Dispensary observation of children with congenital heart defects. Medical examination of patients with heart disease

In most cases, in the second half of the first year of life. According to many authors, by the age of 1 year of life, the oval window closes in only 50-60% of children. It is believed that it can close spontaneously throughout the life of an adult. In place of the closed oval window an oval fossa remains in the form of a depression, occupying up to 28% of the area interatrial septum in the middle part. In cases of non-closure of the embryonic foramen, an open oval window is detected, which is found according to data various authors in 17-35% of adults.

The fundamental anatomical difference between a secondary ASD is that with an ASD there is organic defect - the absence of a greater or lesser part of the septum / minus tissue, while with non-closure of the atrial valve / valve / or insufficiency of the oval valve. At the same time, the presence of a valve does not guarantee the reliability of the obturator function and in some cases may be accompanied by antivalvular flow.

It is believed that in most cases it is practically asymptomatic and it is difficult to identify any specific clinical manifestations. Patients may experience transient cyanosis due to an acute increase in pulmonary vascular resistance during screaming or prolonged breath-holding.

There are no physical findings that indicate PFO unless there are concomitant congenital heart defects. However, it should be suspected in patients with transient generalized cyanosis.

A moderate left-to-right shunt is accompanied by physical findings that are noted in secondary ASD. These findings include a fixed split second heart sound, pulmonary systolic murmur exile.

Literature data demonstrate an ambiguous approach to assessment clinical role minor anomaly. More recently, the point of view on the practical harmlessness of PFO has steadily prevailed, considering it as a variant of the normal development of the interatrial septum. This point of view still exists in the works of some domestic authors, who believe that with this defect there are no hemodynamic disturbances and no surgical correction is required. However, along with the recognition of the anomaly as a practically insignificant anomaly, there are facts indicating the possibility of serious life-threatening complications arising against its background. First of all, this concerns the problem of paradoxical embolism and hypoxemic conditions. They are caused by the activation of pathological blood flows through the interatrial opening. In such cases it functions as an atrial septal defect. The main reason for this is considered to be the incompetence of the oval window valve and the appearance of a “valvular-inferior” PFO, which occurs as a result of stretching of the interatrial septum (during atrial dilatation).

The combination of manifestations of disembryogenesis is natural. This concerns an aneurysm of the interatrial septum. Currently, aneurysm of the interatrial septum is regarded as a combined factor of embolization in persons with PFO.

Diagnostics: EchoCG - a gap is detected in the middle part of the MR, caused by PFO. Color Doppler ultrasound confirms a left-to-right shunt through the PFO.

Differential diagnosis: ASD (primary, secondary, in the coronary sinus area), total anomalous drainage of the pulmonary veins

Tactics for managing individuals when identifying PFO: children with a small shunt need some kind of treatment. Oxygen therapy is indicated for children who experience transient cyanosis, as well as for patients with a right-to-left shunt through pulmonary hypertension.

The activity of children is not limited, with the exception of patients with PFO, who develop cyanosis during exercise.

Observation is carried out for children with transient central cyanosis. They are indicated for transcatheter occlusion of the LLC.

Complications: transient cyanosis, systemic paradoxical embolism, cerebral stroke due to paradoxical embolism.

LLC 2-4 mm, without shunt, and also in the absence of dilatation of the right chambers of the heart and pulmonary hypertension is not a congenital heart defect.

Patent ductus arteriosus

Frequency. PDA is observed among 5-10% of all children with congenital heart disease, if you do not take into account premature newborns, in whom the presence of PDA is a typical problem. In children with a birth weight of less than 1750 grams, the presence of a persistent ductus arteriosus is determined in 45%, and in 80% of children with a body weight of less than 1200 grams.

Pathanatomy. The ductus is usually a vessel that normally exists in utero connecting the trunk of the pulmonary artery and the descending aorta, usually 5-10 mm distal to the orifice of the left subclavian artery. The duct usually has a narrower opening at the pulmonary artery. The size and shape of the duct varies widely.

Clinical manifestations. With a small PDA, patients usually have no symptoms. With a large PDA, signs of heart failure are characteristic: poor weight gain, shortness of breath and tachycardia, frequent respiratory infections, pneumonia.

Physical examination. In patients with a large PDA and a significant left-to-right shunt, hyperreactivity and an increase in heart size upon palpation are determined. Systolic murmur is determined along the left edge of the sternum. The pulsation of the arteries in the extremities may be increased due to a decrease in diastolic pressure. The second tone is normal, but when the pressure in the pulmonary artery increases, its accent is determined. A medium-sized PDA is characterized by a continuous systolic-diastolic murmur.

Echocardiography. Allows visualization of the PDA in most patients. Doppler studies help determine the hemodynamic situation, shunt direction, and pressure gradient.

Figure 3. Diagram of the PDA.

Forecast. Spontaneous closure of the PDA may be delayed in the healthy newborn but is rarely observed after 1 month of life. With a large shunt, heart failure and repeated pneumonia develop, which can lead to death at an early age. Presence of PDA premature newborn in combination with immaturity of the pulmonary parenchyma, it often leads to heart failure, bronchopulmonary dysplasia, and dependence on artificial ventilation. In the absence of treatment (medical or surgical) aimed at closing the PDA, such conditions are accompanied by high mortality.

Treatment. Indomethacin is used to close a PDA in premature newborns. Indomethacin administration is not effective in full-term neonates. The presence of a PDA, regardless of size, is an indication for its surgical closure.

Coarctation of the aorta

Frequency. Narrowing thoracic aorta in the isthmus region (immediately distal to the origin of the left subclavian artery) occurs in 10% of all congenital heart diseases. CA is more often described in males. Bicuspid aortic valve occurs in 2/3 of patients with coronary artery disease. VSD is accompanied by coronary artery disease in 50% of cases. CA is also a component of other complex heart defects, the pathophysiology of which involves an increase in pulmonary blood flow.

Anatomy and physiology. When the aorta is narrowed below the isthmus, the ductus arteriosus continues to supply blood to the descending aorta after birth (the fetal type of circulation persists). As soon as the pressure in the pulmonary artery begins to decrease, blood circulation to organs and tissues below the diaphragm deteriorates sharply, leading to the development of anuria, acidosis and death. Early surgical correction allows you to restore the patency of the aorta. Used as an emergency resuscitation measure intravenous administration prostaglandin E 1, which allows you to maintain patency of the ductus arteriosus for as long as desired. If the narrowing of the aorta is moderate, the child experiences natural closure of the ductus arteriosus. In this case, as a rule, a network of collateral vessels develops connecting the aortic arch with the descending aorta below the coarctation. Despite the collaterals, the pressure in the aorta before coarctation becomes higher than normal, and below the coarctation site it becomes lower than normal. Hypertension in the arms can be severe already in the first months of life, and left ventricular function is often impaired.

Figure 4. Diagram of aortic coarctation.

Clinical manifestations. In newborns, the first clinical manifestation may be anuria, acidosis and circulatory collapse with satisfactory or decreased pressure in the arms and absence of pulse and blood pressure in the legs. At older ages, there is also a difference in blood pressure and pulsation of the arteries of the upper and lower half of the body.

Auscultatory data are scanty. Systolic murmur is easiest to hear on the back in the interscapular area. With developed collateral circulation, the noise can be heard over the entire chest.

Echocardiography in young patients allows for an accurate diagnosis. Visualization of the aortic isthmus in older children is more difficult.

Treatment. Surgical treatment is indicated at any age upon diagnosis, usually in the first months of life. The operation consists of resection of the narrowed area, with restoration of the aortic lumen using an end-to-end anastomosis from the left lateral thoracotomy. In 5-10% of patients, recurrence of coarctation is observed after surgical treatment. The procedure of choice for these patients is balloon dilatation of the narrowed segment.

Tetralogy of Fallot

Frequency. TF is observed in 10% of all children with congenital heart disease. This is the most common cyanotic defect observed after the first year of life.

Pathanatomy. The original description of TF, as a combination of four signs (stenosis of the outflow tract of the right ventricle, VSD, dextroposition of the aorta, hypertrophy of the right ventricular myocardium), was reduced to a description of two main components: VSD and stenosis of the outflow tract of the right ventricle. VSD in TF is large, non-restrictive, occupies the entire subaortic region, usually equal to or greater than the diameter of the aorta. In 3% of cases, multiple VSDs are observed. Obstruction of the outlet of the right ventricle is observed in 75% of patients at the level of the outflow tract. In 30% of children it is associated with pulmonary valve stenosis. In only 10% of patients, stenosis is limited only to the pulmonary valve.

Clinical manifestations. A systolic murmur is heard immediately after birth. Most patients are cyanotic immediately after birth. Dyspnea on exertion and hypoxic attacks develop later in children with moderate cyanosis. Heart failure is not common. Young children with acyanotic TF may be asymptomatic or may have signs of heart failure due to a left-to-right shunt.

Figure 5. Diagram of tetralogy of Fallot.

