Bacterial endocarditis is a dangerous lesion of the heart. Infective endocarditis

Zubov L.A., Associate Professor, Department of Pediatrics, Northern State Medical University, Chief Pediatric Cardiologist, Department of Health, Administration of the Arkhangelsk Region

The problem of disability in children is an urgent problem in medicine, which is argued by convincing international statistics, according to which the number of disabled people in all countries is large and there is a clear tendency to increase it. This problem has been undeservedly overshadowed by pediatricians for a long time, which currently determines the lack of complete statistics, the lack of clear criteria and approaches to determining disability in many diseases.
According to WHO, about 20% of childhood disability and morbidity is due to malformations. Genetic, hereditary diseases, malformations often contribute to the formation of chronic pathology. Congenital heart disease (CHD) is one of the most common pathologies in children, leading to social insufficiency.
Back in 1989, at the International Conference on the X Revision of the ICD, the International Nomenclature of Disorders, Disabilities, and Social Insufficiency was adopted, which in many countries is used to study groups of patients recognized as disabled, creates the prerequisites for organizing a system of state registration of disabled people, through the use of common terminology . Disorders according to the international nomenclature are defined as changes in the structure of the body, in the functions of organs or systems, and, in principle, are disorders at the organ level. Decreased ability to work - a disorder at the personality level - and reflect the point of view of the performance of the function and the usual activity for an individual of a given age. Social insufficiency - occurs as a result of disability and reflects the interaction and degree of adaptation of the individual to environmental conditions, i.e. it manifests itself in the case when something interferes with the performance of the so-called survival functions - orientation, physical independence, mobility, vocational training, economic independence. Disability is a special case of disability or disability, as well as social insufficiency, which received a formal legal status by decision of a special commission.
The limitations of the child's life and the nature of his social insufficiency are determined by the ability to play, the need for assistance with personal care and self-care, the use of auxiliary technical vehicles, etc. Social insufficiency can be due in large part to insufficiency due to limited physical independence, limited education, and limited ability to integrate into society. Severity rubric scale in the nomenclature (difficulties in activity, activity with the help of assistive devices, need for outside help, complete dependence on the presence of another person, etc.) and prognosis scale (from recovery, improvement to persistent or increasing limitations, uncertain prognosis) help in determining disability.

Until recently, when establishing disability for children with CHD, pediatricians mainly took into account the topical diagnosis of the defect. Disability is defined as a limitation of life due to a health disorder, leading to the need for social protection. The basis for recognizing a child as a disabled person is a combination of the following three main factors:
- a health disorder with a persistent disorder of body functions due to diseases, consequences of injuries or defects;
- limitation of life activity (complete or partial loss of the ability to carry out self-service, independent movement, communication, orientation, control one's behavior, learn or engage in gaming activities in accordance with the age norm);
- the need to implement social protection measures.

This means a transition from the old, familiar, simplified scheme: the presence of a clinical diagnosis (CHD) - the establishment of a disability for a child - to a modern, justified scheme: a clinical and functional diagnosis (determining the type, degree of circulatory dysfunction leading to disability) - defining categories and degree of disability; determination of rehabilitation potential, rehabilitation prognosis - social insufficiency - establishment of disability.

Scheme for determining disability in congenital heart defects :

Circulatory dysfunction

Heart failure: congestive, hypoxemic.

Functional classification of the state s-s-s according to NYHA.

Limitation of vital activity (three degrees of severity)

Rehabilitation potential and rehabilitation forecast

UPU classification is based on the nature of anatomical disorders, and also takes into account the degree of hemodynamic disorders and the assessment of clinical status. Anomalies in the development of the heart and great vessels are accompanied by various hemodynamic disorders, which are divided into primary, occurring immediately after the birth of a child, and secondary, resulting from the course of congenital heart disease.

A. Primary hemodynamic disorders.
I. Hypervolemia of the pulmonary circulation with overload: a) right ventricle (atrial septal defect, abnormal drainage of the pulmonary veins); b) left ventricle (open ductus arteriosus, aortopulmonary septal defect); c) both ventricles (ventricular septal defect, transposition of the great vessels).
II. Difficulty in ejection of blood from: a) the right ventricle (various forms of narrowing of the excretory tract of the right ventricle and pulmonary artery); b) left ventricle (various forms of narrowing of the excretory tract of the left ventricle and aorta).
III. Difficulty in filling the ventricles with blood: a) right (narrowing of the right atrioventricular orifice); b) left (congenital narrowing of the left atrio-veitricular opening).
IV. Volume overload of the ventricles of the heart due to congenital valvular insufficiency: a) right (insufficiency of the tricuspid valve and pulmonary valve), b) left (insufficiency of the mitral valve and aortic valve).
V. Hypovolemia of the pulmonary circulation with a simultaneous increase in minute volume in the systemic circulation, due to the early discharge of venous blood into the systemic circulation (tetrad of Fallot, triad of Fallot, some forms of transposition of the great vessels, etc.).
VI. Mixing of venous blood with arterial blood in the absence of a hemodynamically significant discharge of blood from one circulation to another (common atrium, some forms of transposition of the great vessels).
VII. The release of all venous blood into the systemic circulation with extracardiac compensation mechanisms (common arterial trunk).

B. Secondary hemodynamic disorders. They arise as a result of the development of secondary anatomical processes in the vessels of the pulmonary circulation or in the myocardium.
I. An increase in the minute volume of blood of the systemic circulation due to the discharge of venous blood into the arterial blood through pulmonary arteriovenous and arterioarterial shunts. These hemodynamic disturbances are observed with the development of pronounced sclerosis of the vessels of the pulmonary circulation (secondary pulmonary hypertension) with defects in the septa of the heart, an open arterial duct, a defect in the septum between the aorta and the pulmonary artery.
II. Various forms of cardiac decompensation.
III. Arterial hypertension in the vessels of the upper half of the body and hypotension in the lower ones with coarctation of the aorta.

The CHD in the patient is primarily functional shifts of a compensatory order. Chronic hypoxemia and circulatory disorders lead to compensatory restructuring of all body systems. Compensation for perverse circulation is provided by a change in the function of the heart, vessels of the large and small circles, hematopoiesis and the regime of oxidative processes that continue to develop and form. Depending on the anatomical severity of the defect, compensation may be complete or untenable.
In the clinical course of congenital heart defects (regardless of their type), three phases are noted. In the first - the adaptation phase (from the first days of life) - the child adapts to hemodynamic disorders. With the development of adaptive protective mechanisms, the general condition improves and the patient enters the second phase - relative compensation. When all reserves of protective adaptive mechanisms are exhausted, the third phase begins - the terminal phase, which is characterized by a circulatory disorder that cannot be treated.
All heart defects are accompanied by hyperfunction of the myocardium at rest and especially during exercise. Depending on the nature and severity of hemodynamic disorders, tonogenic dilatation or myocardial hypertrophy predominates. In many patients, a continuous load on the myocardium and pathological changes in biochemical, metabolic and energy processes in the heart muscle are accompanied by the development of morphological changes in the myocardium, which leads to heart failure. The degree of myocardial hypertrophy in various congenital heart defects is not the same - it is greater with defects accompanied by an obstruction to the ejection of blood from the ventricles, and less with isolated defects of the atrial and interventricular septa, as well as with non-closure of the ductus arteriosus. The highest degree of myocardial hypertrophy develops in congenital heart defects with significant narrowing in the path of blood flow. In the same parts of the heart that bear the brunt of the functional load of vicious circulation, the development of cardiosclerosis is observed.

One of the compensatory mechanisms in congenital heart defects is pulmonary hypertension. In children with congenital heart defects, accompanied by increased blood filling of the lungs, at the first stages there is an expansion of the vessels of the small circle, which facilitates the work of the right ventricle. However, another protective reflex that prevents the development of pulmonary edema (Kitaev's reflex) causes vasospasm and an increase in pressure in the pulmonary circulation. Initially, pulmonary hypertension is functional in nature, then vascular sclerosis develops and it becomes organic.
Pulmonary hypertension is divided into 3 groups:
1st - systolic pressure in the pulmonary artery 30-35 mm Hg. Art.,
2nd - moderate pulmonary hypertension - pressure over 35 mm Hg. Art., but does not exceed 70% of the aortic,
3rd - severe pulmonary hypertension - pressure over 70% of the arterial pressure. In this case, there may be a discharge of blood from left to right, cross or reverse.
High pulmonary hypertension makes surgical correction of CHD impossible and useless and indicates a poor prognosis.
In children with cyanotic CHD, constant arterial hypoxemia is compensated by an increase in the number of erythrocytes and hemoglobin (200-300 g/l). In the process of compensating for hypoxia, tissue respiration changes with the participation of anaerobic glycolysis. Compensatory reactions in various parts of the cardiovascular system and tissues ensure the growth and development of the body, but they are depleted and decompensation develops. With stenosis, it manifests itself as acute heart failure, with a defect - cardiopulmonary. With some defects, aneurysm, stroke, and septic endocarditis develop.
Thus, in a patient with CHD, all body systems suffer. Protective compensatory mechanisms turn into their opposite, which leads to decompensation, manifested by respiratory and cardiovascular insufficiency, acute cerebrovascular accident.

Circulatory failure (heart failure) with CHD can be congestive and hypoxemic. The most common cardiac causes of heart failure in children are:
A. Left heart obstruction
Left ventricular inflow tract obstruction (intraatrial obstruction):
Cortriatriatum
Supravalvular mitral stenosis
valvular mitral stenosis
Mitral valve atresia (hypoplastic left heart syndrome)
Left ventricular outflow tract obstruction
Subaortic stenosis
Valvular aortic stenosis
Supravalvular aortic stenosis
Coarctation of the aorta
B. Blood shunt from left to right (heart failure associated with increased pulmonary blood flow)
Large VSD
Open ductus arteriosus
The common truncus arteriosus
aorto-pulmonary junction
Abnormal pulmonary venous drainage
Atrial septal defect
B. Myocardial insufficiency
Primary
Dilated cardiomyopathy
Restrictive cardiomyopathy
Hypertrophic cardiomyopathy
Secondary
Abnormal origin of the left coronary artery from the pulmonary artery
Myocarditis
Asphyxia during childbirth
Postoperative dysfunction of the heart muscle

The classification of degrees of circulatory insufficiency adopted in domestic pediatric cardiology is focused mainly on specific clinical manifestations on the part of individual organs (tachycardia, shortness of breath, edema, hepatomegaly), which is clearly not enough to assess the patient's quality of life. Approved by pediatric cardiologists in our region, the functional classification of the states of the cardiovascular system and physical performance, proposed by the New York Heart Association (NYHA), satisfies the tasks of establishing disability to a sufficient extent. At the same time, for children whose hemodynamic stabilization is achieved by prescribing basic medications, a note is made in the diagnosis: “medicated compensated heart failure”.

