Subacute bacterial endocarditis symptoms. A dangerous consequence of blood poisoning is septic endocarditis. Is there a chance of salvation? Treatment of infective endocarditis

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Acute and subacute infective endocarditis (I33.0)

Cardiology

general information

Short description

Infective endocarditis(IE) is an infectious polyposis-ulcerative inflammation of the endocardium Endocardium - the inner lining of the heart, lining its cavities and forming the valve leaflets
, accompanied by the formation of vegetation Vegetations are a secondary morphological element of rashes in the form of uneven papillomatous growths of the epidermis and papillary layer of the dermis
on valves or subvalvular structures, their destruction, dysfunction and the formation of valve insufficiency.

Secondary IE occurs most often. In this form, pathogenic microorganisms affect previously changed valves and subvalvular structures, including in patients with rheumatic heart disease, degenerative changes in the valves, prolapse Prolapse is a downward displacement of any organ or tissue from its normal position; The cause of such displacement is usually weakening of the tissues surrounding and supporting it.
mitral valve, artificial valves.

Primary IE characterized by the development of infectious lesions of the endocardium against the background of unchanged valves.

The mitral and aortic valves are most often affected, less commonly the tricuspid and pulmonary valves. Damage to the endocardium of the right heart is most common among injection drug addicts.

Acute (septic) IE is an inflammatory lesion of the endocardium lasting up to 2 months, caused by highly virulent microorganisms, occurring with pronounced infectious-toxic (septic) manifestations, frequent formation of purulent metastases in various organs and tissues, mainly without immune manifestations, which do not have time to develop due to transience diseases.

Subacute IE- a special form of sepsis Sepsis is a pathological condition caused by the continuous or periodic entry of microorganisms into the blood from a focus of purulent inflammation, characterized by a discrepancy between severe general disorders and local changes and often the formation of new foci of purulent inflammation in various organs and tissues.
lasting more than 2 months, due to the presence of an intracardiac infectious focus, which causes recurrent septicemia, embolism, increasing changes in the immune system, leading to the development of nephritis Nephritis - inflammation of the kidney
, vasculitis Vasculitis (syn. angiitis) - inflammation of the walls of blood vessels
, synovitis Synovitis is an inflammation of the synovial membrane (the inner layer of the joint capsule or osteofibrous canal) that does not spread to the rest of the tissues and elements of the joint.
, polyserositis Polyserositis is inflammation of the serous membranes of several body cavities (pleura, peritoneum, pericardium, and sometimes joints); more common in large collagenoses and tuberculosis
.

Classification

Modern classification proposed by the European Society of Cardiology

Depending on the location of the infection and the presence/absence of intracardiac material:

1. Left-sided IE of the native valve.

2. Left-sided IE of the prosthetic valve (EPV):
- early EPC (< 1 года после операции на клапане);
- late EPC (> 1 year after valve surgery).

3. Right-sided IE.

4. Associated with an IE device (permanent pacemaker or cardioverter-defibrillator).

Depending on the method of infection:

1. IE associated with medical care:
- nosocomial - signs/symptoms of IE appear more than 48 hours after hospitalization;

Non-nosocomial - manifestations of IE occurred less than 48 hours after hospitalization of the patient receiving medical care (living in a nursing home or long-term care, receiving intensive care within 90 days before the onset of IE, home health nursing or intravenous therapy, hemodialysis, intravenous chemotherapy for 30 days before the onset of IE).
2. Community-acquired IE - manifestations of IE occurred less than 48 hours after hospitalization of a patient who did not meet the criteria for nosocomial IE.
3. IE associated with intravenous drug use.

Active IE(process activity criteria):

IE with prolonged fever and positive blood culture or
- active inflammatory morphology detected at surgery or
- a patient receiving antibiotic therapy or
- histopathological data of active IE.

Returnable:
- relapse (repeated episodes of IE caused by the same microorganism< 6 месяцев после начального эпизода);
- reinfection (infection with different microorganisms or a repeated episode of IE caused by the same microorganism > 6 months after the initial episode).

Previously, acute and subacute forms of IE were distinguished. Now it is not recommended to use such terminology, since with the early prescription of antibacterial therapy, the differences in the course of acute and subacute IE are often blurred.

In practice, the following is most often used IE classification:

Clinical and morphological form:
- primary infective endocarditis - occurring on intact heart valves;
- secondary infective endocarditis - arising against the background of existing pathology of the heart valves as a result of previous rheumatic, atherosclerotic lesions or previous infective endocarditis.

By etiological factor:
- streptococcal;
- staphylococcal;
- enterococcal, etc.

According to the course of the disease:
- acute IE - duration less than 2 months;
- subacute IE - duration more than 2 months;
- prolonged IE - is used extremely rarely in the meaning of a mildly manifested subacute course of IE.

Special forms of IE:
- nosocomial IE;
- IE of the prosthetic valve;
- IE in persons with implanted intracardiac devices: pacemaker and cardioverter-difibrillator;
- IE in persons with transplanted organs;
- IE in drug addicts;
- IE in elderly and senile people.

Etiology and pathogenesis

Infective endocarditis (IE) is a multi-etiological disease. Currently, more than 128 microorganisms that cause the pathological process are known.

Frequent causative agents of IE:
- staphylococci;
- streptococci;
- gram-negative and anaerobic bacteria;
- mushrooms.
In the European Union, staphylococci are isolated from 31-37% of patients, gram-negative bacteria - from 30-35%, enterococci - from 18-22%, viridans streptococcus - from 17-20%.
It is not always possible to isolate the pathogen from the blood of patients with IE, and in many cases the true causative agent of the disease remains unknown. In 50-55% of cases in the acute period and in 80-85% of cases in the subacute period, blood cultures are sterile. This may be due to antibacterial therapy preceding blood sampling, imperfect bacteriological equipment for culture, the presence in the blood of bacteria that require the use of special media (anaerobes, satellites and strains of streptococcus with altered properties - thiol- or vitamin B6-dependent, L-form bacteria , Brucella). Special methods are required to isolate viruses, rickettsia, chlamydia, and fungi.

All variants of IE are accompanied by the formation of vegetations, which are most often located on the valve leaflets and less often on the endocardium of the ventricles or left atrium, as well as on the pulmonary or other arteries.
In primary endocarditis, the valve leaflets are often thin, and the free edge of the valves is often thickened due to hemodynamic disturbances or inflammatory infiltration. Loose red-gray vegetations are located along the free edge of the valves, the inner lining of the ascending aorta.

In secondary endocarditis, when the infectious process affects an already altered valve, fresh vegetations are located on fibrously changed or calcified valves, and chordae may be torn off.

There are three phases in the pathogenesis of IE:
- infectious-toxic;
- immunoinflammatory (immune generalization process);
- dystrophic (with dystrophic changes in internal organs).

In IE, the pathogen localizes and multiplies on the heart valves, entering there from the bloodstream during transient or permanent bacteremia. Transient bacteremia often occurs during various infections and during traumatic procedures, including invasive examinations (bronchoscopy, gastroscopy, colonoscopy, etc.), surgical interventions (tonsillectomy, adenoidectomy, surgical manipulations in the oral cavity).
After trauma to oral tissues, virulent streptococci are most often detected in the blood. The “entry gate” of infection in most cases is the oral cavity; odontogenic infection enters the bloodstream after tooth extraction, removal of tooth roots and other manipulations in the oral cavity. Transient bacteremia usually does not lead to the deposition of bacteria on the endocardium of intact valves, however, under certain conditions, bacteria become fixed to the valvular and parietal endocardium.

Against the background of altered reactivity of the whole organism and the valve apparatus, under the influence of etiological factors, interstitial valvulitis occurs Valvulitis - inflammation of the tissues that form the heart valves; clinically detected only after the formation of a defect in the affected valve
, nonbacterial endocarditis. Further, when an infection occurs, an infectious lesion of the valves develops with bacteremia and thromboembolic complications.

Invasion of microorganisms and the occurrence of endocarditis occur predominantly in areas of high pressure gradient, valvular regurgitation and narrowing of intercavitary communications. In this regard, IE is more often observed with defects of the left side of the heart, since the blood pressure in them is 5 times higher than in the right side.

Epidemiology

Recently, there has been an increase in the incidence of primary infective endocarditis (IE) to 41-54% of all cases of the disease.
The annual incidence of IE is 38 cases per 100 thousand population. People aged 20 to 50 years are more likely to get sick. Men get sick 2 times more often than women.
Infection affects the aortic valve in 28-45%, the mitral valve in 5-36%, and both valves in 35% of cases. The aortic valve is most susceptible to intense hemodynamic influences and pressure changes, therefore, at the edges of the valves, in the area of ​​commissures Commissure (adhesion) - a fibrous cord formed between adjacent surfaces of organs as a result of injury or inflammatory process
, microtraumas occur (microbleeds, destruction of the endothelium).
In men, damage to the aortic valve predominates, in women - to the mitral valve.
Endocarditis of the right heart is less common (damage to the tricuspid valve - up to 6%, pulmonary valve - less than 1%), most often it is detected in injection drug addicts, as well as in patients after heart surgery and in cases of long-term use of vascular catheters.

Risk factors and groups

High risk group:
- persons with valve prostheses, including bioprostheses and homografts;
- persons who have had IE (including those who developed IE without previous heart disease);
- patients with complex congenital defects of the “blue” type (tetralogy of Fallot, transposition of great vessels, single ventricle of the heart, etc.);
- patients who have undergone shunt surgery between the systemic and pulmonary circulation (to eliminate hypoxia) for “blue” type defects.

Moderate risk group:
- other congenital heart defects (excluding atrial septal defect, in which the risk of IE is minimal);
- acquired defects of rheumatic and other nature (even after surgical treatment);
- hypertrophic cardiomyopathy;
- mitral valve prolapse with regurgitation.

Clinical picture

Symptoms, course

The main clinical manifestations of infective endocarditis (IE) are conventionally divided into:
- associated with the presence of septic inflammation with characteristic manifestations of an infectious-inflammatory and immunopathological process;
- caused by embolic complications - “transient” abscesses of various organs with a clinic characteristic of damage to a particular organ;

Heart attacks (as a consequence of vascular thrombosis) with development depending on the location of the lesion in the corresponding clinic;
- progressive heart damage with valvular insufficiency, rhythm and conduction disturbances and the development of heart failure.

It should be noted that IE does not always manifest itself with clinical symptoms of an infectious process, so the first complaints of patients may be due to thromboembolic complications with a characteristic clinical picture depending on the affected organ.

Common symptoms of IE:
- fever;
- chills;
- sweating;
- weakness and malaise;
- anorexia Anorexia is a syndrome consisting of a lack of appetite, a feeling of hunger, or a conscious refusal to eat.
, weight loss.

The most common symptom of IE is fever (from low-grade to hectic Hectic fever is a fever characterized by very large (3-5°) rises and rapid declines in body temperature, repeating 2-3 times a day
), which is observed in 85-90% of patients. Against the background of subfebrile body temperature, 1-2-week rises to 39-40 o C can be observed. In some cases, even with severe IE, fever may be absent, for example, with massive intracerebral or subarachnoid hemorrhages, with congestive heart failure, with severe renal failure , in elderly and senile people.

