Rheumatism: characteristics, symptoms, treatment. Rheumatism (rheumatic fever)

I. Rheumatism (rheumatic heart disease) with maximum activity(activity III degree; synonymous with acute rheumatism, continuously recurrent). A. Clinical symptoms (syndrome):
a) pancarditis;
b) acute or subacute diffuse myocarditis;
c) subacute rheumatic heart disease with severe circulatory failure, stubbornly resistant to treatment;
d) subacute or continuously recurrent rheumatic heart disease in combination with symptoms of acute or subacute polyarthritis, pleurisy, peritonitis, rheumatic pneumonia, nephritis, hepatitis, subcutaneous rheumatic nodules, erythema annulare;
e) chorea with pronounced manifestations of activity.

B. An increasing increase in the size of the heart, a decrease in the contractile function of the myocardium, pleuropericardial adhesions (according to the X-ray examination), which undergo regression under the influence of active antirheumatic therapy.

C. Clear electrocardiographic symptoms (rhythm and conduction disturbances), characterized by obvious dynamics and reverse development under the influence of treatment.

D. Changes in the blood system: neutrophilic leukocytosis - above 10,000; ROE - above 30 mm; C-reactive protein - 3-4 plus and above; fibrinogenemia - above 0.9-1.0%; alpha-two-globulins - above 17%; gamma globulins - 23-25%; blood seromucoid - above 0.8-2.0 units; DPA (diphenylamine test) - above 0.350-0.500.

D. Serological indicators: titers of antistreptolysin-0 (ACL-0), antistreptohyaluronidase (ASH), antistreptokinase are 2-3 times higher than normal.

E. Increased capillary permeability II-III degree (if other possible reasons for this are excluded).

II. Rheumatism (rheumatic heart disease) with moderate activity(activity II degree; synonymous with subacute rheumatism)
A. Clinical symptoms (syndrome):
a) subacute rheumatic heart disease in combination with circulatory failure I, I-II degree, slowly responding to treatment;
b) subacute or continuously recurrent rheumatic heart disease in combination with subacute polyarthritis, fibrinous pleurisy, peritonitis, nephritis, erythema annulare;
c) subacute polyarthritis;
d) rheumatic chorea.

B. Radiologically established increase in the size of the heart, pleuropericardial adhesions, undergoing regression under the influence of active antirheumatic therapy.

B. Electrocardiographic symptoms (prolongation of the P-Q interval, rhythm disturbances), signs of coronaritis, disorders coronary circulation characterized by dynamism and disappearance under the influence of antirheumatic therapy.

D. Changes in the blood system: neutrophilic leukocytosis within 8,000-10,000; ROE acceleration within 20-30 mm; C-reactive protein - 1-3 pluses; an increase in globulins in the range of 11.5-16% for alpha-two globulins and 21-23% for gamma globulins; DPA - within 0.250-0.300; seromukoid - within 0.3-0.8 units.

E. Serological tests: increase in titers of streptococcal antibodies, mainly ACL-0 and ASG, 1.5-2 times against the norm.

E. Increased capillary permeability II degree (if other possible causes of this are excluded).

III. Rheumatism with minimal activity(activity I degree)
A. Clinical symptoms:
a) protracted-sluggish current or latent rheumatism (rheumatic heart disease) with preserved or reduced ability to work; with recurrent rheumatic heart disease against the background of a previously developed heart disease, there may be circulatory failure various degrees, as a rule, poorly amenable to active cardiac therapy;
b) protracted sluggish or latent rheumatic heart disease in combination with rheumatic chorea, encephalitis, vasculitis, moreover, subcutaneous rheumatic nodules, annular erythema, persistent arthralgia;
c) rheumatic chorea.

B. Radiographically with primary outpatient rheumatic heart disease, normal or slightly enlarged heart size; pleuropericardial adhesions that are difficult to reverse under the influence of active antirheumatic therapy. With recurrent rheumatic heart disease against the background of a developed heart disease, the x-ray picture may be different, but, as a rule, with an expansion and change in the configuration of the cardiac shadow, sometimes with pleuropericardial adhesions, which, although with difficulty, are amenable to reduction under the influence of active therapy.

C. On the ECG, manifestations of cardiosclerosis (postmyocarditis), coronaritis and coronary circulation disorders can be detected; different kind rhythm disturbances that are difficult to respond to antirheumatic therapy. Electrocardiographic symptoms are usually not expressive, but persistent in terms of dynamics during antirheumatic treatment.

D. Changes in the blood system are usually few and indefinite: ESR is either slightly accelerated (if there is no circulatory failure), or normal, or even slowed down (with circulatory failure); C-reactive protein is either absent or found within one plus; the amount of globulin fractions (mainly gamma globulin) is slightly increased or within high standard; DFA within the high norm; seromukoid within normal limits or lowered.

D. Serological indicators are either within the high norm or slightly elevated. The dynamics of these indicators during the course of the disease and regardless of intercurrent infection is important. Low titers of streptococcal antibodies may be associated with suppression (depletion) of immunological reactivity and do not reflect the true state. Periodic increase titers, especially the gradual increase in titers in the absence of infection, can serve as an indirect confirmation of the activity of the rheumatic process.

E. Increased capillary permeability within the I degree (if other possible reasons for this are excluded).

These indicators represent a synthesis of the clinical and anatomical characteristics or syndrome of the disease, data from X-ray, electrocardiographic, phonocardiographic examination of the patient, routine blood tests, biochemical and serological studies, and determination of capillary permeability. The dominant in determining activity is the clinical and anatomical characteristics of the disease and its dynamics in the process of medical observation and treatment. The given indicators of the activity of rheumatism should not be considered as a kind of mathematical formula, which gives an unconditionally accurate solution to this complex, mostly clinical, problem. The proposed scheme sets the doctor essentially the same tasks as the classification of stages of circulatory insufficiency according to N. D. Strazhesko and V. Kh. Vasilenko. A particularly difficult task faces the doctor when determining the nature of the process in rheumatism with minimal activity, for example, recurrent latent rheumatic heart disease with circulatory failure. The decisive condition To achieve the goal in these conditions, one should recognize a thorough analysis and synthesis of the results of a dynamic study of the entire clinical picture of the disease and all its laboratory parameters.

As for the actual diagnosis of rheumatism, here it may be useful, according to European and American experts, diagnostic criteria Kisel-Jones (D. Jones, 1944) with some additions. (Criteria 6 and 7 among the main ones and 6 and 7 among the additional ones were proposed by A.I. Nesterov).

Kisel-Jones criteria. I. Main: 1) carditis; 2) polyarthritis; 3) chorea; 4) noduli rheumatici; 5) erythema annulare; 6) "rheumatic history"; 7) ex juvantibus evidence.

II. Additional: 1) fever; 2) arthralgia (not arthritis!); 3) leukocytosis; 4) prolongation of the P-Q interval; 5) previous streptococcal infection;
6) serological and biochemical parameters of blood; 7) increased capillary permeability; 8) other signs of the disease (fatigue, nosebleeds, abdominal pain - abdominal syndrome, etc.).

