Prevention of acute rheumatic fever. Acute rheumatic fever

The epidemiology of rheumatic fever is closely related to the epidemiology of A-streptococcal infections of the upper respiratory tract. The high rate of rheumatic fever began to decline even before the use of antibiotics in clinical practice, and the use of antibiotics since the 1950s has rapidly accelerated this process. Thus, in developed countries, the incidence of rheumatic fever has decreased from 100-250 to 0.23-1.88 per 100,000 population. Nevertheless, about 12 million people in the world currently suffer from rheumatic fever and rheumatic heart disease. Most of them live in developing countries, where the incidence of PD ranges from 1.0 per 100,000 population in Costa Rica, 72.2 per 100,000 in French Polynesia, 100 per 100,000 in Sudan, to 150 per 100,000 in China , In some areas, such as Havana (Cuba), Costa Rica, Cairo (Egypt), Martinique and Guadeloupe, where prevention programs have been introduced, there has been a marked decrease in mortality, prevalence and severity of PD and RHD. Sopioeconomic indicators and factors environment play an indirect but important role in the prevalence and severity of rheumatic fever and RHD. Factors such as lack of resources to provide quality health care, low awareness of the disease in society, crowding of the population, can significantly affect the incidence in the population. However, rheumatic fever is not only a problem of socially and economically disadvantaged populations. This was demonstrated by local outbreaks of rheumatic fever. recorded in the 80s and 90s. 20th century in some areas of the USA, Japan and a number of other developed countries of the world.

Causes of acute rheumatic fever

The etiological relationship between GABHS infections and the subsequent development of acute rheumatic fever (ARF) is well established. Despite the lack of evidence of the direct involvement of group A streptococci in tissue damage in patients with acute rheumatic fever, there is significant epidemiological immunological evidence for the indirect involvement of GABHS in the initiation of the disease:

• outbreaks of rheumatic fever closely follow every epidemic of sore throat or scarlet fever;
• adequate treatment of documented streptococcal pharyngitis markedly reduces the number of subsequent attacks of rheumatic fever;
• Appropriate antimicrobial prophylaxis prevents disease recurrence in ARF survivors;
• the presence in most patients with ARF of elevated titers of at least one of the antistreptococcal antibodies.

Rheumatic fever and rheumatic heart disease are observed only after upper respiratory tract infections caused by group A streptococci. Although beta-hemolytic streptococci of serogroups B, C, O and P can cause pharyngitis and be triggers of the host immune response, they are not associated with the etiology of LC.

Streptococcal pharyngitis/tonsillitis is the only infection associated with ARF. For example, there are many descriptions of outbreaks of skin streptococcal infections (impetigo, erysipelas) that were the cause of post-streptococcal glomerulonephritis, but never the cause of rheumatic fever.

The strains of group A streptococcus that colonize the skin were different from the strains that cause rheumatic fever. Bacterial genetic factors may be an important determinant of the site of onset of group A streptococcal infection. The structure of antigens encoding M- and M-like surface proteins of streptococcus is recognized and labeled from A to E. Pharyngeal strains have A-C structure, while all skin strains have a D and E structure.

Another factor influencing pharyngeal localization could be the CD44 receptor, a hyaluronic acid-coupled protein that serves as a pharyngeal receptor for group A streptococci. It has been experimentally shown that after intranasal administration, group A streptococci colonize the oropharynx in normal mice and do not colonize in transgenic mice not expressing CD44.

Many theories try to explain why acute rheumatic fever is associated only with streptococcal pharyngitis, but there is still no exact explanation. The A group of streptococci is divided into two main classes, based on differences in the C-sequences of the M-protein. One class is associated with streptococcal pharyngeal infection, the other (with some exceptions) with the strains most commonly associated with impetigo. Thus, the characteristics of streptococcal strains are decisive in the initiation of the disease. Pharyngeal infection, with its involvement of a large amount of lymphoid tissue, may itself be important in initiating an abnormal humoral response to microbial antigens with the formation of cross-reactivity to body tissues. Cutaneous strains can colonize the pharynx, but they are unable to elicit as strong an immunological response to M-protein as pharyngeal strains.

Rheumatic fever occurs as a result of an abnormal immune response to group A streptococcal pharyngitis. The clinical manifestations of this response and its severity in a particular individual depend on the virulence of the microbe, the genetic susceptibility of the host, and the "suitable" environmental conditions.

One of the well-studied determinants of bacterial virulence is the M-protein. Streptococcal M-protein is located on the surface of streptococcal cells and has structural homology with cardiomyocyte myosin, as well as with other molecules: tropomyosin, keratin, laminin. This homology is thought to be responsible for the histological changes in acute rheumatic carditis. For example, laminin, an extracellular matrix protein secreted by endothelial cells that line the heart valves, is an essential component of valve structure. It also serves as a target for polyreactive antibodies that "recognize" M-protein, myosin and laminin.

Of the more than 130 identified M protein types, M types 1, 3, 5, 6, 14, 18, 19, and 24 are associated with rheumatic fever. These group A streptococcal M types are postulated to have rheumatogenic potential. These serotypes are usually difficult to encapsulate and form large mucoid colonies rich in M-protein. These characteristics enhance the ability of bacteria to tissue adhesion and resistance to phagocytosis in the host organism.

Another virulence factor is streptococcal superantigens. This is a unique group of glycoproteins that can bind class II molecules of the major histocompatibility complex to V-receptors on T-lymphocytes, simulating antigen binding. Thus, T cells become susceptible to antigen-specific and auto-reactive stimulation. In the pathogenesis of rheumatic fever, some fragments of the M-protein and streptococcal erythrogenic exotoxin are considered as superantigens. Streptococcal erythrogenic toxin can act as a superantigen for B cells as well, leading to the production of autoreactive antibodies.

The genetic predisposition of the macroorganism is also necessary for the development of rheumatic fever. This is currently the only explanation for the fact that rheumatic fever occurs in only 0.3-3% of individuals with acute A-streptococcal pharyngitis. The concept of the genetic predisposition of PD has intrigued researchers for over 100 years. All this time, it was believed that the disease gene has an autosomal dominant transmission path, an autosomal recessive one with limited penetrance, or the transmission is carried out by a gene associated with the secretory status of the blood group. Again, interest in the genetics of ARF has grown in connection with the discovery of the histocompatibility complex in humans. Research results suggest that the immune response is genetically controlled, with high reactivity to streptococcal cell wall antigen expressed through a single recessive gene and low reactivity expressed through a single dominant gene. Current data confirm that the genetic control of low response to streptococcal antigen is closely related to class II histocompatibility antigens. However, the relationship between susceptibility to rheumatic fever and HLA class II antigens varies greatly depending on ethnicity. For example, DR4 is more commonly present in Caucasian patients with PD; DR2 - in Negroids, DR1 and DRw6 - in patients from South Africa; DR3 is more commonly found in PD patients from India (who also have a low incidence of DR2); DR7 and DW53 - in patients from Brazil; DQW2 - Mongoloids. Most likely, these genes are located next to the rheumatic fever predisposition gene, possibly at the same locus, but are not identical to it.

Somewhat later, in patients with LC, surface alloantiheps of B-lymphocytes were identified, called D8/17 alloantigens after the name of the clone of monoclonal antibodies with which they were isolated. According to world data, the D8/17 B-lymphocyte alloantigen is identified in 80-100% of ARF patients and only in 6-17% of healthy individuals. The involvement of the alloantigen of B-lymphocytes of patients in the pathogenesis of rheumatic fever continues to be studied. It is most likely that the predisposition to ARF is polygenic, and the D8/17 antigen may be associated with one of the genes responsible for the predisposition; the other may be a histocompatibility complex encoding DR antigens. Although there is no exact explanation, the increased number of D8/17 positive B cells- a sign of a special risk of morbidity with acute rheumatic fever.

The pathogenesis of rheumatic fever

Streptococcal infection begins with the binding of bacterial surface ligands to specific receptors on host cells and the subsequent activation of specific processes of adhesion, colonization, and invasion. Binding of bacterial surface ligands to host surface receptors is a key event in host colonization and is initiated by fibronectin and streptococcal fibronectin-binding proteins. Streptococcal lipoteichoic acid and M-protein also play an essential role in bacterial adhesion. The host organism responds to streptococcal infection by opsonization and phagocytosis. Streptococcal infection in a genetically predisposed organism under appropriate environmental conditions leads to the activation of T- and B-lymphocytes by streptococcal antigens and superantigens, which, in turn, promotes the production of cytokines and antibodies directed against streptococcal N-acetyl-beta-D-glucoses on (carbohydrate) and myosin.

It is believed that damage to the valvular endothelium by anticarbohydrate antibodies leads to increased production of adhesion molecules and an influx of activated CD4+ and CD8+ T cells. Violation of the integrity of the endothelium of the heart valves leads to the exposure of subendothelial structures (vimentin, laminin and valvular interstitium cells), which contributes to the development of " chain reaction» valvular destruction. After the valve leaflets are involved in the inflammation process, thanks to the newly formed microvessels, the valve endothelium is infiltrated with T cells, supporting the process of valve destruction. The presence of T-cell infiltration, even in old mineralized lesions, is indicative of disease persistence and progression of valve injury. Under the influence of pro-inflammatory cytokines, valvular interstitium cells and other valvular components lead to "improper repair" of the valve.