Specific complaints, depending on the location of the lesion, join the general ones in case of heart damage, the development of embolic or thromboembolic complications.

Skin in patients with IE they are pale and have a specific pale gray or yellowish earthy tint. Skin color depends on the severity of anemia, the presence and severity of infectious-toxic hepatitis, and renal failure.
Often rashes appear on the skin, which are quite heterogeneous and are a manifestation of hyperergic hemorrhagic vasculitis or thrombotic and embolic complications. Hemorrhagic rash is localized on the upper and lower extremities, face, mucous membranes and is more often symmetrical in nature.
Petechial rashes up to 1-2 mm in diameter turn pale and disappear after 3-4 days. In case of infection, hemorrhagic rashes become necrotic in nature, followed by scarring.
Patients experience hemorrhagic rashes under the nails (reddish-brown hemorrhages in the form of stripes).
In severe cases of IE, red-purple spots or bruises up to 5 mm in diameter often appear on the palms and soles ( Janeway spots).
If the process is not limited to small vessel vasculitis and perivascular cellular infiltration is observed, characteristic painful reddish nodules up to 1.5 cm in size appear on the palms, fingers, soles and under the nails ( Osler's nodes). If the course of the disease is favorable, they disappear after a few days (sometimes hours); in complicated cases, suppuration is possible.

Quite often observed joint damage(up to 50% of cases). Patients have arthralgia Arthralgia is pain in one or more joints.
without significant enlargement and deformation of the joints. Due to periostitis Periostitis - inflammation of the periosteum (bone shell consisting of dense fibrous connective tissue)
, hemorrhages and embolisms of the vessels of the periosteum develop bone pain. In some cases, bone and joint pain may be the first and only complaint with IE.

Heart damage may be inflammatory in nature with the development of myocarditis and pericarditis (rhythm and conduction disturbances, heart failure). However, in the majority of cases, the main symptom of IE is valve damage:
- aortic valve with the development of its insufficiency - 62-66%;
- mitral - 14-49%;
- tricuspid - 1-5% (in 46% of cases observed in drug addicts who use injection forms of drug administration);
- simultaneous involvement of several valves in the process (combined damage to the aortic and mitral valves is observed in 13% of cases).

Aortic valve damage
High pulse pressure (a significant difference between systolic and diastolic pressure is achieved due to a decrease in diastolic pressure) is the first clinical symptom that allows one to suspect the development of aortic valve insufficiency.
The auscultatory picture is characterized by a diastolic murmur that appears at the beginning of diastole.
Often, damage to the aortic valve is complicated by an aortic root abscess, which is accompanied by impaired AV conduction, signs of pericarditis, and myocardial ischemia (compression of the coronary artery). Myocardial ischemia in IE is quite common and is caused not only by compression of the coronary arteries, but also by coronaritis Coronaritis - inflammation of the coronary arteries of the heart
, decreased blood flow as a result of aortic valve insufficiency or thromboembolic complications. It is possible to develop acute heart failure as a result of insufficiency of coronary blood flow, incompetence of the valve apparatus or fistulization of an abscess.

Specific signs of IE may be absent with the development of parietal endocarditis, which is more often observed in elderly and senile patients, as well as against the background of severe concomitant disease (tumors with metastases and severe intoxication, cerebrovascular accidents, uremia Uremia is a pathological condition caused by retention of nitrogenous wastes in the blood, acidosis and disturbances of electrolyte, water and osmotic balance in renal failure; usually manifested by weakness, apathy, stupor, hypothermia, arterial hypertension
and etc.). In such cases, the diagnosis of IE is often an echocardiographic finding.

Lung damage with IE, as a rule, occurs with damage to the valvular apparatus of the right parts of the heart and is caused by the development of repeated infarction-pneumonia, pulmonary infarction (clinically manifested by pleurisy Pleurisy - inflammation of the pleura (the serous membrane that covers the lungs and lines the walls of the chest cavity)
, hemoptysis, development of pulmonary edema). For IE, the multilocus nature of inflammatory foci in the lungs with varying degrees of resolution is quite specific.

Kidney damage observed in almost all patients with IE. The lesions are of a different nature, the most common are focal and diffuse nephritis, which can lead to amyloidosis Amyloidosis is a disorder of protein metabolism, accompanied by the formation and deposition in tissues of a specific protein-polysaccharide complex - amyloid. Leads to parenchymal atrophy, sclerosis and functional organ failure
kidney Diffuse nephritis has a severe course, usually with the development of renal failure, which largely determines the prognosis of the disease. Complications in the form of renal artery thromboembolism with subsequent infarction or kidney abscess also contribute to the development of renal failure.

Spleen damage occurs in 40-50% of patients with IE. The most common types of damage to the spleen: septic mesenchymal splenitis, the development of an abscess or infarction of the spleen with subsequent fibrosis. For embolism Embolism - blockage of a blood vessel by an embolus (a substrate circulating in the blood that is not found under normal conditions)
arteries of the spleen (4.3% of cases) patients experience pain in the left hypochondrium; an objective examination reveals a peritoneal friction noise in the area of ​​the projection of the spleen and the presence of transudate Transudate is a protein-poor liquid that accumulates in tissue crevices and body cavities during edema.
in the left pleural sinus. In case of splenic abscess (0.9% of cases), persistent fever is typical against the background of adequate antibiotic therapy.

Liver lesions with IE they are characterized by the development of hepatitis, infarction or liver abscess with corresponding clinical manifestations. Possible hepatomegaly Hepatomegaly is a significant enlargement of the liver.
caused by heart failure.

Eye damage with IE it occurs only in 2-3% of cases. May be very severe and lead to partial or complete blindness due to occlusion Occlusion is a violation of the patency of some hollow formations in the body (blood and lymphatic vessels, subarachnoid spaces and cisterns), caused by persistent closure of their lumen in any area.
retinal arteries, edema and optic neuritis. Symptoms characteristic of IE are described:
- Lukin-Libman sign- petechiae Petechia is a spot on the skin or mucous membrane with a diameter of 1-2 mm caused by capillary hemorrhage
with a white center on the transitional fold of the conjunctiva of the lower eyelid;
- Roth spots- white round spots 1-2 mm in size on the fundus (the result of retinal infarctions).

Damage to the central nervous system may develop as a result of infectious-toxic damage (encephalitis or meningitis, immune vasculitis) or complications of IE (heart attacks, hematomas, brain abscesses). The development of infectious psychoses with psychomotor agitation, hallucinations and delusions is possible.

Diagnostics

Diagnostic criteria for infective endocarditis(modified by J.Li, approved by the American Heart Association at Duke University in 2005)

Definite infective endocarditis(IE)

Pathomorphological signs:
- microorganisms identified during bacteriological or histological examination of vegetations, emboli or samples from intracardiac abscesses, or
- pathological changes: vegetations or intracardiac abscesses, confirmed by histological examination, revealing active endocarditis.

For diagnosis, it is sufficient to identify one of the above criteria.

Clinical criteria:

Two big criteria;

One major and three minor criteria;

Five small criteria.

Possible IE:

One big and one small criterion;

Three small criteria.

Excluded IE:

A definite alternative diagnosis that explains the symptoms of the disease, or

Disappearance of symptoms of infective endocarditis during antibiotic treatment in less than 4 days, or

No pathological evidence of infective endocarditis at surgery or autopsy with less than 4 days of antibiotic therapy, or

Insufficient criteria for probable infective endocarditis listed above.

Clinical criteria for IE

Large criteria

1. Positive blood culture: pathogens typical for IE isolated from two separately taken blood samples (viridans streptococci, Streptococcus bovis or NASEK group: Haemophilus spp., Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella spp., Kingella kingae, or Staphylococcus aureus, or community-acquired enterococci) in the absence of a primary focus, or pathogens consistent with IE isolated from a blood culture under the following conditions: at least two positive results from blood samples taken at least 12 hours apart, or three positive results out of three, or a majority of positive results from four or more blood samples (the interval between taking the first and last sample must be at least 1 hour), or a single detection of Coxiella burnetii or an IgG titer to this microorganism >1:800.

2. Evidence of endocardial damage: positive data from transthoracic echocardiography (transesophageal in the presence of prosthetic valves in patients with possible IE according to clinical criteria or when complications in the form of a perivalvular abscess are detected): fresh vegetation on the valve or its supporting structures, or implanted material, or abscess, or new dysfunction of the valve prosthesis, or newly formed valvular regurgitation (the increase or change in the existing cardiac murmur is not taken into account).

Small criteria

1. Predisposition: predisposing cardiac conditions or frequent intravenous injections (including drug and substance abuse).

2. Body temperature 38 °C or higher.

3. Vascular phenomena: emboli of large arteries, septic pulmonary infarctions, mycotic aneurysms Mycotic aneurysm (septic aneurysm) - an aneurysm that develops as a result of bacterial embolism of the arteries’ own vessels or thromboarteritis (thrombophlebitis) in septic diseases
, intracerebral hemorrhages, hemorrhages in the transitional fold of the conjunctiva and Janevier's lesions Janevier's spots are painless, erythematous small spots on the palms and soles
.

4. Immunological phenomena: glomerulonephritis, Osler’s nodes Osler's nodes are painful foci of compaction in the skin and subcutaneous tissue of a reddish color, up to 1.5 cm in size, representing inflammatory infiltrates caused by damage to small vessels
, Roth spots Roth spots are retinal hemorrhages with a white center measuring 1-2 mm in the fundus (the result of retinal infarctions)
and rheumatoid factor.

5. Microbiological data: a positive blood culture that does not meet the major criterion (excluding single positive cultures of coagulase-staphylococci, usually Staphylococcus epidermidis and microorganisms that are not the cause of IE), or serological confirmation of an active infection due to a potential causative agent of IE (Coxiella burnetii, Brucella, chlamydia, legionella).

Instrumental research methods

1. Electrocardiography. Changes in IE are nonspecific. If myocarditis occurs (diffuse or focal), it is possible to identify signs of AV block, smoothness or inversion of the T wave, and depression of the RS-T segment. Thromboembolism in the coronary arteries is accompanied by characteristic ECG signs of myocardial infarction (pathological Q wave, changes in the RS-T segment, etc.).

2.Echocardiography the valve apparatus in IE is of great practical importance, since in many cases it allows us to identify direct signs of the disease - vegetation on the valves if their size exceeds 2-3 mm. There are three types of vegetation: “sessile”, “pedunculated”, “filamentous”.

The main criteria for IE during echocardiography: microbial vegetations, severe regurgitation Regurgitation is the movement of the contents of a hollow organ in the direction opposite to the physiological one as a result of contraction of its muscles.
on the affected valves.
Additional signs: cardiac abscesses, septic damage to internal organs, chordal avulsion, perforation Perforation is the occurrence of a through defect in the wall of a hollow organ.
, rupture of valve leaflets, effusion into the pericardial cavity.