For a reliable nosological diagnosis of rheumatism, a combination of 2-3 main and several additional criteria Kisel-Jones. However, considering it possible to use the modified Kisel-Jones criteria in practical work, it should be emphasized that this scheme, although recognized as a solid basis for the diagnosis of rheumatism, is still only a scheme that cannot take into account the whole variety clinical manifestations this disease and therefore cannot replace the clinical thinking and experience of the doctor. Therefore, it is considered only as a valuable diagnostic technique that helps the doctor purposefully summarize the most important manifestations of the disease.

The problem of rheumatism is extremely relevant in modern clinical pediatrics, since the disease that began in childhood leads to an increase in the number of disabled people among the adult population, often causing disability.

Rheumatism (Sokolsky-Buyo disease) is common disease organism with systemic lesion connective tissue inflammatory nature and involvement in the process of the cardiovascular system and other organs. It is typical for him chronic course and granulomatous development of the inflammatory response.

The concept of "rheumatism" was introduced into medical practice by Ballonius in 1635 in order to distinguish migratory joint pain in rheumatism from gout. The term "yeita" means "tide", as at that time it was believed that in this disease, the disease-causing fluid rushes to the joints. It should be noted that the term "rheumatism", previously widespread in domestic and foreign (especially German) literature, is now less and less used in international literature and WHO publications. In these publications, this disease is referred to as " rheumatic fever» (rheumatic fever). However, it is preferable to use the term "rheumatism", since it refers to the nosological clinical form of the disease, and not its individual symptom, in this case, fever.

EPIDEMIOLOGY. Not so long ago, rheumatism was widespread. But since the end of the 60s, the incidence of rheumatism has progressively decreased, and now these figures have stabilized. In industrialized countries, the incidence of rheumatism is less than 5 per 100,000 population per year, i.e. less than 0.005%. AT developing countries among the population in unfavorable socio-economic conditions, the incidence of rheumatism among children reaches 100 per 100,000 (0.1%).

In industrialized countries, according to the decrease in the incidence of rheumatism, there is a decrease in the incidence of rheumatic heart disease. Thus, the frequency of rheumatic defects among schoolchildren in the 80s was 0.6-0.7 per 1000 in the USA and Japan, respectively. In developing countries, this figure ranges from 1.6 to 18.6 per 1000.

Rheumatism begins mainly in childhood and young age. Under the age of 3 years and older than 30 years, the incidence of primary rheumatism is extremely rare. More than 70% of cases primary morbidity falls on the age of 8-15 years.

The social significance of rheumatism is due to the rather high disability of the population (5% of persons newly recognized as disabled suffer from heart defects of rheumatic origin), the course of the disease, which has a progressive, cyclical nature. Therefore, a very important issue is rational treatment and prevention, preventing disability and exacerbations.

ETIOLOGY. Currently, most researchers involved in the problem of rheumatism believe that rheumatism is the result of the body's interaction with group A beta-hemolytic streptococcus. Beta-hemolytic streptococci are divided into a number of serological groups depending on the characteristics of the polysaccharide antigen that is part of the cell wall. Highest value in human pathology have streptococci belonging to the serogroup A (Streptococcus pyogens). It is the microorganisms of this group that cause rheumatism. Streptococci of other serological groups (B, C, G, F) rarely cause infection and do not cause rheumatism.

Beta- hemolytic streptococcus group A causes a person such infectious diseases like scarlet fever, pharyngitis or tonsillitis, infection skin (impetigo). But rheumatism never occurs after impetigo, but only after scarlet fever, pharyngitis or tonsillitis.

The prevalence of group A streptococci is quite significant and varies widely. Thus, group A streptococcus is found in the pharynx in 10-50% of healthy school-age children (WHO, 1988). The presence of group A streptococcus in the upper respiratory tract may be a sign of acute streptococcal infection or bacterial carriage. These states are differentiated by the titers of antistreptococcal antibodies. With bacteriocarrier, in contrast to active infection, there is no increase in titers of antistreptolysin-0 (ASL-O). AT different countries elevated titers of ASL-0 are found in 15-69% of clinically healthy children, which indicates a previous streptococcal infection.

As evidence that confirms the streptococcal etiology of rheumatism in children, use the following:

1) clinical symptoms of rheumatism appear 2-3 weeks after a pharyngeal infection caused by group A beta-hemolytic streptococcus;

2) streptococci are found in 65% of patients with rheumatism in oral cavity, and in the blood in the active phase, antibodies to streptococcus are detected in 80% of patients;

3) in the blood of patients with rheumatism, antibodies to streptococcus are determined in very high titers;

4) a sharp decline morbidity and recurrence of rheumatism after bicillin prophylaxis.

It should be noted that only certain serotypes of group A streptococcus have "rheumatogenic" potential. More often in patients with rheumatism, the following ten M-types of group A streptococcus are found: 1,3, 5, 6, 14, 18, 19, 24, 27, 29. The concept of "rheumatogenicity" is based on the biological properties of streptococci, various components of which cause the development of pathological reactions leading to rheumatism.

However, although streptococci serve as the etiological factor of rheumatism, they are not causative agents of rheumatism from the point of view of the classical infectious pathology, since only 0.2-0.3 to 3% of people who have had a sore throat or acute pharyngitis fall ill with rheumatism.

PATHOGENESIS. Currently, the toxic-immunological hypothesis of the pathogenesis of rheumatism is generally recognized. There are several mechanisms in the development of rheumatism, which are interconnected within the framework of the toxic-immunological concept of the pathogenesis of the disease.

1. Toxic mechanism - the development of rheumatism is associated with the direct effect of exo- and endotoxins of streptococcus (streptolysins-O and S, streptohyaluronidase, etc.) on cells and tissues. This leads to hemolysis of erythrocytes (with the subsequent occurrence of toxic annular erythema), destruction of lysosomes and the release of proteolytic enzymes that cause depolymerization of connective tissue mucopolysaccharides and impaired capillary permeability. The result is exudation and swelling of the base substance and procollagen.

In addition, streptolysin-0 has cardiotropic activity and uncouples oxidative phosphorylation in the heart muscle.

These changes correspond to the pathomorphological stage of the disease, which is called "mucoid swelling". Changes in this stage are reversible, and with treatment, the structure of the connective tissue can be completely restored.

2. The mechanism of cross-reactive reactions is due to the fact that streptococcal antigens cross-react with antigens of the myocardium, sarcolemma, components of the atrioventricular bundle, etc.

In addition, antibodies formed against various components of streptococcus also react with the tissues of the heart (myocardium), glycoproteins of its valvular apparatus, with cytoplasmic antigens of the neurons of the caudate and subthalamic nuclei of the brain.

These cross-reactions lead to local inflammation in various organs, causing myocarditis, valvular endocarditis, and chorea.

3. The immunocomplex mechanism is associated with the formation of anti-streptococcal antibodies and the formation of immune complexes, which, being deposited on the basement membranes of capillaries, arteries and the synovial membrane, cause their damage. This mechanism leads to an increase in capillary permeability, platelet aggregation and the formation of fibrin-associated microthrombi. As a result of the participation of this mechanism, vasculitis and synovitis are observed in patients with rheumatism, which leads to polyarthritis.

