Infectious endocarditis involving the aortic valve. Endocarditis. Abdominal organs

Infectious endocarditis (IE) is an inflammatory disease of an infectious nature with damage to the heart valves and parietal endocardium, leading to destruction of the valve apparatus. The course of the disease is acute or subacute like sepsis with circulation of the pathogen in the blood, thrombohemorrhagic and immune changes and complications.

Epidemiology of endocarditis

The incidence of IE is registered in all countries of the world and ranges from 16 to 59 cases per 1,000,000 people, in Russia - 46.3 per 1,000,000 people per year and is steadily increasing. Men get sick 1.5-3 times more often than women. The most common endocardial damage occurs at the age of about 50 years, ¼ of all cases are recorded in the age group of 60 years and older.

The increase in the incidence of IE is due to a significant increase in the number of cardiac surgeries, surgical interventions and post-injection abscesses. It is believed that the likelihood of septic endocarditis in people who use non-sterile syringes (for example, drug addiction) is 30 times higher than in healthy people.

Classification of endocarditis

A. According to the course of the disease

acute – from several days to 2 weeks;
subacute infective endocarditis;
chronic relapsing course.

B. According to the nature of the damage to the valve apparatus

primary infective endocarditis (Chernogubovsky form), which occurs on unchanged heart valves;
secondary endocarditis – develops against the background of existing pathology of the heart valves or large vessels (including in patients with artificial valves).

B. By etiological factor

streptococcal,
staphylococcal,
enterococcal,
viral,
other

When making a diagnosis, the following are taken into account: diagnostic status - ECG with a typical picture; process activity – active, persistent or repeated; pathogenesis – IE of own valves; IE of a prosthetic valve, IE in drug addicts. Localization of IE: with damage to the aortic or mitral valve, tricuspid valve, with damage to the pulmonary valve; with parietal localization of vegetation.

Causes and pathogenesis of endocarditis

The causative agents of infective endocarditis are gram-positive and gram-negative bacteria (strepto- and staphylococci, enterococci, Escherichia coli and Pseudomonas aeruginosa, Proteus), less often - fungi, rickettsia, chlamydia, viruses.

Transient bacteremia is noted both in various infections (sinusitis, sinusitis, cystitis, urethritis, etc.), and after a large number of diagnostic and therapeutic procedures, during which the epithelium colonized by various microbes is damaged. An important role in the development of infective endocarditis is played by decreased immunity due to concomitant diseases, old age, therapy with immunosuppressants, etc.

Symptoms of infective endocarditis

Clinical manifestations of IE are varied. In acute endocarditis of streptococcal and staffylococcal etiology, symptoms such as a sudden marked increase in body temperature, severe chills, signs of acute insufficiency of the affected valves and heart failure are noted. Acute endocarditis is considered a complication of general sepsis.

The disease lasts up to 6 weeks from the onset of the disease, and is characterized by rapid destruction and perforation of valve leaflets, multiple thromboembolisms, and progressive heart failure. If surgical intervention is not performed in a timely manner, IE can quickly lead to death.

Subacute infective endocarditis most often develops at the age of 35-55 years and older. Symptoms of the disease usually appear 1-2 weeks after bacteremia.

Initially, symptoms of intoxication are observed: fever, chills, weakness, night sweats, increased fatigue, weight loss, arthralgia, myalgia. The disease can occur in the form of “repeated acute respiratory infections” with short courses of antibiotic treatment.

With a long-term severe course of the disease, some patients exhibit the following characteristic symptoms:

Janeway's sign (Janeway's spots or rashes) is one of the extracardiac manifestations of infective endocarditis: an immunoinflammatory reaction in the form of red spots (ecchymoses) up to 1-4 mm in size on the soles and palms.

Osler's nodes - also a symptom of septic endocarditis - are red, painful lumps (nodules) in the subcutaneous tissue or skin.

Petechial rashes in septic endocarditis are often found on the mucous membranes of the oral cavity, conjunctiva and folds of the eyelids - the Lukin-Libman symptom.

The symptom of “drumsticks” and “watch glasses” is thickening of the distal phalanges of the fingers and the appearance of a convex shape of the nails.

Roth spots - hemorrhages on the fundus with an intact center - are not a pathognomonic symptom.
In patients with infective endocarditis, the pinch symptom (Hecht's symptom) or the tourniquet symptom (Konchalovsky-Rumpel-Leede symptom) are usually positive: when squeezing a skin fold with your fingers or pulling a limb with a tourniquet, hemorrhages appear in this area.

The development of glomerulonephritis, arthritis, myocarditis, and thromboembolic complications is possible.

There are variants of the course of infective endocarditis without fever, with damage to any one organ - nephropathy, anemia.

The presence of endocarditis should be suspected if a murmur appears over the heart area, embolism of the cerebral and renal arteries; septicemia, glomerulonephritis and suspected renal infarction; fever with the presence of prosthetic heart valves; newly developed ventricular arrhythmias; typical manifestations on the skin; multiple or “volatile” infiltrates in the lungs, peripheral abscesses of unknown etiology. The combination of fever and cerebrovascular accident in a young patient is considered a manifestation of infective endocarditis until another etiology of the disease is proven.

Diagnosis of endocarditis

History and physical examination. It is necessary to ask the patient about existing heart defects, surgical interventions on the heart valves during the last 2 months; rheumatic fever, history of endocarditis; previous infectious diseases in the last 3 months; pay attention to skin manifestations - pallor (signs of anemia), ecchymosis.

Ophthalmological manifestations - Roth spots (retinal hemorrhages with a white center, Lukin-Libman spots (petechiae on the transitional fold of the conjunctiva); transient, often unilateral blindness or impaired visual fields.

The most important sign of infective endocarditis is the appearance or change in the nature of heart murmurs as a result of damage to the heart valves.

When an aortic defect is formed, first there is a systolic murmur at the left edge of the sternum and at the V point (Botkin-Erb point), as a result of stenosis of the aortic mouth due to vegetations on the semilunar valves, then signs of aortic insufficiency appear - a gentle proto-diastolic murmur above the aorta and at the V point , worsening when standing and lying on the left side. As the valves are destroyed, the intensity of the diastolic murmur increases, and the second sound in the aorta weakens.

Symptoms of central nervous system damage manifest themselves in the form of confusion, delirium, paresis and paralysis as a result of thromboembolism, meningoencephalitis.

In acute infective endocarditis, signs of severe heart failure are revealed - bilateral moist rales, tachycardia, additional third heart sound, edema of the lower extremities.

Half of the patients have spleno- or hepatomegaly; you can often notice icterus of the sclera and slight jaundice of the skin; lymphadenopathy. The development of thromboembolic infarctions of various organs (lungs, myocardium, kidneys, spleen) is possible.

Widespread myalgia and arthralgia with predominant involvement of the shoulder, knee and sometimes small joints of the hands and feet are observed in 30-40% of cases. Myositis, tendonitis and enthesopathies, septic mono- or oligoarthritis of various localizations are rare.

Laboratory and instrumental studies:

General blood test for acute infective endocarditis - normochromic normocytic anemia, with a shift in the leukocyte formula to the left, thrombocytopenia (20% of cases), accelerated ESR.

In a biochemical blood test, dysproteinemia with an increase in the level of gamma globulins, an increase in CRB by 35-50%.

General urine analysis: macro- and microscopic hematuria, proteinuria, with the development of streptococcal glomerulonephritis - red blood cell casts.

Blood culture is an objective confirmation of the infectious nature of endocarditis when the pathogen is identified, and allows one to determine the sensitivity of the infectious agent to antibiotics.

In 5-31% of cases with IE, a negative result is possible. Serological methods are effective for IE.

ECG - against the background of IE with myocarditis or myocardial abscess - conduction disturbances, less often paroxysms of atrial tachycardia or atrial fibrillation.

EchoCG is performed in all patients with suspected IE no later than 12 hours after the initial examination of the patient. Transesophageal echocardiography is more sensitive for detecting vegetation than transthoracic echocardiography, but is more invasive.

