wall with hypertrophy of lymphoid formations on it, swelling of the lateral ridges and mucus in a small amount. Hyperemia has a bluish tinge. There is a widespread opinion about the mild nature of the course of this form of MI. Depending on the level of fever and the severity of intoxication, mild, moderate and severe forms of the disease are distinguished. In severe form, hyperthermic syndrome, meningism dominate, in children of the first years of life - convulsive syndrome. More often, such patients are regarded as patients with acute respiratory viral infections with convulsive syndrome or serous meningitis at the time of hospitalization, and only inoculation of meningococcus can adequately verify the diagnosis and conduct etiotropic therapy.

We must not forget that often in children nasopharyngitis precedes the development of generalized forms of the disease, including those with a fatal outcome.

The carriage of meningococcus among children of the first years of life is rare, its frequency in groups reaches more than 40% and depends on the specific epidemic situation.

Among the generalized forms, meningococcemia is distinguished, which can occur in mild, moderate, severe and fulminant forms in the form of meningococcal sepsis; meningococcal meningitis and meningococcemia + meningitis.

Meningococcemia is characterized by an acute, sudden onset, the severity criteria are the severity of intoxication, the nature, size, prevalence, presence of necrosis and the duration of the elements of the rash, from which meningococcus can be sown. In a mild form, the elements are represented by roseola, papules, small hemorrhages, which disappear without a trace by the 3rd day of the disease. In the moderate form, the elements are predominantly large, hemorrhagic, with superficial necrosis in the center. The rash is longer - up to 7-10 days. Severe and septic fulminant forms are characterized by extensive hemorrhages on the skin with deep necrosis and their rejection, in which cosmetic defects on the body. These forms are often accompanied by bleeding: uterine, nasal, gastrointestinal, as well as hemorrhages in the fundus. There are lesions of the heart (endocarditis, myocarditis, pancarditis), joints, lungs, liver, kidneys, adrenal glands.

Modern clinical features of meningococcal meningitis are doubtful (up to 40%) or absence (in 15%) of meningeal symptoms. At the same time, one should remember about the equivalent symptoms indicating the likelihood of meningitis - this is "confusion" of consciousness, delirium, hyperesthesia, persistence of vomiting that does not bring relief, "bursting nature" headache, radicular symptoms that provoke a picture of an acute abdomen; in young children, bulging of a large fontanelle, regurgitation, vomiting, diarrheal syndrome, convulsions, a positive symptom of Lessage - “suspension”. At the present stage, the dependence of liquorological changes (pleocytosis and proteinrachia) on the serogroup of the pathogen has been revealed. In the disease caused by serogroup C meningococcus, these rates are significantly higher than in MI caused by meningococcus B.

Among patients with MI of the Department of Neuroinfections of the NIIDI St. Petersburg, it was noted that meningitis developed in persons with a defective premorbid background from the side of the central nervous system perinatal origin. The most common emergencies in meningococcal meningitis in the acute period of the disease were: cerebral edema, intracranial hypertension, infectious toxic shock (ITS), cerebral infarction, subdural effusion, syndrome of inappropriate secretion of antidiuretic hormone, diencephalic dysfunction and sensorineural hearing loss.

With meningoencephalitis, from the first days of the disease, focal symptoms appear against the background of impaired consciousness in the form of damage to individual cranial nerves, cortical and subcortical paresis or paralysis. There may be general or local convulsions. A very severe course is characteristic, an unfavorable prognosis results in epilepsy, hydrocephalus, and a gross delay in psychomotor development. Characterized by high mortality.

Verification of the infection is carried out by bacterioscopic (a smear and a thick drop of blood, cerebrospinal fluid), bacteriological (a smear of mucus from the nasopharynx, culture of blood, cerebrospinal fluid), serological (indirect hemagglutination reaction (RIHA), agglutination reaction (RA), enzyme immunoassay(ELISA)) and express methods (latex agglutination, counter immunoelectrophoresis (VIEF)).

At the present stage, in meningitis, diagnostic monitoring includes neurosonography (NSG), monitoring to assess the state of the ventricles, subarachnoid space, and color Doppler (duplex) mapping to differentiate subarachnoid effusion from subdural. The electroencephalogram (EEG) is dynamically assessed.

