Active and inactive rheumatism: what are the features of these phases of the disease? What is rheumatism

Rheumatism is an infectious-allergic disease (localization of inflammation - in the joints (arthritis) and in the heart (carditis)), in which there is a lesion connective tissue.

Causes of rheumatism: due to streptococcal infection (as an inflammatory response to infection); malnutrition; hypothermia; decreased immunity; heredity (genetic predisposition of the organism).

Rheumatism can occur one to two weeks after suffering a sore throat, scarlet fever, otitis media, erysipelas of the skin, exacerbations of chronic pharyngitis, tonsillitis.

With rheumatism, large joints are more often affected: knee, elbow, shoulder, ankle, but smaller ones can also be involved in the pathological process: wrist, hands. Especially often the disease affects joints that have previously been damaged or subjected to excessive loads(according to the type of activity or sports training).

Symptoms of rheumatism.

Symptoms of rheumatism are very different and are determined by which organs are affected by inflammation.

Symptoms of rheumatism appear 1-2 weeks after an acute streptococcal infection. Early symptoms include pain and stiffness of muscles and joints, redness and swelling of the joints (elbows, knees, ankles (rheumatic arthritis), palpitations caused by inflammation of the heart (carditis), uncontrollable muscle twitches (Sydenham's chorea), rash (erythema annulare), and mild nodes (nodules) under the skin.

Symptoms of acute rheumatism: increased body temperature sometimes up to 40 degrees, increased heart rate, chills, excessive sweating, loss of strength, swollen and painful joints. Larger and more heavily used joints are the first to suffer. Further, the inflammation spreads to the remaining joints, often symmetrically. The joints are very swollen, reddened, hot to the touch, with pressure and movement pain is felt. Usually, the inflammatory process does not lead to stable changes in the joints. The pulse is frequent, arrhythmic, there is pain in the chest, dilatation (expansion) of the heart, sometimes a pericardial friction rub is heard - this indicates heart damage.

Sometimes the symptoms of rheumatism of the joints develop imperceptibly. The body temperature rises slightly, up to 37.1–37.5°C, the pain is not pronounced, it passes quickly, the swelling is small.

Inflammation of the heart (carditis) often begins at the same time as joint pain and fever. At first, inflammation of the heart does not manifest itself with any symptoms or is accompanied by mild fatigue. Inflammation of the heart resolves gradually, usually within 5 months. However, sometimes the valves are irreversibly damaged, and rheumatic heart disease occurs. Typically, the valve between the left atrium and the left ventricle (mitral valve) is damaged. Damage to the valve is accompanied by the appearance of characteristic heart murmurs, which allow the doctor to diagnose rheumatism. Later, usually in middle age, damage can lead to heart failure and atrial fibrillation, an abnormal heart rhythm.

Rheumatism in children occurs in a milder form or chronic, without any special symptoms. Are celebrated general malaise, rapid pulse and pain in the joints, pain is not felt when moving. If there are no signs of heart damage, then the disease rarely ends in death, although with the development of carditis average duration life of the diseased in the future is significantly reduced.

Rheumatism classification:

Active phase of the disease (III degree - high activity, II - moderate, I - minimal activity);

- inactive phase of the disease.

The course of the disease can be: acute, subacute, protracted, continuously relapsing and latent.

Rheumatism manifests itself in 5 syndromes:

Rheumocarditis (cardiac form) - inflammatory damage to the heart with involvement in the process of all membranes of the heart, but primarily the myocardium.

Symptoms: weakness, fatigue, sweating, loss of appetite; pain in the region of the heart of a pulling, stabbing character; temperature rise - more than 38 ° C;

Tachycardia.

Rheumatic polyarthritis (articular form) - inflammatory lesions of the joints, with changes characteristic of rheumatism.

Symptoms: fever, sweating, rapidly increasing joint pain. The joints are swollen, exudate can accumulate in them. Characterized by the symmetry of the lesions of the joints and volatility. Benign course of arthritis, joint deformity does not remain.

Rheumatic chorea (St. Vitus dance) - a pathological process characterized by the manifestation of vasculitis of small cerebral vessels.

Symptoms: restlessness, activity; violation of handwriting, the inability to hold small objects (cutlery), muscle weakness, uncoordinated movements, swallowing, physiological functions are disturbed. Symptoms disappear during sleep. A change in the mental state of the patient: aggressiveness, selfishness, emotional instability appear, or, on the contrary, passivity, absent-mindedness, increased fatigue.

Skin form of rheumatism. Relate:

- annular erythema - pale pink, barely noticeable rashes in the form of a thin annular rim;

- rheumatic nodules - dense, inactive, painless formations located in subcutaneous tissue, articular bags, fascia, aponeuroses.

Rheumatic pleurisy.

Symptoms: pain in the chest during breathing, aggravated by inhalation;

temperature rise; unproductive cough; dyspnea; on auscultation, a pleural rub is heard.

Treatment of rheumatism.

Treatment of rheumatism is aimed at: the destruction of streptococcal infection and its recurrence; reduction of inflammation; limitation of physical activity, which can worsen the condition of inflamed tissues.

- follow a well-chosen diet. Food should be varied, rich in vitamins, proteins, phospholipids.

- strengthen immunity.

- avoid hypothermia.

- engage in exercise therapy ( physical therapy) - only under the supervision and with the permission of a doctor.

With active rheumatism or symptoms severe insufficiency blood circulation must be observed bed rest. The motor mode expands as the activity of the rheumatic process subsides or the circulatory insufficiency decreases. This usually takes about 2 weeks.

Glucocorticoid hormones, voltaren or indomethacin, quinoline substances are used.

Outside the period of exacerbation, a sanatorium treatment is quite likely.

With severe inflammation of the heart tissue, corticosteroids (hormonal drugs), such as prednisone, are prescribed.

At active phase rheumatism, ascorbic acid is prescribed up to 1 g per day, as the activity decreases, the dose is reduced by half.

Folk methods and remedies for the treatment of rheumatism:

- infusion of wormwood: 1 tbsp. 300 ml of boiling water is poured over a spoonful of wormwood and infused in a thermos for 2 hours, filtered. It is used as an external anesthetic for rheumatism, neuralgia and lumbago.

- a bag of hot coarse salt or sand is used to warm up diseased joints.

- infusion of red clover grass for bathing: 50 g of chopped dry red clover grass pour 1 liter of boiling water. Infuse for 2 hours, then strain and pour into the bath. Take a bath at night. Course of treatment: 12–14 baths.

- 200 g of salt are mixed with 100 g of dry mustard, kerosene is added to them - until a creamy mass is obtained. At night, this ointment is rubbed into painful places.

Tincture of lilac flowers: the flowers are poured into a 0.5 liter bottle to the top, then poured with 40% alcohol. Insist in a dark place for 21 days, then filter. Take 30 drops 3 times a day before meals for 3 months.

- infusion of birch leaves: 1 tbsp. a spoonful of dry birch leaves is poured with 1 cup of boiling water, insisted for 6 hours, then filtered. Take ½ cup 2-3 times a day.

- decoction of birch buds: pour 5 g of birch buds with 1 cup of boiling water, boil for 15 minutes on low heat, then leave for 1 hour, strain. Take ¼ cup 4 times a day 1 hour after meals.

- paraffin applications: paraffin is melted to a temperature of 60-65 ° C. The gauze folded in 5-6 layers is lowered into paraffin and applied to the affected joints. The course of treatment is 10-20 procedures.

- include dogwood berries in the diet - as a tonic and tonic.

- infusion of red clover: 20 g of dried clover inflorescences pour 200 ml of boiling water and leave for an hour. Take 2 tbsp. spoons 3 times a day in the treatment of chronic rheumatism.

- application of propolis: for rheumatic pains in the limbs, a preheated propolis cake is applied to the sore spot, wrapped in a warm scarf and kept all night.

- infusion of coniferous dvukoloskovy: 1 tbsp. brew a spoonful of dry grass with 1 cup of boiling water. Leave for 10 minutes, strain. Take 1 tbsp. spoon in the morning and evening before meals.

- therapeutic and prophylactic baths with horseradish roots: grind 70 g of horseradish roots and leaves and put in a gauze bag and dip in a bath with a water temperature of up to 40 ° C. Take a bath at night. The procedure time is 10 minutes.

- daily on an empty stomach drink lemon juice from one or half a lemon, diluted with hot water.

- infusion of raspberries: pour 30 g of raspberries into 200 ml of boiling water. Insist 20 minutes. Drink at night as a diaphoretic 2 cups in 1 dose in the treatment of chronic rheumatism.

- a decoction of corn stigmas: pour 1 teaspoon of a medicinal plant with 1 glass of water and cook over low heat for 10 minutes. Take 2-3 glasses daily for 6-8 weeks.

- infusion of black currant leaves: 12 - 15 currant leaves pour 0.5 liters of boiling water. Insist 15 minutes. Take (on filtering) 0.5 cup 4-5 times a day.

- infusion of garlic: pour 40 g of chopped garlic cloves into 100 ml of vodka. Infuse in a closed vessel in a dark place with room temperature, shaking occasionally, 7-10 days, strain. Take 10 drops 2-3 times a day 20-30 minutes before meals for rheumatism and gout.

- decoction of chamomile: 4 tbsp. spoons of chamomile medicinal medicinal pour 1 cup boiling water, boil for 10 minutes, then strain. Take 1/3 cup 3 times a day after meals in the treatment of rheumatic joint pain.

- an infusion from the collection of herbs: we take in equal parts licorice root, large burdock, medicinal dandelion, medicinal soapwort, willow bark, nettle leaves. 2 tbsp. spoon collection pour 0.5 liters of boiling water, boil for 10 minutes, then leave for 15 minutes, then strain. Take 0.5 - 1 glass every 2 - 3 hours for attacks of rheumatism.

Infusion of burdock roots: 1 tbsp. a spoonful of dried burdock roots is poured with 2 cups of boiling water, insisted for 2 hours, then filtered. Take 0.5 cup 3-4 times a day.

- a decoction of dogwood roots: pour 1 teaspoon of dogwood roots with 200 ml of water, boil for 15 minutes. Take 2 tbsp. spoons 3 times a day.

- infusion from the collection of herbs: 10 g of burdock roots, 10 g of elecampane, pour 1 glass of water and cook for 20 minutes at low heat and with the lid closed. Then insist 4 hours and strain. Take 1 tbsp. spoon 3-4 times a day before meals.

Stenosis of the left atrioventricular orifice (mitral stenosis)

mitral stenosis(stenosis of the left atrioventricular orifice, stenosis of the left venous orifice) is a heart defect in which the narrowing of the left atrioventricular orifice occurs due to thickening and fusion of the valve leaflets, usually caused by rheumatic endocarditis.

Hemodynamic changes in mitral stenosis:

- obstruction of blood flow when passing through a narrowed (stenotic) mitral orifice from the left atrium to the left ventricle during diastole;

Decreased diastolic filling and stroke volume of the left ventricle;

Increased diastolic filling of the left atrium;

Hypertrophy and dilatation of the left atrium, accompanied by a decrease in its contractility;

Deceleration of blood flow and increased pressure in the pulmonary veins (postcapillary, venous hypertension) and pulmonary capillaries;

Reflex spasm of the arterioles of the pulmonary circulation (Kitaev's reflex - "protective vasoconstrictor reflex of the lungs", protecting the capillaries from an excessive increase in pressure in them) with the formation of precapillary pulmonary arterial hypertension;

Systolic overload of the right ventricle, a decrease in the stroke volume of the right ventricle;

Increased diastolic filling of the right ventricle and right atrium;

Hypertrophy and dilatation of the right ventricle and right atrium;

Decreased blood flow and increased blood pressure venous system systemic circulation.

A significant violation of hemodynamics is observed with a significant narrowing of the mitral orifice, when its area decreases to 1.5 cm 2 or less (normally, its cross section is 4-6 cm 2).