Physical examination. 1. Clinical manifestations depend on the degree of obstruction of the right ventricular outflow tract. The less pulmonary blood flow, the more pronounced the hypoxia. The most typical blood oxygen saturation is around 70-75%. Visible cyanosis depends on two factors: the degree of hypoxia and hemoglobin content. The higher the hemoglobin, the earlier cyanosis is noticeable.

2. Intense systolic murmur is heard along the left edge of the sternum. The more severe the obstruction of the right ventricular outflow tract, the shorter and weaker the murmur. The second tone can be unsplit (since there is no pulmonary component) and accentuated (due to an increase in the size and dextroposition of the aorta). In patients with pulmonary atresia, a constant systole may be heard. diastolic murmur PDA or large aortopulmonary collateral vessels. Long-term cyanosis leads to characteristic changes nail phalanges fingers (drum sticks).

Echocardiography. Two-dimensional echocardiography and Doppler ultrasound may be sufficient to make a diagnosis and determine a treatment plan.

Forecast. Children with TF gradually become more cyanotic. Hypoxic attacks can develop in children early age(usually between 2 and 4 months of age) and can cause neurological damage and death. Developmental delay is observed in cases of severe cyanosis. Thromboembolic complications and brain abscesses may develop. Septic endocarditis is one of the possible complications.

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Figure 6. Schematic of TMS.

Strengthening the first tone and diastolic murmur at the apex are caused by increased blood flow through the mitral valve.

X-ray examination: the pulmonary pattern is enhanced, the cardiac shadow has the configuration of an “egg” lying on its side, the heart is enlarged in size due to both ventricles, the vascular bundle is narrow in the anteroposterior projection and expanded in the lateral projection.

ECG: EOS deviation to the right, hypertrophy of the right atrium and right ventricle, left ventricular hypertrophy in the presence of VSD.

FKG: confirms auscultation data. There is no murmur or the systolic murmur of a VSD is recorded.

ECHOCG: the origin of the aorta from the right ventricle, the pulmonary artery from the left, the location of the aorta in front and to the right of the pulmonary artery, visualization of the VSD, ASD or PDA.

Probing of the heart cavities: decreased blood oxygen saturation in the peripheral arteries, origin of the aorta from the right ventricle and the pulmonary artery from the left ventricle, increased pressure in the left ventricle with VSD or pulmonary stenosis.

Course of the disease. According to many authors, 28% of children born with complete TMS die in the first week of life, 52% in the first month of life, 89% by the end of the first year, 7% before the age of 5 years, 2% before the age of 10 years. The causes of death in non-operated patients are: severe hypoxemia, heart failure, concomitant diseases (pneumonia, ARVI, sepsis).

Treatment of patients with TMS is only surgical and, if possible, it should be early. To date, over 50 methods of surgical treatment have been proposed, which are divided into two main types: palliative and corrective.

Newborns who are in critical condition, a closed balloon or knife atrioseptotomy is performed, which allows them to prolong their life. Others palliative operations are excision of the interatrial septum, systemic-pulmonary anastomoses with TMS with PA stenosis.

Radical correction in IR conditions is in the direction venous blood using a patch from the vena cava into the left ventricle, from which the pulmonary artery arises (intra-atrial correction). Movement is also used main arteries with simultaneous transplantation of the ostia of the coronary arteries into the base of the pulmonary trunk. Operative mortality radical correction defect is 15-20%.

Corrected TMS is less common. It accounts for 1-1.4% of all congenital heart defects. With this defect, the aorta departs from the anatomically right ventricle, which receives blood from the left atrium, into which the pulmonary veins flow. The pulmonary artery arises from the anatomically left ventricle, which receives blood from the right atrium, into which the vena cava flows. Corrected TMS itself does not cause hemodynamic disturbances, since arterial blood enters the systemic circle, and venous blood enters the small circle.

CHILDREN AND REHABILITATION OF CHILDREN WITH CHD

Principles of organizing care for newborns with congenital heart disease:

1) timely identification in the maternity hospital of children with suspected congenital heart disease;

2) topical diagnosis of the defect;

4) timely surgical treatment.

All children suspected of having congenital heart disease should be examined by a cardiologist, sent to a specialized hospital and then to cardiology centers to establish a topical diagnosis of the defect. During examination in a hospital (general clinical examination, ECG, FCG, radiography in three projections, EchoCG with Dopplerography, blood pressure measurement in the upper and lower lower limbs, exercise tests and pharmacological tests) a detailed diagnosis must be made, indicating the topic of congenital heart disease, the degree of pulmonary hypertension, the phase of the defect, the functional class, the degree of heart failure, the nature of complications and concomitant diseases. In all cases of congenital heart disease, consultation with a cardiac surgeon is necessary to decide on the indications and timing of surgical correction of the defect.

If there are signs of circulatory disorders, medicinal cardiotonic, cardiotrophic and restorative therapy is carried out. For patients with stage 1-2 heart failure, it is sufficient to carry out only cardiotrophic and restorative therapy (treatment of dystrophy, anemia, hypovitaminosis, immunocorrection). Patients with stage 3-4 HF after active cardiotonic and diuretic therapy (except for patients with TF, hypertrophic subaortic stenosis) and treatment with vasodilators (ACE inhibitors) are discharged under outpatient supervision of a cardiologist and pediatrician. They are recommended to undergo prolonged treatment with maintenance doses of cardiac glycosides, ACE inhibitors, potassium and magnesium supplements, and cardiotrophs.

Patients with congenital heart disease are discharged from the hospital (with the timing of the next planned hospitalization determined) under outpatient supervision by a cardiologist and pediatrician.

Children in the first month of life with congenital heart disease are observed by a cardiologist weekly, in the first half of the year - 2 times a month, in the second - monthly, after the first year of life - 2 times a year. At least once a year, and sometimes more often, the patient should be routinely examined in a hospital, including examined by a cardiac surgeon, for dynamic monitoring, dose adjustment of maintenance therapy, and sanitation of foci of infection. In this case, it is necessary to register an ECG at least once a quarter, an echocardiography twice a year, and a chest x-ray once a year.

Current opinion about a significant restriction motor activity patients with congenital heart disease recent years considered incorrect. Physical inactivity only worsens the functional state of the myocardium, especially against the background of the natural, age-related physical activity of the child’s body. Taking into account the characteristics of each congenital disorder, it is necessary to conduct regular exercise therapy classes according to a lightweight program, therapeutic massage courses, and hardening procedures.

Preventive vaccinations contraindicated in complex cyanotic defects or pale type congenital heart disease with heart failure of 3-4 functional classes, as well as in the presence of signs of current subacute bacterial endocarditis.

Psychological rehabilitation.

Patients with cyanotic heart defects occurring with blood thickening, impaired rheology, polycythemia, for prevention of possible thrombosis, especially in the hot seasons of the year, should consume a sufficient amount of fluid, and also take anticoagulants and antiplatelet agents (chimes, phenylin) in small doses.

Sanitation of chronic foci of infection(consultation with a dentist and otolaryngologist 2 times a year).

Radical elimination of the defect has a significant positive effect on the functional state of the body. Children begin to gain weight, their signs of circulatory disorders significantly decrease, their motor activity increases, and their tendency to recurrent symptoms decreases. respiratory diseases and the likelihood of developing bacterial endocarditis.

To prevent the development of infective endocarditis, it is necessary to isolate risk groups for IE, which includes:

All patients with congenital heart disease, especially with cyanotic congenital heart disease (TF, TMS with pulmonary artery stenosis), with aortic stenosis, bicuspid aortic valve, coronary artery disease, small IVS defects;

Patients with auscultatory form of MVP;

All patients operated on for congenital heart disease, especially with the application of patches made of synthetic material;

Patients with congenital heart disease who underwent catheterization of the cardiac cavities and great vessels, and insertion of pacemakers;

Patients with congenital heart disease who received valve prostheses as a result of surgery;

Patients cured of infective endocarditis.

Patients with operated congenital heart disease in the first 2-6 months are especially at risk for the occurrence of IE. after surgery, with weakened immunity, festering wounds, a tendency to pyoderma and furunculosis, as well as chronic foci of infection.

Primary prevention IE in all children with congenital heart disease and auscultatory form of MVP includes:

Ñ medical examination by a cardiologist with a planned quarterly examination (general blood and urine analysis, blood pressure, ECG), echocardiography - 2 times a year, chest x-ray once a year. Consultation with a dentist and otolaryngologist – 2 times a year.

Ñ in case of accumulation of intercurrent diseases (ARVI, tonsillitis, bronchitis, etc.), it is necessary to carry out antibiotic therapy (penicillins, macrolides orally or intramuscularly for 10 days).

Ñ chronic foci of infection should be sanitized while simultaneously carrying out a full course of conservative treatment.

