Inflammation of the heart, or what is endocarditis? The main symptoms and methods of treatment of the disease. Acute infective endocarditis

Infective endocarditis (IE)- this is an infectious, often bacterial, polypous-ulcerative lesion of the valvular apparatus of the heart and parietal endocardium, accompanied by the formation of vegetations and the development of valve insufficiency due to the destruction of its cusps, characterized by systemic vascular damage and internal organs and thromboembolic complications.

Epidemiology. The incidence of infective endocarditis averages 30-40 cases per 100,000 population. Men get sick 2-3 times more often than women, among the sick people of working age (20-50 years) predominate. Distinguish primary IE developing against the background of intact valves (in 30-40% of cases), and secondary IE, developing against the background of previously altered valves and subvalvular structures (congenital and acquired valvular heart disease, prosthetic valves, prolapse mitral valve, postinfarction aneurysms, artificial vascular shunts, etc.).

In recent years, there has been a steady increase in the incidence of IE, which is associated with the widespread use of invasive methods of examination and surgical treatment, an increase in drug addiction and the number of people with immunodeficiency states.

The features of "modern" infective endocarditis include:

An increase in the incidence of the disease in the elderly and old age(more than 20% of cases).

An increase in the frequency of the primary (on intact valves) form of IE.

The emergence of new forms of the disease - IE of drug addicts, IE of a prosthetic valve, iatrogenic (nosocomial) IE due to hemodialysis, infection of intravenous catheters, hormone therapy and chemotherapy.

Mortality in infective endocarditis, despite the emergence of new generations of antibiotics, remains high level- 24-30%, and in the elderly - more than 40%.

Etiology IE is characterized by a wide range of pathogens:

1. Most common cause diseases are streptococci(up to 60 - 80% of all cases), among which the most common pathogen is viridescent streptococcus(in 30 - 40%). Factors contributing to the activation of streptococcus are purulent diseases and surgical interventions in the oral cavity and nasopharynx. Streptococcal endocarditis is characterized by a subacute course.

In recent years, the etiological role has increased enterococcus, especially in IE in patients undergoing abdominal surgery on abdominal cavity, urological or gynecological operations. Enterococcal endocarditis is characterized by a malignant course and resistance to most antibiotics.

2. In second place in frequency among the etiological factors of IE is Staphylococcus aureus(10–27%), the invasion of which occurs against the background of surgical and cardiosurgical manipulations, with injection drug addiction, against the background of osteomyelitis, abscesses of various localization. Staphylococcal endocarditis is characterized by an acute course and frequent damage to intact valves.

3. The most severe are IE caused by gram-negative microflora(Escherichia, Pseudomonas aeruginosa, Proteus, microorganisms of the NASEC group), which develop more often in injecting drug addicts and people suffering from alcoholism.

4. Against the background of immunodeficiency states of various origins, IE of mixed etiology develops, including pathogenic fungi, rickettsia, chlamydia, viruses and other infectious agents.

Thus, the most frequent gateway of infection are: surgical interventions and invasive procedures in the oral cavity, urogenital area, associated with the opening of abscesses of various localization, heart surgery, including valve replacement, coronary artery bypass grafting, prolonged stay of the catheter in a vein, frequent intravenous infusions, especially injection drug addiction, chronic hemodialysis.

Due to the frequent initiation of antibiotic therapy before testing the blood of patients with IE for sterility, it is not always possible to identify the causative agent of the disease. In 20-40% of patients, the etiology of the disease remains unknown, which makes it difficult to prescribe adequate antibiotic therapy.

Pathogenesis. In the development of IE, the following pathogenetic mechanisms can be distinguished:

1. transient bacteremia, which can be observed during any surgical interventions on the abdominal organs, genitourinary system, on the heart, vessels, organs of the nasopharynx, during tooth extraction. The source of bacteremia can be purulent infections of various localization, invasive studies of internal organs (bladder catheterization, bronchoscopy, colonoscopy, etc.), as well as non-compliance with sterility when injecting drug addicts. Thus, transient bacteremia is common and does not necessarily lead to IE. For the occurrence of the disease, additional conditions are necessary.

2. Endothelial damage develops as a result of exposure to the endocardium of high-speed and turbulent blood flows, due to metabolic disorders of the endocardium in elderly and senile people. In the presence of initial valvular pathology, the risk of bacteremia transformation into IE reaches 90% (according to M.A. Gurevich et al., 2001). Many invasive diagnostic and surgical interventions are accompanied by damage to the endothelium and, therefore, a high risk of developing IE.

3 . In the area of damaged endothelium, most often on the surface of the cusps of the heart valves occurs platelet adhesion, their aggregation and the formation of platelet parietal thrombi with fibrin deposition. Under conditions of bacteremia, microorganisms from the bloodstream are deposited on microthrombi and form colonies. On top of them, new portions of platelets and fibrin are layered, which cover microorganisms from the action of phagocytes and other factors of the body's anti-infective defense. As a result, large polyp-like accumulations of platelets, microorganisms and fibrin are formed on the surface of the endothelium, which are called vegetations. Microorganisms in vegetations have favorable conditions for reproduction and vital activity, which leads to the progression of the infectious process.

4. Weakening of body resistance as a result of various external and internal factors, it is a necessary condition for the development of an infectious focus in the heart under conditions of bacteremia.

5. As a result infectious destruction the tissues of the valve leaflets and subvalvular structures perforate the leaflets, tear off the tendon filaments, which leads to the acute development of insufficiency of the affected valve.

6. Against the background of a pronounced local infectious destructive process in the body, general immunopathological reactions naturally develop (inhibition of the T-system of lymphocytes and activation of the B-system, the formation of circulating immune complexes (CIC), the synthesis of autoantibodies to own damaged tissues, etc.), which leads to immune generalization process. As a result of immune complex reactions, systemic vasculitis, glomerulonephritis, myocarditis, polyarthritis, etc. develop.

7. IE is characterized thromboembolic complications: infected thromboemboli, which are particles of vegetations or a destroyed valve, migrate along the arterial bed of the large or small circle of blood circulation, depending on the damage to the endocardium of the left or right chambers of the heart, and form microabscesses of organs (brain, kidneys, spleen, lungs, etc.).

8. Progression of IE naturally leads to the development heart and kidney failure.

Pathoanatomy. The left parts of the heart are most often affected - the aortic and mitral valves, with IE in drug addicts - mainly the tricuspid valve. Vegetations on the endocardium are detected, consisting of platelets, fibrin and colonies of microorganisms, perforation or detachment of the valves, rupture of tendon chords. Vegetations often occur with valve insufficiency than with valvular stenosis, and are located mainly on the atrial side of the mitral valve or on the ventricular side - the aortic valve. Microaneurysms of vessels, abscesses of internal organs are characteristic.

Classification of IE

Clinical and morphological:

primary IE,

secondary IE.

By etiology: streptococcal, enterococcal, staphylococcal, proteic, fungal, etc.

With the flow:

acute, lasting less than 2 months,

subacute, lasting more than 2 months,

chronic relapsing course.

Special forms of IE:

Hospital (nosocomial)) IE:

prosthetic valve IE,

IE in persons with a pacemaker (pacer),

IE in people on program hemodialysis.

IE in drug addicts

IE in the elderly and senile

Clinical picture:

The current clinical course of IE is characterized by a predominance of

subacute or atypical forms of the disease with blurred clinical symptoms. Sometimes the disease is diagnosed only at the stage of acute destruction of the heart valves or the development of systemic immunopathological processes in the form of vasculitis, glomerulonephritis, etc.

When describing the clinic of IE, domestic scientists (A.A. Demin, 2005) traditionally distinguish 3 pathogenetic stages of the disease, which differ in clinical, laboratory and morphological parameters and principles of treatment:

Infectious-toxic.

Immunoinflammatory.

Dystrophic.