Conduct a survey of a patient with mitral stenosis, identify complaints.

Shortness of breath, asthma attacks (more often at night), cough, hemoptysis, palpitations, pain in the heart area, weakness, fatigue, rarely dysphagia, dysphonia, a feeling of heaviness in the right hypochondrium, edema of the lower extremities, ascites are noted. Complaints of the patient largely depend on the stage of mitral stenosis.

In the first period (the period of compensation of the valvular defect by the left atrium), patients do not complain.

The second period is characterized by decompensation of the left atrium and the development of pulmonary hypertension. Stagnation in the pulmonary circulation is accompanied by the appearance of shortness of breath, palpitations in patients, initially only during physical exertion, and later at rest. With a sharp increase in pressure in the pulmonary capillaries, attacks of suffocation (cardiac asthma) may occur, more often occurring at night, which is associated with the redistribution of blood and its increased flow to the lungs when the patient takes a horizontal position. The appearance of cough and hemoptysis is also associated with hypertension in the pulmonary circulation. At high pulmonary hypertension patients often complain of increased fatigue, rapidly occurring weakness even with little physical exertion, which is associated with a reduced minute blood volume. During exercise, an adequate increase in minute volume does not occur, since a sharp narrowing of the pulmonary arterioles prevents blood flow to the left heart. Pain in the heart with mitral stenosis is rare. They, as a rule, are stabbing, aching in nature, do not have a clear connection with physical activity. Their cause may be stretching of the left atrium, pulmonary artery. Only sometimes typical angina pectoris pains are noted, which are caused by compression of the left coronary artery by an enlarged left atrium. A significant increase in the size of the left atrium can lead to compression of the esophagus, which is accompanied by dysphagia, or to compression of the recurrent nerve with the development of paralysis of the vocal cords and dysphonia (hoarseness of voice). Dysphonia and dysphagia are rare complaints in mitral stenosis.

In the third period, right ventricular failure develops with congestion in big circle blood circulation, in connection with which there are complaints about the severity and dull pain in the right hypochondrium, edema of the lower extremities, and later on ascites. The weakening of the contractile function of the right ventricle can slightly reduce the pressure in the pulmonary artery. At the same time, the patient complains less of shortness of breath, cough, hemoptysis.

Collect anamnesis.

Indications of acute articular rheumatism suffered in childhood or adolescence, repeated attacks of rheumatism in subsequent years, frequent tonsillitis, observation in a rheumatology room or dispensary, the year of formation of heart disease, decompensation of the cardiovascular system in the small and large circles of blood circulation, the presence of others complications of heart disease (atrial fibrillation, thromboembolic syndrome). Outpatient, inpatient treatment and its results, sanatorium treatment, bicillin prophylaxis. The reason for this hospitalization. The presence of rheumatism and heart defects of rheumatic etiology in close relatives of the patient - brothers, sisters, parents.

Identify the symptoms of mitral stenosis in a patient during a general examination.

Patients with mitral stenosis usually take a forced position (orthopnea) - sitting or lying on a bed with a raised headboard. A characteristic feature is facies mitralis: against the background of pale skin, there is a bright purple or crimson blush on the cheeks, the same color of the lips, the tip of the nose. Peripheral cyanosis (acrocyanosis) is noted. With the development of right ventricular heart failure, there are edema or pastosity of the legs and feet. In the formation of a defect in childhood, there may be a lag in physical development, infantilism (mitral nanism). Rarely, anisocoria is detected, which occurs due to compression of the sympathetic nerve by the left atrium.

Examine the area of ​​the heart.

Determine the presence of a heart hump, apex beat, heart beat, and other pulsations in the region of the heart.

Cardiac push - diffuse pulsation in the III-IV intercostal space at the left edge of the sternum and in the epigastric region (epigastric pulsation). The appearance of this symptom is associated with hypertrophy and dilatation of the right ventricle. The cardiac impulse in the epigastric region increases significantly on inhalation, as blood flow to the right ventricle increases, and the heart takes a more vertical position.

heart hump - uniform protrusion of the anterior chest wall above the projection of the heart, associated with hypertrophy and dilatation of the right ventricle. This symptom is observed with mitral stenosis, formed in childhood or adolescence.

Apex beat (limited rhythmic pulsation in the region of the apex of the heart) with mitral stenosis is rarely determined. Characteristically swelling of the neck veins which occurs due to venous congestion due to the development of right ventricular heart failure.

Perform palpation of the heart area.

Determine the presence of a heart beat, apical beat, a symptom of "cat's purr". Place the palm of your right hand on the anterior chest wall, the base of the hand should be in the middle of the sternum, the fingertips should be above the region of the apex of the heart. In patients with mitral stenosis, a pulsation under the palm of the hand is usually determined, localized at the left edge of the lower half of the sternum (cardiac impulse). The pulsation of the anterior chest wall under the fingertips is often weakened (apex beat) or not detected at all due to atrophy of the left ventricle, as well as due to its displacement by an enlarged right ventricle. In the region of the apex of the heart, the symptom of "cat's purr" (diastolic trembling) is also determined, due to low-frequency fluctuations in the blood as it passes through the narrowed mitral orifice. Trembling is easier to determine in the position of the patient on the left side with maximum exhalation.

Do a heart percussion.

Determine the boundaries of relative and absolute cardiac dullness, the configuration of the heart, the width of the vascular bundle, the size of the diameter of the heart. In patients with mitral stenosis, the zone of relative dullness of the heart is shifted upward (due to dilatation of the left atrium and expansion of the pulmonary artery trunk) and to the right (due to dilatation of the right atrium), an increase in the size of the heart diameter due to the right component is noted, the heart acquires a mitral configuration, in which the waist it is smoothed out due to dilatation of the left atrium and cone of the pulmonary artery, the area of ​​absolute cardiac dullness increases due to dilatation of the right ventricle.

Perform auscultation of the heart.

At the listening points, determine the number of heart sounds, additional tones. Assess the volume of each tone at the auscultation points, identify the presence of bifurcation (splitting), accent II tone, noise. In patients with mitral stenosis, pathological symptoms are found at 1 and 3 points of auscultation.

Above the top of the heart (at 1 point of auscultation) are heard:

Reinforced, clapping I tone (more than twice louder than II tone). I tone has different shades of sound, reminiscent of the flapping of a flag flying in the wind.

The opening tone (or opening click) of the mitral valve - occurs 0.06-0.11 seconds after the start of the II tone. The shorter the interval between the II tone and the opening tone of the mitral valve, the higher the atrioventricular pressure gradient and the pronounced stenosis. The mitral valve opening tone does not disappear when atrial fibrillation. It is best heard at the apex of the heart or to the left of the sternum in the IV-V intercostal space on exhalation.

The "quail" rhythm is a three-term rhythm characteristic of mitral stenosis, due to the combination of clapping tone I with tone II and the opening tone of the mitral valve.

Diastolic murmur with presystolic enhancement - most characteristic of mitral stenosis, but can be heard only in presystole (presystolic murmur) or only in the middle of diastole (mid-diastolic murmur). The diastolic murmur begins after the mitral valve opening tone and is due to the movement of blood through the narrowed opening as a result of an increase in the pressure gradient in the left atrium and ventricle. Its intensity is decreasing (decrescendo), since as the left atrium is emptied, the pressure gradient decreases, and blood flow decreases. At the end of diastole, there is a presystolic increase in murmur due to active left atrial systole and increased blood flow. Presystolic noise, thus, is characterized by the increasing intensity (crescendo). With the development of atrial fibrillation, this noise disappears due to a violation of the contractile function of the atria. Diastolic murmur has a low, rumbling timbre, is heard in a limited space at the apex and is not carried anywhere. It is better to listen to it in the position of the patient on the left side, after physical exertion, while holding the breath on exhalation, since in these conditions the heart is closer to the anterior chest wall, and the blood flow through its left sections increases.

At 3 points of auscultation listened to:

Accent II tone over the pulmonary artery, due to increased pressure in the pulmonary circulation.

Splitting or bifurcation of the II tone, associated with non-simultaneous slamming of the valves of the pulmonary artery and aorta due to lengthening of the systole of the right ventricle in conditions of increased pressure in the pulmonary artery.

Diastolic murmur (Graham-Still murmur) - appears due to relative insufficiency of the valves of the pulmonary artery, which develops as a result of dilatation of the fibrous ring of the valves of the pulmonary trunk in patients with mitral stenosis with severe hypertension in the pulmonary circulation. This noise is functional, diastolic, high-frequency, decreasing, quiet, has a blowing character, occurs immediately after the II tone.

In patients with mitral stenosis, pulsus differens (Popov's symptom) is detected (the pulse is not the same on the right and left hands, because with significant dilatation of the left atrium, the left subclavian artery, and the filling of the pulse on the left decreases). The pulse is soft, weak filling, small (due to a decrease in the systolic volume of the left ventricle with a significant degree of narrowing of the mitral orifice), frequent, uneven, arrhythmic (in the presence of atrial fibrillation).

Systolic blood pressure is normal or low (due to a decrease in cardiac output in severe stenosis); diastolic pressure is normal, rarely elevated; pulse pressure is normal or low. Venous pressure in mitral stenosis is increased with a decrease in the contractility of the right ventricle due to congestion in the systemic circulation.

Do a respiratory exam.

When examining the lungs in patients with mitral stenosis, symptoms are determined due to congestion in the pulmonary circulation. On percussion, there is a dull sound in the lower parts of the lungs. On auscultation, weakened vesicular breathing and moist, unvoiced fine bubbling rales are heard in lower sections lungs. Due to the development of congestive bronchitis, hard breathing with dry wheezing can be heard.

Look for ECG signs of mitral stenosis.

In patients with mitral stenosis, the ECG shows signs of hypertrophy of the left atrium, right ventricle, and often signs of atrial fibrillation.

Signs of left atrial hypertrophy:

- broadened P wave (> 0.1 sec.), two-humped P wave with more high second hump in leads I, II, aVL;

An increase in the amplitude and duration of the second (negative) phase of the P wave in lead Vi. In the presence of atrial fibrillation, signs of left atrial hypertrophy on the ECG cannot be detected.

Signs of right ventricular hypertrophy:

- the electrical axis of the heart is deviated to the right or located vertically;

Increasing the height of the R waves in V 1-2 , R ≥ S in V 1-2 ;

Increasing the depth of the S waves in V 5-6;

Expansion of the QRS complex (> 0.1 sec.) in;

Decrease or inversion of the T wave in;

Lowering of the ST segment below the isolevel in V 1-2. ECG changes, in particular in the right chest leads, correlate with the severity of pulmonary hypertension.

Signs of atrial fibrillation:

Irregular rhythm (RR intervals are different);

Absence of P waves before QRS complexes;

Irregular wavy TP isoline, most pronounced in lead V 1 .

Identify FCG signs of mitral stenosis.

On FCG in patients with mitral stenosis, changes are determined above the apex of the heart and above the pulmonary artery.

Above the apex of the heart:

- prolongation of the Q-I tone interval (from the beginning of the Q wave on the ECG to the maximum oscillation of the I tone on the FCG) up to 0.08 sec. and more;

Increase in the amplitude of the I tone (especially on the high-frequency channel);

Mitral valve opening tone after 0.06-0.11 sec. after the beginning of the II tone (especially on the high-frequency channel);

Decreasing-increasing diastolic noise (mesodiastolic with presystolic amplification) between II and I tones (on different frequency channels).

Above the pulmonary artery:

- increase in the amplitude of the II tone;

Splitting or bifurcation of the II tone;

Decreasing diastolic murmur (Graham-Still murmur).

Look for radiological signs of mitral stenosis.

X-ray examination of the lungs:

- expansion of the roots of the lungs, which give a homogeneous shadow, at first with blurred, and with the development of arterial pulmonary hypertension - with clear boundaries (due to dilatation not only of the trunk of the pulmonary artery, but also of its large branches);

Strengthening of the vascular pattern in the lungs (in cases where venous stasis predominates);

Symptom of "breakage of the arteries" or "amputation of the roots" (in cases where pulmonary arterial hypertension predominates); the pulmonary artery and its large branches expand, but the small vessels are constricted, and the pulmonary pattern on the periphery of the lung fields seems to be depleted.