The pathogenetic mechanism described above is the most likely, but so far there is no direct and convincing evidence of the pathogenetic role of cross-reacting antibodies in vivo and there is no suitable animal model for the study of rheumatic fever.

In 2000-2002 European society cardiologists have published data on the possible trigger role of viruses and heat stress proteins in the formation of relapses of rheumatic fever and rheumatic heart disease, but this theory still requires further study.

Thus, the basis of modern ideas about rheumatic fever is the recognition of the etiological role of GABHS and hereditary predisposition to the disease, which is realized by an anomaly of the body's immune response.

Symptoms of rheumatic fever

Rheumatic fever comes in attacks. In 70% of patients, the rheumatic attack subsides, according to clinical and laboratory data, within 8-12 weeks, in 90-95% - 12-16 weeks, and only in 5% of patients the attack lasts more than 6 months, i.e. takes a protracted or chronic course. In other words, in most cases, the rheumatic process has a cyclic course, and the attack ends and, on average, within 16 weeks.

In more than half of the cases, patients complain of shortness of breath, interruptions in the heart, palpitations, which occur against the background of common symptoms of rheumatic fever: fatigue, lethargy, sweating, fever. In adults, pain in the region of the heart of an indefinite nature may appear.

Rheumatic heart disease, rheumatoid arthritis, chorea, erythema annulare, and subcutaneous nodules are great diagnostic features of acute rheumatic fever.

Subcutaneous nodules and erythema annulare

Subcutaneous nodules and erythema annulare are rare manifestations of rheumatic fever, occurring in less than 10% of cases.

Subcutaneous nodules are round, dense, easily displaced, painless formations ranging in size from 0.5 to 2 cm, often localized on the extensor surfaces of the elbow, knee and other joints, in the occipital region and along the tendon sheaths, are extremely rare during the first attack of rheumatic fever. fever. The number of nodules varies from one to several dozen, but usually there are 3-4. It is believed that they are easier to feel than to see. They persist from several days to 1-2 weeks, less often - more than a month. Subcutaneous nodules are almost always associated with cardiac involvement and are more common in patients with severe carditis.

Erythema annulare are transient annular patches with a pale center, usually occurring on the trunk, neck, and proximal extremities. Annular erythema is never localized on the face. Due to the transience of changes and the absence of associated symptoms, erythema annulare may be missed unless specifically looked for, especially in dark-skinned patients. Individual elements can appear and disappear within minutes or hours, sometimes changing shape before the eyes of a specialist, merging with neighboring elements to form complex structures (which is why they are described in some sources as “cigarette smoke rings”). Erythema annulare usually appears at the onset of a rheumatic attack, but it may persist or recur for months or even years, persisting after other manifestations of the disease subside; it is not affected by anti-inflammatory treatment. This cutaneous phenomenon is associated with carditis but, unlike subcutaneous nodules, is not necessarily severe. Nodules and erythema annulare often coexist.

Erythema annulare is not unique to rheumatic fever, but has also been described in sepsis, allergic drug reactions, glomerulonephritis, and in children without any diagnosed disease. It must be distinguished from toxic erythema in febrile patients and juvenile idiopathic arthritis rash. Erythema annulare in Lyme disease (erythema chronicum migrans) can also resemble erythema annulare in rheumatic fever.

Clinical minor criteria for rheumatic fever

Arthralgias and fever are referred to as "minor" clinical manifestations rheumatic fever in the T. Jones diagnostic criteria, not because they are less common than the five major criteria, but because they have less diagnostic specificity. Fever is observed at the beginning of almost all rheumatic attacks and usually ranges from 38.4-40 C. As a rule, there are fluctuations during the day, but there is no characteristic temperature curve. Children who have only mild carditis without arthritis may be subfebrile, and patients with "pure" chorea are afebrile. The fever rarely persists for more than a few weeks. Arthralgia without objective changes is often found in rheumatic fever. Pain usually occurs in large joints and can be mild to very severe (up to the impossibility of movement), it can persist from several days to weeks, varying in intensity.

Although abdominal pain and epistaxis are noted in approximately 5% of patients with LC, they are not considered part of the T. Jones criteria due to the lack of specificity of these symptoms. However, they may be of clinical significance, since they appear hours or days before the development of major manifestations of PD, abdominal pain is usually localized in the epigastrium or umbilical region, may be accompanied by symptoms of muscular protection, and often simulates various acute diseases abdominal organs.

Clinical observation

Patient S., aged 43, consulted at the Moscow City Rheumatology Center on January 20, 2008, where she was referred from the city polyclinic to clarify the diagnosis.

On examination, she complained of general weakness, sweating, fatigue, shortness of breath during physical exertion. In December 2007, she suffered from acute pharyngitis, for which she did not receive antibacterial treatment. After 3-4 weeks, shortness of breath and palpitations appeared with little physical exertion, pain in the precordial region of a different nature, an increase in body temperature up to 37.2 C, an increase in ESR up to 30 mm/h.

From the anamnesis it is also known that since childhood, a cardiologist has been observed for primary prolapse mitral valve, a mesodiastolic click and a late systolic murmur over the apex were constantly heard during auscultation of the heart. Over the past month, the cardiologist noted an increase in systolic murmur with the acquisition of pansystolic sound, which became the basis for suspicion of ARF and referral to a rheumatology center for a consultation.

Objectively: the skin is of normal color, normal nutrition. There are no peripheral edema. Tonsils are hypertrophied, loosened. In the lungs, vesicular breathing, wheezing was not heard. The boundaries of relative dullness of the heart are not expanded. Weakening of the I tone above the apex, a pansystolic murmur is heard with irradiation to the left axillary region and interscapular region of the 5th gradation, as well as systolic murmur over the tricuspid valve and valve pulmonary artery 3rd gradation. Extrasystole. Heart rate - 92 per minute, blood pressure - 130/70 mm Hg. The abdomen is soft and painless on palpation. Percussion liver and spleen are not enlarged.

Clinical blood test from 16.01.08: Hb ~ 118 g/l, leukocytes - 9.4x10 9 /l, ESR - 30 mm/h

General analysis urine dated 16.01.08 without pathological changes. In the immunological analysis of blood dated 16.01.08: C-reactive protein - 24 mg/l, antistreptolysin-O - 600 units.

On the ECG - the normal position of the electrical axis of the heart, sinus rhythm, heart rate - 70 per minute, single atrial extrasystoles, PQ - 0.14 s, QRS - 0.09 s.

With Doppler echocardiography of 20.01.08, both leaflets of the mitral valve protrude into the cavity of the left atrium, the marginal seal of the anterior leaflet, their movements are in antiphase. Fibrous ring - 30 mm, hole size 39x27 mm, peak gradient - 5.8 mm Hg, mitral regurgitation of the 3rd degree. Left atrium 44 mm, dilatation of the left ventricle: end-diastolic size (EDV) - 59 mm, end-systolic size (ESD) - 38 mm, end-diastolic volume (EDV) - 173 ml, end-systolic volume (ESV) - 62 ml, stroke volume - 11 ml, ejection fraction (FB) - 64%. Aorta 28 mm, not changed. The aortic valve is tricuspid, a small marginal seal of the leaflets, the annulus fibrosus is 24 mm, the peak pressure gradient is 4 mm Hg. The right atrium is 48 mm, the right ventricle is slightly dilated (equal to the left in volume), the calculated pressure is 22 mm Hg. The pulmonary artery is moderately dilated, the pulmonary valve is not changed, the fibrous ring is 29 mm, the systolic pressure gradient across the pulmonary artery valve is 3 mm. Hg, no regurgitation. The tricuspid valve prolapses, the annulus fibrosus is 30 mm, the 1st degree of rigurgitation. Conclusion: prolapse of both leaflets of the mitral valve, marginal thickening of the leaflets of the mitral and aortic valves, mitral regurgitation of the 3rd degree, tricuspid regurgitation of the 1st degree, dilatation of the heart cavities.

Taking into account the connection between the worsening condition of the patient with acute pharyngitis and evidence of a past A-streptococcal infection (detection of an increased titer of antistreptolysin-O), an increase in the existing systolic murmur over the apex of the heart, as well as cardiomegaly detected by echocardiography, an increase in the level of C-reactive protein and increase in ESR was diagnosed: "Acute rheumatic fever: carditis medium degree(mitral and aortic valvulitis). Mitral regurgitation of the 3rd degree. Tricuspid regurgitation of the 1st degree. Supraventricular extrasystole. NK 1 st., II FC.

The patient was hospitalized in City Clinical Hospital No. 52, where a streptococcal infection was treated with amoxicillin for 10 days at a dose of 1500 mg / day, diclofenac at a dose of 100 mg / day for 14 days, strict bed rest was observed for 2 weeks with a further expansion of the load regimen . The patient's condition improved, the size of the heart decreased. At the time of discharge from the hospital for outpatient aftercare, the patient had no complaints. In blood tests, ESR was 7 mm/h, C-reactive protein - 5 mg/l, antistreptolysin-O - less than 250 units. Secondary prophylaxis of rheumatic fever with benzathine benzylpenicillin at a dose of 2.4 million units intramuscularly 1 time every 4 weeks was started, which was recommended for the next 10 years.

Classification of rheumatic fever

Currently in Russian Federation adopted a national classification of rheumatic fever.

