Acute flaccid paralysis in children: a guide. Flaccid (peripheral paralysis)

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In the paralytic and early recovery stages, poliomyelitis can be mixed with various diseases, occurring with paralysis, especially of a flaccid nature, as well as with pseudoparalysis caused by damage to joints, muscles and bones.

Of great importance differential diagnosis between polio and polyradiculoneuropathies of various etiologies. The clinical picture of this syndrome (it is often called Guillain-Barre syndrome or ascending Landry palsy) consists of motor disorders, changes in the reflex, sensitive and vegetative spheres. The disease develops at any time of the year, 1-2 weeks after any rise in body temperature, catarrhal symptoms, intestinal disorders or hypothermia.

The disease begins with the patient complaining of pain in the legs, less often in the arms. Small children refuse to stand on their feet and look for a gentle position. Objectively, symptoms of tension and sensitivity disorders of the “stockings” and “gloves” type are noted.

Paresis and paralysis in polyradiculoneuropathies, as well as in poliomyelitis, are of a sluggish nature, but they are usually symmetrical, diffuse, more often expressed in the distal parts of the extremities, the type of distribution of paresis is predominantly ascending; their intensity is mostly expressed moderately. Tendon reflexes decrease or disappear, abdominal reflexes are not caused only with widespread paralysis of the muscles of the trunk and limbs, urination may be occasionally impaired, which does not happen with polio. Sometimes mild, quickly passing pyramidal symptoms may appear, but damage to the cranial nerves is common. The most typical is a symmetrical lesion of the facial muscles, then in terms of frequency of involvement in the pathological process there are IX, X, then III, IV, VI pairs, less often VII and XII.

Table 5

Diagram of types of breathing disorders

At bulbar syndrome, as with deep paralysis of the respiratory muscles, life-threatening respiratory disorders occur.

Autonomic disorders occur in a number of patients in the form of cyanosis, swelling of soft tissues, sweating, and coldness of the extremities. Mild diffuse muscle atrophy is also noted, mainly in the distal extremities. From the first days of the disease, more often in the second week, protein-cell dissociation is detected in the cerebrospinal fluid, mainly due to a significant increase in protein content.

The disease has a favorable course, with almost complete restoration of lost functions due to paralysis.

Bulbar forms of poliomyelitis can be mistaken for diphtheria neuritis, polyneuritis, diphtheria croup and vice versa. For differential diagnosis, it is important that with diphtheria there is often selective damage to the fibers of the glossopharyngeal nerve, sometimes a violation of accommodation, which is not typical for: poliomyelitis. Neuritis in diphtheria is often accompanied by toxic myocarditis. The diagnosis of diphtheria is confirmed by a high titer of diphtheria antitoxins in the patient’s blood serum.

Availability muscle weakness, hypotension, decreased reflexes are observed in myopathies that develop out of connection with the infectious process, without pain. With myopathy, the disease progresses over a long period of time: a “duck walk”, atrophy of the muscles of the trunk, shoulder and pelvic girdle appear, muscle tone and strength decrease, mask-like appearance of the face, and pseudohypertrophy of the muscles of the lower legs.

Myasthenia gravis is characterized by increased fatigue, weakness, “flickering” paresis - a weakening of symptoms during the day with their subsequent intensification after fatigue. The diagnosis can be confirmed by a positive proserine test: after administration of proserine, muscle weakness decreases or disappears.

In extremely rare cases, flaccid paralysis may occur in children vaccinated with live polio vaccine. The approximate risk is 1 case of paralytic disease per 2-3 million doses of vaccine. The disease can develop not only in vaccine recipients, but also in people who have had close contact with vaccinated people. The greatest risk of paralysis occurs after the first dose of oral polio vaccine.

WHO introduced the concept of vaccine-associated polio. According to WHO recommendations, vaccine-associated polio includes cases when:

1) the disease begins from the 5th to the 30th day after taking the live oral polio vaccine (for those who have had contact with the vaccinated, the period is extended to 60 days);
2) the development of flaccid paralysis or paresis without sensory impairment persists for more than 2 months;
3) there is no progression of the disease;
4) a vaccine strain of the polio virus is isolated from the patient and, over the course of the disease, antibody titers to it increase by at least 4 times.

If these conditions do not exist, the illness resulting from oral polio vaccine is recorded as vaccine reaction. The course of vaccine-associated poliomyelitis is favorable.
Kharkov - 1993

The textbook was compiled by: Ph.D., Associate Professor K.K. Makarenko (Head of the Department of Children's Infectious Diseases, KhIUV), Ph.D. V.A. Mishchenko (Associate Professor of the Department of Children's Infectious Diseases;: KHIUV, I.D. Osadchaya (pediatric neurologist, consultant at the Kharkov Regional Children's Infectious Diseases Clinical Hospital).

Flaccid paresis is a decrease in strength in one or more muscles. It develops only secondarily, that is, it is a consequence of one or another disease. In this case, strength can be measured using a special test, which cannot be said about another condition called paralysis.

Depending on how badly the muscles are damaged, there are 5 types of this condition. To determine one degree or another, you can use a scale specially developed for this purpose.

Determination system

Pathology is determined on a five-point scale, which was developed and has been successfully used in neurology for many years.

Five points are given to a person whose muscle strength is completely preserved, that is, there are no signs of paresis.

A score of four is given when the strength is slightly reduced compared to the recent past.

Three points is already a significant decrease in muscle strength.

Two points are given if the patient cannot overcome gravity. That is, he can bend the elbow joint if the arm is lying on the table, but is not able to do this if the arm is hanging along the body.

One point is given when only individual muscle bundles contract, but not the entire muscle.

Zero points – complete absence muscle tone. This condition is also called plegia.

Depending on the root cause of paresis, two forms can be distinguished. The first form is central or spastic. The second form is peripheral, or flaccid paresis. Depending on how many limbs are affected, we can distinguish:

1. Monoparesis, diagnosed in only one arm or only one leg.
2. , diagnosed in the leg and arm on the right or left side of the body.
3. , diagnosed only in the arms or only in the legs.
4. , which covers both arms and legs.

Causes

The main cause of flaccid paresis of an arm or leg is a stroke, which results in an acute disorder of cerebral or spinal circulation. In second place in frequency are tumors of the brain or spinal cord, and head or back injuries.

Other reasons include:

1. Brain abscess.
2. Encephalitis.
3. Disseminated encephalomyelitis.
4. Poisoning with poisons, salts, alcohol.
5. Botulism.
6. Epilepsy.

Most often, identifying this symptom does not require any diagnostic measures, since making the above diagnoses already implies a decrease in muscle strength in a person.