CLASSIFICATION OF THE FUNCTIONAL STATE OF PATIENTS WITH CARDIAC PROFILE PROPOSED BY NYHA
Functional class Nature of change
I Patients with cardiac pathology that does not limit their physical activity. Ordinary physical activity does not cause excessive fatigue, palpitations, shortness of breath, or an angina attack
II Patients with cardiac pathology, which leads to some limitation of physical activity. At rest, they feel good. Ordinary physical activity causes excessive fatigue, palpitations, shortness of breath, or an angina attack.
III Patients with cardiac pathology, which significantly limits their physical activity. At rest, they feel good. Light physical activity causes excessive fatigue, palpitations, shortness of breath, or an angina attack.
IV Patients who do not tolerate any physical activity without deterioration of health. Subjective manifestations of heart failure or anginal syndrome may occur even at rest. Any physical activity leads to a deterioration in well-being.

I functional class indicates the preservation of the functional reserves of the cardiovascular system and high physical performance, the defect is compensated.
II functional class indicates a moderate decrease in heart reserves and performance, reversibility of circulatory disorders.
III functional class reflects a pronounced decrease in heart reserves and performance, decompensation of the defect.
IV functional class reflects a pronounced decrease in heart reserves and performance, irreversible decompensation of the defect and irreversible dystrophic changes in internal organs due to circulatory failure, patients often need outside care.

Minor disorders of the circulatory function, as a rule, do not lead to a significant limitation of life, requiring social protection measures; a decrease in the ability to learn and the ability to play activities in some sick children with CHD may be due not so much to the presence of minor functional disorders, but to the expediency of limiting physical activity during games, sports and the unsuitability of sick children for training in certain professions. CHD, even with a slight violation of the circulatory function, predetermine the expediency of limiting physical activity during gaming and sports, and may also be contraindications for teaching sick children professions, the nature and working conditions of which are associated with severe physical stress and a high level of energy consumption.
Moderate impairment of circulatory function in children can lead to limitations in the ability to self-service - within the 1st tbsp. restrictions; ability to move - within the 1st st. restrictions; ability to learn - within the 1st Art. restrictions; ability to play activities - within the 1st Art. restrictions.
Children with severe NC may have the following limitations of life: the ability to self-service - within the 2nd tbsp. restrictions; ability to move - within the 2nd Art. restrictions; ability to learn - within the 2nd Art. restrictions; the ability to play activities - within the 2nd tbsp. restrictions.
In children with significantly pronounced NC, life restrictions can reach the highest degree: the ability to self-service is within the 3rd tbsp. restrictions; ability to move - within the 3rd Art. restrictions; ability to learn - within the 3rd Art. restrictions; the ability to play activities - 3rd tbsp. restrictions.

Life limitations in children with CHD are more often caused by impairments in the ability to self-service, movement, play activities, and learning. In accordance with the classification, one of three degrees of severity of disability is determined in a child.

Medical criteria for medical and social expertise for various types of CHD can be:
with CHD with a left-right shunt (with increased pulmonary blood flow): ASD, VSD, PDA
CH stage
Degree of pulmonary hypertension
basic conservative therapy (cardiac glycosides, diuretics, ACE inhibitors)
complications: infective endocarditis, pulmonary, cardiac arrhythmias
effectiveness of surgical correction

with CHD with a right-to-left shunt (with reduced pulmonary blood flow): tetralogy of Fallot
Severity of the course (frequency and severity of dyspnea-cyanotic seizures)
Basic conservative therapy (beta-blockers)
The degree of chronic hypoxemia (impaired functions of the central nervous system, degeneration of internal organs)
complications: infective endocarditis, thromboembolism
Radicality and effectiveness of surgical correction (long period of adaptation to new hemodynamic conditions in combined CHD)
postoperative complications;
with CHD without a shunt: CoA, SA
The severity of NK
The degree of chronic insufficiency of cerebral and coronary circulation
complications: stroke, infective endocarditis
Formation of prestenotic aortic aneurysm
Efficiency and complications of surgical intervention.

In the treatment of patients with CHD, the leading place is occupied by timely surgical correction of defects. Cardiac surgical methods can: prevent the development of infective endocarditis (especially with aortic stenosis, patent ductus arteriosus, VSD); prevent a high degree of hypertension of the small circle; prevent thromboembolic complications; ensure a decent quality of life for the child. Long-term observations show that after surgery in more than 90% of cases a stable positive effect is achieved. Given the current results of operations to eliminate congenital malformations, most patients will undergo surgery and reach adulthood. More and more children with congenital heart disease, considered fatal a few years ago, are surviving thanks to advances in medical and surgical treatment.
Despite a significant improvement in the outcome of CHD operations, some problems may remain. The pediatrician should be aware of possible remaining disorders and potential complications that may develop in a child with heart surgery.

Classification of types of CHD correction Based on the likelihood that the patient will require further subsequent surgery, Friedli suggested:
· True complete correction leads to restoration of normal cardiac anatomy and function and is usually possible with secondary atrial septal defects (ASD), simple ventricular septal defects (VSD), patent ductus arteriosus (PDA), aortic coarctation (CoA). Although late complications occasionally occur in some patients in this category, most children can be expected to lead normal lives without reoperation.
· Anatomical correction with residual effects can be performed in patients with Fallot's tetralogy, atrioventricular septal defects, and valvular obstructions corrected by valvotomy or valve repair. In these patients, symptoms and abnormal physiology disappear, but there are residual defects such as valvular insufficiency or arrhythmias that may require further intervention.
Correction requiring prosthetic materials is used in patients who require a channel between the right ventricle and the pulmonary artery, as in pulmonary atresia with VSD, truncus arteriosus, or prosthetic valve replacement. Due to the somatic growth and degeneration of the prosthetic material in this category of patients, a second operation will undoubtedly be required to replace the prosthesis.
· Physiological correction, such as Senning and Mustard operations for TMS, Fontan operations in patients with a three-chamber heart, eliminates abnormalities in cardiovascular physiology, but without eliminating anatomical abnormalities. As a result, these patients almost always develop late complications requiring surgical or conservative intervention.

This classification is useful for predicting the likelihood of a patient experiencing subsequent problems. The most common possible postoperative problems that may occur in some patients after open heart surgery are:
I. Arrhythmias.
Arrhythmias are the most common problem that occurs in children in the postoperative period. Arrhythmia in a patient in the postoperative period may be due to an underlying congenital heart disease (eg, Ebstein anomaly), be the result of surgical correction (eg, ventriculotomy or atrial suture), be the result of conservative therapy (eg, hypokalemia due to the use of diuretics, overdose of digoxin) or a combination of these factors.
Supraventricular arrhythmias such as extrasystoles, atrial flutter and nodal tachycardias are the most common type of arrhythmias in a patient in the postoperative period. They range in severity from benign (isolated supraventricular arrhythmias) to potentially life-threatening (persistent atrial flutter in a Fontan patient). The causes of these arrhythmias may be scarring from an atriotomy incision or elevated atrial pressure due to obstruction of the atrioventricular valve (mitral stenosis) or an inelastic ventricular chamber (Fallot's tetrad, aortic stenosis). A number of surgical procedures, such as the Fontan operation for a three-chambered heart or the Senning and Mustard operations for TMS, result in residual structural and physiological substrates that can lead to supraventricular arrhythmias. These operations require long intra-atrial sutures, creating an environment in which re-entry circuits can spontaneously occur. Elevated atrial pressure is common with both of these surgeries and is also a cause of re-entry arrhythmias. Less commonly complicated by arrhythmia, atrial surgery, such as closure of an ASD and correction of an abnormal pulmonary venous junction, may be seen on examination.
Isolated and infrequent supraventricular arrhythmias are common in both healthy and postoperative patients and are usually benign. Persistent supraventricular arrhythmias such as atrial flutter, atrial fibrillation, and junctional tachycardias require prompt identification and evaluation by a pediatric cardiologist. For a clinically stable patient, treatment begins with correction of abnormalities that are arrhythmogenic (eg, electrolyte abnormalities, drug-induced arrhythmias). Medical treatment is successful in less than 40% of cases. It can be complicated by proarrhythmic effects and common side effects of some drugs, highlighting the need for experienced arrhythmias to be managed. Hemodynamically unstable patients may require electrical cardioversion. Refractory arrhythmias may require more complex intervention, including radiofrequency ablation of the arrhythmogenic focus or antitachycardia pacemakers to suppress ectopic foci of automatism by artificially accelerating the heart rate.
The clinical significance of bradycardias is often underestimated because their symptoms may be absent or mild. Inadequate heart rate may be due to sick sinus syndrome, which is often observed in patients after Mustard and Senning operations (only 20-40% of them have sinus rhythm 5-10 years after surgery). Approximately 20% of patients 5-10 years after Fontan surgery require antiarrhythmic therapy or a pacemaker.
Ventricular arrhythmias in patients in the postoperative period are less common than supraventricular arrhythmias, but often more significant due to serious hemodynamic disturbances and the possibility of sudden death. The causes of such arrhythmias are scarring caused by ventriculotomy or increased intraventricular pressure (with severe pulmonary or aortic valve stenosis, cardiomyopathic ventricles with elevated end-diastolic pressure) and ischemic lesions associated with coronary artery disease or inadequate myocardial protection during surgery. Earlier surgical correction resulting in less severe ventricular hypertrophy and fibrosis may reduce the prevalence of late ventricular arrhythmias in this patient population.

II. Sudden cardiac death.
Certain types of uncorrected CHD that are associated with increased ventricular pressure (aortic stenosis, pulmonary stenosis), hypertrophic cardiomyopathy, or coronary anomalies place the patient at an increased risk of sudden cardiac death. Its prevalence reaches 5 per 1000 patients per year. Of this group of patients, half had previously undergone corrective heart surgery.