Classification of rheumatic fever (APP, 2003)

• * According to the classification of N.D. Strazhesko and V.Kh. Vasilenko.
• ** Functional class of heart failure according to the New York classification.
• *** There may be post-inflammatory marginal fibrosis of the valve leaflets without regurgitation, which is specified using echocardiography.
• **** In the presence of "the first detected heart disease, it is necessary to exclude other causes of its formation, if possible (infective endocarditis, primary antiphospholipid syndrome, valvular calcification of degenerative origin, etc.).

Diagnosis of rheumatic fever

In the anamnesis of patients with suspected rheumatic heart disease, it is necessary to describe in detail the family and sexual history for the presence of rheumatic fever in the next of kin and documented confirmation of this diagnosis, as well as to establish the presence or absence of documented tonsillopharyngitis, scarlet fever, otitis media, rhinitis, anterior cervical lymphadenitis lymph nodes during the last 2-3 weeks. The presence of risk factors should also be taken into account:

• hereditary predisposition (detection of a specific antigen of B-lymphocytes D8 / 17, as well as a high prevalence of class II antigens of the HLA system);
• "vulnerable" age;
• population density;
• unsatisfactory housing and sanitary and hygienic conditions of life (small living space, large families);
• low level of medical care,

Diagnostic criteria for rheumatic fever

To confirm the primary attack of the disease, major and minor criteria for rheumatic fever are needed, laboratory changes and evidence of prior streptococcal infection, as recommended by the 2004 WHO guidelines. In the context of previous streptococcal infection, two major criteria or a combination of one major and two minor criteria are sufficient to warrant the diagnosis of ARF. The diagnosis of recurrent rheumatic fever in a patient with established RHD may be based on minor criteria combined with evidence of recent streptococcal infection.

Criteria for the diagnosis of rheumatic fever and rheumatic heart disease (WHO, 2004, based on the revised T. Jones criteria)

Diagnostic categories	Criteria
0RL (a) Recurrent attacks of rheumatic fever in patients without established RHD(s) Recurrent attacks of rheumatic fever in patients with established RHD Chorea rheumatica; latent rheumatic heart disease (and)	Two major or one major and two minor criteria + proof of past infection with group A streptococci Two major or one major and two minor criteria + proof of previous group A streptococcal infection Two minor criteria + proof of previous group A streptococcal infection (c) No other major criterion or evidence for group A streptococcal infection is required.

(a) - Patients may have polyarthritis (or only polyarthralgia or monoarthritis) and several (3 or more) other minor manifestations, as well as evidence of a recent GABHS infection. Some of these cases may later progress to RL. They can be considered cases of "possible PD" (if other diagnoses are excluded). In these cases, regular secondary prophylaxis is recommended. Such patients should be observed and regularly examined the heart. This cautious approach is especially important for patients of “vulnerable” age.

(b) - Infective endocarditis must be ruled out.

(c) - Some patients with recurrent attacks may not fully meet these criteria.

Laboratory diagnosis of rheumatic fever

In the presence of rheumatic fever in the active phase, using a blood test, an increase in nonspecific "acute phase indicators" is detected, which include:

• neutrophilic leukocytosis (no more than 12,000-15,000);
• dysproteinemia with increased levels of a-2 and y-globulins;
• increase in ESR (already in the first days of the disease);
• increase in the level of C-reactive protein (from the first days of the disease).

Bacteriological examination of a throat swab can detect GABHS, but does not differentiate between active infection and streptococcal carriage.

Evidence of a recent streptococcal infection is an increase in streptococcal antibody titers, determined in paired sera, which is observed during the first month from the onset of the disease, usually persists for 3 months, normalizing after 4-6 months.

Normal, borderline and high numbers of streptococcal antibodies

Instrumental diagnosis of rheumatic fever

An ECG study can detect rhythm and conduction disturbances: transient atrioventricular blockade (PQ prolongation) of the 1st, less often 2nd degree, extrasystole, changes in the tooth to T in the form of a decrease in its amplitude up to the appearance of negative teeth. These ECG changes are characterized by instability and quickly disappear during treatment.

Phonocardiographic study helps to clarify the data of auscultation of the heart and can be used to objectify changes in tones and noises during dynamic observation.

X-ray of organs chest carried out in order to determine cardiomegaly and signs of stagnation in the pulmonary circulation.

EchoCG criteria for mitral valve endocarditis are:

• club-shaped marginal thickening of the mitral valve;
• hypokinesia of the posterior mitral valve;
• mitral regurgitation;
• transient dome-shaped diastolic flexure of the anterior mitral leaflet.

Rheumatic endocarditis of the aortic valve is characterized by:

• marginal thickening of the valve leaflets;
• transient leaflet prolapse;
• aortic regurgitation.

It should be remembered that isolated aortic valve disease without mitral regurgitation murmur is not characteristic of acute rheumatic carditis, but does not exclude its presence.

Diagnosis example

• Acute rheumatic fever: moderate carditis (mitral valvulitis), MR I degree, migratory polyarthritis. NK 0, 0 FK.
• Acute rheumatic fever: mild carditis, chorea. NK 0, 0 FK.
• Recurrent rheumatic fever: carditis, severe RHD: combined mitral heart disease: mild mitral valve insufficiency, mild stenosis of the left atrioventricular orifice. NK IIA, II FC.

Treatment of rheumatic fever

The main goal of the treatment of rheumatic fever is the eradication of beta-hemolytic streptococcus from the nasopharynx, as well as the suppression of the activity of the rheumatic process and the prevention of severe disabling complications of LC (RHD with heart disease).

All patients with suspected acute rheumatic fever should be hospitalized for diagnosis and treatment.

Medical treatment for rheumatic fever

Since the establishment of rheumatic fever, treatment with penicillins is prescribed, which ensures the removal of GABHS from the nasopharynx. Of the penicillins, benzathine benzylpenicillin or phenoxymethylpenicillin are most commonly used. Recommended daily doses of benzathine benzylpenicillin: children - 400,000-600,000 units, adults - 1.2-2.4 million units intramuscularly once. Phenoxymethylpenicillin is recommended for adults at 500 mg orally 3 times a day for 10 days.

Algorithm for the treatment of streptococcal pharyngitis:

• Phenoxymethylpenicillin (Ospen 750) 1.5 g/day, 10 days: 500 mg (tablets) 3 times a day orally or 750,000 IU/5 ml (syrup) 2 times a day.
• Amoxicillin 1.5 g / day, 10 days: - 500 thousand (tablets) 2-3 times a day inside, regardless of food intake.
• Benzathine benzylpenicillin 1.2-2.4 million units intramuscularly once. It is advisable to appoint when:
  • dubious performance of the patient in relation to oral intake antibiotics;
  • the presence of rheumatic fever in the anamnesis of the patient or close relatives;
  • unfavorable social and living conditions;
  • outbreaks of A-streptococcal infection in preschool institutions, schools, boarding schools, colleges, military units, etc.
• Cefalexin - 10 days: - 500 mg 2 times a day inside.
• In case of intolerance to ß-lactam antibiotics - macrolides - 10 days (including azithromycin - 5 days).
• In case of intolerance to ß-lactam antibiotics and macrolides - clindamycin 300 mg 2 times a day orally with plenty of water for 10 days.

Penicillins should always be considered as the drug of choice in the treatment of ARF, except in cases of individual intolerance, when macrolides or lincosamides are prescribed. Of the macrolides, erythromycin 250 mg orally 4 times a day is most commonly used.

Patients with intolerance to both ß-lactams and macrolides are prescribed lincosanides, in particular lipcomycin 0.5 g orally 3 times a day (10 days).

When studying the long-term prognosis of rheumatic fever and analyzing the incidence of heart defects within a year after an attack, according to the Cochrane review, no significant effect of anti-inflammatory treatment was found. However, the conclusion made about the inefficiency of this impact is not sufficiently substantiated, since in the meta-analysis of eight studies cited by the authors, most of them belonged to the 1950s and 1960s. XX o. These works lacked the most important principles of quality clinical practice, for example, the principle of randomization. In this regard, the authors of the meta-analysis consider it necessary to conduct multicenter, randomized, placebo-controlled studies to study the effectiveness of anti-inflammatory effects in rheumatic heart disease.

Rheumatic fever - background

Rheumatic fever is one of the most ancient human diseases: references to it are found in the early literature of China, India, Egypt. In the Book of Diseases by Hippocrates (460-377 BC), a typical rheumatoid arthritis was described for the first time: intermittent inflammation of many joints, with swelling and redness, severe pain, not life-threatening for patients and observed mainly in young people. The first use of the term "rheumatism" for arthritis is attributed to the Roman physician of the 2nd century, Galen. The term "rheumatism" comes from the Greek word "rheumatismos" and means "spreading" (over the body). Being an active representative of the humoral concept of the origin of various diseases, including arthritis, Galen considered these diseases as a kind of catarrh. The great authority of Galen and the slow progress of knowledge in this area contributed to the fact that Galen's understanding of the essence clinical picture The disease lasted until the 17th century, when the work of Baillou (Baillou), who called himself Ballonius, appeared. The study "Liber cle Rheumatismo etpleuritiddorsal" was published posthumously by his nephew only in 1642. It contained a description of the disease. "Rheumatism is all over the body and is accompanied by pains, tension, heat, sweat... in arthritis, the pains recur at regular intervals and at regular intervals."