The main criteria for IE of a prosthetic valve during echocardiography are: microbial vegetation located on the artificial valve or paravalvular, cardiac abscess and signs of “separation” of the prosthesis.
Additional criteria: paraprosthetic fistula, severe regurgitation on paraprosthetic fistulas, prosthetic valve thrombosis, pericardial effusion, septic damage to internal organs.

If the result of transthoracic echocardiography is questionable or negative, as well as in the presence of clinical signs, transesophageal echocardiography should be performed, which, if the result is negative, is repeated after 2-7 days. A repeated negative result is a reason to exclude the diagnosis of IE.

3. Radiography. X-rays of the chest organs with damage to the right side of the heart reveal characteristic changes in the form of multiple infiltrative foci in the lungs resulting from embolic complications. The peculiarity of such infiltrates in IE is their varying degrees of resolution.

Laboratory diagnostics

Blood culture. To detect bacteremia, it is recommended to take separate samples of venous blood in an amount of 5-10 ml at least three times with an interval of 1 hour (regardless of body temperature). If the patient has received a short course of antibiotics, cultures should be done 3 days after stopping the antibiotics. With prolonged use of antibiotics, blood culture may be negative for 6-7 days or more. After identifying the pathogen, it is necessary to determine its sensitivity to antibiotics.

Methodology for microbiological blood testing

It is necessary to take 3 or more blood samples at intervals of 1 hour (regardless of body temperature). For each analysis, blood is taken in 2 containers: with aerobic and anaerobic nutrient media. In adults, blood is taken in an amount of 5-10 ml, and in children - 1-5 ml every Wednesday. Minimum inhibitory concentrations (MICs) must be determined for antibiotics of choice.

Serological techniques and PCR PCR - polymerase chain reaction
-research effective in diagnosing infective endocarditis caused by difficult-to-cultivate Bartonella, Legionella, Chlamydia, Coxiella burnetii and Tropheryma.

General blood analysis:
- normochromic normocytic anemia (with subacute IE);
- leukocytosis or moderate leukopenia, shift of the leukocyte formula to the left;
- thrombocytopenia (in 20% of cases);
- rise in ESR ESR - erythrocyte sedimentation rate (nonspecific laboratory blood indicator, reflecting the ratio of plasma protein fractions)
above 30 mm/h.

Blood chemistry:
- dysproteinemia with an increase in the level of γ-globulins;
- increase in C-reactive protein;
- creatinine (monitoring kidney function);

In 35-50% of patients with subacute IE, rheumatoid factor is detected in the blood serum.

General urine analysis:
- hematuria Hematuria is the presence of blood or red blood cells in the urine.
;
- proteinuria of varying severity;
- red blood cell casts in nephritic syndrome.

Differential diagnosis

In the early stages of infective endocarditis (IE), it must be differentiated from an extensive list of diseases and syndromes. The most important among them are:
- fever of unknown etiology;
- rheumatoid arthritis with systemic manifestations;
- acute rheumatic fever;
- systemic lupus erythematosus;
- polyarteritis nodosa;
- nonspecific aortoarteritis;
- antiphospholipid syndrome;
- infectious diseases occurring with fever, rash and splenomegaly (generalized form of salmonellosis, brucellosis);
- malignant neoplasms (non-Hodgkin's lymphoma, lymphogranulomatosis);
- sepsis.

Rheumatoid arthritis (RA) with systemic manifestations occupies an important place among connective tissue diseases with which it is necessary to carry out a differential diagnosis of IE.
Rheumatoid arthritis is characterized by the development of erosive-destructive lesions of the joints and rheumatoid endocarditis (50-60%).
Subacute IE is characterized by immune complex pathology, damage to the musculoskeletal system (23-60%), manifested by arthralgia, arthritis, tendinitis, enthesopathies, and discitis of the lumbar spine.
In most RA patients with aortic and mitral valve insufficiency, the disease has an asymptomatic and relatively favorable clinical course. In 40-50% of cases, the clinical course of RA is characterized by hectic fever, valve damage, cardiac rhythm and conduction disturbances.
Specific systemic manifestations of RA that are not found in IE: fibrosing alveolitis, lymphadenopathy, autoimmune thyroiditis, Raynaud's syndrome, rheumatoid nodes, Sjögren's syndrome.

Systemic lupus erythematosus(SLE) in its clinical and laboratory manifestations has significant similarities with IE, which makes differential diagnosis difficult. Fever, polyserositis, myocarditis, vasculitis, and glomerulonephritis occur with equal frequency.
With the formation (30-45%) of thrombotic non-infectious endocarditis, difficulties arise in interpreting the ultrasound picture of valve damage. However, with IE, destructive pneumonia often develops, and with SLE, vascular lesions of the lungs in the form of pneumonitis develop.
SLE is confirmed by the absence of pronounced valve destruction and regurgitation, the presence of a negative blood culture and the positive effect of the use of prednisolone and cytostatics.

Nonspecific aortoarteritis(Takayasu disease) occurs with the formation of aortic valve insufficiency caused by aortic dilatation. In this regard, certain difficulties may arise in the differential diagnosis of IE. Takayasu's disease is often characterized by transient paresthesia. Intermittent claudication in young women, vascular murmurs, asymmetry or absence of pulse (usually in the area of ​​the ulnar, radial and carotid arteries), and differences in blood pressure in the extremities are observed. To verify aortoarteritis, data from ultrasound scanning of blood vessels and contrast angiography are required.

Chronic pyelonephritis in the acute stage (especially in older people) has a characteristic clinical picture (fever with chills, anemia, accelerated ESR, sometimes bacteremia), similar to IE involving the kidneys. On the other hand, patients with pyelonephritis may develop IE caused by microflora, most often found in urinary tract infections (Escherichia coli, Proteus, enterococci).

Malignant neoplasms, especially in older people, is quite difficult to differentiate from IE. With tumors of the large intestine and pancreas, hypernephroma, high fever is often observed. In older people, a rough systolic murmur of mitral regurgitation, which is a consequence of chronic coronary heart disease, is often encountered. Also, a protodiastolic murmur of aortic regurgitation of atherosclerotic origin is often heard. In the presence of a tumor, such patients exhibit anemia and accelerated ESR. In such situations, it is necessary to exclude a tumor before settling on the diagnosis of IE. It should be borne in mind that in elderly and senile patients a combination of IE and tumor is possible.
Malignant neoplasms such as lymphomas and lymphogranulomatosis begin with hectic fever, chills, profuse sweating, and weight loss.
The clinical picture of non-Hodgkin's lymphoma is characterized by equally frequent lymphadenopathy of both all lymph nodes and their individual groups. The first symptoms are an increase in one (50%) or two (15%) groups of lymph nodes, generalized lymphadenopathy (12%), signs of intoxication (86-94%). Blood tests reveal: leukocytosis (8-11%) and/or leukopenia (12-20%), lymphocytosis (18-22%), increased ESR (13.5-32%).
The diagnosis is verified based on histological examination of lymph nodes.

Complications

Frequent complications of infective endocarditis:
- from the heart: myocarditis, pericarditis, abscesses, rhythm and conduction disturbances;
- from the kidneys: heart attack, diffuse glomerulonephritis, focal nephritis, nephrotic syndrome, acute renal failure;
- from the lungs - pulmonary embolism PE - pulmonary embolism (blockage of the pulmonary artery or its branches by blood clots, which often form in the large veins of the lower extremities or pelvis)
, heart attack-pneumonia, pleurisy, abscess, pulmonary hypertension;
- from the liver - hepatitis, abscess, cirrhosis;
- from the spleen - splenomegaly, infarction, abscess;
- from the nervous system - acute cerebrovascular accident, meningitis, meningoencephalitis, brain abscesses;
- from the vascular side - vasculitis, embolism, aneurysm, thrombosis.

Fatal complications of infective endocarditis:
- septic shock;
- respiratory distress syndrome;
- multiple organ failure;
- acute heart failure;
- embolisms in the brain, heart.

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Treatment

The basis of treatment for infective endocarditis (IE) is antibacterial therapy, lasting at least 4-6 weeks.
Antibiotics should not be prescribed before the initial blood draw for bacteriological cultures. The days of the recommended duration of antibiotic treatment should be counted from the first day when a bacteriological blood test gives a negative result.
While the causative agent is unknown, empirical therapy regimens are used. If it is necessary to urgently start empirical therapy before receiving the results of bacteriological studies, it is advisable to focus on the severity of the disease and epidemiological situations that are associated with typical pathogens.

In acute IE, the empirical use of oxacillin with gentamicin is justified. For subacute IE, ampicillin or benzylpenicillin with gentamicin should be prescribed.

Choosing an antibiotic regimen for the treatment of IE caused by enterococcus or penicillin-resistant streptococcus

* - for resistant enterococci, oxazolidinone can be used, but only after consultation with a specialized clinic

Choosing an antibiotic regimen for the treatment of IE caused by streptococcus, affecting native or prosthetic valves

* - in particular for patients with allergies to penicillin;
** - alternative - netilmicin 2-3 mg/kg/day 1 time per day (peak concentration level less than 16 mg/l)

Choosing an antibiotic regimen for the treatment of IE caused by staphylococcus

Note

ZS- Staphylococcus aureus (S. aureus)
CONS- coagulase-negative staphylococcus (if it is sensitive to oxacillin, then gentamicin is replaced with oxacillin)
1 - this refers to both an immediate type reaction and a delayed type hypersensitivity
2 - or its analogues
3 - with the exception of “intravenous” drug addicts, for whom a 2-week course is sufficient
4 - intravenous administration of each dose for at least 60 minutes
5 - the total duration of treatment for patients previously treated with oxacillin should be at least 4 weeks; a second course of gentamicin therapy is not carried out
6 - if sensitivity to gentamicin is proven in vitro, then it is added for S. aureus for the full course of therapy, and for CONS - only for the first 2 weeks. If the microorganism is resistant to all aminoglycosides, then fluoroquinolones are used instead of gentamicin.

Antimicrobial therapy for IE with a negative blood culture or if there are indications for urgent initiation of therapy until the type of microorganism is determined

* - aminopenicillin may be added

Before stopping antibiotic treatment:

Transthoracic echocardiography to assess the condition of the heart at the end of treatment;
- dental examination and sanitation of all active sources of odontogenic infection;
- removal of all intravenous catheters;
- teaching the patient the rules for preventing relapse of IE and maintaining careful oral hygiene, informing him about the symptoms of the disease that require urgent consultation with a doctor;
- rehabilitation program for drug addicts.

Immunotropic drugs. In addition to antibiotics, agents that affect the immune system and anti-infective defense are used in the treatment of IE:
- immunoglobulin complexes (normal human immunoglobulin - octagam, endobulin S/D);
- glucocorticoids (for emergency conditions: bacterial shock, allergic reactions to antibiotics, as well as for immune manifestations: severe glomerulonephritis, vasculitis). Prednisolone is prescribed after the initial effect of antibacterial therapy is obtained and is discontinued 1-1.5 weeks before the end of antibiotic treatment.