Chest X-ray - with infective endocarditis of the right heart, multiple or “volatile” infiltrates are observed in the lungs.

Diagnostic criteria for infective endocarditis

The diagnosis of infective endocarditis is based on modified criteria developed by the Duke University Endocarditis Service:

1) positive blood culture;

2) evidence of endocardial damage - data from transthoracic echocardiography - fresh vegetation on the valve, or its supporting structures, or implanted material.

Differential diagnosis of infective endocarditis

Conducted with:

acute rheumatic fever,
systemic lupus erythematosus,
nonspecific aortoarteritis,
exacerbation of chronic pyelonephritis,
some other diseases

Treatment of endocarditis

Treatment goals: elimination of the pathogen, prevention of complications.

Indications for hospitalization: patients without complications and stable hemodynamics - in general wards; patients with severe heart failure and complications are sent to the intensive care unit.

Drug treatment

Antimicrobial therapy begins immediately after diagnosis. Bactericidal antibiotics are used, which are administered parenterally. For unknown pathogens, high-dose empiric antibiotic therapy is performed. All patients with proven streptococcal etiology should be treated in hospital for at least 2 weeks.

Infectious endocarditis caused by Streptococcus viridans, with damage to the valves:

Benzylpenicillin (sodium salt) IV or IM 12-20 million units 4-6 times a day, 4 weeks, or gentamicin 3 mg/kg per day (no more than 240 mg/day) 2-3 times a day ; Ceftriaxone IV or IM 2 g/day once a day, 4 weeks. This therapy allows clinical and bacteriological remission in 98% of cases of IE.

A dosage of gentamicin in mg/kg in obese patients will produce higher serum concentrations than in lean patients. Relative contraindications to the use of gentamicin are patients over 65 years of age, renal failure, and auditory neuritis.

The following are used as alternative antibiotics:

Amoxicillin / clavulanic acid IV or IM 1.2-2.4 g 3-4 times a day, 4 weeks or Ampicillin / sulbactam IV or IM 2 g 3-4 times a day, 4 weeks

Vancomycin is the drug of choice in patients with allergies to penicillin and other lactams. With prolonged intravenous use of vancomycin, fever, allergic rash, anemia, and thrombocytopenia may occur. It has oto- and nephro-toxicity.

Infectious endocarditis caused by Staphylococcus aureus:

Oxacillin IV or IM 2 g 6 times a day, 4-6 weeks + gentamicin IV or IM 3 mg/kg 1-3 times a day (added at the doctor’s discretion for 3-5 days ), 4-6 weeks; or cefazolin or cephalothin IV or IM 2 g 3-4 times a day, 4-6 weeks + gentamicin IV or IM 3 mg/kg 1-3 times a day, 4-6 weeks ; or cefotaxime IV or IM 2 g 3 times a day, 4-6 weeks + gentamicin IV or IM 3 mg/kg 1-3 times a day (added at the doctor’s discretion for 3-5 days), 4-6 weeks; or imipenem / cilastatin IV or IM 0.5 g 4 times / day, 4-6 weeks; or meropenem IV or IM 1 g 3 times a day, 4-6 weeks; or vancomidine IV or IM 1 g 2 times a day, 4-6 weeks; or rifampicin orally 0.3 g 3 times a day, 4-6 weeks.

Penicillin is prescribed in the case of S. aureus that is sensitive to it as an alternative drug: benzylpenicillin (sodium salt) IV 4 million units 6 times a day, 4-6 weeks.

Treatment when methicillin-resistant strains of staphylococci are identified. As a rule, they are resistant to cephalosporins and carbapenems, so the use of these drugs is not advisable: vancomidine IV 1 g 2 times a day, 4-6 weeks; linezolid IV 0.6 g 2 times a day, 4-6 weeks. Linezolid is characterized by high bioavailability, reaching 100%, and good absorption from the gastrointestinal tract; it is suitable for stepwise antimicrobial therapy: starting treatment with intravenous infusions followed by transition to oral forms of drugs.

Treatment of infective endocarditis caused by methicillin-sensitive staphylococcus within 1 year after valve replacement surgery:

Oxacillin IV 2 g 6 times a day, 4-6 weeks + gentamicin IV 3 mg/kg 1-3 times a day, 2 weeks + rifampicin IV 0.3 g 2 times a day (can be administered orally), 4-6 weeks. If you are allergic to penicillin, oxacillin can be replaced with cephalosporins or vancomycin.

If adequate antibiotic therapy is ineffective within a week, with severe hemodynamic disturbances and the development of refractory heart failure, the formation of a myocardial abscess or valve ring, cardiac surgical treatment is indicated - removal of the affected valve followed by its replacement.

Prognosis for endocarditis

With timely antibiotic therapy, the prognosis is quite favorable. With fungal infective endocarditis, the mortality rate reaches 80% or more. In the case of chronic heart failure, the mortality rate is more than 50% in the next 5 years.

Prevention of endocarditis

Antibiotics should be prescribed to patients from high and moderate risk groups: prosthetic heart valve, hemodialysis, complex congenital heart disease, surgical vascular conduits, a history of infective endocarditis, mitral valve prolapse, therapy with corticosteroid drugs and cytostatics, infection of an intravenous catheter, surgical interventions and post-injection abscesses.

INFECTIOUS ENDOCARDITIS, ACUTE AND SUBACUTE is a disease that occurs acutely or subacutely like sepsis, characterized by inflammatory or destructive changes in the valvular apparatus of the heart, parietal endocardium, endothelium of large vessels, circulation of the pathogen in the blood, toxic damage to organs, the development of immunopathological reactions, and the presence of thromboembolic complications.

The cause of this disease is pathogens such as streptococci, staphylococci, enterococci.

For the development of infective endocarditis, the presence of bacteremia, endocardial injury, and weakening of the body's resistance are necessary. Massive entry of the pathogen into the bloodstream and its virulence are necessary but not sufficient conditions for the development of infective endocarditis. In a normal situation, a microorganism in the vascular bed cannot attach to the endothelium, since it is more often absorbed by phagocytes. But if the pathogen is captured “in the network” of a parietal thrombus, the structures of which protect it from phagocytes, then the pathogenic agent multiplies at the site of fixation. Implantation of the pathogen is often in places with slow blood flow, damaged endothelium and endocardium, where favorable conditions are created for the establishment of a colony of microorganisms inaccessible to destruction in the bloodstream.

Acute infective endocarditis occurs as a complication of sepsis, is characterized by the rapid development of valvular destruction and lasts no more than A-5 weeks. Subacute course is more common (lasting more than 6 weeks). A characteristic symptom is a wave-like fever, a high low-grade fever, and fever suppositories against the background of normal or low-grade fever. Skin type like coffee with milk. Endocardial damage is manifested by the development of mitral and aortic defects. Lung damage due to infective endocarditis is manifested by shortness of breath, pulmonary hypertension, and hemoptysis. Enlargement of the liver is associated with the reaction of the organ mesenchyme to the septic process. Kidney damage manifests itself in the form of glomerulonephritis, infectious toxic nephropathy, renal infarction, and amyloidosis. Damage to the central nervous system is associated with the development of meningitis, meningoencephalitis, parenchymal or subarachnoid hemorrhages. Damage to the organs of vision is manifested by the sudden development of retinal vascular embolism with partial or complete blindness, and the development of uveitis.

Diagnostics

Based on complaints, clinic, laboratory data. In a general blood test - anemia, leukocytosis or leukopenia, an increase in ESR, in a biochemical blood test - a decrease in albumin, an increase in globulins, an increase in C-reactive protein, fibrinogen. Positive blood culture for pathogens typical for infective endocarditis. Echocardiography allows you to identify the morphological sign of infective endocarditis - vegetation, assess the degree and dynamics of valvular regurgitation, diagnose valve abscesses, etc.

Differential diagnosis

With rheumatism, diffuse connective tissue diseases, fever of unknown origin.