At the prehospital stage, if meningococcemia is suspected (including a mixed form of MI), therapy should be started immediately at home, followed by hospitalization. The fight against hyperthermia is carried out depending on the type of fever. With a "pink" fever, paracetamol is administered orally or rectally in a single dose of 10-15 mg / kg, if ineffective - ibuprofen (Nurofen) in a single dose of 5-10 mg / kg of body weight. At the same time physical methods cooling, but no more than 30 minutes. In case of inefficiency, a lytic mixture is introduced in the composition: 50% Analgin + antihistamine intramuscularly at the age dose. With a "pale" fever, the patient is warmed, Papaverine or No-shpu or Dibazol + lytic mixture is injected intramuscularly. With pronounced centralization of blood circulation, a 0.25% solution of Droperidol 0.1-0.2 ml / kg in combination with antipyretics is added to the therapy. In case of convulsive syndrome, along with the specified therapy, Relanium (Seduxen, Sibazon) is injected intramuscularly at a rate of 0.1 ml/kg. In the absence of effect, Droperidol is included in therapy in combination with Analgin, sodium hydroxybutyrate. With the debut of meningitis with convulsions, long-term therapy with valproic acid preparations (Konvuleks and others) is planned, which reduces the risk of developing postmeningitis epilepsy. To prevent toxic shock, prednisolone is administered intramuscularly or intravenously (in / in) at a dose of 2 mg / kg. With severe meningeal syndrome - 25% magnesium sulfate 1 ml / year of life or Lasix (furosemide) - 1-2 mg / kg / m. The introduction of an antibiotic during the first hour of transportation is not recommended, and in the case of long-term transportation, the starting drug is chloramphenicol succinate at a single dose of 25 mg/kg, which is administered for no more than 2 days. The patient's condition is assessed under constant monitoring of blood pressure, pulse rate, respiration, diuresis, color and temperature of the skin, an increase in the quantity and quality of exanthema elements and the patient's consciousness. If a fulminant variant of the generalized form of MI is suspected, hospitalization is carried out by the resuscitation team, which conducts immediate resuscitation at home, depending on the degree of septic shock, the algorithm of which is permanently carried out during the transportation of the patient and continues in the intensive care unit (ICU). Important in the algorithm for providing immediate assistance in case of septic shock is the normalization of hemodynamics, microcirculation, the fight against acidosis and hypoxia. Antishock effect is achieved by the introduction of high doses of hydrocortisone in combination with prednisone or its analogues. Infusion therapy is carried out, the composition of which is determined by the indicators of colloid osmotic pressure (albumin 45-52 g / l and sodium 140-145 mmol / l). Base solutions are 5% glucose, saline or Ringer's solution. The ratio of injected colloids/crystalloids is 1:3. Physiological saline is administered to stop hypovolemia, with a sharp drop in blood pressure by jet, and with a moderate decrease in intravenous drip. Under the control of the acid-base state (CBS), 4% sodium bicarbonate is injected intravenously slowly, drip by base deficiency (BE) in an amount equal to body weight (in kg) multiplied by BE and divided by 2. Instenon angioprotectors are prescribed , Cavinton, Actovegin, Vessel Due F (sulodexide), taking into account the development of generalized vasculitis with damage to the vascular endothelium. Oxygenation should be carried out continuously up to mechanical ventilation (ALV), starting from the moment of home care. Penicillin is prescribed at a dose of 300 thousand units / kg of body weight for 6 injections after the abolition of chloramphenicol succinate, and in children under 3 months - 500 thousand / kg for 8 injections. More compliant and alternative to penicillin is ceftriaxone (Rocefin), which is administered once a day intravenously or intramuscularly at a dose of 100-150 mg/kg of body weight for 5 days for meningococcemia, and for meningitis up to 10 days. In severe or prolonged meningitis, levomycetin succinate is administered endolumbally in a single dose of 10-15 mg. In the syndrome of disseminated intravascular coagulation (DIC), Trental, Reopoliglyukin, colloids are prescribed for hypercoagulation, and freshly prepared plasma, proteolysis inhibitors for hypocoagulation. With edema/swelling of the brain, dehydration therapy (Lasix, mannitol 15%) is carried out continuously only after stabilization of the central hemodynamics. With clinical and EEG monitoring of meningitis with epileptic symptoms, anticonvulsant therapy is corrected. With the ineffectiveness of Konvuleks, topiramate (Topamax) is prescribed. Taking into account the duration of antibiotic therapy in high doses, in recent years, a well-established systemic enzyme therapy with Wobenzym has been proposed, which has a potentiating antibiotic, anti-inflammatory, antitoxic, hepatoprotective, immunomodulatory effects, contributing to the elimination of toxic substances, pathogenic immune complexes, immune deposits from tissues and a combination of positive effects shortens the course and reduces the severity of generalized forms of MI.