Ñ minor surgical operations (tonsillectomy, adenectomy, tooth extraction, dental filling of the lower gum level, surgical treatment of boils and other surgical procedures, as well as installation of venous catheters, hemodialysis, plasmapheresis) and other interventions that can cause short-term bacteremia should be carried out strictly according to indications and under the “cover” of antibiotics). Antibiotics (semi-synthetic penicillins or macrolides) are prescribed 1-2 days before surgery and for 3 days after it.

After heart surgery, especially in the first 2 - 6 months, it is necessary to carry out daily thermometry. A general blood and urine test is performed every 10 days during the first month after surgery, 2 times a month during the first half of the year, and monthly during the second half of the year. Registration of ECG and echocardiography is carried out quarterly in the first half of the year, and then 2 times a year, chest x-ray once a year. After discharge from the surgical cardiac center for examination, the child is sent to the inpatient cardiology department after 3 months to consolidate the effect, conduct an examination, a course of immunomodulatory, cardiotrophic and vitamin therapy, and physical therapy.

Particular attention should be paid to the “frozen” curve of weight dynamics, the periodic appearance of low-grade fever in operated patients, pallor, increased sweating, decreased exercise tolerance, increased “old” and the appearance of new heart murmurs, increasing anemia, periodic increasing ESR, moderate leukocyte neutrophilia, dysproteinemia, changes in urine tests. In such cases, it is necessary to perform 2-3 repeated blood cultures for flora, examination and treatment in a hospital.

Spa treatment It is recommended to carry out in local cardio-rheumatology sanatoriums. It is indicated annually for patients with congenital heart disease for 60-120 days a year, before and after surgery. Contraindications for children to stay in a sanatorium: severe circulatory disorders, heart failure of functional classes 3-4, signs of current subacute bacterial endocarditis, less than three weeks after an intercurrent illness and a year after surgery.

Children are not removed from the dispensary register and are transferred under the supervision of a therapist. Careful outpatient follow-up helps prevent the occurrence or progression of complications in children with congenital heart disease in the pre- and postoperative periods.

Friedli suggested classification of types of correction of congenital heart disease based on the likelihood that the patient will require further subsequent surgery:

n True full correction leads to restoration of normal cardiac anatomy and function and is usually possible with secondary defects interatrial septum, ventricular septal defects, patent ductus arteriosus, coarctation of the aorta. Although late complications sometimes occur in some patients, most children are treated normal life without repeated surgery.

n Anatomical correction with residual effects can be performed in patients with tetralogy of Fallot, atrioventricular septal defects and valvular obstructions treated by valvotomy or valve repair. These patients experience resolution of symptoms and abnormal physiology, but retain residual defects such as valve regurgitation or arrhythmias that may require further intervention.

n Correction using prosthetic materials used in patients who require an anastomosis between the right ventricle and the pulmonary artery (pulmonary atresia with VSD). Due to somatic growth and degeneration of the prosthetic material, this category of patients will require reoperation to replace a prosthesis.

n Physiological correction(operations Senning And Mustard regarding transposition of the great arteries, Fontan operation in patients with a three-chamber heart) eliminates disorders cardiovascular physiology, but does not eliminate anatomical disorders. Such patients almost always develop late complications requiring surgical or conservative intervention.

This classification is very useful for pediatricians and pediatric cardiologists to use in practice in order to predict the likelihood of problems in the operated patient and plan further observation.
The number of patients who have undergone surgical correction of congenital heart disease is growing at a rate that far exceeds the growth in the number and workload of pediatric cardiologists. As a result, the local pediatrician will be forced to take on responsibilities in monitoring this complex group patients. The pediatrician must be aware of all remaining disorders and potential complications that may develop in order to promptly refer the patient to a specialist.

We hope that the issues of classification, diagnosis and follow-up of children with congenital heart disease presented in this manual will help to make a timely and correct diagnosis and reduce the incidence of complications in patients with this pathology.

Careful outpatient follow-up helps prevent the occurrence or progression of complications in children with congenital heart disease in the pre- and postoperative periods.

LIST OF REFERENCES USED

1. Belokon of the heart and blood vessels in children // MoscowVol. 1.- p. 447.

2. , Podzolkov heart defects // Moscow – p. 350.

3. Mutafyan heart defects in children // Moscow. – 2002. – p. 330.

5. , Sinkovsky diagnosis of congenital heart defects // Children's diseases of the heart and blood vessels No. 1. – pp. 39-47.

7. Galdin, clinics and diagnosis of heart failure in childhood and principles of its treatment // Bulletin of Arrhythmology. – 2000. - No. 18.-S. 38-40.

8., Tabolin on pharmacotherapy in pediatrics and pediatric surgery. Clinical cardiology // M.-2004.-p.161.

9. Shkolnikova cardiology in Russia at the turn of the century // Bulletin of Arrhythmology. – 2000. - No. 18. – P. 15-22.

10. Wielenga R. P., Huisveld I. A., Bol E. Safety and effects of physical training in chronic heart failuar // Eur. Heart J. – 1999. - No. 20. – P. 872-8

List of abbreviations

AVK – atrioventricular communication;

BP – blood pressure;

APLV – anomalous pulmonary venous drainage;

CHD – congenital heart defect

GLS – main pulmonary trunk;

DDA – double arc aorta;

VSD - ventricular septal defect;

ASD – atrial septal defect;

EVC is the only ventricle of the heart;

IE – infective endocarditis;

CA – coarctation of the aorta;

PDA – patent ductus arteriosus;

TAS – common truncus arteriosus;

MVP – mitral valve prolapse4

SA – aortic stenosis;

PAS – pulmonary artery stenosis;

HF – heart failure;

TMS – transposition of great vessels;

TF – tetralogy of Fallot;

Appendix 1.

Division of congenital heart defects depending on

from the age chronology of the first symptoms

Defects that manifest only in newborns

Defects that manifest primarily in newborns

Defects in newborns, most often not accompanied by hemodynamic disturbances

Defects manifesting in all age groups

1. Hypoplasia of the left half of the heart

2. Pulmonary valve atresia

3. Complete anomalous drainage of the pulmonary veins

4. Prenatal narrowing or fusion of the oval window

1. Complete transposition of the aorta and pulmonary artery

2. Common true truncus arteriosus

3. Two-chambered heart

1. Atrial septal defect

2. Ventricular septal defect

3. Tetralogy of Fallot (except in cases with a

4. 9pulmonary atresia)

2. Coarctation of the aorta

3. Aortic stenosis

4. Pulmonary valve stenosis

5. Tetralogy of Fallot with pulmonary atresia

6. Tricuspid valve atresia

8. Ebstein's disease

abnormal drainage of pulmonary veins

10. Atrioventricular valve

Appendix 2.

Principles of organizing care for newborns with congenital heart disease:

1) timely identification in the maternity hospital of children with suspected congenital heart disease;

2) topical diagnosis of the defect;

4) timely surgical treatment.

All children suspected of having congenital heart disease should be examined by a cardiologist, sent to a specialized hospital and then to cardiology centers to establish a topical diagnosis of the defect. During an examination in a hospital (general clinical examination, ECG, FCG, radiography in three projections, echocardiography with Dopplerography, blood pressure measurements in the upper and lower extremities, exercise tests and pharmacological tests), a detailed diagnosis must be made indicating the topic of congenital heart disease, the degree of pulmonary hypertension , phase of the defect, functional class, degree of heart failure, nature of complications and concomitant diseases. In all cases of congenital heart disease, consultation with a cardiac surgeon is necessary to decide on the indications and timing of surgical correction of the defect.

If there are signs of circulatory disorders, medicinal cardiotonic, cardiotrophic and restorative therapy is carried out. For patients with stage 1-2 heart failure, it is sufficient to carry out only cardiotrophic and restorative therapy (treatment of dystrophy, anemia, hypovitaminosis, immunocorrection). Patients with stage 3-4 HF after active cardiotonic and diuretic therapy (except for patients with TF, hypertrophic subaortic stenosis) and treatment with vasodilators (ACE inhibitors) are discharged under outpatient supervision of a cardiologist and pediatrician. They are recommended to undergo prolonged treatment with maintenance doses of cardiac glycosides, ACE inhibitors, potassium and magnesium supplements, and cardiotrophs.

Patients with congenital heart disease are discharged from the hospital (with the timing of the next planned hospitalization determined) under outpatient supervision by a cardiologist and pediatrician.

Children of the first month Living with congenital heart disease are observed by a cardiologist weekly, in the first half of the year - 2 times a month, in the second - monthly, after the first year of life - 2 times a year. At least once a year, and sometimes more often, the patient should be routinely examined in a hospital, including examined by a cardiac surgeon, for dynamic monitoring, dose adjustment of maintenance therapy, and sanitation of foci of infection. In this case, it is necessary to register an ECG at least once a quarter, an echocardiography twice a year, and a chest x-ray once a year.

The existing opinion about the significant limitation of motor activity of patients with congenital heart disease in recent years is considered incorrect. Physical inactivity only worsens the functional state of the myocardium, especially against the background of the natural, age-related physical activity of the child’s body. Taking into account the characteristics of each congenital disorder, it is necessary to conduct regular exercise therapy classes according to a lightweight program, therapeutic massage courses, and hardening procedures.