X-ray examination of the heart:

1) in direct projection:

Lengthening and bulging of the 3rd arc of the left heart circuit due to an increase in the left atrium;

Bulging of the 2nd arc of the left contour of the heart due to lengthening and bulging of the trunk of the pulmonary artery;

Mitral configuration of the heart (the heart has a flattened waist due to an increase in the left atrium and expansion of the pulmonary artery trunk);

Bulging to the right of the lower arch of the right contour of the heart, formed by the right atrium, displaced dilated and hypertrophied right ventricle;

The right atriovasal angle (the angle between the lower arch of the right heart contour, formed by the right atrium, and the upper arch, formed by the ascending aorta, sometimes the superior vena cava) is above the normal level;

2) in oblique projections:

Deviation of the contrasted esophagus posteriorly along an arc of small radius (no more than 6 cm) by an enlarged left atrium;

Narrowing of the retrosternal space due to enlargement of the right ventricle.

Identify signs of mitral stenosis according to echocardiography.

Echocardiography reveals the following changes:

Unidirectional movement of the anterior and posterior leaflets of the mitral valve forward (normally, the posterior leaflet moves backward during diastole), due to the fact that the more massive anterior leaflet pulls the posterior leaflet fused with it; the movement of the valves acquires a U-shape;

A sharp decrease or disappearance of peak A, reflecting the maximum opening of the valves during atrial systole;

Decreased rate of early diastolic closure of the anterior leaflet;

Decreased range of motion of the anterior leaflet of the valve;

Thickening of the mitral valve due to fibrosis and calcification;

Expansion of the cavity of the left atrium, while the ratio of the aorta / left atrium decreases (normally it is 1);

Expansion of the cavity of the right ventricle.

Complications in mitral stenosis.

1. Atrial fibrillation.

2. Thrombi of the left atrium, including spherical ones.

3. Thromboembolism in the vascular system of the systemic circulation (cerebral vessels, kidneys, spleen, etc.).

4. Thromboembolism in the vascular system of the pulmonary circulation, pulmonary infarction, infarct pneumonia. The causes of thromboembolism in the pulmonary artery system are phlebothrombosis of the veins of the lower extremities, which develop due to congestion in the systemic circulation and low physical activity of patients, as well as blood clots in the right atrium. In addition, local thrombus formation can be observed in the vessels of the small circle, which is facilitated by congestion in the vessels of the lungs and a decrease in blood flow velocity.

5. Left ventricular heart failure (cardiac asthma, pulmonary edema).

6. Right ventricular heart failure.

Rheumatism(Sokolsky-Buyo disease) is a systemic inflammatory disease of the connective tissue with a predominant localization of the process in the cardiovascular system, which develops in connection with an acute infection (group A hemolytic streptococcus) in predisposed persons, mainly children and adolescents (7-15 years old).

• Epidemiology

Rheumatism is registered in all climatic and geographical zones of the world. The data of recent decades have convincingly shown the relationship between the level of primary incidence of rheumatism and the socio-economic development of countries, which is confirmed by its predominant distribution in developing and underdeveloped countries, where 80% of the world's children live. According to the generalized data of I. Padmavati, rheumatism among schoolchildren in developing countries is 6-22 per 1000 child population, while a progressive course of the disease is noted with the formation of multiple heart defects, pulmonary hypertension and early mortality with symptoms of increasing heart failure.

Among the social conditions that play a certain role in the development of the disease, one should name overcrowding in apartments and schools, poor nutrition of children, and a low level of medical care.

In our country, over the past 25 years, morbidity and mortality have decreased by more than 3 times. For example, a prospective 10-year study of the primary incidence of rheumatism showed a decrease from 0.54 per 1000 children. up to 0.18. However, the prevalence of rheumatic heart disease, according to L. I. Benevolenskaya et al. (1981), still remains high (1.4%), which is apparently associated with the accumulation of such patients in older age groups by increasing life expectancy and reducing mortality.

• Pathomorphology

One of the main manifestations of the disease is rheumatic heart disease, specific diagnostic feature which ashofftalalaevskaya granuloma.

Rheumatic granuloma consists of large irregularly shaped basophilic cells of histiocytic origin, sometimes multinucleated, giant multinucleated cells of myogenic origin with eosinophilic cytoplasm, cardiohistiocytes (Anichkov's myocytes) with a characteristic arrangement of chromatin in the form of a caterpillar, lymphoid and plasma cells, mast cells (mast cells), single leukocytes.

Ashofftalalaevsky granules are most often located in the perivascular connective tissue or in the interstitium of the myocardium (mainly the left ventricle), papillary muscle, septum, as well as in the endocardium, vascular adventitia, sometimes in their wall with rheumatic vasculitis. Currently, granulomas in pathological anatomical examination are found much less frequently than previously noted, which is apparently associated with a change in the clinical and morphological "appearance" of rheumatism, with the so-called pathomorphosis.

Another morphological substrate of heart damage in rheumatic heart disease is a nonspecific inflammatory reaction, essentially similar to that in the serous membranes, joints. It consists of edema of the intermuscular connective tissue, sweating of fibrin, infiltration by cellular elements, mainly polymorphonuclear leukocytes and lymphocytes.

In rheumatism, there is also damage to muscle fibers in the form of hypertrophy, atrophy, various types of dystrophy and necrobiotic processes up to complete lysis, followed by regeneration of the functional structures of myocytes when the rheumatic process subsides.

When comparing the data of a morphological study with the degrees of clinical activity of the rheumatic process (according to AI Nesterov), certain patterns were revealed. Thus, the maximum degree of activity is characterized by simultaneous damage to several membranes of the heart and valves. The exudative component of inflammation predominates in the form of thromboendocarditis, exudative and myocarditis, fibrinous pericarditis, which often acquires diffuse character. In addition, diffuse rheumatic endocarditis or valvulitis described by V. T. Talalaev, recurrent warty endocarditis (with a continuous recurrent course) can be detected. Also note the prevalence and severity of mucoid and fibrinoid swelling, multiple "blooming" ashofftalalaevsky granulomas.

With moderate clinical activity, a productive type of reaction predominates, often having a focal character (fibrous endocarditis, interstitial focal myocarditis), "erased" granulomas are detected. As the activity of the process decreases, dystrophic changes in muscle fibers become more important, up to the appearance of small foci of necrobiosis and myolysis. Such foci can be regarded as metabolic necrosis, which is associated with acute heart failure, which is often the cause of death in such patients. The detection of fixed immunoglobulins in the sarcolemma of the myocardial muscle fibers and the adjacent sarcoplasm, as well as in the vessel wall, indicates the role of immune reactions in the damage to the heart parenchyma.

The morphological picture in rheumatic heart disease with a minimum degree of activity of the process according to the materials of biopsies and pathological anatomical studies is different. When studying biopsies, granulomas were often found (data from N. N. Gritsman, in 61.8%) and microsigns of a nonspecific exudative proliferative component. In these cases, more than half of the patients showed signs of activity of the rheumatic process after surgery. In cases of rheumatic heart disease with a minimal degree of activity, which ended in death, granulomas were rarely detected and circulatory disorders and multiple small-focal metabolic necrosis were more often noted.

As a rule, in almost all cases of rheumatic heart disease (with the exception of primary rheumatic heart disease in children), sclerotic processes were found, most pronounced in the endocardium, especially in the valvular apparatus, where severe deforming sclerosis developed.

According to the frequency of lesions, the mitral valve comes first, then the aortic valve, and finally the tricuspid valve. There are insufficiency of the mitral valve, stenosis of the mitral orifice and combined defects with a predominance of one or another type of defect; the process eventually ends in stenosis. The mitral orifice with stenosis can be 2-14 times narrower than normal. In the myocardium, sclerosis of the connective tissue layers most often develops. Fibers of the conducting system may be involved in the sclerotic process.

In the articular tissues in rheumatic polyarthritis, there are processes of disorganization of the connective tissue, exudative inflammation, vasculitis with an outcome in moderate fibrosis. In the subcutaneous tissue, in the area of ​​\u200b\u200bthe joints, rheumatic nodules with a diameter of 0.5-2.5 cm can occur in groups, which disappear without a trace within 2 weeks - 1 month. In the vessels of the microcirculatory bed of the skin, especially in the active phase of the disease, there are inflammatory changes, perivascular accumulations of mast cells of labrocytes, small histiocytic infiltrates.

Serous membranes are constantly involved in the process with high activity of rheumatism, giving a picture of serous, serous-fibrinous and fibrinous inflammation. In addition to a nonspecific inflammatory reaction, fibrinous deposits are organized in the epicardium with the help of large histocytes resembling Ashofftalalaev granuloma cells.

In the interstitium of the skeletal muscle, both exudative proliferative processes with foci of fibrinoid swelling and the reaction of local connective cells, and focal necrosis of muscle fibers with a corresponding cellular reaction from large histiocytes can be observed. Most often, such granulomatous accumulations are detected in the muscles of the pharynx.

In the lungs, changes can be observed that are regarded as rheumatic pneumonia: vasculitis and perivasculitis, infiltration of the alveolar septa with lymphoid-histiocytic elements, protein membranes on the inner surface of the alveoli, in the lumen of the alveoli - serous fibrinous exudate, sometimes with a hemorrhagic tinge, with an admixture of desquamated cells of the alveolar epithelium. In some places there are small foci of fibrinoid necrosis with large cell proliferation around (Masson's bodies).

Kidney damage in rheumatism is a manifestation of systemic vascular damage. Inflammation and sclerotic changes are observed in vessels of all calibers, from the branches of the renal artery to the glomerular capillaries. Observed focal, rarely diffuse, glomerulonephritis.

All departments are involved in the process nervous system. Most of these changes are based on vasculitis, which primarily affects the vessels of the microvasculature. Atrophic and dystrophic changes in ganglion cells, mainly basal ganglia, occur in chorea. In the pia mater, in the stroma of sensitive ganglia, in the endo and perineurium, lymphohistiocytic infiltrates are observed.

With rheumatism in the lymph nodes, spleen, bone marrow, tonsils, i.e., in the "organs of immunogenesis", a plasma cell reaction is noted.

What Causes Rheumatism

Group A hemolytic streptococci are the most common cause of upper respiratory tract and subsequent development of rheumatic fever. One of the conditions for the development of rheumatism is the severity of nasopharyngeal streptococcal infection and its insufficiently effective treatment. Evidence of the importance of streptococcal infection in the development of rheumatism are epidemiological observations, according to which rheumatism most often develops in the first months of the formation of so-called closed teams.

The significance of streptococcal infection in rheumatism is indirectly evidenced by the detection in the vast majority of patients of various anti-streptococcal antibodies - ASL0, ASG, ASA, antideoxyribonuclease B (anti-DNase B) in high titers.

How does acute nasopharyngeal A-streptococcal infection leads to the development of acute rheumatism, is still not well known. One might think that a streptococcal infection, especially a massive one, has a direct or indirect damaging effect on tissues with a huge number of different cellular and extracellular antigens and toxins. Among them, an important role is played by cell wall Mprotein, which is a virulence factor, Tprotein (streptococcus type specificity factor), capsule hyaluronic acid, which can suppress the phagocytic activity of neutrophils, a mucopeptide, which has an "endotoxic" effect, and a cytoplasmic membrane, which contains cross-reacting antigens. with the myocardium, for example, tipone-specific Mprotein. In addition, there is a large group of exoenzymes - metabolic products of streptococcus, which have toxic and antigenic properties. These include streptolysins O and S, streptokinase and hyaluronidase, proteins and deoxyribonuclease B and others, in response to which ppotivpstreptococcal antibodies are produced. with pathogenic activity. Streptococcus exoenzymes can directly cause tissue damage, for example, hyaluronidase - depolymerization of hyaluronic acid, streptokinase - activation of the kinin system involved in the development of inflammation.