After discharge from the hospital, convalescents of generalized forms of MI are under dispensary supervision of a pediatrician and a neuropathologist, during which the consequences of the disease are eliminated by complex rehabilitation methods.

With the carriage of meningococcus and mild nasopharyngitis, hospitalization is carried out only for social reasons and from closed institutions. Ampicillin, Levomycetin are prescribed in age dosages for 4 days, or Rocephin is administered intramuscularly for 3 days at a dose of 125 mg up to 12 years and 250 mg in older people. After 3 days, a bacteriological examination is carried out and, if it is negative, the child is admitted to the team. With prolonged carriage, a second course of antibiotic therapy is carried out in combination with immunorehabilitation drugs. In order to prevent the disease in those who contacted the patient with MI, a therapy similar to the treatment of localized forms is carried out. The team is quarantined for 10 days from the moment of isolation of the patient, in which the supervision of a pediatrician and an ENT doctor is carried out. In the first 5-10 days, emergency prevention of MI is carried out with vaccines A or A + C for children over 1 year old, adolescents and adults. Or if other serogroups of meningococcus are detected within the same time frame, no later than 7 days from the moment of contact, passive prophylaxis with normal immunoglobulin is carried out.

After mild form MI vaccination according to the vaccination schedule can be carried out 1 month after recovery.

After severe and mixed forms of MI, vaccination, in the absence of contraindications from a neuropathologist, can be carried out no earlier than 3 months after recovery.

In order to prevent the spread of meningococcal infection and the formation of group morbidity in organized groups, it is necessary to vaccinate contingents at an increased risk of infection at the age of 1.5 years: those attending preschool institutions; located in institutions with round-the-clock stay (orphanages, orphanages); students of grades 1-2 of general education schools and boarding schools.

The following are registered in Russia: meningococcal vaccines A and A + C (Russia) - capsular specific polysaccharides of meningococci of the corresponding serogroups.

Foreign: Meningo A + C - purified lyophilized polysaccharides of meningococci serogroups A and C; polyvalent meningococcal vaccine with polysaccharides of groups A, C, Y and W 135 (England, USA). The vaccines are weakly reactogenic, harmless and immunologically active, causing an increase in the protective antibody titer from the 5th day after a single injection, with a maximum of their accumulation after 2 weeks. Can be combined in different syringes with other vaccines.

For literature inquiries, please contact the editor.

F. S. Kharlamova, doctor of medical sciences, professor

Meningococcal infection is a contagious disease that is transmitted by airborne droplets, affects the central nervous system, joints, heart muscle and often causes toxic shock. The causative agent of the disease, Neisseria meningitides, is a close relative of the gonococcus, but unlike it, it uses the epithelium of the upper respiratory tract as an entrance gate. Infectiousness in meningococcus is low, so outbreaks of the disease occur in conditions of crowding and close contact: in kindergartens, schools, barracks, boarding schools.

The incidence of meningococcal infection is undulating. The indicator periodically creeps up for several years, after which a steady decline is observed for 8-10 years. In the Russian Federation, the incidence on average remains at the level of 5 cases per 100 thousand of the population, in European countries - up to 3 per 100 thousand, in the countries of Central Africa - 20-25, reaching in unfavorable years up to 800 cases per 100 thousand of the population. African countries form the "meningitis belt" of the planet due to the high prevalence of the disease.

Children and young people under 30 suffer from meningococcal infection, but the disease is most severe in infants under one year old and in people over 60 years old. Sometimes events develop so quickly that a lightning-fast form of the disease is isolated separately. The consequences of meningococcal infection depend on the severity of its course and the prevalence of the pathogen, it can lead to severe disability and death.