III. Residual and recurrent defects.
Children with CHD often have residual defects that are minor and do not affect the long-term outcome of surgical correction. A number of patients have more severe residual defects, either due to elective staged surgical correction (eg, palliative surgery for tetralogy of Fallot) or because of incomplete success of the initial surgery (less than 5% for most defects).
Recurrent malformations such as valvular stenosis or insufficiency, conduit obstruction, or recurrent coarctation of the aorta may occur. Recurrence of an anatomical defect leads to a return of the original symptoms if this problem is not identified and corrected in a timely manner. Although any type of corrected heart defect can recur, certain defects recur more frequently. For example, the prevalence of recurrent aortic coarctation is approximately 10% after repair in a young child. Aortic valve stenosis after balloon valvotomy or open surgical valvuloplasty is rarely permanent, with less than 50% complication-free survival after 10 years of follow-up.

IV. Problems caused by valves and prostheses.
Valvotomy (performed by balloon dilatation of the aortic or pulmonic valve or surgical valvuloplasty of the aortic, pulmonic, mitral, or tricuspid valve) is rarely permanent. Pulmonary valvotomy is the longest, with an expected complication-free survival of 75-80% after 5 years for both surgical and balloon valvotomy in young children. Early results of aortic valvotomy by balloon or open surgery are quite successful in children, although residual aortic stenosis is more common after balloon valvotomy and aortic regurgitation after surgical valvotomy. However, the complication-free survival rate is only 50% at 10 years and less than 33% at 15 years of follow-up in older patients after surgical valvotomy. Late complications include recurrent aortic valve stenosis, clinically significant aortic regurgitation, endocarditis, and the need for reoperation.
Valve replacement is generally avoided in children if there is an alternative to reconstruction, due to the disadvantages of all valve replacement options in the growing child. The valve prosthesis has significant disadvantages:
1. Growing out of the valve. A growing child who receives a prosthetic valve before reaching full height will undoubtedly require valve replacement in the future due to the development of relative stenosis as somatic growth continues and the valve orifice area remains the same.
2. Limited wear resistance of the valve.
3. Thrombogenesis and anticoagulation. The prevalence of systemic thromboembolic events after implantation of a prosthetic valve varies depending on the type of prosthesis used and the position in which the valve is implanted in the heart. Mitral or tricuspid valve prostheses have a 2-fold higher incidence of thromboembolism compared to those implanted in the aortic valve position. Due to the risk of thromboembolism, all patients who have had a mechanical valve implanted should receive anticoagulants.

V. Ventricular dysfunction.
Most patients who have successfully undergone CHD repair usually do not have clinically apparent ventricular dysfunction. However, congenital malformations still cause subclinical changes in the heart, which can progress and cause abnormal ventricular function. It is hypothesized that earlier surgical correction of congenital heart defects results in a lower incidence of ventricular dysfunction, as the patient's heart will be exposed to the abnormal condition for a shorter period of time. There are several potential causes of ventricular dysfunction in these patients:
1. Chronic hemodynamic overload. Chronic pressure and volume overload in malformations such as stenosis or regurgitation of the aortic or pulmonic valve cause ventricular hypertrophy. Over time, chronic hypertrophy leads to myocardial fibrosis, which causes irreversible changes in systolic and diastolic myocardial function.
2. Chronic cyanosis. Chronic cyanosis also leads to myocardial fibrosis due to an imbalance in the oxygen demand determined by the work of the heart and the oxygen content available in desaturated arterial blood. This problem is exacerbated when it occurs in conditions of a hypertrophied ventricle (eg, tetralogy of Fallot).
3. Complications of surgical correction. Open heart surgery requires the heart to be stopped for an extended period of time. Inadequate myocardial protection during this period is usually manifested by early postoperative myocardial dysfunction.
Late consequences of ischemic myocardial injury include regional and global myocardial systolic dysfunction and fibrosis. Ventricular incisions can also alter regional myocardial function due to coronary artery disease.

VI. Endocarditis.
Bacterial endocarditis poses a persistent serious risk for patients with non-operated CHD and, to a lesser extent, for patients with corrected defects. In contrast to the situation a decade ago, when rheumatic malformations were more often associated with an increased risk of endocarditis, now CHD and intracardiac prostheses are the most common comorbidities. In patients with a prosthetic heart valve, the prevalence of both early and late endocarditis varies from 0.3% to 1.0% per patient per year. In patients with unrepaired CHD, the overall risk of endocarditis ranges from 0.1 to 0.2% per patient per year and decreases 10-fold to 0.02% after correction. The risk of endocarditis varies depending on the type of defect. Complex blue-type heart defects represent the highest risk, which is estimated at 1.5% per patient per year. Patients operated on for tetralogy of Fallot remain at an increased risk of endocarditis (0.9% per patient per year) due to the relatively common prevalence of residual VSD and right ventricular outflow obstruction. Patients with a surgically closed VSD (0.1% per patient per year) or bicuspid aortic valve after surgical valvotomy (0.15% - 0.38%) have a moderate risk. Patients with a corrected ASD, VSD, PDA, aortic coarctation, or pulmonary stenosis and those who have had pacemaker implantation have a low risk of endocarditis (up to 0.05% per patient per year).

VII. Growth and development.
Lagging behind in physical development is one of the symptoms of congenital heart disease, which causes the greatest concern among parents. There is a correlation between the degree of stunting and the type of CHD. In children with large left-to-right shunts (i.e., VSD, complete atrioventricular septal defect, etc.), the degree of stunting is consistent with the size of the shunt and the degree of congestive heart failure. In contrast, patients with cyanotic heart disease tend to be more or less stunted, related to the specific defect present, but not to the degree of cyanosis.
Patients with obstructive heart disease, such as aortic or pulmonic valve stenosis, or coarctation of the aorta, are usually not stunted. Infants with severe symptoms of heart failure fail to gain weight due to both reduced calorie intake and increased caloric utilization. Due to tachypnea at rest and fatigue, the baby may become tired during feeding before an adequate amount of calories has been consumed.
Patients with a complete anatomical correction are expected to have a normal growth rate, while patients with an incomplete or staged correction are likely to lag behind. A patient who lags on the growth curve should be evaluated for possible complications of surgery, including unrecognized residual or recurrent defects. Concomitant metabolic or non-cardiac causes of poor weight gain should also be ruled out.
Neuropsychiatric development in most patients who underwent surgery for congenital heart disease is normal, although some have either pre-existing disorders or acquired as a result of complications in the preoperative period and during the operation. Some patients have obvious causes of developmental delay attributable to intrauterine infections, Down's syndrome, and other syndromes associated with mental retardation. Patients with blue malformations have lower intelligence quotient (IQ) and developmental quotient (DQ) compared to healthy children. The duration of cyanosis affects the degree of developmental delay, which indicates the advantage of early correction of these defects. Congestive heart failure in CHD with left-to-right shunts causes developmental delay, but to a lesser extent than that seen in patients with cyanosis.
Patients undergoing open-heart surgery are exposed to a number of influences that can have a profound effect on their subsequent neurological and intellectual development. A cardiopulmonary bypass may pose a risk, especially when deep hypothermia and circulatory arrest are used during surgery. Chronic brain syndromes such as choreoathetosis have been associated with the use of deep hypothermia. There is little data regarding the long-term follow-up of patients who underwent heart surgery in childhood. However, their school performance, including graduation from high school, success at work, and marriage rates are less than those of adults of the same age without CHD. This may be influenced by restrictions from parents and doctors during childhood.

STATE EDUCATIONAL INSTITUTION OF HIGHER PROFESSIONAL EDUCATION CHITA STATE MEDICAL ACADEMY

DEPARTMENT OF POLYCLINIC THERAPY WITH A COURSE OF GENERAL MEDICAL PRACTICE

NONCORONARY HEART DISEASES

TUTORIAL

CHITA, 2008

UDC 616.126-002-022.7:616.127-002:616-002.77:616.11-002

BBK 54.101

Aleksenko, E.Yu. Non-coronary heart disease: a textbook. / E.Yu. Aleksenko, L.P. Sheludko, E.A. Tomina, S.M. Zwinger. - Chita: ICC CHGMA, 2008. - 84 p.

The manual is intended for general practitioners. Contains the necessary information about the etiology, pathogenesis, classification, clinical manifestations, diagnosis, modern principles of treatment, prevention, examination of temporary disability and medical and social examination of non-coronary heart diseases: endocarditis, myocarditis, pericarditis and syndrome-like diseases.

Reviewers :

Aleksenko Yu.I.- Associate Professor of the Department of Internal Diseases of the Dental and Pediatric Faculties, Ph.D.

Luzina E.V.- Associate Professor of the Department of Therapy FPC and PPS, Ph.D.