The role of streptococcal infection (including L forms) in the development of recurrent rheumatic heart disease, in which there may be no pronounced antistreptococcal immune response, is very peculiar, which served as the basis for the search for other etiological factors, for example, viruses or nostreptococcal association virus.

The study of the etiology and pathogenesis of rheumatism is based on two aspects of the problem - Asstreptococcal infection and predisposition to rheumatism. Indeed, all previous experience convincingly testifies to the inseparable connection of these facts.

So, only 0.3-3% of those who have had an acute streptococcal infection fall ill with rheumatism.

In families of patients with rheumatism, the tendency to a hyperimmune antistreptococcal response (ASL0, ASH, ASA, DNase B) and the prevalence of rheumatism and rheumatic heart disease are higher than in the general population, especially among first-degree relatives.

For the occurrence of rheumatism, an individual hyper immune reaction of the body to streptococcal antigens and the duration of this response are important, as evidenced by the dynamic study of antistreptococcal antibodies. The reasons for the long-term persistence of antistreptococcal immune reactions in patients with acute rheumatism require clarification. The role of a genetically determined defect in the elimination of streptococcus from the body is discussed. Apparently, the survival of streptococcus in the body in the form of L-forms of hemolytic streptococcus is also important.

The predisposition to rheumatism is not limited to the special reactivity of antistreptococcal immunity. According to L. I. Benevolenskaya and V. A. Myakotkin, in families of patients with rheumatism, repeated cases of the disease occur 3 times more often than in the population, and rheumatic heart defects even 4 times more often. Concordance for rheumatism among monozygotic twins is also the highest (37%). The significance of family genetic predisposition is confirmed by the data of population genetic studies.

More substantiated is the concept of the polygenic type of inheritance of rheumatism, according to which a significant number of involved genes determines the breadth and variety of clinical manifestations and course options. However, this multifactorial concept does not exclude the search for specific genetic factors that explain individual symptoms of the disease and its course.

Studies of genetic markers have shown that among patients with rheumatism, persons with blood groups A (II), B (III) and AVN non-secretors are more common. In recent years, an intensive study of the relationship of individual rheumatic diseases with the HLA phenotype has been carried out. In particular, J. B. Zapiskie drew attention to the decrease in the frequency of HLA A3 in children with rheumatism, and V. Joshinoja and V. Pope - to the frequent detection of HLA B5. In patients with rheumatism of the Russian population, according to N. Yu. Goryaeva, HLA All, B35, DR5 and DR7 prevailed. At the same time, some researchers paid attention to the increase in the content of HLA DR2 and DR4 in the examined patients. Although these data show differences in the frequency of detection of certain individual immunogenetic markers in rheumatism, however, they allow us to discuss the significance of the DR locus in the structure of multifactorial predisposition in rheumatism and, in particular, to hyperreactivity to streptococcal (group A) antigens and exoenzymes. Other aspects of the genetic predisposition to rheumatism are also discussed. For example, the significance of the increase in the frequency of B-lymphocyte alloantigen 883, found in a number of genetically and geographically distinct populations with acute rheumatic fever (71% versus 17% in controls), the role of monoclonal antibodies D 8/17, which reacted with lymphocytes in almost all 100% patients with acute rheumatic fever and only 10% of patients with other rheumatic diseases. Of particular interest is the concept of recent authors about the genetic determinism of cross-reactivity between B lymphocytes, heart tissues and streptococcal antigens.

Pathogenesis (what happens?) during Rheumatism

Despite the fact that the specific mechanisms of predisposition to rheumatism have not yet been fully disclosed, the incidence of only certain individuals, repeated cases of the disease in "rheumatic" families, the correspondence of the genetic model of rheumatism to polygenic inheritance models allow us to consider predisposition to rheumatism along with streptococcal infection as etiological factors. this disease. In the complex pathogenesis of the development of such classical manifestations of rheumatism as rheumatic heart disease, arthritis, chorea, anular erythema, the greatest importance is attached to immune inflammation, immunopathological processes in which streptococcal antigens and antistreptococcal antibodies are most actively involved, however, the toxic concept also makes a certain contribution to at least in understanding the initial manifestations of pathology. Summarizing numerous literature data, G. P. Matveikov et al. point out that the latter concept is based on a number of actual materials shown in the experiment, indicating the cardiotoxic action of gtpeptolysins, streptococcal proteinase, deoxyribonuclease - "endotoxins" and the combined effect of endo and exotoxins.

The concept of the role of cross-reacting antigens - the antigenic components of streptococcus and body tissues - received the greatest confirmation. Thus, a cross-reaction was found between the group A polysaccharide and epithelial cells thymus, which, according to I. M. Lyampert, is associated with a violation of the functioning of T-lymphocytes with the development of cell-mediated autoimmune reactions. Group A streptococcal antigens cross-react with myocardial antigens. Subsequently, a cross-reaction was found between the components of the streptococcal membrane and sarcolemmal antigens, streptococci and components of the atrioventricular bundle, streptococcal membranes and cytoplasmic neuronal antigens in children with acute rheumatic chorea.

The fact that the severity of the course of rheumatism correlates with the level of antihardial antibodies and that deposits of immunoglobulins and complement are found in rheumatic heart disease indicates the role of immunopathological mechanisms in the development of one of the most important manifestations of rheumatism - rheumatic carditis. Immunopathogenetic mechanisms of rheumatic heart disease in recent years have been confirmed by the discovery of circulating immune complexes in patients. T. A. Ryazantseva et al., V. A. Nasonova et al. and other authors showed that v patients with high content In circulating immune complexes, high titers of ASLb and immunoglobulins, especially IgG, are more often detected, various titers of atrioventricular tricular dissociation and atrioventricular block I-II degree are more often detected. According to A. I. Speransky et al., ASL0 and Q are found in the composition of circulating immune complexes in patients with acute rheumatism, which indicates pathogenetic significance these complexes in the development of myocarditis.

In rheumatism, various autoimmune reactions to such components of the connective tissue and heart valves as structural glycoproteins, proteoglycans, and mucoproteins have also been found.

The pathogenesis of other clinical manifestations of rheumatism (migratory arthritis, skin syndrome) is not well understood. Nevertheless, an immunocomplex mechanism for the development of synovitis and chorea is assumed.

Thus, acute streptococcal infection in some patients causes an increase in the humoral and cell-mediated immune response to various components of streptococcus, promotes the activation of cross-reacting autoantibodies and T cells.

Along with immunopathological mechanisms, inflammation plays an important role in the development of the main clinical manifestations of rheumatism. There is no doubt that rheumatism belongs to the group of those systemic diseases in which inflammation is mediated by chemical mediators, such as lymphomonokines, kinins and biogenic amines, chemotaxis factors, and others, leading to the development of the vascular-exudative phase of acute inflammation. At the initial stages of the development of an inflammatory reaction in rheumatism, a large role belongs to the toxic effects of extracellular products of group A streptococcus on cell membranes, vascular permeability, etc.

Thus, the pathogenesis of rheumatism as a systemic cocv distoconnective tissue disease is complex. Obviously, streptococcus plays an important role in its development, which has a toxic and immunonatological effect on the body and, possibly, causes an autoimmune process. However, these factors can be realized only in a predisposed organism, in which a complex of violations in the system of nonspecific and specific defense is determined. At the same time, antistreptococcal immunity is characterized by a persistent response to streptococcal antigens.

Rheumatism classification:

Successes in the fight against rheumatism in our country, associated with the implementation of a universal unified therapeutic and preventive tactics, are largely due to the widespread introduction into practice of the working classification proposed by A. I. Nesterov. The classification defines the phases of the disease (active, inactive), which became possible due to a thorough study of the activity of the process.

The inactive phase of rheumatism is understood as such a state of health in those who have undergone rheumatism, when clinical and thorough laboratory examination in dynamics fails to reveal any signs of an inflammatory process or impaired immunity. In the inactive phase of rheumatism, the working capacity of patients is preserved, and hemodynamic disturbances are detected with significant physical exertion, if a heart defect has formed.

During the active phase of the disease, three degrees of activity are distinguished:

• maximum (III degree),
• moderate (II degree),
• minimal (I degree),

Differing mainly in the features of the inflammatory process in various organs and systems.

Clinical and functional characteristics and signs of process activity, according to laboratory tests, reflect a pronounced exudative component of inflammation - migratory polyarthritis, severe carditis, serositis, pneumonia, and others, combined with high levels of antistreptococcal immunity and protein content in the acute phase.

At the II degree of activity, the symptoms of carditis predominate, usually moderately pronounced, in combination with subfebrile temperature, volatile polyarthralgia or subacute monooligoarthritis, chorea, etc. Indicators of inflammatory activity are moderate or slightly changed.

Finally, at the I degree of activity, minimally pronounced symptoms of carditis are detected clinically and only on the ECG and FCT; all laboratory parameters are normal or some of them are slightly changed.

If the III degree of activity of the process always indicates the onset of the disease or its exacerbation, then the II and I degree of activity can be either at the beginning of the disease or during its exacerbation, or develop under the influence of treatment. Dynamic determination of clinical and laboratory parameters allows you to more accurately determine the degree of activity. From these positions, the specification of the degree of activity of the rheumatic process is an indicator of the real state of the patient, which determines the nature and duration of therapeutic measures.

The classification of rheumatism reflects the clinical and anatomical characteristics of individual lesions; its essence will be stated in the description of the clinical picture of the disease. The inactive phase of the disease is characterized by the consequences transferred manifestations rheumatism in the form of myocardiosclerosis, formed heart disease, non-cardiac adhesive changes. Recognition of "inactive" manifestations of past rheumatism is of great practical importance, determining the labor activity of the patient, the possibility of curing him from rheumatism, albeit with residual changes, for example, with cardiosclerosis, moderate heart disease.

The column "character of the course" lists the main variants of the course, the recognition of which is based on the clinical and temporal principle of the severity of the onset and duration of the course of the primary rheumatic process or its exacerbation.

In the acute course of rheumatism, its acute onset is also observed with fever, polyarthritis, rheumatic heart disease, and other manifestations, with high laboratory activity indicators and a rapid and often complete (within 2-3 months) effect of anti-inflammatory therapy.

Subacute rheumatism may also present with a sudden onset, as in acute rheumatic fever, but with less febrile reaction and persistent polyarthritis and less responsive to anti-inflammatory therapy. The same can be noted in relation to rheumatic heart disease. However, more often the disease begins as if gradually - with subfebrile temperature, monooligoarthritis, with a predominance of myocarditis and endocarditis in the clinic, a tendency to a longer course of up to 3-6 months from the onset of an attack with periodic exacerbations.

A protracted course is most characteristic of recurrent rheumatism, more often observed in women with a formed heart disease. With this variant of the course, rheumatic heart disease prevails in the clinical picture of the disease, accompanied by unstable low-grade fever and polyarthralgia. The activity of the pathological process is usually minimal or moderate, the duration of the disease is often more than 6 months, without bright exacerbations and remissions. Anti-inflammatory therapy is ineffective.

These three variants are the most common in modern rheumatism - the first two in primary and the last in recurrent. The following two variants of the course are rarely observed - continuous and latent.

The continuous recurrent course of rheumatism is characterized by an undulating course. Each exacerbation most often begins acutely with the involvement of all membranes of the heart and (or) with polyserositis, the development of vasculitis (pulmonary, renal, cerebral), oligoarthritis and fever, accompanied by laboratory indicators of high or moderate activity of the pathological process. Anti-inflammatory antirheumatic therapy has an incomplete effect, the disease acquires a protracted course, without a tendency to develop remission. A continuously relapsing course is usually characteristic of recurrent rheumatism with formed heart defects and often significantly aggravates the clinical picture of the disease and prognosis. thromboembolic complications caused by embolic processes (usually with atrial fibrillation), vasculitis with chronic disseminated intravascular coagulation syndrome.