Pathogen

Meningococcus is a round, gram-negative bacterium, immobile, does not form spores. In human cells, it is located in pairs, forming structures similar in appearance to coffee beans. This organization of bacteria is called a diplococcus. Young meningococci have thin and delicate filaments on the surface of the cell wall, with which they attach to epithelial cells.

Bacteria secrete a large amount of aggressive substances that contribute to their penetration into the blood and various tissues of the body. For example, hyaluronidase breaks down the main component of connective tissue - hyaluronic acid, due to which collagen bundles are loosened and a passage for meningococcus is formed. cell wall bacteria is the strongest toxin for the human body. It negatively affects the central nervous system, kidneys, heart muscle and causes a powerful activation of the immune system.

The causative agent is unstable in the external environment. It quickly dies when heated, under the influence of ultraviolet radiation, during processing disinfectants. The most favorable conditions for its life are high humidity (70-80%) and air temperature in the range of 5-15 degrees C, in which it retains its activity for up to 5 days. For this reason, the incidence increases significantly in the cool season - from February to April, subject to warm and snowy winters.

The source of infection is a sick person or a carrier. The carriage of meningococcus does not manifest itself subjectively, so the person does not know that he is dangerous to others. The causative agent is localized in the nasopharynx, is released outward with droplets of saliva when talking, coughing, sneezing. It has been noted that with the accumulation of carriers of about 20% in the population, mass outbreaks of meningococcal infection occur. Patients with meningitis or a common form of the infection are more contagious, but they tend to be isolated from society and pose a danger only to their caregivers.

The mechanism of the development of the disease

Meningococcus enters the mucous membrane of the nasopharynx of a susceptible person and is firmly fixed on it. Further interaction between the macroorganism and the microorganism depends on the activity of the immune system and the aggressiveness of the toxins of the pathogen. If local immunity is well expressed, then the carriage of meningococcal infection develops: bacteria multiply moderately in the nasopharynx and are released into the external environment in small quantities. After some time, they leave the body.

If the virulence of meningococcus is sufficient to penetrate deep into the mucous membrane, meningococcal develops. Bacteria destroy the cells of the body, release aggressive substances into the tissues, which entails a reaction of the vessels and the immune system. The blood rushes intensely to the site of inflammation, its liquid part goes into the mucous membrane - hyperemia and edema are formed. They are designed to limit the pathological focus and prevent further spread of the pathogen.

Sensitive nerve endings in the area of ​​inflammation react to biologically active substances that secrete destroyed cells and send a pain impulse to the brain, like a distress signal. It is further enhanced by bacterial toxins and the pressure of edematous tissues on the receptor. As a result, a person feels pain and sore throat.

If the inflammatory reaction has not stopped meningococcus in the nasopharynx, it penetrates into the blood and lymphatic vessels. In the blood of the pathogen, immune cells and protective proteins are attacked, which is why most of the microorganisms die with the release of a dangerous toxin. In situations where the forces are approximately equal, the disease ends at this stage, manifesting itself with a rash and intoxication.

diseases caused by meningococcus

If the immune cells waste their potential before they destroy all the bacteria, then incomplete phagocytosis occurs. The leukocyte captures meningococcus, but cannot digest it, so the pathogen remains viable and travels through the body in this form. Further development of events depends on where the bacteria penetrate. Penetrating through the meninges, they cause purulent arthritis through the joint capsule, and iridocyclitis into the iris of the eyeball.

Meningococci settle in the peripheral blood vessels and damage their vascular wall due to which blood rushes into the tissues. So, a hemorrhagic rash is formed on the skin, which is a local hemorrhage.

A large amount of meningococcal toxin in the blood leads to paralytic vasodilation in the periphery and a sharp drop blood pressure. There is a redistribution of blood flow: blood is deposited in small vessels and does not flow in sufficient quantities to vital organs - the brain, heart, liver. Infectious-toxic shock develops - a deadly condition.