In addition, increased vascular permeability, exudation and destructive changes in the connective tissue contribute to the formation of fibrinoid, which is deposited in the tissues in the form of foci. This corresponds to the second stage of pathomorphological changes - the stage of fibrinoid swelling (or necrosis). The changes occurring at this stage are irreversible.

4. Autoimmune mechanism - as a result of a violation of the regulatory function of T-lymphocytes and a hyperergic reaction of B-lymphocytes in patients with rheumatism, autoantibodies arise in response to tissue damage. They react with myocardial fibrils, cause necrosis and exacerbate myocarditis.

In places of deposition, there is an increase in the production of lymphokines that stimulate fibroblasts. This leads to the formation of rheumatic granuloma (Ashoff-Talalaev granuloma), which corresponds to the third stage of pathomorphological changes - granulomatosis.

The last pathomorphological stage is sclerosis and hyalinosis of the connective tissue. It is at this stage that rheumatic nodules occur.

The above mechanisms of development of the rheumatic process are observed in patients with primary rheumatism. With subsequent attacks of rheumatism, the ratio between these mechanisms changes.

CLASSIFICATION. The variety of clinical manifestations of rheumatism and the resulting need for a differentiated approach to the understanding and treatment of this disease determine the need for a unified classification of the disease.

The first attempt to classify rheumatism was made in 1934 by the All-Union Antirheumatic Committee. Then, in connection with the development of knowledge and ideas in the field of rheumatology, the classification was repeatedly revised and supplemented. At present, the classification variant approved in 1964 at the All-Union Symposium on the Classification of Rheumatism and Infectarthritis (Moscow) and based on the proposals of Academician of the USSR Academy of Medical Sciences A.I. Nesterov (Table 33).

According to this classification, two phases are distinguished in the clinical picture of rheumatism: active and inactive, and the activity of the inflammatory process is characterized by three degrees of activity, depending on their severity: I, II and III. We will describe the activity criteria in more detail below.

Depending on the clinical and anatomical lesion, the nature of the damage to the heart (primary rheumatic carditis, recurrent rheumatic heart disease, rheumatism without obvious cardiac changes is indicated, while the presence of a defect is found out and the valve is called, rheumatic myocardiosclerosis) and other organs and systems (polyarthritis, serositis, chorea, encephalitis, vasculitis, nephritis, hepatitis, pneumonia, etc.).

The classification also indicates the nature of the course of the disease: acute, subacute, protracted (sluggish), continuously recurrent, latent.

Acute course - the process begins acutely, with rapid development clinical symptoms, usually with maximum activity. Clinical manifestations are mainly due to exudative inflammation both in the heart and in other systems. Patients can accurately report the date of onset of the disease. The duration of the active phase is up to 8 weeks.

Subacute course - the disease begins gradually, and the activity of the inflammatory process does not exceed II degree. This is the most common course of the disease. The onset of the disease is indistinct; when interviewed, patients find it difficult to name even the month of the onset of the disease. The duration of the active phase is 2-4 months. The results of therapy can not always be accurately determined.

A protracted sluggish course is characterized by a gradual onset, minimal activity, which persists for a long time, despite the ongoing treatment, but without an obvious change in clinical and laboratory parameters.

Continuously relapsing course - with it, each subsequent relapse occurs before the previous exacerbation passes into an inactive phase. It is the most severe, torpid course of rheumatism. Heart disease is characteristic, circulatory failure is expressed. Complex therapy gives a temporary effect, relapses usually occur already against the background of ongoing treatment.

(A.I. Nesterov, 1964)

The latent course is characterized by a latent, difficult to detect course of the disease, but, despite the asymptomaticity of the disease, fresh rheumatic granulomas are detected, and “accidental” detection of valvular heart disease is also characteristic (according to Talalaev’s definition - “ outpatient form"rheumatism).

The classification also indicates the state of blood circulation. There are four degrees of circulatory failure in patients with rheumatism (according to G.F. Lang):

H0 - no circulatory failure, there are no objective and subjective signs of functional circulatory disorders;

HI - circulatory insufficiency of the 1st degree: signs of circulatory insufficiency are absent at rest and appear during physical exertion (walking, squatting, etc.) in the form of shortness of breath and tachycardia;

HII - circulatory failure of the II degree, congestion in the lungs or big circle circulation:

HIIA - changes are less pronounced (stagnation in the lungs, moderate enlargement of the liver, swelling of the feet by the end of the day);

HIIB - congestion in the systemic circulation is pronounced (significant enlargement of the liver, edema, ascites), but they are reversible and treatable;

HIII - a severe disorder of hemodynamics, irreversible and not amenable to treatment, circulatory failure of the III degree.

If possible, the main localization of the lesion should be clarified (myocardium, endocardium, pericardium, pancarditis, coronaritis) and the number of attacks should be indicated.

According to the classification, it is necessary to clarify the degree of activity of the rheumatic process. Criteria for determining the degree of activity of rheumatism are presented in table 34.

Table

(A.I. Nesterov, 1964)

Note. CRP - C-reactive protein;

DPA - diphenylamine (test);

SC - sialic acids

The inactive phase of rheumatism is understood as such a state of health in those who have undergone rheumatism, when, with clinical and laboratory examination in dynamics, it is not possible to identify any signs of an inflammatory process or impaired immunity. The working capacity of patients is preserved, and hemodynamic disturbance is detected with significant physical exertion, if a heart disease has formed. According to N.A. Belokon and M.B. Kuberger (1987), one can speak of an inactive phase no earlier than 6 months after the disappearance of clinical and laboratory signs of process activity, since morphological changes persist much longer than clinical and laboratory ones.

This classification, as already mentioned, is generally accepted for use in our country. However, in contrast to this classification, by the WHO Expert Committee (1988), patients who have had rheumatism are not further considered as patients with "rheumatism in the inactive phase", although they all need long-term bicillin prophylaxis.

In addition, WHO experts (1988) believe that there is no "continuously relapsing" course of rheumatism. In their opinion, frequent relapses Rheumatism in children is the result of improper secondary prevention of the disease. There are also objections to criteria for disease activity. According to the considered classification, the activity of the disease is clinical concept and is determined by the parameters of the clinical and laboratory picture. But clinical activity disease does not always coincide with the intensity of the pathoanatomical process in the heart and other organs.

CLINICAL MANIFESTATIONS. Clinical manifestations of the disease in children are polymorphic and varied.

Rheumatism usually occurs 2-3 weeks after a sore throat or pharyngitis. Patients complain of lethargy, weakness, sweating. To initial manifestations rheumatism in children should be attributed to a sudden increase in body temperature, symptoms of intoxication, arthralgia or polyarthritis.

Although the disease affects various organs and tissues, the leading one is the defeat of the heart, which is described as carditis. Depending on the location of the lesion, there may be endo-, myo- or pancarditis. The most natural in rheumatism is endomyocarditis. Pancarditis develops only in severe cases the course of the disease.

Consider the most important clinical signs of endocarditis in children.