Outstanding physician of the 17th century. Sydenham a little later, Baiilou clearly characterized rheumatoid arthritis: strong pain in the joints; this pain moves from place to place, in turn in all joints, and finally affects one joint with redness and swelling, ”Sydenham is credited with the first description and recognition of chorea as a rheumatic disease.

The first reports of heart damage in rheumatic diseases of the joints appeared at the end of the 18th century, but these facts were considered as an ordinary combination of two different diseases, and not as a single disease.

The English physician Pitcairn (1788) was one of the first to recognize the connection between rheumatic fever and heart disease. For the first time, Pitcairn noted the frequent involvement of the heart in rheumatism. He assumed a common cause of disease of the heart and joints and coined the term "cardiac rheumatism".

NI. Sokolsky and Zh. Buyo (Bouillaud) at the same time, but independently of each other, established a direct organic connection between rheumatic fever and rheumatic heart disease. Most scientists of that time attached paramount importance to the development of endocarditis and pericarditis in rheumatism, Professor of Moscow University G.I. Sokolsky in his work "On rheumatism muscle tissue heart "(1836) singled out the clinical and anatomical forms of rheumatic heart disease - myocarditis, endocarditis and pericarditis, giving special attention to rheumatic myocarditis, ßouillaud in the Clinical Guide to Heart Diseases (Paris, 1835) and the Clinical Guide to Articular Rheumatism and the Law of Coincidence inflammation of the heart with this disease ”(Paris, 1840) noted the high prevalence of rheumatic heart disease in the form of valvulitis and pericarditis and formulated his famous law of coincidence of rheumatic arthritis and heart disease.

The works of Bouillaud and G.I. Sokolsky in the history of the development of the doctrine of rheumatic fever had the value of a scientific feat and became a turning point in the understanding of this disease. From a historical and scientific point of view, the definition of rheumatic fever as Sokolsky-Buyo's disease is quite justified.

In 1894, Romberg found in 2 deceased patients significant infiltrates at the site of attachment of the valves, and in the myocardium - numerous small calluses from the connective tissue, confirming rheumatic myocardial damage. This was later proven in the classic work of Aschoff, who described rheumatic granulomas in the myocardium in 1904. W.T. Talalaev (1929) has an exceptional merit in studying the stages of development of the rheumatic process. “The significance of the developed by Ashoff and V.T. Talalaev morphological criteria for rheumatic heart disease, - wrote A.I., Nesterov, - is so great that rheumatic granulomas are rightfully called ashoff-talalaevsky, "

Many prominent clinicians of the XX century. devoted themselves to studying the problems of rheumatic fever and rheumatic heart disease (RHD) (Botkin S.P., Davydovsky I.V., Nesterov A.I., Strukov A.I. and others). For the clinical and anatomical characteristics of rheumatic heart disease in children, the studies of M.A. Skvortsova. In 1944 T. Jones (Jones) presented the first classification of RL, which is used in an improved form to this day. However, when studying domestic literature, it was possible to establish that 5 years before the appearance of the work of T. Jones, the outstanding Soviet pediatrician A.A. Kissel described the 5 main criteria of T. Jones, calling them "absolute signs of rheumatism." He argued that “for rheumatism, the absolute signs are rheumatic nodules, circular erythema, chorea, and a special form of arthritis, which quickly passes from one joint to another. The presence of only one of these signs finally decides whether the child has rheumatism. Perhaps, a completely peculiar heart lesion in rheumatism should also be attributed to the absolute signs, since we do not observe such a clinical picture with heart damage in children from other causes. Damage to the heart of rheumatic origin is characterized by the constant progression of heart disease, and often the patient does not complain about anything. This feature almost never occurs in case of damage to the heart of another origin.

The discovery in 1958 by the French scientist J. Dass of the main histocompatibility system and the clinical development of the topic “Association of HLA c various diseases” turned out to be prerequisites for studying the relationship of HLA with rheumatic fever. In 1976 Academician A.I. Nesterov wrote that "modern concepts of rheumatism are devoid of something very important, intimate, probably embedded in the individual characteristics of the molecular structure of lymphocytes or the characteristics of an individual gene pool." This statement of the largest Russian scientist, a world-famous rheumatologist, turned out to be prophetic. Since 1978, a new direction in studying the mechanisms of predisposition to rheumatic fever has been emerging abroad and in our country.

Thanks to the work of the outstanding scientist and our teacher, Academician A.I. Nesterov, additions were developed to diagnostic criteria rheumatic fever, which increased their differential diagnostic significance. A deep study of the etiology, clinic and diagnosis of rheumatic fever allowed A.I. Nesterov to put forward the problem of an active pathological process and develop a classification of the degrees of activity of the rheumatic process, approved at the symposium of socialist countries in 1964 and which served as the basis for creating similar classifications for other rheumatic diseases. He wrote: “Each new classification is not a completely complete system of knowledge and experience, but only a key stage of scientific progress, which, as knowledge accumulates, will be replaced by a new stage that opens and explains new facts and new scientific and practical horizons.” Taking into account the etiological role of streptococcus in the development of rheumatic fever at the Institute of Rheumatism of the USSR Academy of Medical Sciences (GU "Institute of Rheumatology of the Russian Academy of Medical Sciences"), created by Academician A.I. Nesterov, developed an original method of bicillin-aspirin prevention of recurrence of the disease.

Established in different countries ideas about the essence of rheumatic fever and its clinical and anatomical forms gave rise to various designations of the disease in the historical aspect: “rheumatic fever” (rheumatic fever) of Anglo-Saxon authors, “acute articular rheumatism” (rhumatisme areiculaire aigu) or, less commonly, Buyo’s disease (maladie de Bouillaud) by French authors, rheumatic fever or acute rheumatic fever by German authors. It is now generally accepted to refer to the disease as rheumatic fever.

To date, acute rheumatic fever is one of the few rheumatic diseases whose etiology has been proven. Undoubtedly, this disease is caused by group A beta-hemolytic streptococcus (GABHS). According to the figurative expression of Academician A.I. Nesterov, "without streptococcus, there is neither rheumatism nor its relapses."

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Acute rheumatic fever (ARF) is a dangerous disease that mainly affects children or young people under 20 years of age. In Russia, recently, pathology has been diagnosed extremely rarely, mainly residents of Asia are affected by it.

As a result of infection with streptococcal infection in persons with a hereditary factor, an acute inflammatory process of connective tissues develops, which spreads to the heart, joints, nervous system and brain. Without timely treatment, this disease can cause severe complications.

Features of the disease

The disease develops against the background of acute tonsillitis, tonsillitis or scarlet fever caused by aggressive group A beta-hemolytic streptococci. This type of infection is extremely toxic and dangerous because it provokes the development of an autoimmune process, as a result of which immunity works against its own cells of the heart and blood vessels. This only happens if the body has a genetic predisposition to rheumatism.

According to statistics, the pathology is observed mainly in females and is transmitted genetically from relatives of the first line of kinship. Acute rheumatic fever is often referred to as a disease of social disadvantage. This is due to the fact that the predisposing factors are:

• living conditions in which a large number of young people live in one room (students);
• countries in which medical care is of a low level, there is no sanitary culture;
• poor nutrition and living conditions, low material level.

In the bulk of people after suffering a disease caused by streptococcus, strong immunity is developed. And in individuals who are genetically predisposed, there is no immune response, and with secondary infection, a complex autoimmune inflammatory process begins.

Streptococcus antigens, circulating with the bloodstream throughout the body, are deposited in the tissues and blood vessels of the heart - vascular system, causing inflammation due to high toxicity. This leads to the development of progressive rheumatism. If on early stage treatment does not begin, then an irreversible process of necrosis of cells and collagen fibers develops, which causes a severe form of sclerosis.

Disease classification

ORL is classified according to several indicators:

• depending on the phase of the disease;
• according to clinical indicators;
• according to the degree of involvement in the inflammatory process of various body systems.

Primary and recurrent rheumatic fever

The primary form of the disease begins suddenly, has pronounced symptoms and an active inflammatory process. If timely therapeutic assistance is provided, treatment can be quick and effective.

Re-infection as a result of hypothermia, stress causes a relapse and a progressive course of rheumatism.

Classification according to the manifestations of the disease

The disease can proceed with varying degrees of intensity:

1. acute form- has a sudden onset, an active process and polysyndromic lesions;
2. subacute degree- inflammation develops gradually over several months, has blurred symptoms, a process of moderate activity and a low effect of therapy;
3. protracted form- characterized by a long sluggish inflammatory process;
4. latent course- has no symptoms, is found in the diagnosis of heart disease;
5. recurrent rheumatic fever has an undulating clinical course, with phases of exacerbation and remission, damage to internal organs occurs quite quickly.

The severity of inflammation

The disease has different degrees of damage to internal organs:

1. heart disease may or may not develop, but the heart is involved in the inflammatory process, which is fraught with myocardiosclerosis and rheumatic heart disease;
2. joints, respiratory organs, kidneys, skin are involved in the inflammatory process, neurorheumatism may develop;
3. the clinical picture is characterized by polyarthritis, chorea, carditis, subcutaneous nodules and erythema annulare;
4. persistent circulatory disorders, causing heart failure.

serous membranes and internal organs are rarely affected, more often with the re-development of rheumatism. The joints and the cardiovascular system are mainly affected.

Causes of the disease

There are two main causes of rheumatic fever.

