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Lecture notes, cheat sheets
Hospital pediatrics. Rheumatism in children and adolescents. Clinic, diagnosis, treatment (lecture notes)
Directory / Lecture notes, cheat sheets Table of contents (expand) LECTURE No. 16. Rheumatism in children and adolescents. Clinic, diagnosis, treatment Rheumatism is a systemic inflammatory disease of connective tissue with characteristic damage to the heart. Etiology, pathogenesis. The main etiological factor in acute forms of the disease is b-hemolytic streptococcus of group A. In patients with protracted and continuously recurrent forms of rheumatic carditis, it is often not possible to establish a connection between the disease and streptococcus. In the development of rheumatism, particular importance is attached to immune disorders. It is assumed that sensitizing agents in the body (streptococcus, viruses, nonspecific antigens, etc.) can lead in the first stages to the development of immune inflammation in the heart, and then to a violation of the antigenic properties of its components with their conversion into autoantigens and the development of an autoimmune process. Genetic predisposition plays a special role in the development of rheumatism. Classification. It is necessary to identify the previously inactive or active phase of the disease. Activity can be minimal (I degree), moderate (II degree) and maximum (III degree). To determine the degree of activity, the severity of clinical manifestations, as well as changes in laboratory parameters, are used. Classification according to the localization of the activity of the rheumatic process (carditis, arthritis, chorea, etc.), the state of blood circulation and the course of the disease. There is an acute course of rheumatism, a subacute course, a protracted course, a continuously relapsing course and a latent course of the disease. Isolation of the latent course is justified only for retrospective characteristics of rheumatism, latent formation of heart disease, etc. Clinic. Most often, the disease develops 1-3 weeks after a sore throat, sometimes another infection. In case of relapses, this period may be shorter. Relapses of the disease often develop after any intercurrent diseases, surgical interventions, or physical overload. A manifestation of rheumatism is a combination of acute migratory and completely reversible polyarthritis of large joints with moderately severe carditis. The onset of the disease is acute, violent, rarely subacute. Polyarthritis develops quickly, accompanied by remitting fever up to 38-40 0 C with daily fluctuations of 1-2 0 C, severe sweating, but more often without chills. The first symptom of rheumatic arthritis is acute pain in the joints, growing and intensifying with the slightest passive and active movements. The pain is accompanied by swelling of the soft tissues in the joint area and at the same time effusion appears in the joint cavity. The skin over the affected joint is hot, there is sharp pain when palpating the joint, the range of motion is limited due to pain. A characteristic feature is symmetrical damage to large joints - most often the knee, wrist, ankle, and elbow. The “volatility” of inflammatory changes is typical, manifested in the rapid and reverse development of arthritic manifestations in some joints and the same rapid increase 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 accompanying defect, is not severe, with complaints of mild pain or unpleasant, unclear sensations in the heart area, slight shortness of breath during exertion, and rarely - complaints of interruptions in the functioning of the heart, palpitations. On percussion, the heart is of normal size or moderately enlarged to the left; on auscultation and on FCG, satisfactory sonority of tones is characteristic, a slight muffling of the 1st tone, sometimes a 3rd tone is recorded, rarely a 4th tone, a soft muscular systolic murmur at the apex of the heart and projections of the mitral valve. Blood pressure is normal or moderately reduced. The ECG shows flattening, widening and jaggedness of the P wave and the QRS complex, rarely there may be an extension of the PQ interval by more than 0,2 s, in some patients a slight shift of the S-T interval is recorded downward from the isoelectric line and a change in the T wave, becoming low, negative, less often biphasic (primarily in leads V1-V3). Extrasystoles, 2-3 degree atrioventricular block, intraventricular block, and junctional rhythm rarely appear. Diffuse