Complaints. The first symptoms usually appear 1 to 2 weeks after the episode of bacteremia. It - fever and intoxication. In subacute endocarditis, the disease begins with subfebrile temperature, which is accompanied by general weakness, chilling, sweating, fatigue, decreased appetite, and palpitations. During this period, the correct diagnosis, as a rule, is not established. The resulting symptoms are regarded as a viral infection, myocarditis, tuberculosis intoxication, etc.

A few weeks later, a hectic or persistent fever is established with a rise in body temperature to 38-39 ° C and severe chills, night sweats, weight loss of 10-15 kg, headaches, arthralgia and myalgia. Cardiac complaints appear and progress: shortness of breath during physical exertion, pain in the heart, persistent tachycardia. Despite the expressiveness clinical symptoms, the diagnosis of IE in the absence of signs of a formed heart disease may not yet be established. At this time, the identification of vegetations on the valves using echocardiography may be decisive. With the development of a defect in the affected valve, signs of left or right ventricular failure quickly appear, which is accompanied by characteristic physical and instrumental findings, making the diagnosis of IE obvious. With the formation of heart disease against the background of perforation of the valve leaflets and destruction of valve vegetations, thromboembolic complications often occur with the development of ischemic stroke, infarction of the spleen, kidneys (with left-sided IE) and lungs (with right-sided IE), which is accompanied by characteristic complaints. Fungal IE is characterized by thromboembolism in the arteries of the extremities with the development of mycotic aneurysms or foot necrosis.

In a later immuno-inflammatory stage, complaints appear that indicate the development of glomerulonephritis, hemorrhagic vasculitis, myocarditis, arthritis, etc.

objectively comes to light pallor skin with a grayish-yellowish tint (“coffee with milk” color), which is associated with anemia characteristic of IE, involvement of the liver and hemolysis of erythrocytes. Patients lose weight rapidly. Characteristic changes in the terminal phalanges of the fingers are revealed in the form "drum sticks" and nails by type "watch glasses" developing sometimes already after 2 - 3 months of the disease. On the skin of patients (on the front surface chest, on the limbs) can be observed petechial hemorrhagic eruptions(painless, not blanching when pressed). Sometimes petechiae are localized on the transitional fold of the conjunctiva of the lower eyelid. Lukin spots or on the oral mucosa. In the center of small hemorrhages in the conjunctiva and mucous membranes there is a characteristic zone of blanching. similar in appearance Roth spots are determined on the retina during the study of the fundus. On the soles and palms of the patient, painless red Janeway spots with a diameter of 1 - 4 mm. Perhaps the appearance of linear hemorrhages under the fingernails. Characteristic Osler's nodules Painful, reddish, pea-sized growths in the skin and subcutaneous tissue on the palms and soles associated with the development of thrombovasculitis. Positive pinching symptoms (Hechta) and Rumpel–Leede–Konchalovsky test, which indicate increased fragility of small vessels due to vasculitis. During the test, a blood pressure cuff is applied to the upper arm and a constant pressure of 100 mmHg is created in it for 5 minutes. With increased vascular permeability or thrombocytopathy (decrease in platelet function), more than 10 petechiae appear below the cuff in an area limited by a diameter of 5 cm.

Lymph node examination often reveals lymphadenopathy.

With the development of heart failure, external signs congestion in the systemic or pulmonary circulation

(orthopedic position, cyanosis, swelling of the legs, swelling of the neck veins, etc.).

With thromboembolic complications, characteristic external signs are also revealed: paralysis, paresis, signs of pulmonary embolism, etc.

Cardiac manifestations of IE:

In the acute course of IE and the rapid destruction of the affected valve, acute left ventricular or right ventricular failure develops with characteristic objective signs. Damage to the aortic valve is noted in 55 - 65% of cases, mitral valve - in 15 - 40%, simultaneous damage to the aortic and mitral valves - in 13%, tricuspid valve - in 1-5%, but among drug addicts this localization is detected in 50% of patients .

Percussion and auscultatory signs of valvular defects in primary IE, the nature of the pulse and blood pressure generally correspond to the physical manifestations of rheumatic heart disease.

It is difficult to diagnose IE associated with existing congenital or rheumatic heart disease. In differential diagnosis, along with the history and characteristic extracardiac signs of IE, the appearance of new or changes in previously existing heart murmurs due to the formation of new heart defects is taken into account.

Changes abdominal organs are manifested in an increase in the liver and splenomegaly (in 50% of patients) associated with generalized infection and frequent thromboembolic infarcts of the spleen.

Complications of IE:

Abscess of the annulus of the valve and its destruction.

diffuse myocarditis.

Heart failure, including acute with valve destruction.

Thromboembolism (in 35–65%) of patients.

Myocardial abscess, septic pulmonary infarction, spleen, brain.

Glomerulonephritis leading to chronic renal failure.

Diagnostics:

1. Complete blood count detects leukocytosis with a shift of the leukoformula to the left, an increase in ESR up to 50-70 mm / hour, normochromic anemia due to bone marrow suppression. An increase in ESR usually persists for 3–6 months.

2. Biochemical blood test reveals a pronounced dysproteinemia due to a decrease in albumin and an increase in the content of α 2 and γ-globulins, the content of fibrinogen, seromucoid increases, C-reactive protein appears, positive sedimentary tests - formol, sublimate, thymol. In 50% of patients, rheumatoid factor is detected.

3. Blood culture for sterility may be decisive in confirming the diagnosis of IE and choosing an adequate antibiotic therapy. To obtain reliable results, blood sampling should be carried out before the start of antibiotic therapy or after a short-term withdrawal of antibiotics in compliance with all the rules of asepsis and antisepsis by puncture of a vein or artery. In the area of the puncture of the vessel, the skin is treated twice with an antiseptic, the vein should be palpated with sterile gloves, 5–10 ml of venous blood is taken from the vein in 2 vials with nutrient media and immediately sent to the laboratory.

In acute IE, blood is taken three times with an interval of 30 minutes at the height of fever; in subacute IE, blood is taken three times within 24 hours. If after 2-3 days the growth of the flora is not obtained, it is recommended to sow 2-3 more times. With a positive result, the number of bacteria is from 1 to 200 in 1 ml of blood. Their sensitivity to antibiotics is determined.

4. Electrocardiography may reveal signs of focal or diffuse myocarditis, thromboembolism in the coronary arteries is accompanied by ECG signs of myocardial infarction, thromboembolism in the pulmonary artery (PE) will be manifested by ECG signs of acute overload of the right ventricle.

5. Echocardiography in many cases, it allows to identify direct signs of IE - vegetation on the valves, if their size exceeds 2-3 mm, to assess their shape, size and mobility. There are also signs of rupture of the tendon chords, perforation of the valve leaflets, and the formation of valvular heart defects.

Septic (infectious) endocarditis is caused by pathogenic microorganisms, predominantly by bacteria. Pathology affects the inner surface of the heart (endocardium), in particular, one or more heart valves, endocardium on inner surface walls or interventricular septum.

The outcome of the process can be acute valvular insufficiency, leading to pulmonary edema or impaired peripheral circulation, as well as damage to the heart muscle. Untreated, infective endocarditis often leads to lethal outcome.

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Reasons for development

Different variants of the disease have different causes.

Etiological factors of endocarditis:

heart valve disease, especially the mitral valve, caused by rheumatism (30% of cases);

Mitral valve endocarditis in rheumatic fever

congenital heart defects (15% of cases):, and others;
with significant regurgitation;
degenerative valve diseases caused by atherosclerosis, with syphilis, as well as a congenital anomaly - a bicuspid aortic valve.

75% of cases are caused by streptococci, 25% by staphylococci (these are more aggressive microorganisms).

Prosthetic valve endocarditis usually develops as a result of suppuration and fistula formation and is combined with valvular insufficiency. As a result, complications may occur: shock, heart failure, stroke, and others. Early endocarditis is more often caused by staphylococci, late - by streptococci.