Endocarditis. The rheumatic process most often affects the heart valves and proceeds in the form of rheumatic valvulitis. Patients are characterized by complaints of discomfort in the region of the heart, fever, palpitations, dizziness. During the examination, pallor of the skin, pulsation cervical vessels. On palpation - the pulse of satisfactory filling, not tense, tachycardia. On percussion, the borders of the heart are within age norms. Auscultatory heart sounds are somewhat weakened, a systolic murmur is heard at the apex, which at first is soft, short, musical, inconsistent, and becomes coarse as the valves are damaged.

Myocarditis. Mandatory component rheumatic carditis. There are complaints of indefinite pain in the region of the heart, weakness, fatigue, palpitations, shortness of breath. On examination, pallor of the skin and mucous membranes, "blue" under the eyes, cyanosis of the lips or nasolabial triangle are revealed. On palpation - the pulse of weak filling, the apical impulse is weakened, tachycardia at the onset of the disease is replaced by bradycardia. Percussion, the borders of the heart, as a rule, are shifted to the left or in all directions, depending on the severity of the inflammatory process (focal or diffuse myocarditis). On auscultation, the heart sounds are weakened, especially the first one, a systolic murmur is heard. Its cause is considered to be relative insufficiency of the mitral valve (due to the expansion of the heart, hypotension of the heart muscles, in particular papillary ones).

Sometimes, due to lengthening (weakening of the myocardium) and shortening (due to tachycardia) of systole, embryocardia is observed, i.e. alignment of the duration of systole and diastole.

To confirm the diagnosis of myocarditis great importance have data instrumental examination. On the ECG, myocarditis is characterized by a violation of atrioventricular conduction in the form of a prolongation of the P-R interval, a decrease in the voltage of the QRS teeth (indicating a severe course of the process), as well as possible violation rhythm.

Pericarditis. It indicates, as a rule, pancarditis, as it is combined with the involvement of all membranes of the heart in the inflammatory process. The appearance of pericarditis in the rheumatic process is clinically expressed in sudden deterioration general condition sick. Typical complaints about sharp pain in the region of the heart, shortness of breath appears (even at rest), a dry and obsessive cough (reflex) is often noted.

Draws attention on examination forced posture child ( sitting position with the torso tilted forward), cyanosis of the skin. The objective picture depends on which pericarditis is dry (fibrinous) or exudative.

With dry (fibrinous) pericarditis, the boundaries of the heart are not displaced, and auscultation reveals a “pericardial friction noise”, resembling a crunch of snow, which is heard in the systole and diastole phase and is not associated with heart sounds.

With exudative pericarditis, the pulsation in the region of the heart disappears, the apex beat is not detected, the boundaries of the heart are displaced in all directions, its tones are significantly weakened, barely audible, especially in the sitting position.

Polyarthritis is one of the leading clinical manifestations of rheumatism. Its severity is different - from pain (polyarthralgia) to swelling and redness of the joints and unbearable pain (arthritis). In the modern course of rheumatism, polyarthralgia is essentially regarded as the equivalent of rheumatic polyarthritis.

Rheumatic polyarthritis is characterized by:

1) multiple lesions of the joints, mainly large (ankle, knee, elbow, wrist, etc.), less often - small (joints of the foot, hands, etc.);

2) symmetrical damage to the joints;

3) migratory, "flying" damage to the joints (an inflammatory reaction appears and disappears very quickly);

4) absence of deformation or any functional changes in the affected joints;

5) the rapid disappearance of manifestations against the background of the use of anti-inflammatory therapy.

Chorea. A characteristic feature of the course of rheumatism in children. Chorea is considered a kind of subcortical and partially cortical encephalitis. The morphological substrate of this lesion is associated with vasculitis and degenerative changes in the striopalidar system of the brain. It is with these lesions that the manifestations characteristic of chorea are associated.

At objective examination can be installed typical symptoms chorea. First of all, it changes mental condition child: emotional instability, absent-mindedness, fatigue, passivity appear, school performance worsens. Simultaneously arise movement disorders which are manifested by hyperkinesis, grimacing, slurred speech (dysarthria). These disorders are usually aggravated by excitement.

In addition, there is a disorder of coordination of movements. This is manifested by a violation of handwriting, the inability to hold table setting items while eating, instability in the Romberg position, negative finger-nose and knee-heel tests.

Chorea is also characterized by muscular hypotension. In this regard, there are symptoms of “flabby shoulders” (when lifting a child under the armpits, only the shoulders rise, the head goes deep between them), “penknife” (bent in knee joint the leg can be easily brought to the chin), “folding arm” (when the arm is bent in elbow joint forearm touching shoulder).

When examining the neurological status, there is an increase in tendon reflexes, especially knee reflexes ( positive symptom Gordon), there is a pronounced clonus of the feet.

Chorea usually affects children 5-10 years of age and girls of puberty.

Annular erythema. Usually appears on the trunk and limbs, less often - on the legs, neck, face. These are pale pink rashes in the form of a thin annular rim with a clear outer and less clear inner edges. In the center of the ring, the skin is not changed. Rings of erythema are often intricately combined with each other, resembling garlands or lace patterns. Annular erythema is not accompanied by any subjective sensations and usually disappears without a trace.

Rheumatic nodules. Painless formations ranging in size from 2 mm to 1 cm, rounded, dense, located in the fascia, tendons, in the subcutaneous tissue. Favorite localization is the extensor surface of the elbow, knee, metacarpophalangeal joints, the area of ​​the ankles, the spinous processes of the vertebrae, etc. Nodules appear imperceptibly as a result of the formation of granuloma and sclerosis. Usually within 1-2 months they undergo reverse development without residual effects.

Damage to other organs and systems is manifested by rheumatic pneumonia, pleurisy, abdominal syndrome, kidney damage, serositis, etc.

To determine the activity of the inflammatory process, laboratory tests such as determining the number of leukocytes, ESR, the content of seromucoid, sialic acid, fibrinogen, alpha-1- and alpha-2-gamma globulins, C-reactive protein, and indicators of the diphenylamine reaction are used.

DIAGNOSTIC CRITERIA FOR RHEUMATISM. The diagnosis of rheumatism is sometimes extremely difficult to establish. This is a clinical diagnosis, and there are no sufficiently convincing methods for its diagnosis, and the severity clinical symptoms different and not always sufficient for a timely diagnosis.

Diagnostic criteria for rheumatism were first formulated by the Russian pediatrician A.A. Kisel (1940), who identified five "absolute" signs of it: rheumatic nodules, annular erythema, chorea, migratory polyarthritis, carditis.

In 1944, a list of signs for the diagnosis of rheumatism was published, subdividing them into "major" and "minor" criteria. The basis of such a division is the diagnostic significance of a particular indicator. Clinical signs, the most significant for diagnosis, were called "major", and less characteristic - "small" criteria (see diagram).

These criteria were later revised in 1956 and 1982 under the auspices of the American Rheumatic Association. In this form, they were adopted by the WHO Expert Committee (1988):

The scheme of diagnostic criteria for rheumatism (AA Kisel - T.T.D. Jones)

"Big" criteria:

Polyarthritis

erythema annulare

Rheumatic nodules

"Small" criteria:

A) Clinical:

1. Fever

2. Arthralgia

3. History of rheumatism (or previous rheumatism)

B) Laboratory:

1. Acute phase reactants ( increase in ESR, PSA, leukocytosis)

2. Prolongation of the P-R interval

The presence of two "major" or one "major" and two "small" criteria indicates high probability rheumatism in children. Moreover, the diagnosis of rheumatism is acceptable only if there are "large" clinical criteria. However, for the final decision on the diagnosis of rheumatism, data confirming a streptococcal infection are needed. These include:

1) increased titer of antistreptococcal antibodies (ASL-0, etc.);

2) sowing from the pharynx of group A streptococcus;

3) recent scarlet fever.