The variant of chronic rheumatism is classified as latent, in which it is not possible to detect clinical and laboratory signs of activity. Fundamentally latent rheumatism can be primary and secondary. Primarily latent rheumatism is recognized by accidental detection of usually mitral heart disease in examined individuals, for example, in epidemiological studies (primarily latent). Secondarily latent rheumatism can be established in patients when signs of progression of rheumatic heart disease are detected during dynamic observation and treatment, as well as when signs of morphological activity are found in the atrial ears removed during heart surgery, in biopsy specimens of other parts of the heart. Recognition of secondary latent rheumatism (usually rheumatic heart disease) is extremely important, since it aggravates, without treatment, cardiac pathology and significantly worsens the results of the operation. As for primary latent rheumatism, it is necessary to exclude the possibility of other causes of heart disease (viral valvulitis, for example).

And, finally, the last column of the working classification presents the nomenclature of the functional state of blood circulation according to Strazhesko-Vasilenko with the subdivision of circulatory insufficiency into I, IIA, PB and III stages.

Thus, the working classification of rheumatism makes it possible to assess the phase of rheumatism in a diverse way and specify the activity both in terms of clinical and morphological manifestations and laboratory-documented indicators, assess the nature of the course and, finally, the functional state of the heart of the main organ of the pathological process in rheumatism - and thus the prognosis.

Symptoms of Rheumatism

Clinical picture:

Despite the polymorphism of clinical manifestations characteristic of rheumatism, a wide range of course options, this disease has a number of features, namely:

• connection with a previous acute streptococcal infection;
• the presence of "absolute signs of rheumatism", according to A. A. Kisel - Kisel-Jones criteria;
• tendency to develop heart disease.

In the development of rheumatism, three periods can be distinguished. The first period lasts 2-4 weeks after streptococcal infection, is asymptomatic or with symptoms characteristic of prolonged convalescence. The second period is a clinically obvious disease with the development of polyarthritis, carditis, and other clinical, morphological and immunobiochemical changes characteristic of primary rheumatism. The third period - diverse manifestations of recurrent rheumatism with the progression of the severity of heart defects and the development of hemodynamic disorders. This characteristic of rheumatism reflects all stages of its development - from the initial to the final, accompanied by functional insufficiency of the most affected organ - the heart.

Rheumatic arthritis remains one of the main clinical manifestations and diagnostic criteria, predominantly primary rheumatism, rarely recurrent, in which polyarthralgia predominates.

Rheumatic polyarthritis is characterized by lesions predominantly of the knee, ankle, elbow, shoulder and, less frequently, wrist joints, the migratory nature of joint damage. There is a quick effect after administration acetylsalicylic acid and other non-steroidal anti-inflammatory drugs with the disappearance within a few days, and often hours of all articular manifestations.

The severity of rheumatic polyarthritis is different - from unbearable pain, swelling and redness of the skin to a barely noticeable defiguration, which can be paid attention only because of severe pain. In the modern course of rheumatism, especially recurrent, sharp flying polyarthralgia can essentially be considered as the equivalent of rheumatic migratory polyarthritis.

Usually, rheumatic polyarthritis undergoes complete regression, however, with frequent recurrence, chronic post-rheumatic arthritis of Jacques rarely develops in patients with heart disease, characterized by damage to the small joints of the hands and feet, ulnar deviation of the hands in combination with flexion of the metacarpophalangeal joints and extreme hyperextension of the distal interphalangeal. In recent years, it has been established that Jacques' chronic seronegative arthritis is also observed in other chronic diseases with predominantly tendon-muscular and periarticular pathology, for example, chronic systemic lupus erythematosus.

Rheumatic carditis determines the nosological specificity of rheumatism and the outcome of the disease as a whole, being the most common symptom of the disease, one of its main criteria.

Rheumatic carditis is characterized by the involvement of all membranes of the heart in the pathological process, while myocardial damage is an early and almost obligatory symptom, against which endocarditis and pericarditis develop. Rheumatic pancarditis (formerly a frequent manifestation of rheumatism in children and adolescents) is now extremely rare. Early recognition of rheumatism and active anti-inflammatory therapy significantly mitigated the course of carditis, but did not change its essence - outcomes in heart defects. Since against the background of current myocarditis it is not always easy to recognize val vulitis, and even more so parietal or chordal endocarditis and (or) erased leaking pericarditis, the term "rheumatic carditis" has become widespread in the clinic as a generalizing concept of heart damage in rheumatism, obliging, however, the doctor to use all the methods of laboratory and instrumental diagnostics available to him in order to recognize the rheumatic process in any of the membranes of the heart. Many years of clinical experience shows that rheumatic heart disease is characterized by consistent involvement of the myocardium, pericardium and endocardium in the pathological process, although there may be various combinations that ultimately determine the clinical and instrumental manifestations of the disease.

Three forms of rheumatic heart disease - severe, moderate and weak, corresponding to such morphological definitions known in the past as diffuse and focal rheumatic heart disease. Advantage clinical classification consists in the fact that it reflects the clinical and laboratory instrumental signs of the severity of active carditis, and its disadvantage is the applicability of these criteria mainly to primary rheumatic carditis and recurrent rheumatic carditis without heart disease. With recurrent rheumatic heart disease against the background of a formed heart disease and hemodynamic disorders, determining the form of rheumatic heart disease is extremely difficult. But apparently clinical significance such a release is not significant, since it is known that as rheumatic heart disease recurs and heart disease progresses, there is a tendency for rheumatism to protracted and latent course, in which moderate or often mild rheumatic heart disease is usually observed.

Severe rheumatic heart disease is usually found in acute and subacute primary rheumatism. His clinic is determined by widespread inflammation of one, two, rarely three membranes of the heart (pancarditis). With severe rheumatic heart disease, patients are concerned about shortness of breath and palpitations during movement, and with involvement in the process of the pericardium - pain.

An objective examination reveals tachycardia that does not correspond to body temperature, but often there may be bradycardia. As a rule, patients have moderate hypotension, a distinct increase in percussion of the borders of the heart to the left or in all directions. According to auscultation and phonocardiographic examination, heart sounds are muffled, weakened and (or) deformed I tone, systolic (high-frequency) murmur, less often mesodiastolic murmur at the apex of the heart, pathological III and IV tones with the occurrence of protodiastolic and protodiastolic gallop rhythms. diagnostic significance is the appearance of protodiastolic aortic murmur, pericardial friction murmur, as well as radiological and echocardiographic symptoms of pericardial effusion.

Severe carditis is also characterized, according to ECG data, by a violation of the function of excitability and repolarization processes, a slowdown in atrioventricular conduction, a prolongation of the electrical systole, and a change in the atrial complex.

When conducting effective anti-inflammatory therapy (Fig. 11), the dynamism of clinical, radiological, electro and phonocardiographic signs is characteristic.

Moderately expressed rheumatic heart disease develops with primary and recurrent rheumatism, its acute and subacute course.

Of practical importance is the recognition of moderately severe rheumatic heart disease in the primary protracted course of rheumatism, which is characterized by a high incidence of heart defects due to the frequent combination of myocarditis and valvulitis in such patients. Patients often complain of persistent cardialgia and palpitations. Percussion expanded left border of the heart, which is confirmed by x-ray enlargement of the left ventricle in primary rheumatism, and recurrent - a decrease in the size of the heart in the process of anti-inflammatory therapy.

On auscultation and on PCG, I tone is weakened, distinct III tone, systolic and transient diastolic murmurs. On the ECG - violations of the processes of repolarization, intraventricular conduction, sinus arrhythmia. There are violations of the contractile function of the myocardium. Attention is drawn to the low dynamism of all clinical and instrumental indicators under the influence of anti-inflammatory therapy.

Weakly expressed rheumatic carditis can be observed in any variant of the course of primary and recurrent rheumatism. In acute and subacute course of primary rheumatism, clinical and laboratory signs of high activity of the process are characterized by extracardiac syndromes, and in recurrent rheumatic heart disease, a mild process (carditis) against the background of heart disease can be obscured by hemodynamic disorders.

Patients with mild primary rheumatic carditis do not complain, and objectively only a retrospective analysis after the treatment allows us to catch the dynamics of the size of the left border of the heart. With a known alertness of the doctor, patients can detect a tendency to tachycardia, or rather lability of the pulse, a slight muffling of tones (on FKG - an unsharp decrease in the amplitude of the first tone), a weak systolic murmur recorded as a mid-frequency murmur.

On the ECG, there are signs of deep and persistent disorders of atrioventricular conduction, blockade of the legs of the atrioventricular bundle, rhythm disorders such as atrial fibrillation, extrasystole, paroxysmal tachycardia, diffuse changes in the myocardium.

Recurrent rheumatic heart disease retains the features of the primary, but the process is more difficult and as new exacerbations occur, it increasingly occurs with combined and combined heart defects, acquiring a chronic protracted or latent course with an unstable effect of antirheumatic therapy. To a certain extent, progressive circulatory failure, which is not so rare in these cases, requires the exclusion of recurrent rheumatism, although it may be associated with acute metabolic necrosis in the myocardium.

Rheumatic lung disease develops mainly in children with acute or continuously recurrent course of rheumatism in the form of rheumatic pneumonia or pulmonary vasculitis, usually against the background of severe carditis (pancarditis).

Rheumatic pneumonia manifested by increased shortness of breath, fever, an abundance of different-sized voiced wet rales on one or both sides of the lungs in the absence of dulling of the lung sound. Radiologically, local strengthening, thickening and deformation of the lung pattern with multiple small foci of compaction is determined. With a bilateral basal process, a typical pattern of "butterfly wings" is formed. The dynamism of clinical and radiological changes under the influence of antirheumatic therapy is characteristic.

Rheumatic pulmonary vasculitis characterized by cough, often hemoptysis, shortness of breath. Usually, in patients in the absence of any percussion changes in the lungs, a significant amount of voiced moist rales is heard, and diffuse enhancement of the pulmonary pattern is determined radiologically. With the development of vasculitis, the effectiveness of anti-inflammatory therapy is observed. However, it is not always easy to make a differential diagnosis with congestion in the lungs, especially with recurrent rheumatic heart disease against the background of heart disease.

Rheumatic pleurisy- one of the most frequent manifestations of rheumatic polyserositis, often occurring at the onset of the disease simultaneously with migratory polyarthritis and accompanied by pain during breathing, pleural friction noise in the area of ​​exudate accumulation and fever. Pleurisy with a large effusion is currently extremely rare, mainly in children with a rapid course of rheumatism, more often a small effusion in the sinuses or adhesions (pleurolia fragmyalnmr, pleroperchka "dial") are detected x-ray examination. There is a rapid reverse development of changes under the influence of anti-inflammatory treatment. Only with a continuously recurrent flow against the background of heart defects, recurrent unilateral pleurisy is observed.

kidney damage in rheumatism are varied from transient toxic post-infectious nephritis to glomerulonephritis and congestive kidney in severe heart failure. The low-manifest symptomatology of rheumatic glomerulonephritis is the main reason for the rare diagnosis of this systemic symptom of rheumatism in the clinic.

Abdominal syndrome meets seldom, mainly at children's age, at an acute course of primary or returnable rheumatism. Clinical symptoms characterized by the sudden onset of diffuse or localized abdominal pain, accompanied by nausea, rarely vomiting, stool retention or increased frequency. The pains are migratory in nature, varying in severity, accompanied by fever, slight tension abdominal wall, pain on palpation. The basis of the abdominal syndrome is rheumatic peritonitis, so the abdominal syndrome is often combined with polyarthritis and serositis of other localizations. Peritoneal symptoms disappear after a few days, usually there are no relapses.