Preventive vaccinations are contraindicated in complex cyanotic defects or pallid congenital heart disease with heart failure of functional classes 3-4, as well as in the presence of signs of current subacute bacterial endocarditis.

Psychological rehabilitation.

Patients with cyanotic heart defects, occurring with thickening of the blood, impaired rheology, polycythemia, to prevent possible thrombosis, especially in the hot seasons of the year, should consume a sufficient amount of fluid, and also take anticoagulants and disaggregants (chimes, phenylin) in small doses.

Sanitation of chronic foci of infection (consultation with a dentist and otolaryngologist 2 times a year).

To prevent the development of infective endocarditis, it is necessary to identify risk groups for IE, which include:

All patients with congenital heart disease, especially cyanotic ones, all patients operated on for congenital heart disease, especially with patches made of synthetic material; - patients with congenital heart disease who received valve prostheses as a result of surgery; - patients cured of infective endocarditis.

Patients with operated congenital heart disease in the first 2-6 months are especially at risk for the occurrence of IE. after surgery, with weakened immunity, festering wounds, a tendency to pyoderma and furunculosis, as well as chronic foci of infection.

Primary prevention of IE in all children with congenital heart disease is medical examination by a cardiologist with a planned quarterly examination (general blood and urine analysis, blood pressure, ECG), echocardiography - 2 times a year, chest x-ray once a year. Consultation with a dentist and otolaryngologist - 2 times a year; in case of intercurrent diseases (ARVI, tonsillitis, bronchitis, etc.), it is necessary to carry out antibiotic therapy (penicillins, macrolides orally or intramuscularly for 10 days).

Minor surgical operations (tonsillectomy, adenectomy, tooth extraction, dental filling of the lower gum level, surgical treatment of boils and other surgical procedures, as well as installation of venous catheters, hemodialysis, plasmapheresis) and other interventions that can cause short-term bacteremia should be carried out strictly according to indications and under the “cover” of antibiotics). Antibiotics (semi-synthetic penicillins or macrolides) are prescribed 1-2 days before surgery and for 3 days after it.

After heart surgery, especially in the first 2 - 6 months, it is necessary to carry out daily thermometry. A general blood and urine test is performed every 10 days during the first month after surgery, 2 times a month during the first half of the year, and monthly during the second half of the year. Registration of ECG and echocardiography is carried out quarterly in the first half of the year, and then 2 times a year, chest x-ray once a year. After discharge from the surgical cardiac center for examination, the child is sent to the inpatient cardiology department after 3 months to consolidate the effect, conduct an examination, a course of immunomodulatory, cardiotrophic and vitamin therapy, and physical therapy.

Spa treatment It is recommended to carry out in local cardio-rheumatology sanatoriums. It is indicated annually for patients with congenital heart disease for 60-120 days a year, before and after surgery. Contraindications for children to stay in a sanatorium: severe circulatory disorders, heart failure of functional classes 3-4, signs of current subacute bacterial endocarditis, less than three weeks after an intercurrent illness and a year after surgery.

Children are not removed from the dispensary register and are transferred under the supervision of a therapist. Careful outpatient follow-up helps prevent the occurrence or progression of complications in children with congenital heart disease in the pre- and postoperative periods.

During the first phase of the vice frequency of examination by a pediatrician of children with congenital heart disease without hemodynamic disturbances 2 times a year; after inpatient treatment, 6 months monthly, then once every 2 months up to a year.. A cardio-rheumatologist examines the child 2-4 times a year, with severe course(blue type defect, pulmonary hypertension, etc.) 1 time every 1-2 months. Consultation with a dentist and ENT doctor 2 times a year, other specialists - as indicated. The cardiac surgeon consults the child when making a diagnosis, then according to indications. Children who have undergone operations for congenital heart disease, including palliative ones, are examined once every 2-3 months in the first year after the intervention, then 1-2 times a year.

Examination methods: blood tests, urine tests 2 times a year, X-ray examination 1 time a year, Echo-CG, ECG 1 time every 6 months. Other studies according to indications.

Indications for hospitalization: clarification of the diagnosis of congenital heart disease, the appearance of decompensation symptoms, severe hypoxemic crises, the development of complications, intercurrent diseases. Surgical debridement of foci of chronic infection no earlier than 6 months after surgery for heart disease. Contraindications for surgical debridement of foci of infection are the presence of symptoms of decompensation, hemorrhagic diathesis in children with the third phase of blue defect, complications from the central nervous system.

One of the leading tasks of rehabilitation of congenital heart disease is compensation of heart failure. The regimen for a child with congenital heart disease provides for widespread use fresh air both at home and outdoors. The temperature should be maintained between 18-20 degrees with frequent ventilation. A child’s participation in outdoor games with other children should be determined not by the nature of the defect, but by its compensation and the child’s well-being. Children suffering from congenital heart disease limit their own motor activity. In the presence of congenital heart disease with unimpaired hemodynamics, children study in weakened groups in kindergarten, and in preparatory groups at school. If there are hemodynamic disturbances, a special group is permanently assigned, exercise therapy. After heart surgery, exemption from physical education for 2 years, permanent exemption for symptoms of cardiac or pulmonary insufficiency. Twice a year (spring and autumn) a course of treatment is carried out with cardiotropic drugs: riboxin, cocarboxylase, ATP, corhormone, intercordin, potassium orotate, glutamic acid, vitamin therapy.

Physical education classes in the absence of hemodynamic disorders - in the preparatory group, in the presence of hemodynamic disorders - in special group constantly or exercise therapy. After heart surgery, exemption from physical education for 2 years.

Dispensary observation Before transfer to an adult clinic, after surgical treatment, the issue of medical examination is decided individually. Health group III-V.

MITRAL DEFECTS

Clinical examination

Patients with valvular heart defects are observed by a family doctor or local physician during consultations with a rheumatologist and cardiologist according to the nosological principle in the groups “rheumatic fever”, “rheumatic arthritis”, “Bechterew’s disease”, “systemic lupus erythematosus”, etc.

The frequency of inspections is at least 4 times a year. The scope of the examination is a clinical analysis of blood, urine, X-ray examination of the chest organs, ECG, FCG, echocardiography, biochemical blood tests - acute phase reactions, glycosaminoglycans. If necessary, consultations with an ENT specialist, dentist, ophthalmologist, neurologist. If indicated, consult a cardiac surgeon.

Complex therapeutic measures determined by the underlying disease leading clinical symptom complexes- heart failure, arrhythmias, etc.

Criteria for the effectiveness of clinical examination: reducing the frequency of relapses of the disease, reducing the period of temporary disability, the number of patients on disability.

Mitral stenosis is a common acquired heart defect. It can be observed in a “pure” form or in combination with mitral valve insufficiency.

Etiology. Almost all cases of mitral stenosis are a consequence of rheumatism. Quite often, the history of such patients (up to 30-60% of cases) does not contain obvious rheumatic attacks, however, there should be no doubt about the rheumatic origin of the defect.

Mitral stenosis usually forms at a young age and is more often observed in women.

Pathogenesis. Hemodynamic changes . In humans, the area of ​​the left atrioventricular opening varies between 4-6 cm 2 . It has a significant reserve area, so only reducing it by more than half can cause noticeable hemodynamic changes.

The narrowed mitral orifice serves as an obstacle to the expulsion of blood from the left atrium, therefore, to ensure normal blood filling of the left ventricle, a number of compensated mechanisms are activated.

The pressure in the atrium cavity increases (from 5 mmHg to 25 mmHg). This increase in pressure leads to an increase in the pressure difference between the left atrium and the left ventricle, resulting in easier passage of blood through the narrowed mitral orifice. Left atrial systole lengthens and blood enters the left ventricle for a longer time. These two mechanisms - an increase in pressure in the left atrium and an extension of the systole of the left atrium at first compensate negative influence narrowed mitral orifice on intracardiac hemodynamics.



A progressive decrease in the orifice area causes a further increase in pressure in the cavity of the left atrium, which simultaneously leads to a retrograde increase in pressure in the pulmonary veins and capillaries. In some patients (30%), a further increase in pressure in the left atrium and pulmonary veins due to irritation of baroreceptors causes a reflex constriction of arterioles (Kitaev reflex). This protective reflex protects the pulmonary capillaries from excessive increases in pressure and sweating of the liquid part of the blood into the cavity of the alveoli. Subsequently, prolonged spasm of arterioles leads to the development morphological changes. This creates a second barrier to blood flow, thereby increasing the load on the right ventricle. As a result, its hyperfunction and hypertrophy reach pronounced degrees. A significant increase in pressure in the pulmonary artery and right ventricle makes it difficult to empty the right atrium, which is also facilitated by a decrease in the ventricular cavity due to its pronounced hypertrophy. The difficulty of expelling blood from the right atrium causes an increase in pressure in its cavity and the development of hypertrophy of its myocardium.