Of the antistreptococcal antibodies, the determination of ASL-O titers, which are usually elevated in 80% of patients with rheumatism, has the greatest diagnostic value. Only in patients with chorea, and in the first 2 months from the onset of the disease, there is a low or borderline level of ASL-O. The level of ASL-O is considered elevated if it corresponds to at least 250 units. Todd in adults and at least 333 units. in children over 5 years of age.

For increase diagnostic value these parameters, it is necessary to investigate paired sera, for which blood is taken at intervals of 2-4 weeks. In this case, an increase in antibody titer by two or more dilutions is diagnostic sign recent streptococcal infection.

The above diagnostic criteria for rheumatism are intended to diagnose the disease only in the active phase.

A very common mistake is premature, before the appearance of distinct symptoms of rheumatism, the appointment of anti-inflammatory drugs (salicylates, corticosteroids). As a result, a fuzzy clinical picture, allowing only to assume the diagnosis of rheumatism. Obviously, it is impossible to reduce the severity of the symptoms of rheumatism until they become sufficiently clear. Otherwise, setting correct diagnosis will be difficult.

DIFFERENTIAL DIAGNOSIS. According to the above criteria for the diagnosis of rheumatism, the classical forms of the disease are recognized quite clearly. But for successful treatment and prevention, it is important to establish an accurate diagnosis in cases where the symptoms are poor. There is evidence of the similarity of rheumatism with 26 different diseases.

If a patient with rheumatism has severe polyarthritis, it becomes necessary to exclude juvenile rheumatoid arthritis(YURA) (Table 35). JRA, in contrast to rheumatic polyarthritis, is characterized by the presence of persistent pain syndrome in the area of small joints hands, feet, spine; prolonged pain for several weeks and even months, not amenable to treatment with anti-inflammatory drugs; stiffness of movements in the affected joints, especially in the morning; development of deformities of the affected joints; muscle atrophy in the area of ​​the affected joint; no changes in the heart for a long time; changes on the x-ray of the joints (osteoporosis, expansion of the joint space, ankylosis, etc.).? Table 35

The presence of carditis in a patient with rheumatism requires differential diagnosis with non-rheumatic carditis (Table 36). Differences between non-rheumatic carditis and rheumatism: connection with the transferred ARVI and the occurrence of the disease directly against its background (at the height of the underlying disease); absence of articular syndrome at the onset of the disease; the presence of a more pronounced pain syndrome in the region of the heart, complaints are of a colored emotional nature; non-formation of valvular heart disease; the absence or weak severity of laboratory signs of the activity of the process, despite the rather pronounced signs of carditis, and the titers of antistreptococcal antibodies are not increased or do not increase in the dynamics of the disease.

Table

Significant polymorphism of the clinical symptoms of rheumatism, systemic lesions of the connective tissue require differential diagnosis with systemic lupus erythematosus (SLE). In patients with SLE, in contrast to patients with rheumatism, there are skin rashes in the form of a "butterfly" on the face; enlarged lymph nodes and spleen; high activity of the process and a motley clinical picture of the disease, and in 50% of children LE-cells are found in the blood and in almost all children (95%) - antinuclear antibodies.

Many of these signs are common to children and adults. But still, some features of the course of rheumatism are noted in children:

1) a more severe course of the process due to a pronounced exudative component of inflammation;

2) cardiac forms of rheumatism are more common;

3) more frequent relapses of the disease;

4) rheumatic rash and rheumatic nodules are much more common;

5) the presence of chorea, which adults do not have;

6) polyserositis is more often noted;

7) the constant activity of the interictal period is maintained;

8) the so-called "dry decompensation" is characteristic with an increase in the liver without leg edema, which occurs in adults;

9) children more often than adults develop rheumatic pneumonia;

10) heart disease is more often formed.

Currently, the number of children with rheumatic heart disease has decreased by more than 2 times. The incidence of acquired heart defects in children with rheumatism is 10-15%. The most common acquired heart disease in children is mitral valve insufficiency (60%), the second place is occupied by combined mitral valve disease (mitral valve insufficiency and stenosis of the left venous orifice) - in 15%, the third place - isolated aortic insufficiency- in 10% of children.

PRINCIPLES OF TREATMENT OF CHILDREN WITH RHEUMATISM.

The basis for the treatment of children with rheumatism is the principle of complex staged therapy. The implementation of this principle is achieved by the fact that patients are treated in a hospital, treated in a rheumatic cardiology sanatorium and observed by a cardiorheumatologist in a polyclinic. All patients with rheumatism must be hospitalized and, if possible, isolated.

Treatment of patients with rheumatism includes the following main links:

1) organization of the regime - establish bed rest for 2-3 weeks or more, depending on the severity of carditis and the characteristics of the course. After the elimination of signs of carditis, the child is transferred to a semi-bed rest (allowed to get up at the table, for procedures, to the toilet), and then - to the training mode;

2) ensuring a balanced diet - it should be complete, fortified, easily digestible, high-calorie.

Assign table number 10 (according to Pevzner), according to which the child is limited (reduced) the amount of table salt, fluid intake and additionally assigned foods rich in potassium (baked potatoes, raisins, dried apricots, prunes);

3) the appointment of etiotropic therapy, taking into account the recognition of the etiological role of group A streptococcus in the development of rheumatism.

Penicillin is injected intramuscularly at 600,000 - 2,000,000 IU per day (in 4 divided doses) for 2 weeks (100,000 IU per 1 kg of body weight), then bicillin-5 intramuscularly for 4-6 weeks. Children weighing less than 30 kg are prescribed a dose of 600,000 IU, more than 30 kg - 1,200,000 IU.

With intolerance to penicillin drugs, erythromycin is indicated. It is prescribed for children weighing less than 25 kg at a dose of 40 mg per 1 kg of body weight per day (not more than 1 g) in 2-4 doses, more than 25 kg - 250 mg 4 times a day;

4) inclusion in pathogenetic therapy drugs that act on key links in pathogenesis. For this purpose, drugs with anti-inflammatory activity are used. Apply:

4.1) Non-steroidal anti-inflammatory drugs:

A) acetylsalicylic acid is prescribed at 60-100 mg per 1 kg of body weight, but not more than 2 g per day in 4 doses after meals, washed down with milk (to reduce the likelihood of developing stomach ulcers). full dose acetylsalicylic acid apply for 3-4 weeks, and then reduce it by half and continue taking it for 6 weeks;

B) indomethacin (methindol) - at a dose of 2.5-3 mg per 1 kg per day (within 50-100 mg);

C) voltaren (ortofen) - 3-3.5 mg per 1 kg of body weight per day (75-150 mg per day);

D) brufen (ibuprofen) is a less active non-steroidal anti-inflammatory agent and can be used with moderate or minimal process activity in daily dose 400-800 mg. The advantage of the drug is that it does not have side effects.