List of abbreviations ………………………………………………………………………….5

1. Infective endocarditis……………...………………………...………….…7

1.1 Classification and terminology of infective endocarditis………..….….7

1.2 Etiology and pathogenesis……………………………………………………..........9

1.3 Diagnosis of infective endocarditis……………………………….......10

1.4 Differential diagnosis…………………………………………………..15

1.5 Treatment of infective endocarditis……………………………………......19

1.6 Prevention of infective endocarditis…………………………………24

1.7 Examination of working capacity…………………………………………….......27

2. Myocarditis………………………………………………………………….……..29

2.1 Etiology…………………………………………………………………….…30

2.2 Myocardial pathology……………………………………………………….31

2.3 Classification of myocarditis….……………………..…………………………32

2.4 Diagnosis of myocarditis…………………………………………………..……..34

2.5 Differential diagnosis……………………………………………….….39

2.6 Treatment of myocarditis……………………………………………………………40

2.7 Examination of working capacity………………………………………….……..44

2.8 Clinical examination………………………………………………………………….44

3. rheumatic fever………………………………………………………46

3.1 Terminology and diagnostics…………………………………………………..46

3.2 Primary prevention of ARF………………………………………………………52

3.3 Treatment of ARF……………………………………………………………………….53

3.4 Secondary prevention of ARF…………………………………………………...54

3.5 Classification………………………………………………………………….…54

3.6 Examination of working capacity………………………………………………………………………55

3.7 Medical examination………………………………………………………………..57

4. Pericarditis………………………………………………………………….……58

4.1 Classification of pericarditis…………………………………………………..58

4.2 Pathogenesis of pericarditis………………………………………………………………59

4.3 Acute pericarditis……………………………………………………………….60

4.4 Chronic pericarditis…………………………………………………………64

4.5 Specific forms of pericarditis………………………………………….68

4.6 Rare forms of pericardial diseases……………………………………………………………………77

4.7 Prevention and rehabilitation………………………………………………...80

4.8 Examination of working capacity…………………………………………………………80

Literature……………………………………………………………………………….82

LIST OF ABBREVIATIONS

AV block - atrioventricular block

BP - blood pressure

ADNA B - antideoxyribonuclease B

ALT - alanine aminotransferase

ASG - antistreptohyaluronidase

ASA - antistreptokinase

ASL-O - antistreptolysin O

AST - aspartate aminotransferase

GABHS - group A beta-hemolytic streptococcus

HIV - human immunodeficiency virus

VEM - bicycle ergometry

GC - glucocorticoids

DNA - deoxyribonucleic acid

ACE inhibitor - angiotensin-converting enzyme inhibitor

IE - infective endocarditis

CS - corticosteroid

CPK - creatine phosphokinase

LDH - lactate dehydrogenase

LV - left ventricle

FUE - fever of unknown etiology

LS - medicine

MB - CPK - myocardial fraction of creatine phosphokinase

MK - mitral valve

INR - international normalized time

ITU - medical and social expertise

NK - circulatory failure

NSAIDs - non-steroidal anti-inflammatory drugs

NCD - neurocirculatory dystonia

ARF - acute rheumatic fever

RA - rheumatoid arthritis

RL - rheumatic fever

RNHA - hemagglutination neutralization reaction

RNA - ribonucleic acid

RPS - rheumatic heart disease

RSK - complement fixation reaction

SBP - systolic blood pressure

SLE - systemic lupus erythematosus

HF - heart failure

ESR - erythrocyte sedimentation rate

CRP - C-reactive protein

SJS - systemic scleroderma

FK - functional class

FKG - phonocardiography

HRHD - chronic rheumatic heart disease

CEC - circulating immune complexes

HR - number of heartbeats

ECG - electrocardiogram

EchoCG - echocardiography

INFECTIOUS ENDOCARDITIS

Currently, infective endocarditis (IE) is a significant problem in cardiology. The prevalence of this disease in economically developed countries ranges from 25 to 93 people per 1,000,000 population.

IE more often develops in the working-age population due to the epidemic of injection drug addiction, the widespread use of cardiac surgery, invasive medical manipulations and studies, and other reasons. There are special forms of the disease:

in Russia from 1990 to 2001. the number of drug addicts increased by 16.5 times and amounted to 45.2-48.7 per 100 thousand of the population (approximately 3.5-4 million). The annual incidence of infective endocarditis among drug addicts exceeds 5-6%. Complications of surgical treatment of heart defects, arrhythmias and conduction disorders are prosthetic valve IE (12-18%) and IE in patients with an implanted pacemaker (1-8%). After program hemodialysis, IE develops in 1.7-5.1% of patients, organ transplantation - in 7.7-18% of recipients. Increased mortality (60-100%) persists, largely due to the species composition of pathogens.

In patients with infective endocarditis, the pathological process involves the cardiovascular system, liver, spleen, lungs, kidneys, nervous system, etc., which largely determines the polymorphism of the clinical picture. Therefore, the duration of diagnosis verification is 3.8-10 months. In 40% of patients, the disease remains unrecognized for a long time or is not diagnosed at all.

Despite a wide range of modern antibiotic therapy, there is a high mortality from infective endocarditis, which, according to various studies, ranges from 18 to 36%. Early diagnosis of the disease is problematic, and the pathomorphosis of the disease undergoes significant changes.

Among the many dangerous diseases of the heart, bacterial endocarditis can be distinguished, since this disease is infectious and, if not treated in time, can cause many complications, including heart failure. Why the disease develops, how it is treated and what is dangerous, we will understand further.

What it is?

Bacterial endocarditis (backendocarditis) is a lesion of the inner lining (membrane) of the heart. It has a septic character, that is, it is caused by an infection. You can clearly see how a healthy endocardium differs from an infected one in the following picture:

In backendocarditis, microorganisms that are present in the human body penetrate the membrane, where they initialize an active population. Most often these are the following types of bacteria:

• staphylococcus;
• enterococcus;
• streptococcus;
• Pneumococcus;
• coli.

Specialists in recent years have noted a change in the composition of infectious pathogens, as the number of primary acute endocarditis with staphylococcal nature has increased. It is noted that when infected with Staphylococcus aureus, backendocarditis develops in almost 100% of cases.

In addition to bacteria, fungi can also cause the disease, regardless of the age group of the patient. As a rule, this occurs in the case of prolonged antibiotic treatment in the postoperative period or with long-standing venous catheters.

Medical studies show that men are more susceptible to backendocarditis. Female patients with this disease are 2 times less common.

Types and stages of development

According to the type of flow, there are three main types of backendocarditis:

• Spicy. In this case, the patient is sick for up to 2 weeks, given that he will be given proper treatment. With this type of disease, there is a possibility of such a consequence as the development of a defect in the valvular apparatus.
• Subacute. May take up to 3 months. Its characteristic difference from the previous species is that ulcers form on the heart, as well as thrombotic growths, which greatly complicates the consequences of the lesion.
• Chronic. It is not treated, and therefore the patient can suffer for years from the symptoms of the disease and its exacerbations.

The disease is also divided into two types depending on the presence or absence of background pathology:

• Secondary. It develops against the background of rheumatic heart disease. This is due to the fact that there is already an inflammatory process in the shell of the heart, so it is vulnerable to the effects of pathogenic microorganisms. So, in 90% of the patient, against the background of a defect, it develops.
• Primary. Occurs against the background of intact valves. As a rule, this happens if complications arise in the body after SARS. It is also possible that the disease is the result of severe stress or overwork.

In the case of intact heart valves, the primary form develops. If there are other diseases, for example, rheumatic lesions of the heart, then a secondary one develops.

Causes of the disease

Bacteria that attack the heart enter the body orally, so the cause of the development of the disease can be:

• Diseases caused by bacterial infection. It can be both diseases of the epidermis, and sinusitis, otitis, tonsillitis. These diseases can be triggered by the following types of bacteria: streptococci, enterococci and staphylococci.
• Performing some surgeries. For example, tooth extraction.

As such, there are no other causes for the development of bacterial endocarditis, but there are several risk factors that can lead to the development of the disease for no apparent reason:

• heart disease;
• (primary lesion of the heart muscle);
• artificial heart valve;
• scars on the heart valve as a result of past diseases of the cardiovascular system.

In general, backendocarditis is most susceptible to people with damaged heart valves or those replaced with artificial ones. Often the disease develops in drug addicts, because the valves of their hearts become as vulnerable as possible under the influence of drugs.

Symptoms

The described disease has many signs, and therefore it is difficult to recognize it immediately. The most striking and frequently encountered of them include:

• symptoms of intoxication of the body: nausea and vomiting, pre-syncope, fever, gastrointestinal upset, clouding of consciousness;
• a single sharp increase in temperature (up to 39-40 degrees);
• rashes on the skin and mucous membranes of varying severity, which may be accompanied by severe itching and redness;
• obvious and severe deformity of the limbs, especially fingers and toes;
• persistent shortness of breath;
• dry persistent cough without improvement (most often caused by an infection that enters the lungs);
• gray, pale or yellow-green skin tone;
• unreasonable and sudden loss of body weight;
• decreased efficiency and attention, fatigue, loss of working capacity.

The occurrence of certain symptoms and their intensity is determined by the following important factors:

• the state of the immune system;
• the phase of the development of the disease;
• the type of bacteria that caused the disease;
• the general health of the person.

For some, the symptoms appear gradually and at first may not even cause any discomfort. Such a development of the disease is dangerous because patients do not attach importance to the symptoms that have arisen, and the disease progresses, and this leads to neglected conditions. In others, on the contrary, the disease makes itself felt sharply and forces you to immediately take prompt measures.

Diagnostic Measures

With the above symptoms, you need to contact a cardiologist. The specialist will conduct a series of diagnostic measures in order to accurately diagnose:

1. Gather a general picture of the patient's health status. In particular, he will check the body for the presence of chronic infections and analyze the transferred surgical interventions, if any.
2. Conduct instrumental and laboratory studies. If a high content of leukocytes is found in the blood test, as well as a sharp increase in ESR (erythrocyte sedimentation rate), then this is a signal of backendocarditis.
3. He will conduct an important study to confirm the diagnosis - multiple blood cultures. It is needed in order to detect the pathogen and its type. Blood sampling for culture is best done at the peak of the patient's febrile state.
4. It will also take into account the indicators of a biochemical blood test. With bacterial endocarditis, changes in the protein spectrum of the blood and immune status were noticed. Hemolytic activity is reduced.
5. Do an echocardiogram. This research method is used to diagnose and confirm the diagnosis, since it allows you to identify vegetations on the heart valves, and this is a clear sign of bacterial endocarditis.

If the diagnosis is difficult, the doctor may additionally prescribe an MRI and MSCT of the heart.

How is it treated?

Treatment is carried out in a hospital, where the patient stays at least until the general state of health improves. He is prescribed bed rest, diet and drug therapy.

Immediately after blood culture, the patient is prescribed antibacterial drugs based on the type of infectious agent. Most often, a broad-spectrum antibiotic is selected, which allows not only to cope with the disease itself, but also with background problems in the body.

It is more difficult to treat endocarditis, the causative agent of which was a fungus. In such cases, the drug Amphotericin B (Amphotericin B), designed for a long course of treatment, is prescribed.

If against the background of endocarditis there are diseases such as nephritis, polyarthritis or myocardial disease, non-hormonal anti-inflammatory agents are added to the main drug therapy. These include Indomethacin and Diclofenac.

If drug treatment does not give positive results or improve the patient's condition, then a surgical operation is prescribed. The specialist performs prosthetics of the heart valves, and also cuts out part of the damaged parts of the organ. Instead of surgery, plasmapheresis or ultraviolet blood irradiation can be used.

Pediatric backendocarditis

Most often, endocarditis occurs in children under 2 years of age, while the disease cannot be congenital, but is only acquired. The transferred infectious diseases of both the child and the mother at the time of gestation contribute to the development of the disease.

A distinctive symptom of backendocarditis in children is a change in the color of the skin. It may acquire a pale gray or yellow-green tint. In addition, with children's backendocarditis, the following symptoms occur:

• acute toxicosis;
• endocardial damage;
• blockage of blood vessels by blood clots.