The doctor must examine the patient and interview him. The main complaints are identified, from what period the strength in the arms or legs began to decrease, and whether anyone in the family has similar symptoms.

After this, a neurological examination is performed on a five-point scale, which reveals flaccid paresis lower limbs and assess the general condition muscular system. After this is carried out general analysis blood and, if necessary, toxicological tests.

From others diagnostic procedures– electroencephalography, CT scan, magnetic resonance angiography. If necessary, a neurosurgeon is consulted.

Treatment

Acute flaccid paresis is not a separate disease, but only a consequence of other, more serious diseases. Therefore, treating it alone will not give any results. First of all, it is necessary to identify and direct treatment to the cause that caused this condition.

For example, it may require surgical removal of a tumor or hemorrhage caused by a stroke. The same method is used to remove the abscess (abscess) and begin antibiotic therapy.

Treatment can use drugs that improve blood circulation, lower blood pressure, and improve metabolism. Antibacterial therapy may also be carried out if infections of the brain or spinal cord have been diagnosed. For botulism - administration of serum. And, of course, drugs that improve nerve conduction are always used.

It turns out that the treatment of flaccid foot paresis will depend entirely on what causes the pathology, and the therapy itself must be strictly individual.

During treatment, massage, exercise therapy, physiotherapy and other procedures are required that are aimed at preventing the muscles from atrophying.

It is very rare to be completely cured, so in most cases the patient receives disability.

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And the motor nuclei of the cranial nerves to the axon terminals. Since no efferent impulse can reach the muscle without passing the peripheral motor neuron, peripheral paralysis is characterized by loss of all movements - voluntary and involuntary. The muscle is deprived of both impulse and non-impulse (trophic) influence from the peripheral motor neuron.

The occurrence of peripheral paralysis leads to the impossibility of muscle tone (muscle atony), reflexes (areflexia) and to disruption of trophic processes (degenerative muscle atrophy). Regressive bio-chemical, structural and physical processes, as a result of which their function is disrupted. Thus, when stimulated by an electric current, the muscle responds with a slow worm-like contraction, like smooth muscle. The damaged peripheral motor cell shows signs of increased excitability, which leads to sporadic contractions of motor units, which are called fascicular twitches. They are very characteristic of such peripheral motor neuron diseases as amyotrophic lateral sclerosis, cervical myelopathy, and syringomyelia.

Denervated muscles also become hypersensitive (denervation hypersensitivity), which is manifested by spontaneous contractions of individual muscle fibers, sometimes difficult to detect visually. However, fasciculations and fibrillations are well identified using EMG.

Spinal cord lesion

In the anterior horns of the spinal cord along the vertical spinal axis there are motor neurons that innervate different regions. From level C I -C IV and partially C V, the muscles of the neck and the diaphragm muscle (C IV), C V -C VIII (there are 8 spinal segments in the cervical spinal cord) and partially the thoracic Th I belt are innervated upper limbs and themselves, Th I -Th XII - muscles of the trunk, lumbar L I -L V, partially Th XII and sacral S I - II - the belt of the lower extremities and the lower extremities themselves, S III - IV - sphincters of the bladder and anus . According to the level of damage to the segments of the spinal cord or the peripheral structures emanating from them, peripheral paralysis will be noted. In a clinical setting, the doctor has to solve the inverse problem, namely: by the localization of peripheral paralysis, determine the topic of damage to the nervous system.

Lesions of the spinal cord are usually characterized by bilaterality: upper or lower paraplegia, tetraplegia (paresis).

Cranial nerve damage

When the motor structures of the cranial nerves are damaged at any level - from the nucleus to the terminal and axon - peripheral paralysis occurs in the muscles of the tongue, pharynx, larynx and soft palate (caudal group of cranial nerves, bulbar syndrome), masticatory muscles (trigeminal nerve), facial (facial) and external muscles of the eye (oculomotor group of cranial nerves).

Breathing disorders

In patients with signs of damage to the spinal cord and other parts nervous system Breathing disorders often occur. They can be called: Material from the site

• decompensation of previous pulmonary and cardiac pathology (chronic obstructive processes in the lungs, etc.);
• secondary respiratory disorders due to bulbar lesions and impaired pharyngeal reflex, retraction of the tongue, flow of saliva, mucus and food entering the upper respiratory tract with the development of atelectasis and pneumonia;
• somatic complications in the form of hypostatic pneumonia on the side of hemiplegia;
• central respiratory disorders with damage to the medulla oblongata (tachypnea, periodic types of respiratory distress, apnea);
• damage to the fibers of the corticonuclear pathway ending on the peripheral motor neurons of the respiratory muscles (diaphragm, intercostal muscles), with loss of voluntary control of breathing and the risk of sudden death during sleep;
• damage to peripheral motor neurons at level C IV and the thoracic spinal cord.

Flaccid paralysis(paresis) develops when a peripheral (lower) neuron is damaged in any area: anterior horn, root, plexus, peripheral nerve. In this case, the muscles lose both voluntary and involuntary, or reflex, innervation. Flaccid paralysis syndrome is characterized by the following signs[Duus P., 1995]:

Lack or decrease in muscle strength;
- decreased muscle tone;
- hyporeflexia or areflexia;
- muscle wasting or atrophy.

Hypotonia and areflexia develop due to interruption of the arc of the monosynaptic stretch reflex and a disorder of the mechanism of tonic and phasic stretch reflexes. Muscle atrophy is caused by a violation of the trophic influence from the anterior horn on the muscle fibers, develops several weeks after denervation of the muscle fibers and can be so pronounced that after several months or years only the connective tissue remains intact in the muscle.

Restorative measures for the development of flaccid paresis or paralysis are aimed, firstly, at restoring (if possible) the function of a peripheral neuron, and secondly, at preventing the development of muscle tissue atrophy and preventing contractures.

Improving nerve tissue function

Achieved by prescribing neutrotrophic and vasoactive drugs:

• nootropil/piracetam (capsules/tablets 0.4 g-0.8 g three times a day or 20% solution 5-10 ml intramuscularly or intravenously);
• Cerebrolysin (3-5 ml intramuscularly or intravenously);
• actovegin (5-10 ml intramuscularly or intravenously drip once or twice a day; 1 ml contains 40 mg of the active substance);
• trental (in pills, 0.1 g three times a day, or 5 ml intravenously drip once a day; 1 ml contains 0.02 g of the active substance);
• vitamin B1 (solution of thiamine chloride 2.5% or 5% or thiamine bromide 3% or 6%, 1 ml intramuscularly daily, once a day);
• vitamin B12 (400 mcg once every 2 days intramuscularly, can be taken simultaneously with vitamin B1, but not in the same syringe).

