Antibiotics that are active against staphylococci must be included in the empiric antibiotic regimen. All drugs are administered intravenously. The choice of drug depends on the severity of the patient's condition and the sensitivity spectrum of pathogens isolated in the area. A beta-lactam antibiotic (oxacillin or nafcillin) is usually given or, if infection with methicillin-resistant Staphylococcus aureus is suspected, vancomycin. If gram-negative pathogens are common in the area, an aminoglycoside is added. In infective endocarditis caused by methicillin-sensitive staphylococcus, use oxacillin or nafcillin, 1.5-2 g every 4 hours for 4 weeks. In a serious condition, an aminoglycoside is sometimes added in the first 2 weeks of treatment - usually gentamicin, 1.5 mg / kg every 8 hours. Bacteremia stops faster, but otherwise there is no increase in the effectiveness of treatment. For penicillin allergy or infection caused by methicillin-resistant strains of Staphylococcus aureus, vancomycin is used, 1 g every 12 hours. For infective endocarditis caused by other pathogens, therapy depends on sensitivity to antibiotics. Usually the course lasts 4 weeks.
There is no consensus regarding the surgical treatment of infective endocarditis in drug addicts, as well as in patients of other groups. Indications for surgery in them are the same as in other patients: persistent heart failure, unopened myocardial abscess, ineffectiveness of antibiotic therapy, especially in candidal and other fungal endocarditis. The nature of the operation depends on which valve is affected. In severe tricuspid valve endocarditis, excision of the tricuspid valve is effective. With endocarditis of the mitral or aortic valve, their prosthetics are required; in most cases it is safe, but if the patient continues to inject drugs, then there is a constant risk of infective endocarditis. Therefore, the feasibility of such operations is highly controversial. The issue of valve replacement should be decided jointly by the attending physician, the cardiac surgeon and the patient himself.
scientific article on the topic INFECTIOUS ENDOCARDITIS IN INTRAVENOUS DRUG addicts: A REVIEW Science of Science
Infectious endocarditis in intravenous drug addicts: a review
Karpin V.A., Doctor of Medical Sciences, Doctor of Philosophy, Professor
Zulfigarova B. T., post-graduate student Shuvalova O. I., candidate of medical sciences, assistant Kuzmina N. V., doctor of medical sciences, professor
Dobrynina I.Yu., Doctor of Medical Sciences, Professor Nelidova N.V., Candidate of Medical Sciences, Associate Professor
Burmasova A.V., Candidate of Medical Sciences, Senior Lecturer Gromova G.G., Candidate of Medical Sciences, Senior Lecturer (Surgut State University of the Khanty-Mansiysk Autonomous Okrug - Yugra)
INFECTIOUS ENDOCARDITIS IN IV DRUG ADDICTS: A REVIEW
Introduction. According to official statistics, the number of drug addicts is growing from year to year in the world. Over the past 5 years, it has increased 4 times. As you know, drug addiction causes suppression of the immune system and a decrease in the body's resistance, which leads to the frequent development of purulent-inflammatory processes. The widespread use of drugs using the intravenous route of administration has led to a significant increase in the number of post-injection infectious complications, often accompanied by a generalization of the purulent process with the development of sepsis.
The period from the mid-90s was marked by the progression of a new form of infective endocarditis (IE) for us - infective endocarditis in intravenous drug users (IEVN). The incidence of IEVI in recent years is several times higher than the incidence of IE among individuals with predisposing factors such as rheumatism or an artificial valve. Among drug addicts, the incidence of IE is 2 to 5% annually. Based on long-term observations, 63% of patients hospitalized for IE were intravenous drug addicts. With intravenous administration of drugs, IE develops in 6.4% of patients.
What are the features of infective endocarditis of injecting drug users that make it possible to distinguish it into a special group?
Etiology. The microbial landscape in IE has undergone significant dynamics over many years of observation. As for IEVN, here the authors are practically unanimous: Staphylococcus aureus predominates in the spectrum of pathogens - Staphylococcus aureus. The source of infection is most often the skin of patients: multiple injections contribute to the colonization of the skin by Staphylococcus aureus. It is a highly invasive microorganism capable of infecting intact valve endothelium. At the same time, IE of the left heart, as a rule, based on previous valvular lesions, is more often caused by streptococci. In the group represented by people who did not use drugs, this pattern
was absent - in most cases, polymicrobial associations prevailed in various variants. An important feature of IEVN is the high frequency (up to 85%) of pathogen detection in blood cultures. A negative blood culture usually indicates errors in the sampling or examination of the material. According to IEVI, true negative blood cultures are rare and account for only 5%.
Staphylococcus aureus, isolated from the blood of IE patients with drug addiction, in most cases, was characterized by high virulence and resistance to antibacterial drugs.
Pathogenesis. IEVN is characterized by damage to the right chambers of the heart: a characteristic feature is the involvement of the tricuspid valve in the pathological process, according to various authors, from 46 to 86% of cases. According to the data, 61% of patients with isolated IE of the tricuspid valve were intravenous drug users.
Most authors agree that IEVN is characterized by damage to an unchanged, intact heart valve. At present, no sufficiently convincing explanations have been found, what is the mechanism for the development of IE of the tricuspid valve in the absence of its previous changes. In experiment, normal heart valves are highly resistant to infection. There is the most common opinion that frequent intravenous injection of any drugs is accompanied by the appearance in the blood of a large number of tiny particles and air bubbles that “bombard” the surface of the endocardium, causing its microtrauma, primarily on the tricuspid valve located on the path of blood flow coming from superior vena cava. With the abuse of intravenous injections, prerequisites are created for the attachment of infection and the occurrence of IE of the right chambers of the heart. This mechanism explains the well-known fact that the tricuspid valve is predominantly affected in drug addicts who prefer the intravenous route of drug administration, while in all other cases, the mitral and aortic valves, which experience the greatest functional load, are primarily affected. A certain role is also played by the pronounced virulence and adhesive activity of Staphylococcus aureus, as well as the widespread violation of asepsis in the domestic environment.
A certain role in the pathogenesis of IEVN is played by a violation of the immune system during prolonged use of narcotic drugs.
Clinical features of IEVN. Young age is a feature of IEVN, while the majority of patients with modern IE are characterized by "aging". Men are more often ill.
In the clinical picture of IEVN, most authors distinguish two leading points - an acute course and polysyndromicity. The severity and severity of the course of the disease are very characteristic of a staphylococcal infection. The leading syndromes are infectious-toxic (75-92%) and thromboembolic (65-78%).
Auscultatory symptoms of tricuspid valve insufficiency usually appear in the later stages of the disease. This is due to the peculiarities of the morphology of the valvular apparatus of the heart and the nature of intracardiac hemodynamics. The dimensions of the tricuspid foramen are relatively large, and the pressure in the cavity of the right ventricle is about 5 times less than in the left one. Even with partial destruction of the tricuspid valve, the resulting tricuspid insufficiency is relative, patients tolerate it satisfactorily due to compensatory mechanisms and a small volume of blood returning to the right atrium.
Myocarditis in injecting drug users develops twice as often as in IE patients who do not use drugs (78.8% vs. 37.2%); The toxic effect of Staphylococcus aureus explains the frequent development of severe myocardial dystrophy in this group of patients.
The development of such a formidable complication of IE of the right heart chambers as septic thromboembolism of the branches of the pulmonary artery with the subsequent development of pneumonia, often destructive and often recurrent, is a kind of "visiting card" of the IEVN. In some cases, pulmonary manifestations of the disease become dominant, and pneumonia can become the leading manifestation of IEVI, significantly complicating timely diagnosis. In addition, multiple repeated embolism of the pulmonary artery branches gradually leads to the development of pulmonary hypertension, dilatation of the right heart, an increase in tricuspid regurgitation and right-sided heart failure with the formation of chronic cor pulmonale. According to data, destructive forms of pneumonia developed in 52% of patients and, as a rule, were caused by Staphylococcus aureus.
Diffuse glomerulonephritis, which is more pronounced in drug addicts, is a frequent complication of IEVN. It can be assumed that this is due to immunological disorders caused by long-term drug intoxication. They are also more likely to have splenomegaly.
echocardiographic features. Echocardiographic examination is the cornerstone of the diagnosis of IEVN. When fever occurs in intravenous drug users, physical and laboratory tests may be ineffective in detecting IE. A key finding on echocardiography is the combination of vegetations with tricuspid regurgitation. It should be emphasized that, in contrast to left-sided IE, where not only transthoracic, but also more informative transesophageal access is practically mandatory, the advantage of the latter in the study of the tricuspid valve (TC) for identifying vegetations is not so clear. Usually with transthoracic echocardiography, it is possible to obtain a fairly high-quality image of the TC, since it is located close enough to the ultrasound transducer. In addition, the vegetation on the TC is usually quite large. This allowed some authors to doubt the appropriateness of using a transesophageal study in patients with suspected endocarditis of the right heart. So, according to the data, during transthoracic echocardiography in patients with IEVN, vegetation was detected in 86% of patients.
associated infections. Viral hepatitis. The liver is often affected in drug addicts with IE. In patients of this group, not only prolonged drug intoxication is important, but also a high risk of infection with viral hepatitis, especially viral hepatitis C. The risk of infection in this contingent is 6090%, while in ordinary groups it does not exceed 5%. According to the data, viral hepatitis C was diagnosed in 57% of patients, viral hepatitis B - in 15%, a combination of B and C - in 28%. The authors believe that the addition of viral hepatitis contributes to the recurrent course of IEVN. The relative rarity of viral hepatitis B in these patients is explained by the rapid elimination of hepatitis B virus in the presence of hepatitis C virus.
HIV infection. Patients with IE suffering from intravenous drug addiction are often infected with the human immunodeficiency virus (HIV). From 40 to 97.2% of patients with IEVN are HIV-infected. The predominance of HIV-seropositive patients in the environments
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Similar scientific papers on the topic "Science"
A. V. Burmasova, I. Yu. Dobrynina, B. T. Zulfigarova, V. A. Karpin, N. V. Kuzmina, N. V. Nelidova, and O. I. Shuvalova - 2014
Infective endocarditis in injecting drug users.
Its cause is
Staphylococcus aureus (more than 50%), streptococci and enterococci (about 20%), fungi (6%). In some cases
Pseudomonas aeruginosa develops. Quite often found
From the above, it can be seen that in most cases, the microorganisms that cause
development of infective endocarditis, are opportunistic. Therefore, only one
infection and bacteremia are not enough to damage the heart valves. Availability required
predisposing conditions that contribute to the formation of infective endocarditis. They can
divided into two main groups.
Firstly, these are various conditions accompanied by changes in the intracardiac
Secondly, factors predisposing to the development of bacteremia, not related to
damage to the heart and blood vessels.
In accordance with the nature of hemodynamic disorders, three risk groups can be distinguished
development of infective endocarditis.
High risk patients:
Prosthetic heart valves (highest risk!).
History of infective endocarditis;
Blue combined congenital heart defects (single ventricle,
dextraposition of the main arteries, tetralogy of Fallot);
Open ductus arteriosus;
Bicuspid aortic valve with stenosis or insufficiency;
Rheumatic aortic defects;
Mitral insufficiency, including in combination with stenosis;
Defects of the interventricular septum;
Residual effects after heart surgery (valvular stenosis and insufficiency,
intracardiac shunt).
Artificial aortopulmonary shunts (conduits). Patients at moderate risk:
Mitral valve prolapse with mitral regurgitation or leaflet thickening;
Mitral stenosis without insufficiency;
Tricuspid valve defects;
Stenosis of the valve of the pulmonary artery;
Bicuspid aortic valve without hemodynamic disturbances;
Calcification of the aortic valve, mitral ring;
The first six months after heart surgery for a defect without residual effects.
Patients at this risk:
Mitral valve prolapse without mitral regurgitation and leaflet thickening;
Minor valvular regurgitation in the absence of organic heart disease;
Isolated atrial septal defect of the ostium secundum type;
Atherosclerosis of the aorta, coronary arteries;
Condition six months or more after heart surgery for a defect without
Implanted pacemakers and defibrillators;
Condition after coronary artery bypass grafting;
Past Kawasaki disease or rheumatism without valvular disease.