Disease classification

The interaction of meningococcus with the human body proceeds according to various scenarios, each of which requires a special approach and treatment. In this regard, in 1976, Academician Pokrovsky developed a classification of meningococcal infection, which doctors use to this day. According to her, they distinguish:

Localized forms:

• The carriage of meningococcus is asymptomatic;
• Acute nasopharyngitis - manifested by symptoms of acute respiratory infections;
• Pneumonia - the clinic does not differ from other bacterial ones.

Generalized forms:

Clinical manifestations

From the moment of infection to the onset of symptoms of meningococcal infection, it takes from 1 to 10 days, on average, the incubation period lasts 2-4 days.

Nasopharyngitis

The disease begins acutely with scanty mucous secretions,. The temperature rises only in half of the patients, does not exceed 38.5 degrees C. It is accompanied by signs of intoxication: aching muscles and joints, headache, lack of appetite, lethargy. The fever lasts no more than 4 days, after which the patient quickly recovers.

When examining the pharynx, hyperemia of the posterior pharyngeal wall is visible, from 2-3 days of illness it becomes granular due to the reaction of small lymphoid follicles. The tonsils, their arches, and the uvula remain unchanged, although in children under 3 years of age, inflammation also extends to them.

Meningococcemia

The presence of meningococcus in the blood causes a rapid and powerful immune response, which immediately affects the patient's condition. The disease begins acutely with a sharp rise in temperature to 39 degrees C and above. There are signs of severe intoxication: chills, pain in the lower back, muscles, joints, headache, severe weakness. The patient may vomit without abdominal pain, and there is no appetite.

hemorrhagic rash with meningococcemia

6-24 hours after the rise in temperature, the most characteristic sign of meningococcemia appears - hemorrhagic rash. Initially, it may look like pink spots, pinpoint hemorrhages, which quickly transform into large, irregularly shaped bruises. The elements of the rash have a different shape and size, bulge somewhat above the surface of the skin, and are sensitive when touched. Most often they are located on the thighs, buttocks, shins and feet and have a star-shaped outline.

The rash falls asleep for 1-2 days, after which the reverse development of its elements begins. Small ones are pigmented and completely disappear after a while, large ones can leave behind retracted scars. The early appearance of a rash (up to 6 hours after the rise in temperature) and the location of its elements on the face, upper half of the body are signs of an extremely severe course of meningococcemia. Sometimes it ends with necrosis of the tip of the nose, fingers and toes.

The presence of meningococcus in the blood is fraught with the development of a formidable complication - infectious-toxic shock.. It usually begins in the first hours from the onset of the disease and, without emergency assistance, inevitably leads to the death of the patient. The first signs of an incipient shock are a marbled pallor of the skin, a drop in body temperature and blood pressure.. The patient gradually loses consciousness and plunges into a coma, death occurs from insufficient blood supply to the brain, heart and liver.

Another dangerous complication meningococcemia is the Friederichsen-Waterhouse syndrome. It develops when the adrenal cortex dies under the influence of a massive hemorrhage into it. The patient stops producing adrenal hormones, which are responsible for water-salt metabolism and maintaining blood pressure. As a result, he dies from dehydration or heart failure.

Meningitis

Meningococcal meningitis begins with a rise in temperature to 38.5-39.5 degrees C and headache, which increases significantly by the end of the first day of illness.

meningitis symptoms

The pain in the head is bursting in nature, most often localized in the fronto-temporal or occipital regions, but can cover the entire skull as a whole. Pain is aggravated by bright light, loud sounds, when changing the position of the body. Often it is accompanied by vomiting with a fountain, which does not bring relief and occurs without previous nausea.

first sign of meningitis in a baby

By the end of the first day, symptoms of irritation of the meningeal membrane (meningeal signs) appear. These include soreness of the posterior neck muscles, the inability to fully straighten the leg in knee joint with flexed hip. In infants, the first signs of meningitis are considered to be a complete refusal to eat, a constant monotonous cry, and a bulging fontanel on the head. If you take a sick baby by the armpits, he bends his legs to the body - this is a symptom of suspension.

On the 3rd-4th day of the disease, in the absence of antibacterial treatment, the patient takes the characteristic position of the "pointing dog". He lies on his side, bending his legs and throwing his head back, while his back is strongly arched and tense. In children, this posture is more common and more pronounced than in adults. By the same time, consciousness becomes cloudy, the patient is inhibited, does not respond to questions or answers in monosyllables. In some cases, hearing is turned off, paralysis develops eyeballs, limbs, swallowing muscles. Often, meningococcal meningitis is combined with meningococcemia, which is manifested by a hemorrhagic rash on the skin.