If the anatomical integrity of the peripheral nerves is compromised, neurosurgical intervention may be indicated.

Preventing the development of muscle atrophy

This is a very important task, since degeneration of denervated muscle fibers develops very quickly and is often irreversible. By the time innervation is restored (either through natural reinnervation or through neurosurgical intervention), atrophy can reach such a pronounced degree that muscle function can no longer be restored. Therefore, measures to prevent the development of muscle atrophy with impaired innervation should begin as early as possible. For this purpose, massage (classical, acupressure, segmental), therapeutic exercises, electrical stimulation of nerves and muscles are prescribed.

Massage

It is aimed at stimulating muscles, so techniques include fairly intense rubbing, deep kneading, and impact on segmental zones. However, massage of paretic muscles should not be done with great force. The massage should be moderate and short-lived, but carried out over many months (short breaks are taken between courses). Rough, painful techniques can cause increasing muscle weakness. They also use acupressure using a tonic technique. The toning method of acupressure is carried out by applying vibrating, short, quick stimulation with the fingertip sequentially to a number of points that stimulate the desired movement. The topography of recommended points of influence for stimulating active muscle contractions is presented in table 4.5. and on Fig.4.6.

Note: Cun is a unit of measurement individual for each person, equal to the distance between two folds formed when bending the second and third phalanges of the middle finger on the left hand in men and on the right hand in women.

Physiotherapy

Aimed at restoring movements of weakened muscles. Initially, in the complete absence of active movements, passive movements are used in all joints of the paretic segment or limb. Passive movements are performed with a small amplitude simultaneously with the volitional sending of a motor impulse to the patient for this movement. To teach the patient at least minimal active muscle tension, exercises with electromyographic feedback can be very effective.

When muscle contractions appear, special attention begins to be paid to active exercises with strictly individual dosing of gradually increasing physical activity. Initially, with severe paresis, active movements are performed under easier conditions. To do this, they use techniques aimed at lightening the weight of the limb and reducing the friction force: movements are made in a horizontal plane, on a smooth surface. Another way to get relief is to exercise in water. The patient is taught dosed muscle tension and relaxation, gradual increase and decrease in effort, differentiation of different degrees of effort (for this, visual aids can be used to help the patient analog scales and columns, dynamometer indicators). As muscle strength is restored, training exercises begin to be used. In order to increase the load on the muscles, multiple repetitions of the movement, an increase in the speed of movement and the length of the lever, and resistance to the movement are used (the resistance can be provided by a trainer or a partner; rubber bandages, expanders, and block exercise machines with a suspended load are also used to create resistance). The exercise should cause some fatigue, but not overwork of the working muscles. Intensive, prolonged physical exercise, since paretic muscles are characterized by rapid fatigue, and an overdose of exercise leads to an increase in muscle weakness. The load is increased gradually as muscle strength increases.

Electrical stimulation

Electrical stimulation plays a special role in the treatment of flaccid paralysis. Electrical stimulation of motor nerves and muscles refers to the use of electric current with the aim of initiating or strengthening the activities of these structures [Bogolepov V.M. et al., 1985]. Electric current, changing the concentration of tissue ions near the cell membrane and changing its permeability, acts like natural biocurrents. The therapeutic effect of electrical stimulation is associated with increased blood flow to contracting muscles and improvement venous outflow, which is accompanied by a local increase in metabolic and plastic processes, as well as an increase functional activity central nervous system. However, the therapeutic effect of electrical stimulation entirely depends on how correctly the parameters of the stimulating electrical current are selected. The choice of exposure parameters, in turn, is determined by the degree of disruption of the muscle innervation and the condition of the muscle tissue. Therefore, electrical muscle stimulation should always be preceded by a diagnostic study of the degree of muscle denervation. The main question to be resolved is the question of the presence of a complete (anatomical or functional) or partial interruption of the nerve, since with a intact or only partially damaged nerve, stimulation of the muscle must be carried out through the nerve, whereas with complete denervation of the muscle one must limit itself to stimulation of the muscle itself. This issue can be resolved using electromyography and/or electrodiagnostics.

Currently, the main diagnostic method for determining the level and degree of damage to nerve conductors is electromyography in its modern versions (stimulation, needle). Let us recall that the main electromyographic signs of partial nerve damage are a decrease in the velocity of excitation (during demyelination) and/or a decrease in the amplitude of the M-response (a sign of axonopathy), as well as changes in the structure of action potentials of motor units. Signs of complete interruption of a peripheral nerve include the absence of an M response when the nerve is stimulated, as well as spontaneous activity recorded in the muscle at rest. Damage to a motor neuron at the level of the anterior horns of the spinal cord is characterized by the appearance of fasciculations at rest, and with active contraction - a sparse interference curve with individual high-amplitude discharges of long duration.

Classical electrodiagnostics, which has been used for more than 100 years to study peripheral nerves, is gradually losing its diagnostic value due to the advent of more informative electromyography. However, as a method for selecting the optimal parameters of the stimulating current, electrodiagnostics still retains its importance. In addition, in the absence of electromyography capabilities, electrodiagnostics can help determine the degree of denervation or reinnervation of the muscle. Some modern physiotherapeutic devices combine the capabilities of both electrodiagnostics and electrical stimulation.

Based on the results of electrodiagnostics, the presence or absence of a reaction of degeneration of the neuromuscular system is revealed, the rheobase and chronaxy are determined, and a force-duration curve is constructed for the affected muscle, or a curve of the relationship between the time of the current and its intensity necessary to obtain threshold excitation. The data obtained are used to guide the selection of electrical stimulation current parameters.

For electrical stimulation They use constant pulse currents with a rectangular, exponential or half-sinusoidal pulse shape with a duration of 1 to 300 ms, modulation of these pulses in a series of different durations and frequencies, and a current strength of up to 50 mA. Alternating sinusoidal modulated currents with carrier frequencies of 2000 and 5000 Hz can also be used when modulated with low frequencies from 10 to 150 Hz, current strength up to 80 mA.

Let us recall that in a healthy striated muscle, excitation under the influence of current develops quickly, under the influence of short impulses, and in order to obtain a contraction it is necessary to quickly turn on the current, since a smooth increase in current due to the great adaptive ability healthy nerves and muscles does not lead to a motor effect. When exposed to impulses applied at a frequency of more than 20 per 1 sec, tetanic contraction occurs in a healthy muscle as a result of the summation of individual excitations by the neuromuscular apparatus. The most powerful muscle contraction in a healthy muscle occurs at a pulse frequency of 60-100 Hz, but with such stimulation muscle fatigue quickly develops. When used more than low frequencies fatigue develops to a lesser extent, but the strength of muscle contraction also decreases. Nerve damage and muscle denervation are characterized by a decrease or absence of the response of the nerve and muscle to stimulation by a series of frequently following impulses (i.e., to stimulation with tetanizing current), a decrease or absence of the nerve response to direct current stimulation, and a temporary increase in muscle excitability during stimulation with single impulses direct current followed by a gradual extinction of this reaction, a perversion of the polarity of the reaction to galvanic current.