Subacute infective endocarditis

Subacute infective endocarditis (PIE) in most cases is diagnosed in a comprehensive clinical picture. From the moment the first clinical symptoms appear until diagnosis is made, it often takes 2-3 months. 25% of all cases of PIE are diagnosed during cardiac surgery or autopsy.

PIE Clinic. In classic cases, fever with chills and increased sweating comes first. An increase in body temperature from subfebrile to hectic occurs in 68-100% of patients. Often the fever has a wave-like character, which is associated either with a respiratory infection or with an exacerbation of a chronic focal infection. Staphylococcal PIE is characterized by fever, chills that last for weeks, and profuse sweating. In some patients with PIE, body temperature rises only at certain times of the day. At the same time, it can be normal when PIE is combined with glomerulonephritis, renal failure, severe cardiac decompensation, especially in older people. In such cases, it is advisable to measure the temperature every 3 hours for 3-4 days and not prescribe antibiotics.

Sweating can be both general and local (head, neck, front half of the body, etc.). It occurs when the temperature drops and does not bring improvement in well-being. With streptococcal sepsis, chills are observed in 59% of cases. In most cases, it is impossible to identify the entrance gates of infection during PIE. Thus, fever, chills, and increased sweating are a characteristic triad of subacute sepsis.

Among the phenomena of intoxication, loss of appetite and performance, general weakness, weight loss, headache, arthralgia, and myalgia are noted. In some patients, the first symptom of the disease is embolism in the vessels of the systemic circulation. Embolism in the vessels of the brain is interpreted as an atherosclerotic lesion in the elderly, which makes timely diagnosis difficult. During inpatient observation, such individuals are found to have an increase in temperature, anemia, and an increase in ESR to 40-60 mm/hour. Such a clinic is observed in streptococcal sepsis.

At the onset of the disease, symptoms such as shortness of breath, tachycardia, arrhythmia, and cardialgia are rarely diagnosed. Approximately 70% of patients with PIE have pale skin with a yellowish tint (“coffee with milk”). Petechiae are found on the lateral surfaces of the body, arms, and legs. It is quite rare to have a positive Lukin-Libman symptom. Osler's nodes are located on the palms in the form of small, painful red nodules. Hemorrhagic rashes occur with subacute staphylococcal sepsis. Necrosis may develop due to hemorrhages in the skin. The above-mentioned skin changes are caused by immune vasculitis and perivasculitis. Mono- and oligoarthritis of large joints, myalgia and arthralgia are diagnosed in 75% of patients. Over the past decades, the clinic of primary PIE has changed, skin lesions are becoming less common.

The pathognomonic symptom of PIE is heart murmurs, which occur due to valve damage with the development of aortic regurgitation. Diastolic murmur, which is best heard in a sitting position with the body tilted forward or to the left, has diagnostic significance. With the gradual destruction of the aortic valve leaflets, the intensity of the diastolic murmur along the left edge of the sternum increases, and the second sound above the aorta becomes weaker. There is a decrease in diastolic blood pressure to 50-60 mm Hg. Art. with a significant difference in pulse pressure. The pulse becomes high, fast, strong (altus, celer, magnus) - Corrigan's pulse. The borders of the heart shift to the left and down. Aortic valve insufficiency can develop within 1-2 months.

Much less often, the mitral or tricuspid valve is affected in primary PIE. Damage to the mitral valve is indicated by the presence and increase in intensity of systolic murmur at the apex of the heart with a weakening of the first sound. Due to mitral regurgitation, the cavity of the left ventricle (LV) and atrium later increases. Damage to the tricuspid valve with insufficiency is diagnosed in drug addicts. Of diagnostic significance is the increase in systolic murmur over the xiphoid process of the sternum, which intensifies at the height of inspiration, preferably on the right side (Rivero-Corvalo symptom). Often tricuspid insufficiency is combined with recurrent thromboembolism of small and medium branches of the pulmonary artery. In secondary PIE, bacterial inflammation of the valves develops against the background of rheumatic or congenital heart disease. Since destructive processes occur when intracardiac hemodynamics are disturbed, during dynamic observation the intensity of the noise increases or a new valve noise appears. Sometimes a peculiar musical noise may be heard - a “bird squeak”. Its appearance is caused by perforation of the valve leaflets, and acute left ventricular heart failure may develop. The purulent-metastatic process from the valves can spread to the myocardium and pericardium with the development of myopericarditis. Damage to the myocardium and pericardium is indicated by an increase in chronic cardiac decompensation, arrhythmia, heart block, pericardial friction noise, etc.

An important syndrome of PIE is thromboembolic and purulent-metastatic complications. Purulent metastases reach the spleen (58.3%), brain (23%), lungs (7.7%). Cases of embolism of the spinal cord with paraplegia, coronary vessels of the heart with the development of myocardial infarction, and the central retinal artery with blindness in one eye have been described. With embolism, the spleen is moderately enlarged in size, and on palpation on the right side it is soft and sensitive. Sharp pain is observed with perisplenitis or splenic infarction. Enlargement and damage to the spleen are diagnosed using methods such as computed tomography, ultrasound, and scanning.

In second place after damage to the spleen is kidney damage. Gross hematuria with proteinuria and severe pain in the lower back are characteristic of thromboembolism and microinfarction of the kidney. In some cases, primary IE begins as diffuse glomerulonephritis (“renal mask PIE”). It is characterized by microhematuria, proteinuria, and increased blood pressure. Of great importance in glomerulonephritis is immune complex inflammation with the deposition of immune deposits on the basement membrane. Kidney damage in PIE worsens the prognosis due to the risk of developing chronic renal failure.

Changes in the blood depend on the severity of the septic process. Acute IE is characterized by rapidly progressive hypochromic anemia with an increase in ESR to 50-70 mm/h, which develops over 1-2 weeks. Hypo- or normochromic anemia is diagnosed in half of patients with PIE, and a decrease in hemoglobin levels occurs within several months. With cardiac decompensation, there is no increase in ESR. The number of leukocytes ranges from leukopenia to leukocytosis. Significant leukocytosis indicates the presence of purulent complications (abscess pneumonia, heart attacks, embolisms). In acute IE, leukocytosis reaches 20-10 to the ninth power/l with a shift to the left (up to 20-30 band neutrophils).

Of the auxiliary diagnostic methods, urine examination is of particular importance, in which proteinuria, cylindruria, and hematuria are found. In the blood there is dysproteinemia with a decrease in albumin levels, an increase in alpha-2 and gamma globulins up to 30-40%. PIE is characterized by hypercoagulation of the blood with an increase in the level of fibrinogen and C-protein. Electrocardiography reveals extrasystolic arrhythmia, atrial fibrillation and flutter, and various conduction disturbances in persons with myopericarditis.

Other news

Infectious endocarditis is an inflammatory process of infectious origin that affects the inner lining of the heart (endocardium), which lines its chambers and valves.

The incidence of infective endocarditis, according to various authors, ranges from 3 to 10 cases per 100,000 population. Women get sick half as often as men.

Infectious endocarditis is an infectious polyposis-ulcerative inflammation of the endocardium

Causes and risk factors

For the development of infective endocarditis, a combination of several factors is necessary:

damage to the endothelium of blood vessels and endocardium;
transient bacteremia (temporary circulation of pathogenic or opportunistic microorganisms in the bloodstream);
decreased general immunity;
disturbance of hemodynamics and hemostasis.

The cause of transient bacteremia usually lies in a source of chronic infection in the body or in the performance of invasive (that is, damage to the integrity of the skin) medical procedures.

The most common causative agent of the subacute form of infective endocarditis is viridans streptococcus.

The acute form of the disease can be caused by:

Staphylococcus aureus;
Pneumococcus;
enterococcus;
coli.

Infectious endocarditis caused by fungal infection, anaerobic and gram-negative pathogens is very difficult. Fungal endocarditis is caused by long-term antibiotic therapy or a catheter left in the vein for a long time.