rheumatic myocarditis is manifested by significant inflammation of the myocardium with severe swelling and, consequently, dysfunction. From the onset of the disease, the patient is bothered by severe shortness of breath, which forces him to assume a position of orthopnea, constant pain in the cardiac region, and rapid heartbeat. Characterized by “pale cyanosis” and swelling of the neck veins. The heart is diffusely dilated, with a weak apical impulse. The tones are sharply muffled, very often a clear third tone (protodiastolic gallop rhythm) and a distinct, but significantly soft systolic murmur are heard. The pulse quickens, the filling is weak. Blood pressure is reduced. Venous pressure rises quickly, but in combination with collapse it also decreases. The ECG shows a decrease in the voltage of all waves, flattening of the T wave, a change in the S-T interval, and atrioventricular block. The outcome of rheumatic myocarditis in the absence of adequate treatment can be myocardial cardiosclerosis, which often characterizes the degree of prevalence of myocarditis. With focal cardiosclerosis, myocardial functions are not impaired. Diffuse myocardial cardiosclerosis is characterized by signs of decreased contractile function of the myocardium, which is manifested by a weakening of the apical impulse, muffled tones (especially I), and systolic murmur. Rheumatic endocarditis, which is the cause of the development of rheumatic heart defects, has very few clinical symptoms. A significant symptom on auscultation is a clear systolic murmur with sufficient sonority of tones and the absence of signs of severe myocardial damage. In contrast to the murmur associated with myocarditis, endocardial murmur is rough, but can sometimes have a musical tone. The sonority of endocardial murmur increases when the patient's position changes or after exercise. Reliable signs of endocarditis are the variability of existing murmurs and especially the emergence of new ones when the boundaries of the heart do not change. Diastolic murmurs disappear easily and quickly; they are sometimes heard at the very beginning of a rheumatic attack on the projection of the mitral valve, as well as on the vessels; in part they can also be associated with endocarditis. Deep endocarditis of the leaflets or aortic valve in some patients is reflected on the echocardiogram: thickening of the leaflets, their " shaggy", multiple echoes from them. Pericarditis is rare in rheumatism clinics. Dry pericarditis is clinically manifested by constant pain in the heart area and a pericardial friction rub, which is often heard along the left edge of the sternum. The intensity of the murmur during auscultation varies; it is often detected in both phases of the cardiac cycle. The ECG reveals an upward shift of the S-T interval in all leads at the very beginning of the disease. With further development, these intervals return to the isoelectric line, and biphasic or negative T waves are also formed simultaneously. Dry pericarditis itself is not capable of causing enlargement 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 separation of the inflammatory layers of the pericardium and the accumulating exudate. Clinical manifestations include shortness of breath, which worsens when the patient lies down. The area of the heart with a large amount of exudate swells, the intercostal spaces are smoothed, the apex beat is not palpable. The heart is significantly enlarged and takes the shape of a trapezoid or round graphite. The pulsation of the contours during fluoroscopy is small. On auscultation, the tones and noises are dull (as there is effusion). The pulse is frequent, small in filling; blood pressure is reduced. Venous pressure is always increased, swelling of the cervical and peripheral veins appears. The electrocardiogram is the same as for dry pericarditis; an additional symptom may be a noticeable decrease in the voltage of the QRS complex. Echocardiography, which determines the presence of fluid in the heart sac, is of particular diagnostic importance. When the skin is affected, annular erythema is practically characteristic, which is pink ring-shaped elements that never itch and are located mainly on the skin of the inner surface of the arms and legs, as well as the abdomen, neck, and torso. It is found in only 1-2% of patients. The “rheumatic nodules” described in the old manuals are now almost never encountered. Erythema nodosum, hemorrhages, and urticaria are also not typical. With kidney damage, mild