Incomplete emptying of the right ventricle during systole leads to
an increase in diastolic pressure in its cavity. The developing dilatation of the right ventricle and the relative insufficiency of the tricuspid valve slightly reduce the pressure in the pulmonary artery, but the load on the right atrium increases to an even greater extent. As a result, decompensation develops in a large circle.

Clinic. From the analysis of the pathophysiological features of the defect, it follows that the clinical picture of the disease at different stages of its development will differ in some features. However, all patients with mitral stenosis should have objective signs, depending solely on the characteristics of the valve lesion.

Complaints. If mitral stenosis is not pronounced and is compensated by increased work of the left atrium, then patients may not complain. They are able to perform quite significant physical activity. When pressure in the pulmonary circle increases, complaints of shortness of breath during physical activity appear. Another complaint is a cough, dry or with a small amount of mucous sputum, often mixed with blood. With high pulmonary hypertension, patients often complain of fatigue and weakness, because there is no adequate increase in cardiac output.

When congestion occurs in the pulmonary circulation, patients often complain of palpitations during physical activity. Sometimes angina pain. Their cause may be: 1) stretching of the left atrium; 2) stretching of the pulmonary artery; 3) compression of the left coronary artery enlarged left atrium.

Objective data.

Inspection. The appearance of a patient with moderately severe stenosis does not present any peculiarities. As the symptom of pulmonary hypertension increases, a typical facies mitralis is observed: against the background of pale skin, a sharply defined “mitral” blush of the cheeks with a somewhat cyanotic tint.

Visually, the area of ​​the heart bulges - a “heart hump” is observed. This symptom is associated with hypertrophy and dilatation of the right ventricle and with its increased impacts on the anterior chest wall.

Noteworthy is the absence of the apical impulse, since the left ventricle is pushed aside by the hypertrophied right ventricle.

Palpation. If, after preliminary physical exercise, the patient is placed on his left side, then when holding the breath during the exhalation phase, diastolic tremors can be detected at the apex of the heart - “cat purring.” This symptom is caused by low-frequency vibrations of the blood as it passes through the narrowed mitral orifice. In the 2nd intercostal space to the left of the sternum, palpation with the palm of the hand during the exhalation phase can determine the intensification (emphasis) of the 2nd tone. Nesterov B.S. (1971) describes the symptom of “two hammers”: if you place your hand on the heart area so that the palm is projected onto the apex, and the fingers are projected onto the area of ​​the second intercostal space to the left of the sternum, then the clapping 1st tone is felt by the palm as the first “hammer”, and the accented second tone is perceived by the fingers as the blow of the second “hammer”.

In the upper part of the epigastrium, pulsation can be observed, depending on hard work hypertrophied right ventricle: during inspiration, this pulsation increases sharply, as blood flow to the right ventricle increases.

Percussion. With percussion relative dullness the heart is enlarged upward due to the left atrial appendage and to the right due to the right atrium.

Auscultation. Provides the most significant signs for diagnosis, since the detected phenomena are directly related to impaired blood flow through the mitral orifice.

Tone I is strengthened (clapping). This depends on the fact that in the preceding diastole the left ventricle is not filled sufficiently with blood and contracts quite quickly. At the apex, the opening sound of the mitral valve (opening click) is also heard immediately following the second sound. The clapping 1st tone in combination with the 2nd tone and the opening tone will create a characteristic melody at the apex of the heart - the “quail rhythm”.

Typical auscultatory symptoms of mitral stenosis include diastolic murmur. The murmur is associated with the movement of blood through a narrowed mitral orifice due to a pressure gradient from the left atrium to the left ventricle.

Pulse is usually not an indicator characteristic changes. The pulse is slightly less than normal filling as a result of a decrease in cardiac output.

R logic research. The purpose of this study is to more accurately determine the enlarged sections of the chambers of the heart, as well as to determine the condition of the small circle vessels.

ECG turns out to be very valuable in diagnosing mitral stenosis and assessing the stage of its course. The purpose of the ECG is to detect hypertrophy of the left atrium and right ventricle, the presence of rhythm disturbances.

Signs of left atrial hypertrophy: 1) double-apex P wave in lead I, AVL, V4-6; 2) in lead V1 there is a sharp increase in amplitude and duration of the second phase of the P wave; 3) an increase in the time of internal deviation of the P wave by more than 0.06 seconds.

Signs of right ventricular hypertrophy: 1) deviation of the electrical axis of the heart to the right in combination with a shift in the ST interval and a change in the T wave in AVF, III; 2) in the right chest leads the R wave increases, and in the left chest leads the S wave increases.

FKG- graphic recording of heart sounds and cardiac murmurs. The value of PCG increases in conditions when, during auscultation, it is difficult to attribute the auscultated murmur to one or another phase of the cardiac cycle.

ECHO-KG is currently essential for the diagnosis of mitral stenosis.

Diagnostics.

Direct signs: 1) clapping I tone; 2) the tone of the mitral valve opening (opening click); 3) diastolic murmur; 4) diastolic tremor (palpation); 5) ECHO-CG - signs of mitral stenosis.

Indirect signs: 1) R-logical and ECHO-CG signs of left atrium enlargement; 2) on the ECG - hypertrophy of the left atrium; 3) shortness of breath on exertion; 4) attacks of cardiac asthma; 5) pulsation in the epigastrium due to the right ventricle; 6) R-logical and ECHO-CG signs of right ventricular hypertrophy.

Treatment. There are no specific conservative treatments for mitral stenosis. Circulatory failure is treated using generally accepted methods (cardiac glycosides, diuretics, potassium supplements). With an active rheumatic process - antirheumatic drugs, antibiotics. Surgical method treatment - commissurotomy.

Surgical treatment is only a component in a complex complex rehabilitation measures patients with rheumatic heart defects. 3-4 weeks after the operation, patients return to pediatricians and therapists for further rehabilitation and consolidation of the effect achieved by the operation.

Strict recording and systematic monitoring of patients in clinics and dispensaries is carried out in order to timely prevent and identify exacerbations of rheumatism, circulatory compensation disorders, and the state of the coagulation system.

In the first 2-3 months after surgery, children must be examined weekly, then up to a year - at least once a month. With uncomplicated course postoperative period Control examinations of patients in surgical clinics are carried out 6 months after surgery, then annually, and if necessary, more often.

A three-year continuous course of treatment with bicillin-5 is recommended for all operated patients, and in subsequent years - seasonal spring and autumn courses of antirheumatic therapy. In children, it is advisable to receive continuous antirheumatic treatment until growth is complete. Sanitation of foci of infection in cases of tonsillitis, otitis, dental caries, gastrointestinal diseases. If operations are necessary for these diseases, protective 10-14-day courses of antibiotic treatment are advisable.

If the operation was performed with incomplete correction of the defects or there are pronounced secondary changes in the lungs, myocardium and other organs, individual treatment with cardiac glycosides, diuretics, enzymes and vitamins under the control of blood electrolytes and ECG is indicated.

You are allowed to attend school 2-3 months after the operation. In adolescents and in the long term after surgery, already in mature age patients have to deal with employment issues. In most cases, with uncomplicated mitral stenosis and adequate commissurotomy, in the first 6 months it is advisable to assign disability group II, and subsequently - group III with limitation physical activity. One year after the operation, it is possible to restore working capacity without any restrictions.

In case of residual defects and complicated operations with symptoms of circulatory compensation disorders, the issue of working ability after 6 months after the operation is decided on an individual basis. It is advisable to maintain disability group II or III for the period necessary to fully stabilize compensation.

Patients with prosthetic heart valves usually undergo surgical treatment in more severe (IV) stages of the disease and, in addition to persistent antirheumatic therapy, usually require treatment with cardiac glycosides, diuretics and anticoagulants.

After discharge from the hospital, they should be sent to specialized sanatoriums.

In order to prevent thromboembolism after replacement of the left atrioventricular valve, it is necessary to constantly use anticoagulants indirect action with maintaining the prothrombin index at 50-70%. The dose is selected individually, treatment is carried out in the hospital and on an outpatient basis under the control of blood coagulation.

The prothrombin index is monitored monthly, and more often if it fluctuates and the dose of the anticoagulant changes.

In case of increased bleeding (hemorrhage, hematuria, menorrhagia), as well as the need for planned surgery (tonsillectomy, tooth extraction, etc.), it is necessary to reduce the dose of the anticoagulant and increase the prothrombin index to 70-75%. It is not advisable to completely discontinue the drug.

When examining the working capacity of patients with valve prostheses, it is necessary to remember that operations are performed in severely ill patients with pronounced secondary changes in the heart and other organs. Therefore, the operation cannot completely restore the child’s ability to work, as after eliminating the stenosis using a closed technique. Due to the difficulties of solving this problem in lately More and more attention is being paid to objective methods and quantitative assessment of work ability.