Naproxen, mefenamic acid and other drugs are also used. The mechanism of action of these drugs is associated with inhibition of the enzyme prostaglandin synthetase, which prevents the synthesis of prostaglandins, which are known to have a pronounced inflammatory potential.

4.2) Steroid anti-inflammatory drugs: prednisolone, triamcinolone, dexamethasone, etc. Used in the presence of severe carditis or life threatening carditis.

Prednisolone is prescribed in a daily dose of 1-2 mg per 1 kg of body weight (at a dose of 40-60-90 mg per day). The full dose of the drug is used for 2-3 weeks (until a clear clinical effect), and then constantly reduced with its complete cancellation after 6-8-10 weeks.

The mechanism of action of glucocorticoids is to stabilize cell membranes, including lysosomes, inhibition of collagen depolymerization, inhibition of fibroblast activity, and inhibition of the antigen-antibody reaction.

Quinoline drugs (delagil, plaquenil) also have an anti-inflammatory effect and antiproliferative effect. However, they are characterized by a late therapeutic effect, which limits the therapeutic possibilities of these drugs.

To normalize vascular permeability, apply:

A) galascorbin, ascorutin, ascorbic acid;

B) antihistamines- tavegil, suprastin, diazolin, fenkarol, peritol, etc.

For normalization metabolic disorders in the heart muscle and other tissues are used: panangin, asparkam, riboxin, phosphaden, cardiac glycosides (digoxin, etc.), B vitamins, etc.

In the treatment of chorea, in addition to non-steroidal anti-inflammatory drugs (Voltaren, indomethacin, etc.), the following is prescribed:

A) bromine preparations (1% sodium bromide solution);

B) phenobarbital 0.01-0.13-0.05 g 2-3 times a day for 2 weeks, then only at night for another 2 weeks;

C) seduxen, chlorpromazine;

D) vitamins B. (5% solution of 0.5-1 ml / m), B6 ​​(5% solution of 0.5-1 ml / m), per course - 15-20 injections;

E) physiotherapy procedures: bromine electrophoresis on collar zone, electrosleep;

E) warm coniferous baths at a water temperature of 37 ° C, 5-7 minutes, 8-10 baths per course.

The duration of treatment depends on the duration of the active phase of the disease. Average duration the acute phase of rheumatism is 6-12 weeks.

PREVENTION OF RHEUMATISM. The main directions for the prevention of rheumatism are based on recognition as etiological factor beta-hemolytic streptococcus group A. Prevention of rheumatism is divided into primary, secondary and current.

Primary prevention is a complex of state, public and individual events aimed at preventing the primary incidence of rheumatism. Primary prevention measures are aimed at:

A) effective treatment of acute streptococcal infections caused by group A streptococcus (tonsillitis, pharyngitis, scarlet fever), prevention of their spread and reduction of contacts;

B) to increase the natural resistance and adaptive capabilities of the body to the adverse effects of the external environment.

Since rheumatism develops most often after an acute streptococcal infection, its timely diagnosis and early active antibacterial therapy are especially important.

Patients with acute streptococcal infection should be isolated. Treatment should be with penicillin for 5-7 days. Penicillin is administered intramuscularly at 100,000 IU per 1 kg of body weight per day (or preschool children at 300,000-350,000 IU per day and up to 450,000 IU per day for school-age children), and then with an interval of 5-6 days 2 times bicillin-5 is injected intramuscularly at a dose of 600,000-900,000 IU (if body weight is less than 30 kg) or at a dose of 1,200,000 IU (if body weight is more than 30 kg).

If it is impossible to organize intramuscular administration of penicillin (bicillin), phenoxymethylpenicillin is prescribed per os 250 mg 4 times a day for 10 days (if the body weight is more than 20 kg) or 125 mg 4 times a day (if the child's body weight is less than 20 kg) .

You can also use ampicillin, cephalosporin antibiotics, dicloxacillin.

In case of intolerance to penicillin preparations, erythromycin is prescribed 250 mg 4 times a day, for children weighing less than 25 kg - 40 mg per 1 kg in 2-4 doses (but not more than 1 g per day) for 10 days.

Treatment of streptococcal infections is ineffective and contraindicated with sulfa drugs, tetracycline, chloramphenicol.

After suffering an acute streptococcal infection, the child should be under the supervision of a local pediatrician for 1 month, since usually symptoms of rheumatism most often appear during this period.

A very important link in primary prevention is the prevention of the spread of streptococcal infection. This is achieved by isolating the patient, observing the rules of personal hygiene, ventilation and wet cleaning of the room, systematic quartzing of rooms, the use of air purifiers, etc.

The complex of restorative measures includes: systematic hardening of the body, physical education and sports, adherence to the daily routine, the correct alternation physical activity and rest, sufficient stay for fresh air nutrition, taking multivitamins, etc.

An important preventive measure is the treatment of foci of chronic infection. All foci of chronic streptococcal infection, especially in the nasopharynx (tonsillitis, pharyngitis, sinusitis, sinusitis), must be carefully sanitized. Tonsillectomy is performed under the protection of penicillin, which is prescribed 2-3 days before surgery and within 7-10 days after surgery in appropriate doses for the age.

Mandatory sanitation of teeth affected by caries is necessary, although streptococci are not found in teeth affected by caries. The same applies to periodontitis.

As mentioned above, for the occurrence of rheumatism is important genetic predisposition and familial streptococcal infection. Therefore, especially thorough primary prevention should be carried out for children from families in which there are patients with rheumatism, since they are at risk due to their predisposition to rheumatism.

Secondary prevention of rheumatism is a system preventive measures aimed at preventing relapses and progression of the disease in people who have had rheumatism.

The most important link in secondary prevention is bicillin prophylaxis, which has been used in our country since 1958. This made it possible to reduce the frequency of relapses in the first years of bicillin prophylaxis by 8-10 times.

Secondary prevention is the regular administration of antibacterial drugs(usually penicillin preparations) to patients who have had rheumatism, in order to prevent seeding and / or infection with group A streptococcus of the upper respiratory tract. For the purpose of secondary prevention, long-acting penicillin preparations are used - bicillin, to which, as confirmed by the work of microbiologists, resistant strains of streptococcus are not formed even with prolonged use.

Currently, for secondary prevention, the drug bicillin-5 is used, which is a mixture containing 1 part of benzylpenicillin novocaine salt and 4 parts of dibenzylethylenediamine salt of benzylpenicillin (bicillin-1).

There are two main methods of secondary prevention of rheumatism, which are outlined by the WHO Expert Committee (1988):

A) regular year-round intramuscular injection of bicillin-5 once every 3-4 weeks;

B) year-round daily antibiotics per os (penicillin, sulfazine, erythromycin).

The most effective is the regular intramuscular injection of bicillin-5 of prolonged action. It is administered intramuscularly to children weighing less than 30 kg at a dose of 600,000 IU once every 3 weeks, for children weighing more than 30 kg - at a dose of 1,200,000 IU once every 4 weeks.