proteinuria and hematuria are detected (due to generalized vasculitis and damage to the renal glomeruli and tubules). Damage to the nervous system and sensory organs. Lesser chorea, the most typical “nervous form” of rheumatism, is observed mainly in children, especially girls. Minor chorea is characterized by a combination of emotional lability with muscle hypotonia and violent movements of the torso, facial muscles and limbs. Minor chorea occurs with relapses, but by the age of 17-18 it almost always ends. A feature of this form may be relatively minor damage to the heart, as well as slightly expressed laboratory indicators of the activity of rheumatism. Diagnosis: based on medical history, clinical and laboratory data. In the blood test, neutrophilic leukocytosis with a shift to the left, thrombocytosis, an increase in ESR to 40-60 mm/h. An increase in titers of antistreptococcal antibodies is characteristic: antistreptohiapuronidase and antistreptokinase more than 1: 300, antistreptolysin more than 1: 250. The height of titers of antistreptococcal antibodies and their dynamics do not indicate the degree of activity of rheumatism. In a biochemical study, an increase in the level of plasma fibrinogen above 4 g/l, globulins above 10%, g-globulins - above 20%, seromucoid - above 0,16 g/l, the appearance of C-reactive protein in the blood test. In many cases, biochemical activity indicators parallel the ESR value. There are broad diagnostic criteria for rheumatism: polyarthritis, carditis, ring erythema, chorea, rheumatic nodules. There are minor diagnostic criteria for rheumatism: fever, arthralgia, previous rheumatism, the presence of rheumatic heart disease, increased ESR, a 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 major diagnostic criteria and one minor diagnostic criterion or one major and two minor diagnostic criteria, but only if both of the following evidence simultaneously exist can a previous streptococcal infection be judged: recent scarlet fever (which is an undisputed streptococcal disease); culture of group A streptococcus from the pharyngeal mucosa; increased titer of antistreptolysin O or other streptococcal antibodies. Treatment. Maintain bed rest for 3 weeks or more. The diet shows a limitation of table salt, carbohydrates, and a sufficient introduction of proteins and vitamins. Exclusion of allergenic products. Antibacterial therapy with benzylpenicillin, sodium salt is used for 2 weeks, then long-acting drugs - bicillin-5, in case of penicillin intolerance - replacement with cephalosporins, macrolides. Vitamin therapy and potassium supplements are prescribed. Pathogenetic therapy: glucocorticoids, prednisolone. Non-steroidal anti-inflammatory drugs (indomethacin, voltaren). Aminoquinoline preparations (rezoquin, delagil) - for sluggish, protracted and chronic course. Immunosuppressants are rarely used. Symptomatic treatment of heart failure is carried out. When indicated, diuretic therapy is prescribed. Antirheumatic drugs have practically no effect on the manifestation of minor chorea. In these cases, it is recommended to add luminal or other psychotropic drugs such as aminazine or seduxen to the therapy. Of great importance for the management of patients with chorea minor is a calm environment, a positive attitude from others, and instilling in the patient confidence in a complete recovery. If necessary, it is necessary to take measures to prevent the patient from self-harm due to violent movements. Treatment in a hospital is 1,5-2 months, then treatment in a local sanatorium for 2-3 months, where chronic foci of infection are treated and follow-up with a local pediatrician and cardio-rheumatologist. Prevention: primary correct treatment of streptococcal infection, sanitation of foci of chronic infection, balanced nutrition. Secondary prevention includes bicillin-drug prophylaxis for all patients, regardless of age and the presence or absence of heart disease, who have undergone a significant rheumatic process. The prognosis is favorable. Author: Pavlova N.V. << Back: Helminthiasis in children. Clinic, diagnosis, treatment, prevention (Ascariasis. Alveococcosis. Hookworm disease (hookworm and necatoriasis). Diphyllobothriasis. Opisthorchiasis. Teniosis. Trichocephalosis. Fascioliasis. Echinococcosis. Enterobiasis) >> Forward: Broncho-obstructive syndrome. Clinic, diagnosis, treatment. Respiratory failure. Clinic, diagnosis, treatment (Acute bronchitis. Respiratory failure)
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