Aggression of beta-hemolytic streptococcus A - type

The main factor disease-causing, is a strain of streptococcal infection A - type. Most often this occurs against the background of transferred ENT - diseases:

• purulent tonsillitis;
• scarlet fever;
• pharyngitis.

This strain is highly contagious and toxic, as soon as pathogenic microorganisms invade the circulatory system, the work of the body's immune system is disrupted. As a result, a rheumatic attack of its own cells begins, affecting the joints, heart and other organs.

hereditary factor

Despite the high pathogenicity of the strain, not everyone is at risk of getting rheumatism. And only those who have a specific antigen in the body, thereby determining a hereditary predisposition to acute rheumatic fever.

Symptoms of acute rheumatic fever

As a rule, the first signs of fever occur 2 weeks after the infection. First, the patient's condition improves, the period of false recovery may be accompanied by sluggish symptoms in the form of weakness and slightly enlarged lymph nodes. It is at this moment that specific antibodies are synthesized and the disease develops.

The majority of children and adolescents in the acute period of the disease experience the following symptoms:

• a sharp increase in body temperature up to 40 0 ​​С;
• development of pain syndrome in the joints of different localization: pain can occur in the knees, elbows and in the area hip joints, constantly moving;
• periarticular tissues turn red and swell;
• there are signs of rheumatic heart disease: pain in the chest, arrhythmia, low blood pressure.

In young children, symptoms are more pronounced than in adolescents and adolescents. They have mild symptoms.

• body temperature does not exceed 38.5 0 С;
• pain in the joints is less pronounced, swelling and inflammation do not always accompany pain;
• symptoms of rheumatic heart disease are blurred.

Primary fever is manifested by vivid symptoms:

Skin rashes in the form of red dense nodules occur only in children, are localized on the chest, back, under the skin in the area of ​​​​the joints and disappear within a month.

How the disease is diagnosed

Due to the similar symptoms to other diseases, the diagnosis of ARF is often difficult. If signs of carditis are observed, first of all, to determine the diagnosis, it is carried out:

1. Echocardiogram in Doppler mode, which allows you to determine at what speed and in what direction the blood moves in the veins and arteries, as well as the pressure in the vessels. The study of the state of the coronary vessels and structural changes in the heart gives an idea of ​​the degree of damage to the valves and the inflammatory process of the heart membrane.
2. Electrocardiogram captures everything pathological changes heart rate, which indicates the state of the heart muscle.

A laboratory blood test is mandatory, the indicators of which give an idea of ​​the following:

• at increased speed erythrocyte sedimentation (ESR) and an increased amount of reactive protein, which characterizes inflammation in the liver, it can be concluded that acute inflammation develops in the body;
• in rheumatic fever, a blood test is performed for the presence of antibodies against streptococci (they are elevated).

In addition, a swab is taken from oral cavity for bacteriological examination for the presence of a hemolytic streptococcal agent. To exclude other heart diseases, it is also carried out differential diagnosis. Based on a comprehensive examination of the patient, the doctor prescribes treatment.

Treatment of acute rheumatic fever

The goal of treatment is to:

• eliminate the cause of the disease;
• normalize metabolic processes in the body and stabilize the work of damaged organs, as well as significantly increase immunity;
• affect the patient's condition by eliminating the symptoms.

Most patients are hospitalized, especially children. They require strict bed rest for 21 days and a dietary diet. Depending on the patient's condition, the doctor prescribes drug treatment and physiotherapy. In severe cases, surgery may be required.

Medical

For streptococcal infections, only antibiotics are used. These can be penicillin preparations, and in case of individual intolerance they are replaced with macrolides or lincosamides.

The first 10 days, antibiotics are used as injections, and then tablets are prescribed.

If carditis is diagnosed, apply hormone therapy using glucocorticosteroids. This is done under the strict supervision of a doctor.

For symptomatic treatment use the following drugs:

• - to eliminate pain and inflammation in the joints, the course of treatment can last up to 2 months;
• Digoxin - as a stimulant for the normalization of myocardial function;
• Asparkam - with dystrophic changes in the heart;
• Lasix - as a diuretic for swelling of tissues;
• Immunostimulants to improve the protective reactions of the body.

The duration of treatment and dosage is determined by the doctor. It depends on the condition and age of the patient.

Surgical intervention

Operative treatment is carried out only in case of severe heart disease. Then the attending physician decides on the need for surgical treatment. The patient may undergo plastic surgery or prosthetic heart valves.

Physiotherapy

Physiotherapy procedures are carried out in parallel with the main treatment:

• paraffin and mud applications;
• UHF heating;
• treatment with infrared rays;
• radon and oxygen baths.

At the stage of recovery, a course of therapeutic massage is prescribed, which should be carried out by a specialist.

Nutrition Features

Given that this disease activates allergic reactions due to metabolic disorders, it is necessary to introduce a dietary diet and follow a number of rules:

• limit the consumption of fast carbohydrates;
• exclude fatty;
• reduce the amount of salt in cooking;
• be sure to eat proteins and vegetable fats;
• the diet should be rich in vitamins and minerals;
• cooking method - boiling, stewing, baking, all ingredients must be soft;
• diet - fractional, at least 6 times a day, liquid - no more than 1 liter.

The patient's menu should be designed in such a way that the body receives all the necessary vitamins and minerals, the deficiency of which occurs during the period of illness.

What are the consequences of the disease and complications

With timely diagnosis and adequate therapy, the prognosis is usually positive, but some patients may experience serious complications:

• development of a chronic form of the disease, heart disease, mitral valve atrophy;
• in children in 10% of cases there is a prolapse or stenosis, heart failure;
• arrhythmia, tachycardia;
• risk of developing endocarditis.

Death is extremely rare, but the consequences can be serious.

Impact on immunity

The immune system consists of a complex of tissues, blood vessels, human organs, which provide the body's ability to resist diseases due to the secreted immune cells.

As a result of the high toxicity of group A beta-hemolytic streptococcus, specific antibodies are formed that destroy the body's immune cells and affect not only connective tissues, but also neurons. Thus, inflammation develops throughout the body in various organs, and the affected immune cells begin to destroy not hostile agents, but their own. As a result of the lesion, necrosis develops, and the proliferation of connective tissues begins, forming scars and causing irreversible processes that disrupt the function of the organ.

How does rheumatic fever progress in children?

Acute rheumatic fever in children is more severe than in adults and often has complications. Basically, the heart and joints suffer, irreversible processes develop, which in the future can cause disability. Children are more likely to develop heart disease, carditis and stenosis.

Treatment of adolescents is difficult because often there is an allergic reaction to medications that are necessary for the treatment of the disease. Incorrect acceptance or rejection medicines causes resistance of microorganisms to antibiotics, which is fraught with a chronic form of the disease and the occurrence of relapses. For this purpose, children who have previously had a fever should periodically take prophylactic courses of penicillin.

Rheumatic fever and pregnancy

According to statistics, women are more prone to rheumatism, so not a single representative of the weaker sex is immune from this disease, especially at a young age.

If infection occurs during pregnancy, doctors recommend interrupting it, as the consequences can be unpredictable for both the fetus and the mother.

Previous ARF may present with complications during pregnancy. An increasing load on the heart with an increase in the term can worsen the condition of the pregnant woman and cause pulmonary edema during childbirth. The greatest danger is valvular heart disease, which can develop during pregnancy.

In order to minimize the risks during gestation and delivery, pregnancy planning is necessary. As a rule, such women are C-section, and during the whole pregnancy they are observed in the hospital. Contraindication for pregnancy and childbirth is only the acute phase of the disease.

What preventive measures can be taken

Preventive measures should be started in healthy children. They are as follows:

• increased immunity - good nutrition, sports, hardening procedures;
• when infected bacterial infection it is necessary to carry out treatment until the complete recovery of the child;
• prevent children from being in a large crowd of peers, monitor the health of family members.

If the child has already been ill with acute rheumatic fever, the recommendations of doctors are as follows:

• constant supervision by a doctor;
• once every 21 days it is necessary to inject penicillin;
• treat all diseases in a timely manner.

In this case, preventive measures must be observed for 5 years, provided that there are no complications. If heart disease has developed, such patients are observed for life.

Acute rheumatic fever or rheumatism is inflammatory disease connective tissue caused by group A beta-hemolytic streptococcus in genetically predisposed individuals. Most often, children and young people from 7 to 20 years old get sick.

The term " rheumatism" was officially replaced by " acute rheumatic fever to emphasize that this is an acute inflammatory process that begins after a streptococcal infection (tonsillitis, pharyngitis, scarlet fever) and is its complication.

Cause of rheumatism

The trigger for the development of rheumatism is group A beta-hemolytic streptococcus. Streptococcal infection has a direct toxic effect on the heart and triggers an autoimmune process when the body produces antibodies against its own tissues, primarily the heart and cells of the vascular wall. But this can only happen in an organism genetically predisposed to rheumatic fever. Girls and women (up to 70%) and first-degree relatives get sick more often.

In economically developed countries, the incidence of rheumatism is negligible. Among the social conditions contributing to the occurrence of the disease include:

Crowding during living and learning;
- low level of sanitary culture and medical care;
- Poor material and living conditions, insufficient food.