Microorganisms circulating in the bloodstream penetrate into the cavities of the heart and adhere to the endocardium. This process is called adhesion, the conditions for its occurrence are immunity disorders, as well as congenital or acquired defects of the valve apparatus.

Infectious endocarditis is fraught with serious complications that can lead to death: acute heart failure, septic shock, multiple organ failure, etc.

Hemodynamic disturbances caused by heart defects contribute to the occurrence of microtraumas of the endocardium and valves. Through these injuries, infectious agents penetrate the endocardium. Microbial colonies very quickly destroy the valves, as a result of which they can no longer perform their functions, and the patient develops rapidly progressive heart failure.

Against the background of infective endocarditis, immune damage occurs to the endothelium (inner layer) of the capillaries of the mucous membranes and skin. This is manifested by symptoms of hemorrhagic capillarotoxicosis or thrombusculitis.

Forms of the disease

Depending on the cause of its occurrence, infective endocarditis occurs:

primary - an infectious process in the endocardium develops against the background of initially unchanged valves;
secondary - an infection in the endocardium develops against the background of an existing pathology of the valve apparatus or blood vessels.

Based on the nature of the course, the following forms of infective endocarditis are distinguished:

acute – occurs as a complication of medical manipulations on blood vessels, the heart or an acute septic condition, lasts 1.5-2 months;
subacute – occurs with insufficiently active treatment of the underlying disease or acute form of endocarditis, lasts more than 2 months;
protracted – characterized by a slow course and the absence of an obvious primary purulent-septic focus.

According to the activity of the inflammatory process, infective endocarditis can be active or inactive (healed).

The inflammatory-destructive process can be limited (only the heart valve leaflets are affected) or extend beyond the affected valve.

Stages of the disease

The clinical course of infective endocarditis is divided into several stages:

Infectious-toxic. It is characterized by transient bacteremia and the formation of microbial vegetations (colonies) on the heart valves and endocardium.
Immune-inflammatory (infectious-allergic). Symptoms of damage to internal organs are characteristic, that is, signs of splenomegaly, nephritis, hepatitis, myocarditis.
Dystrophic. Develops against the background of progressive heart failure and septic process. It manifests itself as severe irreversible damage to internal organs, including myocardial necrosis.

Without treatment, infective endocarditis is fatal within 1.5–6 months from the onset of the first symptoms.

Symptoms

The acute form of infective endocarditis is clinically characterized mainly by signs of toxemia and bacteremia. These include:

severe general weakness;
increased fatigue;
decreased appetite;
weight loss;
dyspnea;
an increase in body temperature to high levels, which is accompanied by tremendous chills;
profuse sweating when body temperature drops;
Iron-deficiency anemia;
sallow skin color;
petechiae (pinpoint hemorrhages) on the mucous membranes and skin;
pinch symptom (bruise formation due to minor skin trauma).

Against the background of infective endocarditis, most patients experience damage to the heart muscle itself (myocarditis). When auscultating the heart, functional murmurs are heard, the appearance of which is explained by valve damage and anemia.

Damage to the aortic and (or) mitral valve leaflets is accompanied by the appearance and progression of signs of their insufficiency, as well as heart failure.

In subacute infective endocarditis, thrombotic deposits are torn off from the leaflets of the affected heart valves, which can result in embolism of the blood vessels of the spleen, kidneys, and brain with the formation of infarction (necrosis) of these organs. The examination reveals:

enlarged liver and spleen (hepatosplenomegaly);
polyarthritis;
diffuse (less often focal) glomerulonephritis.

Diagnostics

When collecting anamnesis, special attention should be paid to previous medical interventions and the presence of foci of chronic infection. Confirmation of the diagnosis of infective endocarditis is carried out according to laboratory and instrumental examination of the patient, including:

general blood test (leukocytosis, shift of the leukocyte formula to the left, significant increase in ESR);
bacteriological blood culture with determination of sensitivity to antibiotics. This analysis is repeated several times, and blood sampling is best done at the height of the fever;
blood chemistry. There are changes in the immune status (the concentration of anti-tissue antibodies increases, the hemolytic activity of complement decreases) and the protein spectrum (the concentration of α-globulins increases, and subsequently γ-globulins);
EchoCG. Helps visualize microbial vegetations with a diameter of more than 5 mm on heart valves;
magnetic resonance or multislice computed tomography. Allows you to assess with a high degree of accuracy the condition of the valves, as well as the entire heart as a whole.

Treatment

In case of infective endocarditis, the patient is hospitalized; strict bed rest is indicated. An important element of therapy is the organization of proper nutrition. The diet should be balanced in the content of nutrients, vitamins and microelements, and consist of easily digestible dishes.

The main treatment is medication. Antibiotics are prescribed taking into account the sensitivity of the microflora; broad-spectrum antibiotics are used until the results of the antibiogram are obtained.

The incidence of infective endocarditis, according to various authors, ranges from 3 to 10 cases per 100,000 population. Women get sick half as often as men.

Treatment of infective endocarditis of fungal etiology is carried out with amphotericin B over a long course (up to several months). In complex drug therapy of the disease, other agents with antimicrobial properties (antistaphylococcal globulin, antistaphylococcal plasma, dioxidine) can also be used.

Methods of extracorporeal detoxification are indicated (intravascular ultraviolet irradiation of blood, plasmapheresis, hemosorption).

In the presence of concomitant diseases (nephritis, polyarthritis or myocarditis), non-steroidal anti-inflammatory drugs are added to the treatment regimen.

If the heart valves are destroyed with the development of their insufficiency after the inflammatory process subsides, surgical intervention to replace the valves is performed.

Possible complications and consequences

The most dangerous complications of infective endocarditis that can lead to death are:

acute heart failure;
respiratory distress syndrome;
embolism in the vessels of the brain or heart;
septic shock;
multiple organ failure.

Forecast

The prognosis for infective endocarditis is always serious. Without treatment, the disease ends in death within 1.5–6 months from the onset of the first symptoms. With timely antibiotic therapy, the mortality rate is 30%. In approximately 15% of patients, infective endocarditis takes a chronic course, in which periods of remission are followed by periods of exacerbation.

Prevention

Patients at risk for the development of infective endocarditis (with congenital or acquired heart defects, prosthetic valves, vascular pathology, foci of chronic infection in the body) should be under medical supervision.

To prevent the occurrence of bacteremia during invasive medical procedures, broad-spectrum antibacterial drugs should be prescribed.

Also, to prevent the development of infective endocarditis it is necessary:

regularly sanitize foci of chronic infection in the body;
avoid bacterial and viral infections, and if they occur, carry out timely treatment;
avoid hypothermia;
adhere to proper nutrition;
carry out hardening procedures.

Video from YouTube on the topic of the article:

Infective endocarditis (IE) is a serious disease with a high mortality rate. Without treatment, the mortality rate for IE is 100%. In recent years, there has been a significant increase in the number of patients with endocarditis in our country and abroad. According to various authors, today the incidence has increased in the elderly and senile, as well as among people under the age of 30 who use intravenous drugs.

It is known that IE is a disease of an infectious nature with the primary localization of the pathogen on the heart valves, parietal endocardium, occurring with manifestations of systemic infection, vascular complications and an immune reaction.

Traditionally, the development of IE is associated with the presence of “intracardiac” risk factors, which include congenital and acquired heart defects, the presence of prosthetic valves, valve prolapse and other anomalies. In recent years, patients with focal infection, as well as people who have had invasive research methods, including the installation of a subclavian catheter, have been classified as high-risk individuals. A special risk group consists of drug addicts who practice intravenous drug administration, in whom IE occurs with damage to intact heart valves.