The main requirement for electrical stimulation is to achieve maximum results with the least damaging and irritating effect of the current. In this regard, the selection of such parameters of the stimulating current as frequency, duration, shape and amplitude of pulses is very important.

Pulse frequency: Tetanic muscle contractions are the most physiological and effective. Therefore, we must strive to carry out stimulation not with single, slightly physiological contractions (twitching) of the muscle, but by inducing tetanic contractions. Only in cases where even the longest pulses of tetanizing current (40 ms) do not cause tetanic contraction, as a last resort, stimulation is carried out with single, possibly shorter pulses of galvanic current.

Pulse duration: The shorter the pulse duration, the less irritating the effect of the current. An increase in pulse duration, especially over 60 ms, is accompanied by a significant increase in pain. Therefore, we must strive to use the shortest possible pulses.

Pulse amplitude (current): There is a linear relationship between the strength of the current and the strength of the muscle contraction caused. However, as the current increases, its irritating effect also increases.

Pulse shape: for a denervated muscle, the adaptive abilities of which are reduced, a smoothly increasing current is used (the most adequate is the exponential shape of the pulses).

With partial denervation of the muscle, the muscle is stimulated through the nerve; with complete denervation, the muscle is stimulated directly. When stimulating a muscle through a nerve, an active electrode (1-4 cm square in size) is placed on the motor point of the nerve or muscle (the motor point of the nerve is the area where the nerve is located most superficially and is accessible to influence; the motor point of the muscle is the place corresponding to the level of entry motor nerve into the muscle, or the place where the nerve branches into small branches, the area of ​​greatest excitability of the muscle). The second electrode (100-150 cm2 in size) is placed in the projection of the spinal cord segment corresponding to the nerve along the midline of the body. When stimulating the muscle directly, both electrodes are placed above the muscle: one above its abdomen, the second at the junction of the muscle and the tendon.

Muscle contraction should alternate with periods of rest. The ratio of the time of current and pauses, depending on the state of the muscle, varies within 1:2-1:4. The specific stimulation mode should be based on the results of electrodiagnostics, reflecting functional state muscle tissue. Electrical stimulation should not cause muscle fatigue.

Stimulation of very weakened muscles is carried out for a very short time - 2-3 minutes three times over half an hour, at low current strength (there is no need to achieve distinct contractions). Weakened muscles need to be helped by reducing the effects of gravity and friction. In the presence of voluntary muscle contractions, it is advisable to combine the action of the current with the patient’s volitional efforts aimed at performing muscle contractions. As muscle strength increases, the duration of the electrical stimulation procedure increases to 15-20 minutes with short 2-3 minute breaks for rest. The current intensity should ensure that good, distinct contractions are obtained. Sometimes additional load is introduced in the form of overcoming gravity or resistance.

It is important to remember that the muscle must be stimulated from its stretched initial state so that under the influence of the current it can contract. Undifferentiated contraction of many muscles at the same time and severe pain indicate that the procedure was performed incorrectly.

It is necessary to stimulate muscles with impaired innervation daily and for a long time, until reinnervation occurs. Periodic breaks are necessary because long-term use electrical stimulation may cause irritation skin. In parallel with electrical stimulation, it is advisable to prescribe drugs that improve muscle trophism - ATP, riboxin, vitamin E. The main contraindications for electrical stimulation include malignant neoplasms, fever, acute inflammatory processes, a tendency to bleeding, and severe heart rhythm disturbances.

Prevention of the formation of contractures and sprains of the tendon-ligamentous apparatus

It is achieved by using removable plaster splints or orthoses. Orthoses should be light, not restrict remaining movements, not compress the underlying tissues, especially in areas with impaired sensitivity, and not impair blood circulation in the limb. The orthosis must hold the limb or its segment in a position in which there is no overstretching of the affected muscle and its tendons: for example, in case of paralysis of the extensor muscles of the hand and fingers, an extensor splint is applied for the fingers and wrist joint; in case of paralysis of the muscles that perform dorsal extension of the foot, a splint is applied to hold the foot in the middle position.

Poliomyelitis (infantile paralysis) is caused by a virus and is a highly contagious viral infection. In its most serious form, polio can cause rapid and irreversible paralysis; until the late 1950s, it was one of the most dangerous infectious diseases and often occurred in epidemics. Post-polio syndrome or post-polio progressive muscular atrophy can occur 30 years or more after the initial infection, gradually leading to muscle weakness, wasting, and pain. Polio can be prevented by building immunity and is now virtually extinct in developed countries; however, the risk of disease still exists. Polio is still common in many countries around the world, and there is no way to cure it; therefore, until the polio virus is eradicated, vaccination remains the main method of protection.

In summer and early autumn, when polio epidemics most often occur, parents first of all remember it when their child gets sick. The disease, like many other infections, begins with general malaise, fever and headache. Vomiting, constipation, or mild diarrhea may occur. But even if your child has all these symptoms, plus leg pain, you should not rush to conclusions. There's still a good chance it's the flu or a sore throat. Of course, you call a doctor anyway. If he is away for a long time, you can reassure yourself this way: if the child can lower his head between his knees or tilt his head forward so that his chin touches his chest, he probably does not have polio. (But even if it fails these tests, it is still not proof of disease.)
Despite significant progress in eradicating polio in our country, the problem of diseases accompanied by acute flaccid paralysis (AFP) has not lost its relevance. Pediatricians often encounter various infectious diseases of the brain, spinal cord, and peripheral nerves. The study of the structure of neuroinfections indicates that lesions of the peripheral nervous system occur in 9.6% of patients, infectious diseases of the spinal cord - in 17.7%. Among the latter, acute infectious myelopathies predominate, while acute paralytic vaccine-associated poliomyelitis, acute myelopathy, and enceare much less common. In this regard, in modern conditions it is necessary to pay special attention differential diagnosis AFP, monitoring the epidemic situation, which will avoid overdiagnosis, improve treatment results, and reduce the frequency of unfounded registration post-vaccination complications.

Acute paralytic poliomyelitis is a group of viral diseases united according to the topical principle, characterized by flaccid paresis, paralysis caused by damage to motor cells in the anterior horns of the spinal cord and the nuclei of the motor cranial nerves of the brain stem.