Phenoxymethylpenicillin is used per os no 250 mg 2 times a day, sulfazine - 0.5 g per day (if body weight is less than 30 kg) or 1 g per day (if body weight is more than 30 kg).

An important aspect of secondary prevention is the establishment of its duration. The likelihood of recurrence of rheumatism depends on a number of factors, such as the time elapsed since past illness, age of the patient, condition environment etc. Than less age child with primary rheumatism, the greater the likelihood of relapse. It is shown that after the onset of puberty, the frequency of relapses decreases with age. Largest number relapses occur in the first 5 years after suffering primary rheumatism. In addition, in patients with rheumatism with severe carditis, relapses occur more often than in patients without heart damage.

A) in patients who did not have carditis during the primary rheumatic attack, secondary prophylaxis should be carried out for 5 years and until they reach the age of 18;

B) patients with predominant carditis at the first attack of rheumatism, secondary prevention should be carried out until they reach the age of 25 and longer if environmental conditions or other risk factors require it.

With these recommendations in mind, seasonal prophylaxis recommended after a 3-year period should obviously be recognized. ongoing prevention, outdated, and the simultaneous appointment of acetylsalicylic acid or other non-steroidal anti-inflammatory drugs in the form of monthly courses in spring and autumn is scientifically unfounded and unsafe.

Current prevention of rheumatism is aimed at treating any emerging intercurrent diseases in patients with rheumatism until complete recovery and normalization of blood counts. This applies to patients who have had a primary rheumatic attack, acute streptococcal diseases (tonsillitis, pharyngitis, etc.), as well as acute respiratory viral infections (flu, etc.). In this case, be sure to prescribe penicillin preparations or other antibiotics, taking into account tolerance.

When extracting a tooth in children who have had a rheumatic attack, penicillin is administered intramuscularly the day before and in the next 3 days: preschool children - 400,000-600,000 IU, school-age children - 600,000-1,200,000 IU per day. If it is impossible intramuscular injection penicillin on an outpatient basis, phenoxymethylpenicillin is prescribed orally or bicillin-5 is administered intramuscularly before tooth extraction.

In addition, in patients with rheumatism, all dental procedures or manipulations that cause bleeding, including the removal of tartar, require prophylaxis, especially in the presence of gum disease.

Depending on the degree of risk, patients when performing dental procedures are shown:

A) with a moderate degree of risk, the appointment of 2 g of amoxicillin or 2 g of phenoxymethylpenicillin per os 1 hour before surgery and 2 g per os after 6 hours;

B) with a high degree of risk (severe valvular damage, previous endocarditis), intramuscular (or intravenous) administration of 1 g of amoxicillin and 80-100 mg of gentamicin before the intervention and

1 g amoxicillin (intramuscularly, intravenously or per os) after 6 hours;

C) with an allergy to penicillin, as well as if recently (within

2 weeks) administered penicillin or carried out long-term prophylaxis with this antibiotic, it is recommended 1.5 g of erythromycin per os 1 hour before the intervention and 0.5 g per os after 6 hours.

Rheumatism in children is systemic pathology autoimmune nature. It affects the synovial membranes of the joints, the heart, skin, nervous and urinary system.

Pathology is dangerous for its complications. These are heart defects, irreversible changes in the structure of valves, heart attacks, including other organs - the spleen, kidneys. The disease is characterized by a progressive and relapsing course. The treatment is long.

The bulk of small patients with rheumatism are children from 7 to 15 years old. In preschool children, this disease is rarely diagnosed.

Diagnosis of pathology is difficult. But there are a number of features that distinguish childhood rheumatism from the manifestations of the disease in adult patients.

Reminder for parents:

1. Leading pathological processes - carditis - inflammatory processes affecting the tissues of the heart.
2. Infants are more likely to develop heart defects than older patients.
3. Polyarthritis develops much less frequently than in adults.
4. More often diagnosed are chorea, rashes, rheumatic fever in children, the appearance of rheumatoid nodules on the skin.
5. The course of the disease is severe, with episodes of recurrence of the inflammatory process, but in general, the treatment of childhood rheumatism is more effective than in patients of other age groups.

Causes and symptoms

The main reason for the development of the disease in childhood considered to be affected by some species of streptococci.

• Acute respiratory and viral diseases that causes group A hemolytic streptococcus. Simple infection is not enough. To activate rheumatism, the immune defense must fail. This occurs when untimely or not quality treatment nasopharyngeal pathologies.
• Heredity - if there were cases of the disease in the family history, then the probability of developing the child is quite high.
• Chronic inflammatory diseases of the nasopharynx.
• Some influence on the onset of pathology is exerted by constant hypothermia, stress factors, and poor eating habits.

The first symptoms of rheumatism in children appear in the period from a week to a month after an infectious or viral disease.

Clinical manifestations of rheumatism:

1. Rheumocarditis - weakness, shortness of breath, pallor up to cyanosis is noted. The inflammatory process captures all the membranes of the heart, but only one area can be affected - the myocardium, pericardium.
2. Polyarthritis - initially large and medium-sized joints of the legs are affected. Small joints are the last. There is symmetry in the location of the inflamed joints.
3. Chorea minor - a violation manifests itself in girls. The kid becomes irritable, whiny, gait is disturbed, handwriting changes, speech becomes slurred. In severe cases, the baby can not serve himself on his own.
4. Ring erythema - swelling in the form of white or pinkish rings. Doesn't itch, doesn't flake. The main location on the abdomen.
5. Acute rheumatic fever resolves in children with fever.
6. Nodules on the head and in the projection of the tendons connecting the joints with the muscles.

These are the main symptoms of rheumatism in children, determined in pediatrics. Dangerous recurrence of the disease, developing a year after the first episode of pathology. Symptoms in the second episode are more aggressive and may be accompanied by heart failure, disturbances in the functioning of the valvular apparatus of the heart.

Phases and degrees

Currently, the method of A.I. is used to classify the stages of the pathological process. Nesterov. It was developed back in 1964 and is being revised. But the new classification criteria are not yet presented in the WHO protocols.

There are 2 phases of the disease - active and inactive or remission.

Active phase or rheumatic attack

In pathogenesis, a primary or secondary round of the disease is distinguished. Acute rheumatic fever in children begins 7-15 days after the illness. The temperature rises to critical values, signs of carditis are noted - pain in the heart, shortness of breath, polyarthritis.

There are 3 degrees of severity of the active phase:

1. Minimal damage - there is no exudate, the inflammatory process is mild, the temperature is subfibrile or normal. Laboratory indicators or within the normal range, or increased slightly.
2. Moderate severity - symptoms of moderate severity, rheumatic fever may or may not be present. Laboratory indicators are increased, but not critical. Leukocytosis is in the range of 8-10 units, ESR - from 20 to 40 units.
3. Severe form - an acute inflammatory process, the presence of exudate, obvious signs of heart damage, active polyarthritis. Laboratory indicators indicate a severe lesion - ESR from 40 units and above, the presence of streptococcal antibodies exceeds normal performance 5 times. The differential diagnosis and medical history are not difficult to establish.

If a severe clinic is observed, then the child must be hospitalized in a hospital.

Inactive phase

The inactive phase is a state of remission. Symptoms subside, but there may be pain in the heart, slight indicators of fever. In rare cases, there is a slow destruction of the valvular system of the heart.