This paper summarizes the experience of diagnosing and managing patients with IE on the basis of the general therapeutic department of the Alexander Hospital in St. Petersburg for the period 1998-2003. Diagnosis of the disease was carried out in accordance with Duke criteria. The diagnosis of IE was assessed as reliable if two main criteria were present, namely:

when a pathogen typical for IE is isolated from a patient’s blood culture;
when determining echocardiographic signs of endocardial damage - mobile vegetations on the heart valves, abscesses in the area of the valve prosthesis; formation of intracardiac fistulas, etc., in combination with three and/or five auxiliary criteria, which included vascular complications (embolism of large arteries, septic pulmonary infarctions, intracranial hemorrhages, etc.), immunological phenomena (glomerulonephritis, Osler’s nodes, hemorrhagic vasculitis and etc.), as well as febrile fever, hepato-splenomegaly and other manifestations of systemic infection.

We examined 105 patients with IE, of which in 80 people aged 18 to 30 years (first group), the main risk factor for the disease was injection drug addiction.

In the second group of patients (25 people), the main predisposing factors for the development of IE were congenital and acquired heart defects, as well as prosthetic valves.

In people of the older age group, an additional risk factor was degenerative-dystrophic changes in the heart valves.

The relationship between the nature of heart valve damage and risk factors for IE is presented in.

According to an echocardiographic study, 100% of patients in the first group had mobile vegetations on the leaflets of the tricuspid valve (TV), which was accompanied by the formation of its insufficiency of degrees I-III.

In the second group of patients with IE, there was damage to the left chambers of the heart with the formation of vegetations on the leaflets of the aortic and mitral valves. Isolated damage to the mitral valve was observed in two people with rheumatic heart disease (mitral stenosis), in one patient with a congenital ventricular septal defect, and in a single case of an obstructive form of hypertrophic cardiomyopathy.

Among elderly and senile people, nine people (36%) had isolated damage to the aortic valve in the absence of signs of aortic stenosis. Along with this, in five patients (20%) aged from 72 to 87 years, IE developed against the background of an aortic defect of atherosclerotic origin, and in all five, combined damage to the aortic and mitral valves was detected. Degenerative-dystrophic changes in other heart valves were detected in 100% of patients in the older age group.

The formation of vegetations on the aortic valve leaflets was observed in two patients with the tertiary form of syphilis against the background of an existing aortic defect associated with a specific process in the aorta.

In two cases, we observed the development of endocarditis of prosthetic valves.

When comparing the results of blood cultures in two groups of patients, significant differences were determined both in the frequency of microbial flora isolation and in the species composition of endocarditis pathogens. According to our data, the causative agent of IE in drug addicted patients in 71.3% of cases (57 people) was Staphylococcus aureus, while in the second group, along with coccal flora, gram-negative microorganisms were more often found (28%). Negative blood culture results were observed significantly less often in the first than in the second group of patients with IE: 18.7% and 56%, respectively. Data regarding the etiological structure of IE in the studied groups of patients are presented in.

Clinical characteristics and features of the course of IE

The clinical course and nature of complications of infective endocarditis largely depend on the localization of valve vegetations - in the right or left chambers of the heart, as well as the degree of virulence of the causative agent of the disease.

The course of IE in drug addicted patients was particularly severe and polysyndromic. The reason for hospitalization in most patients was acute complications of the underlying disease. A significant proportion of patients were admitted to the intensive care unit of the hospital with clinical symptoms of unilateral or bilateral multifocal pneumonia, the cause of which was septic thromboembolism of the branches of the pulmonary artery (72% of patients). The course of pneumonia was accompanied by severe respiratory failure, often with the development of respiratory distress syndrome (RDS) and foci of destruction in the lungs (12%). Manifestations of secondary nephropathy, which were found in 100% of patients in the first group, were sometimes mistakenly interpreted as an exacerbation of chronic glomerulo- or pyelonephritis, urolithiasis, which served as a reason for hospitalization of these patients in the urological and nephrological departments.

In the second group of patients, the main reason for hospitalization was prolonged febrile fever in combination with anemia and hepatolienal syndrome. Along with this, in five people (20%) the reason for hospitalization was progressive heart failure.

The main clinical syndromes observed in patients with IE of the first and second groups are presented in.

According to our observations, a characteristic feature of the clinical course of IE in drug addicted patients was a high incidence of septic pulmonary embolism with the formation of multiple foci of infiltration in the lungs. In many patients, pulmonary thromboembolism was recurrent (31.3% of patients) and was often complicated by the development of destructive foci in the lungs.

The formation of vegetations in 100% of patients of the first group was accompanied by tricuspid valve insufficiency of the I-III degree with the formation of regurgitant flows. At the same time, in most patients there were no severe disturbances of central hemodynamics associated with TC dysfunction. In this group of patients, a characteristic clinical feature was the reversible nature of hemodynamic disorders during therapy. Acute heart failure with dilatation of the heart cavities and a decrease in ejection fraction to 40% or lower was observed in 28 patients (35.3%) due to the addition of acute myocarditis or against the background of concomitant damage to the heart valves.

Secondary nephropathy was one of the most common syndromes in the first group of patients with IE. Acute renal failure was observed in 16 patients, and in 10 of them it was reversible and was associated with acute disseminated intravascular coagulation syndrome, as well as acute heart failure with edema. Infectious-toxic nephropathy was recorded in 73.8% of cases and was accompanied by urinary syndrome - hematuria, proteinuria, leukocyturia - with a sufficient level of glomerular filtration.

A characteristic feature of IE in the second group was the subacute course of the disease with a long period of fever at the prehospital stage, and in the elderly and senile age the fever was subfebrile in nature with rare rises in temperature to febrile levels.

Most patients with subacute infective endocarditis (PIE) were admitted to the hospital at the stage of a developed clinical picture of the disease with clinical signs of thromboembolism of vessels in the systemic circulation. In this group of patients, the most common complications should be recognized as cerebral embolism with the development of ischemic and hemorrhagic strokes, embolism of the renal vessels with pain and hematuria, as well as the formation of acute focal changes in the myocardium associated with embolism of the coronary vessels or covering the mouths of the coronary arteries with vegetations .

Septic thromboembolism of cerebral vessels was often accompanied by the development of purulent meningoencephalitis with a fatal outcome. At the same time, blood cultures of 56% of patients in the second group did not show growth of microbial flora. Noteworthy is the fact that septicemia in patients with positive blood culture results in 28% of cases was caused by gram-negative microflora. In this category of patients, the source of bacteremia was foci of chronic infection in the genitourinary system, and in two patients (according to autopsy) bilateral apostematous nephritis was detected.

A significant number of patients with PIE (62%) showed signs of acute circulatory failure with congestive wheezing in the lungs, pulmonary hypertension, enlarged cardiac cavities and peripheral edema.

In this group of patients, prerenal azotemia and acute renal failure associated with the development of acute circulatory failure were observed more often than in the first group.

Acute diffuse myocarditis, typical manifestations of which were various rhythm disturbances, was diagnosed in 27% of patients in the second group.

Anemia with a decrease in hemoglobin level to 80 g/l or less was detected in 100% of patients in the second group. A significant increase in ESR (more than 45 mm/h) was observed in 85.8% of patients with subacute IE.

Skin changes in the form of hemorrhagic rashes, Henoch-Schönlein purpura, as well as other manifestations of immune inflammation in both groups of patients were uncommon - 6.3 and 4% in the first and second groups, respectively.

Treatment of patients with IE

Conservative therapy of patients with IE was carried out using broad-spectrum antibiotics in combination with detoxification, anticoagulant and metabolic therapy. As part of antibacterial therapy, patients received cephalosporins of III-IV generations in combination with aminoglycosides and metronidazole. From the group of cephalosporins, the following were prescribed: ceftriaxone (Longacef) 2 g per day intravenously (IV), or cefotaxime (Talcef) 2 g per day IV, or cefepime (Maxipim) 2 g per day IV in combination with aminoglycosides ( amikacin in a daily dose of 1.5 g intravenously) and metronidazole 1.5-2 g per day intravenously. If such therapy was ineffective or there were contraindications to the above drugs, antibiotics of the lincosamine group were used: clindamycin 1.2 g per day IV or lincomycin 3 g per day IV in combination with fluoroquinolones (ciprofloxacin 400 mg per day i.v. /V). In the intensive care unit, therapy was carried out for five to seven days with imipinem (thienam) at a dose of 2-4 g per day intravenously or rifampicin at a daily dose of 0.45-0.6 g intravenously. The average duration of antibiotic therapy in the study group of patients was 28 + 3.5 days.