Video: meningococcal meningitis

Diagnostics

Diagnosis of meningococcal infection is carried out by doctors of various specialties, which depends on the form of the disease and its manifestation. With acute nasopharyngitis, patients usually turn to a local therapist, an ENT doctor, with a rash - to an infectious disease specialist, a dermatovenereologist, with headaches, paralysis - to a neurologist. Cases of severe meningococcal infection are diagnosed in departments providing emergency assistance. However, like any infectious disease, it belongs primarily to the competence of the infectious disease specialist.

The doctor examines the patient, collects an anamnesis, studies complaints. Epidemiological data play an important role: if over the past 10 days a patient has had prolonged contact with a person with nasopharyngitis or a case of meningococcal infection has been detected in his team, then meningococcal infection has occurred with a high degree of probability. An acute onset of the disease, a rise in temperature, the presence of a hemorrhagic rash on the skin, meningeal signs, and impaired consciousness also speak in favor of the diagnosis.

All patients with signs of meningitis undergo a lumbar puncture. to get cerebrospinal fluid (CSF) for analysis. With meningococcal infection, cerebrospinal fluid flows out under pressure that is higher than normal, has a yellow or yellow-green color. It is cloudy due to the high content of protein and cellular elements.

The following methods are used to confirm the diagnosis:

If necessary, instrumental methods of research are connected. An ECG is performed if there is a suspicion of toxic damage to the heart, CT or MRI of the brain when signs of focal lesions of the central nervous system appear (paralysis, hearing loss).

Treatment

Patients with meningococcal infection are hospitalized in an infectious diseases hospital or in intensive care (with infectious-toxic shock). The term of hospitalization is up to 30 days in case of a severe form of the disease. At the time of treatment, the patient is shown a diet with a predominance of easily digestible protein, some fluid restriction and table salt. Elements of the skin rash are treated with local antiseptics - fucorcin, brilliant green, potassium permanganate solution.

Medical treatment includes:

Recovery criteria include:

• Normal body temperature for more than 5 days;
• Absence of inflammatory changes in the nasopharynx;
• The disappearance of the rash;
• Absence of headache and meningeal signs;
• Normalization of blood counts;
• Negative bakposev and PCR-study of cerebrospinal fluid.

Follow-up after recovery

After discharge from the hospital, the patient must be observed by a local general practitioner for a year. During this period, a sick person needs to take a general blood test 4 times (1 time in 3 months), if necessary, he is shown an ECG, CT and MRI of the brain. 5 days after discharge, a bacteriological examination is repeated, for which a swab is taken from the nasopharynx. With a negative result, a person is allowed to join the team and work.

Any vaccines are contraindicated for an ill person within 3 months after recovery. For one year, he should not sunbathe in the sun, change the climate zone drastically, overheat in a bath or sauna.

Prevention of meningococcal infection

If a patient with meningococcal infection is detected in the team, quarantine is imposed for 10 days, during which all its participants are examined for the carriage of meningococcus, thermometry and throat examination are performed daily. Besides, All contacts should be given prophylactic antibiotics: rifampicin 600 mg 2 times a day for 2 days, ciprofloxacin 500 mg intramuscularly once.

Specific prophylaxis is the introduction of a special anti-meningococcal vaccine. Since 2013, it has been included in the national vaccination calendar of the Russian Federation. It is administered intramuscularly to healthy children older than 2 months twice with an interval of 2 months. Emergency vaccination is carried out in the first 5 days after contact with a patient with meningococcal infection. The planned introduction is shown to first-year students living in a hostel, conscript soldiers.

Vaccination against meningococcal infection is carried out by vaccines:

1. Dry vaccine meningococcal polysaccharide A ("Menugate");
2. Vaccine meningococcal polysaccharide A + C;
3. Tetravalent meningococcal vaccine (against serotypes A, C, Y, W-135) - "Mentsevax".

In addition, a combined intramuscular vaccine against Hemococcus and Pneumococcus is produced. Persistent immunity is formed during the 1st month after vaccination.