The principles and recommendations for the rehabilitation of these patients, developed by J. A. Bendet and co-authors, have the following expression in quantitative characteristics: the workload of the working day for patients with valve prostheses should not exceed one third of the maximum tolerated energy expenditure, determined using a stress test. Moreover, the initial load power during the test should not exceed 0.98 kJ/min (100 kgm/min). If well tolerated, it increases to 170 per minute. The assessment of labor capabilities can be carried out according to the criteria proposed by N. M. Amosov and Y. A. Bendet, who distinguish 5 groups according to the threshold load.

The first (workable) - with a load tolerance of more than 7.35 kJ/min (750 kgm/min) for women and 8.82 kJ/min (900 kgm/min) for men.

The second (moderately limited) - with a load tolerance of 4.90-7.35 kJ/min (501-750 kgm/min) for women and 5.88-8.82 kJ/min (601-900 kgm/min) for men.

The third (significantly limited) - with a load capacity of 2.94-4.90 kJ/min (301-500 kgm/min) for women and 2.94-5.88 kJ/min (301-600 kgm/min) for men.

The fourth (inoperative) - with load tolerance in the range of 0.98-2.94 kJ/min (100-300 kgm/min) for women and men.

And finally, the fifth (requiring care) group includes patients with exercise tolerance of less than 0.98 kJ/min.

Women's magazine www.

Rheumatism is the most familiar name for this inflammatory disease, although in the literature it is sometimes called Sokolsky-Buyo disease or rheumatic fever, which does not change its essence at all.

About 30-40 years ago, the spread of rheumatism was quite widespread. Mainly, among the sick were frequently and long-term ill children from 6 to 14-15 years old, with foci of chronic infection (tonsillitis), low immunity and a hereditary predisposition to cardiac pathology. The appearance of the first attack in adulthood is no exception, but the onset of the disease in adults is quite rare.

Modern medicine knows many ways to combat this very serious illness, the path of which is aimed directly at heart damage and the formation of valve defects. Diagnostic search using new methods and high-precision equipment, effective medications and effective preventive measures make it possible to stop the pathological process at the beginning of its inception.

Causes of rheumatic fever

The greatest importance in the formation of the inflammatory process of connective tissue with subsequent damage to various membranes of the heart belongs to β-hemolytic streptococcus (group A), which often settles in the upper respiratory tract to provoke an acute respiratory viral disease with reduced immunity. That is why quite often rheumatism debuts after a sore throat or other related pathological conditions.

Despite the high incidence of acute respiratory viral infections and tonsillitis in children, not everyone develops rheumatism, so it is believed that hemolytic streptococcus alone is not enough for the development of the disease. We need conditions and prerequisites that will assist the infectious agent to defeat the body.

Low or, conversely, excessively high (hyperimmunoreactivity) immune response, genetically programmed predisposition, poor living conditions and unfavorable factors external environment leave a person unprotected and open pathogenic microorganisms the road to the connective tissue of the heart, which has an antigenic composition similar to streptococcus. Immune reactions begin to take place in the membranes of the heart, accompanied by the formation of anticardiac immunoglobulins (autoantibodies) aimed at the tissue of one’s own heart, and not at fighting the enemy. As a result, the titer of unnecessary antibodies increases, and the heart is damaged.

In addition, the occurrence of the rheumatic process is often associated with the presence of certain leukocyte alloantigens, inherited from parents, and the formation of cross-reacting immunoglobulins aimed at streptococcus, but capable of interacting with HLA system antigens (tissue antigens). This phenomenon is called molecular mimicry and is considered very significant in the development of autoimmune processes, which include rheumatism.

What follows from the classification

The rheumatic process usually affects different organs and systems. Many people associate the development of the disease with articular syndrome, which, however, holds second place after damage to the connective tissue of the heart, which has the status of leader. The course of the disease almost always involves damage to the heart, namely its membranes. But depending on which of them “liked” more for a permanent place of residence, rheumatic carditis (the general name of the pathology) can be presented as:

  • Endocarditis;
  • Myocarditis;
  • Pericarditis;
  • Pancarditis (all membranes are affected simultaneously).

In addition, the classification of rheumatism may involve division according to other parameters:

  1. An acute rheumatic process of high activity with a sudden onset, characterized by pronounced symptoms that require a quick response and intensive treatment that gives a good effect;
  2. Subacute moderate active form diseases with an attack duration of up to six months, less pronounced clinical manifestations and therapeutic effect;
  3. Monotonous protracted process, no different high activity, lasting more than six months and manifesting itself in most cases as one syndrome;
  4. Continuously relapsing wave-like course, which is characterized by severe exacerbations and incomplete remissions, numerous syndromes and progression of pathology of many organs;
  5. The latent variant of rheumatism goes unnoticed by the patient, since neither clinical, nor laboratory, nor instrumental methods diagnostics do not indicate a hidden inflammatory process. The disease is detected only after a defect has formed in the heart.

It should be noted that in children the course of rheumatism is more acute and severe than in adults. Subacute and latent variants are much less common, and the acute period is accompanied by symptoms of severe intoxication and organ damage (heart, joints, brain). Sometimes, against the background of fever, several systems are involved in the process at once.

In children in the acute phase, the disease can last up to 2 months from the onset of the attack, and in the active phase its course can last up to a year.

The subacute and latent course of the disease, as a rule, is an accidental finding during examination and, unfortunately, often belated, since the acquired heart defect has already managed to form and even manifest itself clinically, which became the reason for the examination.

A continuously relapsing process in childhood is considered very unfavorable in terms of prognosis, since in the vast majority of cases it leads to the formation of valvular heart disease.

Clinical picture of the disease

Since inflammation first of all begins to disable the cardiovascular system, it is advisable to consider the symptoms of rheumatism primarily from this position and divide them into cardiac (primary) and extracardiac.

It should be noted that the symptoms of the very first attack, when there is no defect yet, are distinguished by the most striking and distinct signs rheumatic lesions, That's why clinical picture The disease can be represented as an outbreak of acute rheumatic fever (ARF):

  • Acute onset (rheumatic attack), occurring a week or two after a sore throat, acute respiratory viral infection or any adenoviral infection;
  • High body temperature, sometimes reaching 40°C;
  • Migratory arthritis, sometimes serositis (inflammation of the serous membrane).

However, it is not so rare that the rheumatic process begins with low-grade fever, pain that intensifies when walking (climbing stairs) and slight swelling in the knee joints(in one or both).

The initial symptoms of the disease very little characterize its further course, so you should not try to predict the prognosis. The most reasonable thing in this situation would be to consult a doctor, because for the development of the rheumatic process, even one hour can play a role and prevent terrible complications in the form of a defect, myocardiosclerosis or heart failure. We should not forget that the latent course very often contributes to the silent and imperceptible formation of valve defects, so treatment should be started as early as possible.

Considering that rheumatism is a systemic diseases, the main feature of which is the active involvement of various organs in the process, it is characterized by multi-syndrome, so it is advisable to consider all the nuances from this point of view.

Damage to joints and heart

Missing a clear picture of active rheumatism at the first stage can complicate its diagnosis in the future, when a heart defect is formed, blood circulation is impaired, and the pathological process has turned into a chronic relapsing course. Therefore, it is very important not to miss the first attack, not to attribute it to another disease, and to prevent the involvement of the heart and the formation of irreversible consequences.

Since the acute onset of the disease has already been described above, we can move on to the forms of the rheumatic process and their manifestations:

Nervous system response

Basically, what people mean by rheumatic fever is serious illnesses hearts. Obviously, this is true, however, although to a lesser extent, the process can also affect other organs. For example, if primary rheumatism reaches the nervous system, then there is a possibility of developing chorea minor, which is also among the leaders, since it confidently holds 3rd place in frequency of occurrence in children, where for some reason it gives preference to girls.

The classic course of the disease can last up to 3 months, but usually this line does not pass; however, recently, chorea minor has also begun to “disguise”, like many other diseases. Instead of the classic form of minor chorea, you can often find an erased version, the course of which drags on and becomes wavy. But, basically, chorea minor has five significant signs that determine its diagnosis:

  • The appearance of random violent muscle movements. This phenomenon is scientifically called choreic hyperkinesis and can occur anywhere (neck, face, torso, upper and lower limbs);
  • Disorder of coordination of movements, which the child ceases to control and finds it difficult to do something purposefully (walk or stand in one place);
  • The predominance of muscle hypotonia with general dystonia of muscles, which sometimes become flabby and change so much that they resemble paralysis;
  • The phenomena of vegetative-vascular dystonia with chorea minor are not uncommon;
  • Inherent in minor chorea emotional lability is the result of psychopathological disorders that arose against the background of the rheumatic process, and not a feature of adolescence or the costs of education.

Other changes in the nervous system in Sokolsky-Buyo disease (encephalitis) are considered an extremely rare case and are characteristic primarily of childhood.

