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Lecture № 16. Rheumatism in children and adolescents. Clinic, diagnosis, treatment



Rheumatism is a systemic inflammatory disease of connective tissue with a characteristic lesion of the heart.

Etiology, pathogenesis. The main etiological factor in acute forms of the disease is b-hemolytic group A streptococcus. In patients with prolonged and continuously recurring forms of rheumatic heart disease, it is often impossible to establish the association of the disease with streptococcus. In the development of rheumatism, particular importance is attached to immune disorders.

It is suggested that sensitizing agents in the body (streptococcus, viruses, nonspecific antigens, etc.) can lead in the first stages to the development of immune inflammations in the heart, and then to the violation of the antigenic properties of its components, converting them into autoantigens and the development of an autoimmune process. A special role in the development of rheumatism is played by genetic predisposition.

Classification. It is necessary to identify previously inactive or active phase of the disease.

Activity can be minimal (I degree), medium (II degree) and maximum (grade III). To determine the degree of activity, the severity of clinical manifestations is used, as well as changes in laboratory indicators.

Classification of the localization of the activity of the rheumatic process (carditis, arthritis, chorea, etc.), the state of circulation and the course of the disease.

Isolate acute course of rheumatism, subacute flow, prolonged course, continuously recurrent course and latent course of the disease. Isolation of latent flow is justified only for retrospective characteristics of rheumatism: latent formation of heart disease, etc.

Clinic. Most often the disease develops 1-3 weeks after the angina, sometimes - another infection. With relapses, this period may be less. Relapses of the disease often develop after any intercurrent diseases, surgical interventions, physical overload. The manifestation of rheumatism is the combination of acute migratory and reversible full polyarthritis of large joints with moderately expressed carditis. The onset of the disease is acute, violent, rarely subacute. Polyarthritis develops rapidly, accompanied by remitting fever up to 38-40 C with diurnal fluctuations of 1-2 C, severe sweating, but more often without chills.

The first symptom of rheumatic polyarthritis is acute joint pain, which increases and intensifies with the slightest passive and active movements. To the pain, puffiness of the soft tissues in the joint region joins and at the same time there is an effusion in the joint cavity. Skin over the affected joint is hot, with palpation of the joint sharp soreness, the volume of movements is limited due to pain.

A characteristic feature is the symmetrical lesion of large joints - often knee, wrist, ankle, elbow. Typical "volatility" of inflammatory changes, manifested in the rapid and reverse development of arthritic manifestations in some joints and the same rapid growth in other joints. All joint changes disappear without a trace even without treatment, they last no more than 2-4 weeks.

Rheumatic myocarditis, if there is no concomitant defect, is mild, with complaints of mild pain or uncomfortable, vague sensations in the heart, minor dyspnea in exercise, rarely with complaints of heart failure, palpitations. With percussion, the heart of normal size or moderately enlarged to the left, with auscultation and on the PCG, a satisfactory sonority of tones is characteristic, a slight muffling of 1 tone, sometimes 3 tons, rarely 4 tons, mild systolic murmur at the apex of the heart and projection of the mitral valve. Blood pressure normal level or moderately reduced. On the ECG - flattening, broadening and serration of the P wave and the QRS complex, there can rarely be an extension of the PQ interval of more than 0.2 s, in some patients a small shift of the S-T interval from the isoelectric line to the bottom of the isoelectric line and a change in the T wave become low, less often two-phase (first of all in the leads V1-V3). Rarely appear extrasystoles, atrioventricular blockade of the 2-3rd degree, intraventricular blockade, nodal rhythm.

Diffuse rheumatic myocarditis is manifested by significant inflammation of the myocardium with its pronounced edema and, consequently, a violation of function. Since the beginning of the disease, the patient is concerned about pronounced dyspnea, which causes the position of orthopnea to take place, there is a constant pain in the heart area, rapid heart rate. Characteristic "pale cyanosis", swelling of the cervical veins. The heart is diffusely widened, a weak apical impulse. The tones are sharply muffled, very often a clear III tone is heard (the proto-diastolic rhythm of the gallop) and a distinct but significantly mild systolic noise. The pulse is fast, weak filling. Blood pressure is lowered. Venous pressure rises rapidly, but in combination with collapse also decreases. On the ECG, a decrease in the voltage of all the teeth, a flattening of the T wave, a change in the interval S-T, an atrioventricular block are recorded. The outcome of rheumatic myocarditis in the absence of adequate treatment can be myocardial cardiosclerosis, which often characterizes the prevalence of myocarditis. With focal cardiosclerosis, myocardial functions are not impaired. Diffuse myocarditis cardiosclerosis is characterized by signs of a decrease in the contractile function of the myocardium, which is manifested by weakening of the apical impulse, by muffling the tones (especially I), systolic murmur. Rheumatic endocarditis, which is the cause of the development of rheumatic heart disease, has very little clinical symptoms.

An essential symptom is at auscultation clear systolic noise with sufficient sonority of tones and absence of signs of pronounced myocardial damage. In contrast to noise associated with myocarditis, endocardic noise is coarse, but sometimes it can have a musical tinge. The soundness of endocardic noise increases when the posture changes patient or after a load.

Significant signs of endocarditis are the variability of already existing noises and especially the appearance of new ones with unchanged boundaries of the heart. Diastolic noises quickly and easily disappear, they are heard sometimes at the very beginning of a rheumatic attack on the projection of the mitral valve, as well as on the vessels, and in part may also be associated with endocarditis. Deep endocarditis of the valves or aortic valve in some patients is reflected in the echocardiogram: thickening of the valves, their "shaggy", multiple echoes from them.
Pericarditis in the clinic of rheumatism is rare.