Etiology. The etiological structure of infectious diseases of the nervous system is diverse. Among etiological factors“wild” polioviruses type 1, 2, 3, vaccine polioviruses, enteroviruses (ECHO, Coxsackie), herpesviruses (HSV, HHV type 3, EBV), influenza virus, mumps virus, diphtheria bacillus, borrelia, UPF (staphylococcus , gram-negative bacteria).

Of particular interest is spinal paralysis caused by the “wild” polio virus, which belongs to the picornavirus family, a genus of enteroviruses. The pathogen is small in size (18-30 nm) and contains RNA. Virus synthesis and maturation occur inside the cell.

Polioviruses are not sensitive to antibiotics and chemotherapy. When frozen, their activity persists for several years, in a household refrigerator - for several weeks, at room temperature - for several days. At the same time, polio viruses are quickly inactivated when treated with formaldehyde, free residual chlorine, and do not tolerate drying, heating, ultraviolet irradiation.

The polio virus has three serotypes - 1, 2, 3. Its cultivation in laboratory conditions is carried out by infecting various tissue cultures and laboratory animals.

Causes

Poliomyelitis is caused by a viral infection with one of three forms of the polio virus.

The virus can be transmitted through contaminated food and water or through contaminated saliva during a cough or sneeze.

The source of infection is a sick person or carrier. The greatest epidemiological significance is the presence of the virus in the nasopharynx and intestines, from where it is released in external environment. In this case, the release of the virus in feces can last from several weeks to several months. The nasopharyngeal mucus contains the polio pathogen for 1-2 weeks.

The main routes of transmission are nutritional and airborne.

In conditions of mass specific prevention sporadic cases were reported throughout the year. Mostly children under seven years of age were ill, of whom specific gravity of early age patients reached 94%. The infectiousness index is 0.2-1%. Mortality among unvaccinated people reached 2.7%.

In 1988, the World Health Organization raised the question of the complete eradication of polio caused by the “wild” virus. In this regard, 4 main strategies have been adopted to combat this infection:

1) achieving and maintaining a high level of population coverage with preventive vaccinations;

2) carrying out additional vaccinations on national immunization days (NDIs);

3) creation and operation of an effective epidemiological surveillance system for all cases of acute flaccid paralysis (AFP) in children under 15 years of age with mandatory virological examination;

4) carrying out additional “cleaning up” immunization in disadvantaged areas.

At the time of the adoption of the Global Polio Eradication Program, the number of patients in the world was 350,000. However, by 2003, thanks to ongoing activities, their number dropped to 784. Three regions of the world are already free from polio: American (since 1994), Western Pacific (since 2000) and European (since 2002). However, polio caused by wild poliovirus continues to be reported in the Eastern Mediterranean, African and South-East Asia regions. India, Pakistan, Afghanistan, and Nigeria are considered endemic for polio.

Since December 2009, an outbreak of polio caused by type 1 poliovirus has been registered in Tajikistan. It is assumed that the virus came to Tajikistan from neighboring countries - Afghanistan, Pakistan. Taking into account the intensity of migration flows from the Republic of Tajikistan to the Russian Federation, including labor migration and active trade relations, the “wild” polio virus was imported into the territory of our country, and cases of polio in adults and children were registered.

Russia began implementing the Global Polio Eradication Program on its territory in 1996. Thanks to maintaining a high level of vaccination coverage among children in their first year of life (more than 90%) and improving epidemiological surveillance, the incidence of this infection in Russia has decreased from 153 cases in 1995. up to 1 - in 1997. By decision of the European Regional Certification Commission in 2002. Russian Federation received the status of a polio-free territory.

Before the transition to the use of inactivated polio vaccine, diseases caused by vaccine polioviruses were recorded in Russia (1 - 11 cases per year), which usually occurred after the first dose of live OPV was administered.

Diagnostics

Medical history and physical examination.

Blood tests.

Lumbar puncture (spinal tap).

Laboratory diagnostics. Only based on the results of virological and serological studies can a final diagnosis of polio be made.

The following are subject to virological testing for polio in the laboratories of regional centers for epidemiological surveillance of polio/AFP:

- sick children under 15 years of age with symptoms of acute flaccid paralysis;

- contact children and adults from foci of poliomyelitis and AFP in the case of late (later than the 14th day from the moment of detection of paralysis) examination of the patient, as well as if there are people around the patient who arrived from areas unfavorable for poliomyelitis, refugees and internally displaced persons (one-time) ;

- children under the age of 5 years who arrived during the last 1.5 months from the Chechen Republic, the Republic of Ingushetia and applied for medical care to medical and preventive institutions, regardless of the profile (once).

Patients with clinical signs of poliomyelitis or acute flaccid paralysis are subject to mandatory 2-fold virological examination. The first fecal sample is taken within 24 hours of diagnosis, the second sample is taken 24-48 hours later. The optimal volume of feces is 8-10 g. The sample is placed in a sterile special plastic container. If delivery of selected samples to regional center When polio/AFP surveillance is carried out within 72 hours of collection, samples are refrigerated at 0 to 8°C and transported to the laboratory at 4 to 8°C (reverse cold chain). In cases where the material is planned to be delivered to the virology laboratory at a later date, the samples are frozen at a temperature of -20 °C and transported frozen.

The frequency of virus isolation in the first two weeks is 80%, in the 5th-6th week - 25%. No permanent carriage was detected. Unlike the Coxsackie and ECHO viruses, the polio virus is isolated extremely rarely from the cerebrospinal fluid.

At deaths material is collected from the cervical and lumbar extensions of the spinal cord, the cerebellum and the contents of the colon. With paralysis lasting 4-5 days, it is difficult to isolate the virus from the spinal cord.

The following are subject to serological examination:

— patients with suspected polio;

- children under the age of 5 years who arrived during the last 1.5 months from the Chechen Republic, the Republic of Ingushetia and sought medical care in medical institutions, regardless of their profile (one time).

For serological study Take two samples of the patient’s blood (5 ml each). The first sample should be taken on the day of the initial diagnosis, the second - after 2-3 weeks. Blood is stored and transported at a temperature of 0 to +8 °C.

RSC detects complement-fixing antibodies to the N- and H-antigens of poliovirus. In the early stages, only antibodies to the H-antigen are detected, after 1-2 weeks - to the H- and N-antigens, in those who have recovered - only N-antigens.

During the first infection with poliovirus, strictly type-specific complement-fixing antibodies are formed. Upon subsequent infection with other types of polioviruses, antibodies are formed predominantly to heat-stable group antigens, which are present in all types of polioviruses.