Other symptoms that may occur are identical to those that appear in adult patients. In rare cases, children have a symptom such as Janeway spots. They are not painful and appear on the palms and feet.

About 14 days pass from the moment the bacteria-causative agents enter the body until the development of the disease, and after that the first symptoms are found in the child. A correct diagnosis cannot be made without special diagnostic measures, which were described above.

Treatment of pediatric bacterial endocarditis includes small doses of Penicillin and other broad-spectrum antibiotics, which are selected individually after a complete examination and identification of a specific type of pathogen. Sometimes aspirin and other anti-inflammatory drugs are additionally prescribed. As in the case of adult patients, if drug therapy fails, surgical intervention is prescribed.

To prevent bacterial endocarditis in a child, it is important to monitor his condition and timely eliminate the consequences of caries, sinusitis, tonsillitis and other infectious diseases.

Complications

Backendocarditis is dangerous precisely because of the many complications that can even lead to death. These complications include:

• septic shock;
• cerebral embolism;
• respiratory distress syndrome;
• acute heart failure;
• cardiac embolism.

As a result of backendocarditis, heart failure of the following stages may develop:

1. Acute. Lasts at least 6 weeks. During inflammation, the ventricles and the heart muscle are affected. As a result of acute failure, heart cells die.
2. thrombotic. It is characterized by the occurrence of blood clots in the left and right ventricles of the endocardium. As a result, the growth of young connective tissue and the development of foci of sclerosis.
3. Fibrous. It is characterized by narrowing of the heart chambers. There is a risk of developing heart disease.

In addition, the transferred disease gives complications from some organs:

• kidney: renal failure, nephrotic syndrome;
• hearts: , heart disease, ;
• lungs: abscess, pulmonary hypertension, pneumonia;
• liver: hepatitis, cirrhosis;
• spleen: organ rupture, abscess;
• nervous system: meningitis, brain abscess, stroke;
• vessels: aneurysms, thrombosis, thrombophlebitis.

Video: what can lead to bacterial endocarditis?

Why it is important to treat caries, sinusitis and other infectious diseases in order to protect your heart from the penetration of infectious microorganisms, learn from the video:

Bacterial endocarditis is a disease that should be taken seriously. At the first symptoms, you should seek medical help and undergo an examination. Only timely measures will help to avoid the negative consequences of the disease for the whole organism.

The most significant changes in the epidemiology of infective endocarditis have occurred in the last 10-15 years.

If earlier IE often affected young people, then in the recent period there has been a clear increase in the number of infective endocarditis in older age groups. At the same time, the vast majority of them did not have previous valvular lesions, but were often subjected to diagnostic invasive procedures. The frequency of infective endocarditis depends on social conditions. In developing countries, where the role of rheumatism remains high, IE is more common in young people than in older people. In developed countries, the incidence is 3-10 cases per 100,000 patient years, with 1.5-2.5 cases among young people, and 14.5 cases per 15,000 people in older age groups (70-80 years).

Mortality from infective endocarditis is 11-27% during inpatient treatment. In the early post-stationary period, mortality remains very high, reaching 18-40%.

Men get sick more often than women 2 times.

Frequency. Infective endocarditis occurs with a frequency of 0.03-0.3%

Types of infective endocarditis

It is customary to distinguish 4 principles underlying the definition of the type of infective endocarditis:

• process localization; valve type (artificial, natural);
• the place of occurrence of the disease (hospital, outside the hospital, connection with the introduction of drugs);
• process activity;
• recurrent infective endocarditis or reinfection.

Causes of infective endocarditis

Acute infective endocarditis is most often caused by bacteria: Staphylococcus aureus, pyogenic streptococcus, gram-negative bacteria (Proteus, Pseudomonas aeruginosa, NASEK group).

Over a century of research into the diagnosis and treatment of infective endocarditis, it has been established that virtually all bacteria can cause the disease. However, only those bacteria that cause bacteremia are of particular importance: they have the ability to persist in the bloodstream for a long time, have an increased ability to colonize on the endocardium and form a biofilm on artificial surfaces.

Such abilities are possessed, first of all, by staphylococci, streptococci, enterococci. These microorganisms are mentioned in the beginning - middle of the XX century. and in the latest works of the beginning of the XXI century. It has been established that the ability to colonize the endocardium is regulated by the presence of the adhesin protein on the surface of the microorganism. Among many adhesins, collagen-, fibrin- and fibronectin-binding adhesins are the most important.

Thus, the beginning of colonization can be described by the term "adherence", which is carried out by adhesins located on the surface of the bacterium. However, micro-organisms in the blood are necessary for the "sticking" to take place. The source of bacteremia immediately preceding IE is rarely identifiable in practice.

The source of bacteremia was identified in 48% of patients with IE of natural valves and in 41% of patients with IE of artificial valves. In patients with natural valvular IE, the source of infection is often the oral cavity. Dental pathology became the source of the disease in 17% of patients. Diseases of the skin, genitourinary system and gastrointestinal tract led to IE in 8%, 2% and 9% of patients, respectively. In patients with infective endocarditis of artificial valves, a different picture was observed. Most often, the source of bacteremia is medical interventions (14% of patients). In second place were diseases of the genitourinary system (11%), and diseases of the oral cavity - only 3%. Apparently, this is due to the fact that the preoperative period involves the sanitation of foci of infection.

Transient bacteremia is often caused by typical oral and intestinal microbiota. The frequency of bacteremia after dental procedures ranges from 10 to 100%. In everyday life, the vast majority of healthy people may experience transient bacteremia when brushing their teeth. Experts from the American Heart Association have studied clinical and bacteriological parallels, i.e. the most characteristic microflora that led to infective endocarditis in patients with various clinical conditions and diseases was determined.

The etiology of IE in patients with an artificial valve depends on the time that has passed since the moment of prosthetics. Early IE is most often caused by coagulase-negative staphylococci (30-41%), Staph, aureus (8-24%), gram-negative bacteria - 10-15%, enterococci - 3.3-10%, fungi - up to 10%, streptococcus viridans - less than 1%.

Late infective endocarditis causes a spectrum of pathogens close to the spectrum of natural pathogens.

Differences in flora in the early period of the disease seem to be due to a significant number of medical interventions and frequent hospitalizations.

The modern view of pathogenesis defines the stages: 1st stage - the penetration of flora from the source of infection into the bloodstream and the development of persistent bacteremia. This stage occurs when the immune status changes. 2nd stage - fixation of the microorganism on the surface of the valve, endocardium. At this stage, a large role belongs to the previous changes in the valve, both of an organic nature and resulting from the damaging effect of the blood jet, which is forced to move at a different speed and turbulent due to valve defect, which creates all the conditions for the introduction of bacteria into the endocardium. Damage to the valve leaflets can occur with mechanical damage to the electrodes of the pacemaker, degenerative processes due to age-related changes. Degenerative changes in valve leaflets are detected in 50% of patients older than 60 years without a clinical picture of infective endocarditis. Stage 3 - initial valve changes - local signs of inflammation: swelling, exudation, etc. 4th stage - the formation of immune complexes (production of autoantibodies to the altered tissue structure), which are deposited in various organs and determine the systemic nature of the disease: damage to the heart, kidneys, liver, blood vessels.

The pathogenesis of infective endocarditis is characterized by the following syndromes.

1. intoxication syndrome. Starting from the 1st stage of the disease, bacteria in the patient's body cause intoxication, manifested by weakness, fever, increased ESR, leukocytosis and other typical manifestations of intoxication.
2. An increase in the bacterial mass, on the one hand, steadily maintains the severity of intoxication, and on the other hand, promotes the growth of vegetations on the valves; the growth of vegetations leads to the separation of their fragments and embolic syndrome.
3. Septic emboli contribute to the generalization of the process and the introduction of infection into almost all organs. The embolus causes mechanical occlusion of the vessel, which leads to regional blood flow disorders (acute cerebrovascular accident (ACV), embolic myocardial infarction, kidney infarction, embolic retinal damage, etc.).
4. autoimmune syndrome. Circulating immune complexes lead to vasculitis, polyserositis, glomerulonephritis, capillaritis, and hepatitis.
5. Syndrome of multiple organ failure. First of all, terminal renal failure and acute heart failure are the main causes of deaths in IE.

Symptoms of the debut of the disease

The manifestations of infective endocarditis at the onset of the disease are varied and depend both on previous changes in the valves and on the type of microorganism that caused the disease.

Infective endocarditis debuts as a clinical picture of an acute infectious disease, accompanied by fever, severe intoxication, multiple organ damage, and rapidly onset circulatory failure. Equally, the debut of the disease is manifested by a slight fever, unexpressed symptoms, which makes it difficult to diagnose the disease. In such a situation, a patient complaining of weakness, loss of body weight, makes a long journey through doctors of various specialties, until the appearance of specific valve changes becomes apparent. More than 90% of patients report fever, weakness, decreased appetite, weight loss, sweating, myalgia. In 85% of patients, a characteristic murmur of mitral, aortic or tricuspid insufficiency appears in the early stages of the disease.

Typical hemorrhages, glomerulonephritis, hepatosplenomegaly are noted in approximately 30% of patients with IE. Approximately one third of patients develop embolic syndrome of varying severity. The complexity of the clinical picture of the onset of the disease requires the doctor to assume a possible IE in the following situations.

1. The appearance of "new" noises in the auscultatory picture of the heart. Change in the auscultatory picture of a pre-existing heart disease.
2. The appearance of an embolism in the absence of an obvious source of emboli.
3. The appearance of fever in a patient with an artificial valve installed with a pacemaker.
4. The onset of fever in a patient previously treated for infective endocarditis.
5. Fever in a patient with congenital heart disease.
6. Fever in an immunocompromised patient.
7. Fever following procedures predisposing to bacteremia.
8. Fever in a patient with congestive heart failure.
9. The appearance of fever in a patient with Osler's nodules, hemorrhages, embolism.
10. The appearance of fever on the background of hepatolienal syndrome.

The manifestation of IE is manifested by a number of typical symptoms; their detection in patients allows to optimize diagnostics.

Most common for infective endocarditis:

• systemic inflammation syndrome: fever, chills, night sweats, left shift leukocytosis, anemia, positive blood cultures;
• intoxication syndrome: weakness, loss of appetite, myalgia, arthralgia, weight loss;
• hemodynamic syndrome: the formation of valvular heart disease with previously unchanged valves and the formation of combined valvular disease;
• autoimmune lesion syndrome: glomerulonephritis, myocarditis, hepatitis, vasculitis;
• thromboembolic syndrome: embolism in the brain, intestines, spleen, kidney, retina.