Symptoms of rheumatism

In typical cases, the first attack of rheumatic fever begins 2-3 weeks after a streptococcal infection. Suddenly or gradually, against the background of general malaise, the body temperature rises to 37 degrees, the temperature quickly rises to 38-39 degrees. Temperature rises in rheumatism are accompanied by chills, sweating. There are signs of polyarthritis (inflammation of the joints): swelling, redness of the joints, pain at rest and during movement. Rheumatism affects large joints (knee, ankle, elbow, shoulder). Rheumatic polyarthritis is characterized by: symmetry (simultaneously affects both knees or both ankle joints), the sequence and volatility of the lesion (inflammation quickly passes from one joint to another). Complete reversibility of joint inflammation, restoration of joint function within 2 days after taking NSAIDs (aspirin).

The temperature increase in rheumatism lasts 2-5 days and normalizes when the arthritis subsides. Sometimes at the beginning of the disease, unstable rashes appear on the skin of the trunk and extremities. They look like pink rings - annular erythema. Rashes appear and disappear without leaving traces. A characteristic, for rheumatism, but extremely rare symptom (up to 3% of cases) is subcutaneous rheumatic nodules. They have a size from a grain to a pea, dense, painless, localized on the affected joints, the back of the head.

The main manifestation of rheumatism is heart damage - carditis, the severity of which depends on the outcome of rheumatic fever. There are prolonged stabbing, aching pains in the region of the heart, shortness of breath with little physical exertion, palpitations, and disturbances in the work of the heart. The outcome of carditis in 25% of cases is the formation of heart disease.

Rheumatic chorea is a manifestation of damage to the nervous system. There are chaotic involuntary twitching of the limbs and mimic muscles, grimacing, slurring of speech, impaired handwriting, inability to hold a spoon and fork while eating. Symptoms completely disappear during sleep. Chorea with rheumatism lasts 2-3 months.

The duration of rheumatic fever averages 6-12 weeks. This is the period during which the acute inflammatory process goes through all stages. Rheumatic fever lasting more than 6 months is considered to be protracted. A new episode of rheumatism often occurs in the first 5 years after the first attack, and over time, its likelihood decreases. The emergence of new attacks depends on the occurrence of repeated streptococcal infections.

Diagnosis of rheumatism.

1. Complete blood count - signs of inflammation (leukocytosis - an increase in the number of leukocytes and accelerated ESR).
2. Biochemical analysis blood - an increase in the content of fibrinogen, C-reactive protein - indicators of the acute phase of inflammation.
3. Serological studies detect antistreptococcal antibodies in high titers.
4. Bacteriological examination: detection of group A beta-hemolytic streptococcus in throat swabs.
5. Electrocardiography - reveals violations of the heart rhythm and conduction, an increase (hypertrophy) of the heart.
6. Doppler echocardiography reveals signs of damage to the heart valves, pumping function and myocardial contractility, the presence of pericarditis.

Diagnosis of rheumatism is undoubted in the presence of a formed heart disease. In the absence of heart disease, the following criteria are used:

The presence of 2 major criteria or 1 major and 2 minor criteria, combined with evidence of a previous streptococcal infection, suggests a high likelihood of rheumatism.

Treatment of rheumatism.

Success in the treatment of rheumatic fever and the prevention of heart disease development is associated with early detection of the disease and individualized treatment. Therefore, it is necessary to contact your doctor (family doctor, pediatrician, therapist) when the first signs of inflammation appear. Treatment of rheumatic fever is carried out in a hospital. If carditis is suspected, bed rest is mandatory. In rheumatism, a diet rich in vitamins and protein is prescribed, with restriction of salt and carbohydrates. Etiotropic (antistreptococcal) treatment of rheumatism is carried out - antibiotics are prescribed according to the developed schemes.

Anti-inflammatory treatment - hormones (glucocorticoids - prednisolone) and NSAIDs (non-specific anti-inflammatory drugs - aspirin, diclofenac), depending on the degree of activity of the process.

The next stage - patients undergo rehabilitation (restorative) treatment in a specialized center (sanatorium).

The third stage is dispensary observation by a family doctor (pediatrician, therapist). Every year, the patient is examined by a rheumatologist, an ENT doctor, and laboratory research, ECG, echocardiography.

Complications of rheumatism.

The main complications include:

1. Formation of heart disease.
2. Development of congestive heart failure.
3. Violation of the heart rhythm.
4. Thromboembolism.
5. The occurrence of infective endocarditis (inflammation of the inner lining of the heart).

Chronic rheumatic heart disease (heart disease) is a disease in which the valves of the heart, its partitions are affected, leading to dysfunction of the heart, the formation of heart failure. Occurs after rheumatic carditis. The progression of heart disease can occur under the influence of repeated attacks of rheumatic fever. All patients with heart defects are consulted by cardiac surgeons and are subject to referral for surgical treatment to specialized clinics.

Primary prevention of rheumatism is the prevention of the onset of rheumatic fever in a healthy child. It includes measures aimed at increasing immunity (good nutrition, hardening, physical education), prevention of streptococcal infection (improvement of people who surround the child, elimination of crowding), timely and complete treatment streptococcal diseases.

Secondary prevention of rheumatism is the prevention of recurrence and progression of rheumatic fever that has already occurred. It includes: dispensary observation, timely treatment of foci of chronic infection, administration of benzathine benzylpenicillin intramuscularly 1 time in 3 weeks. The duration of secondary prevention for each patient is set strictly individually, but not less than 5 years after the last attack, for patients who have had rheumatic fever without carditis and for life for patients with a formed heart disease.

Consultation of a doctor on the topic of rheumatism:

Question: How is the treatment and prevention of rheumatism in pregnant women carried out?
Answer: The occurrence of acute rheumatic fever in pregnant women is extremely rare, but if a disease occurs, a woman must be urgently hospitalized in the therapeutic department of a hospital or in a maternity hospital specialized in cardiovascular pathology. Secondary prophylaxis with penicillin in pregnant women who have had rheumatic fever is necessary, especially in the first trimester of pregnancy, when the likelihood of an exacerbation of the disease is high.

Therapist Vostrenkova I.N.

There are no strictly specific reasons, there is a predisposition of the anatomy and physiology of the joint itself or factors leading to inflammation itself:

• Connective tissue diseases of an autoimmune nature - psoriasis, rheumatism, systemic lupus erythematosus.
• Metabolic disorders - diabetes mellitus.
• Water-salt imbalance - gout.
• Diseases of a general nature, in which the joint is affected a second time - tuberculosis, syphilis, gonorrhea, sepsis.
• Occupational hazard, due to the need for static tension of the elbow joint - accountants, chess players, scientists, writers, engineers, truck drivers, engravers and jewelers, dental technicians. Work associated with physical labor - construction workers and agricultural workers.
• The consequences of sports amateur or professional activities, fraught with constant regular microtraumas - tennis, volleyball, basketball, hockey.
• An untreated or undiagnosed unnoticed joint injury that ended in mini-scarring, but with impaired tissue physiology.
• Infection from the body by contact, with open injuries; hematogenous way - with blood, in a septic condition; by the lymphogenous route - with chronic catarrhal viral diseases of the genitourinary or respiratory systems.
• Intentional or household, acute or chronic injury, ending with hemarthrosis and secondary inflammation - dislocations, subluxations, fractures, damage to muscles and tendons.
• Oncological diseases of a malignant or benign nature.

Causes

In each case, the causes of the inflammatory process in the elbow joint may be different, but the most common of all are the following:

• consequences of professional activity. This disease is observed when the labor duties of a person are associated with excessive loads performed by the elbow joint, or if the hands are constantly and for a long time in an uncomfortable position. An example would be, for example, professions such as musicians or drivers;
• injury. In most cases, the elbow area suffers from a direct blow or bruise. The disease is also observed after sprains. The result of all unsuccessful falls and bruises are often fractures, blows, torn ligaments, bruises, dislocations, etc.;
• excessive loads on the elbow area. In most cases, this cause of inflammation is observed in athletes who are constantly involved in weightlifting or enhanced exercise on weight machines;
• infection. Most often, the infection spreads throughout the body from some superficial injury and reaches the muscles of the elbow.

Treatment

Only a qualified doctor can diagnose the disease. To establish an accurate diagnosis, a blood test is taken from the patient, x-rays are taken of the damaged area, if there is liquid in the elbow bag, then it is also taken for analysis.

In each case, the patient is assigned mandatory rest, the injured hand must be in complete immobility. If necessary, various dressings, scarves, tourniquets and dressings are used for this.

Drug treatment is always prescribed in each case only individually. To eliminate the infectious process, the patient is prescribed a course of anti-inflammatory drugs, antibiotics and special physiotherapy (electrophoresis, UHF, heat therapy). To relieve the pain and edematous process, non-steroidal anti-inflammatory drugs are prescribed - Ortofen, Movalis. But in difficult cases, the doctor can also prescribe a hormonal anti-inflammatory drug - Diprospan.

External treatment is carried out with ointments: Fastum, Relif, Vishnevsky ointment and others.

In that unpleasant case, if the patient has suppuration in the elbow joint, then he is prescribed a surgical operation, during which the joint cavity is cleaned and washed. If necessary, a special drainage is placed to remove excess fluid.

Alternative treatment of inflammation of the elbow joint is also allowed, but this therapy should be carefully discussed with the attending doctor.

Symptoms

In the case when the patient begins inflammation of the elbow joint, the symptoms this disease may appear in different ways. When internal inflammation or bursitis is observed, the symptoms are as follows:

• sharp pain in the elbow area;
• redness skin in the area of ​​pain;
• swelling and swelling of the elbow;
• the formation of a soft seal in the painful part, which is able to change its shape with light pressure.