Rheumatic chorea refers to the main manifestations of rheumatism ("an absolute sign", according to the definition of A. A. Kisel). Chorea minor develops mainly in children and adolescents, more often girls, and pregnant women with rheumatism. The clinical symptoms of chorea are very characteristic. suddenly changing mental condition child: selfishness, emotional instability develops, or, on the contrary, passivity, absent-mindedness, fatigue, aggressiveness. At the same time, motor restlessness with hyperkinesis and muscle weakness with muscle hypotension occur. Hyperkinesias are manifested by grimacing, slurred speech, dysarthria, impaired handwriting, inability to hold table setting items while eating, general motor restlessness, uncoordinated erratic movements. Sometimes muscular hypotension is of primary importance, as a result of which the child cannot sit, walk, the process of swallowing, physiological functions, etc. are disturbed (pseudo-paralytic form of chorea). Among the individual clinical signs of chorea, they describe the symptoms of "flabby shoulders" (when lifting the patient by the armpits, the head sinks deep into the shoulders), Czerny (retraction of the epigastric region when inhaling), "Filatov's eye and tongue" (the inability to simultaneously close the eyes and stick out the tongue), " choreic hand" - flexion in the carpal beam and extension in the metacarpophalangeal and interphalangeal joints of the arm extended forward. Gordon (delayed reverse flexion of the lower leg in the event of a knee reflex as a result of tonic tension of the quadriceps femoris muscle). Choreic hyperkinesias are aggravated by excitement, less often by physical exertion, and disappear during sleep. Tendon reflexes in chorea minor are somewhat increased, sometimes a mild clonus of the feet is detected, with muscle hypotension there are no reflexes.

From non-specific manifestations nervous system damage in rheumatism, they describe rheumatic vasculitis with one or another localization of damage to various parts of the nervous system, hypothalamic syndrome, etc.

Skin lesions in rheumatism, which is based on rheumatic vasculitis, usually manifests with erythema annulare and rheumatic nodules, which are pathognomonic signs of the disease (the main diagnostic criterion). However, in recent years, skin lesions have been observed extremely rarely.

Clinically erythema annulare - pale pink, barely noticeable rashes in the form of a thin annular rim with a clear outer and less clear inner edges. Elements merge into bizarre shapes on the shoulders and torso, less often on the legs, neck, and face. Skin rash is not accompanied by any subjective sensations and usually disappears without a trace.

Rheumatic nodules ranging in size from millet to beans are dense, inactive, painless formations located in the fascia, aponeuroses, along the periosteum, articular bags, in the subcutaneous tissue. Favorite localization is the extensor surfaces of the elbow, knee, metacarpophalangeal joints, ankles, spinous processes of the vertebrae, etc. Rheumatic nodules appear imperceptibly for patients and also quickly disappear or undergo reverse development within 1-2 months without residual effects.

Diagnosis of Rheumatism

• Laboratory data

To determine the activity of the inflammatory process, laboratory tests such as determining the number of leukocytes and ESR, the content of seromucoid proteins, fibrinogen, ni and aaglobulins, CRP, etc. are used.

Detection of circulating antibodies in high titers to streptolysin, streptokinase, streptohyaluronidase is an additional diagnostic criterion. The highest titers of circulating antistreptococcal antibodies are detected in the acute course of rheumatism and the III degree of activity of the process. The presence of a hyperimmune response to streptococcus can be established more often with the simultaneous determination of ASL0, ACT, ACK, antiDNase B.

The diagnosis is sometimes extremely difficult to establish. This is due to the fact that the main clinical most commonly observed signs of rheumatism, such as carditis and polyarthritis, are not specific to rheumatism. big diagnostic value have chorea, erythema annulare, and roar. matic nodules, but chorea occurs no more than 15% of sick children, and annular erythema and nodules in only 1.5% of sick children.

All this led to the fact that clinicians began to use generalized diagnostic criteria for rheumatism.

Diagnostic criteria for rheumatism were first formulated by the Soviet pediatrician A. A. Kisel, who identified five "absolute" signs of rheumatism: rheumatic nodules, erythema annulare, chorea, migratory polyarthritis and carditis. Later, the same five signs were classified by Jones as the main criteria for rheumatism.

The following are the American Heart Association - AHA diagnostic criteria for rheumatism.

Axial (large) manifestations:

• carditis, characterized by an expansion of the boundaries of the heart, the presence of systolic or diastolic murmurs above the apex of the heart, effusion pericarditis with typical changes in the boundaries and configuration of the heart, pericardial friction noise and characteristic electrocardiographic parameters, the development of circulatory failure in a child or in an adult under the age of 25 years with absence of other reasons;
• polyarthritis, manifested by pain in the joints, limitation of movement, swelling, redness, a feeling of heat;
• chorea with characteristic "involuntary twitching of the mimic muscles of the face and limbs;
• subcutaneous nodes - small dense, almost painless formations the size of a pea or nut, localized in the subcutaneous tissue near the joints (usually found in childhood, youth or young age);
• annular erythema (erythema annulare) - recurrent rashes of pink annular shape with uneven contours; their color weakens from the periphery to the center; observed on the lateral surface of the chest, neck, upper limbs, rarely on the cheeks, more common in childhood, adolescence and young age; erythema is unstable, relieved by heat;
• rheumatic history - - an indication of the chronological relationship of the disease with a recent nasopharyngeal (streptococcal) infection, repeated tonsillitis or catarrh of the upper respiratory tract, the presence of patients with rheumatism among family members, neighbors in the school desk or workplace in the workplace;
• efficacy of ex juvantibus antirheumatic therapy given for 35 days.

Additional manifestations.

• temperature rise;
• adynamia, rapid fatigue,
• irritability, weakness;
• pale skin and vasomotor lability;
• sweating;
• nose bleed;
• abdominal syndrome.

According to the AHA recommendations, minor diagnostic criteria for rheumatism include: fever, arthralgia, history of rheumatism, prolongation of the PR interval, increased erythrocyte sedimentation rate, and elevated CRP. In addition, special criteria have been identified, which include previous infection with hemolytic streptococcus.

Special, mainly laboratory, indicators:

• leukocytosis (neutrophilic);
• dysproteinemia (increased ESR, hyperfibrinogenemia, the appearance of SRV, an increase in the content of uglobulins, serum mucoproteins, glycoproteins);
• pathological serological indicators: streptococcal antigen in the blood, increased titers of ASL0, ACK, ASH; 4) increased capillary permeability.

Finding two main criteria or one main and two additional criteria in a patient is enough to make a diagnosis of rheumatism.

However, this statement is true if the main manifestations of the disease are chorea, annular erythema or rheumatic nodules. With polyarthritis or carditis, the diagnosis of rheumatism can only be made if there are a larger number of both basic and additional criteria. In particular, the Kisel-Jones criteria in everyday practical work used to diagnose acute or subacute rheumatism in children and young people.

For the recognition of a protracted (primarily protracted), erased, atypical, latent course of rheumatism, AI Nesterov (1976) proposed a syndromic diagnosis of primary rheumatism.

The first clinical epidemiological syndrome includes data indicating the association of the disease with streptococcal infection.

The second clinical-immunological syndrome includes: a) unmotivated recovery delay general condition a patient after a nasopharyngeal infection, fatigue, palpitations, arthralgia, unstable subfebrile condition; b) increased titers of streptococcal antibodies, change cellular immunity, symptoms of autoimmunization, identification of biochemical signs of inflammation (dysproteinemia, increased ESR, the appearance of CRP, etc.).

Finally, the third syndrome, cardiovascular, detected using clinical, instrumental, radiological and other research methods, confirms the presence of carditis and extracardiac localizations of the rheumatic process.

Clinical experience shows that syndromic diagnosis makes it possible to recognize primary rheumatism at the very beginning of its development and thus provide targeted treatment.

Diagnostic criteria for rheumatism, suitable for epidemiological studies and outpatient diagnostics, have acquired great practical importance.

The most informative signs of rheumatism and their combinations, calculated in threshold values ​​of the sums of diagnostic coefficients (in bits), were combined into 10 syndromes. The table includes a group of symptoms that exclude rheumatism.

The syndrome of "history of joint damage", as well as the selected 15 signs (33-47) for the diagnosis of carditis, etc., turned out to be important. At the same time, the share of syndromes varies in the developed criteria. Heart disease and chorea are evaluated by the maximum number of arbitrary units, and carditis, polyarthritis, skin lesions found in an isolated form in a patient may indicate probable rheumatism, but their combination makes the diagnosis of rheumatism certain. However, it must be borne in mind that, no matter how great the significance of diagnostic schemes. they do not replace the medical thinking, the diagnostic work of the doctor, who must recognize (and put into the scheme) a symptom, characterize the identified "syndrome of joint damage in anamnesis" and conduct a differential diagnosis of this process with related diseases.

• Differential Diagnosis

Differential diagnosis of rheumatism in early stages disease is based on the detection of polyarthritis (monoligoarthritis) and carditis.

Naturally, the relationship of the disease with streptococcal infection, the age of the patient, a family history of rheumatic fever, and the features of the clinical picture of polyarthritis (the presence of liarthralgia) should be taken into account. However, rheumatic arthritis must be differentiated from reactive arthritis, primarily iersiniozny and salmonella, juvenile rheumatoid arthritis, hemorrhagic vasculitis and etc.

To exclude juvenile rheumatoid arthritis (JRA), you can use the criteria proposed by A. V. Dolgopolova et al. For JRA, especially important are such signs as the “persistence” of arthritis from the onset of its onset, the involvement of other joints in the process, including small, often symmetrical nature of the lesion. The main difference between rheumatic polyarthritis and JRA is the migratory nature of the first and the persistence of the second. Typical for rheumatic polyarthritis are rapid (in the first 7-10 days) addition of carditis, high titers of antistreptococcal antibodies, the effectiveness of acetylsalicylic acid, etc.

Hemorrhagic vasculitis may begin with polyarthritis, clinically no different from rheumatic, but the appearance of purpura in combination with abdominal pain, and later renal pathology helps to establish the correct diagnosis.

With the development of primary rheumatic carditis, a differential diagnosis is made with numerous non-rheumatic myocarditis (viral, bacterial, etc.).

The features of the syndrome of primary rheumatic heart disease include:

• the presence of a chronological relationship of the disease with nasopharyngeal streptococcal infection (classical tonsillitis, pharyngitis);
• Existence latent period(2-4 weeks) between the end of the previous streptococcal infection and the first clinical manifestations of rheumatic heart disease;
• predominant occurrence of the disease at the age of 7-15 years;
• acute or subacute onset of the disease, even in cases that subsequently evolve into a primary protracted course of the disease;
• frequent detection at the onset of the disease of polyarthritis or severe polyarthralgia;
• passive nature of cardiac complaints;
• relatively frequent detection of a combination of myocarditis, pericarditis, valvulitis, "high mobility" of symptoms of inflammatory heart disease;
• a clear correlation of the severity of clinical manifestations of rheumatism with laboratory indicators of the activity of the rheumatic process.

Non-rheumatic myocarditis is characterized by: chronological relationship with viral infections(most often), stressful influences; shortening or absence of a latent period after an infection; development of myocarditis in middle and old age; gradual development of the disease; absence of articular syndrome at the onset of the disease; active, emotionally colored nature of complaints in the region of the heart, the absence or weak severity of laboratory signs of the activity of the process with severe clinical manifestations of carditis; the presence of symptoms of asthenia, vegetative dystonia, violations of thermoregulation at the onset of the disease.

Functional cardiopathies, although rare, must be differentiated from recurrent lingering rheumatic heart disease in middle-aged women (who were often misdiagnosed with rheumatism in childhood). Functional cardiopathies are characterized by pain in the region of the heart, palpitations, interruptions, sensations of "fading", "stopping" the heart, "lack of air" and others that are not characteristic of patients suffering from myocarditis. Often, cardiac complaints appear or sharply increase against the background of vegetative-vascular crises, proceeding according to the sympathetic-adrenal and, less commonly, vagoinsular type. The contrast between the abundance and brightness of subjective manifestations and the scarcity of objective data is characteristic. The prescribed anti-inflammatory therapy does not improve the condition of patients, and corticosteroid therapy even worsens, while sedatives, especially sympatholytic ones, cause a good therapeutic effect. The absence of a formed heart disease with indications of numerous "attacks of rheumatism" in childhood and the predominance of subjective manifestations over objective manifestations in the clinical picture of the disease make it possible to diagnose functional cardiopathy.