The manifestation of the disease is regulated by the type of pathogen. Thus, staphylococcal IE is characterized by significant intoxication, hectic fever, pronounced severity of the condition, the rapid appearance of "screenings" - septic embolism; fungal infective endocarditis is characterized by a pattern of occlusion of large arteries. A typical picture of infective endocarditis, described by W. Osler at the beginning of the 20th century. characteristic of viridescent streptococcus.

The main conclusion of the analysis of the clinical picture of the onset of the disease is a wide palette of symptoms and syndromes, which cannot be algorithmized even at the beginning of the 21st century. Its interpretation requires high professionalism of the doctor.

Prognostic value of clinical symptoms of the onset of the disease

Hospital mortality in patients with IE ranges from 9.6 to 26%. The extremely high mortality rate, even in the era of antibiotic treatment and early surgical intervention, requires the introduction of a preliminary prognostic assessment of the symptoms of the onset of the disease into everyday practice. This will allow optimizing the treatment of the disease, for example, considering surgical treatment as the main one already in the onset of the disease. The prognostic assessment of symptoms is based on 4 factors: the clinical portrait of the patient; extracardiac manifestations of the disease; characteristics of the causative agent of the disease; echocardiogram results. The prognosis is always more difficult when infective endocarditis is localized on the valves of the "left" heart, and a patient with rapidly progressive circulatory failure, glomerulonephritis and verified S. aureus flora has a high risk of death and requires surgical treatment at the earliest stages of the disease. The risk of death in such patients reaches 79%. Low EF values ​​or their rapid decrease in a short time, diabetes mellitus, cerebrovascular accident (embolism to other organs is possible) increase the risk of death by more than 50%. Thus, in the modern tactics of patient management, the principle of early prognostic assessment of the condition of patients is clearly formed to form a group of patients requiring the earliest possible surgical treatment.

The presence of at least one of the symptoms is sufficient to assess the patient's prognosis as severe.

Symptoms in the post-debut period

One of the most common symptoms of the disease is fever. The degree of increase in body temperature is different. With an acute onset of the disease, as a rule, fever reaches a high level, and the difference between the maximum and minimum body temperature can reach 2-3 ° C. With a subacute onset of the disease, the temperature is subfebrile. Debilitated patients may not have fever. The absence of fever is considered as a prognostic indicator of the severe course of the disease. In severe cases, fever is accompanied by chills and profuse sweats. Most often, all / about the rise in temperature occurs at night, which leads to the "flickering out" of the patient.

Along with fever, symptoms characteristic of circulatory failure appear - shortness of breath, tachycardia. The basis of circulatory failure is not only disturbed intracardiac hemodynamics due to the destruction of valves, but also developing myocarditis. The combination of myocarditis and destruction of the valve leaflets leads to the rapid formation of remodeling of the heart chambers. During this period, a doctor who regularly listens to the heart, in addition to characteristic noises, determines a decrease in the volume of the first tone at the 1st auscultation point. This refers to the signs of a severe prognosis. In the same period, a change in skin color is possible. S.P. Botkin, W. Osler described this color as the color of coffee with milk and attached great importance to it. In the modern clinic, this symptom has lost its significance and is not even mentioned in the manuals as diagnostically important.

Each patient notes arthralgia, myalgia. Pain is systemic and usually symmetrical. Local pain is not typical and requires the exclusion of embolism or the onset of osteomyelitis.

Every third patient clearly shows signs of rapid weight loss. This is an important symptom reflecting the degree of intoxication and the severity of the prognosis. Observations of patients with infective endocarditis have shown that excess adipose tissue before the disease is associated with the number of deaths.

Every seventh patient notes headaches and rise in blood pressure. Its increase is based on developing glomerulonephritis, which is accompanied by proteinuria, a decrease in glomerular filtration rate and an increase in creatinine levels. Control of the glomerular filtration rate is mandatory for all patients with infective endocarditis, as it allows you to adequately calculate the doses of administered antibiotics. During the period of a detailed clinical picture, the doctor traditionally expects to detect characteristic manifestations of the disease on the periphery - Osler's nodules, Roth's spots, hemorrhages of the nail bed, Janeway's spots. These stigmata of the disease were of great importance in the pre-antibacterial era, but they are rare in the modern clinic, their frequency<5%.

S.P. Botkin attached great importance to palpation of the spleen, highlighting several types of density of its edge, which allows assessing the severity of the disease. In the era of antibiotic treatment of IE, severe splenomegaly can be noted in less than 5% of patients.

Thus, the clinical picture of infective endocarditis has changed significantly. The clinic is dominated by a high frequency of erased forms, intoxication syndrome, syndrome of autoimmune lesions and syndrome of hemodynamic disorders. Virtually no symptoms of shock.

With an adequately selected antibacterial drug, fever can be stopped up to 7-10 days. Persistence of fever for a long time indicates the presence of an infectious agent S. aureus or the addition of a nosocomial (secondary) infection or the presence of an abscess.

Normalization of temperature does not mean the cure of the patient. In many ways, the clinical picture of the post-debut period of the disease consists of complications of the disease. Typical complications of infective endocarditis are circulatory failure, uncontrolled infectious process (abscess, aneurysm, fistula, vegetation growth, temperature persistence > 7-10 days), embolism, neurological manifestations, acute renal failure. One complication is observed in 70% of patients, two complications at the same time - in 25% of patients.

In drug addicts, the tricuspid valve is most often affected with the development of septic thromboembolism in the vessels of the small circle (multiple bilateral infarct pneumonia with decay).

Treatment of infective endocarditis

Antimicrobial treatment

This treatment is the mainstay of treatment for infective endocarditis. It was antibiotics that turned IE from an absolutely incurable deadly disease into a treatable one. In recent decades, significant developments have taken place in the study of the flora that causes IE, which made it possible to formulate the main trends in the modern antibacterial treatment of infective endocarditis.

1. Growing resistance of pathogens to the antibiotics used, an increase in the number of strains of oxacillin-resistant staphylococci have been noted everywhere. For example, in the Russian Federation, the incidence of oxacillin-resistant S. aureus is 33.5%. The same figure in the US has doubled in 5 years. Between 2002 and 2007, the incidence of vancomycin-resistant enterococci increased from 4.5% to 10.2%. The general trend is the widespread registration of multiresistant strains of staphylococcus, enterococcus, pneumococcus and other microorganisms. This has led to a decrease in the effectiveness of traditional antibiotic treatment regimens for infective endocarditis.
2. The fact of survival of microflora after antibacterial treatment in vegetations and in bacterial films covering the artificial valve has been proven. The bacteria in them are practically protected from antibacterial drugs. Experts see a solution to this problem in increasing the duration of treatment from 2 to 4-6 weeks for IE of own valves and up to 6 months for IE of prosthetic valves.
3. Emphasis is placed on the early use of a regimen of a combination of antibacterial drugs, which should be discussed in all cases of persistent fever against the background of antibacterial treatment.
4. The widespread organization of a high-quality microbiological service is emphasized, which allows choosing etiologically justified antibacterial treatment as soon as possible. It is many times more effective than empirical antibiotic treatment of IE with an unknown pathogen.
5. In severe cases of infective endocarditis, the combination of antibacterial and surgical treatment followed by correction of the antibacterial treatment regimen after surgery based on PCR material of vegetations and emboli was recognized as the most effective.

Treatment of infective endocarditis with antibiotics is divided into two fundamentally different approaches. A - treatment of IE with an identified pathogen and B - treatment of IE with an unknown pathogen.

Treatment of infective endocarditis with an established pathogen

Streptococcal infective endocarditis

Penicillin-sensitive streptococci

The tactics of choosing the mode of antibiotic use depends on the value of the minimum inhibitory concentration (MIC). If the IPC<0,125 мг/л (в 90% случаев неосложненного течения инфекционного эндокардита), то двухнедельное лечение пенициллином в комбинации с цефтриаксоном или гентамицином (или нетимицином) оптимально. Назначая аминогликозиды (гентамицин, нетимицин), следует удостовериться, что функция почек сохранена. При умеренном снижении их функции или исходно нормальных показателях можно обсуждать режим использования гентамицина 1 раз в день. Больным с аллергией на?-лактамные антибиотики показан ванкомицин.

The widely discussed antibiotic teicoplanin lacks conclusive effective evidence.

Penicillin-resistant streptococci

If MIC > 0.125 mg/l, but<2,0 мг/л, то стрептококки относительно резистентны. Если МПК >2.0 mg/l, then such a strain is recognized as absolutely resistant. In a number of recommendations, strains are recognized as absolutely resistant if the MIC > 0.5 mg / l. Recently, there has been a significant increase in strains absolutely resistant to penicillins, exceeding the level of 30%. The clinical picture of such infective endocarditis is characterized by the severity of the course, mortality is 17%. Despite the common basic antibiotics in the treatment of IE penicillin-resistant and penicillin-susceptible strains, the duration of treatment and the combination of antibacterial drugs are distinguished. The short treatment regimen is excluded. The duration of treatment increases from 2 weeks for penicillin-sensitive strains to 4 weeks for penicillin-resistant strains. With a high MIC, vancomycin becomes the drug of choice. Any form of resistance (relative or absolute) implies a duration of treatment with aminoglycosides up to 4 weeks along with basic drugs.

Infective endocarditis caused by these pathogens is relatively rare in the modern clinic. Given the high incidence of meningitis (characteristic of Strept. Pneumonia), it is important to determine how to treat infective endocarditis, if it is associated or not associated with meningitis. In cases where meningitis is absent, treatment tactics are determined at the level of the IPC (strain sensitive, relatively sensitive, resistant). When combined with meningitis, penicillin should be excluded because of its low ability to penetrate into the cerebrospinal fluid.

The drug of choice in this situation is ceftriaxone.

P-hemolytic streptococci have a number of features:

• group A is characterized by a relatively mild course of the disease and, as a rule, is represented by strains sensitive to penicillin;
• group B began to be detected in patients recently;
• for microorganisms of groups B, C and G, a high incidence of abscesses is characteristic. In this regard, the issue of surgical treatment must be addressed from the first days of the disease.