Anticoagulants. In patients with IE who were constantly taking indirect anticoagulants before the disease, these drugs should be replaced with heparin. It is recommended to interrupt the use of anticoagulants in patients with staphylococcal IE of the prosthesis in the event of embolism in the vessels of the central nervous system during the first 2 weeks of antibiotic treatment.

Conditions requiring consideration of surgical treatment for IE:

Heart failure;

Fungal IE;

IE caused by bacteria resistant to antibiotics; left-sided IE caused by gram-negative bacteria;

Persistent bacteremia with positive blood culture one week after starting antibiotic treatment;

One or more embolic episodes during the first 2 weeks of antibiotic therapy;

EchoCG signs of valve destruction - perforation, rupture, fistula or large paravalvular abscess; other indications are large, more than 10 mm, vegetation on the anterior leaflet of the mitral valve, persistence of vegetation after an episode of embolism and increase in size of vegetation despite appropriate antimicrobial therapy;

IE of the prosthesis.

The essence of surgical intervention for IE is the sanitation of the heart chambers and radical correction of intracardiac hemodynamics. For this purpose, mechanical removal of infected tissue is carried out, followed by rational antibiotic therapy. If necessary, prosthetics of the affected valve is performed. The best results are observed in patients operated on in the early stages of IE, with preserved myocardial reserve.

Previously suffered infective endocarditis;
- surgically formed systemic or pulmonary vessels;

Diseases with an average risk of IE:
- acquired valvular heart defects;
- congenital heart defects of the “non-cyanotic” type;
- mitral valve prolapse with severe regurgitation or significant thickening of the valve (myxomatous degeneration);

Hypertrophic cardiomyopathy.

Bronchoscopy with a rigid endoscope;

Esophageal dilatation or sclerotherapy for esophageal varices;

Surgical interventions or manipulations for obstruction of the biliary tract;
- lithotripsy;
- cystoscopy (for urinary tract infections);

Biopsy of the urinary tract or prostate gland;

Transurethral resection of the prostate gland;

Interventions on the urethra (including bougienage);
- dental procedures accompanied by a risk of damage to the oral mucosa or gums;

Tonsillectomy, adenoidectomy;

Gynecological operations and childbirth in the presence of infection.

Prophylactic antibiotic regimens

Interventions in the oral cavity, respiratory tract, esophagus:
- no allergy to penicillin: amoxicillin 2 g (children - 50 mg/kg) orally 1 hour before the intervention;
- there is no possibility of oral administration: amoxicillin or ampicillin 2 g (children - 50 mg/kg) intravenously 30-60 minutes before the intervention;
- allergy to penicillin: clindamycin 600 mg (children - 20 mg/kg) or azithromycin/clarithromycin 500 mg (children - 15 mg/kg) 1 hour before the intervention;

Interventions on the genitourinary organs or gastrointestinal tract:
1. If you are not allergic to penicillin:
- high-risk groups: amoxicillin or ampicillin 2 g intravenously + gentamicin 1.5 mg/kg intravenously 30-60 minutes before the intervention, 6 hours later - amoxicillin or ampicillin 1 g orally;
- medium-risk groups: amoxicillin or ampicillin 2 g (children - 50 mg/kg) intravenously 30-60 minutes before the intervention or amoxicillin 2 g (children - 50 mg/kg) orally 1 hour before the intervention.
2. If you are allergic to penicillin:
- high-risk groups: vancomycin 1 g (children - 20 mg/kg) 1-2 hours before the intervention + gentamicin 1.5 mg/kg intravenously or intramuscularly;
- medium-risk groups: only vancomycin 1 g (children - 20 mg/kg) 1-2 hours before the intervention.

Information

Sources and literature

1. Diagnosis and treatment of internal diseases: Hand. for doctors / ed. Komarova F.I., M.: Medicine, 1996
   1. "Infective endocarditis" Gogin E.E., Tyurin V.P. - pp. 300-318
2. Tatarchenko I.P., Komarov V.T. Infective endocarditis: current course, diagnosis and treatment, Penza: PGIUV, 2001
3. Shevchenko Yu.L. Surgical treatment of infective endocarditis, St. Petersburg: Nauka, 1995
4. "Guidelines on Prevention, Diagnosis and Treatment of Infectious Endocarditis. Executive Summary" Horstkotte D, Follath F, Gutschik E, Lengyel M et al. Eur Heart J 2004; 25 (Issue 3)
5. "Guidelines on Prevention, Diagnosis and Treatment of Infectious Endocarditis. Full Text" Horstkotte D, Follath F, Gutschik E, Lengyel M et al. Eur Heart J, 2004
6. “Features of modern infective endocarditis” Gurevich M.A., Tazina S.Ya., “Russian Medical Journal”, No. 8, 1999
7. "Features of the modern course of infective endocarditis" Gurevich M.A., "Clinical Medicine", No. 6, 1997
8. "Modern treatment of infective endocarditis" Beloborodov V.B., "Russian Medical Journal", No. 10, 1999
9. "Modern infective endocarditis" (Part 2) Tazina S.Ya., Gurevich M.A., "Clinical Medicine", No. 1, 2000

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Endocarditis is an inflammation of the lining of the heart, in most cases affecting the valves and cells that line the surface of the vessels adjacent to the heart.

The most dangerous and fast-acting variant of endocarditis is septic. In the old classification it was called acute endocarditis. Most often, the cause of its occurrence is cardiac surgery, catheterization of the heart chambers, and prosthetics. 10% of all heart surgeries are complicated by endocarditis. The period of occurrence of complications is 14-30 days. In this case, the pathogens are nosocomial strains. In the vast majority of cases, staphylococci, Pseudomonas aeruginosa and fungi are found in the culture.

Subacute septic endocarditis

Subacute septic endocarditis is a protracted, sluggish chronioseptic process with localization of the infectious focus on valves disfigured by old rheumatic, syphilitic, congenital, traumatic defects, or previously unchanged.

The causative agent of the disease is most often viridans streptococcus, less often staphylococci, pneumococci, and Candida fungi. Often the disease is preceded by the entry into the blood of low-virulent agents that normally populate the oral cavity, nasopharynx, upper respiratory tract, etc. Passing bacteremia is observed after tooth extraction, tonsillectomy, catheterization of the urinary tract, after childbirth, abortion, etc. Normally, this bacteremia goes away without a trace after a few days.

Organic valvular heart disease is the main predisposing condition for the settling of septic infection on the valves, just as in the classical experiments of Vysokovich, preliminary mechanical damage to the valves turned out to be a necessary condition for obtaining experimental endocarditis when bacteria were introduced into the blood.

Subacute septic endocarditis is often preceded by various infectious diseases, tonsillitis, complications after abortion, and sometimes after surgical interventions and injuries.

For the disease to occur, a decrease in the body's resistance due to previous sensitization is important. The incidence also increases during natural disasters, wars, etc. It is also possible to obtain an experimental model of the disease - this is sepsis in a previously sensitized organism. Often the disease develops in patients with rheumatic heart defects, in the presence of changes in the inner lining of the arteries. More rarely, the disease affects the intact heart.

Features of the disease

• The endocardium is affected.
• There is systemic involvement of the reticuloendothelial system, causing generalized vascular damage.
• Other organs of the reticuloendothelial system (liver, spleen) are also involved.
• When bacteria enter the blood, they first settle on the heart valves, most often on the aortic valves. In the future, the valves themselves become a source of infection, less often the mitral valve suffers, and even the tricuspid valve.

Symptoms of subacute septic endocarditis

The disease occurs at different ages (6-75 years), but most often in young people (21-40 years). Often characterized by gradual development. Manifestations are initially uncharacteristic (malaise, fatigue, headache, increased sweating, low-grade fever), and periodic improvement in general condition is noted. The clinical picture consists of general septic symptoms (fever, chills, excessive sweating); symptoms of heart disease (tachycardia, expansion of the boundaries of the heart, changes in the sonority of tones and the appearance of noise with the gradual development of a typical picture of heart disease, most often aortic); symptoms of vascular damage (petechiae, thromboembolism). The appearance of petechiae is very characteristic of prolonged septic endocarditis; petechiae with a white center on the conjunctiva of the lower eyelid are typical (Lukin-Libman symptom). Hemorrhagic rashes are often wavy in nature and have a symmetrical location. Sometimes Osler's nodes appear (reddish skin lumps up to 1.5 cm in diameter, painful to the touch and located on the palms, fingers, soles, under the nails).

Acute septic endocarditis

Acute septic endocarditis develops as a septic complication of a number of protracted infectious diseases: pneumonia, gonorrhea, meningococcal infection, brucellosis and essentially any other infection, as well as one of the secondary localizations of surgical (wound) and obstetric sepsis - after trauma, osteomyelitis, carbuncle, puerperal thrombophlebitis, etc. The causative agents are most often hemolytic streptococcus, Staphylococcus aureus, pneumococcus, gonococcus, meningococcus, Brucella, influenza bacillus, etc., which are found on the heart valves and in the blood.

The valvular lesion is warty-ulcerative in nature with a predominance of decay. Even with ordinary microscopy, bacteria are found in the thickness of the valves. Most often, the aortic valves are affected, then the mitral valve, and relatively often the tricuspid valve, in particular with pneumonia and gonorrhea. Compared with subacute septic endocarditis, valves that were not previously damaged by another process are somewhat more often affected, apparently due to the more pronounced virulence of microbes that have a greater ability to settle on healthy valves.

The disease occurs at any age, somewhat more often in men. In relation to the actual pathogenesis of the disease, one should take into account the neuroreflex and neurotrophic influences, which are discussed in the section on subacute septic endocarditis.

Symptoms of acute septic endocarditis

The disease occurs as a general septic process; manifestations of septic endocarditis may not come to the fore. The fever is septic in nature, chills, profuse cold sweats, anemia, pronounced neutrophilic leukocytosis with a shift to the left, and significantly accelerated ESR are observed. Hemolytic streptococcus is cultured from the blood. There are multiple petechiae and hemorrhages on the skin. The spleen and liver are soft and enlarged on palpation, signs of emerging aortic valve insufficiency, glomerulonephritis, and multiple embolisms appear. Acute septic endocarditis can develop against the background of previous rheumatic valve disease.

Bacterial endocarditis is an inflammatory process in the inner lining of the heart caused by the influence of pathological microorganisms, the main one of which is streptococcus. Often, endocarditis is a secondary manifestation that develops against the background of other diseases, but it is bacterial damage to the membrane that is an independent disorder. It affects people of any age group, which is why endocarditis is often diagnosed in children. A distinctive feature is that men suffer from this disease several times more often than women.

The main cause of the disease is the penetration of a pathogenic bacterium into the body, in most cases it is viridans streptococcus, a little less often, pneumococcus and. Predisposing factors for the adhesion of a particular microorganism to the endocardium are, in a child, secondary lesions of the heart valves. Risk groups include people with a ventricular septal defect or coarctation of the aorta. In addition, the disease develops in people with a weakened immune system, the elderly, or when leading an unhealthy lifestyle.