Other organs also suffer from rheumatism

Damage to other organs during the rheumatic process occurs with varying frequency (usually rare) and manifests itself:

  1. Ring-shaped erythema (pale pink rash on the skin of the arms, legs and torso), which is more characteristic of primary rheumatism and is even considered one of its diagnostic signs;
  2. The appearance of rheumatic nodules in the form of painless formations of various sizes, round and inactive. They are localized mainly on the extensor surfaces of small and large joints(metacarpophalangeal, elbow, knee, etc.) and tendons (heel, ankle area, etc.). However, rheumatic nodules are given important role in diagnostics, therefore they belong to significant criteria establishing a diagnosis;
  3. A very rare occurrence for Sokolsky Buyo disease is rheumatic pulmonary vasculitis and rheumatic pneumonitis, which are treated primarily with antirheumatic drugs, since antibiotics give weak healing effect. But the development of rheumatic pleurisy, which gives adhesive phenomena, is observed in approximately a third of patients and is detected by chest x-ray;
  4. Abdominal syndrome in the form of peritonitis, which in rheumatism is characteristic mainly of childhood and adolescence and manifests itself: a sudden increase in body temperature, cramping abdominal pain, nausea, sometimes with vomiting, constipation or increased frequency of stools;
  5. Kidney damage that occurs in acute period rheumatic fever and characterized by enormous difficulties in the diagnostic search.

Dependence of rheumatic fever on gender and age

At primary school age, with the same frequency for boys and girls, an acute onset of the rheumatic process with bright and multi-syndromic symptoms is more typical, where polyarthritis and rheumatic carditis are often accompanied by chorea, erythema and nodules.

In adolescents, the disease proceeds somewhat differently: it “loves” girls more, it begins with slowly developing rheumatic carditis, against which a heart defect often develops, and the disease itself becomes protracted and relapsing.

A special group of patients with rheumatism consists of young men who have left childhood and adolescence, entered adolescence and, in most cases, are able to pay military duty to their homeland. Of course, when a young man arrived during this period already with a certain baggage of rheumatic diseases, his presence in the ranks of recruits was called into great doubt. Another question is if the disease overtook the young man at this age. The anxiety of the parents and the guy himself is quite understandable, so they are eager to learn more about the disease itself and its prospects.

In adolescence, the disease is characterized predominantly by acute onset (ARF) with clearly defined syndromes:

  • Rheumatic carditis;
  • Polyarthritis;
  • Ring-shaped erythema.

Most likely, the disease at this age, with timely treatment, will end in complete recovery and will not remind itself in the future. But there are exceptions to every rule: heart disease develops in 10-15% of young people.

As for adults, they practically do not get sick with acute rheumatic fever. But cases of recurrent rheumatic carditis (mainly in women) are not so rare occurrence. Cardiac pathology acquires a protracted, progressive nature and after 10-15 years it manifests itself as concomitant and combined heart defects. Simple measures can save the situation and improve the prognosis for future life: clinical observation, adequate treatment and preventive measures.

Video: story about childhood rheumatism

How to recognize the rheumatic process?

The very first steps in a diagnostic search are:

  • Collection of a rheumatic history, where special emphasis is placed on infections suffered in the recent past;
  • Examination of the patient to identify symptoms of rheumatism: polyarthritis, rheumatic carditis, chorea, etc.);
  • Auscultation (appearance or intensification of murmurs in the area of ​​the apex of the heart or aorta, rhythm disturbance);

An important role in the diagnosis of rheumatism is assigned to a blood test to determine:

  1. Erythrocyte sedimentation rate - ESR and values leukocyte formula(usually a detailed analysis is prescribed immediately);
  2. C-reactive protein (normally negative);
  3. Titer of antibodies directed to streptococcus (antistreptolysin - ASL-O) and intensively “multiplying” in rheumatism;
  4. Rheumatoid factor (RF), which is normally negative.

Primary activities also include:

  • Taking material from the throat for the purpose of inoculating it and identifying β-hemolytic streptococcus (its presence says a lot);
  • Electrocardiogram (an extended P-Q interval indicates a heart defect of rheumatic origin);
  • X-ray methods usually provide little information during the first attack of rheumatism, but are used to diagnose changes characteristic of severe rheumatic carditis in children and young people;
  • Ultrasound examination (ultrasound), as a rule, establishes the presence or absence of a defect.

Treatment of Sokolsky–Buyo disease

The fight against rheumatic fever involves combined treatment and long-term observation, so in healing process There are 3 stages:

  1. Active phase, requiring hospital stay;
  2. Outpatient treatment at the place of residence with a cardiologist;
  3. A period of long-term follow-up and prevention of relapse of the disease.

For rheumatism, the patient is usually prescribed antimicrobial (antibiotics) and anti-inflammatory drugs (nonsteroidal anti-inflammatory drugs and corticosteroids), but their dosages and regimens are calculated depending on the form, phase, and course of the disease. NSAIDs (non-steroidal anti-inflammatory drugs) are considered a good and effective medicine for rheumatism, so in recent years preference has been given more often to this group. In addition to anti-inflammatory, NSAIDs have a good analgesic effect, which is important when articular form rheumatism.

If the course is unfavorable, there is a need for long-term complex therapy or timely surgical intervention(heart disease), therefore, in the case of rheumatic fever, it is better to rely on the doctor’s opinion, visit him more often and follow all recommendations.

The task of the second stage in adults consists of treatment in a clinic and referral from this stage to a cardiological sanatorium. It is better to immediately direct children and adolescents to a rheumatological sanatorium, bypassing outpatient treatment.

The third stage usually lasts for years and consists of scheduled visits to a cardiologist, examinations, and preventive measures aimed at preventing relapse.

However, it is important to note that long-term prevention is secondary prevention. But you need to start the primary one immediately and immediately. It consists in eliminating foci of chronic infections and very vigorous treatment of acute pathological processes caused by streptococcus.

Prevention of rheumatism at home

Tablets and other forms medications, which are actively used in hospitals, do not want to be used at home, so patients learn folk remedies treatment of rheumatism and do it at home. Of course, this is possible if rheumatism has not done a lot of things and proceeds slowly without any particular exacerbations, although patients, as a rule, still take anti-inflammatory tablets with an analgesic effect from the pharmacy in reserve.

What does unofficial (traditional) medicine offer us?

As a pain reliever, for example, people recommend a warm (not hot!) bath with chamomile (infusion). Although, probably, even without chamomile, a warm bath will have a beneficial effect on “rheumatic”? Especially if you take it in the evening before bed.

For pain relief, you can use a mixture of alcohols: camphor (50 g) and ethyl (100 g), to which you should add the beaten whites of two eggs, mix well and rub into sore joints. Or you can use for such purposes a gruel of grated potatoes, which can be placed on a sore spot on a linen cloth.

Used as a seasoning, celery is said to help with rheumatism. To do this, the plant is boiled and drunk in small doses.

Rosehip is generally considered a medicinal plant, so it is also used for rheumatism. To do this, take 1.5 cups of its leaves and roots crushed in a coffee grinder, pour it with a bottle of vodka, leave for a week, but do not forget, since the future medicine needs to be shaken periodically. When it is ready, strain and drink 1 tbsp. spoon three times a day a quarter of an hour before meals. If everything goes well, then the dose can be increased to 2 tablespoons, but remember that this is still a vodka solution, it’s not hard to get used to it.

In fact, you can find it on the Internet different recipes Treatments for rheumatism are sometimes, to put it mildly, exotic. For example, in the initial stage of the rheumatic process (most likely, we are talking about the joint form), they suggest applying bees to the sore spot. Bee venom, of course, has anti-inflammatory properties, but often produces an allergic reaction that must be taken into account.

Sokolsky-Buyo disease is treated with earthworms, ant baths or goat droppings, wine, fasting and much more, but such treatment, as a rule, has a local effect, but does NOT affect the cause of the rheumatic process - streptococcal infection. And while remaining in the body, it very often affects the valve apparatus of the heart. Therefore, all preventive measures, first of all, should be aimed at increasing natural immunity(compliance with the work and rest regime, balanced diet, saturating the body with vitamin C, etc.), the fight against streptococcus, adequate treatment of tonsillitis, sanitation of foci of chronic infection. However, of all the listed points, diet for patients and their relatives probably comes first.

Nutrition for rheumatic fever is practically no different from that for other cardiovascular pathologies. The patient is still in the hospital set up with table No. 10, which is not advisable to change in the future. This diet involves limiting fatty, salty, fried and smoked foods; preference is given to steamed dishes containing a sufficient (but not excessive!) amount of proteins, carbohydrates (better in fruits than in cakes), fats (without them at all, too). impossible), vitamins and microelements.

The presence of a parental history of rheumatic fever is a reason to examine children and strengthen control over their health.

Video: rheumatism in the program “Live Healthy!”

What is heart disease (congenital and acquired)

Diagnostics

Diagnosis of heart defects begins with an examination of a pregnant woman. Listening to heartbeats allows you to suspect a heart defect in the fetus. The woman is examined by specialists to determine the viability of the unborn child. Immediately after birth, neonatologists examine the baby, listen to the baby’s heart murmurs, and monitor the first hours and days of life. If necessary, they are transferred to specialized children's centers.