For all groups, the choice of streptococcal regimen depends on the IPC. The regimen of short treatment is contraindicated categorically.

Infective endocarditis due to staphylococcus aureus

Infective endocarditis caused by S. aureus is characterized by a severe course and rapid destruction of the valve. IE caused by coagulase-negative strains is characterized by the formation of a perivalvular abscess, metastatic septic complications. If the staphylococcal flora is verified, then the duration of treatment should exceed 4 weeks and reach 6 weeks.

When identifying staphylococcal flora, the most important issue for the clinician is the question of the sensitivity of the flora to methicillin. Methicillin-resistant flora is characterized by severe course and high mortality. The leading drug, the drug of choice in the treatment of staphylococcal IE is oxacillin. The high efficacy of oxacillin in left-sided staphylococcal IE of its own valves with an uncomplicated course was proven with a treatment duration of 4 weeks, with complications of infective endocarditis, a treatment duration of 6 weeks. For uncomplicated staphylococcal infective endocarditis of the right heart valves, a 2-week course of treatment is recommended. Clinically, there is no convincing evidence of the clinical efficacy of gentamicin in staphylococcal IE, however, the agreed position of experts allows adding gentamicin to oxacillin treatment for 3-5 days for IE of natural valves and up to 2 weeks for IE of prosthetic valves.

The inclusion of rifampicin in the combined antibacterial treatment of infective endocarditis is due to the fact that rifampicin is highly effective against bacterial films covering the metal surfaces of pacemakers and artificial valves. In patients with an allergic reaction to penicillin (not an anaphylactic type of reaction), 4th generation cephalosporins are possible. With an anaphylactic reaction to penicillin, only vancomycin with gentamicin is possible.

Patients with methicillin-resistant and vancomycin-resistant staphylococci formed a special niche in the treatment of infective endocarditis. Monitoring of the flora in patients with IE shows that in the last 3-5 years, the level of resistance has been rapidly increasing. With resistance to methicillin, the drug of choice is vancomycin. The appointment of other groups (in practice, carbapenems are prescribed in these situations) is erroneous, because MRSA are resistant to them. The prognosis of a patient with IE caused by vancomycin-resistant strains is severe. In this situation, it is possible to use menezolid. The role of a new antibiotic quinupristin dalfopristin (synercyte), a new cyclic lipopeptide - daptomycin (6 mg/kg per day intravenously) is being studied. In all cases of resistance to vancomycin, the patient should be managed in conjunction with a clinical pharmacologist.

In case of prosthetic valve IE, the doctor needs to accurately determine the date of the operation. If staphylococcal infective endocarditis developed before 1 year, then it was caused by coagulase-negative methicillin-resistant staphylococcus aureus. In this situation, the combination of vancomycin with rifampicin and gentamicin for 6 weeks is optimal. If the strain is resistant to gentamicin or other aminoglycosides, a fluoroquinolone should be added instead of the aminoglycoside in the combination of three antibiotics.

Enterococcal infective endocarditis

Enterococcal infective endocarditis in 90% of cases is caused by Enterococcus faecalis and much less often by E. faecium. Both strains are characterized by extremely low sensitivity to antibiotics, which obviously requires decent treatment for up to 6 weeks and a mandatory combination of antibacterial drugs based on the synergism of the bactericidal activity of penicillins, vancomycin with aminoglycosides. The essence of this combination is that penicillins and vancomycin increase the permeability of the enterococcus membrane for aminoglycosides. Increased permeability leads to the creation of a high concentration of drugs in the ribosomes inside the cell, which leads to a pronounced bactericidal effect. US (AHA) and European guidelines differ on the choice of the first drug in the treatment of enterococcal infective endocarditis. In the United States, penicillin is recommended at a dose of up to 30 million IU / day. In European recommendations, the drug of choice is amoxicillin, 200 mg/kg per day, intravenously, or ampicillin at the same dose. The second drug of choice for combination treatment is gentamicin. If the flora is resistant to gentamicin, it should be replaced with streptomycin at a dose of 15 mg / kg per day intravenously or intramuscularly every 12 hours, monitoring of kidney function is mandatory. The elimination of enterococcal flora is effective only with a combination of penicillins and aminoglycosides.

In a number of patients, resistance to the penicillin series is noted; in these situations, the penicillin preparation is changed to vancomycin. When the Enterococci strain is polyresistant, including to vancomycin, it is advisable to start treatment with minezolid, 1200 mg/day, intravenously, in 2 doses.

The following points are important for practice:

• only two aminoglycosides, gentamicin and streptomycin, have synergistic action with penicillins, other aminoglycosides do not have such an effect;
• if enterococcal infective endocarditis is caused by E. faecalis resistant to penicillin, vancomycin and aminoglycosides, then the duration of treatment should exceed 8 weeks;
• a combination of two?-lactam antibiotics is possible - ampicillins with ceftriaxone or carbapenem (glipenem) with ampicillin. However, this experience has been little studied, evidence class 2C.

Infective endocarditis due to the NASEK group

A number of gram-negative microorganisms are united in the NASEC group. In total, these microorganisms cause from 5 to 10% of all cases of infective endocarditis of the natural valves. A distinctive feature of NASEK is slow growth, which makes it difficult to determine the minimum inhibitory concentration. A number of microorganisms from the NASEC group secrete β-lactamases, which makes it difficult to use unprotected penicillins as first-line drugs. The effectiveness of ceftriaxone at a dose of 2 mg per day for 4 weeks has been proven.

For strains that do not produce β-lactamase, ampicillin, 12 g per day, IV, 4-6 doses, plus gentamicin, 3 mg/kg per day, in 2 or 3 doses, has been shown to be effective. Duration of treatment - 4 weeks.

The effectiveness of the fluoroquinolone ciprofloxacin, 400 mg, intravenously 2 times a day, on NASEC is less than that of the combination of aminopenicillin + aminoglycoside.

In 2007, the International Infective Endocarditis Group reported IE caused by non-NASEC gram-negative flora. Such IE was detected in 49 (8%) of 276 patients with IE included in the registry. The severity of the course of the disease allows researchers to recommend surgical treatment as early as possible + treatment with p-lactam antibiotics along with aminoglycosides.

Infective endocarditis caused by rare pathogens

In the vast majority of cases, rare pathogens are not detected by conventional methods, and the patient falls into the category of infective endocarditis with an unidentified pathogen. In the last year, such pathogens include microorganisms. Despite their rarity, a special bacteriological examination after negative blood cultures is mandatory.

The duration of infective endocarditis caused by rare forms of microorganisms has not been established. Bacteriostatic drugs doxycycline, erythromycin are used in the treatment of infective endocarditis only in this situation.

Empiric Treatment

When the flora that caused infective endocarditis could not be identified, or microbiological analysis is not possible, or the patient is waiting for laboratory results, the doctor needs to determine the choice of antibacterial drug. When making a decision, it is necessary to know whether there is a valve prosthesis, when it was installed, whether the patient has previously (when) received antibacterial treatment (which one), whether there is intolerance to p-lactam antibiotics.

In these situations, it is recommended to start treatment with ampicillin - sulbactam, 12 g / day, in combination with gentamicin. In case of intolerance to penicillin, vancomycin is prescribed in combination with ciprofloxacin and gentamicin. In prosthetic valve IE, the combination of vancomycin with rifampicin and gentamicin is effective. It is expedient to add cefipime to this combination if the prosthesis was performed 2 months before the disease, and the probability of gram-negative aerobes addition is high.

Prevention of infective endocarditis

First of all, the prevention of infective endocarditis should be carried out in patients with altered valves, i.e. with heart defects, regardless of whether they have been operated on or not.

As priority measures, foci of infection of any localization are sanitized. When extracting a tooth, tonsillectomy, installing a urinary catheter and removing it, any urological surgery, fibrogastroscopy, colonoscopy, it is necessary to prophylactically use antibiotics in short courses. If the patient is diagnosed with intolerance to penicillin drugs, amoxicillins are used, 2 g 1 hour before the intervention (ampicillin is possible). With intolerance to aminopenicillins, macrolides are used.

For interventions in the urogenital area, fibrocolonoscopy, gastroscopy in patients with a high risk of infective endocarditis, it is advisable to prophylactically treat with a combination of drugs: ampicillin, 2.0 g intravenously + gentamicin, 1.5 mg/kg intravenously one hour before manipulation and one hour after manipulation, give orally ampicillin, 2.0 g. In patients with moderate risk, you can limit the use of this combination only before the intervention. In case of intolerance to aminopenicillins in patients with high and moderate risk, it is advisable to use it and vancomycin in the treatment regimen 1-2 hours before the intervention.

Survival and mortality in patients with infective endocarditis

Survival for 10 years is 60-90%; The 20-year milestone is experienced by 50% of cured patients. Survival depends on a number of factors. It is higher at an earlier onset of the disease, in patients undergoing surgical treatment. Large mortality in the long term is associated with NK.

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Symptoms and treatment of infective endocarditis

Comparison of valves in disease

Our heart is an important and very complex organ, which is quite easily subject to changes, unfortunately, of a negative nature. One such change is infective endocarditis. E a disease in which inflammation occurs in the inner lining of the heart. This inner membrane, i.e. connective tissue, lines the valves and cavities of the heart. The course of this disease helps to understand the explanation of the causes of its occurrence.

The reasons

The name of this disease well reflects the essence of the pathological process, because various infectious agents can excite the disease.

1. Staphylococci. Today, it is increasingly possible to meet an infectious type of endocarditis, which is caused by staphylococcus aureus. Usually its course is the most severe in comparison with other pathogens. Also, its course is nosocomial in nature, that is, this type of disease often occurs when vascular catheters, fistulas, and arteriovenous nodes become infected.

streptococci

Streptococci. Infective endocarditis caused by Str. Viridaris, is characterized by a gradual slow onset. Often this applies to modified valves. Endocarditis caused by Str. Boyis. It usually develops against the background of gastrointestinal pathology, and more specifically, it is intestinal polyposis, colon or stomach cancer, duodenal ulcer or stomach ulcer. If the causative agent is β-hemolytic streptococcus, then the patient most likely suffers from diabetes mellitus or another heart disease. The course of this form is usually severe.

Salmonella. They rarely cause endocarditis. If the same weight occurs, it concerns damaged aortic and mitral valves. Salmonella can also infect the vascular endothelium.

Meningococcus. This form of the disease is also rare, but its development occurs against the background of meningitis. A valve is damaged that was not previously damaged.