In some cases, the disease may not show any symptoms for quite a long time, particularly in older people and people with weakened immune systems. But in most cases, signs such as an increase in body temperature, a decrease in appetite are expressed, against the background of which body weight sharply decreases. In addition, the disease is characterized by dangerous consequences.

Diagnosis of the disease consists of performing a large number of laboratory and instrumental examinations of the patient, which consist of assessing the performance of the heart and its valves. Treatment of the disease is based on the prescription of medications and surgery, which, in turn, requires special training.

Etiology

The main cause of bacterial endocarditis is the pathological effect of certain microorganisms. Currently, more than one hundred and twenty causative agents of this disorder are known. But most often the disease is formed under the influence of candida and enterococcus. Risk factors for this disease include:

• congenital or acquired heart valve defects;
• the presence of artificial valves in a person;
• sagging valve flaps;
• purulent-inflammatory processes in the body;
• individual features of the heart structure;
• maintaining an unhealthy lifestyle, in particular with regular use of large amounts of drugs;
• previously performed invasive diagnostic techniques;
• indiscriminate use of antibiotics;
• harmful working conditions that reduce human immunity;
• performing treatment of any disease using surgery;
• infectious processes in the oral cavity;
• natural labor in the presence of infection of the birth canal is the main risk of endocarditis in children.

The development of the disease occurs approximately according to this pattern - the heart valves are initially affected, after which the endocardium is involved in the inflammatory process. Next, the blood clot breaks off, against which the disease develops.

Varieties

Depending on the course, this disorder is divided into several forms:

• acute– characterized by a sudden and sharp onset, and the duration of the disease is approximately two weeks;
• I'll make it more acute– lasts for several months until a diagnosis is made;
• chronic- characterized by a rather long course. It lasts for several years and is very difficult to treat.

In addition to dividing the disease according to the time it occurs, there is another classification of the disease, depending on its course:

• infectious-toxic;
• immuno-inflammatory;
• dystrophic.

Depending on the factors causing the disease, it is divided into:

• primary– occurred on undamaged valves;
• secondary– develops against the background of already developed cardiac pathologies, previously suffered infective endocarditis or.

Classification of the occurrence of such a disease in children:

• congenital– formed during intrauterine development. Often, if the expectant mother has an acute or chronic course of infectious disorders;
• acquired- found in children in the first two years of life, quite often on intact valves. In children over two years of age, as in adults, this disease develops for a reason.

Symptoms

In some cases, symptoms may be completely absent, particularly in older people or those with weakened immunity. The clinical manifestation of bacterial endocarditis depends on the form of the disease. Thus, the symptoms of acute endocarditis are:

• a significant increase in body temperature, up to a feverish state;
• increased sweating;
• severe chills;
• body – lethargy and headaches;
• subcutaneous hemorrhages, as well as a similar process on the mucous membranes or fundus of the eye;
• small nodules form on the fingers of the upper limbs, which cause pain;
• heart failure.

Subacute bacterial endocarditis is expressed by such symptoms as:

• fever;
• increased sweating;
• chills;
• muscle weakness and pain;
• severe loss of body weight;
• change in skin color. The skin becomes similar in color to coffee with milk;
• the appearance of a hemorrhagic rash;
• sleep disturbance;
• decrease in the amount of urine excreted per day;
• the formation of small painful nodules under the skin;
• separation of the nail plates.

During diagnosis, an increase in the size of the spleen, and less often the liver, is detected.

Complications

Bacterial endocarditis is a dangerous disease that can cause severe and irreparable complications, especially if treatment is not started in time. The formation of consequences is due to the accumulation of bacteria cells, which, in turn, form scabs. As the disease progresses, scabs may break off and travel to other organs. This is what leads to complications such as:

• or ;
• lack of oxygen supply to internal organs;
• abscesses of the heart cavities;
• dysfunction of heart valves;
• recurrence of the disease;
• blood clot formation;
• pathologies of cerebral circulation.

In addition, there are a number of complications that develop after medical intervention. These consequences include:

• acute heart and kidney failure;
• stroke;
• violation of the blood clotting process;
• atrioventricular block.

Diagnostics

Since bacterial endocarditis is a serious condition, when the first symptoms occur, it is necessary to seek help from specialists. The earlier the diagnosis is made, the more positive the prognosis of the disease will be.

Diagnostic measures for such a pathology involve a large number of instrumental diagnostic studies. But before prescribing them, the attending physician needs to carry out several manipulations. The first is to study the patient’s life history and medical history. This is necessary to search for predisposing factors for the onset of the disease. Next, a thorough examination is carried out, in particular the skin, as well as the mucous membranes of the mouth and eyes. This is done to determine the presence and intensity of symptoms. In addition, it is necessary to find out the first time of their manifestation.

Thus, the specialist will find out the full picture and stage of the disease in each patient.

Only after this are laboratory tests prescribed:

• general clinical blood and urine tests are carried out to identify concomitant diseases that may negatively affect the course of the underlying disease;
• biochemical study of blood - the level of uric acid and cholesterol is assessed, which may indicate internal damage to some organs;
• determination of blood clotting ability;
• immunological blood test - to search for antibodies to pathological microorganisms and own cells;
• bacterial culture - performed to determine the pathogen;
• PCR diagnostics.

Instrumental diagnostic techniques include:

• ECG - to detect possible heart rhythm disturbances;
• phonocardiograms – assessment of heart murmurs, which may correspond to a heart defect;
• X-rays of the chest area - the procedure makes it possible to determine the volume of the heart, identify blood stagnation or pulmonary infarction;
• EchoCG is the main way to diagnose bacterial endocarditis. It helps determine the size of the cavities and the thickness of the heart muscles, and also identifies heart defects;
• transesophageal echocardiography - a study of the heart in which a sensor is inserted into the esophagus. Prescribed only in cases where the previous method did not provide sufficient information;
• SCT is a procedure for taking several images in different projections and at different depths. Allows you to obtain the most accurate image of the organ being examined;

Thanks to the above studies, the doctor prescribes effective treatment tactics.

Treatment

The beginning of treatment for such a disease is carried out immediately, after diagnostic measures have been carried out. Comprehensive elimination of the disease includes the prescription of medications and surgery. The basis of drug therapy is:

Medical intervention is indicated in almost half of the cases when such a disorder is diagnosed. There are several ways to carry out the operation, depending on the timing of its implementation:

• emergency – performed within 24 hours from the moment the diagnosis is confirmed. Indications for this type of operation are acute heart failure and detection of bacteria that are poorly responsive to drug therapy;
• urgent – ​​carried out within several days of the patient’s hospital stay;
• deferred – carried out after a two-week course of antibiotics.

The goals of performing a particular operation are the complete elimination of structures containing the pathogen, replacement of damaged valves with biological or mechanical ones. Every tenth patient dies during surgery.

Prevention

Prevention of bacterial endocarditis involves eliminating pathological microorganisms. To prevent a person from having problems with such a dangerous disease, it is necessary to adhere to several rules:

• timely elimination of inflammatory processes of bacterial origin;
• prophylactic use of antibiotics;
• compliance with safety rules for people with heart defects.

The prognosis of bacterial endocarditis depends on several factors - the age group of the patient, the presence of complications, the type of bacteria that causes it, and diagnostic results. The acute course of the disease, in the absence of treatment, ends in death in a month, subacute - in six months. If antibiotics are taken in a timely manner, every fourth patient dies, and with secondary damage to the artificial valve, every second patient dies. In elderly patients, the prognosis is sadder, since it develops into a chronic form with frequent exacerbations.

It was first described more than 100 years ago. At different times it was called Osler's disease, Jacques' disease, etc. Often the disease occurs against the background of rheumatic heart disease.

Previously, subacute septic endocarditis was considered as an evolution of rheumatism, but then it was shown that it can also affect the intact heart. Now it is considered as an independent disease.

ETIOLOGY:

Subacute septic endocarditis is often preceded by various infectious diseases.

diseases, sore throats, complications after abortions, sometimes after surgical interventions

The causative agent of the disease is most often viridans streptococcus, less often staphylococci, pneumococci, and Candida fungi. Often the disease is preceded by the entry into the blood of low-virulent agents that normally populate the oral cavity, nasopharynx, upper respiratory tract, etc. Passing bacteremia is observed after tooth extraction, tonsillectomy, catheterization of the urinary tract, after childbirth, abortion, etc. Normally, this bacteremia goes away without a trace after a few days.

For the disease to occur, a decrease in the body's resistance due to previous sensitization is important. The incidence also increases during natural disasters, wars, etc. It is also possible to obtain an experimental model of the disease - this is sepsis in a previously sensitized organism. Often the disease develops in patients with rheumatic heart defects, in the presence of changes in the inner lining of the arteries. More rarely, the disease affects the intact heart.

FEATURES OF THE DISEASE:

1. The endocardium is affected.

2. There is systemic involvement of the reticuloendothelial system, causing generalized vascular damage.

3. Other organs of the reticuloendothelial system (liver, spleen) are also involved.

4. When bacteria enter the blood, they first settle on the heart valves, most often on the aortic valves. In the future, the valves themselves become a source of infection, less often the mitral valve suffers, and even the tricuspid valve.

FEATURES OF MORPHOLOGICAL CHANGES IN THE DISEASE:

There is necrobiosis, fibrinoid swelling, predominantly ulcerative endocarditis, and ulcerative-warty endocarditis may occur. In this case, proliferation is practically not expressed, which leads to rapid deformation of the valve. The liver is affected: phenomena of septic hepatitis are observed. Pulp hyperplasia occurs in the spleen, and necrosis may form. When the kidneys are damaged, focal or diffuse nephritis occurs. Generalized systemic vascular damage, mainly of small caliber, is often observed. And toxicoallergic vasculitis occurs.

There may also be thromboembolic complications, mainly in the systemic circulation. Which is caused by polypous-ulcerative endocarditis (and in rheumatism - only polypous endocarditis).

CLINIC:

The clinic consists of:

1. Generalized vasculitis.

2. Valve lesions such as thrombotic endocarditis.

3. Sepsis.

Previously, there was an acute onset of the disease with chills and high fever. Currently, a subacute course is more often observed: the disease begins gradually, low-grade fever, severe weakness, sweating, loss of appetite, weight loss, chills.

An external examination reveals pale skin with a yellowish tint. Hemorrhagic syndrome is characteristic: petechiae, bruises, nosebleeds, retinal hemorrhages, and sometimes subarachnoid hemorrhages. Petechiae are most often found on the skin in the collarbone area, at the base of the nail bed, on the conjunctiva of the eyes and the oral mucosa.

Causes of hemorrhagic syndrome:

Violation of the permeability of the vascular wall (vasculitis).

Enlargement of the spleen and disruption of its function, which

manifests itself as thrombocytopenia. Pronounced inhibition of hematopoiesis: anemia, pallor.