With internal inflammation of the bag of the elbow joint, a fluid is produced that makes it difficult to move the hand. The person feels lack of movement and muscle resistance.

In the case when the patient suffers from external inflammation (epicondylitis), then the symptoms are different:

• crackling sounds in the elbow area when it moves;
• aching pain, which is aggravated by the movement of the ligaments. As a rule, if the patient is at rest and does not move his hand, then pain is not present;
• there is swelling in the area of ​​the affected elbow.

Together with all the above signs, a person may feel nausea, weakness of the body, headache, increased body temperature.

Cervical osteochondrosis

Degenerative-dystrophic changes in the cervical spine lead to pain in the elbow.

The reason is that the destroyed tissues of the intervertebral discs infringe on the nerve, the pain radiates to the arm and elbow joint.

With cervical osteochondrosis, pain in the elbow is a concomitant symptom that worsens at night. The pain syndrome is intense, it is problematic to bend the arm or take it behind the back. In addition, there is numbness of the limb.

Treatment is aimed at eliminating the underlying disease - taking NSAIDs, chondroprotectors, muscle relaxants, vasodilators. Mandatory physiotherapy and exercise therapy.

Physiotherapy

Physiotherapy treatment is aimed at relieving pain and inflammation, as well as muscle tension. After the end of the acute period, apply:

• Paraffin-ozocerite applications;
• Ultraphonophoresis of hydrocortisone;
• Local cryotherapy;
• Extracorporeal shock wave therapy.

In the acute period of epocondylitis, for pain relief and inflammation relief, doctors prescribe high-intensity pulsed magnetotherapy, infrared laser radiation and percutaneous electroanalgesia with the Eliman-401 apparatus.

Tennis elbow disease or lateral (external) epicondylitis of the elbow joint is a common disease of the musculoskeletal system. The monotonous repetition of the same movements, during which the elbow joint is actively involved and there is a serious load on the forearm and hand, causes inflammation at the site of attachment of these muscles to the lateral (outer) epicondyle. Tennis players do this all the time. As a rule, the leading hand suffers. Therefore, the name tennis elbow syndrome was assigned to the disease. However, it also occurs in ordinary people.

To prevent this type of injury, preventive purposes kinesiology taping of a tennis player's elbow is used.

In the area of ​​frequent damage:

• People, professional activity which involves the repeated execution of monotonous hand movements (painters, artists, doctors, builders, drivers, musicians, cooks, etc.);
• People aged 40-60 years;
• Athletes (tennis players, weightlifters, wrestlers, boxers).

Causes of the disease:

• Excessive tension of the muscles of the hand, leading to regular microtrauma of the muscles and tendons and, as a result, to the development of inflammation;
• Age-related dystrophic processes in the muscle and tendon;
• Genetic weakness of the ligamentous apparatus;
• Other diseases of the musculoskeletal system;

Sometimes it happens that the disease appears without any apparent reason (sudden epicondylitis) or after a single intense overload of the forearm. Often the disease becomes chronic, as it proceeds quite easily and many people simply do not go to the hospital.

How is elbow bursitis treated?

Bursitis is considered occupational disease athletes. With bursitis, the periarticular capsule becomes inflamed from injury or microdamage due to prolonged stress on the joint.

Bursitis develops as an inflammation of the elbow joint in the presence of:

• sports or domestic injuries (bruises, sprains, fractures);
• long-term presence of the elbow and hand in the same forced position (rocking a small child, playing musical instruments);
• mechanical impact on the hands;

This inflammation does not affect such a joint as the maxillotemporal. It is typical for the elbow and shoulder. Bursitis is not always immediately recognizable, as it may first appear as a normal edema. Gradually accumulated inside the synovial fluid begins to interfere with movements. Then there is pain, local fever, redness of the skin around the site of inflammation.

According to the form of the course of the disease, serous bursitis and purulent are distinguished. To cure bursitis, you need to go through a difficult diagnostic procedure in the form of a puncture of the joint. The opinion that bursitis can be cured by folk methods is erroneous. Folk preparations reduce swelling and inflammation, relieve pain in the affected area. But the disease can be completely cured not by folk, but only by therapeutic means or by surgery.

Forms of the disease and characteristic symptoms

The acute form of bursitis is characterized by a sudden onset of the inflammatory process, which manifests itself the day after the injury. In the area of ​​the top of the elbow there is a slight swelling, soft to the touch consistency. Edema is painful, which manifests itself both during palpation of the affected area, and at rest. Inflammation is accompanied by general poor health, weakness and fever. Day after day, for one week, the edema grows, giving a person tangible discomfort and restricting movement in the joint. Such a patient should immediately seek medical help and undergo a course of treatment prescribed by a doctor in order to avoid the transition of the disease to a relapsing form, when even a minor factor leads to a new round of inflammation after an apparent recovery.

A feature of the chronic form is not a sharp, but the gradual development of edema of small sizes.

A person does not immediately pay attention to the unusual condition of the elbow, so the disease can last for years in a sluggish form. The long course of the inflammatory process negatively affects the joint itself, causing pathological changes in it.

Chronic bursitis is dangerous for the health of the joint

If an infection was introduced into the synovial sac (most often from the outside as a result of a bite or cut), then the pathogen begins to multiply inside the periarticular pocket, causing first serous and later purulent inflammation. It is accompanied by a sharp rise in temperature, up to the heat. The place of edema is hot to the touch. Septic, or infectious, bursitis is dangerous possible development necrosis of the walls of the articular bag and infection in the general bloodstream.

Purulent bursitis - an advanced case of septic inflammation of the synovial bag

Thus, common symptoms of bursitis include:

1. Edema: This is usually the first sign that the patient notices. The skin on the back of the elbow may be loose, so swelling may not be noticed at first. In some cases, the edema grows rapidly and is immediately visible. The tumor may be the size of a golf ball at the tip of the elbow.
2. Pain: as the bursa is stretched, the pain in the elbow increases, especially when flexing. As a rule, with extension, the pain decreases or is absent. But there is a category of people with ulnar bursitis who do not experience pain in principle, regardless of whether their arm is bent or straightened.
3. Redness or pronounced warmth on the back of the elbow: may indicate an infection.
4. Sensitivity in and around the elbow.
5. Pus: In advanced cases of infectious inflammation, the presence of yellow or white, thick, cloudy exudate in the infected elbow is characteristic.

Treatment of inflammation of the elbow joint

Effective treatment of the elbow joint, both traditional and folk remedies

But it is important to remember that self-medication can cause serious harm to your health. To avoid this, before treating the disease with classical or folk remedies, you should immediately consult a doctor, at its first manifestations.

Treatment with traditional means for elbow disease largely depends on the course and cause of the disease.

The main traditional methods of treatment of bursitis and epicondylitis:

• alternating warm and cold compresses;
• tight bandage;
• antibiotic therapy (purulent inflammation of the articular bag);
• painkillers;
• non-steroidal anti-inflammatory drugs;
• compresses, ointments (with traumatic bursitis);
• physiotherapy treatment.

Also, if necessary, can be used: surgical treatment, or intra-articular hormonal injections. Most often, such methods are used for complicated bursitis, when suppuration occurs in the synovial bag.

Treatment of bursitis and epicondylitis with folk remedies includes:

• compresses from potatoes or cabbage;
• compresses with decoctions of anti-inflammatory herbs (calendula, plantain, etc.);
• vodka compresses with Vishnevsky's ointment;
• lotions from propolis tincture;
• intake of celery infusion.

Inflammation of the elbow joint, the treatment of which, possibly, with folk remedies, should not be acute or infectious. Otherwise, complex therapy is used.

It should be remembered that the treatment of folk methods of bursitis, without consulting a doctor and careful diagnosis, is unacceptable. Otherwise, the disease can become complicated and go into a form that requires surgical treatment and drainage.

All the detailed manipulations of the hands are performed by a small but complex elbow joint. It consists of the articular heads of the three bones of the upper limb - the diaphysis of the humerus and the epiphyses of the ulna and radius, which are surrounded by the articular capsule and lined with a synovial membrane. The cells of this tissue secrete a special fluid to smooth movements in the joint, and cushioning during sudden movements and heavy lifting.

Inflammation is classified according to several parameters:

1. By type of pathogen: specific (Koch's wand, gonococcus, treponema) and non-specific (streptococcal and staphylococcal infection, viral infection).
2. According to the type of flow: acute, which, in turn, is detailed according to the type of exudate accumulating in the focus of inflammation: serous, hemorrhagic and purulent; subacute and chronic - fibrous.
3. By localization:
   • arthritis - affecting all elements of the joint without irreversible changes;
   • arthrosis - degeneration, partial or complete destruction of the articular complex;
   • the defeat of the capsule is called bursitis, from the Latin word "bursa" - a bag;
   • the pathological process in the muscles and tendons surrounding the elbow joint is called epicondylitis.

Causes of bursitis and its treatment video

Most patients recover safely from bursitis. The best prevention is to lead a healthy lifestyle with moderate exercise and the use of protective elbow pads as needed.

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Diseases and their symptoms.

Symptoms are usually precisely localized in the joint area: pain of a different nature, swelling, induration (infiltration), redness, dysfunction in a different range, reddening of the skin of the elbow.

Bursitis.