Septic endocarditis of a prosthetic mitral valve

Intravenous drug use-induced endocarditis can be caused by a variety of organisms, including staphylococci, enterococci, corynebacteria, fungi, legionella, and many others.

Classification

Endocarditis can have several variants of the course, remaining one of the main diseases, the untimely diagnosis of which is life-threatening. There are such types of pathology:

valvular endocarditis, acute and subacute;

Acute verrucous endocarditis

prosthetic valve endocarditis, early and late;
endocarditis caused by intravenous drug use.

There is also a variant associated with the installation of a pacemaker, and nosocomial, that is, that occurred in a hospital during the treatment of other diseases.

The classic division of endocarditis into acute and subacute is now blurred due to wide application antibiotics and a large number of patients with immunosuppression. However, the acute course is more characteristic of the rapid damage to the normal valve caused by Staphylococcus aureus or group B streptococcus.

In Fig. 1: the prosthetic valve is infected with the pathogen Enterococcus; rice. 2-4: artificial valves infected Staphylococcus aureus, in fig. 4 extensive destruction of heart tissue with aortic root abscess.

Already affected valves are involved in the subacute process. Its manifestations are less pronounced, and the pathology can develop over several months. The main pathogens are group A hemolytic streptococci or enterococci.

Prosthetic valve endocarditis accounts for up to 10% of cases. 5% of prosthetic valves become infected. Mechanical prostheses become infected in the first 3 months after installation, and the biological inflammatory process develops a year or more later (late endocarditis). Mitral prostheses are more susceptible to infection than aortic ones.

Early prosthetic valve endocarditis develops in the first 2 months after surgery. It is caused mainly by staphylococci, but streptococci, Candida fungi, enterococci can also become its cause.

Intravenous drug use endocarditis affects healthy valves, mostly the tricuspid valves. The most common pathogen is staphylococcus aureus.

Damage symptoms

In 90% of patients, the temperature rises, fever is sometimes noted, it can be intermittent. 85% of patients have a heart murmur.

Half of the patients have the so-called classic signs of endocarditis:

(small subcutaneous hemorrhages) - a common but non-specific sign;
subungual hemorrhages in the form of dark red lines;
Osler's nodules: subcutaneous formations, often located in the area of \u200b\u200bthe fingertips;
Jenway spots: painless lesions on the palmar surfaces and soles.

a) Jenway spots; b) subungual hemorrhages; c) Osler's nodules; d) Lukin-Libman symptom (conjunctival hemorrhage).

In 40% of patients, neurological disorders are noted:

ischemic stroke;
intracerebral hemorrhage;
multiple microabscesses of the brain.

Other possible symptoms endocarditis:

heaviness in the area under the left rib due to an increase in the spleen;
rigidity neck muscles, inability to tilt the head forward;
mental disorders, delirium;
paralysis, speech disorders;
hemorrhages in the conjunctiva of the eye;
pale skin;
pulmonary rales, cough;
abnormal heart rhythm;
rubbing noise of the pleura or pericardium, determined by listening.

With a subacute variant of endocarditis, the symptoms are nonspecific:

a slight increase in temperature;
lack of appetite;
weight loss;
flu-like symptoms;
muscle pain;
chest pain when breathing (due to pleural effusion);
headache;
heaviness in the right hypochondrium, vomiting, abdominal pain.

Possible complications of septic endocarditis:

, inflammation of the heart bag (pericarditis), cardiac arrhythmias;
circulatory failure;
aneurysm of the sinus of Valsalva;
abscess of the heart muscle or aortic root;
vascular embolism, mycotic aneurysms;
arthritis, myositis;
glomerulonephritis, kidney failure;
stroke;
abscess or or mesentery.

For the causes and symptoms of septic endocarditis, see this video:

Diagnostics

Recognition of septic endocarditis and its causes - Long procces. Diagnosis takes into account clinical, microbiological, pathomorphological and echocardiographic characteristics.

Major criteria according to microbiological blood analysis:

single simultaneous release of two pathogens;
isolation of one microorganism in two samples taken more than 12 hours apart;
three or more positive tests obtained more than 1 hour apart.

Major echocardiographic criteria:

detection of growths (vegetations) on valves, surrounding tissues, valve prostheses;
abscess of the heart muscle;
insufficiency of the prosthetic valve;
acute valvular insufficiency.

Echocardiography of IE: the arrow shows a long mobile vegetation located on the right coronary cusp of the aortic valve

Small Criteria:

heart disease or injection drug use;
temperature 38 degrees or more;
vascular symptoms, for example, pulmonary infarction, cerebral or conjunctival hemorrhage, Jenway spots;
immunological signs: Osler's nodules, Roth's spots (damage to the retina), glomerulonephritis and a positive test for rheumatoid factor;
isolation from the blood of microorganisms that do not meet the major criteria, or the detection of antibodies to them during a serological study in the appropriate condition of the patient;
results of cardiac ultrasound that do not contradict the proposed diagnosis, but do not match the major criteria.

Diagnosis Criteria for IE

The final diagnosis is made on the basis of the following data:

the presence of two major criteria;
or 1 major and 3 minor criteria;
5 small signs.

Treatment

The mainstay of therapy for septic endocarditis is antibiotics. Before their appointment, it is necessary to take from 3 to 5 blood tests with an interval of 60 to 90 minutes for the subsequent isolation of the pathogen.

Then the introduction begins antibacterial drug selected according to clinical guidelines.

After receiving the result of the analysis, it is possible to correct the therapy - replacing the antibiotic with a more effective one.

Depending on the course of the disease, the following are prescribed:

penicillins, in particular semi-synthetic in combination with clavulanic acid;
cefazolin, ceftriaxone;
gentamicin;
vancomycin;
streptomycin;
carbapenems.

Treatment of IE depending on the causative agent

Medicines are administered by intravenous infusion or injection for 4 to 6 weeks or longer.

In the presence of a mechanical valve prosthesis or deep vein thrombosis, anticoagulant therapy with warfarin is additionally prescribed.

About 20% of patients require surgical intervention. Operation necessary in such cases:

congestive circulatory failure refractory to conventional treatment;
fungal endocarditis (except for those caused by histoplasma);
detection of microbes in the blood after 3 days of antibiotic administration;
the spread of microorganisms to other organs;
break ;
conduction disturbances caused by an abscess of the interventricular septum;
transition of inflammation from the aortic valve to the mitral valve;
early prosthetic valve endocarditis;
pacemaker infection.

Damaged artificial devices are removed, the affected valve is replaced.

Forecast

It depends on the severity of the disease and the presence of complications. General indicator mortality is 14.5%.

Cure rate for previously healthy valve disease:

streptococci - 98%;
enterococcus and staphylococcus in drug addicts - 90%;
hospital staph infection – 60%;
gram-negative aerobes and fungi - about 50%.

If the valve prosthesis is affected, the cure rate is 10% less. On average, it is possible to cure 60% of patients with early prosthesis endocarditis and 70% with late ones.

Factors that worsen the prognosis:

elderly age;
involvement of the aortic valve;
development of heart failure;
stroke;
concomitant diabetes mellitus.

Prevention

Up to 25% of cases of septic endocarditis are associated with interventions that lead to a short-term entry of microbes into the blood vessels. Only half of these patients previously belonged to the risk group. Therefore, only about 10% of cases of endocarditis can be prevented by prescribing prophylactic antibiotics.

The main source of infection is gum inflammation, so maintaining oral health serves in the best possible way primary prevention diseases.

Risk groups for the development of endocarditis:

prosthetic valve;
previous endocarditis;
condition after heart transplantation;
congenital heart defects with a high pressure gradient.

Patients at risk need endocarditis prophylaxis before such interventions:

any procedure that damages the gums or the oral mucosa;
any intervention with damage to the respiratory mucosa;
procedures on inflamed skin, the musculoskeletal system (opening an abscess, treating a fracture, and so on).