The group of increased risk of developing bacteremia includes, first of all, injectable
drug addicts. At the same time, infection of the drug solution itself is rarely the cause of the disease,
more often the pathogen penetrates from the skin when it is punctured.
infected skin ulcers, the need for medical procedures on the urinary tract and
large intestine, long standing central vein catheters. In about 1/3 of cases, infectious
endocarditis of the elderly has a nosocomial (hospital) genesis.
Separately, it is necessary to single out groups of patients receiving program hemodialysis, as well as
suffering from diabetes.
The pathogenesis of infective endocarditis is a sequential chain of events,
starting with the formation of an aseptic parietal thrombus at the site of endocardial injury and ending with
inflammatory bacterial destruction of the valve as a result of infection and
formation of heart disease.
The prerequisite for the disease is damage to the endocardium by turbulent blood flow in persons
having risk factors. As a result of platelet adhesion and subsequent fibrin deposition
sterile vegetations are formed, which in essence are parietal blood clots. Beloved
the place of their appearance are areas of high pressure in the left parts of the heart, as well as
physiological narrowing in the locations of the heart valves. In the presence of anomalies such as
ventricular septal defects, bicuspid aortic valve, risk of endocardial injury
increases. Experimental studies have shown that endocardial injury is
an indispensable condition for the development of infective endocarditis, since on the intact endocardium aggregation
platelets do not occur.
The second indispensable condition for the occurrence of the disease should be considered the presence in the blood
bacteria that can colonize the endocardium. If the bacterial membrane contains surface
polysaccharides and proteins from the class of adhesins facilitates the binding of bacteria to the formed on
damaged endocardium with sterile blood clots.
As a result, a classic inflammatory process develops, leading to destruction
valves with the formation of heart disease.
An early morphological manifestation of infective endocarditis is the appearance of
characteristic vegetation containing platelets, fibrin, inflammatory cells and erythrocytes. Subsequently
the onset of destruction of the endocardium, ulceration and abscess formation is possible.
According to the ICD-10, infective endocarditis is classified under category 133. From this
classification excludes rheumatic endocarditis.
133 - Acute and subacute endocarditis.
133.0 - Acute and subacute infective endocarditis.
133.9 - Acute endocarditis, unspecified.
In accordance with the old classifications, acute, subacute and chronic
infectious (bacterial) endocarditis.
Modern classifications include bacteriological: clinical,
activity and morphological characteristics.
With positive results of bacteriological, immunological, morphological
methods in the diagnosis, the etiological characteristics of the disease must be noted. If with
using all available methods to determine the type of pathogen is not possible, then the diagnosis should
characterize IE as "microbiologically unspecified".
Endocarditis is considered active if cultures are positive,
accompanied by fever, as well as signs of activity, confirmed morphologically during
operation time. In other cases, endocarditis is considered inactive.
If eradication has not been carried out in full, it is possible to develop a recurrent
infective endocarditis with the appearance of characteristic signs of activity.
Clinical symptoms develop within the first two weeks after the episode,
causing bacteremia. The disease begins with malaise and fever. The latter may be
insignificant, however, with highly virulent pathogens, the disease begins acutely with a rise
temperatures up to 39°C and above. Characterized by arthralgia, pain in the muscles and lower back.
The skin is pale, yellowish (color "coffee with milk"). Objectively
petechial rashes on the skin, conjunctiva, oral mucosa are noted. Spots are noted
Rota - oval retinal hemorrhages with a white dot in the center and Janeway spots - small
hemorrhagic spots on the palms and feet, slightly resembling nodules. With a long course
disease develops a symptom of "drum sticks".
Auscultatory noted heart murmur, indicating the formation of heart disease.
Palpation and percussion of the abdomen can reveal an enlarged spleen.
The severe course of the disease is characterized by thromboembolic complications,
formation of septic aneurysms.
Additional methods include, first of all, bacteriological
blood test, which gives positive results in 95% of cases. Crops are carried out twice
after 12 hours. In cases where antibiotic therapy cannot be delayed, blood sampling
carried out at intervals of minutes from different veins within 3-6 hours preceding the start
treatment. The results are considered positive if bacteria are present in two cultures taken from 12-
hourly intervals, or in most crops taken three or four times.
Other laboratory data are characterized by accelerated ESR, normo- or hypochromic anemia.
Leukocytosis and changes in the leukocyte formula are mainly determined in acute endocarditis. AT
Urinalysis revealed proteinuria and microhematuria.
Of the instrumental methods, the leading diagnostic study is
echocardiography. It is necessary to determine the nature and size of vegetation, their localization, presence and
expression of regurgitation. In the early stages, the information content of transthoracic echocardiography may be
low. (45% positive results). At the same time, the use of a transesophageal probe allows
increase the sensitivity of the method up to 90-93%.
Summarizing all of the above, we can determine the following diagnostic criteria
infective endocarditis proposed by Durack D. et al (1994):
Positive blood culture results with isolation of typical pathogens;
Echocardiographic signs of IE (vegetation, abscesses, newly appeared
paravalvular or valvular regurgitation).
Cardiac lesions predisposing to IE or injection drug use;
Temperature rise > 38°C;
Vascular changes (embolism of large arteries, pulmonary infarctions, intracranial
hemorrhages, subconjunctival hemorrhages, Jsynway spots);
Immunological changes (glomerulonephritis, Osler's nodules, Roth's spots,
Isolation of the pathogen that does not meet the main criterion or serological
signs of infection with a typical pathogen;
Echocardiographic signs of endocarditis that do not meet the main criterion.
Undoubted infective endocarditis is detected in the presence of two main criteria
or one main and three additional, or in the presence of five additional criteria.
The diagnosis of probable IE is made in the presence of one main and one additional
criterion, or only three additional ones.
A diagnosis is considered rejected if there are not enough criteria to
confirmation of a “possible” endocarditis, the presence of another disease in the patient, or with complete
the disappearance of symptoms of the disease with short-term (less than four days) antibiotic therapy.
Examples of the formulation of the diagnosis
1. Streptococcal infective endocarditis. active phase. Combined aortic
heart disease (aortic stenosis, aortic valve insufficiency). Chronic cardiac
failure. PA stage. FKZ.
2. Infective endocarditis of unspecified etiology with combined mitral
aortic heart disease (mitral valve insufficiency, aortic stenosis). inactive phase.
Chronic heart failure. Stage I. FKZ. Differential diagnosis is carried out in
fever, the cause of which cannot be quickly determined, since the typical clinical
a picture with the formation of valvular disease may not develop from the first days of the disease.
First of all, these are lesions of the heart of a rheumatic nature. In case it is about
acute rheumatic fever, the diagnosis is usually not difficult due to the presence
typical diagnostic criteria for rheumatism (see Part I, p. 128).
A great difficulty is the identification of secondary infective endocarditis against the background of
pre-existing heart disease. In this case, an important role is played by the collection of anamnesis, a thorough
tracking auscultatory symptoms, the presence of other clinical signs of endocarditis.
blood culture studies.
Heart valve disease often accompanies systemic diseases of the connective tissue.
tissues such as systemic lupus erythematosus, polyarteritis nodosa, antiphospholipid syndrome,
nonspecific aortoareritis (Takayasu's disease),
Fever of unknown origin may occur with malignant neoplasms,
especially in the elderly, exacerbation of previously undiagnosed chronic pyelonephritis.
Treatment of infective endocarditis is primarily aimed at eradication.
bacterial flora that caused the disease. It should be said that. despite the current
time of a fairly wide range of antibacterial drugs, therapy of this category of patients
still remains a difficult task.
The main principle of therapy for infective endocarditis is the earliest possible
start of antibiotic therapy. In this case, the duration of treatment is 4-6 weeks. The choice of drug is determined
culture results, but in most cases a bactericide should be used. More often
only penicillins, cephalosporins and vancomycin are used. When determining the dose of antibiotic
evaluate the minimum inhibitory and bactericidal concentrations.
Until culture results are available in patients with iodoacute infective endocarditis
non-prosthetic valves are prescribed antibiotics that are effective against enterococci, since
the latter are more resistant than streptococci (ampicillin 12 g/day, sometimes in combination with
gentamicin 3 mg/kg/day).
Therapy for acute infective endocarditis begins with an effective against
Staphylococcus aureus vancomycin (30 mg/kg/day). For injection drug addicts, I add! gentami-
qin in standard dosages.
If the results of the blood culture are available, the choice of the drug is specified. Since the main
the microorganism that causes valvular damage in non-addicted patients is
penicillin-sensitive viridescent C1 reptococcus (MIC ≤ 0.1 μg / ml), then therapy is started
the appointment of benzylpenicillin in the ground. units/day, ceftriaxone at a daily dose of 2 g.
gentamicin at a daily dose of 3 mg/kg/day potentiates the effect. If you are allergic to this drug, treatment
start with vancomycin.
In case of moderate sensitivity of streptococci to penicillin (MIC ≥ 0.1 μg / ml, but
Ulanova Veronika Ivanovna Infective endocarditis in people with drug addiction
^ Clinical characteristics of infective endocarditis in drug dependent individuals
The reason for hospitalization of most patients was acute complications of the underlying disease. A significant part of the patients were admitted to the intensive care unit of the hospital with a clinic of unilateral or bilateral multifocal pneumonia, the cause of which was septic thromboembolism of the branches of the pulmonary artery. Secondary nephropathy with the development of acute renal failure (ARF) was the reason for hospitalization in 7 patients, and in most cases this complication was mistakenly interpreted as an exacerbation of chronic glomerulo- or pyelonephritis, as well as urolithiasis. Acute thrombophlebitis of peripheral veins, accompanied by fever and pain syndrome, was the reason for admission of patients to the hospital in 5.5% of cases. Relatively rare causes of hospitalization of drug addicted patients were arthritis of the joints of the lower extremities, as well as complications of IE associated with erosive and ulcerative lesions of the gastrointestinal tract (2.7 and 0.9%, respectively).
^ Clinical picture of heart damage in drug addicted patients with infective endocarditis
^ Clinical characteristics of complications of infective endocarditis in people with drug dependence
^ Clinical characteristics of infective endocarditis
^ Outcomes of infective endocarditis in drug dependent and non-drug dependent patients
^ Factors affecting the outcome of infective endocarditis in drug dependent and non-drug dependent patients
Infective endocarditis in drug addicts
INFECTIONS OF THE CARDIOVASCULAR SYSTEM
INFECTIOUS ENDOCARDITIS
Classification
Depending on the main pathogens and the associated features of antibiotic therapy, infective endocarditis is divided into the following main categories:
- infective endocarditis of natural valves;
- infective endocarditis in drug addicts using the intravenous route of administration of narcotic substances;
- infective endocarditis of artificial (prosthetic) valves:
- early (developing within 60 days after surgery) - more often due to valve contamination or as a result of perioperative bacteremia;
- late (developing more than 2 months after surgery) - may have the same pathogenesis with early infective endocarditis, but a longer incubation period; may also develop as a result of transient bacteremia.
Depending on the nature of the course of the disease, they are distinguished spicy and subacute infective endocarditis. However, the subdivision of bacterial etiology is the most significant, as this determines the choice of AMP and the duration of therapy.
Main pathogens
Infective endocarditis can be caused by a variety of microorganisms, but the vast majority are streptococci and staphylococci (80-90%).
The most common pathogens of infective endocarditis are presented in Table. one .
Table 1. Etiology of infective endocarditis
Infective endocarditis in injecting drug users: treatment
In a serious condition, confidence in the diagnosis of infective endocarditis of the left heart and (or) radiographic signs of septic embolism of the branches of the pulmonary artery, empirical antibiotic therapy is started after taking blood for culture.
It is not necessary for all injecting drug addicts with fever alone. In many cases, it is wiser to wait for the results of blood cultures under conditions of careful observation: in some patients, another serious illness is diagnosed during this time, in others, the fever turns out to be due to a mild illness or a pyrogenic or allergic reaction to the drug and disappears within a day.