Clinical examination of preschool and school age necessarily includes an examination by a pediatrician and auscultation of the heart. If unclear noises are detected, children are referred to a cardiologist, they undergo electrocardiographic and ultrasound examination heart (ultrasound) and large vessels. A more objective method for studying cardiac murmur is phonocardiography. The sounds are recorded and subsequently transcribed. It is possible to distinguish functional noise from organic noise.

Ultrasound and Doppler echocardiography of the heart allow you to visually evaluate the work of different parts of the heart, valves, determine the thickness of the muscle, and the presence of reverse blood flow.

X-ray examination helps diagnose enlargement of individual parts of the heart and aorta. Sometimes this is done by contrasting the esophagus. In this case, the patient takes a sip of the contrast agent, and the radiologist observes its progress. In certain heart defects, enlarged chambers cause deviation of the esophagus. Based on this feature, we can establish the presence of anatomical defects.

More functional and structural damage, we will analyze the main symptoms of heart defects separately for different forms of the disease.

Acquired heart defects

This disease is the most common cause of disability and mortality in young people.

By primary diseases vices are distributed:

  • about 90% - rheumatism;
  • 5.7% - atherosclerosis;
  • about 5% are syphilitic lesions.

Other possible diseases, leading to disruption of the structure of the heart - prolonged sepsis, trauma, tumors.

Heart disease in adults can be associated with any of the listed diseases. Most often occur valve defects. Under the age of 30 - insufficiency of the mitral and tricuspid valves. Syphilitic aortic insufficiency appears between 50 and 60 years of age. Atherosclerotic defects occur at 60 years of age and older.

Mechanism of functional disorders

As a result of valve insufficiency, blood ejected during systole (contraction) from one section to another or into large vessels partially returns, meets the next portion, overwhelms the entire section of the heart, causing stagnation.

When the heart opening is narrowed, the same difficulties are created. Through a narrow opening, blood hardly passes into the vessels or the next chamber of the heart. Overfilling and stretching occurs.

Acquired heart defects develop gradually. The heart muscle adapts, thickens, and the cavity in which excess blood accumulates expands (dilates). Up to certain limits, these changes are compensatory in nature. Then the adaptive mechanism “gets tired” and circulatory failure begins to form.

The most common defects of this group:

  • mitral valve insufficiency;
  • mitral stenosis;
  • aortic valve insufficiency;
  • narrowing of the aortic mouth;
  • insufficiency of the tricuspid (tricuspid) valve;
  • narrowing of the right atrioventricular orifice;
  • pulmonary valve insufficiency.

Characteristic functional disorders and symptoms of acquired defects

Mitral valve insufficiency refers to rheumatic heart defects. Mitral valve(bicuspid) is located between the left atrium and the ventricle. This is the most common valve defect (3/4 of all). Only in 3.6% of cases is it observed in its “pure” form. This is usually a combination of valve damage and stenosis of the left atrioventricular orifice (the passage between the left atrium and the ventricle). Such combined defect also called " mitral disease hearts."

The rheumatic process leads to wrinkling of the valve flaps and shortening of the tendons that ensure their functioning. As a result, a gap remains through which blood, when the left ventricle contracts, returns back to the atrium. During the next contraction, the ventricle receives more blood. As a result, its cavity expands and the muscles thicken. The adaptive mechanism does not cause disturbances in the well-being of patients and allows them to perform their usual work. Decompensation develops due to the addition of stenosis due to the ongoing activity of the rheumatic process.

The first symptoms in children appear after a sore throat. The child complains of fatigue during physical education lessons, shortness of breath, and palpitations. Children stop taking part in games. In adults, the first signs of decompensation are shortness of breath when walking, especially when going uphill, and a tendency to bronchitis.

The patient's appearance is characteristic: lips with a bluish tint, blush on the cheeks. In babies, due to an increased cardiac impulse, a protrusion of the chest can form, it is called a “heart hump”. When examining and listening to the heart, the doctor diagnoses characteristic murmurs. The prognosis for the course of the disease is favorable if it is possible to stop the attacks of rheumatism at the stage of valve insufficiency and prevent the development of stenosis.

Mitral stenosis is a narrowing of the left atrioventricular opening. The most common rheumatic defect. About 60% of cases are observed in a “pure” form. The inability to push blood into the ventricle leads to expansion of the left atrium to enormous sizes. As a compensatory mechanism, the right ventricle dilates and thickens. It is he who supplies blood through the lungs to the left atrium. Failure of the device leads to stagnation of blood in the lungs.

Shortness of breath - main symptom this vice. Children grow up pale and physically underdeveloped. Over time, a cough appears with foamy sputum containing blood, palpitations, and pain in the heart. This symptom is especially characteristic after exertion or overwork. Small stagnant veins surrounding the lung tissue are ruptured.

The patient is pale, the cheeks, tip of the nose, lips and fingers are cyanotic. Heart pulsation is visible in the epigastrium. Changed breathing can be heard in the lungs. Diagnosis is not difficult. A dangerous complication is that blood clots form in the stretched left and right atria. They can pass through the bloodstream and cause infarctions of the kidneys, spleen, brain, and lungs. The same reason contributes to the development of atrial fibrillation. With the rapid progression of rheumatism, patients become disabled due to severe complications.

Aortic valve insufficiency occurs during a long course of rheumatism, syphilis, chronic sepsis, and is the result of severe atherosclerosis. The valves become dense and inactive. They do not completely close the outlet through which blood flows from the left ventricle to the aorta. Part of the blood returns to the ventricle, it expands sharply, and the muscles thicken. Circulatory failure first occurs of the left ventricular type (cardiac asthma, pulmonary edema), then right ventricular manifestations join (as with mitral stenosis).

Patients are pale, strong pulsation of the neck vessels is visible, and the symptom of head swaying along with pulsation is characteristic. Complaints of dizziness, headache, pain in the heart area are associated with insufficient oxygen supply. A change in blood pressure is characteristic: the upper numbers are increased, the lower ones are significantly reduced. The prognosis is related to the course of the underlying disease.

Insufficiency of the tricuspid valve, located between the right parts of the heart, does not occur in its “pure” form. This defect is formed as a consequence of compensation for mitral stenosis. Manifestations of the defect are observed against the background of other symptoms. You can attach special importance to swelling and puffiness of the face, bluishness of the skin upper half torso.

According to the data, other acquired forms of defects account for medical statistics about 1%.

Congenital heart defects

Congenital defects are complex disorders of cardiac development in the fetus at the embryonic stage. There are no exact indications about the reasons for the occurrence yet. A certain role has been established for infection of the maternal organism in the initial stage of pregnancy (influenza, rubella, viral hepatitis, syphilis), lack of protein and vitamins in the diet of the expectant mother, and the influence of background radiation.

The most common defects are non-union:

  • ductus botallus;
  • interventricular septum;
  • interatrial septum.

Rare defects: narrowing of the pulmonary artery, aortic isthmus.

An isolated defect occurs in isolated cases. In most children, abnormal development leads to complex combined anatomical changes in the heart.

An open botal duct is necessary during the uterine period of development. It connects the pulmonary artery and the aorta. By the time of birth, this path should be closed. The defect is more common in women. It is characterized by blood transfusion from the right ventricle to the left and vice versa, expansion of both ventricles. Clinical signs are most pronounced with a large hole. When small, they can go unnoticed for a long time. Treatment is only surgical; the duct is sutured and completely closed.

A ventricular septal defect is a patent opening up to two cm in diameter. Due to high pressure in the left ventricle, blood is driven to the right. This causes dilatation of the right ventricle and pulmonary congestion. The left ventricle also enlarges compensatoryly. Even in the absence of complaints, patients have characteristic murmurs when listening to the heart. If you put your hand in the area of ​​the fourth intercostal space on the left, you can feel the symptom of “systolic trembling”. Treatment for decompensation of the defect is only surgical: the hole is closed with synthetic material.

Atrial septal defect accounts for up to 20% of all cases of congenital defects. Often included in combined defects. Between the atria there is an oval foramen, which closes in early childhood. But in some children (usually girls), it never closes. On the side of the left atrium, the opening is covered by a leaf of the valve and presses it tightly, since there is more pressure here. But with mitral stenosis, when the pressure in the right side of the heart increases, blood flows from right to left. If the hole is not completely closed even by the valve, then mixing of blood occurs, overflowing the right parts of the heart. Treatment of the defect is only surgical: a small defect is sutured, a large defect is covered with a graft or prosthetic materials.

Complications of congenital nonunions include unusual thromboembolism.

For diagnosis in these cases, X-ray examination with a contrast agent is used. Introduced into one chamber of the heart, it passes through open ducts to another.

Particularly difficult to treat are combined defects of four or more anatomical defects (tetralogy of Fallot).

Surgical treatment of congenital defects is currently carried out on early stages to prevent decompensation. Clinical observation of patients requires constant protection from infection, control of nutrition, and physical activity.

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