When examining the digestive organs, genital or urinary systems, antibiotics are not needed.

Usually assigned penicillin antibiotic 1 or 2 hours before the procedure and 6 hours after the first dose. With intolerance to this group, erythromycin, clindamycin, gentamicin can be used.

To avoid the development of the disease, you should:

treat chronic inflammatory pathologies;
strengthen the immune forces of the body;
do not use intravenous injections unnecessarily, especially when using non-sterile syringes.

Septic endocarditis is a lesion of the heart valve, leading to circulatory failure, vascular embolism, damage to the brain, kidneys, and other organs. This pathology requires long-term treatment antibiotics and sometimes surgery. With an incorrectly chosen treatment strategy or a severe course of the disease, there is a possibility of a fatal outcome.

About the diagnosis, treatment and prevention of septic endocarditis, see this video:

Classification of infective endocarditis

By origin, primary and secondary infective endocarditis are distinguished. Primary usually occurs in septic conditions various etiologies against the background of unchanged heart valves. Secondary - develops against the background of an already existing pathology of blood vessels or valves with birth defects, rheumatism , syphilis , after valve replacement surgery or commissurotomy .

According to the clinical course, the following forms of infective endocarditis are distinguished:

acute - duration up to 2 months, develops as a complication of an acute septic condition, severe injuries or medical manipulations on the vessels, heart cavities: nosocomial (nosocomial) angiogenic (catheter) sepsis. It is characterized by a highly pathogenic pathogen, severe septic symptoms.
subacute - lasting more than 2 months, develops with insufficient treatment of acute infective endocarditis or the underlying disease.
protracted.

Do drug addicts clinical features infective endocarditis are young age, rapid progression of right ventricular failure and general intoxication, infiltrative and destructive lung damage.

In elderly patients, infective endocarditis is caused by chronic diseases of the digestive system, the presence of chronic infectious foci, and damage to the heart valves. There are active and inactive (healed) infective endocarditis. According to the degree of damage, endocarditis occurs with limited damage to the leaflets of the heart valves or with a lesion that extends beyond the valve.

The following forms of infective endocarditis are distinguished:

infectious-toxic - characterized by transient bacteremia, adhesion of the pathogen to the altered endocardium, the formation of microbial vegetations;
infectious-allergic or immune-inflammatory - are characteristic Clinical signs lesions of internal organs: myocarditis, hepatitis, nephritis, splenomegaly;
dystrophic - develops with the progression of the septic process and heart failure. The development of severe and irreversible lesions of internal organs is characteristic, in particular, toxic degeneration of the myocardium with numerous necrosis. Myocardial damage occurs in 92% of cases of prolonged infective endocarditis.

Symptoms of infective endocarditis

The course of infective endocarditis may depend on the duration of the disease, the age of the patient, the type of pathogen, and also on previous antibiotic therapy. In cases of highly pathogenic pathogen ( Staphylococcus aureus, gram-negative microflora), an acute form of infective endocarditis and early development of multiple organ failure are usually observed, and therefore the clinical picture is characterized by polymorphism.

The clinical manifestations of infective endocarditis are mainly due to bacteremia and toxinemia. Patients complain of general weakness, shortness of breath, fatigue, lack of appetite, weight loss. A characteristic symptom of infective endocarditis is fever - a rise in temperature from subfebrile to hectic (exhausting), with chills and profuse sweating(sometimes, in pouring sweats). Anemia develops, manifested by pallor of the skin and mucous membranes, sometimes acquiring an "earthy", yellowish-gray color. There are small hemorrhages (petechiae) on the skin, mucous membrane of the oral cavity, palate, on the conjunctiva of the eyes and eyelid folds, at the base of the nail bed, in the collarbone region, arising from the fragility of the blood vessels. Damage to the capillaries is detected with a mild injury to the skin (a pinch symptom). Fingers take the form of drumsticks, and nails - watch glasses.

Most patients with infective endocarditis have damage to the heart muscle (myocarditis), functional murmurs associated with anemia, and valve damage. With damage to the leaflets of the mitral and aortic valves, signs of their insufficiency develop. Sometimes there is angina, occasionally there is a friction rub of the pericardium. Acquired valvular disease and myocardial damage lead to heart failure.

In the subacute form of infective endocarditis, embolisms of the vessels of the brain, kidneys, and spleen occur with thrombotic deposits that have come off the cusps of the heart valves, accompanied by the formation of heart attacks in the affected organs. Hepato- and splenomegaly are found, on the part of the kidneys - the development of diffuse and extracapillary glomerulonephritis, less often - focal nephritis, arthralgia and polyarthritis are possible.

Complications of infective endocarditis

Fatal complications of infective endocarditis are septic shock, embolism to the brain, heart, respiratory distress syndrome, acute heart failure, multiple organ failure.

With infective endocarditis, complications from the internal organs are often observed: kidneys (nephrotic syndrome, heart attack, renal failure, diffuse glomerulonephritis), heart (valvular heart disease, myocarditis, pericarditis), lungs (heart attack, pneumonia, pulmonary hypertension, abscess), liver ( abscess, hepatitis, cirrhosis); spleen (heart attack, abscess, splenomegaly, rupture), nervous system (stroke, hemiplegia, meningoencephalitis, brain abscess), blood vessels (aneurysms, hemorrhagic vasculitis, thrombosis, thromboembolism, thrombophlebitis).

Diagnosis of infective endocarditis

When collecting an anamnesis, the patient finds out the presence of chronic infections and past medical interventions. The final diagnosis of infective endocarditis is confirmed by instrumental and laboratory data. In a clinical blood test, a large leukocytosis and a sharp increase in ESR. Multiple blood cultures to identify the causative agent of infection have an important diagnostic value. Blood sampling for bacteriological culture is recommended at the height of fever.

The data of a biochemical blood test can vary widely in one or another organ pathology. With infective endocarditis, there are changes in the protein spectrum of the blood: (α-1 and α-2-globulins increase, later - γ-globulins), in the immune status (the CEC, immunoglobulin M increases, the total hemolytic activity complement, increases the level of anti-tissue antibodies).

A valuable instrumental study for infective endocarditis is EchoCG, which allows you to detect vegetations (more than 5 mm in size) on the heart valves, which is a direct sign of infective endocarditis. More accurate diagnosis is carried out using MRI and MSCT of the heart.

Treatment of infective endocarditis

With infective endocarditis, treatment is mandatory inpatient, until improvement general condition the patient is prescribed bed rest, diet. The main role in the treatment of infective endocarditis is given to drug therapy, mainly antibacterial, which is started immediately after blood culture. The choice of antibiotic is determined by the sensitivity of the pathogen to it, it is preferable to prescribe antibiotics a wide range actions.

In the treatment of infective endocarditis, penicillin antibiotics in combination with aminoglycosides have a good effect. Fungal endocarditis is difficult to treat, so amphotericin B is prescribed for a long time (several weeks or months). They also use other agents with antimicrobial properties (dioxidin, antistaphylococcal globulin, etc.) and non-drug methods of treatment - autotransfusion of irradiated blood with ultraviolet radiation.

At comorbidities(myocarditis, polyarthritis, nephritis) non-hormonal anti-inflammatory drugs are added to the treatment: diclofenac, indomethacin. In the absence of the effect of drug treatment, it is indicated surgical intervention. Prosthetic heart valves are performed with excision of damaged areas (after the severity of the process subsides). Surgical interventions should be carried out by a cardiac surgeon only according to indications and accompanied by antibiotics.

Prognosis for infective endocarditis

Infective endocarditis is one of the most severe cardiovascular diseases. The prognosis for infective endocarditis depends on many factors: existing valve lesions, the timeliness and adequacy of therapy, etc. The acute form of infective endocarditis ends without treatment. fatal after 1 - 1.5 months, subacute form - after 4-6 months. With adequate antibiotic therapy, mortality is 30%, with infection of prosthetic valves - 50%. In older patients, infective endocarditis is more indolent, often not immediately diagnosed, and has a poorer prognosis. In 10-15% of patients, the transition of the disease to a chronic form with relapses of exacerbation is noted.