Antibiotics that are active against staphylococci must be included in the empiric antibiotic regimen. All drugs are administered intravenously. The choice of drug depends on the severity of the patient's condition and the sensitivity spectrum of pathogens isolated in the area. A beta-lactam antibiotic (oxacillin or nafcillin) is usually prescribed, or if an infection with methicillin-resistant strains of Staphylococcus aureus is suspected. vancomycin. If gram-negative pathogens are common in the area, an aminoglycoside is added. With infective endocarditis caused by methicillin-sensitive staphylococcus aureus. use oxacillin or nafcillin. 1.5-2 g every 4 hours for 4 weeks. In severe cases, sometimes an aminoglycoside, usually gentamicin, is added in the first 2 weeks of treatment. 1.5 mg / kg every 8 hours. Bacteremia stops faster, but otherwise there is no increase in the effectiveness of treatment. With an allergy to penicillins or an infection caused by methicillin-resistant strains of Staphylococcus aureus. vancomycin is used. 1 g every 12 hours. In infective endocarditis caused by other pathogens, therapy depends on sensitivity to antibiotics. Usually the course lasts 4 weeks.
There are reports of the cure of uncomplicated infective endocarditis of the right heart with a beta-lactam antibiotic in combination with an aminoglycoside in 2 weeks. Such a scheme may be appropriate, since it is difficult to provide a safe venous access for a long time. Most experts consider it necessary to administer intravenous antibiotics throughout treatment, although this often requires the placement of an indwelling central venous catheter.
The prognosis of staphylococcal endocarditis of the right heart in injection drug addicts is favorable. Antibiotic resistance and death are rare.
With endocarditis caused by other pathogens and lesions of the left heart, the prognosis is worse, the morbidity rate and mortality are higher.
There is no consensus regarding the surgical treatment of infective endocarditis in drug addicts, as well as in patients of other groups. Indications for surgery in them are the same as in other patients: persistent heart failure. unopened myocardial abscess. ineffectiveness of antibiotic therapy, especially in candidal and other fungal endocarditis. The nature of the operation depends on which valve is affected. In severe tricuspid valve endocarditis, excision of the tricuspid valve is effective. With endocarditis of the mitral or aortic valve, their prosthetics are required; in most cases it is safe, but if the patient continues to inject drugs, then there is a constant risk of infective endocarditis. Therefore, the feasibility of such operations is highly controversial. The issue of valve replacement should be decided jointly by the attending physician, the cardiac surgeon and the patient himself.
Features of infective endocarditis in drug addicts
Infective endocarditis (IE) in drug addicts (with intravenous drug use) has become a serious problem for internists in recent years due to the peculiarity of morphological and clinical symptoms that create difficulties for timely diagnosis, selection of optimal therapy, and poor prognosis.
A number of patients observed in specialized narcological institutions develop fever, often due to pneumonia, cellulitis, osteomititis, skin infections, etc. D 10-16% of hospitalized patients have IE, which is responsible for death (2-8% of cases) . Usually the disease is acute, the initial manifestation is a persistent fever.
As a rule, there are no systemic embolic and microvascular phenomena, which is explained by the predominant lesion of the tricuspid valve in drug addicts.
More often, the disease debuts as a pulmonary pathology, which is the result of multiple septic embolisms (in 75%) with the development of pneumonia, heart attacks, and pleurisy. In half of the patients, the main complaint, in addition to fever, is cough, thoracalgia, hemoptysis (the result of heart attacks).
Characteristic murmurs of tricuspid insufficiency are absent at the beginning (according to the literature data), but later they are detected in 50% of patients, while a mesosystolic murmur is heard at the lower part of the sternum on the left, which increases on inspiration.
As a rule, there is no heart failure. Petechiae and splenomegaly are observed in 50% of patients.
Some patients may have toxic encephalopathy and focal neurological symptoms (the result of aneurysms or brain abscess formation).
Thus, the diagnosis of right-sided endocarditis, characteristic of drug addicts, is
special difficulties. The diagnosis of IE is based on a combination of anamnesis data, the originality of clinical, bacteriological, and radiological results of a lung examination. Valuable is the ECHO-KG study in febrile patients with an indeterminate diagnosis. Unfortunately, vegetation at the onset of the disease is not detected in all patients.
Typical are x-ray studies with the detection of multiple focal changes of a progressive nature with the formation of cavities, which sometimes leads to a false diagnosis, in particular, tuberculosis, which occurred in our patient.
The cause of the disease in drug addicts is most often Staphylococcus aureus, while in many cases it is resistant to a number of antibiotics. Multiple organisms are often found. In 5% of patients with IE (right-sided), bacteriological cultures are negative, but on the other hand, false-negative results are possible.
In recent years, mixed infections among drug addicts have become increasingly common. So, IE can occur in persons carriers of the hepatitis virus (more often B).
Recently, in the therapeutic department of the 64th City Clinical Hospital, we observed and for the first time diagnosed IE in 5 aged drug addicts. Four of them had primary tricuspid valve endocarditis, one had secondary IE (against the background of congenital aortic disease). Two patients categorically denied intravenous drug use, but one, after the discovery of the hepatitis B virus, admitted himself, and the narcologist confirmed this fact in the other. Three patients were cured of IE. One patient with viremia and liver cirrhosis left the hospital ahead of schedule. One (19 years old) died (in addition to IE, a venereologist diagnosed her with secondary syphilis, confirmed by serological tests).
Infective endocarditis in drug addicts
Infective endocarditis of the tricuspid valve is much less common than infective endocarditis of the aortic and mitral valves. At the same time, when discussing the features of infective endocarditis of the right atrioventricular valve, we should first of all note that the vast majority of cases are associated with intravenous drug administration.
Intravenous drug users (IVD) constitute a special group of patients who are increasingly admitted to the hospital with a diagnosis of infective endocarditis.
With the growth of intravenous drug addiction, the incidence of infective endocarditis is also growing. For example, according to the Moss and Munt Center, between 1994 and 2000, 63% of 116 patients admitted to hospital for infective endocarditis based on the Durak criteria were intravenous drug users. Of these, 86% were diagnosed with involvement of only the right side of the heart, while 14% also had involvement of the left side of the heart. Right-sided infective endocarditis is characterized by high morbidity and mortality, which causes significant economic damage.
The fact that in most cases intravenous drug users have right-sided infective endocarditis has not yet received an exact explanation. It is believed that repeated non-sterile injections play the largest role in damage to the tricuspid valve and pulmonic valve. However, immune disorders that occur in drug addicts are also of some importance.
Mostly young men are ill (mean age 20-30 years) with an initially intact tricuspid valve. In some cases, reinfection is noted - a repeated lesion of the tricuspid valve after an already transferred infective endocarditis. Such cases cause certain difficulties in diagnosis using echocardiography. In the case of right-sided endocarditis, the tricuspid valve is almost always affected, much less often - the pulmonary artery valve, both valves are extremely rarely involved in the process. It is also known about the rare possibility of damage to other endocardial structures, such as the Eustachian valve.
In most cases of right-sided infective endocarditis, the blood culture is positive. In 70% of infective endocarditis, Staphylococcus aureus is the etiological factor, the remaining cases are caused by streptococci or, less commonly, gram-negative flora, fungi, or diphtheroids. Pseudomonas infection is often diagnosed with multivalvular disease. Quite rarely (usually due to non-sterile injections) other, unusual, pathogens or polymicrobial infections occur. A negative blood culture usually indicates blood sampling against the background of antibiotic therapy. The cause of right-sided IE with negative blood culture may be Bartonella spp., which is isolated from urban homeless residents.
The frequency and characteristics of the course of infective endocarditis in various types of drug addiction have not been studied. In Western countries, infective endocarditis is thought to occur more frequently in cocaine users, who require more injections, than in heroin addicts. Information on the prevalence of HIV infection among drug addicts diagnosed with infective endocarditis varies greatly (58-76%). However, it has now been proven that the presence of HIV is an independent risk factor for the development of infective endocarditis, and in such patients, involvement of the right heart is even more common.
Common manifestations of infective endocarditis in drug addicts are persistent fever, bacteremia, and multiple pulmonary embolisms. At the same time, the symptoms of embolism are scarce and of little specificity (chest pain, shortness of breath, cough, hemoptysis). Crucially, unlike infective endocarditis in non-users of intravenous drugs, in whom the severity of clinical symptoms almost always correlates with the severity of valve injury, symptoms of infective endocarditis in intravenous drug users may be sparse, even with large vegetation size and severe tricuspid regurgitation. regurgitation.
The course of right-sided endocarditis in drug addicts has other features. Noises associated with right side pathology are often difficult to auscultate. In most patients with right-sided infective endocarditis, a systolic murmur is heard, but most often it is mild, nonspecific, and originates from the left side of the heart.
Complications of right-sided infective endocarditis can be cardiac and pulmonary. In the event of peripheral arterial embolism or sudden onset of neurological symptoms in such patients, involvement of the left heart and paradoxical embolism should be excluded. The combination of multiple chest x-ray infiltrations, fever, and bacteremia in drug addicts should always prompt a search for right-sided infective endocarditis.
Septic pulmonary embolism and its consequences (heart attack, lung abscess, bilateral pneumothorax, hydrothorax, and empyema) are common complications of right heart infective endocarditis. Often, drug addicts with infective tricuspid valve endocarditis are admitted to the hospital with abscessing pneumonia that is resistant to antibiotic therapy, which, however, is quickly cured after prosthetics of the affected valve.
In addition, some patients develop mycotic aneurysms of the branches of the pulmonary artery, often complicated by pulmonary hemorrhage, often fatal. Multiple repeated embolism of the branches of the pulmonary artery gradually leads to the development of pulmonary hypertension, dilatation of the right chambers of the heart and right-sided heart failure. Emboli large enough to dramatically increase pulmonary artery pressure and form acute cor pulmonale are rare. The dilated right atrium (RA) is a substrate for the development of supraventricular arrhythmias, primarily atrial fibrillation. Paravalvular abscesses may form. Vasculitis rarely complicates the course of right-sided infective endocarditis.
With a functioning oval window and discharge of blood from right to left, due to significantly increased pressure in the right atrium, hypoxemia occurs, and if an embolus penetrates through the arteriovenous message, paradoxical embolism occurs.
Complications of infective endocarditis caused by Staphylococcus aureus, such as extracardiac infections, thromboembolism, and severe sepsis, are more common in IV drug users than in non-drug users. At the same time, mortality among drug addicts may be lower, since they are usually young people with fewer comorbidities. However, after normalization of groups by age and comorbidities, mortality in them did not differ significantly.
Although sensitivity and specificity studies of the Durak criteria for infective endocarditis of the right heart have not been performed, any of the existing echocardiographic phenomena in the right heart, in combination with a positive blood culture of a typical microorganism, should be interpreted as right-sided infective endocarditis.
However, there are some limitations to the use of the Durak criteria for infective endocarditis of the right heart chambers. Thus, intravenous drug addiction is only a small criterion. From a clinical point of view, it is important that auscultatory symptoms in intravenous drug users with a first episode of endocarditis, with normal or slightly elevated right ventricular pressure, low flow rate and slight turbulence of the flow of tricuspid regurgitation, may be very scarce. Immunological and vascular manifestations related to Durak's minor criteria are also less common than in left-sided infective endocarditis. Small criteria include septic pulmonary embolism.
X-ray examination of the chest organs reveals changes in the lungs associated with septic embolism in 55% of cases of right-sided infective endocarditis, so this study is of particular importance in such patients.
Echocardiography remains the basis for the diagnosis of right-sided infective endocarditis. The key finding is a combination of vegetation with tricuspid and/or pulmonary (less commonly) regurgitation. Often, the diagnosis of infective endocarditis is difficult due to anatomical features such as the Chiari network or protruding Eustachian valve. It is especially difficult to make a differential diagnosis with transthoracic examination.
It must be remembered that drug addicts often have the consequences of a previous infective endocarditis with damage to the tricuspid valve. A frequent outcome of tricuspid valve endocarditis is its destruction with insufficient closure of the valves and severe regurgitation. Therefore, in itself, the identification of valve damage and even vegetation does not always mean the presence of an active infection. As a differential feature, old, sterile vegetation usually has a high echo density and may be calcified.
However, in some cases it is impossible to determine whether the infection has recurred or whether there are only consequences of a previous infective endocarditis. In this regard, it must be understood that infective endocarditis is a condition in which echocardiographic findings must always be interpreted in the context of clinical findings. The discovery of new tricuspid regurgitation in drug addicts or an increase in existing regurgitation in the absence of other explanations always requires the exclusion of infective endocarditis.