Bursitis is manifested by various symptoms, depending on the aggression and severity of inflammation. From subtle swelling and mild pain during extension, to a significant increase in the joint, redness, sharp throbbing and arching pain, suffering from joint function. With suppuration or a sharp exacerbation, a violation of the general condition is possible - subfebrile temperature, chills, weakness, headaches and loss of appetite. In the case of purulent inflammation, there is a danger of the transition of the articular abscess to the phlegmon of the hand, and damage to the muscles and bones directly - myositis and osteomyelitis, with the occurrence of fistulas and necrotic tissue fusion. Chronic bursitis, on the other hand, is characterized by tissue compaction, the formation of nodules and limitation of function during exercise.

Epicondylitis.

Epicondylitis is external and internal, and the symptoms will correspond to localization: disturbance and pain during extension and flexion. Often the lesion is asymmetrical - in accordance with the working hand, which is in a constant long-term load. Also distinguish: lateral and medial form. Lateral - called the "tennis player's hand", characteristic of the age after 30 years, occurs with certain complex-directed movements, inherent in tennis players, lumberjacks and painters. The medial is called "golfer's elbow" when actively used and movements that strain the forearm.

Arthritis.

Arthritis is characterized by early dysfunction, all signs of inflammation. Depending on the stage, the whole palette of pain is sharp, cutting, dull and aching. Severe stiffness and stiffness of the joint, to complete immobility and inability to move the arm at the elbow. Inflammatory painful contracture of the muscular-ligamentous apparatus. With suppuration, fluctuation and cyanosis of the tissues surrounding the joint are observed.

Complications of bursitis

Complications of bursitis include:

• secondary infection, which may develop after aspiration or steroid injection;
• secondary septic (infectious) arthritis;
• sepsis (blood poisoning) and osteomyelitis (purulent-necrotic process in the bones) sometimes occur as a result of severe septic bursitis, especially with a late diagnosis;
• fistulas (a pathological opening in the body) may develop after spontaneous rupture or surgical drainage of the periarticular sac;
• recurrence of bursitis is more likely with a recurrence of the injury that caused the inflammation.

Chronic pain in the joint and the associated decrease in its functionality can be caused by the inflammatory process in the persistent course of bursitis.

Causes and symptoms of development

Elbow diseases can be recognized by a variety of causes. This disease occurs in people of different age categories, regardless of gender. Everyone can be exposed to risk factors.

Causes

The causes of the disease of the ulnar structure can be:

• untreated injuries;
• sprain;
• excessive loads of a permanent nature;
• prolonged support on the elbow;
• hypothermia;
• transferred infectious diseases;
• heredity.

Main symptoms

Symptoms vary depending on the type of disease. Whereas bursitis is inflammation of the internal structures of the elbow structure (bursae), epicondylitis is inflammation of the external structures of the elbow joint.

The main symptoms of inflammation of the articular bag:

• swelling of the joint capsule (soft elastic swelling of a rounded shape);
• difficulty in movement;
• pain during flexion and extension of the arm;
• crunching when moving;
• local, and sometimes a general increase in temperature.

The main symptoms of epicondylitis:

• pain when turning the forearm, as well as rotational movements;
• sharp intense pain on palpation;
• the pain is localized in the affected area.

Treatment how to do it right

Immobilization and preparations

The treatment regimen is determined by the doctor. Self-medication is dangerous. In complex injuries, it is recommended to immobilize the limb by applying a fixator. If there are inflammatory processes in the elbow joint, the arm should also be rested. For infections caused by bacteria, antibiotic therapy is prescribed. Severe pain can be removed by an injection of Novocaine. It is also recommended to use the following anti-inflammatory and analgesic tablets and liniments:

The drug will eliminate pain and relieve inflammation.

• "Voltaren";
• "Diclofenac";
• "Dolobene";
• "Dolgit";
• "Nimedar";
• "Fastum";
• "Indovazin";
• "Ibuprofen";
• "Analgin".

Physiotherapy

Physiotherapy treatment of the elbow muscle and other tissues includes procedures such as:

• magnetotherapy;
• laser therapy;
• infrared irradiation;
• electrophoresis;
• diadynamic therapy;
• thermal wraps with ozocerite or paraffin;
• phonophoresis;
• shock wave therapy of the elbow joint;
• cryotherapy.

Treatment with folk methods

The tool has anti-inflammatory properties.

1. Take 50 g of propolis and vegetable oil.
2. Steam the ingredients in a water bath until a uniform consistency.
3. Cool down.
4. Lubricate the elbow joint, tie on top with polyethylene and a warm cloth.

For oral administration, a tincture of cinquefoil is used, prepared as follows:

1. Take a few crushed plant roots.
2. Add 0.5 l of vodka.
3. Insist 21 days.
4. Take 10 ml 3 r. per day.

Also useful are decoctions and infusions of elecampane, oak or willow bark, birch leaves and buds. Warm baths with a decoction of pine needles or the addition of essential oils with lavender extract. It should be remembered that the folk method can be treated as an adjuvant, but not replace traditional treatment.

Acute rheumatic fever is one of the most severe complications (synonymous names for the pathology are rheumatic heart disease, Buino-Sokolsky's disease).

This disease is manifested by inflammatory damage to the connective tissue fibers and is characterized by lesions predominantly of the heart and articular tissues (lesions of the central nervous system and skin on this moment rarely recorded).

It should be noted that the likelihood of developing the disease and the severity of its course largely depend on the presence of predispositions to the development of streptococcal infections. Also, the disease is 2.5 times more common in women.

Acute rheumatic fevers are one of the most common causes of hospitalization of patients under the age of twenty-four in cardiology departments. The most common acute rheumatic fever develops in patients from seven to fifteen years. In older patients, repeated attacks of fevers of rheumatic origin and chronic pathologies of the heart valves are more often recorded.

Attention. It should be noted that acquired heart defects, often resulting from acute rheumatic fever (ARF), are the leading causes of deaths in cardiac patients under the age of thirty-five.

For reference. Acute rheumatic fever is a post-infectious complication of streptococcal tonsillitis or pharyngitis, manifested as systemic inflammatory lesions of connective tissue fibers.

At the same time, ARF affects mainly the heart (carditis) and articular tissues (polyarthritis). Less common is the development of rheumatic chorea (damage to the tissues of the central nervous system) and annular erythema or rheumatic nodes (rheumatic lesions of the skin).

The development of ARF symptoms is a consequence of the development of autoimmune responses to antigens of streptococcal genesis, similar to the autoantigenic structures of the affected cells of the body.

Acute rheumatic fever - causes

The cause of the development of this disease is streptococci of beta-hemolytic types from group A.

For reference. At the same time, it must be taken into account that not all strains of streptococci are capable of leading to the development of ARF. Most often, ARF develops after suffering streptococcal diseases (tonsillitis, pharyngitis, etc.).

Streptococcal strains that cause streptococcal pyoderma of the impetigo type are unable to lead to the development of acute rheumatic fevers.

Usually, acute rheumatic fever in children is recorded much more often than in adults.

The symptoms of ARF have been described since ancient times, however, earlier this disease proceeded, as a rule, with the development of chorea. Modern acute rheumatic fever occurs mainly with:

• asymptomatic manifestations;
• a decrease in the incidence of severe lesions of the heart valves;
• isolated cases of damage to the central nervous system;
• low incidence of protracted and latent cases of the disease;
• an increase in the incidence of the disease among patients older than twenty years.

Risk factors for the formation of ARF are:

• the age of the patient is from five to twenty years;
• the presence of hereditary predispositions to the occurrence of diseases of streptococcal origin;
• living in areas with low temperatures and high levels of humidity;
• the presence of chronic foci of infection of streptococcal origin or the frequent development of acute infections;
• the presence of congenital pathologies of the cardiovascular system or autoimmune pathologies, accompanied by a systemic lesion of connective tissue fibers;
• burdened family history (frequent streptococcal infections in close relatives, pathologies of the cardiovascular system in relatives, family cases of acute rheumatic fevers, etc.);
• prematurity (in small and premature children, ARF is recorded more often in the future);
• the presence of carriage of B-lymphocyte alloantigens;
• the patient has the 2nd or 3rd blood group;
• the patient has high levels of neopretins and antibodies to cardiolipins;
• living in economically unfavorable regions;
• poor nutrition, beriberi, exhaustion;
• chronic lack of sleep and overwork;
• alcoholism or drug use, etc.

It should also be emphasized that due to the irrationally conducted antibiotic therapy and a high frequency of self-treatment, there was an increase in the number of antibiotic-resistant strains of beta-hemolytic streptococci.

Acute rheumatic fever - etiology

ARF develop after suffering diseases of streptococcal etiology. In most patients with ARF, in the most acute phases of the disease, high titers of antibodies to streptococcal agents are detected in the blood.

It should be noted that acceptance antibacterial agents with a high level of antistreptococcal activity helps prevent the development of repeated attacks of rheumatic fever.

In children in the neonatal period and patients under four years of age, infections of streptococcal etiology are rarely recorded.

Attention! The peak incidence is observed among patients from seven to fifteen years.

The transmission of infection of streptococcal origin is carried out by airborne droplets. The contact-household transmission mechanism (common household items, toys) is less commonly implemented.

Patients with acute streptococcal infections are the main source of infectious agents; less commonly, infection occurs from healthy carriers of streptococcal infections. The risk of infection from a healthy carrier is more often realized in people living with the carrier in the same apartment.