Prevention of infective endocarditis

Persons with an increased risk of developing infective endocarditis are subject to the necessary monitoring and control. This applies, first of all, to patients with prosthetic heart valves, congenital or acquired heart defects, vascular pathology, with a history of infective endocarditis, with foci of chronic infection (caries, chronic tonsillitis, chronic pyelonephritis).

The development of bacteremia can accompany various medical manipulations: surgical interventions, urological and gynecological instrumental examinations, endoscopic procedures, tooth extraction, etc. For a preventive purpose, a course of antibiotic therapy is prescribed for these interventions. It is also necessary to avoid hypothermia, viral and bacterial infections (flu, tonsillitis). It is necessary to carry out sanitation of foci of chronic infection at least 1 time in 3-6 months.

Endocarditis is an inflammation that affects the inner lining of the heart called the endocardium. The disease occurs unpredictably, causing heart failure. As a rule, it is not independent disease, but is a particular manifestation of other diseases, and in most cases - infections.

What is this disease?

internal inflammation lining of the heart is called endocarditis. Often it also affects the valvular apparatus and the layer of cells that cover the surface of adjacent vessels. Often people who take narcotic drugs in the injection method of use, tricuspid valve endocarditis develops, presented in the form of 3 connecting plates between the right atrium and the right ventricle of the heart.

Features of the course of the disease and treatment depend on the type of endocarditis, which, due to the appearance, can be infectious (bacterial, septic) or non-infectious. In addition, endocarditis is classified according to anatomical features, because changes can complement each other depending on etiological factor and immunological state of the body.

For an accurate diagnosis, it is necessary to consult a doctor who will be guided not only by the clinical manifestations of endocarditis, but also by the results of various studies.

It is not worth delaying the examination, since heart disease and heart failure can develop, and in 30% of cases endocarditis is fatal.

General symptoms

Regardless of the type, endocarditis is often accompanied by such manifestations:

raising body temperature to high limits;
the development of chills;
pain in the joints and muscles;
general intoxication of the body, causing weakness throughout the body, severe weight loss, chronic headaches, etc .;
increased blood clotting with further formation of blood clots, and in the worst case, a heart attack;
heavy sweating;
lethargy;
the acquisition of grayish skin with characteristic red spots;
headaches that have a growing character;
the formation of reddish painful nodules on the hands.

If the patient suffers from a heart disease, his shortness of breath will increase - at first it will manifest itself during physical exertion, but then it will become permanent. On average, the heartbeat will be about 120 beats per minute.

In chronic endocarditis, symptoms persist for about six months. During this period, the patient loses a lot of weight, the fingers take on the appearance of drumsticks, while the nails grow dull and become convex. Hemorrhages appear on the fingers and toes, reddish nodules form.

Types of endocarditis due to development

Endocarditis can be infectious, that is, it can occur when the endocardium is damaged by microbes and toxins, as well as non-infectious, that is, it can occur due to injuries and other reasons. More often endocarditis is infectious nature, but it is worth considering the features of each type.

Infectious

It develops if the pathogen enters the bloodstream, and the human immunity is weak to fight them. Endocarditis is caused by gram-negative and anaerobic microorganisms, as well as fungi. As a rule, they affect the body with prolonged use of antibiotics, in the postoperative period, or with catheters standing in the veins for a long time.

There are three forms of development of infective endocarditis:

Infectious-toxic. Bacteria enter the bloodstream, begin to multiply there, forming growths-vegetations.
Infectious-allergic. With a decrease in immunity resistance, internal organs (kidneys, spleen, liver, myocardium) are affected.
Dystrophic. It manifests itself if the septic process and heart failure progress. It has a severe development and causes damage to internal organs, including toxic myocardial degeneration with necrosis.

The exact characterization of endocarditis depends on its type:

Spicy. Occurs as a complication of sepsis. Rapid valvular destruction develops and lasts no more than 5 weeks. Manifested by the following reactions:
tormented by fever, and body temperature ranges from 37.5 to 39 degrees;
the skin acquires a dark shade (coffee with milk);
develops defect of the mitral and aortic valve;
from the side pulmonary system shortness of breath, hemoptysis and pulmonary hypertension;
the liver increases in size, kidney damage occurs with the development of glomerulonephritis;
damage to the central nervous system occurs due to the development of meningitis;
the organ of vision is affected by the development of retinal vascular embolism with complete and partial blindness.
Subacute or chronic (protracted). As a rule, its causative agents are streptococci and staphylococci, and less often - enterococci, pneumococci, E. coli. Diagnosed within six weeks of onset clinical picture, unfortunately, already on the operating table or after an autopsy in the morgue. Has the following characteristics:
in the usual case, the first to appear is fever, chills and sweating, while the temperature has a wave-like character, so you might think that the patient has a common cold or chronic infection;
the skin takes on a pale appearance, possibly with a yellowish tint, and hemorrhages are also poured out on it, which can later cause the development of necrosis with hemorrhage under the skin;
in some patients, especially the elderly, the temperature may rise at certain hours or against the background of developing glomerulonephritis, but generally remain within the normal range, so the temperature should be measured at least 7-8 times a day for 3 weeks;
general intoxication develops, therefore, weight loss and a decrease in working capacity occur, anemia develops and the erythrocyte sedimentation reaction increases to 40 mm / h, and such manifestations are noted - weakness, fatigue, dizziness, headaches.

Elena Malysheva will tell in detail about septic endocarditis in her program “Live Healthy”:

In general, endocarditis proceeds like sepsis, causing destructive and inflammatory changes in the heart, parietal endocardium and large vessels. In addition, they develop an immunopathological reaction and toxic damage to organs, and also provoke thromboembolic complications.

non-infectious

The disease is also called non-bacterial thromboendocarditis. It is caused by platelet or fibrin clots that form on the heart valves and adjacent endocardium. Their appearance is not due to infection, but to organ damage, circulation of immune complexes, vasculitis, or hypercoagulability.

Such endocarditis is asymptomatic, but it can be diagnosed by signs characteristic of arterial embolism, including fever and a heart murmur. Wherein pain will be observed from the damaged organs - the brain, kidney or spleen.

Classification of anatomical types of endocarditis

According to the anatomical sign, endocarditis is of the following types:

Warty. It develops with rheumatic disease, lupus erythematosus (Libman-Sachs endocarditis), after an infectious disease with the development of intoxication. With it, warty thrombi appear over the affected endocardium due to destruction of the endothelial lining.
recurrent warty. As a rule, it is observed in rheumatism. On the deformed valve, mucoid and fibrinoid swellings, thrombic overlays and granulomatosis appear.
diffuse(valvulitis). The only difference from the previous species is that granulomatosis is rarely observed, thrombotic overlays do not appear at all, and the endothelium is not damaged.
fibroplastic. Its development is rheumatic pains. It is characterized by early fibrosis or thickening of the tissue with scarring. At autopsy, the patient has an enlarged heart, thickened septa, and possible fibrin threads on the pericardium.
Acute ulcerative. Develops with sepsis. Destructive processes are launched, large and rough ulcers are formed on the endocardium. Blood circulation is disturbed due to changes in the structure of the endocardium. The inflammatory process very actively passes from the valves to other tissues of the heart, which leads to massive thrombus formation.
Polyposis-ulcerative. This is one of the forms of sepsis, which is called protracted septic endocarditis. In rare cases, it can occur with other infections, such as brucellosis. In ulcerative endocarditis, the heart valves are the primary focus, and the pathogen, entering the bloodstream, quickly spreads to other organs. It is characterized by destructive thrombotic changes against the background of valve sclerosis.