Fungal endocarditis. It develops in patients who have undergone surgery on the vessels or the heart, have had a fungal infection, as well as in drug addicts who inject drugs intravenously. Immunodeficiency states that have different etiologies contribute to the development of the disease, for example, it can be HIV infection.

Pseudomonas aeruginosa

Pseudomonas aeruginosa. This pathogen affects pre-modified and intact valves located on both the right and left sides of the heart. The disease caused by Pseudomonas aeruginosa is severe, and it is difficult to treat.

Microorganisms of the NASEK group. The lesion extends to the prosthetic valves, and in this case the disease develops a year after the prosthesis was made. Also, the lesion may affect pre-modified natural valves.

Brucella. Usually this form occurs in those people who have had contact with animals affected by brucellosis. In this case, the lesion usually captures the tricuspid and aortic valves. General analysis of peripheral blood reveals leukopenia.

Classification of infective endocarditis also includes the differentiation of the disease according to several factors. There are two clinical and morphological forms of infectious endocarditis.

1. Primary form. Occurs in conditions of a septic nature, which have a different etiology. The lesion usually affects intact heart valves.
2. secondary form. It develops against the background of a pathology that is already present in the valves or vessels, as well as in diseases such as syphilis, rheumatism. The secondary form can manifest itself after valve prosthetics.

According to the clinical course, infective endocarditis is divided into three types.

1. Acute course. Duration - two months. It is a consequence of medical manipulations on the cavities of the heart or vessels or an acute septic condition.
2. Subacute flow. The duration stretches over two months. It arises due to the fact that the treatment of the acute form was ineffective and insufficient.
3. Prolonged flow.

Symptoms

The symptoms of infective endocarditis depend on factors such as the age of the patient, the duration of the disease, and the form of the disease. Also, manifestations may depend on previous antibiotic therapy.

Symptoms of the disease can be shortness of breath, weakness, fatigue

Clinical manifestations are due to toxinemia and bacteremia. Generally speaking, patients complain of shortness of breath, weakness, fatigue, weight loss, loss of appetite, fever. There is pallor of the skin, small hemorrhages in the region of the collarbones, on the mucous membrane of the oral mucosa, on the conjunctiva of the eyes and in some other places. If mild skin trauma occurs, capillary damage is found. This condition is also called a pinch symptom. It is worth paying attention to the shape of the nails and fingers. Nails become like watch glasses, and fingers like drumsticks.

In many patients, endocarditis is accompanied by heart muscle damage and functional murmurs, which are associated with valve damage and anemia. If the leaflets of the aortic and mitral valves are damaged, there will be signs of their insufficiency. Angina pectoris and pericardial rub may occur.

In the previous subheading, we discussed the causative agents of endocarditis. It is important to understand that each of them, starting to act in the patient's body, manifests itself in individual symptoms. Understanding this helps to more accurately determine the form of the disease. Consider some pathogens, but now from the side of the signs that are inherent in them.

Staphylococci

Staphylococci. The process that they cause is quite active. There is hectic fever, accompanied by profuse sweats. There are many foci of metastatic infection. Extensively developing hemorrhagic skin rash, suppuration rash and necrosis. Brain damage may occur. There is a slight enlargement of the spleen. This, as well as its soft texture, makes it impossible to feel it. Despite this, ruptures of the spleen and its septic infarcts often occur. Endocarditis often develops in the left side of the heart, where the aortic and mitral valves are equally affected. In this case, there is a high body temperature, severe intoxication, chills.

Streptococci. Much depends on the specific type of streptococcus. For example, infective endocarditis caused by Str. pyogenes, is manifested by high body temperature, severe intoxication, pustular skin diseases during the time that preceded the development of endocarditis.

Fungal endocarditis. Characteristic clinical features are thromboembolism in large arteries, signs of endophthalmitis or chorioretinitis, fungal lesions of the oral mucosa, esophagus, genital organs and urinary tract.

Now let's summarize all the listed symptoms by listing them:

• general weakness and malaise;
• loss of appetite, weight loss;
• dyspnea;
• rise in temperature to 40 degrees, accompanied by severe sweating and severe chills;
• pallor of the mucous membranes and skin, the skin acquires an earthy and yellowish tint;
• small hemorrhages on the mucous membranes of the mouth, on the skin, in the eyelids and sclera;
• fragility of blood vessels;
• modification of fingers and nails.

If any of these symptoms begin to be observed, you should immediately consult a doctor. If endocarditis is not detected in time, serious complications may develop, a person may even die. Of course, the doctor will not diagnose immediately. First, it is necessary to conduct a thorough diagnosis of the state of the patient's body, which will help to establish the form of the disease and prescribe a more effective treatment.

Diagnostics

Diagnostics includes several methods. To begin with, it is important to take a blood test from the patient. Infective endocarditis in this case is detected by the following indicators:

• normochromic moderate anemia;
• leukocytosis and shift of the leukocyte formula to the left;
• an increase in ESR, which can persist even despite effective treatment for six months: at the same time, if the ESR is normal, this does not mean that infective endocarditis can be ruled out;
• increased concentration of sialic acids.

For diagnosis, you need to undergo a series of examinations

The patient also takes a urine test. In endocarditis, this analysis reveals proteinuria and microhematuria, even if there are no obvious signs of kidney damage. If glomerulonephritis develops, hematuria and proteinuria will be most pronounced.

There is such a thing as blood culture. This is a culture of microbes that is isolated from the blood. This study also helps in identifying endocarditis and its form. For example, subacute endocarditis is defined by persistent bacteremia. In this case, the number of bacteria is in the range from one to two hundred ml. To detect bacteremia, it is necessary to take venous blood three times in a volume of about twenty milliliters. The interval between the first and third blood sampling should be one hour. If the pathogen is identified, it is important to determine how sensitive it is to antibiotics.

Of course, it is important to determine the state of the heart itself. For this, two research methods are used.

1. ECG. Conduction disorders such as sinoatrial block or AV block may be identified. If an embolic lesion of the coronary arteries occurs, infarct changes may occur.
2. EchoCG vegetation. Their size should be about five millimeters, then they can be identified. The most sensitive method for detecting vegetations is transesophageal echocardiography. This method also allows you to identify abscesses, perforation of the valves and rupture of the sinus of Valsalva. Echocardiography is good to use in order to monitor the effectiveness of treatment and the dynamics of the process.

Treatment

Benzylpenicillin

Treatment of infective endocarditis is usually carried out in a complex, which is based on adequate antimicrobial therapy. Since gram-positive flora often becomes the causative agent, the doctor may begin treatment with the appointment of benzylpenicillin, the dose of which is from 12 to 30 units per day. The course usually lasts about four weeks. If endocarditis is caused by viridescent streptococcus, a combination of aminoglycosides with penicillin can have a good effect. For example, a doctor may prescribe gentamicin. Semi-synthetic penicillins can also be used.

Enterococcal endocarditis usually develops due to interventions in the gastrointestinal tract or genitourinary tract. In this case, the cephalosporin is not very effective, so ampicillin or vancomycin is used, combining it with aminoglycosides.

It is difficult to treat endocarditis, which is caused by gram-negative flora, Pseudomonas aeruginosa, Escherichia coli, and so on. In this case, cephalosporins of the third and second generation, ampicillin, carbenicillin are used, combining them with aminoglycosides. Dosages are applied large for about six weeks.

These drugs, of course, are not the only ones that are used in the treatment of endocarditis. There are other medicines that have antibacterial properties. It could be dioxin.

If immunological manifestations are severe, and antibiotics have an insufficient effect on ongoing processes, the doctor may add hormones to the treatment. In any case, the doctor has recommendations for the treatment of endocarditis. The new version was released in 2009, there are versions published in 2012 and at other times. Only the doctor himself can effectively apply this knowledge for the benefit of the patient.

In addition, a decision may be made about surgical treatment. It includes the removal of vegetations and prosthetic valves.

The indications for surgery are as follows:

• large and mobile vegetations on the valves, which is determined during the ultrasound of the heart;
• abscesses of the valve ring and myocardium;
• progressive heart failure, observed with severe valve defects and not decreasing with drug therapy;
• early relapses of endocarditis;
• recurrent thromboembolic syndrome.

Effects

In order to understand the consequences of infective endocarditis, it is necessary to determine which target organs are involved and how exactly they are affected.

1. Heart. From the side of the heart, the following negative changes can occur: aneurysm, abscess, heart attack, pericarditis, myocarditis, arrhythmia, heart failure.
2. Vessels: aneurysm, vasculitis, hemorrhages, thrombosis, thromboembolism.
3. Kidneys. Perhaps the development of renal failure. infarction, diffuse glomerulonephritis, focal nephritis and nephrotic syndrome.
4. The defeat of the nervous system includes an abscess, meningoencephalitis, cyst, transient circulatory disorders of the brain.
5. The lungs can undergo abscess, infarction, pneumonia, and pulmonary hypertension.
6. Spleen: infarction, rupture, abscess, splenomegaly.
7. Liver: hepatitis.

The disease can affect both all and individual organs.

The lesion can affect both all target organs and some of them. In general, the prognosis depends on factors such as existing valvular lesions, the adequacy and timeliness of the therapy, and so on. If the acute form is not treated, death occurs after about a month and a half, and in the subacute form after six months. If antibiotic therapy is adequate, then mortality is observed in thirty percent of cases, and if infection of prosthetic valves occurs, then in fifty percent of cases.

In older patients, the disease progresses sluggishly. Often it is detected at a later date, so the prognosis is worse. Infectious endocarditis is one of the major causes of death among children. Infective endocarditis in children often develops due to the wrong behavior of parents, both before pregnancy and during pregnancy. To save the lives of both adults and children, it is very important to follow preventive measures.

Prevention

Preventive measures are important both for those who want to completely prevent the onset of the disease, and for those who have already been diagnosed. For individuals belonging to the latter group, prevention is important so that endocarditis does not progress and does not pass into other, more serious forms. For such people who are at high risk, it is important to regularly see doctors and monitor their health.

It is important to avoid bacterial and viral infections: tonsillitis, flu, etc.

Of course, a healthy lifestyle has never harmed anyone, so it is necessary to monitor what kind of food enters our body, whether it is active enough and whether the rest and work regimen is correct. All these factors will help maintain the state of your heart at the proper level, which will prolong life and save you and your loved ones from unnecessary problems.