Usually, transthoracic echocardiography can obtain a high-quality image of the tricuspid valve, since most drug users have a fairly good ultrasound window. Thus, there is no need for routine TEE in all patients with right-sided infective endocarditis. The need for TEE arises in the diagnosis of paravalvular abscesses and unusual forms of right-sided infective endocarditis, such as involvement of the pulmonic valve or Eustachian valve.
In the absence of echocardiographic signs of infective endocarditis and its high clinical probability, the study is repeated after a week. If repeated negative results are obtained and the likelihood of infective endocarditis (especially with staphylococcal bacteremia) remains high, TEE is performed.
Another form of infective endocarditis can be considered infective endocarditis associated with the presence of an intracardiac device (for example, a pacemaker). This condition has a number of features, including those due to the characteristics of the patient population in which it most often occurs. In most cases, these are elderly patients with a large number of concomitant diseases. Associated with this is the ambiguity of symptoms and poor prognosis. Infective endocarditis associated with the presence of an intracardiac device should be suspected if unusual symptoms are present, especially if they develop in elderly patients with a pacemaker (pacer).
In the case when infective endocarditis is suspected in a patient with a pacemaker and a lead in the right heart or with an artificial valve, TEE is usually indicated, since transthoracic examination often causes diagnostic difficulties. Treatment of this condition is impossible without removal of the intracardiac device.
Infective endocarditis (IE) is an infectious polyposis-ulcerative inflammation of the endocardium, accompanied by the formation of vegetations on the valves or subvalvular structures, their destruction, dysfunction and the formation of valve insufficiency. Most often, pathogenic microorganisms affect previously altered valves and subvalvular structures, including in patients with rheumatic heart disease, degenerative changes in valves, MVP, and artificial valves. This is the so-called secondary infective endocarditis. In other cases, an infectious lesion of the endocardium develops against the background of unchanged valves (primary infective endocarditis).
In recent years, the frequency of primary IE has increased to 41-54% of all cases of the disease. There are also acute and subacute infective endocarditis. Sufficiently common in the past, a prolonged course of endocarditis is now a rarity. The mitral and aortic valves are most often affected, less often the tricuspid and pulmonary valve. The defeat of the endocardium of the right heart is most typical for injection drug addicts. The annual incidence of infective endocarditis is 38 cases per 100 thousand of the population, and people of working age (20-50 years) are more likely to get sick.
In the last decade, many authors have noted an increase in the incidence of IE, which is associated with the widespread use of invasive medical equipment, more frequent surgical interventions on the heart, an increase in drug addiction and the number of people with immunodeficiency states. Mortality in IE remains at the level of 40-60%, reaching 80% in elderly and senile patients. These data highlight the difficulties in timely diagnosis and effective treatment of the disease.
What causes infective endocarditis:
Infective endocarditis is a polyetiological disease. Currently, more than 128 microorganisms are known as pathogens. Common causative agents of IE include staphylococci, streptococci, gram-negative and anaerobic bacteria, and fungi. In the EU countries, staphylococci are isolated from 31-37% of patients, gram-negative bacteria - from 30-35%, enterococci - from 18-22%, streptococcus viridans - from 17-20%. The predominance of staphylococci, streptococci and gram-negative bacteria in the microbial landscape of the disease is indicated by many American and Canadian authors.
Studies conducted in the 90s in thirty US hospitals showed the following ratio of IE pathogens: starh. aureus - 56%, str. viridans - 31%, starh. epidermidis - 13%, enterococci and other bacteria - 5.6% of cases. According to domestic authors, the proportion of staphylococci is 45-56%, streptococci - 13-25%, enterococci - 0.5-20%, anaerobic bacteria - 12%, gram-negative bacteria - 3-8%, fungi - 2-3 % of positive blood cultures.
The type of pathogen largely determines the lethality from IE. If in the 1950s and 1960s viridescent streptococcus prevailed, then in the last decades of the 20th century, the main causative agents of infective endocarditis were epidermal and Staphylococcus aureus, which are isolated from 75-80% of patients with a positive blood culture. Mortality in IE caused by Staphylococcus aureus is 60-80%.
In recent decades, among the causative agents of IE, the proportion of gram-negative bacteria of the NASEC group (4-21%) and fungi (up to 4-7%) has increased. Yeast-like and true fungi (of the genus Candida, Aspergillus), which have a pronounced affinity for the endocardium, often act as pathogens. Mortality in fungal IE reaches 90-100%, and in IE caused by gram-negative microflora - up to 47-82%.
In the 80-90s, the number of cases of IE caused by anaerobic (8-12%) microflora increased. Anaerobic endocarditis is characterized by high activity of the infectious process, resistance to antibiotic therapy, increased hospital mortality (up to 46-65%). The features of the course of anaerobic endocarditis include the frequent (41-65%) formation of thrombophlebitis, thromboembolism in the vessels of the lungs, heart and brain.
Representatives of the genera Staphylococcus, Streptococcus, Enterococcus, Escherichia, Salmonella, Shigella, Proteus, Klebsiella, Yersinia, Candida, Aspergillus are of primary importance among the causative agents of IE.
ETIOLOGICAL VARIANTS OF ENDOCARDITIS
Staphylococci
In the last decade, the most common IE caused by Staphylococcus aureus (Staph. aureus). It differs significantly from other etiological variants in its characteristic clinical features: as a rule, it has a severe course with high process activity and hectic fever with profuse sweats, with the appearance of multiple foci of metastatic infection; it is mostly nosocomial (occurs during hospital stay due to infection of vascular catheters, arteriovenous shunts and fistulas); valve perforation often develops, followed by heart failure; hemorrhagic skin rash is extensive, necrosis and suppuration of rashes are often observed; typical brain damage (embolism of the cerebral arteries, brain abscesses, meningoencephalitis); the spleen is rarely palpable due to its soft consistency and slight increase, but septic infarcts of the spleen and its ruptures are often observed; endocarditis develops both on damaged (rheumatic, atherosclerotic, congenital heart defects) and intact valves, artificial valves, and endocarditis of artificial valves is usually caused by coagulase-negative staphylococci; endocarditis of the left half of the heart develops more often with the same frequency of damage to the mitral and aortic valves; severe course of the disease with high body temperature, chills, severe intoxication, rapid destruction of the valvular apparatus of the heart (there is predominantly acute pneumococcal endocarditis, less often subacute); more frequent damage to the aortic valve compared to other heart valves; the presence of a large vegetation on the affected valve (this sign is diagnosed using an ultrasound examination of the heart); an increase in the frequency of pneumococcal strains resistant to antibiotic therapy; frequent development of purulent foci (abscesses of the brain, myocardium, pleural empyema); high mortality (30-40%).
streptococci
There are some clinical features of infective endocarditis caused by various types of streptococcus. For endocarditis caused by Str. viridaris, are characteristic: often slow, gradual onset; development of endocarditis mainly on previously modified valves; a high incidence of immunocomplex pathology (nephritis, vasculitis, arthritis, myocarditis); lethality is about 10%.
Certain features are also inherent in endocarditis caused by Str. boyis: frequent presence in patients of a previous pathology of the gastrointestinal tract (cancer of the stomach or large intestine, gastric or duodenal ulcer, intestinal polyposis); development of heart failure in most patients; rare thromboembolic complications; high lethality (27%). For endocarditis caused by Str. pyogenes, are characterized by severe intoxication, high body temperature, pustular skin diseases in the period preceding the development of endocarditis, rapid damage to the heart valves (most often mitral), high mortality (18-20%).
Endocarditis caused by beta-hemolytic streptococcus develops more often in patients with diabetes mellitus, chronic alcoholism and with any previous heart disease (for example, rheumatic heart disease). This etiological variant of endocarditis is characterized by a severe course, thromboembolic complications (they are observed in almost 1/2 of patients). Mortality reaches 11-13%.
There are some clinical features of endocarditis caused by Str. agalactiae is a member of group B streptococci. This microorganism is part of the normal microflora of the oral cavity, urogenital and gastrointestinal tract. Under the influence of Str. agalactiae in the patient's body, the synthesis of fibrinolysin is disrupted, large vegetations are formed and systemic embolisms develop. In addition, septic musculoskeletal manifestations (arthritis, myositis, osteomyelitis) are extremely characteristic. Often there is a combination of endocarditis caused by Str. agalactiae, with malignant neoplasms of the colon.
Microorganisms of the NASEC group
Microorganisms of the NASEK group, which are representatives of the normal flora of the oropharynx and respiratory tract, cause subacute endocarditis of previously altered natural valves and endocarditis of prosthetic valves (in this case, endocarditis develops more often 1 year after prosthetics). Natural valve endocarditis caused by NASEK microorganisms is characterized by large vegetations and frequent systemic embolisms. Microorganisms of this group grow slowly on special media and blood culture should be incubated for 3 weeks. A characteristic feature of endocarditis caused by Haemophilus spp. is the development of the disease in women aged 20-40 years with the predominant localization of the process on the mitral valve.
Pseudomonas aeruginosa
Pseudomonas aeruginosa is one of the representatives of the gram-negative flora, most often causing endocarditis. In this case, intact and previously modified valves of both the left and right halves of the heart are involved. The course of endocarditis is severe with severe destruction of valves and the development of heart failure. The "entrance gates" of infection are the urogenital tract, infected wounds and burns. Pseudomonas aeruginosa endocarditis is very difficult to treat due to the high resistance of the pathogen to antibiotic therapy. Pseudomonas aeruginosa often causes infective endocarditis in intravenous drug users, affecting the tricuspid valve.
Brucella
Brucellous endocarditis is rare in people who have been in contact with farm animals with brucellosis. In this variant of endocarditis, the aortic or tricuspid valve is more often affected, an aneurysm of the sinus of Valsalva may develop, atrioventricular conduction disorders are often observed, and the pericardium is often involved. A general analysis of peripheral blood usually reveals leukopenia.
meningococci
Meningococcal endocarditis is now very rare. It usually develops against the background of a meningitis clinic and, as a rule, affects the previously undamaged mitral valve. Characteristic features of meningococcal endocarditis: high body temperature, arthralgia, hemorrhagic rash, large vegetations on the affected valve, hemorrhagic exudative myocarditis.
Salmonella
Salmonella endocarditis is a rare variant of infective endocarditis that affects pre-damaged mitral and aortic valves with rapid development of their destruction, frequent formation of blood clots in the atria. Salmonella also affects the vascular endothelium (endarteritis) with the development of aneurysms.
Fungal endocarditis
It usually develops in people who have undergone surgery on the heart and large vessels, as well as in drug addicts who inject drugs intravenously and in patients with a fungal infection. Contribute to the development of fungal endocarditis immunodeficiency states of various etiologies, in particular, due to cytostatic therapy, HIV infection. It is difficult to diagnose fungal endocarditis, because blood cultures are not always positive, especially in Aspergillus endocarditis (hemocultures are positive in Aspergillus endocarditis in 10-12% of patients, in candidiasis - in 70-80% of cases), and it is necessary to use a special cultivation technique.
The characteristic clinical features of fungal endocarditis are: thromboembolism in large arteries (cerebral, coronary, gastrointestinal tract, lower extremities), and thromboembolism is often the first clinical manifestation of the disease; signs of chorioretinitis or endophthalmitis (detected during ophthalmoscopic examination); symptoms of fungal infection of the mucous membranes of the oral cavity, esophagus, urinary tract, genital organs; large sizes of vegetation on the valves, reaching a diameter of 2 cm or more (a sign is determined by echocardiography), with aspergillus endocarditis, vegetations may not be located on the valves, but near the wall, therefore they may not be detected by ultrasound; predominant damage to the aortic valve (the aortic valve is affected in 44% of cases, the mitral valve - in 26%, the tricuspid valve - in 7% of cases), however, in streets with prosthetic valves, aortic valve damage is observed 4 times more often compared to the mitral valve; the formation of myocardial abscesses (more than 60% of patients, especially with Aspergillus endocarditis); severe course and high mortality (more than 50%).