How is it diagnosed?

Important components in the diagnosis of endocarditis, in addition to clinical symptoms, are laboratory tests:

General analysis blood. Allows you to see the shift of the leukoformula to the left and a decrease in leukocytes, a decrease in the level of hemoglobin, an acceleration in the level of the reaction of mastering erythrocytes.
Blood chemistry. It will show an increase in the globulin fraction of plasma proteins, C-reactive protein and changes in rheumatoid factor.

Often, if infective endocarditis is suspected, blood is sown for sterility for diagnostic purposes. For the accuracy of the results, 2-3 crops are carried out.

General urine analysis. In it, protein and leukocytes will be increased.
ECG (electrocardiogram). The study makes it possible in the early stages to see signs of left ventricular hypertrophy, ventricular or atrial extrasystole, cardiac arrhythmias. Atrial fibrillation can also be seen on an ECG study, but this is less common.
Echo-KG (echocardiography). It is prescribed for suspected infective endocarditis. The examination allows you to see heart defects and changes in the state of the valvular apparatus, to identify calcification and rupture of the valve leaflet. Echocardiography is used to determine surgery.

When diagnosing and further treatment consultation with a cardiologist is mandatory.

Treatment measures

Treatment can be carried out in the cardiovascular, rheumatological or infectious department and depends on the type of endocarditis. It can be of two types:

conservative

It involves the use of drugs to eliminate the cause of the disease and its symptoms. In most cases, drug therapy is enough for a complete recovery, but bed rest and diet are often also prescribed.

The main thing in the treatment will be antibiotic therapy and preferably a broad spectrum of action:

Antibiotics are used to treat acute infective endocarditis to kill the pathogen. Treatment with antimicrobial drugs is prescribed as soon as the patient arrives and donates blood to the bacterial culture. After determining the pathogen, drugs are prescribed to eliminate them:
green streptococcus - Benzylpenicillin, Ceftriaxone, Ampicillin, Gentamicin, Amoxicillin (clavulanic acid);
Staphylococcus aureus - Oxacillin, Cefazolin, Imipenem, Vancomycin, Linezolid;
enterococci - Benzylpenicillin, Ampicillin, Gentamicin;
pneumococcus - Linezolid, Cefotaxime, Levofloxacin;
pathogens from the HACEK group - Ampicillin, Ceftriaxone, Gentamicin;
Pseudomonas aeruginosa - Ceftazidime;
fungal infections - Amikacin, Meropenem, Amphotericin B, Flucytosine.

To normalize the work of the heart of a patient with chronic endocarditis, beta-blockers, diuretics, cardiac gliclazides, and antagonists are prescribed.
For the treatment of non-infectious endocarditis, Heparin sodium or Warfarin is often prescribed, but the main and main thing is to reduce the load on the heart. The final choice of treatment is determined by the cardiologist.

After the course of treatment, all clinical manifestations of the disease disappear, and urine and blood tests show normal results.

Surgical

The main goal of the surgeon is to prevent dangerous complications. At surgical treatment defects that have arisen with endocarditis are eliminated.

Surgery carried out only strictly according to the following indications:

accumulation of a purulent component in the region of the endocardium;
bacterial endocarditis;
increasing heart failure, not treated with medication.

During surgical treatment, the valve apparatus is replaced with an artificial one.

Prevention of endocarditis

aim preventive measures is to prevent damage to the heart infectious diseases, tonsillitis, surgical interventions. It is aimed at improving activities, which boil down to compliance with doctor's prescriptions. In this case, you must remember the following rules:

limit physical stress on the heart;
avoid stress;
observe therapeutic diet- table 10 and 10a, which requires limiting the use of salt, spicy and fried foods, alcoholic beverages, but it is recommended to use low-fat broths, soups, hard pasta, vegetables in any form, boiled lean meat or fish.

Endocarditis is complex and serious illness of cardio-vascular system. It is important to recognize it in time, for which you need to contact medical institution where all the necessary diagnostic studies and prescribe treatment taking into account the individuality of the patient and the characteristics of his immune system.

Endocarditis is an inflammation that occurs in the inner lining of the heart, the endocardium. The disease does not always proceed with obvious signs: it is characterized by a slight malaise, an increase in temperature to low numbers, less often - discomfort in the heart. At the same time, it is characterized by an unpredictable course: at any time, inflammation of the endocardium can cause thromboembolism of the arteries of vital organs, acute heart failure, dangerous arrhythmias, and damage to internal organs. In addition, the disease can recur.

Usually, endocarditis occurs as a complication of inflammation of the tonsils, kidneys, lungs, myocardium and other diseases, so it is rarely diagnosed. But there is also an independent pathology - infective endocarditis. It develops when microorganisms enter the endocardium.

Most often it is bacteria, so the disease used to be called "bacterial endocarditis". Now that fungi have become more common in blood cultures, this name for the disease is considered obsolete. Infective endocarditis is also called septic endocarditis, because here, as in sepsis, microorganisms are found in the blood, which should normally be sterile.

What is the endocardium and why is its inflammation dangerous?

The endocardium that becomes inflamed in endocarditis is several layers of cells:

The endocardium lines the walls of the heart from the inside, forms folds - the valve flaps, as well as the tendon chords attached to them and the papillary muscles pulling the chords. It is this shell of the heart that is the separator between blood and internal structure hearts. Therefore, in the absence of inflammation, it is designed so that there is no significant friction of blood against the heart walls, and there is no deposition of blood clots here. This is achieved by the fact that the surface of the endothelium is covered with a layer of glycocalyx, which has special, athrombogenic properties.

The endocardium of the heart valves from the side of the atria is denser. This is provided large quantity collagen fibers in the muscular-elastic layer of the membrane. From the side of the ventricles, the muscular-elastic layer is 4-6 times thinner, contains almost no muscle fibers. The valves between the cavities of the heart and the vessels (pulmonary trunk, aorta) are thinner than the atrioventricular valves. The endocardium covering them is thicker at the base of the valve, but the valves themselves no longer show any layering. There are very few muscle fibers on the valves that close the entrance to the vessels.

The nutrition of the deepest endocardium bordering on the myocardium comes from the vessels that make up its structure. The remaining departments receive oxygen and the necessary substances directly from the blood, which is located in the heart cavities.

Directly below the endocardium is the heart muscle - the myocardium. It is responsible not only for contractions of the heart, but also for right rhythm these contractions: in the myocardium there are “paths” of cells, some of which produce, while others transmit further electrical impulses, obliging the necessary parts of the heart to contract.

When it enters the blood enough microbes (bacteria or fungi), they naturally end up inside the cavities of the heart. If a person's immunity is sufficiently weakened, then microorganisms settle on the endocardium (especially on the valves between the left atrium and the ventricle, as well as at the entrance from the left ventricle to the aorta) and cause inflammation there. The inflamed endocardium grows, thrombotic masses are deposited on it. This form of the disease is called "warty endocarditis" and is more characteristic of a rheumatic process.

Thrombotic masses can break off at any time and enter the arteries that feed the internal organs with the blood flow. So a stroke, a heart attack of the spleen, intestines, lungs and other organs can develop.

Due to the increase in the mass of the valve by blood clots and scar tissue, it ceases to perform its function normally - to prevent the reverse flow of blood. Because of this, a condition called "chronic heart failure" develops.

Microorganisms that have settled on the valves, chordae, or surface of the papillary muscles can cause endothelial ulcers (ulcerative endocarditis). If this leads to the development of a “hole” in the valve or a detachment of the chord, the heart “loses control” over its own processes. This is how acute heart failure develops, proceeding according to one of the scenarios: either pulmonary edema, shortness of breath and a feeling of lack of air, or a sharp decrease in pressure, increased heart rate, a panic state with possible loss consciousness.