In childhood, the primary protracted course of rheumatic heart disease must be distinguished from mitral valve prolapse. Characteristic of mitral valve prolapse is the aus cultative picture - the presence of a click in the projection area of ​​the mitral valve in the middle of systole and the late systolic murmur of mitral regurgitation following it. The size of the heart is small. The diagnosis of mitral valve prolapse is confirmed by echocardiography, which establishes excessive movement of the mitral valve leaflets into the left atrial cavity during systole. As a rule, this pathology is not accompanied by a violation of intracardiac hemodynamics, but in some cases, especially in young women and girls, complaints of cardialgia, shortness of breath, and palpitations may appear.

With recurrent rheumatic heart disease against the background of a formed heart disease, especially aortic one, it is necessary to exclude infective endocarditis. In this case, bacterial infections should be taken into account in the immediate anamnesis - infected injuries, purulent infections, etc. With infective endocarditis, patients complain of pronounced weakness, weight loss, chilling, sweating , bone and muscle pain, persistent arthralgia or mild migratory arthritis, periarthritis. Symptoms of infective endocarditis include: prolonged remittent, sometimes intermittent fever with chills, profuse sweating, pale skin, symptoms of deformed nails ("watch glasses"), or nail phalanges(like "drum sticks"), symptoms of Lukin-Libman, a tendency to thromboembolism, the development of diffuse glomerulonephritis, vasculitis. Liver enlargement not related to circulatory failure - almost the same common symptom with this disease, as well as splenomegaly. An important diagnostic value is attached to persistent progressive anemia, detection of rheumatoid factors, significant hypergammaglobulinemia, detection of bacteremia.

In some cases of recurrent, often protracted, rheumatic heart disease, it becomes necessary to conduct a differential diagnosis with severe progressive variants of Abramov-Fiedler myocarditis, in which pallor of the skin, puffiness of the face, and cyanotic gray skin tone are observed. The patient's anxiety is typical. often caused by intense prolonged pain in the heart, increasing shortness of breath, weakness, poorly amenable to drug therapy, progressive circulatory failure. As a rule, tachycardia, hypotension, a significant increase in the size of the heart (often cor bovinum), deafness of heart sounds are found. Along with muscle systolic murmur in some patients, one can hear mesodiastolic murmur, gallop rhythm. Relatively often, paroxysms of atrial fibrillation, extrasystole are detected, less often - paroxysmal tachycardia, complete or persistent atrioventricular blockade. characteristic feature such forms of myocarditis are deep electrocardiographic changes in the form of a variety of rhythm disturbances, changes in intraventricular conduction, blockade of the legs of the atrioventricular bundle, severe violations atrioventricular conduction up to complete transverse blockade. X-ray reveals a pronounced increase in all parts of the heart, a decrease in the amplitude of the pulsation along the contour of the heart to areas of adynamia during X-ray kymography. A discrepancy between the severity of the condition and the almost complete absence of changes in blood tests typical of the acute phase of the inflammatory process is characteristic.

Rheumatism Treatment

Success in the treatment of rheumatism and prevention of the development of heart disease is associated with early recognition and individualized treatment based on the assessment of the course, the degree of activity of the pathological process and the severity of carditis, the nature of valvular heart disease, the state of the myocardium, other organs and tissues, the profession of the patient, etc. .

AT in general terms such a program consists of antimicrobial and anti-inflammatory therapy, measures aimed at restoring immunological homeostasis, organizing a rational balanced diet and adapting to physical activity, as well as preparing for workload, timely surgery patients with complex heart defects.

All patients during the active phase of rheumatism associated with past Astreptococcal infection are shown penicillin, which has a bactericidal effect on all types of Astreptococcus. This task is met by a 10-day treatment of angina and a two-week prescription of penicillin during the active phase of rheumatism, followed by a switch to a prolonged preparation of bicillin5. Recommended doses - 1,200,000-1,500,000 IU of potassium or sodium salt, 200,000 IU every 4 hours for 5 days with angina and 2 weeks with rheumatism. In the future, it is advisable to introduce bicillin5 at a dose of 1,500,000 IU. Children are prescribed an age-appropriate dose - 400,000-600,000 IU / day. In case of intolerance to penicillin, erythromycin 250 mg 4 times a day can be prescribed according to the same administration regimen as penicillin. The use of sulfonamides and tetracycline drugs for angina and rheumatism is not justified, firstly, because they have only a bacteriostatic effect (stop cell division) and, secondly, contribute to the formation of resistant strains.

Among other measures aimed at reducing streptococcal effects on the body, we can recommend placing patients in small wards, regular ventilation and systematic ultraviolet irradiation of the wards, and strict adherence to personal hygiene measures. In addition, it is necessary to identify chronic tonsillitis, conduct a thorough conservative treatment and, if necessary, surgical removal of the tonsils.

The anti-inflammatory drugs currently used to treat the active phase of rheumatism include glucocorticosteroid drugs, salicylic, indol derivatives, phenylacetic acid derivatives, etc.

Of the entire large group of glucocorticosteroids in clinical practice prednisolone is most widely used, and in recurrent rheumatic heart disease against the background of heart disease, triamcinolone (polcortolone). In urgent cases, to obtain a quick effect, prednisolone hydrochloride is used in 1 ml ampoules. containing 30 mg of the drug, sodium salt dexamethasone-21-phosphate, available in 1 ml ampoules (4 mg of the drug), or 6methylprednisolone (methipred, urbazone).

Prednisolone at a dose of 20-30 mg / day is indicated for primary rheumatic heart disease (especially with pronounced and moderately pronounced), with polyserositis and chorea. From our point of view, the development of valvulitis is also an indication for treatment with these drugs.

With recurrent rheumatic heart disease with III and II degree of activity of the process, the presence of severe or moderate carditis, corticosteroid drugs are also necessary, including the development of heart failure due to active carditis. In these cases, triamcinolone at a dose of 12-16 mg / day is preferred as a drug that has less ability to disrupt electrolyte balance. Corticosteroid drugs are not recommended for grade I activity and mild carditis due to increased dysmetabolic processes in the myocardium.

Prednisolone at a dose of 20-30 mg / day (or another drug at an equivalent dose) is prescribed until a therapeutic effect is achieved, usually for 2 weeks, and then the dose is reduced by 2.5 mg (half a tablet) every 5-7 days. The entire course of treatment lasts G / 2-2 months (only 600-800 mg per course). Withdrawal in rheumatism is not observed, although mild signs of increased activity with dose reduction seem to occur, mainly in the form of arthralgia, a slight increase in laboratory tests in the acute phase of the inflammatory process. In these cases, the reduction in the dose of the drug should be somewhat suspended. Stop hormone therapy usually during the patient's stay in the hospital.

Due to the effect of corticoid drugs on water-salt metabolism, the treatment complex should include potassium chloride 3-4 g / day, panangin and others, with fluid retention - aldosterone antagonists (veroshpiron up to 6-8 tablets per day), diuretics (lasix according to 4080 mg / day, furosemide 40-80 mg / day, etc.), with euphoria - tranquilizers, etc. However, these side effects rarely require discontinuation of the drug, with the exception of the formation of a steroid ulcer, which casuistically rarely develops with rheumatism, if the drug is not assigned to patients with "ulcerative anamnesis".

Non-steroidal anti-inflammatory drugs have found wide application in active rheumatism.

At present, the most widespread are the average doses of acetylsalicylic acid - 3-4 g / day, less often 5 g / day and above. Indications for the appointment of salicylates:

• minimal degree of activity, moderately and mild carditis, mainly myocarditis;
• prolonged course of rheumatism, suspicion of latent treatment, in which the dynamics of clinical and laboratory parameters under the influence of treatment makes it possible to recognize this variant of the course;
• long-term treatment with subsidence of the activity of the process and the abolition of corticosteroids, as well as after discharge from the hospital;
• recurrent rheumatic heart disease against the background of severe heart defects and circulatory failure, since salicylates do not retain fluids, prevent a tendency to thrombosis, and stimulate the respiratory center;
• prevention of exacerbation of rheumatism in the spring and autumn periods and especially after intercurrent infections (in combination with antibiotics).

Acetylsalicylic acid is prescribed but 1 g 3-4 times a day after meals for 1-3 months or more with good tolerance and the condition of careful monitoring of side effects.

Derivatives of indolacetic acid - indomethacin - have been successfully used in rheumatism for more than 20 years. Indomethacin has a pronounced therapeutic effect: the subjective symptoms of carditis (cardialgia, palpitations, shortness of breath) disappear by the 8-10th day of treatment and the objective symptoms - by the 14-16th day. Polyarthritis and polyserositis disappear even faster. Noted positive influence drug for cerebrovasculitis and pulmonary vasculitis. The positive dynamics was the brightest in III-II degree of rheumatism activity, severe and moderate carditis. The advantage of indomethacin is the possibility of its administration in suppositories to those patients who had a history of peptic ulcer or chronic gastritis. The daily dose of indomethacin in suppositories is 100 mg (administered twice at 50 mg or 100 mg at night). Indomethacin on the first day is given orally in capsules containing 25 mg of the drug, 1 or 2 after meals (required!) To avoid irritating the gastrointestinal tract. With good tolerance, the dose is increased to therapeutic (75-100 mg), less often 125-150 mg with a significant exacerbation of the course. In this dose, the drug is prescribed for the entire period of treatment in the hospital. In acute and subacute course, treatment continues for another month on an outpatient basis. With a protracted course of the disease, it is necessary to take indomethacin after discharge from the hospital for at least 2-3 months (6 months each) until the laboratory indicators of the activity of the inflammatory process are completely normalized, and with a continuously relapsing course - for several months and even years at 50-75 mg / day (as in the treatment of patients with ankylosing spondylitis). Indomethacin can be prescribed to patients with recurrent endocarditis on the background of heart disease and heart failure, since it does not retain fluid.

Contraindications: pregnancy and lactation, gastric ulcer, ulcerative colitis, allergic reactions. It is not recommended to prescribe the drug to drivers of cars and persons of similar professions because of the property of the drug to reduce attention and cause dizziness.

Voltaren is also an active non-steroidal anti-inflammatory drug. The comparative clinical efficacy of voltaren and indomethacin showed that the former is not inferior to it in anti-inflammatory activity, but has a minimal effect on the gastrointestinal tract, since voltaren is available in 25 mg tablets with a coating that is resistant to the action of gastric juice. As B. S. Dzhusenova showed, under the influence of voltaren, as well as indomethacin, on the 2-3rd day the body temperature decreased to normal, polyarthralgia disappeared, subjective signs of rheumatic heart disease (on the 5-7th day), and rhythm disturbances were not detected after 2 -4 days of treatment, a little later (on the 7th-9th day) the final part of the ventricular complex on the ECG returned to normal. Auscultatory symptoms of carditis already on the 15-20th day significantly decreased. When taking Voltaren, side effects are small: individual intolerance in the form of ordinary allergic reactions, occasionally headache, epistaxis, microhematuria.

Ibuprofen (Brufen), as a less active anti-inflammatory non-steroidal drug, can be used with moderate and especially minimal process activity at a dose of 800-1200 mg for a long time, mainly in outpatient practice with a protracted course of rheumatism.

With a protracted and continuously relapsing course of rheumatism, non-steroidal anti-inflammatory therapy, as a rule, is combined with multi-month and, if necessary, long-term use of aminoquinoline derivatives - delagil or hydroxychloroquine (plaquenil), respectively, 0.25 g and 0.2 g 2 times a day after meals for a month , and then 0.2 g after dinner as needed under medical supervision ( side effects- gastralgia, visual impairment, leukopenia, dermatitis, etc.).