Pathogenesis (what happens?) during Infective Endocarditis:
The pathogenesis of IE is rather complex and not fully understood. A schematic diagram of the pathogenesis of IE can be represented as follows: congenital, acquired defects of the heart valves increase in the rate and appearance of turbulence of the transvalvular blood flow mechanical damage to the endothelium of the valves deposition of platelets and fibrin on the damaged areas of the endocardium formation of chronic non-infectious endocarditis with thrombotic vegetations transient bacteremia against the background of a decrease in the body's reactivity adhesion and colonization of pathogenic bacteria in fibrino-platelet vegetations, inflammation of the endocardium, formation of microbial vegetations, destruction of valves, development of heart failure, a systemic infectious process with embolic, thrombohemorrhagic, immunocomplex lesions of internal organs and tissues (Figure 1).
As the initial mechanisms of pathogenesis, endocardial damage, bacteremia, adhesion, reproduction, colonization of pathogenic bacteria on the valves are distinguished. The main role in the development of IE belongs to the destruction of the endocardium, bacteremia. Experimental studies indicate that cardiac catheterization for several minutes causes sensitivity of the endocardium to microbial aggression for many days.
Electron microscopy data made it possible to trace the sequence of formation of the pathological process. It was found that under the influence of regurgitant blood flow, the shape and structure of endothelial cells change, intercellular permeability increases, and endothelial desquamation occurs. Pores are formed between endotheliocytes through which lymphocytes and macrophages penetrate. An increase in the size of the pores, a decrease in the athrombogenic properties of the endocardium enhances the adhesion of bacteria. At the site of detachment of dystrophically changed cells, intensive thrombus formation occurs. The endocardium is covered with activated platelets, “sewn” with fibrin fibers.
Damage, deendothelialization of the endocardium enhance the adhesion of bacteria, the formation of a covering layer of platelets, fibrin. A “zone of local agranulocytosis” inaccessible to phagocytes is created, which ensures the survival and reproduction of pathogenic microorganisms. In the process of ongoing bacterial colonization, the growth of the platelet-fibrin matrix, microbial thrombi are formed, vegetations, damage and destruction of the valve occur.
Figure 1. Scheme of the pathogenesis of IE.
Factors that enhance the adhesion of bacteria to the endocardium can be divided into local and general. The composition of the local includes congenital and acquired valve changes, impaired intracardiac hemodynamics. Birth defects increase the risk of bacteremia transforming into IE by up to 92%. Predisposing conditions for the onset of the disease create mechanical, biological artificial valves. Common factors include violations of the body's resistance, pronounced changes in immunity that develop during immunosuppressive therapy in drug addicts, alcoholics, the elderly and patients with changes in the HLA histocompatibility system.
The formation of IE occurs against the background of bacteremia, endocardial injury, and a decrease in body resistance. Bacteremia plays a leading role. The sources of bacteremia can be foci of chronic infection, invasive medical examinations and manipulations (bronchoscopy, gastroscopy, colonoscopy, surgical interventions), tonsillectomy, adenoidectomy, opening and drainage of infected tissues, dental procedures.
The development of IE depends on the massiveness, frequency, species specificity of bacteremia. The risk of developing the disease is especially high with repeated “minimal” or “massive” bacteremia due to surgical operations. staph bacteremia. aureus is a 100% risk factor for IE due to increased adhesion and peptidoglycan binding of the endocardium of these bacteria. Significantly lower virulence in epidermal staphylococcus and streptococci. The chance of developing IE in pneumococcal bacteremia is approximately 30%.
There are certain patterns in the localization of infection, due to a violation of intracardiac hemodynamics during the formation of a defect. Such anatomical formations in case of valve insufficiency are the surface of the MV from the side of the left atrium, the surface of the AC from the side of the aorta, the chord. With non-closure of the interventricular septum, the endocardium of the right ventricle in the region of the defect is more often affected.
Persistent bacteremia stimulates the immune system, triggering the immunopathological mechanisms of inflammation. Changes in immunity in IE are manifested by hypofunction of T-lymphocytes, hyperfunction of B-lymphocytes, polyclonal production of autoantibodies. Complement activation mechanisms are disrupted, circulating immune complexes are formed. In modern studies, a significant pathogenetic role of an increase in the concentration of CEC with deposition in target organs is confirmed. Undoubted attention deserves an increase in the concentration of interleukins 1, 6, 8 and tumor necrosis factor, the pro-inflammatory activity of which, along with the induction of an acute phase response, is involved in the development of systemic manifestations of IE.
Thromboembolism contributes to the generalization of the infectious process, the formation of heart attacks, and organ necrosis. Pulmonary embolism develops in 52-67% of patients with IE with a predominant lesion of the right heart chambers. Vessel obstruction is accompanied by humoral disorders resulting from the release of biologically active substances from platelet aggregates in a thrombus (thromboxane, histamine, serotonin).
With PE, “dead” spaces are formed in the lungs (several segments or a lobe) that are not perfused by mixed venous blood. Shunting of mixed venous blood in the lungs increases significantly. A decrease in the carbon dioxide voltage gradient between mixed venous and arterial blood, an increase in the concentration of carbon dioxide in arterial blood causes arterial hypoxemia.
An increase in total pulmonary vascular resistance to blood flow is one of the main mechanisms for the formation of arterial pulmonary hypertension in patients with IE. Changes in hemodynamics and blood rheology cause inadequate perfusion of vascular zones, gas exchange disorder. Reduced oxygen delivery to lung tissue, accumulation of tissue metabolites and toxic products of anaerobic processes are the cause of pulmonary infarction.
In the development of chronic HF in patients with IE, several pathogenetic mechanisms are distinguished: the formation of valve insufficiency (s), septic damage to the myocardium, pericardium, changes in hemodynamics, rhythm disturbance, conduction, fluid retention associated with impaired renal function. An important link in the pathogenesis of heart failure is an increase in afterload with a long-term increase in peripheral vascular resistance. Vasoconstriction causes maintenance of systemic arterial pressure, optimizes reduced cardiac output.
MV insufficiency causes dilatation, hypertrophy of the left parts of the heart, increased pressure in the vessels of the pulmonary circulation, decompensation of the left ventricular type, right ventricular hypertrophy, and heart failure in a large circle. Damage to the aortic valve contributes to the development of diastolic overload of the left ventricular hypertrophy, dilatation of the left ventricle of relative MV insufficiency (“mitralization of the defect”) hypertrophy, dilatation of the left atrium, stagnation of blood in the pulmonary circulation, decompensation of the left ventricular type of hypertrophy, dilatation of the right heart, right ventricular HF. Severe tricuspid valve insufficiency causes dilatation, right atrial hypertrophy, dilatation, right ventricular hypertrophy due to increased blood volume from the right atrium entering its cavity, venous stasis in the systemic circulation.
With IE, microcirculation and rheological properties of blood change. Intravascular coagulation occurs, which in its development goes through four stages. The first stage of hypercoagulation and compensatory hyperfibrinolysis begins in the affected organ, coagulation-active substances are released from the cells, and the activation of coagulation spreads to the blood. The second stage of increasing consumption coagulopathy and intermittent fibrinolytic activity is characterized by a decrease in the number of platelets, the concentration of fibrinogen in the blood. The third stage of defibrinogenation and total, but not permanent fibrinolysis (defibrinogenation-fibrinolytic), corresponds to complete DIC. The fourth stage is the stage of residual thrombosis and occlusion.
The causes of microcirculation disorders are microthrombosis, remodeling of microvessels. The change in the geometry of the vessels begins as an adaptive process in violation of hemodynamics, increased activity of tissue, humoral factors. Subsequently, vascular remodeling contributes to the progression of circulatory disorders. Changes in microcirculation are due to increased aggregation of platelets, erythrocytes. In left ventricular heart failure against the background of perivascular edema, erythrocyte aggregation, local erythrostasis, and blood flow fragmentation occur.
A special role is given to increased activity of plasma hemostasis. The significance of hyperfibrinogenemia, as an independent factor in reducing the rheological properties of blood and the progression of IE, has been substantiated in clinical and experimental studies. Important in violation of microhemodynamics is the formation of microthrombi. Hemorheological changes cause a decrease in the perfusion properties of blood, increase hemodynamic disorders in the periphery. Tissue hypoxia increases, aerobic metabolism is activated. Tissue hypoxia in chronic HF reduces myocardial contractility and increases pre- and afterload.
During IE, several pathogenetic phases are distinguished: infectious-toxic (septic), immuno-inflammatory, dystrophic. The first phase is characterized by transient bacteremia with adhesion of pathogenic bacteria to the endothelium and the formation of microthrombotic vegetations. The second phase is manifested by multiple organ pathology (endovasculitis, myocarditis, pericarditis, hepatitis, nephritis, diffuse glomerulonephritis).
Under the influence of endogenous toxins, decompensation of organs and systems occurs, metabolism is disturbed, and the body disintegrates as a biological whole. During the dystrophic phase, severe, irreversible changes in the internal organs are formed.
These pathogenetic phases are typical for all clinical and morphological forms and variants of the course of the disease. However, the pathogenesis of secondary IE has some peculiarities. Congenital heart disease increases the functional load on the cardiovascular system and valves, endothelium is damaged. The function of organs rich in reticuloendothelial tissue is subject to inhibition. The nonspecific resistance of the organism decreases. Transient bacteremia causes the formation of a primary infectious focus.
Against the background of a decrease in overall resistance, a chronic inflammatory process is formed. Sensitization of the organism by bacterial antigens develops. The myocardium is damaged by cardiac antibodies. During bacteremia from foci of chronic infection, bacteria adhere to the altered valves. A secondary septic focus is formed in the heart, which is the basis for the development of secondary IE.
Infective endocarditis with damage to the right chambers of the heart develops after damage to the TC by a subclavian catheter, with sounding of the heart, prolonged standing of the Swan-Ganz catheter, and frequent intravenous injections. The widespread use of vascular catheterization for the purpose of intensive infusion therapy increases the number of cases of thrombophlebitis, thrombosis, infection, followed by the development of sepsis.
It should be noted that 30% of subclavian vein catheters reach the cavity of the right atrium of the heart and injure the cusps of the TC. The installation of endocardial electrodes for pacing in some cases is the cause of an infectious lesion of the TC. The reason for the development of IE in the right chambers of the heart can be bullets, fragments of other firearms that have been in the heart for a long time.
Secondary IE with damage to the right chambers of the heart often develops with a ventricular septal defect, an open ductus arteriosus (22%). The development of IE is due to damage to the endocardium by regurgitant blood flow. With high small defects of the interventricular septum, a thin stream of blood injures the septal leaflet of the TC. In the case of an open ductus arteriosus, the endocardial surface of the pulmonary trunk is injured in the area of the defect. Thus, in recent decades, the most common cause of primary IE is sepsis, intravenous drug addiction, and the secondary cause is congenital heart disease.
For the development of IE in drug addicts, endocardial damage is typical with frequent intravenous injections. During injections of self-produced drugs, air bubbles damage the tricuspid valve endocardium in 100% of cases. The endocardium is injured, its roughness occurs. Damaged areas serve as a place of adhesion, platelet aggregation, followed by the formation of blood clots. Violation of asepsis contributes to the development of bacteremia, infection of the damaged areas of the endocardium with Staphylococcus aureus (70-80%). The reason for its affinity for the TC endocardium in drug addicts is not entirely clear.
Changes in immunity, nonspecific resistance are the key mechanisms of the pathogenesis of this form of the disease. According to the study of the immune status in patients with IE with damage to the right heart chambers, a decrease in T-helpers, an increase in T-suppressors, and a decrease in the activity of natural killers were revealed. These changes are caused by inhibition of the reactivity of the immune system due to the depletion of functional reserves. An increase in the concentration of TNF, a cytokine that plays a key role in the development of immune-inflammatory reactions of the body, was registered.
Among the numerous effects of TNF, attention is drawn to its effect on the collagen of valves of types 1, 3, 4, constituting 50-70% of its mass. Tumor necrosis factor inhibits the transcription of the collagen gene, thereby reducing the synthesis of the latter by fibroblasts. In addition, TNF stimulates the production of collagenase, which is involved in the degradation of valvular collagen. Denatured collagen fragments induce the production of inflammatory mediators by macrophages, induce and maintain the inflammatory process.
The number of drug addicts and patients who use vascular catheters for a long time is large. However, not everyone develops IE. In this regard, the genetic aspects of predisposition have been studied. According to the study of the HLA phenotype (according to the antigens of loci A, B), the most likely markers of genetic predisposition to IE with damage to the right chambers of the heart are the antigen of the HLA B35 system, the A2-B35 haplotype.