The presence of bacteria or fungi in the blood causes the activation of immunity, as a result of which antibodies are formed to these microorganisms, the complement system (several immune proteins) is activated. Antigens of microbes combine with antibodies and complement proteins, but are not destroyed (as it should be in the norm), but are deposited around the vessels of many organs: kidneys, myocardium, joints, individual vessels. This causes inflammatory-allergic reactions, resulting in glomerulonephritis, arthritis, myocarditis or vasculitis.

Statistics

In 2001, the incidence of infective endocarditis was reported as 38 cases per 100,000 population. Now it is indicated that the incidence of this disease is less - 6-15 per 100 thousand people. At the same time, mortality remains high - 15-45% (on average - 30%), especially in the elderly.

Endocarditis often affects people of working age - 20-50 years old, as well as children. The incidence of men and women is the same.

Causes of endocarditis and its classification

Depending on the initial state of the inner heart membrane, infective endocarditis of the heart is primary and secondary. Both of them are caused by such microorganisms:

bacteria: green (is the main cause of subacute endocarditis) and pneumonic streptococci, Staphylococcus aureus and enterococcus (cause an acute inflammatory process), coli, mycobacterium tuberculosis, pale treponema (with syphilis), brucella, some gram-negative and anaerobic bacteria;
mushrooms, usually Candida. Such a microflora usually appears when a person has been treated with antibiotics for a long time, or he has had a venous catheter for a long time (in the treatment of any diseases);
some viruses;
some simple ones.

Only primary endocarditis is one that occurs on normal, healthy valves, and secondary - on valves affected by rheumatism or prolapse, on artificial valves and those near which there is a pacemaker. Recently, the incidence of primary endocarditis has begun to increase. It reached 41-55%.

Microorganisms enter the human blood in the following ways:

through a wound of the skin or mucous membranes, when it was contaminated with microbes in a person with reduced immunity or with an installed artificial valve or pacemaker;
when performing various invasive methods of examination and treatment: catheterization of peripheral veins for the introduction of contrast into them (for performing angiographic studies), endoscopic and open interventions, abortions, cystoscopy and even extraction (pulling out) of teeth when a foreign surface comes into contact with blood;
from any source of bacterial or fungal inflammation (for example, from the lungs with pneumonia, abscess of the tonsils, gangrene of the extremities) - subject to reduced immunity, especially if it is combined with valvular pathology;
with any infection (microorganisms always enter the bloodstream and pass through the heart): respiratory tract, maxillary sinuses, kidneys, joints, intestines, and so on, if a person has an artificial valve or pacemaker;
when using injection drugs (in this case, the endocardium of the right heart is most often affected), when sterility is not observed;
during the installation of prostheses or implants, especially when it comes to installing artificial heart valves or a pacemaker;
during any heart surgery.

It is more likely that the microbe will “stick” to the endocardium and cause an inflammatory process in it in the elderly, drug addicts, people with immunodeficiencies, including those who have immunodeficiencies due to cancer treatment. More susceptible to the development of endocarditis and people who constantly take alcohol.

There are also local factors contributing to the development of this disease. These are heart defects - congenital and acquired (especially defects of the interventricular septum and coarctation of the aorta), artificial valves. There is evidence that in the presence of valvular pathology, any entry of a certain amount of bacteria into the blood (even with a tooth root cyst or tonsillitis) in 90% of cases can cause infective endocarditis.

If everything is in order with the heart valves, then when bacteria enter the blood, it is more likely that endocarditis will develop in older people with arterial hypertension, coronary artery disease, cardiomyopathies, Marfan's syndrome. A higher risk of developing endocarditis is in a person who has already had this disease once, even if it did not leave visible, ultrasound-detectable traces on the inner lining of the heart.

If the disease occurs when the causative agent of the disease is found in the blood and there is already damage to the internal organs, this is - septic endocarditis, which is also called infectious and bacterial. When it occurs as a complication of streptococcal lacunar or follicular inflammation of the tonsils, or streptococcal glomerulonephritis, it is called rheumatic endocarditis. There is also tuberculous, syphilitic, traumatic and post-infarction inflammation of the myocardium.

Depending on the course, any endocarditis can be:

acute: lasts about 2 months;
subacute, which lasts 2-4 months, is usually a consequence of an undertreated acute process;
chronic (protracted), "stretching" for more than 4 months. This is a rare type of infective endocarditis, but a fairly common type of disease of rheumatic origin.

According to the defeat of the valves, allocate:

mitral valve endocarditis;
inflammation of the aortic valve;
tricuspid valve endocarditis;
inflammation of the pulmonary valve.

The last 2 valves, located in the right side of the heart, are most often inflamed in injection drug addicts.

The activity of the process may also appear in the diagnosis. Endocarditis will be considered active if a person has a fever in combination with the release of microorganisms during a blood culture or bacteriological examination valves (if heart surgery was performed). If the first episode of endocarditis has ended, and no symptoms have been observed for a year or more, then the re-development of inflammation of the endocardium, with the release of another pathogen from the blood or valves, will be called "recurrent endocarditis". If, despite treatment, symptoms of the disease are present for 2 months or more, and the same microbe is sown from the blood, this is called persistent endocarditis.

If endocarditis has developed after heart surgery, it is divided into:

early: occurs in the first year after the intervention. Means that the infection occurred nosocomial;
late: developed when a year had passed after the operation. Caused by community microflora.

The choice of antibiotic therapy and the prognosis depend on the latter classification. So, if infection occurred with nosocomial microflora, in the first 72 hours of being in a hospital, mortality can reach 40-56%.

Endocarditis in children has an additional classification. It is divided into:

congenital, which is formed even in the prenatal period when the fetus is infected;
acquired, which arose after childbirth: either due to the same reasons as in adults, or when infected during childbirth or immediately after them.

In children older than 2 years, most cases of endocarditis develop on the background of congenital or acquired heart disease.

Symptoms

Signs and symptoms of endocarditis depend on its type (infectious, rheumatic, syphilitic, tuberculous) and are dictated by the course of the disease. So, if acute endocarditis has developed, then the symptoms will be as follows:

high body temperature (up to 39.5 ° C);
during the rise, the temperature of a person beats a strong chill;
profuse sweating;
pain in all joints and muscles;
lethargy;
headache;
the skin becomes grayish with a slight yellowness, sometimes red spots appear on it;
reddish painful nodules appear on the fingers;
hemorrhages in a conjunctiva are noted.

Subacute infective endocarditis occurs with the following symptoms:

elevated body temperature - up to 38.5 ° C;
chills;
worsening sleep;
weight loss;
skin color becomes "coffee with milk";
red rash on the body;
small painful nodules appear under the skin,

but the main difference from the acute process is that this symptomatology is observed for 2 months or more.

The chronic process is characterized by the same symptoms (only the temperature is usually up to 38 ° C) for six months or more. During this time, a person loses a lot of weight, his fingers take on the appearance of drumsticks (expanded in the area of \u200b\u200bthe nail phalanges), and the nails themselves grow dull and become convex (reminiscent of watch glasses). Hemorrhages may appear under the nails, and painful reddish nodules the size of a pea are sure to be found on the fingers and toes, palms and soles.

When a heart defect is formed, shortness of breath appears: first during exercise, then at rest, pain behind the sternum, the heart beats more often (up to 110 beats per minute or more) regardless of temperature.

If glomerulonephritis or kidney infarction develops, edema appears on the face, urination is disturbed (usually there is less urine), urine changes color to reddish, pain in the lower back appears.

If, against the background of the main symptoms, severe pain develops in the left hypochondrium, this indicates that one of the branches of the arteries that feed the spleen is clogged, and part or all of this organ dies.

With the development of pulmonary embolism, there is a sharp feeling of lack of air, pain behind the sternum. Against this background, a violation of consciousness is rapidly growing, and the skin (especially on the face) acquires a purple hue.