Lukin-Lidman syndrome - hemorrhagic petechiae on the mucous membranes and under the nails. Sometimes red, painful nodules, first described by Osler (Osler's node), are found, which arise from damage to the capillaries. With a long course of the disease, nails in the form of watch glasses and fingers in the form of drumsticks are found. Mild jaundice is caused by the occurrence of toxic hepatitis (cafe-au-lait skin). Liver enlargement (hepatomegaly) can be associated with two reasons: toxic hepatitis, heart failure.

At the beginning of the disease, the temperature is hectic with strong swings, significantly debilitating the patient. However, low-grade fever is also possible. Symptoms of heart damage gradually develop:

The first to be affected is the aortic valve. Its deficiency is formed. A systolic murmur occurs over the aorta.

If the myocardium (myocarditis) suffers, then the symptoms of heart failure will come to the fore.

Arrhythmias occur.

It is possible to form tears and perforations of the leaflets, rupture of the chordae or papillary muscles, which sharply worsens hemodynamics.

The disease is especially severe with thromboembolic complications associated with endocarditis:

Myocardial infarction due to embolism in the coronary artery.

Kidney infarction when an embolus enters the kidney vessels.

Infarction of the spleen, sometimes with subsequent development of an abscess.

Cerebral embolism - stroke.

Embolism of the vessels of the intestines and extremities with corresponding symptoms.

Common to these complications is pain and a collapsed state. Signs of inflammation are increasing. The temperature reaction is pronounced. The function of the corresponding organ suffers sharply.

In the case of long-term subacute septic endocarditis, the kidneys suffer. There are:

1. Focal nephritis, which is manifested by urinary syndrome, proteinuria, hematuria, casts in the urine.

2. Diffuse glomerulonephritis - manifested by arterial hypertension, mild edema. The temperature may decrease, which is sometimes a reason for the erroneous diagnosis of glomerulonephritis as an independent disease.

LABORATORY DIAGNOSTICS:

1. Repeated blood cultures are performed, especially at the height of fever and chills. In approximately 40% of cases, staphylococcus is sown, in 60% - viridans streptococcus and other pathogens. This is an absolute sign of the disease.

2. Clinical blood test:

There is moderate normochromic anemia without reticulocytosis;

Tendency to leukopenia with a large shift to the left to young neutrophils. In rheumatism, leukocytosis is observed, which is important for differential diagnosis;

Leukocytosis in septic endocarditis can be observed in the case of thromboembolic complications.

Eosinophilia;

Monocytosis;

Thrombocytopenia;

A common sign is toxic granularity of leukocytes;

ESR sharply increased to 50-70 mm/hour;

An electropherogram of blood proteins reveals normal or hypergamma-globulinemia;

The formol test is typically positive;

3. False positive reaction of Wasserman, Kahn.

4. Urinalysis is most informative in cases of long-term progression, when nephritis is already developing: proteinuria, microhematuria.

5. Tests to identify hemorrhagic syndrome: pinch symptom, tourniquet symptom.

6. Sometimes rheumatoid factor is detected in the blood, and a decrease in complement levels is noted.

Anemia, leukopenia, thrombocytopenia are associated with the phenomena of hypersplenism.

DIFFERENTIAL DIAGNOSTICS:

1. Carry out with rheumatism. Rheumatism is characterized by:

With rheumatism, pain in the joints is noted, their visible changes in 30% of cases. It is not arthralgia that is possible, but polyarthritis.

Mitral defects form more often, and aortic defects only with repeated attacks.

The conduction systems of the heart are disrupted, and atrioventricular block often occurs (prolongation of the PQ interval).

There are no symptoms of hemorrhagic diathesis.

In rheumatism, hypersplenism is not observed.

There is no thickening of the nail phalanges in the form of drumsticks.

The kidneys are practically not affected.

In doubtful cases, blood cultures for rheumatism are sterile.

Determination of antibody titer (antistreptolysin and antihyaluronidases) helps in differential diagnosis.

2. Systemic lupus erythematosus (SLE). It is characterized by:

Mostly women suffer, and subacute septic endocarditis occurs more often in men.

The serous membranes are often affected and pericarditis and pleurisy occur.

Erythema on the face in the form of a butterfly.

Blood cultures are sterile.

There are no thromboembolic complications.

LE sockets in the blood.

3. Diffuse glomerulonephritis:

With it there is no period of prolonged preceding fever.

With glomerulonephritis, heart disease does not form.

There is no splenomegaly.

There are no thromboembolic complications.

Blood culture is sterile.

4. Syphilitic aortitis:

There are no signs of hemorrhagic diathesis.

There is no enlargement of parenchymal organs.

There are symptoms of syphilitic aortitis and signs of damage to other organs (nervous system, bone).

TREATMENT:

Hospitalization is required. Strict bed rest is indicated. The diet is without special restrictions, but if there are signs of heart failure, the amount of NaCl is limited.

1. Antibiotic therapy: during treatment, it is necessary to repeatedly determine the sensitivity of the flora to the selected drug. If you are sensitive to penicillin (viridans streptococcus), it is prescribed in large doses: 10 million units/day. i/m. If penicillin causes allergic reactions, then cephalosporin antibiotics are prescribed: Cefalotin, Cephaloridin, etc. Penicillin is usually combined with Streptomycin, which allows the daily dose of Penicillin to be reduced. Lincomycin is effective against Staphylococcus aureus. For gram(-) pathogens, the use of Neomycin and Kanamycin is indicated.

If within 3-4 days the use of an antibiotic does not produce an effect, it is replaced with another one or a combination of antibiotics is prescribed. Possible intravenous administration of drugs.

2. Desensitizing agents: Diphenhydramine, Pipolfen.

3. Glucocorticoids: Prednisolone is prescribed at a dose of 20-30 mg/day. within 7-10 days. Start taking the drug 2-3 days after the course of desensitizing therapy.

4. General restorative therapy: vitamins, fractional blood transfusions.

5. Drugs that reduce the permeability of the vascular wall: vitamin “C” 2-4 g/day. , Rutin 0.1 3 times/day, Calcium gluconate (chloride), vitamin "K".

THANATOGENESIS:

Increasing heart failure;

Generalization of sepsis;

Aortic valve insufficiency almost always develops. 35% of patients lose their ability to work.

Rheumatism is an infectious-allergic disease, which is based on inflammation and disorganization of connective tissue. The main cause of rheumatism is considered to be beta-hemolytic streptococcus group A. Upon first contact with this microorganism, the patient usually suffers from tonsillitis or pharyngitis ( in childhood). Without qualified drug treatment, the initial disease goes away within 1 to 2 weeks. However, then comes the most dangerous phase.

The human immune system begins to produce antibodies against the pathogen. In some cases, this reaction becomes excessively strong ( hyperergic immune response). In such patients, antibodies begin to attack connective tissue cells ( mainly in the cardiovascular system). This inflammation is called rheumatism.

In rheumatic endocarditis, the following structures of the heart are most often affected:

• mitral valve;
• aortic valve;
• tricuspid valve ( usually in combination with other localizations);
• chordae tendineae;
• parietal ( parietal) endocardium;
• deep layers of the myocardium.

Injuries

Allergic reaction

Intoxication

Infection

The most common causative agents of bacterial endocarditis are:

• Viridans streptococcus (Streptococcus viridans) - approximately 35 - 40% of cases. It is the most common causative agent of infective endocarditis.
• Enterococcus (Enterococcus) – 10 – 15%. It normally lives in the human intestine, but under certain conditions it can become pathogenic ( pathogenic).
• Staphylococcus aureus (Staphylococcus aureus) – 15 – 20%. It can live on the skin or in the nasal cavity of healthy people. Causes severe infective endocarditis with severe valve damage.
• Streptococcus pneumoniae- 15%. This microorganism is the causative agent of pneumonia, sinusitis or meningitis in children. In the absence of qualified treatment, endocardial damage may occur.
• Other streptococci and staphylococci– 15 – 20%. These pathogens usually cause endocarditis with a favorable prognosis without serious damage to the valves.
• Bacteria from the HACEK group (Haemophylus, Actinobacillus actinimycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae) – 3 – 7%. This group of microorganisms was combined because of their high tropism ( affinity) specifically to the endocardium of the heart. Their common feature is difficulty in diagnosis, because all bacteria of the HACEK group are difficult to cultivate on nutrient media.
• Gram-negative bacteria – 5 – 14% (Shigella, Salmonella, Legionella, Pseudomonas). These bacteria rarely infect the endocardium. Usually, in addition to heart symptoms, there are also dysfunctions of other organs and systems.
• Fungal infections- 15%. Fungal infections also rarely affect the endocardium. The problem in such patients is the need for long-term treatment with antifungals. Due to the danger of complications, doctors often resort to surgical treatment.
• Other pathogens. In principle, endocarditis can be caused by almost all known pathogenic bacteria ( chlamydia, brucella, rickettsia, etc.). In approximately 10–25% of cases, it is not possible to isolate the causative agent of the disease, although all the symptoms and diagnostic tests speak in favor of infective endocarditis.
• Combination of several infectious agents (mixed form). It is rarely recorded and usually leads to a severe, protracted course of the disease.

An important feature of bacterial endocarditis is the formation of so-called vegetations on the valve leaflets. Most often they occur in the left side of the heart. Vegetations are small accumulations of microorganisms attached to the valve. Usually, at the first stage, a small thrombus forms at the site of endocardial damage. Subsequently, it is to it that the first infectious agents attach. As they multiply and the inflammatory process intensifies, the vegetation may increase. If they have a flat shape and are firmly attached to the sash, then they are called fixed. Mobile vegetations resemble pedunculated polyps in structure. They seem to hang on the valve leaf and move depending on the blood flow. Such vegetations are the most dangerous, since the separation of this formation leads to its entry into the bloodstream and acute thrombosis. Severance of large mobile vegetations is a fairly common cause of serious complications and even death in infective endocarditis. The severity of the consequences depends on the level at which vessel thrombosis occurs.

Separately, fibroplastic eosinophilic Loeffler's endocarditis should be considered. The reasons for its development are unknown. With this disease, the parietal pericardium is predominantly affected, which distinguishes it from other variants of the disease. It is assumed that complex allergic reactions play a role in the development of Loeffler's endocarditis.

Types of endocarditis

Infective endocarditis can be divided into two main groups:

• Primary infective endocarditis. Primary is a form of the disease in which bacteria circulating in the blood linger on the leaflets of a healthy valve ( any of the valves) and caused inflammation. This form is quite rare, because a healthy endocardium is little susceptible to pathogens.
• Secondary infective endocarditis. Secondary endocarditis is called endocarditis, in which the infection reaches already damaged heart valves. This form of the disease is much more common. The fact is that narrowing of the valves or their improper operation disrupts the normal flow of blood. There are turbulences, stagnation of blood in certain chambers of the heart, or an increase in internal pressure. All this contributes to microscopic damage to the endocardium, where bacteria from the blood easily penetrate. Defects that predispose to secondary infection of the heart valves are rheumatic process, patent ductus arteriosus, septal defect, and other congenital or acquired heart defects.