Dry pericarditis is clinically manifested by constant pain in the heart and pericardial friction noise, which is often heard along the left edge of the sternum. The intensity of noise in auscultation is different, often it is determined in both phases of the cardiac cycle. The ECG reveals a shift in the interval of S-T upward in all leads at the very beginning of the disease. With further development, these intervals return to the isoelectric line, and also two-phase or negative teeth T are formed. Dry pericarditis itself is not capable of inducing augmentation of the heart.

Exudative pericarditis is a further stage in the development of dry pericarditis. The main first clinical sign of the appearance of effusion is the disappearance of pain due to the disconnection of inflammatory papillary sheets, accumulating exudate.

Clinical manifestations in the form of dyspnea, which increases when the patient lies down. The region of the heart with a large amount of exudate swells, the intercostal space is smoothened, the apical impulse is not palpable. The heart is considerably enlarged and takes the form of a trapezoid or round graphite. Pulsation of contours with fluoroscopy is small. At auscultation, tones and noises are deaf (as there is effusion). Pulse is frequent, small filling; arterial pressure is lowered. Venous pressure is always increased, swelling of cervical and peripheral veins appears. The electrocardiogram is the same as with dry pericardial, an additional symptom may be a noticeable decrease in the voltage of the QRS complex. Of particular diagnostic importance is echocardiography, which establishes the presence of fluid in the heart bag. When the skin is affected, the annular erythema, which is pink ring-shaped elements that never itch, is located mainly on the skin of the inner surface of the hands and feet, as well as the abdomen, neck, and trunk. It is found only in 1-2% of patients. "Rheumatic nodules", described in the old manuals, now almost never occur. Also, nodular erythema, hemorrhage, urticaria are not characteristic. With lesions of the kidneys, weakly expressed proteinuria and hematuria are revealed (due to generalized vasculitis and lesion of the renal glomeruli and tubules). Disorders of the nervous system and sensory organs. Small chorea, the most typical "nervous form" of rheumatism, is observed mainly in children, especially in girls. Small chorea is characterized by a combination of emotional lability with muscle hypotension and violent movements of the trunk, mimic muscles and limbs. Malignant chorea is recurring, but by 17-18 years it almost always ends. A feature of this form can be a relatively small lesion of the heart, as well as slightly expressed laboratory indices of activity of rheumatism.

Diagnosis: based on anamnesis, clinical and laboratory data. In the analysis of blood neutrophilic leukocytosis with a leftward shift, thrombocytosis, an increase in ESR up to 40-60 mm / h. Characteristic growth of anti-streptococcal antibody titres: antistreptogyapuronidase and antistreptokinase more than 1: 300, antistreptolysin more than 1: 250. The height of anti-streptococcal antibody titers and their dynamics does not show the degree of activity of rheumatism. In a biochemical study, an increase in plasma fibrinogen level above 4 g / l, globulins above 10%, y-globulins above 20%, seromucoid - above 0.16 g / l, the appearance of a C-reactive protein in a blood test. In many cases, biochemical activity indicators are parallel to the value of ESR. There are large diagnostic criteria for rheumatism: polyarthritis, carditis, annular erythema, chorea, rheumatic nodules. There are small diagnostic criteria for rheumatism: fever, arthralgia, past rheumatism, rheumatic heart disease, increased ESR, positive reaction to C-reactive protein, prolongation of the P-Q interval on the ECG.

The diagnosis can be considered reliable if the patient has two large diagnostic criteria and one small diagnostic criterion or one large and two small diagnostic criteria, but only if both of the following evidence exist simultaneously, one can judge of a prior streptococcal infection: scarlet fever (which is an uncontested streptococcal disease); sowing group A streptococcus from the pharyngeal mucosa; increased titer of antistreptolysin O or other streptococcal antibodies.

Treatment. Observe bed rest for 3 weeks or more. The diet shows the restriction of table salt, carbohydrates, sufficient intake of proteins and vitamins. Exclusion of products that cause allergization. Antibacterial therapy of benzylpenicillin, sodium salt is used 2 weeks, then long-acting drugs - bicillin-5, with penicillin intolerance - replacement with cephalosporins, macrolides. Prescribe vitamin therapy, potassium preparations. Pathogenetic therapy: glucocorticoids, prednisolone. Non-steroidal anti-inflammatory drugs (indomethacin, voltaren). Preparations of aminoquinoline (resichin, delagil) - for sluggish, prolonged and chronic course. Immunosuppressants are rarely used. Symptomatic therapy of heart failure is performed. With the indications prescribed diuretic therapy. On the manifestation of small chorea, antirheumatic drugs practically do not affect. In these cases, it is recommended to add luminal or other psychotropic drugs such as aminazine or seduxen to the therapy. Great importance for the management of patients with small chorea has a calm environment, a positive attitude of others, suggesting the patient a certainty of full recovery. When necessary, measures must be taken to prevent the self-harm of the patient due to violent movements.

Treatment in a hospital is 1,5-2 months, then treatment at a local sanatorium is 2-3 months, where chronic foci of infection are treated and dispensary supervision is performed by a district pediatrician and a cardiorevmatologist.

Prevention: primary correct treatment of streptococcal infection, sanation of foci of chronic infection, rational nutrition. Secondary prophylaxis includes carrying out bicillin-medication prophylaxis to all patients regardless of age and the presence or absence of heart disease after a reliable rheumatic process. The forecast is favorable.

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Lecture № 16. Rheumatism in children and adolescents. Clinic, diagnosis, treatment

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