Symptoms of infective endocarditis develop in three stages:

Infectious-toxic: bacteria enter the bloodstream, "land" on the valves, begin to multiply there, forming growths - vegetation.
Infectious-allergic: due to the activation of immunity, internal organs are affected: myocardium, liver, spleen, kidneys.
Dystrophic. At this stage, complications develop both from the internal organs and from the myocardium (areas of the heart muscle die off in 92% of cases of prolonged inflammation of the endocardium).

Infective endocarditis in children develops as an acute process and is very similar to SARS. The difference is that with ARVI, the complexion should not change to yellowish, and pain in the heart should not be noted.

If endocarditis is rheumatic, then it usually develops after a sore throat, glomerulonephritis, in which beta-hemolytic streptococcus was isolated (in the first case, from the surface of the tonsils, in the second, from the urine). After the disease has subsided, after a while the person notes weakness, fatigue, and malaise. Again (after a sore throat or inflammation of the kidneys), the temperature usually rises to 38 ° C, but may be higher. There are also unpleasant sensations in the region of the heart. Against this background, other signs of rheumatism may also be noted: a temporary increase and soreness of large joints, passing by itself.

Complications

One of the most formidable complications of endocarditis is embolism - a detachment of a section of an overgrown valve, a thrombus or a thrombus with a section of the valve with a further "journey" of this particle through the arteries. The embolus (or thromboembolus) will stop where it will exactly match the diameter of the artery.

If the detachment of the particle occurred in the left parts of the heart, then embolization of the vessels of a large circle develops - one of the internal organs may suffer: intestines, spleen, kidneys. They develop a heart attack (that is, the death of the site).

If a thrombus or unstable (poorly fixed) vegetation is located in the right sections, the embolus blocks the vessels of the small circle, that is, the pulmonary artery, resulting in a lung infarction.

Also, due to endocarditis, the following complications can be observed:

Acute heart failure.
Formation of heart disease.
Myocarditis.
Pericarditis.
Chronic heart failure.
Kidney damage: glomerulonephritis, nephrotic syndrome, renal failure.
Spleen lesions: abscess, enlargement, rupture.
Complications from the nervous system: stroke, meningitis, meningoencephalitis, brain abscess.
Vascular lesions: inflammation, aneurysms, thrombophlebitis.

Diagnostics

Diagnosis of endocarditis is based on data:

listening to the heart: first, systolic murmur is determined, then diastolic;
determining the boundaries of the heart: they expand to the left (if the valves in the left parts of the heart are damaged) or to the right (if vegetations are found in the right parts);
ECG: if there is irritation by the inflamed endocardium of the myocardial pathways, the cardiogram determines the rhythm disturbance;
Ultrasound of the heart (echocardioscopy): this is how vegetations (growths) on the valves, and thickening of the endocardium and myocardium are determined. By ultrasound with dopplerography, one can judge the function of the heart and indirectly - the pressure in the small circle;
bacteriological examination of blood (sowing it on various nutrient media);
blood tests by PCR method: this is how some viruses and bacteria are determined;
rheumatic tests: in order to distinguish infective endocarditis from rheumatic;
If necessary, magnetic resonance or CT scan chest with a targeted study of the heart.

An accurate diagnosis of infective endocarditis is made when there is a specific ultrasound picture of the heart, and in addition, the pathogen is determined in the blood. If all the symptoms point to this disease, a microbe is detected in the blood, but there are no significant changes on echocardioscopy, the diagnosis is “questionable”.

When the pathogen is not detected in the blood, but the ultrasound picture is beyond doubt, the diagnosis is written that infective endocarditis is either “culture-negative” (that is, bacteriological culture did not reveal anything), or “PCR-negative” (if PCR was not isolated pathogen).

Treatment

Since the disease in question is characterized by unpredictability and unexpected development of complications, treatment of endocarditis should be carried out only in a hospital. It includes the required intravenous administration antibiotics according to the scheme applied according to the latest orders of the Ministry of Health. Usually these are broad-spectrum antibiotics with a special focus on streptococcus viridans and Staphylococcus aureus ("Vancomycin", "Zyvox"); often a combination of 2-3 drugs is used.

Prior to the start of treatment with antibiotics from a peripheral vein, a three-fold blood sampling for sterility is performed. Based on its results (they are received on about 5 days), a change in the antibacterial drug can be made.

The course of antibiotics is from 4 to 12 weeks. Their cancellation is carried out only after the normalization of temperature, laboratory parameters and after they receive a negative bacteriological culture three times against the background of a trial withdrawal of antibacterial drugs.

In addition to antibiotics are prescribed:

blood thinners (heparin);
glucocorticoids;
antifungal agents;
inhibitors of proteolytic enzymes;
antistaphylococcal plasma or immunoglobulin;
drugs needed to treat a particular complication of endocarditis;

If a drug treatment within 3-4 weeks is ineffective, then in order to remove the foci of infection inside the heart and avoid the progression of heart failure and the development of thromboembolism, an operation is performed. The intervention involves the removal of the affected valves with the subsequent installation of their prostheses.

Surgical intervention can also be applied urgently (within a day after the diagnosis). It can save a life if developed:

acute heart failure,
valve walls torn off
valve perforation has occurred
fistulas, abscesses, or valve pseudoaneurysms have developed,
during the first week of therapy, mobile growths appeared on the valves more than 10 mm in diameter,

but the risk from such an operation is also extremely high.

After the operation, a person receives antibiotics for 7-15 days. He is in the hospital, on bed rest.

After endocarditis, the motor mode expands, but physical exercise remain banned. Diet - table number 10 with the restriction of salt, liquids, the complete exclusion of alcohol, cocoa, chocolate, coffee, as well as spicy, fatty and smoked foods.

Forecast

Infective endocarditis is a disease whose prognosis is conditionally unfavorable. In people without immune deficiency, malformations and diseases of the heart and its valves, it is more favorable, especially under the condition of early diagnosis of the disease and the urgent start of powerful antibiotic therapy. If a person has endocarditis, chronic heart disease or a suppressed immune system, life-threatening complications can develop.

The prognosis also worsens if:

symptoms of the disease began to appear after admission to the hospital (where either invasive diagnostics or operations were performed, including those on the heart) - within the first 72 hours;
if gram-negative flora, Staphylococcus aureus, Cochiella or Brucella insensitive to antibiotics, fungal flora are sown from the blood (from the valves).

With infective endocarditis involving the right heart, a better outcome can be expected.

Rheumatic endocarditis is more favorable for life: acute heart failure and thromboembolism are less typical for it. But heart disease in this pathology develops in the vast majority of cases.

Prevention

Prevention of endocarditis is as follows:

it is necessary to adhere to sufficient physical activity and follow the rules of a healthy diet in order to be examined and treated with invasive methods as little as possible;
it is important to sanitize the foci of infection in a timely manner: treat diseased teeth, wash the lacunae of the tonsils when chronic tonsillitis, ensure the outflow of contents from the sinuses - with chronic sinusitis;
if you still have to be treated, you need to do it not at home or in dubious offices, but in specialized clinics;
if work or life involves frequent trauma, care must be taken to maintain sufficient immunity. To do this, it is important to eat right, move enough, maintain the hygiene of your skin and external mucous membranes;
in the event of an injury, correct antiseptic treatment wounds and, if necessary, a visit to the doctor;
if, due to heart disease, a heart operation was needed, the installation of an artificial valve or a pacemaker, after which blood thinners were prescribed, they cannot be arbitrarily canceled;
if the doctor prescribes antibiotics for any reason, you need to take them for as many days as prescribed. From the 5th day of taking antibiotic therapy, you need to ask the doctor about the need to prescribe antifungal drugs;
antibiotic prophylaxis is important before starting any invasive treatment. So, if the operation is planned, it is better to start administering drugs 12-24 hours before it (especially if the intervention will be carried out on the organs of the oral cavity or intestines). If you had to resort to emergency operation antibiotics should be administered as soon as possible after admission to the hospital.