PH detects virus-neutralizing antibodies in the early stages of the disease; it is possible to detect them during the hospitalization of the patient. Virus-neutralizing antibodies can be detected in urine.

RP in agar gel reveals precipitins. Type-specific precipitating antibodies can be detected during the recovery period and circulate long time. To confirm the increase in antibody titers, paired sera are examined with an interval of 3-4 weeks; a dilution of the serum that is 3-4 times or more higher than the previous one is taken as a diagnostic increase. The most effective method is ELISA, which allows short time determine class-specific immune response. It is mandatory to carry out PCR to detect RNA viruses in individual feces and cerebrospinal fluid.

Symptoms

Fever.

Headache and sore throat.

Stiff neck and back.

Nausea and vomiting.

Muscle pain, weakness, or spasms.

Difficulty swallowing.

Constipation and urinary retention.

Bloated belly.

Irritability.

Extreme symptoms; muscle paralysis; difficulty breathing.

Pathogenesis. The entry point for infection in polio is the mucous membrane of the gastrointestinal tract and upper respiratory tract. The virus multiplies in lymphatic formations back wall pharynx and intestines.

Overcoming the lymphatic barrier, the virus penetrates the blood and is carried by its current throughout the body. Fixation and reproduction of the polio pathogen occurs in many organs and tissues - lymph nodes, spleen, liver, lungs, heart muscle and, especially, in brown fat, which is a kind of virus depot.

Penetration of the virus into the nervous system is possible through the endothelium of small vessels or along peripheral nerves. Distribution within the nervous system occurs along cell dendrites and possibly through intercellular spaces. When the virus interacts with cells of the nervous system, the most profound changes develop in motor neurons. The synthesis of polioviruses occurs in the cytoplasm of the cell and is accompanied by suppression of the synthesis of DNA, RNA and proteins of the host cell. The latter dies. Within 1-2 days, the titer of the virus in the central nervous system increases, and then begins to fall and soon the virus disappears.

Depending on the state of the macroorganism, the properties and dose of the pathogen, the pathological process can stop at any stage of viral aggression. In this case, various clinical forms of poliomyelitis are formed. In most infected children, due to the active reaction of the immune system, the virus is eliminated from the body and recovery occurs. Thus, with the inapparant form, there is a nutritional phase of development without viremia and invasion into the central nervous system, with the abortive form, there are nutritional and hematogenous phases. For clinical options, accompanied by damage to the nervous system, is characterized by a sequential development of all phases with damage to motor neurons at different levels.

Pathomorphology. Morphologically, acute poliomyelitis is most characterized by damage to large motor cells located in the anterior horns of the spinal cord and the nuclei of the motor cranial nerves in the brain stem. In addition, the pathological process may involve the motor area of ​​the cerebral cortex, the nuclei of the hypothalamus, and the reticular formation. In parallel with damage to the spinal cord and brain, the soft meninges are involved in the pathological process, in which it develops acute inflammation. At the same time, the number of lymphocytes and protein content in the cerebrospinal fluid increase.

Macroscopically, the spinal cord appears swollen, the border between the gray and white matter is blurred, and in severe cases, the cross section shows retraction of the gray matter.

Microscopically, in addition to swollen or completely disintegrated cells, unchanged neurons are found. This “mosaic” pattern of damage to nerve cells is clinically manifested by an asymmetric, random distribution of paresis and paralysis. In place of dead neurons, neuronophagic nodules are formed, followed by the proliferation of glial tissue.

Classification

According to modern requirements, the standard definition of polio and acute flaccid paralysis (AFP) is based on the results of clinical and virological diagnostics (Appendix 4 to Order M3 of the Russian Federation No. 24 dated January 25, 1999) and is presented as follows:

- acute flaccid spinal paralysis, in which the “wild” polio virus is isolated, is classified as acute paralytic poliomyelitis (according to ICD 10 revision A.80.1, A.80.2);

- acute flaccid spinal paralysis that occurred no earlier than the 4th and no later than the 30th day after taking the live polio vaccine, in which the vaccine-derived poliovirus was isolated, is classified as acute paralytic polio associated with the vaccine in the recipient (according to ICD 10 revision A .80.0);

- acute flaccid spinal paralysis that occurs no later than the 60th day after contact with a vaccinated person in which vaccine-derived poliovirus is isolated is classified as acute paralytic poliomyelitis associated with a vaccine in a contact (according to ICD 10 revision A.80.0). Isolation of vaccine-derived poliovirus in the absence of clinical manifestations doesn't have diagnostic value;

- acute flaccid spinal paralysis, in which the examination was not carried out completely (the virus was not isolated) or was not carried out at all, but residual flaccid paralysis is observed by the 60th day from the moment of their onset, is classified as acute paralytic poliomyelitis, unspecified (according to ICD 10 revision A .80.3);

- acute flaccid spinal paralysis, in which a full adequate examination was carried out, but the virus was not isolated and no diagnostic increase in antibodies was obtained, is classified as acute paralytic poliomyelitis of another, non-poliomyelitis etiology (according to ICD 10 revision A.80.3).

Isolation of a “wild” strain of the virus from a patient with catarrhal, diarrheal or meningeal syndromes without the occurrence of flaccid paresis or paralysis is classified as acute non-paralytic poliomyelitis (A.80.4.)

Acute flaccid spinal paralysis with the release of other neurotropic viruses (ECHO, Coxsackie viruses, herpes viruses) refers to diseases of a different, non-poliomyelitis etiology.

All these diseases, based on the topical principle (damage to the anterior horns of the spinal cord), appear under the general name “Acute poliomyelitis”.

Classification of polio

Based on the severity of the process, mild, moderate and severe forms of polio are distinguished. The course of the disease is always acute, and the nature can be smooth or non-smooth, depending on the presence of complications (osteoporosis, fractures, urolithiasis disease, contracture, pneumonia, bedsores, asphyxia, etc.).

Clinic. The incubation period for polio is 5-35 days.

The spinal form of polio in children occurs with greater frequency than other paralytic forms. In this case, more often the pathological process develops at the level of the lumbar thickening of the spinal cord.

During the course of the disease, there are several periods, each of which has its own characteristics.

The preparalytic period is characterized by an acute onset of the disease, worsening general condition, increased body temperature to febrile levels, headache, vomiting, lethargy, adynamia, meningeal signs. General infectious, cerebral and meningeal syndromes can be combined with catarrhal or dyspeptic symptoms. In addition, it is noted positive symptoms tension, complaints of pain in the back, neck, limbs, pain on palpation of nerve trunks, fasciculations and horizontal nystagmus. The duration of the preparalytic period is from 1 to 6 days.