The structural basis for changes in the reactivity of the immune system in patients are violations of the spatial organization of the complex: T-cell receptor - immunogenic peptide - protein of the major histocompatibility complex. In the development of the disease, the combination of the genetic determinism of the immune system defect with the modification of histocompatibility antigens by infectious agents, chemicals (drugs, antibiotics) and other factors is important.
The development of prosthetic valve IE is due to many reasons: endocardial trauma during surgery, bacteremia, decreased body resistance, and changes in immunity. During the prosthetics of artificial valves, infection occurs, which is determined by the physical properties, the chemical composition of the implanted valve, and the adhesion of bacteria on the suture material. Increased adhesion of staphylococci on intracardiac sutures determines the composition of pathogens of early IEPK (staphylococcus epidermidis, staphylococcus aureus).
In 50% of cases of early PVE, the postoperative wound is the source of bacteremia. In the pathogenesis of late IEPK, transient bacteremia, which occurs during intercurrent infections (36%), dental procedures (24%), operations (12%), and urological studies (8%), is of key importance. Additional sources of infection are arterial systems, intravenous, urethral catheters, heart patches, endotracheal tubes.
Infection begins with abacterial thrombotic deposits, which then become infected with transient bacteremia. Large hemodynamic loads are the cause of the development of IE of an artificial valve located in the mitral position. Inflammation begins with the cuff of the prosthesis, the annulus fibrosus. Further, annular, annular abscesses are formed, paraprosthetic fistulas are formed, and the prosthesis is torn off.
Thus, the development of infective endocarditis is due to immunodeficiency, primary or secondary damage to the endocardium, and incoming bacteremia. The further course of the disease is mediated by a complex of pathogenetic mechanisms that are formed as a result of systemic vascular damage, multiple thromboembolism, immunocomplex reactions, changes in central and intracardiac hemodynamics, and disorders of the blood coagulation system.
Symptoms of Infective Endocarditis:
CLASSIFICATION
In the international classification of diseases of the 10th revision (1995), there are:
133.0. Acute and subacute infective endocarditis:
Bacterial,
Infectious without detailed specification,
Slowly flowing
Malignant,
Septic,
Ulcerative.
An additional code (B 95-96) of the list of bacterial and other infectious agents is used to designate an infectious agent. These rubrics are not used in primary disease coding. They are intended to be used as additional codes when it is appropriate to identify the causative agent of diseases classified elsewhere.
B 95. Streptococci and staphylococci as the cause of diseases classified elsewhere:
At 95.0. Group A streptococci as the cause of diseases classified elsewhere.
At 95.1. Group B streptococci as the cause of diseases classified elsewhere.
At 95.2. Group D streptococci as the cause of diseases classified elsewhere.
At 95.3. Streptococcus pneumoniae as the cause of diseases classified elsewhere.
At 95.4. Other streptococci as the cause of diseases classified elsewhere.
At 95.5. Unspecified streptococci as the cause of diseases classified elsewhere.
At 95.6. Staphylococcus aureus as the cause of diseases classified elsewhere.
At 95.7. Other staphylococci as the cause of diseases classified elsewhere.
At 95.8. Unspecified staphylococci as the cause of diseases classified elsewhere.
B 96. Other bacterial agents as the cause of diseases classified elsewhere:
At 96.0. Mycoplasma pneumoniae as the cause of diseases classified elsewhere Pleura-pneumonia-like-organism.
At 96.1. Klebsiella pneumoniae as the cause of diseases classified elsewhere.
At 96.2. Escherichi coli as the cause of diseases classified elsewhere.
At 96.3. Haemophilus influenzae as the cause of diseases classified elsewhere.
At 96.4. Proteus (mirabilis, morganii) as the cause of diseases classified elsewhere.
At 96.5. Pseudomonas (aeruginosa, mallei, pseudomallei) as the cause of diseases classified elsewhere.
At 96.6. Bacillus fragilis as the cause of diseases classified elsewhere.
B 96.7. Clostridium perfringens as the cause of diseases classified elsewhere.
At 96.8. Other specified bacterial agents as the cause of diseases classified elsewhere.
Table 1 presents the clinical classification of infective endocarditis by A.A. Demin and V.P. Drobysheva (2003). The authors identify the etiological section, course options, outcomes, clinical and morphological forms, pathogenetic stages of the development of the disease. Variants of damage to the heart, vessels of the kidneys, liver, spleen, lungs, nervous system are given. Great attention should be paid to risk stratification, predictors of embolic complications.
Table 1 Classification of infective endocarditis
| Etiological characteristics | Course, stage, outcomes | Clinical and morphological form | Target Organs: Lesions | Risk stratification |
| Gram-positive bacteria: staphylococci streptococci enterococci Gram-negative bacteria Pseudomonas aeruginosa Microbial coalitions Rickettsia Viruses | Flow: subacute Stage: infectious-toxic immunoinflammatory dystrophic Degree of activity: high(III) moderate(II) minimum(I) outcomes: recovery remission treatment failure recurrence | Primary(on intact valves) Secondary with valvular and vascular injuries): rheumatic, atherosclerotic, lupus, syphilitic, traumatic defects and arteriovenous aneurysms, commissurotomy, artificial vascular anastomoses, shunts in chronic hemodialysis, transplanted heart valves | Heart Key words: infarction, malformation, abscess, aneurysm, myocarditis, arthymia, pericarditis, heart failure Vessels Key words: vasculitis, thromboembolism, thrombosis, hemorrhages, aneurysm kidneys: focal nephritis, diffuse glomerulonephritis, nephrotic syndrome, heart attack, renal failure Liver: hepatitis Spleen Key words: plenomegaly, infarction, abscess, rupture Lungs Key words: pneumonia, abscess, infarction, pulmonary hypertension Nervous system: CVA, transient cerebrovascular accident, meningoencephalitis, abscess, cyst | High risk factors (grade III): involvement of more than 5 target organs, perivalvular abscesses and / or destruction of valves, Staphylococcus aureus in blood culture with AK lesions, multivalvular lesions, a large number of CF, involvement of all valve leaflets, NYHA HF III-IV FC Moderate risk factors (grade II): defeat 3-5 organs |
In a serious condition, confidence in the diagnosis of infective endocarditis of the left heart and (or) radiographic signs of septic embolism of the branches of the pulmonary artery, empirical antibiotic therapy is started after taking blood for culture. It is not necessary for all injecting drug addicts with fever alone. In many cases, it is wiser to wait for the results of blood cultures under conditions of careful observation: in some patients, another serious illness is diagnosed during this time, in others, the fever turns out to be due to a mild illness or a pyrogenic or allergic reaction to the drug and disappears within a day.
Antibiotics that are active against staphylococci must be included in the empiric antibiotic regimen. All drugs are administered intravenously. The choice of drug depends on the severity of the patient's condition and the sensitivity spectrum of pathogens isolated in the area. A beta-lactam antibiotic (oxacillin or nafcillin) is usually prescribed, or, if infection with methicillin-resistant strains of Staphylococcus aureus is suspected, vancomycin. If gram-negative pathogens are common in the area, an aminoglycoside is added. In infective endocarditis caused by methicillin-sensitive staphylococcus, use oxacillin or nafcillin, 1.5-2 g every 4 hours for 4 weeks. In a serious condition, an aminoglycoside is sometimes added in the first 2 weeks of treatment - usually gentamicin, 1.5 mg / kg every 8 hours. Bacteremia stops faster, but otherwise there is no increase in the effectiveness of treatment. For penicillin allergy or infection caused by methicillin-resistant strains of Staphylococcus aureus, vancomycin is used, 1 g every 12 hours. For infective endocarditis caused by other pathogens, therapy depends on sensitivity to antibiotics. Usually the course lasts 4 weeks.
There are reports of the cure of uncomplicated infective endocarditis of the right heart with a beta-lactam antibiotic in combination with an aminoglycoside in 2 weeks. Such a scheme may be appropriate, since it is difficult to provide a safe venous access for a long time. Most experts consider it necessary to administer intravenous antibiotics throughout treatment, although this often requires the placement of an indwelling central venous catheter.
The prognosis of staphylococcal endocarditis of the right heart in injection drug addicts is favorable. Antibiotic resistance and death are rare.
With endocarditis caused by other pathogens and lesions of the left heart, the prognosis is worse, the morbidity rate and mortality are higher.
There is no consensus regarding the surgical treatment of infective endocarditis in drug addicts, as well as in patients of other groups. The indications for surgery are the same as in other patients: persistent heart failure, unopened myocardial abscess, ineffectiveness of antibiotic therapy, especially in candidal and other fungal endocarditis. The nature of the operation depends on which valve is affected. In severe tricuspid valve endocarditis, excision of the tricuspid valve is effective. With endocarditis of the mitral or aortic valve, their prosthetics are required; in most cases it is safe, but if the patient continues to inject drugs, then there is a constant risk of infective endocarditis. Therefore, the feasibility of such operations is highly controversial. The issue of valve replacement should be decided jointly by the attending physician, the cardiac surgeon and the patient himself.
Endocarditis
General information
Endocarditis- inflammation of the connective tissue (inner) shell of the heart, lining its cavities and valves, often of an infectious nature. Manifested by high body temperature, weakness, chills, shortness of breath, cough, chest pain, thickening of the nail phalanges like "drumsticks". Often leads to damage to the heart valves (usually aortic or mitral), the development of heart defects and heart failure. Relapses are possible, mortality in endocarditis reaches 30%.
Infective endocarditis occurs when the following conditions are present: transient bacteremia, damage to the endocardium and vascular endothelium, changes in hemostasis and hemodynamics, impaired immunity. Bacteremia can develop with existing foci of chronic infection or invasive medical manipulations.
The leading role in the development of subacute infective endocarditis belongs to green streptococcus, in acute cases (for example, after open heart surgery) - to Staphylococcus aureus, less often Enterococcus, pneumococcus, Escherichia coli. In recent years, the composition of infectious causative agents of endocarditis has changed: the number of primary acute endocarditis of a staphylococcal nature has increased. With bacteremia Staphylococcus aureus, infective endocarditis develops in almost 100% of cases.
Endocarditis caused by gram-negative and anaerobic microorganisms and fungal infection are severe and do not respond well to antibiotic therapy. Fungal endocarditis occurs more often with prolonged antibiotic treatment in the postoperative period, with long standing venous catheters.
Adhesion (sticking) of microorganisms to the endocardium is facilitated by certain general and local factors. Among the common factors are severe immune disorders observed in patients with immunosuppressive treatment, in alcoholics, drug addicts, and the elderly. Local include congenital and acquired anatomical damage to the heart valves, intracardiac hemodynamic disorders that occur with heart defects.
Most subacute infective endocarditis develops with congenital heart disease or with rheumatic lesions of the heart valves. Hemodynamic disturbances caused by heart defects contribute to valve microtrauma (mainly mitral and aortic), changes in the endocardium. On the valves of the heart, characteristic ulcerative-warty changes develop that look like cauliflower (polypous overlays of thrombotic masses on the surface of ulcers). Microbial colonies contribute to the rapid destruction of the valves, their sclerosis, deformation and rupture can occur. The damaged valve cannot function normally - heart failure develops, which progresses very quickly. There is an immune lesion of the endothelium of small vessels of the skin and mucous membranes, leading to the development of vasculitis (thrombovasculitis, hemorrhagic capillary toxicosis). Characterized by a violation of the permeability of the walls of blood vessels and the appearance of small hemorrhages. Often there are lesions of larger arteries: coronary and renal. Often, the infection develops on the prosthetic valve, in which case the causative agent is most often streptococcus.
The development of infective endocarditis is facilitated by factors that weaken the immunological reactivity of the body. The incidence of infective endocarditis is constantly increasing worldwide. The risk group includes people with atherosclerotic, traumatic and rheumatic damage to the heart valves. Patients with ventricular septal defect, coarctation of the aorta have a high risk of infective endocarditis. Currently, the number of patients with valve prostheses (mechanical or biological), artificial pacemakers (pacemakers) has increased. The number of cases of infective endocarditis is increasing due to the use of prolonged and frequent intravenous infusions. Drug addicts often suffer from infective endocarditis.