For each patient, this phase has an individual duration and can vary from several months to several years. If within 5 years the child has not developed a relapse, then he is removed from the dispensary.

Diagnosis and treatment

Diagnostics is complex. Obligatory examination by a doctor - pediatrician, rheumatologist, cardiologist. Special attention should be given to signs of chorea, the formation of subcutaneous nodes, family history.

Required clinical tests blood. General indicators are determined - leukocytosis, erythrocyte sedimentation rate, the presence of antibodies to streptococcal infection, the permeability of the vascular wall.

Instrumental diagnostic methods:

• X-ray of the chest area - signs of a decrease in the contractile function of the heart muscles, a change in the configuration of the organ are determined.

Treatment tactics depend on the severity of the disease. In the inactive phase, the emphasis is on prevention and recovery, general health improvement, reducing the likelihood of relapse. AT acute stage hospitalization is indicated. This will stop the process in a short time.

What the doctor will prescribe:

• Preparations NSAID groups in tablets or by injection, in severe cases, corticosteroids. Duration of admission nonsteroidal drugs ranges from 1.5 to 2 months. Corticosteroids - 2 weeks in loading doses, then gradually reduced.
• Antibiotics at the doctor's choice - as a rule, penicillins are prescribed. The duration of antibiotic therapy is from 10 to 14 days.
• In the presence of chronic tonsillitis it is shown to supplement the treatment with antibiotics of other pharmacological groups - macrolides, cephalosporins.
• Quinoline drugs - have an immunosuppressive and anti-inflammatory effect. The duration of therapy is from 1.5 to 2 years.

At chronic tonsillitis removal of the tonsils. Surgical intervention is carried out no earlier than 2 months after the cessation of the active inflammatory process.

Rehabilitation and care of children with rheumatism

Rehabilitation consists in the use of spa treatment. In this case, continue drug therapy started in the hospital. shown physiotherapy, general firming procedures.

Caring for a baby requires patience and care from parents. During treatment, bed rest is indicated, which may further depress earlier active child. An important point in the organization of care is warmth, since babies diagnosed with rheumatism are intolerant of cold. Do not use heavy blankets, it is better to put warm pajamas on the child. Because of the pain syndrome, the child can delay the processes of defecation and urination. Therefore, you need to monitor the frequency of the stool.

With a decrease in the severity of the inflammatory process, it is recommended to engage in calm craft games, read, and make applications. Parents should try to distract the baby from depressive thoughts and moods.

A diet for rheumatism is following the principles of a healthy diet. Fried, smoked, spicy dishes are prohibited. You should not be zealous with sweets. Dairy dishes, vegetables, lean meat are essential elements of the diet. Perhaps the baby will have a reduced appetite. Do not insist, but offer!

Forecast and prevention

Prevention of rheumatism in children consists in the qualitative treatment of pharyngitis and other diseases of the nasopharynx. The main cause of these pathologies is streptococcal infection, which can cause a primary or secondary round of rheumatism. If antibiotics are indicated, follow full course treatment.

If the child has already been ill, it is important to prevent a secondary round of the disease. For this, it is recommended to administer the antibiotic "Bicillin" once a week for 5 years after recovery.

Forecasts for rheumatism and the consequences are individual and depend on the degree of damage to the structures of the heart. If the disease is acute, but there are no manifestations of carditis, then with proper treatment, complete recovery occurs. At inflammatory processes in the heart, valvular defects occur in 25% of patients. Fatal outcome from the effects of rheumatism present stage development of medicine is 4%.

Recognizing rheumatism alone is difficult. Alternative methods of treatment can do more harm than help. If you suspect a pathology, you should immediately seek medical help.

Rheumatism is a general inflammatory process involving connective tissue caused by group A beta-hemolytic streptococcus.
Acute rheumatic fever is a systemic inflammatory disease of the connective tissue with predominant localization in the cardiovascular system. developing in predisposed persons in connection with an infection caused by group A beta-hemolytic streptococcus.

Classifications

1. Classification by A.I. Nesterov (1964)

2. Congress of rheumatologists of the USSR, 1985.
BUT. Active rheumatism(rheumatism in the active phase)
- without involvement of the heart (rheumatoid arthritis, polyarthritis, chorea)
- with involvement of the heart (primary rheumatic carditis, recurrent rheumatic heart disease without defect or with defect)

3. International statistical classification X revision.
Acute rheumatic fever:
- no heart failure
- with heart failure
- chorea
chronic rheumatic diseases

Pathogenesis of immune diseases

Stage I: immune complex formation, complement activation
P stage: migration of macrophages and mast cells, alteration processes and microcirculation disorders
Stage III: violations of blood coagulation processes with the development of microthrombosis and micronecrosis

Stages of the rheumatic process

1. Alterative-exudative (3-4 weeks)
2. Proliferative (1-5 months)
3. Development of rheumatic sclerosis (5-6 months)
"The whole rheumatic process takes about 6 months" (V.T.Talalaev)

Streptococcus pathogenicity factors

1. M-protein - has antigenic properties, reduces the activity of leukocyte ATPase, promotes resistance to phagocytosis.
2. Streptolysin - S - has a direct toxic effect on erythrocytes, platelets, myocardial and kidney cells by increasing the permeability of their cell and lysosomal membranes.
3. Streptolysin O - induces the production of cytotoxic antibodies,
4. Streptohyaluronidase - increases the permeability of tissues for toxins
5. Streptoproteinase - causes the destruction of the protein-mucopolysaccharide complex - the main substance of the connective tissue.
6. Hyaluronic acid- component of the capsule, which has hydrophilic properties, prevents phagocytosis.

Criteria for rheumatism

(A.A. Kisel - T. Jones - World Association of Cardiology - WHO (1988))
Large: carditis, polyarthritis, chorea. erythema annulare and subcutaneous nodules
Small: fever. arthralgia. the presence of a defect or rheumatic fever in the anamnesis, ECG changes
The diagnosis is reliable in the presence of 2 major and 1 or 2 minor features and is probable in the presence of 1 major and 2 minor.
WHO reservation: association with streptococcal infection is mandatory within the time period characteristic of the development of an immune disease (10-14 days).

Formulation of the diagnosis:

Rheumatism. a / f, 1 tbsp. activity. Recurrent endomyocarditis. Combined mitral defect with a predominance of stenosis. Myocardial cardiosclerosis. Permanent form of atrial fibrillation. HNK PA Art.
Rheumatism, n / f. Combined aortic defect with predominance of stenosis. Myocardial cardiosclerosis. HNK PA Art.

Examination plan:

1. General blood test
2. 2-hour thermometry
3. Protein fractions
4. C-pretein
5. Titers of antistreptolysin-o.antistreptohyaluronidase and antistreptokinase
6. ECG
7. FCG, ECHOCG, Doppler ECHOCG.

Treatment:

1. Ward mode (or bed)
2. Penicillin 150000 units. after 3 hours for 7-10 days. (then bicillin-3 1500000 units 1 time per week, then bicillin - 5 1500000 units 1 time in 3 weeks)
3. Voltaren (diclofenac sodium) 50 mg 3 times a day