The paralytic period is marked by the appearance of flaccid paralysis or paresis of the muscles of the limbs and torso. Supporting diagnostic signs this stage are:

- sluggish nature of paralysis and its sudden appearance;

- rapid increase in movement disorders over a short period of time (1-2 days);

- damage to proximal muscle groups;

- asymmetrical nature of paralysis or paresis;

- absence of disturbances in sensitivity and function of the pelvic organs.

At this time, changes in the cerebrospinal fluid occur in 80-90% of patients with poliomyelitis and indicate the development of serous inflammation in the soft meninges. With the development of the paralytic stage, general infectious symptoms fade away. Depending on the number of spinal cord segments affected, the spinal form can be limited (monoparesis) or widespread. The most severe forms are those accompanied by impaired innervation of the respiratory muscles.

The recovery period is accompanied by the appearance of the first voluntary movements in the affected muscles and begins on the 7-10th day after the onset of paralysis. If 3/4 of the neurons responsible for the innervation of any muscle group die, the lost functions are not restored. Over time, atrophy increases in these muscles, contractures, joint ankylosis, osteoporosis, and limb growth retardation appear. The recovery period is especially active during the first months of the disease, then it slows down somewhat, but continues for 1-2 years.

If after 2 years the lost functions are not restored, then they speak of a period of residual effects (various deformities, contractures, etc.).

The bulbar form of polio is characterized by damage to the nuclei of 9, 10, 12 pairs of cranial nerves and is one of the most dangerous variants of the disease. In this case, there is a disorder of swallowing, phonation, pathological secretion of mucus in the upper respiratory tract. Of particular danger is the localization of the process in the medulla oblongata, when damage to the respiratory and cardiovascular centers poses a threat to the patient’s life. Harbingers of an unfavorable outcome in this case are the occurrence of pathological breathing, cyanosis, hyperthermia, collapse, and impaired consciousness. Damage to the 3rd, 4th, 6th pairs of cranial nerves in polio is possible, but less common.

The pontine form of polio is the most mild, but cosmetic defect The child may have it for the rest of his life. Clinical characteristics this form of the disease involves damage to the nucleus facial nerve. In this case, immobility of the facial muscles on the affected side suddenly occurs and lagophthalmos, Bell's symptoms, “sails”, and pulling of the corner of the mouth to the healthy side when smiling or crying appear. The pontine form of polio most often occurs without fever, general infectious symptoms, or changes in the cerebrospinal fluid.

The meningeal form of poliomyelitis is accompanied by damage to the soft meninges. The disease begins acutely and is accompanied by a deterioration in general condition, an increase in body temperature to febrile levels, headache, vomiting, lethargy, adynamia, and meningeal signs.

Symptoms characteristic of the meningeal form of poliomyelitis are pain in the back, neck, limbs, positive symptoms of tension, pain on palpation of the nerve trunks. In addition, fasciculations and horizontal nystagmus may be observed. The electromyogram reveals subclinical damage to the anterior horns of the spinal cord.

When conducting spinal tap The cerebrospinal fluid usually flows out under pressure and is transparent. His research reveals:

— cell-protein dissociation;

— lymphocytic pleocytosis (the number of cells increases to several hundred per 1 mm3);

- normal or slightly increased content squirrel;

- increased sugar content.

The nature of changes in the cerebrospinal fluid depends on the timing of the disease. Thus, the increase in cytosis may be delayed and in the first 4-5 days from the onset of the disease the composition of the cerebrospinal fluid remains normal. In addition, sometimes, in the initial period, a short-term predominance of neutrophils in the cerebrospinal fluid is observed. After 2-3 weeks from the onset of the disease, protein-cell dissociation is detected. The course of the meningeal form of poliomyelitis is favorable and ends with complete recovery.

The inapparent form of polio is characterized by the absence clinical symptoms with the simultaneous isolation of a “wild” strain of the virus from feces and a diagnostic increase in the titer of antiviral antibodies in the blood serum.

The abortive form or minor disease is characterized by an acute onset, the presence of general infectious symptoms without involvement of the nervous system in the pathological process. Thus, children may experience fever, moderate lethargy, decreased appetite, and headache. Often the listed symptoms are combined with catarrhal or dyspeptic symptoms, which serves as the basis for the erroneous diagnosis of acute respiratory viral or intestinal infections. Typically, the abortive form is diagnosed when a patient is hospitalized from the outbreak and receives positive results of a virological examination. The abortive form proceeds benignly and ends with complete recovery within a few days.

The development of vaccine-associated poliomyelitis is associated with the use of live oral vaccine for mass immunization and the possibility of reversing the neurotropic properties of individual clones of vaccine virus strains. In this regard, in 1964, a special WHO committee determined the criteria by which cases of paralytic poliomyelitis can be classified as vaccine-associated:

- onset of the disease no earlier than the 4th and no later than the 30th day after vaccination. For those who have been in contact with a vaccinated person, this period is extended to the 60th day;

- development of flaccid paralysis and paresis without impaired sensitivity with persistent (after 2 months) residual effects;

— absence of progression of the disease;

- isolation of a polio virus similar in antigenic characteristics to the vaccine virus and at least a 4-fold increase in type-specific antibodies.

Treatment

Rest in bed is necessary until severe symptoms subside.

Painkillers may be used to reduce fever, pain, and muscle spasms.

Your doctor may prescribe betanekol to combat urinary retention and antibiotics to treat an associated bacterial infection urinary canal.

A urinary catheter, a thin tube connected to a bag to collect urine, may be needed if control of bladder was lost due to paralysis.

Artificial respiration may be required if breathing is difficult; In some cases, surgery to open the throat (tracheotomy) may be necessary.

Physiotherapy is necessary in cases of temporary or permanent paralysis. Mechanical devices such as braces, crutches, wheelchairs and special boots can help you walk.

Combination of professional and psychological therapy can help patients adjust to the limitations imposed by the disease.

Treatment of polio in the acute period should be etiotropic, pathogenetic and symptomatic.

The development of clinical variants of polio with damage to the nervous system requires mandatory, as early as possible hospitalization of the patient, providing careful care and constant monitoring of basic vital functions. A strict orthopedic regimen must be followed. Affected limbs are given physiological

position with the help of plaster splints and bandages. The diet must meet the child’s age-related needs for basic ingredients and includes the exclusion of spicy, fatty, and fried foods. Particular attention should be paid to feeding children with bulbar or bulbospinal forms, since due to impaired swallowing there is a real threat of developing aspiration pneumonia. Tube feeding of the child allows you to avoid this dangerous complication.

As for drug treatment, an important point is to limit intramuscular injections as much as possible, which contribute to the worsening of neurological disorders.