Detoxification therapy included intravenous infusions of rheopolyglucin, hemodez, polarizing mixtures in combination with loop diuretics. The volume of administered fluid averaged 2-2.5 liters per day. During the entire period of infusion therapy, the functional state of the kidneys, electrolyte composition of the blood, and daily diuresis were monitored. In the intensive care unit, CVP monitoring was carried out in all patients. Infusion therapy was carried out throughout the entire acute period of the disease until the manifestations of intoxication syndrome were relieved. The average course duration was 22 + 4.5 days.

The development of pulmonary embolism, especially in combination with signs of acute disseminated intravascular coagulation syndrome in the hypercoagulable stage, served as the basis for prescribing anticoagulant therapy. The initial dose of heparin was 10 thousand units intravenously, in a stream, then - 1000 units per hour intravenously, drip with a transition to subcutaneous administration up to 30 thousand units per day. Heparin was administered under the control of coagulogram parameters and blood clotting time. At the same time, intravenous transfusions of fresh frozen plasma were carried out at a rate of 300 ml per day with the addition of 2500-5000 units of heparin. Severe anemia (Hb less than 80 g/l, Ht ≤25) was corrected by red blood cell transfusions (five to seven doses). In the presence of hypoproteinemia, the administration of solutions of amino acids, albumin or native plasma was used. Identification of clinical and radiological signs of pulmonary edema against the background of recurrent septic pulmonary embolism served as an indication for the prescription of corticosteroids (prednisolone from 120 to 200 mg per day intravenously). Therapy with direct-acting anticoagulants in combination with cryoplasma transfusions was carried out until there was a sustained improvement in hemostasis. The criteria for normocoagulation were the level of fibrinogen in plasma 3-4 g/l, the absence of thrombocytopenia, normalization of CVV, aPTT, thrombin time, as well as negative paracoagulation tests. According to our data, relief of the manifestations of acute DIC at the hypercoagulation stage in 75% of patients was observed on the seventh to tenth day from the start of complex therapy.

Some patients developed resistance to the ongoing antibacterial therapy, which was characterized by an increase in intoxication, febrile fever, progressive anemia, as well as blood cultures of the causative agent of IE - Staphylococcus aureus - in 65% of cases. During X-ray examination of this category of patients, foci of destruction of lung tissue were detected with a high frequency, and in three patients there was purulent effusion in the pleural cavity.

Long-term use of broad-spectrum antibiotics in 70.3% of patients (38 people) was accompanied by the development of side effects of antibacterial therapy. Candidiasis of the oral cavity, pharynx, esophagus, as well as intestinal dysbiosis of stage III-IV was detected in 36 patients (66.7%). The use of antibiotics with hepatotoxic properties (cephalosporins, lincosamines, metronidazole) in two patients (3.7%) with chronic hepatitis C and B led to the progression of liver failure, which was accompanied by high fermentemia (ALT 1500 IU, AST 1000 IU) and jaundice.

The development of congestive heart failure with the appearance of acrocyanosis, moist rales in the basal parts of the lungs, peripheral edema in combination with cardiomegaly and a drop in ejection fraction to 50-45% was observed in five patients (9.3%) against the background of massive infusion therapy.

Long-term anticoagulant therapy in 20.4% (11 people) of observations was accompanied by an increase in plasma tolerance to heparin, which was clinically expressed in the development of peripheral phlebothrombosis, while we did not observe heparin-induced thrombocytopenia in the examined group of patients.

Positive results of conservative therapy were obtained in 70.2% of patients (56 people) with TC lesions and only in 32% of patients (6 people) from the second group. The outcome of IE in both groups of patients was the formation of heart valve insufficiency.

Hospital mortality for IE in drug addicts was 29.4% (24 people), while in patients with damage to the left chambers of the heart (second group) the mortality rate was 68% (19 people).

According to autopsy data, the main causes of death in patients with IE were:

septicopyemia with the formation of purulent foci in the liver, kidneys, spleen, brain with the development of multiple organ failure (46.2%);
heart failure due to polyposis-ulcerative endocarditis with destruction of the heart valves, as well as acute myocarditis with dilatation of the heart cavities (39.4%);
secondary nephropathy with the development of renal failure, pulmonary edema, cerebral edema (14.4%).

Thus, the characteristic features of IE in people with drug addiction are an acute course of the disease with damage to the right chambers of the heart and relapses of septic pulmonary embolism. The causative agent of IE in 71.3% of injection drug users is highly virulent Staphylococcus aureus. The formation of tricuspid valve insufficiency of degrees I-III has become the most common complication of IE in drug addicts. Moreover, most patients do not experience severe disturbances of central hemodynamics leading to the development of acute circulatory failure.

Subacute IE in patients with predisposing heart diseases, as well as in elderly and senile people, occurs with predominant damage to the left chambers of the heart, and monovalvular damage predominates in the older age group. The presence of concomitant pathology in people over 60 years of age masks the course of the underlying disease, which is responsible for late diagnosis and high mortality of patients. The protracted course of IE is characterized by low inoculability of the pathogen compared to acute forms of the disease. The development of thromboembolism of vessels in the systemic circulation is a characteristic clinical feature of subacute IE.

A positive effect from conservative therapy is observed in the majority of patients with IE with TC lesions, while in subacute endocarditis of the left chambers of the heart, conservative therapy is ineffective in most patients.

Hospital mortality in both groups of patients is due to dissemination of the pathogen with the formation of purulent foci and multiple organ failure, as well as the development of acute circulatory failure and secondary nephropathy.

Literature

Butkevich O. M., Vinogradova T. L. Infective endocarditis. - M., 1997.
Simonenko V. B., Kolesnikov S. A. Infective endocarditis: current course, diagnosis, principles of treatment and prevention. - Wedge. Med., 1999. - 3. - P. 44-49.
Tazina S. Ya., Gurevich M. A. Modern infective endocarditis. - Wedge. med., 1999. - 12. - pp. 19-23.
Bansal R. C. Infective endocarditis. Med Clin North America 1995; 79 (5): 1205-1239.
Bayer A. S., Bolger A. F., Taubert K. A. et al. Diagnosis and management of infective endocarditis and its complications. Circulation 1998; 98: 2936-2948.
McKinsey D. S., Ratts T. E., Bisno A. I. Underlying cardiac lesions in adults with infective endocarditis. The changing spectrum. Amer J Med 1987; 82: 681-688.
Lamas C. C. Eykyn S. J. Suggested modifications to the Duke criteria for the clinical diagnosis of native valve and prosthetic valve endocarditis: analysis of 118 pathologically proven cases. Clin Infect Dis 1997; 25: 713-719.
Durack D. T., Lukes A. S., Bright D. K. et al. New criteria for diagnosis of Infective Endocarditis Utilization of Specific Echocardiographic Finding. Amer J Med 1994; 96: 200-209.
Tyurin V.P., Dubinina S.V. Infectious endocarditis in elderly and senile people. - Wedge. Med., 2000. - 4. - P. 53-56.

V. I. Ulanova
V. I. Mazurov, Doctor of Medical Sciences, Professor
Medical Academy of Postgraduate Education, St. Petersburg

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HISTORICAL DATA

Subjective data

Upon admission, he complained of spontaneous shortness of breath at rest and poor sleep.

At the time of supervision, he made no complaints.

History of the development of the present disease

The patient considers himself sick since October 13, 2015. The onset of the disease is acute. The patient noted shortness of breath, increased sweating, and paroxysmal pain in the lower third of the sternum radiating to the epigastrium. On 10/15/15 he called an ambulance due to shortness of breath, without previous physical activity. MUZ EMS was delivered to the emergency department of the First City Clinical Hospital named after. HER. Volosevich with suspected ACS and pulmonary embolism. The patient had not previously consulted a doctor about the present disease.