Classification of infective endocarditis
By origin, primary and secondary infective endocarditis are distinguished. Primary usually occurs in septic conditions of various etiologies against the background of unchanged heart valves. Secondary - develops against the background of an already existing pathology of blood vessels or valves with congenital malformations, rheumatism, syphilis, after valve replacement surgery or commissurotomy.
According to the clinical course, the following forms of infective endocarditis are distinguished:
- acute - duration up to 2 months, develops as a complication of an acute septic condition, severe injuries or medical manipulations on the vessels, heart cavities: nosocomial (nosocomial) angiogenic (catheter) sepsis. It is characterized by a highly pathogenic pathogen, severe septic symptoms.
- subacute - lasting more than 2 months, develops with insufficient treatment of acute infective endocarditis or the underlying disease.
- protracted.
In drug addicts, the clinical features of infective endocarditis are young age, rapid progression of right ventricular failure and general intoxication, infiltrative and destructive lung damage.
In elderly patients, infective endocarditis is caused by chronic diseases of the digestive system, the presence of chronic infectious foci, and damage to the heart valves. There are active and inactive (healed) infective endocarditis. According to the degree of damage, endocarditis occurs with limited damage to the leaflets of the heart valves or with a lesion that extends beyond the valve.
The following forms of infective endocarditis are distinguished:
- infectious-toxic - characterized by transient bacteremia, adhesion of the pathogen to the altered endocardium, the formation of microbial vegetations;
- infectious-allergic or immune-inflammatory - clinical signs of damage to internal organs are characteristic: myocarditis, hepatitis, nephritis, splenomegaly;
- dystrophic - develops with the progression of the septic process and heart failure. The development of severe and irreversible lesions of internal organs is characteristic, in particular, toxic degeneration of the myocardium with numerous necrosis. Myocardial damage occurs in 92% of cases of prolonged infective endocarditis.
Symptoms of infective endocarditis
The course of infective endocarditis may depend on the duration of the disease, the age of the patient, the type of pathogen, and also on previous antibiotic therapy. In cases of a highly pathogenic pathogen (Staphylococcus aureus, gram-negative microflora), an acute form of infective endocarditis and early development of multiple organ failure are usually observed, and therefore the clinical picture is characterized by polymorphism.
The clinical manifestations of infective endocarditis are mainly due to bacteremia and toxinemia. Patients complain of general weakness, shortness of breath, fatigue, lack of appetite, weight loss. A characteristic symptom of infective endocarditis is fever - a rise in temperature from subfebrile to hectic (exhausting), with chills and profuse sweating (sometimes, heavy sweating). Anemia develops, manifested by pallor of the skin and mucous membranes, sometimes acquiring an "earthy", yellowish-gray color. There are small hemorrhages (petechiae) on the skin, mucous membrane of the oral cavity, palate, on the conjunctiva of the eyes and eyelid folds, at the base of the nail bed, in the collarbone region, arising from the fragility of the blood vessels. Damage to the capillaries is detected with a mild injury to the skin (a pinch symptom). Fingers take the form of drumsticks, and nails - watch glasses.
Most patients with infective endocarditis have damage to the heart muscle (myocarditis), functional murmurs associated with anemia, and valve damage. With damage to the leaflets of the mitral and aortic valves, signs of their insufficiency develop. Sometimes there is angina, occasionally there is a friction rub of the pericardium. Acquired valvular disease and myocardial damage lead to heart failure.
In the subacute form of infective endocarditis, embolisms of the vessels of the brain, kidneys, and spleen occur with thrombotic deposits that have come off the cusps of the heart valves, accompanied by the formation of heart attacks in the affected organs. Hepato- and splenomegaly are found, on the part of the kidneys - the development of diffuse and extracapillary glomerulonephritis, less often - focal nephritis, arthralgia and polyarthritis are possible.
Complications of infective endocarditis
Fatal complications of infective endocarditis are septic shock, embolism to the brain, heart, respiratory distress syndrome, acute heart failure, multiple organ failure.
With infective endocarditis, complications from the internal organs are often observed: kidneys (nephrotic syndrome, heart attack, renal failure, diffuse glomerulonephritis), heart (valvular heart disease, myocarditis, pericarditis), lungs (heart attack, pneumonia, pulmonary hypertension, abscess), liver ( abscess, hepatitis, cirrhosis); spleen (heart attack, abscess, splenomegaly, rupture), nervous system (stroke, hemiplegia, meningoencephalitis, brain abscess), blood vessels (aneurysms, hemorrhagic vasculitis, thrombosis, thromboembolism, thrombophlebitis).
Diagnosis of infective endocarditis
When collecting an anamnesis, the patient finds out the presence of chronic infections and past medical interventions. The final diagnosis of infective endocarditis is confirmed by instrumental and laboratory data. In a clinical blood test, a large leukocytosis and a sharp increase in ESR are detected. Multiple blood cultures to identify the causative agent of infection have an important diagnostic value. Blood sampling for bacteriological culture is recommended at the height of fever.
The data of a biochemical blood test can vary widely in one or another organ pathology. With infective endocarditis, there are changes in the protein spectrum of the blood: (α-1 and α-2-globulins increase, later - γ-globulins), in the immune status (the CEC, immunoglobulin M increases, the total hemolytic activity of the complement decreases, the level of anti-tissue antibodies increases) .
A valuable instrumental study for infective endocarditis is EchoCG, which allows you to detect vegetations (more than 5 mm in size) on the heart valves, which is a direct sign of infective endocarditis. More accurate diagnosis is carried out using MRI and MSCT of the heart.
Treatment of infective endocarditis
In case of infective endocarditis, the treatment is necessarily inpatient, until the general condition of the patient improves, bed rest and diet are prescribed. The main role in the treatment of infective endocarditis is assigned to drug therapy, mainly antibacterial, which is started immediately after blood culture. The choice of antibiotic is determined by the sensitivity of the pathogen to it, it is preferable to prescribe broad-spectrum antibiotics.
In the treatment of infective endocarditis, penicillin antibiotics in combination with aminoglycosides have a good effect. Fungal endocarditis is difficult to treat, so amphotericin B is prescribed for a long time (several weeks or months). They also use other agents with antimicrobial properties (dioxidin, antistaphylococcal globulin, etc.) and non-drug methods of treatment - autotransfusion of irradiated blood with ultraviolet radiation.
With concomitant diseases (myocarditis, polyarthritis, nephritis), non-hormonal anti-inflammatory drugs are added to the treatment: diclofenac, indomethacin. In the absence of the effect of drug treatment, surgical intervention is indicated. Prosthetic heart valves are performed with excision of damaged areas (after the severity of the process subsides). Surgical interventions should be carried out by a cardiac surgeon only according to indications and accompanied by antibiotics.
Prognosis for infective endocarditis
Infective endocarditis is one of the most severe cardiovascular diseases. The prognosis for infective endocarditis depends on many factors: existing valvular lesions, timeliness and adequacy of therapy, etc. The acute form of infective endocarditis without treatment ends in death after 1–1.5 months, the subacute form - after 4–6 months. With adequate antibiotic therapy, mortality is 30%, with infection of prosthetic valves - 50%. In older patients, infective endocarditis is more indolent, often not immediately diagnosed, and has a poorer prognosis. In 10-15% of patients, the transition of the disease to a chronic form with relapses of exacerbation is noted.
Prevention of infective endocarditis
Persons with an increased risk of developing infective endocarditis are subject to the necessary monitoring and control. This applies, first of all, to patients with prosthetic heart valves, congenital or acquired heart defects, vascular pathology, with a history of infective endocarditis, with foci of chronic infection (caries, chronic tonsillitis, chronic pyelonephritis).
The development of bacteremia can accompany various medical manipulations: surgical interventions, urological and gynecological instrumental examinations, endoscopic procedures, tooth extraction, etc. For a preventive purpose, a course of antibiotic therapy is prescribed for these interventions. It is also necessary to avoid hypothermia, viral and bacterial infections (flu, tonsillitis). It is necessary to carry out sanitation of foci of chronic infection at least 1 time in 3-6 months.
As a manuscript
Ulanova
Veronika Ivanovna
Infective endocarditis in people with drug dependence
(clinical and morphological study)
14.01.04 - internal diseases
14.03.02 - pathological anatomy
A V T O R E F E R A T
dissertations for a degree
doctors of medical sciences
St. Petersburg
The work was carried out at the St. Petersburg Academy of Postgraduate Education of the Federal Agency for Health and Social Development
Scientific consultants:
Mazurov Vadim Ivanovich
Doctor of Medical Sciences
Professor Zinzerling Vsevolod Alexandrovich
Official opponents:
Corresponding Member of the Russian Academy of Medical Sciences Honored Scientist of the Russian Federation
Professor Simonenko Vladimir Borisovich
doctor of medical sciences professor Nesterko Andrey Onufrievich
doctor of medical sciences professor Ariel Boris Mikhailovich
Leading organization: Academician I. P. Pavlov St. Petersburg State Medical University.
The defense of the dissertation will take place on February 20, 2012 at ___ o'clock at a meeting of the council for the defense of doctoral and master's theses
D 215.002.06 at the Federal State Educational Institution of Higher Professional Education "Military Medical Academy. S. M. Kirov” Ministry of Defense of the Russian Federation (194044, Academician Lebedev St., 6).
The dissertation can be found in the fundamental library of the Federal State Educational Institution of Higher Professional Education “VMedA im. S. M. Kirov "at the address: 194044, st. Acad. Lebedeva, 6.
Scientific Secretary of the Dissertation Council
doctor of medical sciences professor
A. E. Filippov
GENERAL DESCRIPTION OF WORK
The relevance of research. Infective endocarditis (IE) is one of the most urgent problems of modern clinical medicine. In recent years, there has been a significant increase in the number of patients with infective endocarditis both in our country and abroad. Analysis of the pathomorphism of IE indicates a steady increase in the number of its primary forms. Over the past decades, there has been an increase in the number of elderly and senile patients with IE. According to most researchers, the increase in the incidence is associated both with the difficulties of early diagnosis and with an increase in the number of risk factors for the development of this disease. The widespread use of invasive research methods (vascular catheters, angiographic and intracardiac procedures), as well as an increase in the number of surgical interventions on the heart, is associated with an increased risk of developing infective endocarditis. Along with this, a high incidence of IE is recorded among people who use intravenous drugs. According to the Federal Drug Control Service (FSKN), the number of drug addicts in Russia currently exceeds 6 million people, and the number of drug addicts registered in drug dispensaries of the Russian Federation is 500 thousand people. In this regard, the problem of infective endocarditis, which develops in people who use intravenous drugs, seems to be relevant. Of particular importance is the study of the etiological factors of this disease and the characteristics of the clinical course of IE in drug addicted patients who are HIV-infected and have concomitant viral hepatitis C and B. A number of studies have established a relatively favorable clinical course of infective endocarditis in HIV-infected patients (Moss R., Munt B., 2003; Pulvirenti J. J., 1996; Hoen B. et al., 2002; Arshad A., 2000).
Along with this, according to B. D. Prendergast (2003), G. D'Amati et al. (2001), P. Rerkpattanapipat et al. (2000), in HIV-infected patients with IE, destructive processes in the endocardium are more often observed, which are accompanied by perforation of the leaflets of the heart valves, rupture of the chords and papillary muscles.
The clinical significance of concomitant chronic hepatitis C and B in HIV-infected drug addicts with infective endocarditis seems to be insufficiently studied. The results of the study by A. H. Mohsen et al. (2003), D. M. Patrick et al. (2001), D. Vlahov et al. (1994) showed that in this group of patients, along with pathological changes caused by the course of a generalized bacterial infection, there are also morphological signs of severe viral liver damage. According to other authors, chronic hepatitis C and B with a moderate and minimal degree of activity does not significantly affect the clinical course and the level of hospital mortality in drug addicted patients with IE (Moss R., Munt B., 2003; Stein M. D. et al., 2001; Sulkowsky M. S. et al., 2000).
According to the literature, the significance of S. aureus as a factor in hospital mortality in this group of patients has not been finally determined, and the clinical picture of infective endocarditis in them has not been sufficiently studied. Information about the incidence and prevalence of antibiotic-resistant strains of Staphylococcus aureus in HIV-infected drug addicted patients with IE with chronic hepatitis C and B is also controversial (Demin A. A. et al., 2000; Ako J. et al., 2003; Bouza E et al., 2001; Cabell C. H. et al., 2002).