• spicy;
• subacute;
• chronic ( protracted).

Acute infective endocarditis

Subacute infective endocarditis

Chronic ( protracted) infective endocarditis

The following groups of patients are predisposed to the chronic course of the disease:

• Newborns and infants. The prevalence of chronic endocarditis in children is explained by congenital heart valve defects. In these cases, infection and its development on the endocardium is usually a matter of time.
• People who inject drugs. This category of people has a high probability of toxic damage to the endocardium and infection. In addition, as treatment progresses, germs may be reintroduced. Often such patients have mixed infections.
• People who have undergone heart surgery. Diagnostic or therapeutic manipulations in the heart cavity always pose a risk of endocardial injury. In the future, this creates favorable conditions for the formation of an infectious focus.

In chronic infective endocarditis, periods of remission and relapse are usually observed. Remissions represent improvements in the patient's condition and the disappearance of acute symptoms. During this period, patients mainly show signs of damage to the valves, but the infectious focus in the heart is not eliminated. Relapse is a sharp deterioration in the patient’s condition associated with the activation of infection and the development of an acute inflammatory process. A similar course is also observed in rheumatic endocarditis.

In some countries, in addition to acute, subacute and chronic forms of endocarditis, an abortive variant of the course is also distinguished. It is characterized by rapid and lasting recovery ( no relapses). This outcome is the most favorable, since the valve apparatus of the heart does not have time to suffer due to inflammation. Abortive course is observed in infectious and toxic endocarditis, when the disease was diagnosed at an early stage and timely treatment was started.

Rheumatic endocarditis has a slightly different classification. It is not based on the duration of the disease ( because it's always long), but on the nature of changes in the heart valves. They allow you to assess the intensity of the inflammatory process and prescribe the correct treatment.

Rheumatic endocarditis is divided into four types:

• Diffuse endocarditis. In this case, a change in the structure of the connective tissue occurs over the entire surface of the valve. Its valves thicken, making it difficult for the heart to function normally. Small granulomas can be found on the surface ( usually appear on the left ventricular side on the cusps of the mitral or aortic valve). Characterized by simultaneous damage to connective tissue in several places, including chords and parietal endocardium. Timely treatment of such endocarditis at the stage of connective tissue swelling helps to avoid irreversible changes. If granulomas have already appeared, there is a high risk of fusion or shortening of the valve leaflets. Such changes are called rheumatic heart disease.
• Acute warty endocarditis. This form of the disease is characterized by detachment of the superficial layer of the endocardium. At the site of the lesion, thrombotic masses and fibrin are deposited, which leads to the appearance of specific formations, so-called warts. They look like small light brown or gray tubercles. In some cases, a sharp growth of these formations is observed with the formation of entire conglomerates on the valve leaflet. Unlike vegetations in infective endocarditis, these formations do not contain pathogenic microorganisms. However, if microbes circulate in the blood, such warts may become infected with the development of secondary infective endocarditis and a deterioration in the patient’s general condition. If inflammation can be stopped in the early stages, then the formations on the valve leaflets do not increase. In this case, there is practically no risk of blood clot rupture and serious disruption of the heart.
• Recurrent verrucous endocarditis. This type is characterized by changes similar to those in acute wart endocarditis. The difference lies in the course of the disease. Formations on the valves appear periodically, during exacerbation of rheumatism. Persistent fibrin deposits are observed when calcium salts are included. Such formations are clearly visible during echocardiography ( echocarliography) or x-rays that help confirm the diagnosis.
• Fibroplastic endocarditis. This form is the final stage of the three previous variants of the course of rheumatic endocarditis. It is characterized by pronounced changes in the valve flaps ( their shortening, deformation, fusion). These changes are irreversible and require surgical treatment.

With Loeffler's endocarditis, the following stages are distinguished:

• Spicy ( necrotic) stage. The inflammatory process affects the endocardium of both ventricles and ( less often) atria. Not only the superficial layer in contact with the blood is affected, but also the deep layers of the myocardium. A large number of eosinophils are found in the inflamed tissue ( type of leukocyte). The duration of this stage is 5 – 8 weeks.
• Thrombotic stage. At this stage, inflammatory foci in the endocardium begin to become covered with thrombotic masses. Because of this, the walls of the heart chambers thicken and their volume decreases. There is a gradual coarsening of the endocardium, during which more connective tissue fibers appear in its thickness. The underlying myocardium thickens due to hypertrophy ( increase in volume) muscle cells. The main problem at this stage is a pronounced decrease in ventricular volume.
• Stage of fibrosis. When the connective tissue in the endocardium has formed, the wall loses its elastic properties. There is an irreversible decrease in the volume of the heart, a weakening of its contractions and damage to the chordae tendineae, which also affects the functioning of the valves. In this case, the picture of chronic heart failure comes to the fore.

Symptoms of endocarditis

Symptoms and signs of heart failure in various forms of endocarditis

The following symptoms are in favor of infective endocarditis:

• increased body temperature;
• increased sweating;
• skin manifestations;
• ocular manifestations;
• headaches and muscle pain.

Increased body temperature

The absence or slight increase in temperature (despite an acute infectious process) can be observed in the following groups of patients:

• aged people;
• stroke patients;
• patients with severe heart failure;
• when the level of uric acid in the blood increases.

Chills

Increased sweating

Skin manifestations

Patients with endocarditis may experience the following skin manifestations of the disease:

• Petechial rash. The elements of the rash are small red spots that do not rise above the surface. They are formed due to pinpoint hemorrhages due to damage to the vascular wall. The rash can be localized on the chest, torso, limbs and even on the mucous membranes ( hard and soft palate). In infective endocarditis, a small grayish area may be located in the center of the petechial hemorrhage. The rash usually lasts for several days before disappearing. In the future, without adequate treatment, repeated rashes may occur.
• Janeway spots. The spots are intradermal bruises measuring 2–5 mm that appear on the palms or soles. They can rise 1–2 mm above the surface of the skin and can be felt through the surface layers.
• Pinch symptom. A slight pinch of the skin on the limb leads to the appearance of pinpoint hemorrhages. This helps detect capillary fragility due to vasculitis ( vascular inflammation).
• Konchalovsky-Rumpel-Leede test. This test also proves the fragility of capillaries and the increased permeability of their walls. To artificially induce pinpoint hemorrhages, apply a cuff or tourniquet to the limb. Due to compression of the superficial veins, the pressure in the capillaries increases. After a few minutes, elements of a rash appear below the site where the tourniquet was applied.
• Osler's nodes. This symptom is typical for chronic endocarditis. Nodules are dense formations on the palms, fingers and soles, which can reach 1 - 1.5 cm in diameter. When pressing on them, the patient may complain of moderate pain.

Ocular manifestations

Headaches and muscle pain

Rheumatic endocarditis is characterized by signs of damage to the heart valves. In the early stages, patients may not complain. Diagnosis of the disease is possible only with a thorough examination by a cardiologist or laboratory tests. In later stages, valve deformation leads to symptoms of heart failure. Distinctive signs of the rheumatic process are sometimes damage to other organs and systems. This disease is rarely limited to cardiac manifestations only. In this regard, patients often present complaints that are not characteristic of endocarditis.

With rheumatic valve damage, symptoms of damage to the following organs and systems may be observed:

• Joints. Joint inflammation may develop in parallel with endocarditis or precede it. The disease usually affects large and medium-sized joints of the limbs ( shoulder, elbow, knee, ankle). Symptoms and complaints include pain, limited mobility and slight swelling in the affected area.
• Kidneys. Kidney damage due to endocarditis is manifested by impaired urine filtration. In this case, signs of bleeding may appear in the blood. Moderate pain in the kidney area is also characteristic.
• Damage to the serous membranes. In some cases, rheumatism can cause diseases such as pericarditis and pleurisy. This will make the diagnosis of endocarditis somewhat difficult due to similar manifestations.
• Skin damage. Erythema nodosum and ring-shaped erythema are typical for rheumatism. Sometimes rheumatoid nodules appear deep in the skin. These lesions are localized mainly in the area of ​​the joints affected by the disease.

Diagnosis of endocarditis

In the diagnosis of endocarditis of any origin, the following research methods are used:

• general examination of the patient;
• lab tests;
• bacteriological tests;
• instrumental examination methods.

General examination of the patient

During a general examination, the doctor collects data about the disease in the following ways:

• History taking. Taking an anamnesis is very important in diagnosing endocarditis of any etiology, as it helps to understand where the disease came from. Most often, it is possible to find out that the first cardiac symptoms were preceded by infectious diseases. Then endocarditis can be explained by the entry of bacteria into the heart and the development after some time of characteristic manifestations of the disease. In rheumatic endocarditis, the first symptoms are preceded by a sore throat or pharyngitis ( usually 2 – 4 weeks before the first signs of rheumatism). In addition, the doctor asks the patient about other chronic pathologies or previous operations, as they may predispose to the development of endocarditis.
• Visual inspection. Visual examination of patients with endocarditis may provide little information. However, with infectious forms, a characteristic rash or other skin symptoms may appear. In rheumatic endocarditis, the patient's joints are examined, looking for signs of inflammation. In addition, patients with chronic endocarditis experience general exhaustion, pale skin, and changes in the shape of fingers and nails.
• Palpation. Palpation during examination of the heart provides almost no information important for the diagnosis. If endocarditis develops against the background of sepsis, the doctor can palpate enlarged lymph nodes in various parts of the body. Palpation also includes measuring the pulse and determining the apical impulse. The latter is a point on the anterior chest wall where cardiac contractions are projected. With severe valve pathology, this point may be displaced.
• Percussion. Percussion involves beating the heart through the anterior chest wall. With its help, an experienced doctor can accurately determine the boundaries of the cardiac sac and the heart itself. Percussion is usually performed while lying on your back and is a painless procedure that takes 5 to 10 minutes. In patients with endocarditis, there is often an extension of the left border to the left ( due to hypertrophy of the left ventricular muscle).
• Auscultation. Auscultation is listening to heart sounds using a stethoscope. It can provide information about valve operation. The first auscultatory changes usually appear no earlier than 2–3 months of the disease, when a heart defect begins to form. The most typical sign is weakening of the first and second sounds at the listening points of the mitral and aortic valves.