Past illnesses

In childhood, he was diagnosed with chronic glomerulonephritis of unknown etiology, which led to the development of chronic renal failure. Since 2013, systemic hemodialysis has been carried out.

Denies the presence of infectious, venereal, mental, endocrine diseases, tuberculosis and allergic reactions. He rarely suffered from respiratory infections.

Life story

Born in 1973 in the city of Novodvinsk, in a complete family, the only child. He graduated from 8 classes of secondary school. Received secondary specialized education as a cook. He began working at the age of 20, but as a result of illness was forced to change jobs. He did not serve in the army - he was a reserve private. Currently, he is disabled in group 1 due to chronic renal failure, is not officially employed, and sometimes works part-time as a driver. Lives alone, single, no children. Housing conditions are satisfactory, nutrition is nutritious and regular.

Family history: Compounded heredity: the patient’s mother suffered from ischemic heart disease, died from stroke, ischemic stroke.

Allergy history: denies the presence of allergies.

Presence of bad habits: nicotine addiction - smoking since age 20, no drug addiction, alcohol in moderation.

OBJECTIVE INVESTIGATION - PRESENT CONDITION

At the time of admission, the patient was in a moderate condition. At the time of supervision the condition is satisfactory. The patient's position is active, consciousness is clear, mood is depressed.

Normosthenic physique. Normothermia. Height 163 cm, weight 70 kg. Skin of normal color, clean; elasticity and turgor are normal. Hair and nails are normal.

Subcutaneous tissue is moderately developed (BMI 20.9). The skin fold under the shoulder blade is 2 cm, on the shoulder - 2 cm, on the abdomen - 4 cm. The lymph nodes are not enlarged, painless, not fused with the surrounding tissues, the skin over them is clean, not hyperemic.

The muscular and musculoskeletal systems are well developed, there were no fractures during his life, movements in the joints were fully preserved.

There is no peripheral edema.

Respiratory system

On examination, breathing is free and even. NPV 22-24 per minute. The type of breathing is mixed, the rhythm is correct. The chest is of regular shape, symmetrical, both halves participate in the act of breathing, the intercostal spaces are not widened. There is no runny nose.

On palpation, the pain points are painless, the chest is resistant, voice tremor is the same over symmetrical areas of the right and left lungs.

Topographic percussion: the boundaries of the lungs are within normal limits. The width of the Krenig margins is 5 cm on the right and 5 cm on the left. The mobility of the pulmonary edge along the mid-axillary line of the left lung is 6 cm, the right lung is 6 cm.

Comparative percussion: a clear percussion sound is determined over the symmetrical areas of the right and left lungs.

Auscultation: weakened vesicular breathing, hard in the lower parts, no wheezing.

Circulatory organs

The apex beat is not visually determined, the cardiac hump, pulsation of peripheral vessels, swelling and pulsation of the jugular veins are not observed. The pulse on the radial arteries is rhythmic, 85 beats/min, full, moderate tension, synchronous. The pulsation of the brachial, radial and temporal arteries is preserved and is the same on both sides.

Palpation: an apical impulse is detected in the 5th intercostal space 2 cm inward from the midclavicular line, with an area of 2-3 cm2, of moderate strength, low.

Percussion: The boundaries of OST and AST are not expanded. The width of the vascular bundle is 6 cm.

Auscultation: muffled heart sounds, presence of systolic and protodiastolic wheezing. The heart rhythm is correct. Blood pressure 125/85 mm Hg. Art.

Digestive organs

Examination of the oral cavity during examination of the oral mucosa revealed no pathology; the color is pale pink, the tongue is covered with a white coating, and is moist. Your teeth.

When examining the abdominal area: round in shape, not swollen, symmetrical, involved in the act of breathing, no retractions/bulges were detected, the venous network is clearly visible.

Auscultation: peristalsis sounds in the intestinal projection.

Percussion: tympanitis of varying heights is determined over the entire surface of the abdomen, liver dimensions according to Kurlov: 7x9x9 cm - within normal limits. Free fluid in the abdominal cavity is not detected.

On superficial palpation of the abdomen, the anterior abdominal wall is not tense, no pain or muscle separation is detected.

With deep palpation: the sigmoid, transverse colon and greater curvature of the stomach are palpated. The spleen could not be palpated. The lower edge of the liver protrudes from under the costal arch.

The stool is regular and formed.

urinary system

No asymmetry of the lumbar regions or swelling was detected. It was not possible to palpate the kidneys and bladder in a standing or lying position. The symptom of effleurage is negative.

The act of urination is painless and regular. Urine is light, without impurities (according to the patient)

Endocrine system and sensory organs

The skin color is pale. The skin is dry, turgor is reduced. Palms are dry.

Height corresponds to age and gender. The body is developed proportionally. Fat layer and male-type hair growth. No stretch marks were found on the hips or abdomen.

Nervous system

Patient Pankov S.G. is in a clear consciousness, oriented in time (unmistakably names the date), space (realizes where he is), environment (remembers what happened to him), personality (names himself, date of birth, age, name, etc.).

He makes contact, is critical, and is in a cheerful mood. He does not notice memory loss (when asked to repeat what was said a few minutes ago, he repeats it without error). Speech activity is normal.

No neck rigidity was detected, Kernig's sign was negative. Sleep is normal 7-8 hours a day, easily transitions from sleep to wakefulness. There is no dizziness or headaches. Unconditioned reflexes are preserved.

ADDITIONAL DATA

1. General blood test

WBC - leukocytes - 13.5 * 109/l

LYM# -- absolute lymphocyte content - 1.8*109/l.

LYM% -- relative (%) content of lymphocytes - 0.146%.

MXD# -- absolute content

Monocytes= 11%

Basophils=1%

Eosinophils - 2%

HGB - hemoglobin concentration - 103 g/l

RBC -- absolute content of erythrocytes - 3.8 * 1012 g/l

MCH -- average hemoglobin content in an individual red blood cell - 27.1 pg

PLT -- absolute platelet count - 264*109/l

ESR - 61 mm/h

Conclusion:

2. Biochemical analysis of blood plasma

Urea - 18.47 mmol/l (N - 5.2 -8.3)

Creatinine - 836.94 µmol/l (N 62.00-106.00)

Sodium - 143.88 mmol/l (N 136.0-146.0)

Potassium - 6.14 mmol/l (N - 3.40-4.5)

Total bilirubin - 8.70 µmol/l (N 0.00-21.00)

Total protein - 69.11g/l (N 66.00-87.00)

C-reactive protein - 42.50 mg/l (N 0.00-5.00)

AST - 12.18 (N 0.00-38.00)

ALT - 14.25-14.19(N 0.00-41.00)

Thymol test - 2.40 (N 0.00-5.00)

INR - 1.09 (N 0.80-1.20)

Prothrombin time - 14.3 (N 12-16 sec)

D-dimers - 1.45 μg/ml (N 0.00-0.50)

3. Conclusion: a sharp increase in the content of C-reactive protein, urea, creatinine and D-dimers, which indicates severe intoxication and inflammation in the body.

Blood gases (10/15/15)

pH/blood gases

	32.0 mmHg
	55.1mmHg
Acid-base status


Oximetry




Electrolytes


Calculated values

Conclusion: decompensated metabolic alkalosis.

4. Microbiological examination (catheter culture) (10.20.15)

Conclusion: microbiological examination of blood and determination of sensitivity to antibiotics dated 10/16/15 - sensitivity - amoxicillin/clavuanate, cefepime, ciprofloxacin, vancomycin, clindamycin.

5. EchoCS (10/15/15)

Conclusion: the opening of the anterior valve leaf is limited. On the non-coronary cusp (+LKS?) of the aortic valve there is a floating formation of medium echogenicity measuring about 12*6 mm (vegetation)

6. SCT of the chest (28.10.15)

Conclusion: Small left-sided hydrothorax. Lymphadenopathy of the intrathoracic lymph nodes.