The basis of the treatment of rheumatism is a system of staged treatment - a hospital - a clinic - a resort.

In the hospital, active anti-inflammatory therapy is carried out, bicillin prophylaxis and rehabilitation are started, controlling the physical performance of the patient. After the activity of the rheumatic process decreases and the patient's condition improves, they are transferred to the second stage, which involves sending the child and adolescent to a specialized rheumatological sanatorium, and an adult patient to a local cardiological sanatorium or a polyclinic under the supervision of a rheumatologist. The main goal of the second stage is to continue treatment with non-steroidal anti-inflammatory drugs (individually selected in a hospital), aminoquinoline derivatives (for chronic rheumatism), bitschlin 5, and rehabilitation.

The third stage includes dispensary observation and preventive treatment patient with rheumatism. Dispensary tasks:

• implementation medical measures aimed at the final elimination of the active rheumatic process;
• carrying out symptomatic therapy of circulatory disorders in patients with heart defects, solving issues of surgical correction of defects together with a cardiac surgeon;
• resolving issues of rehabilitation, working capacity and employment;
• implementation of primary prevention of rheumatism and secondary prevention relapses of the disease.

Rheumatism Prevention

The main goal of primary prevention of rheumatism is to organize a set of individual, social and national measures aimed at eliminating the primary incidence of rheumatism. These include the promotion of systematic and reasonable hardening of the body, the further development of physical culture and sports among the population, the fight against overcrowding in homes, schools, kindergartens, public institutions, the implementation of extensive individual and public sanitary measures that reduce the possibility of streptococcal infection of the population and, first of all, children teams.

An important point is the timely recognition and effective treatment of an acute infection caused by (3-hemolytic streptococcus group A. For this purpose, parenteral (or oral) administration of penicillin is prescribed at a daily dose of 1,200,000 IU for adults, up to 300,000 IU for preschool children and up to 450,000 IU children of school age for 5 days, and then with an interval of 5-6 days, bicillin5 is administered twice at a dose of 600,000 IU / day.

Along with the treatment of acute Astreptococcal infections, it is important preventive measure are hardening, increasing resistance to infection. Of no small importance in the primary prevention of rheumatism was the systematic implementation of state measures aimed at improving the standard of living, improving housing conditions, classes in schools in one shift, etc.

Secondary prevention of rheumatism is aimed at preventing relapse and progression of the disease in people who have had rheumatism. For this purpose, secondary year-round prophylaxis with bicillin5 is recommended, carried out by monthly, and according to the latest WHO recommendations, three-week injections of bicillin5 at a dose of 1,500,000 IU for adults and school-age children and 750,000 IU every 2 weeks for preschool children. According to the Instructions for the Prevention of Rheumatism and its Relapses in Children and Adults, all patients who have undergone a significant rheumatic process over the past 5 years, and, according to individual indications, those who have suffered a rheumatic attack for more than 5 years (without damage to the heart and with carefully sanitized foci chronic infection), during the first 3 years, round-the-clock, and in the next 2 years, spring-autumn seasonal prophylaxis of relapses with bicillin in the same doses is carried out. If there are signs of the formation of valvular heart disease, a prolonged or continuously recurrent course of chorea, foci of chronic streptococcal infection, as well as recurrent rheumatic heart disease, year-round bicillin prophylaxis is recommended for 5 years.

Patients with rheumatism of pregnant women from the first weeks are observed by a rheumatologist and an obstetrician who decide whether to continue or terminate the pregnancy. For pregnant women who have had rheumatism or have active manifestations of it, bicillin5 is prescribed from 8-10 weeks of gestation until delivery, the duration of bicillin prophylaxis in postpartum period depends on the activity and characteristics of the course of the rheumatic process.

Along with the bicillin prophylaxis of relapses in all patients with rheumatism and threatened by rheumatism (family members of patients) during acute respiratory diseases, angina, exacerbation of a chronic infection, current prevention is carried out, consisting of a 10-day treatment with penicillin in the same way as with angina. Penicillin is prescribed to patients with rheumatism before and after surgical interventions(tonsillectomy, tooth extraction, abortion, etc.).

Certain rescues during bicillin prophylaxis arise in connection with the possibility of developing allergic reactions. According to WHO (1968), the frequency of all allergic complications to the administration of penicillin preparations in different countries over the previous 12 years was 0.7-10%. These complications include severe reactions ( anaphylactic shock etc.) were noted only in 0.015-0.04% of cases. Thus, the low frequency of severe allergic reactions is unlikely to be an obstacle to widespread bicillin prophylaxis. However, the possibility of their occurrence indicates the need for careful identification of persons with hypersensitivity to penicillin, compliance with appropriate precautions. Mandatory conditions are the conduct of bicillin prophylaxis in a room well equipped for anti-shock measures, training of personnel in their quick and accurate implementation.

Long-term experience of rheumatologists in most countries has shown that prolonged administration of antibiotics penicillin series prolonged action is so far the only effective drug method for preventing recurrence of rheumatism. The success of bicillin prophylaxis depends on the regularity of its implementation. Bicillin prophylaxis is most effective in patients with acute and subacute rheumatic fever. Patients with clinical variants of the course of the disease and chronic circulatory failure require not only long-term antibacterial, but also long-term anti-inflammatory and aminoquinoline therapy, which in these cases plays the role of secondary prevention of exacerbation. Much attention should be paid to measures that contribute to the restoration of disturbed reactivity, compensation of the function of the cardiovascular system. For this purpose, resort factors are used in the staged treatment of patients with rheumatism.

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Rheumatism appears with an allergenic effect of streptococcus after transferred infections. The characteristic symptoms are inflammation of the heart, joints, brain, skin, and lungs. Timely treatment perfectly copes with the disease without causing serious complications.

What is rheumatism?

Chronic disease has been known to mankind for a long time. Even the famous Hippocrates described methods of treating rheumatism. Medical scientists had long disputes about what causes pathology, and only in the nineteenth century Sokolsky and Buyno unraveled the etiology of the disease.

Risk of getting sick systemic disease children between the ages of seven and fifteen are most commonly affected. Very rarely, rheumatism appears in old age in immunocompromised individuals.

According to statistics, girls get rheumatic fever much more often than teenage boys. The peak incidence occurs in primary school age and up to thirteen years. Outbreaks of rheumatism begin after epidemics of tonsillitis or scarlet fever, chronic pharyngitis.

Children's body subject to regular attack infectious agent, after recovery, it enters the stage of allergic susceptibility to streptococcus. This happens when the development of the immune system of the developing organism is imperfect.

It is noted that residents of Eastern Europe, Asia and Australia are more likely to suffer from rheumatism, in North America and the western part of Europe, cases of the disease are much less common. Every eighth out of ten patients has acquired heart defects, this fact is due to the special susceptibility of the heart muscle to the streptococcal strain.

Reasons for the appearance

The preceding condition after which a person develops rheumatism is infection Streptococcus organism.

These diseases include:

• frequent sore throats;
• scarlet fever;
• chronic tonsillitis;
• pharyngitis.

Influence pathogen very toxic to the body. Streptococcus produces foreign proteins that are similar in structure to the protein component found in the membranes of the brain, heart muscle and valves. This factor explains the pathogenic effect of the bacterium on the heart, brain, as well as the skin and joints.

Chief rheumatologist: "If the joints of the arms and legs begin to hurt, urgently exclude from the diet ...

Not every infected person can get rheumatism, the vast majority of them recover completely with the formation of immunity to an infectious disease. Three people out of a hundred are affected by rheumatism.

In this case, desensitization of the body to streptococcus occurs against the background of provoking factors:

• unfavorable state of the environment;
• decrease in the body's defenses with poor immunity;
• poor nutrition, a state of hypovitaminosis;
• living in one area a large number of people;
• low social status.

One of the fundamental roles is played by genetic predisposition. From generation to generation, a person inherits D8 / 17 B-cell antigens, as well as antigens compatible in histology of the second class. The presence of specific proteins in cells when attacked by a microorganism gives impetus to the development of rheumatism with an additional negative influence of external factors.

Classification of rheumatism

Rheumatism is divided into phases and stages depending on the clinical picture of the pathology.

Phases of rheumatism:

• inactive - there are no symptoms, when conducting a blood test, there are no laboratory signs of the presence of the disease;
• the active phase, which, in turn, can be minimally active (the disease proceeds in a mild form), moderate activity (clinical picture with moderate manifestations), severe degree of the disease (symptoms are bright, all organs and systems that can be involved in pathology are affected) .

According to the degree of the course of rheumatism, there are:

1. Acute rheumatism is characterized by a sudden onset with a sharp rise in body temperature, the development of a vivid picture of the pathology involving all organs susceptible to damage. Timely treatment gives a positive result.
2. In the subacute course of rheumatism, the manifestations are less pronounced, and therapeutic measures do not give quick positive results. The disease lasts from three to six months.
3. Protracted rheumatism lasts from six months, but not more than twelve months. In this case, the pathology develops slowly, the signs of the disease are mild.
4. The latent course does not manifest itself clinically, the rheumatic factor is not detected in the blood, the latent process is dangerous, imperceptible by the development of complications. Often, heart valve disease can be diagnosed earlier than rheumatic fever.
5. The recurrent form proceeds for a long time with the appearance of acute attacks with severe manifestations of the disease, there is an exacerbation in the off-season (spring, autumn). During the remission period, there is no lull in symptoms. The disease continues to progress rapidly, quickly affecting the internal organs.

Rheumatism can manifest itself as a complex of syndromes characteristic of it with damage to the heart, skin, membranes of the brain, joints and lungs, and involvement in the process of one organ. In severe cases, the process can spread to the kidneys, blood vessels.

Symptoms of the disease

Signs of developing rheumatism can be seen a week later, in some cases twenty-one days after an infectious pathology. A person has a sharply understood temperature up to high values preceded by severe chills.

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The joints become painful and slightly swollen, accompanied by an unpleasant ache. The patient feels weakness, he develops symptoms of tachycardia, the work of the sweat glands intensifies.

After a short period of time, the symptoms are gaining strength:

• all joints swell, become hot and red on imaging, with severe pain on palpation and local pressure;
• from the side of the heart, there is a rapid heartbeat and heart rhythm failure, pain behind the sternum.

The acute course is accompanied by damage to the connective tissue in different organs. There are five characteristic syndromes of rheumatism.

rheumatic heart disease

Damage to the muscles of the heart is observed in eight out of ten patients with rheumatism. Inflammation manifests itself stabbing pains in the heart, palpitations, arrhythmia, shortness of breath, palpitations, cough during exercise. A person becomes lethargic, quickly gets tired, he has no appetite, apathy appears.

Body temperature does not rise above 38 degrees. The heart increases in size, adapting to the stress of general inflammation. There is a decrease blood pressure, sweating. When listening, pathological noises and gross violations of the heart rhythm are diagnosed.

In severe cases, gross violations of cardiac activity are observed:

• heart pain intensifies;
• shortness of breath is present at rest;
• the pulse becomes quiet;
• there are signs of impaired peripheral circulation;
• complication may be cardiac asthma or pulmonary edema.

Rheumopoliarthritis

Inflammation in the joints appears simultaneously with changes in the heart. The lesion begins with large joints.

All the signs of classic inflammation appear:

• severe pain when moving at rest, in small joints the symptom is volatile: it appears in one or the other joint;
• joints swell, often symmetrically;
• the skin over the sore spot becomes red and hot on palpation;
• motor function is impaired.

The condition is complicated by the fact that many joints hurt, the body temperature rises to 39 degrees, fluctuations in values ​​during the day can reach one degree. In this case, the patient becomes weak, there is fragility of blood vessels with frequent bleeding from the nose.

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.
A. 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, processes of alteration 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 - a 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 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 a 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