As etiotropic agents for meningeal and paralytic forms, it is necessary to use antiviral drugs (pleconaril, isoprinosine pranobex), interferons (viferon, roferon A, reaferon-ES-lipint, leukinferon) or inducers of the latter (neovir, cycloferon), immunoglobulins for intravenous administration.

Pathogenetic therapy acute period provides for inclusion in complex therapy:

— glucocorticoid hormones (dexamethasone) in severe forms for health reasons;

- vasoactive neurometabolites (trental, actovegin, instenon);

— nootropic drugs (gliatilin, piracetam, etc.);

— vitamins (A, B1, B6, B12, C) and antioxidants (vitamin E, mexidol, mildronate, etc.);

- diuretics (diacarb, triampur, furosemide) in combination with potassium-containing drugs;

- infusion therapy for the purpose of detoxification (5-10% solutions of glucose with electrolytes, albumin, infucol);

- inhibitors of proteolytic enzymes (Gordox, Ambien, Contrical);

- non-narcotic analgesics (for severe pain);

— physiotherapeutic methods (paraffin or ozokerite applications on the affected limbs, UHF on the affected segments).

The appearance of the first movements in the affected muscle groups marks the beginning of the early recovery period and is an indication for the prescription of anticholinesterase drugs (prozerin, galantamine, ubretide, oxazil). As the pain syndrome is relieved, exercise therapy, massage, UHF are used, then electrophoresis, electromyostimulation with pulsed current, hyperbaric oxygen therapy.

After discharge from the infectious diseases department, the course of treatment with the medications described above continues for 2 years. The optimal solution should be considered the treatment of polio convalescents in specialized sanatoriums.

It is not yet known whether the infection can be stopped once it has started. On the other hand, many infected children do not suffer from paralysis. Many who are temporarily paralyzed then make a full recovery. Most of those who do not recover permanently make significant improvement.

If mild paralysis is observed after the acute phase of the disease, the child should be under constant medical supervision. Treatment depends on many factors. At each stage, the decision is made by the doctor, and there is no general rules. If paralysis persists, various operations are possible to restore the mobility of the limbs and protect them from deformation.

Prevention

When there are cases of polio in your area, parents start asking how to keep their child safe. Your local doctor will give you the best advice. There is no point in panicking and depriving children of all contact with others. If there are cases of the disease in your area, it is wise to keep children away from crowds, especially indoor areas such as shops and cinemas, and away from swimming pools that are used by many people. On the other hand, as far as we now know, it is not at all necessary to prohibit a child from meeting close friends. If you take care of him like this all your life, you won’t even allow him to cross the street. Doctors suspect hypothermia and fatigue increase susceptibility to the disease, but both are wise to avoid at all times. Of course, the most common case of hypothermia in the summer is when a child spends too much time in the water. When he begins to lose his color, he should be called out of the water - before his teeth chatter.
. There are a number of vaccines that are recommended to be given at two months of age, then again at four and 18 months, and a booster dose when the child starts school (between four and six years of age).

Immunization of children is the basis of the polio eradication strategy, and the level of vaccination coverage during routine immunization should be at least 95% among children of decreed ages in accordance with the Preventive Vaccination Calendar.

National days immunization is the second important component of the polio eradication strategy. The goal of these campaigns is to stop the circulation of wild poliovirus by immunizing as quickly as possible (within a week) all children in the most vulnerable age group. high risk diseases (usually children under three years of age).

In Russia, National Polio Immunization Days covering about 4 million children under 3 years of age (99.2-99.5%) were held for 4 years (1996-1999). Immunization was carried out in two rounds, with an interval of one month, with live oral polio vaccine (OPV), with vaccination coverage of at least 95% of the number of children indicated age groups located in this territory.

The main preventive drug both in our country and throughout the world is live vaccine Seibina (ZVS), recommended by WHO. In addition, imported vaccines Imovax Polio (Sanofi Pasteur, France), Tetracoc (Sanofi Pasteur, France) are registered in Russia. The Pentaxim vaccine (Sanofi Pasteur, France) is under registration. The listed vaccines are inactivated polio vaccines. Vaccines are stored at 2-8 °C for 6 months. An opened bottle should be used within two working days.

Currently, for immunization of the child population against polio, OPV is used - oral types 1, 2 and 3 (Russia), IPV - Imovax Polio - inactivated enhanced (types 1, 2, 3) and Pentaxim (Sanofi Pasteur, France).

Vaccination begins at the age of 3 months three times with an interval of 6 weeks with IPV, revaccination at 18 and 20 months, and at 14 years with OPV.

The dose of domestically produced live vaccine is 4 drops per dose. It is administered orally an hour before meals. It is not allowed to drink the vaccine, eat or drink within an hour after vaccination. If regurgitation occurs, a second dose should be given.

Contraindications to VPV vaccination are:

- all types of immunodeficiency;

— neurological disorders due to previous VPV vaccinations;

- Availability acute diseases. In the latter case, vaccination is carried out immediately after recovery.

Non-severe illnesses with an increase in body temperature up to 38 °C are not a contraindication for VPV vaccination. If diarrhea is present, vaccination is repeated after stool normalization.

The oral polio vaccine is considered the least reactogenic. However, when using it, the possibility of an adverse post-vaccination event cannot be excluded. The greatest degree of risk is observed during primary vaccination and during contact infection of non-immune children.

It is possible to prevent the occurrence of vaccine-associated polio in children, especially from risk groups (IDF, born from HIV-infected mothers, etc.), by using inactivated polio vaccine for initial vaccination or by full course immunization.

According to epidemiological indications, additional immunization is carried out. It is carried out regardless of previous preventive vaccinations against polio, but not earlier than 1 month after the last immunization. Children under the age of 5 years are subject to a single immunization with OPV (the age composition of children can be changed), who communicated in epidemic foci with patients with polio, diseases accompanied by acute flaccid paralysis, if these diseases are suspected in the family, apartment, house, preschool educational and medical -preventive institution, as well as those who communicated with those arriving from polio-prone areas.

Nonspecific prevention of polio infection involves hospitalization and isolation of the patient, and monitoring contact children under 5 years of age for 20 days. According to epidemiological indications, a one-time virological examination of contacts is carried out. In the epidemic focus of POLI/AFP, after hospitalization of the patient, final disinfection is carried out.

In adults, polio vaccination is recommended only before traveling to areas where polio is common.

Contact your doctor immediately if you or your child experience symptoms of polio or if you may have been infected with the virus and have not yet been vaccinated.

Contact your doctor to get the polio vaccine if you have not been vaccinated and plan to travel to areas where polio is common.

Attention! Call " ambulance” if someone is having difficulty breathing or has paralysis of a limb.