7. X-ray of the chest organs (15.10.15)

Conclusion: pulmonary congestion

8. Ultrasound of the veins of the lower extremities (10/15/15)

Conclusion: blood flow along the SBV, BV, GBV, PV, and PVV are preserved. With CTC, staining is complete. When compressed, the veins collapse.

9. Ultrasound examination of BCA (22.10.15)

Conclusion: Occlusion of the right IJV. Suspicion of non-occlusive thrombosis of the right subclavian and brachiocephalic veins.

10. ECG (3.11.15)

Conclusion: sinus tachycardia with heart rate 120 beats per minute. EOS is deviated to the left. BPVLNPG. LVH with diastolic overload of the left ventricle. Load on the left atrium. Single extrasystole.

endocarditis aortic valve

Differential diagnosis

Thus, during the examination, a diagnosis of infective endocarditis of staphylococcal etiology was made. The leading syndrome for differential diagnosis is respiratory failure syndrome.

The following diseases are associated with the presence of respiratory failure syndrome: pulmonary embolism (PE), pneumonia.

Pulmonary embolism (PE) is a sudden blockage of the branches or trunk of the pulmonary artery by a thrombus (embolus) formed in the right ventricle or atrium of the heart, the venous bed of the systemic circulation and carried with the bloodstream.

Upon admission to the emergency department, an x-ray examination of the chest organs was performed, which did not reveal changes characteristic of pulmonary embolism, that is, on the x-ray we did not see any acute dilatation of the right parts of the heart, nor an increase in the diameter of the pulmonary artery (bulging of its cone), nor pronounced local depletion pulmonary vascular pattern; in addition, an increased position of the dome of the diaphragm in the area of pulmonary embolism was not detected.

The risk factor for pulmonary embolism was also excluded - varicose veins of the lower extremities, which creates conditions for stagnation of venous blood and the formation of blood clots. On the day of admission to the emergency department, the patient underwent an ultrasound of the veins of the lower extremities, which did not reveal any pathologies.

Impaired respiratory function is also characteristic of pneumonia.

Pneumonia is an inflammation of the lung tissue, usually of infectious origin with predominant damage to the alveoli (the development of inflammatory exudation in them) and the interstitial tissue of the lung

We can also exclude this diagnosis using chest x-ray. The X-ray picture of pneumonia is characterized by the presence of darkening on the segments of the lungs. After performing this study, we did not find any characteristic changes in the lungs that could help us make a diagnosis of pneumonia.

Since we excluded these diseases, the patient was sent for a more detailed examination of the chest organs, namely the heart, and an EchoCS was performed. Based on the results of this examination, a final diagnosis was made - infective endocarditis of the oartic valve.

CLINICAL DIAGNOSIS

Drug therapy

1) Rp.: Heparini 5ml (25.000 ED)

D.t.d. No. 5 inamp.

S. Administer 5,000ED subcutaneously 4 times daily.

Used for the prevention and treatment of thromboembolic diseases and their complications due to the installation of a catheter in the subclavian vein.

Shown for the same purpose

Rp: Fraxiparini 0.6 ml

D.t.d. No. 10 in amp.

S: inject subcutaneously in a lying position into the abdominal area, alternating between the right and left sides of the abdomen

2) Rp.: Tab.Digoxini0.25

S. 1 tablet orally. 1 per day

The drug increases the refractoriness of the atrioventricular node, which leads to a decrease in heart rate (HR), lengthens diastole, improves intracardiac and systemic hemodynamics

3) Rp.:Vancomycini 1.0

D.t.d N5 in flaconis

S. administer 1 bottle intravenously 2 times a day for 6 weeks.

Since a diagnosis of infective endocarditis of staphylococcal etiology was made, antibacterial therapy is mandatory.

4) Rp.: Tabl. Lasics 0.04

S.take 1 tablet 2 times a day

As a result of chronic renal failure and heart failure, edema may develop; the use of a diuretic is necessary to remove fluid from the body.

Mode - general (free)

Diet - table No. 10: limit the consumption of salt, fatty and spicy foods, alcohol. Introduce low-fat soups, boiled meat and fish, vegetables, milk and dairy products, and pasta into the diet.

On 10/30/15, a council of doctors decided to perform an urgent operation to replace the aortic valve.

The prognosis for the patient at this stage of treatment cannot be determined. The final prognosis for life and work will be made after the scheduled operation.

I slept well that night. The condition is satisfactory. The mood is cheerful. He has no complaints. Stool and urination are normal. There is no shortness of breath at rest or at night. There is no swelling. Body temperature 36.7. Heart rate 78 beats/min, blood pressure 130/70 mmHg, respiratory rate 18. Auscultation: rales are heard in the area of the apex of the heart, in the projection of the aorta. The abdomen is soft, without pain.

The condition is satisfactory. The mood is cheerful. He makes no complaints. Temperature 36.5. Heart sounds are rhythmic with heart rate 80 beats/min, blood pressure 110/75 mmHg, respiratory rate 20. No shortness of breath. The skin is clean. The liver is not enlarged. Heart failure does not worsen. There are no focal neurological symptoms.

The patient underwent FGDS. The condition is satisfactory. The mood is sluggish. Complaints of weakness. Body temperature 36.8. Heart rate 75 beats/min, blood pressure 120/70 mmHg, respiratory rate 18. No shortness of breath. There is no swelling. The liver is not enlarged. Therapy continued.

The patient was transferred to the vascular surgery department for aortic valve replacement surgery. The condition is satisfactory. The mood is cheerful. Appetite and sleep are good. He makes no complaints. Body temperature 36.6. Heart rate 78 beats/min, blood pressure 120/80 mmHg, respiratory rate 20.

Patient - born 1973 (41 years old), disabled group 1

On 10/15/15, the EMS team delivered him to the emergency department of the First City Clinical Hospital named after E.E. Volosevich. On 11/10/15, by decision of the medical commission, he was transferred to the vascular surgery department.

Main disease: 1. Primary infective endocarditis of the aortic valve of staphylococcal etiology and the formation of grade 3 aortic regurgitation.

2. Chronic glomerulonephritis. Nephrosclerosis. CKD stage 5. Program hemodialysis since 2013

Complication of the underlying disease: chronic heart failure 2A, FC2. Thrombosis of arteriovenous fistula from 2013. Permanent catheter since 2014. Occlusion of the right IJV. Suspicion of non-occlusive thrombosis of the right subclavian and brachiocephalic veins. Catheter replacement dated 10.2015. Anemia of mild severity of combined genesis, epocrine-dependent.

Doctors from the EMS team diagnosed PE. Since 2013, he has been on program hemodialysis. A general blood test shows signs of inflammation, leukocytosis, increased ESR, and mild anemia. EchoCG revealed an increase in the cavity of the RA, LA, and LV. Dilatation of the pulmonary artery. Increased pulmonary artery pressure 1st degree. Changes in the MV leaflets - compaction, limited opening of the anterior leaflet, 2nd degree regurgitation. Changes in AC - vegetation measuring 12*8 mm, regurgitation of the 3rd degree.

Therapy performed: intramuscular lasix, diclofenac; IV CPS + magnesium sulfate + sodium chlorine; digoxin, carnitine, pentoxifylline, lasix; SC heparin, fraxiparin. Program hemodialysis.

The medical commission decided to perform an operation to replace the aortic valve.

On November 10, 2015, the patient was transferred to the cardiovascular surgery department for aortic valve replacement surgery.

observation by a therapist, cardiologist,

control of the blood coagulation system; control of AST, ALT, cholesterol, LDL

adherence to a hypolipid diet (exclude pork, mayonnaise, fatty dairy products, offal, bone broths, lard; increase grains, fish, vegetables and fruits in the diet)

take (concor, lorista, cardiomagnyl 75 mg in the morning after meals, veroshpiron, furosemide, xarelto, warfarin, digoxin, prestarium, amplodipine, atorvastatin 10 mg in the evening under control)

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