Lab tests

In general and biochemical blood tests in patients with endocarditis, the following changes can be detected:

• Anemia. Anemia is a decrease in the level of hemoglobin in the blood to less than 90 g/l. Most often it is observed in the subacute course of infective endocarditis. Anemia in these cases is normochromic ( blood color index in the range of 0.85 – 1.05). This indicator reflects how saturated red blood cells are with hemoglobin.
• Red blood cell level largely depends on the severity of the infection. Both a decrease and an increase can be observed. The norm for women is 3.7 - 4.7 X10 12, and for men - 4.0 - 5.1 X10 12 cells per 1 liter of blood.
• Increased erythrocyte sedimentation rate ( ESR). This indicator changes already in the first stages of the disease as the inflammatory process develops and remains elevated for several months ( even with a favorable course of the disease). The norm is up to 8 mm/h in men and up to 12 mm/h in women. With age, the normal limits can increase to 15 – 20 mm/h. In patients with endocarditis, this figure sometimes reaches 60–70 mm/h in the infectious version. Rheumatic inflammation can also lead to an increase in ESR. A normal value for this indicator in endocarditis is relatively rare, but does not exclude the diagnosis.
• Leukocytosis. The number of leukocytes in the blood is usually increased. The norm is 4.0 – 9.0 X10 9 cells per 1 liter of blood. In cases of severe bacterial endocarditis, leukopenia may also occur ( decreased white blood cell count). The so-called leukocyte formula is shifted to the left. This means that young forms of cells predominate in the blood. Such changes are characteristic of an active inflammatory process.
• Dysproteinemia. Dysproteinemia is a violation of the proportion between blood proteins. With infectious and rheumatic endocarditis, an increase in the amount of gamma globulins and alpha-2 globulins may be observed.
• Increased concentration of sialic acids and C-reactive factor. These indicators indicate the presence of an acute inflammatory process. They can be increased in both infectious and rheumatic endocarditis.
• Increased creatinine levels in a biochemical blood test is observed in approximately a third of patients with infective endocarditis.
• Increased levels of seromucoid and fibrinogen in the blood is observed in some forms of endocarditis.

Specific tests to confirm rheumatic inflammation are:

• determination of antistreptohyaluronidase titer;
• determination of antistreptokinase titer;
• determination of antistreptolysin-O titer;
• rheumatoid factor ( antibodies against the body's own cells that appear after a streptococcal infection).

There are usually no significant changes in urine analysis. In severe heart failure in the later stages of the disease, oliguria may occur ( decreased urine production). It is explained by a weakening of the pumping function of the heart, due to which the kidneys do not maintain the pressure necessary for normal filtration. In rheumatism with damage to the kidney tissue, traces of blood may be present in the urine.

Bacteriological tests

When collecting blood for bacteriological culture, the following principles are followed:

• In acute endocarditis, three blood samples are taken at intervals of half an hour. In subacute cases, it is possible to take three samples during the day. Repeated cultures increase the reliability of the study. The fact is that microbes that accidentally got into the sample can also grow on the nutrient medium. Triple testing eliminates the possibility of such accidental contamination.
• With each vein puncture, 5–10 ml of blood is taken. Such a large number is explained by the fact that the concentration of bacteria in the blood is usually very low ( 1 – 200 cells in 1 ml). A large blood volume increases the likelihood that bacteria will grow on the nutrient medium.
• It is advisable to take blood samples before starting antibiotic therapy. Otherwise, taking antimicrobial drugs will greatly reduce the activity of bacteria and reduce their concentration in the blood. The result will be a false negative test. If the patient is not in critical condition, it is even practiced to temporarily stop antibiotic therapy to conduct bacteriological blood cultures.
• Blood sampling is done only in sterile gloves with sterile disposable syringes. The skin at the site of vein puncture is treated with an antiseptic solution twice, because it has a particularly high concentration of microbes that can contaminate the sample.
• The collected blood is immediately transported to the laboratory for culture.
• If no colonies grow on the nutrient media within 3 days, the analysis can be repeated.

An alternative to bacteriological analysis is to conduct serological tests. They determine the presence of antibodies to various microbes in the blood or directly detect microbial antigens. The disadvantage of such a study is that it is not possible to create an antibiogram.

Instrumental examination methods

The following instrumental diagnostic methods are of greatest importance for endocarditis:

• Electrocardiography ( ECG). Electrocardiography is based on measuring the strength and direction of bioelectric impulses in the heart. This procedure is completely painless, takes 10 – 15 minutes and allows you to get results immediately. With endocarditis in the early stages of the disease, changes on the ECG will be present only in 10–15% of cases. They are expressed in disturbances in the contraction of the heart muscle, instability of the heart rhythm and signs of myocardial ischemia ( lack of oxygen). These changes are not specific and more often indicate the presence of certain complications of endocarditis.
• Echocardiography ( EchoCG). This method is based on the penetration of ultrasonic waves into the thickness of the soft tissues of the heart. Reflecting from structures of varying densities, these waves return to a special sensor. As a result, an image is formed. On it you can notice vegetations or forming blood clots, characteristic of endocarditis. In addition, the places of fusion of the valves and the peculiarities of the deformation of their valves are visible. EchoCG is recommended to be repeated at different stages of the disease to recognize the first signs of heart defects.
• Radiography. In radiography, images are obtained by passing x-rays through the chest. It cannot be used to find changes specific to endocarditis. However, this method allows you to quickly notice stagnation in the pulmonary circulation and an increase in the volume of the heart. The study is prescribed at the first visit to the doctor to detect signs of cardiac pathology in general.
• Ultrasonography ( Ultrasound), CT scan ( CT) and magnetic resonance therapy ( MRI). These studies are not so often used to diagnose endocarditis directly due to their high cost ( CT and MRI). However, they can be indispensable in searching for complications of this disease. In particular, we are talking about detached blood clots. They can clog the arteries of the limbs, internal organs or even the brain, creating a serious threat to the life and health of the patient. For urgent treatment, it is necessary to determine the exact location of the blood clot. This is where cardiac ultrasound, CT and MRI can help. Sometimes they are also used to detect joint changes in rheumatism, which helps in making a diagnosis.

Generally accepted criteria for the diagnosis of bacterial endocarditis

One of the serious problems in diagnosing endocarditis is identifying its root cause in the early stages of the disease. Doctors often have to decide whether they are dealing with an infection or rheumatic fever. The fact is that the treatment in these two cases will be different. Correct diagnosis at the initial stages will allow earlier initiation of drug therapy, which will prevent complications and eliminate the threat to the patient’s life.

The main differences between bacterial and rheumatic endocarditis

As a rule, none of the above symptoms or tests can accurately determine the origin of endocarditis. However, a comprehensive assessment of the patient’s condition and comparison of all manifestations of the disease contribute to making the correct diagnosis.

Treatment of endocarditis

Depending on the type of disease and leading symptoms, treatment can be carried out in the rheumatology, infectious diseases or cardiovascular department. Consultation with a cardiologist is indicated for any form of endocarditis. The course of treatment must be agreed upon with the same specialist.

Direct treatment of endocarditis is largely determined by the stage of the disease and the nature of the inflammatory process. Misdiagnosis often leads to incorrect treatment. Medical errors are recognized as the most common cause of chronic infective endocarditis.

The following methods are used in the treatment of endocarditis:

• conservative treatment;
• surgery;
• prevention of complications.

Conservative treatment

Treatment of acute infective endocarditis involves taking antibiotics to kill the causative agent. Antimicrobial drugs are prescribed 1 to 2 hours after patients arrive, immediately after taking blood for bacteriological analysis. Until the results of this analysis are available ( usually a few days) the patient takes a drug selected empirically. The main requirement for it is a wide spectrum of action. After identifying the specific pathogen, the appropriate drug is prescribed.

Antibiotics used in the treatment of bacterial endocarditis

To complete the course of treatment and discontinue antibiotics, the following criteria must be met:

• stable normalization of body temperature;
• lack of colony growth on blood culture;
• disappearance of acute clinical symptoms and complaints;
• decrease in the level of ESR and other laboratory parameters to normal.

Further treatment is aimed at eliminating the inflammatory process itself. For this purpose, glucocorticosteroid drugs are used. The standard treatment regimen includes prednisolone 20 mg per day. The drug is taken after breakfast in one sitting orally ( in tablet form). Glucocorticosteroid drugs are also used to reduce acute inflammation in other forms of endocarditis. The main purpose of taking them is to prevent the formation of heart disease.

In addition to antimicrobial and anti-inflammatory treatments aimed at the underlying causes of endocarditis, patients are often prescribed a number of heart medications. They help restore the pumping function of the heart and fight the first signs of heart failure.

To maintain normal heart function in patients with chronic endocarditis, the following groups of drugs are used:

• angiotensin-converting enzyme inhibitors;
• aldosterone antagonists;
• beta blockers;
• diuretics ( diuretics);
• cardiac glycosides.

Surgery

Indications for surgical treatment of endocarditis are:

• increasing heart failure, which cannot be corrected with medication;
• accumulation of pus in the endocardial area ( in the thickness of the myocardium or near the fibrous ring of the valve);
• bacterial endocarditis in people with a mechanical heart valve;
• massive vegetations on the valve flaps ( high risk of thromboembolism).

Sanitation of an infectious focus in endocarditis consists of three stages:

• mechanical refurbishment– removal of vegetations, as well as irreversibly damaged structures and valves is carried out;
• chemical remediation– treatment of the heart chambers with an antiseptic;
• physical rehabilitation– treatment of inaccessible tissues with low-frequency ultrasound.

In the case of bacterial endocarditis, even open surgical sanitation of the heart does not always guarantee complete destruction of the infection. Therefore, surgical treatment in no case implies the abolition of drug treatment. It is only an addition to achieve a faster effect and correct irreversible disorders.

Prevention of complications

An important element of prevention is proper nutrition. The diet for endocarditis is not very different from the diet for any other cardiovascular disease ( diet number 10 and 10a). These diets are aimed at reducing the load on the heart and preventing atherosclerosis. The latter can lead to narrowing of the coronary arteries and deterioration of oxygen supply to the myocardium.

Diet number 10 recommends limiting salt intake ( no more than 5 g per day), fatty and spicy foods, alcohol. All of these foods directly or indirectly increase the load on the heart muscle and worsen heart failure.

Patients who have had endocarditis or are undergoing treatment are recommended to consume the following products:

• bran bread;
• low-fat soups;
• boiled meat or fish;
• vegetables in any form;
• pasta;
• most confectionery products ( except for dark chocolate);
• milk and dairy products.

Consequences and complications of endocarditis

The main consequences and complications of endocarditis are:

• chronic heart failure;
• thromboembolism;
• protracted infectious process.

Chronic heart failure

This problem can be solved by implanting an artificial heart valve. If the endocarditis that destroyed the valve is completely cured, the prognosis for such patients remains favorable.

Thromboembolism

If a thrombus has formed in the right parts of the ventricle, it enters the pulmonary circulation. Here it gets stuck in the vascular network of the lungs, disrupting gas exchange. Without urgent help, the patient quickly dies. This localization of a blood clot is called pulmonary embolism.

If a blood clot forms in the left side of the heart, it enters the systemic circulation. Here it can get stuck in almost any part of the body, causing corresponding symptoms. When the arteries of internal organs or the brain are blocked, there is almost always a danger to the patient’s life. If an artery in a limb becomes blocked, it can lead to tissue death and amputation.

Most often, blood clots from the left ventricle lead to blockage of the following vessels:

• splenic artery;
• cerebral arteries ( with the development of stroke);
• arteries of the limbs;
• mesenteric arteries ( with impaired blood supply to the intestines);
• retinal artery ( leads to irreversible vision loss (blindness)).

Protracted infectious process