According to most researchers, conservative therapy is one of the main directions in the treatment of IE (Tatarchenko I. P., Komarov V. T., 2000; Shlyapnikov S. A., 2002; Bayer A. S. et al., 1998; Baddour L. M. et al., 2005; Cabell C. H., Abrutyn E., 2002). Along with this, the regimens of etiotropic therapy, as well as the timing of the complex treatment of IE in drug addicts, have not been finally determined. According to L. M Baddour et al. (2005), it is advisable to treat uncomplicated IE in people with drug dependence with oxacillin in combination with gentamicin for 6 weeks, while other authors report the possibility of a short course of antibiotic therapy not exceeding 2 weeks (Moss R., Munt B. 2003; Riedemann N. C. et al. 2003; Chang F. Y. et al., 2003; Rubinstein E. et al., 1998).
According to a number of authors, in drug-addicted patients with IE with isolated lesions of the tricuspid valve, surgical methods of treatment are required in more rare cases than in patients with involvement of the left heart chambers due to the rare development of heart failure and an adequate response to antibiotic therapy, which makes it possible to attribute drug therapy to the main methods of treating IE in this group of patients (Chang F. Y., 2000; Moss R., Munt B., 2003; Corti M. E. et al., 2004; De Alarcon A., Villanueva J. L., 1998; Delahaye F. et al., 2002; Espinosa Parra F. J., 2000, Frater R. W., 2000, Hoen B. et al., 2002). According to most researchers, the main reasons for the lack of cardiac surgical treatment of drug addicted patients are patients' refusal to undergo surgery, as well as the development of purulent-septic complications and continued drug use (Valencia E., Miro J., 2004; Wilson L. E. et al., 2002; Tak T et al., 2002; Carrel T., 1993; Pulvirenti J. J. et al., 1996; Hoen B., 2002).
In the works of recent years, data on the effect of systemic enzyme therapy on the clinical course of IE in drug addicts, as well as the definition of indications for its appointment, are not fully reflected (Beloborodov V. B., 1998; Koshkin V. M. et al., 2004; Banker D. D., 1998; Cabell C. H., Abrutyn E., 2002).
The actual problem of IE in drug addicted patients remains the prognosis of the disease and the identification of factors that determine hospital mortality of HIV-infected patients with concomitant chronic hepatitis C and mixed hepatitis C and B. According to the results of a study by M. Faber et al. (1995), A. De Alarcon et al. (1998), E. Valencia (2004), the level of in-hospital mortality in patients with IE with isolated lesions of the tricuspid valve in the absence of surgical treatment ranges from 2.9 to 10%, while other researchers report that mortality from IE caused by aureus staphylococcus is more than 20% (Cabell C. H et al., 2002; Chang F. Y. et al., 2003; Cicalini S. et al., 2001).
Thus, the study of the clinical and morphological picture of infective endocarditis in people with drug addiction, elucidation of the impact on the course of the disease of HIV infection, chronic hepatitis C and mixed hepatitis C and B, analysis of the survival of drug addicted patients with IE in order to establish factors affecting the outcome disease, as well as clarifying the tactics of conservative treatment of this group of patients with the use of systemic enzyme therapy drugs is an important scientific direction and is of great practical importance.
The purpose of the study was to study the features of the clinical course and morphogenesis of infective endocarditis in HIV-infected injection drug addicts with concomitant chronic hepatitis C and mixed hepatitis C and B, as well as the development of methods for their treatment using systemic enzyme therapy.
Research objectives
1. To study the clinical course of infective endocarditis in HIV-infected drug addicts with chronic hepatitis C and mixed hepatitis C and B and compare it with the clinical picture of infective endocarditis in people without drug addiction, HIV infection and viral hepatitis.
2. To study the etiological factors of infective endocarditis in the group of drug addicts, HIV-infected patients with chronic viral hepatitis and compare the data obtained with the etiological factors in patients without drug addiction, HIV infection and viral hepatitis.
3. To analyze autopsy data from HIV-infected drug addicts with chronic viral hepatitis who died from complications of infective endocarditis, and compare the data obtained with the morphological picture of infective endocarditis in patients without drug dependence, HIV infection and chronic hepatitis C and mixed hepatitis C and V.
4. To establish the features of the clinical course and pathomorphism of infective endocarditis in HIV-infected drug addicts with chronic viral hepatitis C and mixed hepatitis C and B.
5. To determine the factors influencing the outcomes and prognosis of infective endocarditis in drug-dependent HIV-infected patients with chronic viral hepatitis and in patients without drug addiction, HIV infection and chronic hepatitis.
6. To study the effect of systemic enzyme therapy drugs on the clinical course and prognosis of infective endocarditis in people with drug dependence, to conduct a comparative analysis of the main clinical and laboratory data in patients treated with Wobenzym as part of the complex therapy of IE and in the control group.
7. To develop a tactic for the conservative treatment of infective endocarditis using systemic enzyme therapy in drug-addicted HIV-infected patients with chronic viral hepatitis C and mixed hepatitis C and B.
Provisions for defense
1. Infective endocarditis in drug addicts is characterized by a predominant lesion of the right chambers of the heart. The features of the clinical course of infective endocarditis in these patients are asymptomatic manifestations of heart damage, rare development of heart failure, and partially reversible hemodynamic disturbances against the background of ongoing conservative therapy.
2. The acute course of infective endocarditis in HIV-infected patients is characterized by a rarer development of purulent pleurisy, meningitis and pericarditis than in patients without drug addiction and HIV infection. Recurrent septic pulmonary embolism with the formation of multiple foci of infarction pneumonia is one of the most common complications of infective endocarditis in drug addicts.
3. Staphylococcus aureus, resistant to beta-lactam antibiotics of the penicillin series, is the most common causative agent of infective endocarditis in drug addicts, and in patients without drug addiction and HIV infection, opportunistic microflora, including gram-negative microorganisms, predominates in the etiology of the disease.
4. The main factors determining the outcome of infective endocarditis in people with drug addiction are the size of vegetations on the leaflets of the tricuspid valve, the development of left ventricular failure, DIC, as well as destructive processes in the lungs and high degrees of tricuspid valve insufficiency, and in patients without drug addiction and HIV infection, risk factors for death include heart failure, cerebral embolism, and embologenic myocardial infarction.
5. The morphological picture of infective endocarditis in people with drug addiction is characterized by the formation of thrombo-ulcerative lesions of the heart valves, the formation of multiple foci of infiltration in the lungs as a result of septic thromboembolism of the branches of the pulmonary artery, the presence of foci of purulent fusion in the myocardium, as well as secondary septic endovasculitis and severe dystrophic changes in organs and tissues.
6. The inclusion of systemic enzyme therapy in the complex treatment of drug addicted patients with infective endocarditis can improve the course of the disease, reduce the duration of the period of bacteremia, and also reduce the frequency of relapses of septic pulmonary embolism.
Scientific novelty of the research associated with the identification of the features of the clinical course of infective endocarditis in drug-addicted HIV-infected patients, which include the acute course of the disease, recurrence of septic pulmonary embolism with the formation of multiple foci of infarction pneumonia and the development of high-grade respiratory failure. Along with this, it was found that the clinical picture of heart damage in these patients is characterized by low symptoms, rare development of heart failure, as well as partially reversible nature of central hemodynamic disorders against the background of ongoing conservative therapy.
It has been established that the presence of systemic immunosuppression in HIV-infected drug-dependent patients with IE is accompanied by the formation of severe dystrophic and alterative changes in organs and tissues, widespread septic vasculitis with secondary circulatory disorders and the development of multiple organ failure.
As a result of the analysis of survival according to Cox, the main factors determining hospital mortality in HIV-infected drug-dependent patients with IE with chronic hepatitis C and B were identified, which include severe destructive lung lesions, high-grade tricuspid valve insufficiency, and the development of DIC. Based on the mathematical model proposed for the first time, the dependence of the degree of survival of drug-addicted patients with IE on the size of vegetations on the tricuspid valve leaflets was proved.
For the first time, the effect of systemic enzyme therapy drugs on the clinical course and outcome of IE in people with drug dependence was studied. A positive effect of SET preparations on the course of the systemic inflammatory process in drug-addicted patients with IE was established, which is due to their anti-inflammatory and anti-edematous effects. Along with this, in patients with recurrent septic thromboembolism of the branches of the pulmonary artery, a positive effect of Wobenzym on the rheological properties of blood associated with the fibrinolytic and antiaggregatory effects of drugs of this group was proved.
Practical significance
As a result of a comparative clinical and morphological study, it was found that infective endocarditis in people with drug addiction is characterized by an acute course with a predominant lesion of the right heart chambers, a significant number of complications, among which septic pulmonary embolism is the most common syndrome. The main causes of high hospital mortality in HIV-infected drug addicts have been identified, including severe dystrophic and alterative changes in organs and tissues due to the course of a generalized infection, as well as the development of septic vasculitis, acute DIC and secondary circulatory disorders. Based on a comparative analysis of the main clinical syndromes in drug-dependent patients with IE and in patients without drug dependence, it was shown that drug-resistant heart failure is a rare complication of IE in people with drug dependence. Comparative analysis of clinical data, results of complex therapy and outcomes of infective endocarditis in the group of drug addicted patients and in patients of the control group made it possible to establish that the majority of drug addicted patients have an adequate response to ongoing conservative therapy.
The inclusion of systemic enzyme therapy preparations in the complex therapy of infective endocarditis has a positive effect on the clinical course of the disease due to a reduction in the duration of bacteremia, relief of the systemic inflammation syndrome at an earlier time, and a decrease in the frequency of recurrence of embolism of the branches of the pulmonary artery, which reduces the period of inpatient treatment of drug addicted patients.
Establishment of the main predictors of hospital mortality in infective endocarditis in people with drug dependence, which include the size of microbial vegetations on the heart valves, the presence of left ventricular failure, severe destructive lung lesions and high-grade tricuspid valve insufficiency, makes it possible to predict the course and outcome of the disease in these patients.
On the basis of the departments of general therapy and cardiology of the Alexander Hospital for the period 1996–2008. personally conducted a clinical examination and treatment of 165 patients with infective endocarditis, identified the features of the course of IE, and developed an algorithm for laboratory and instrumental studies in drug-addicted patients with IE and in the control group. Statistical processing of the obtained data was carried out using the model of proportional risks of death according to Cox, and a mathematical model was created for the influence of the size of vegetations on the tricuspid valve leaflets on the prognosis of IE in people with drug addiction.
Based on the results of macro- and microscopic examination of the sectional material, clinical and morphological comparisons were made, which made it possible to establish the main causes of lethal outcomes of IE in drug addicted patients, as well as to determine the significance of HIV infection and chronic hepatitis C in the thanatogenesis of this group of patients.
The use of systemic enzyme therapy preparations (Wobenzym) in the complex treatment of IE in people with drug dependence has been introduced into clinical practice.
Implementation of work results
The results of the study are used in the practical work of the cardiosurgical and therapeutic departments of St. Petersburg Medical Academy of Postgraduate Education, the departments of the therapeutic profile of the Alexander Hospital, the City Rheumatology Center of St. Petersburg, the North-Western Rheumatology Center, and are also introduced into the treatment and diagnostic process of the Department of Rheumatology of the Leningrad Regional Clinical Hospital.
Forms of implementation: 3 textbooks on the clinic, diagnosis and treatment of infective endocarditis have been published. The research materials are introduced into the lecture material and the educational process for the improvement of doctors at the Department of Therapy and Rheumatology. E. E. Eikhvald, Department of Cardiovascular Surgery, Department of Cardiology, Department of Therapy and Clinical Pharmacology of St. Petersburg MAPO, in teaching students at the Department of Pathology of the Medical Faculty of St. Petersburg State University, and are also used in the training of interns and clinical residents at the same departments .
Materials and methods of research
A clinical examination of 165 patients with infective endocarditis was carried out, 110 of them were injection drug addicts. All patients were divided into three groups. The first group consisted of 63 HIV-infected drug addicts with chronic hepatitis C and mixed hepatitis C and B. The second group consisted of 47 HIV-infected drug addicts without chronic hepatitis. The third (control) group included 55 patients without drug addiction, HIV infection and chronic hepatitis.
Infective endocarditis in patients of groups I and II was characterized by a predominant lesion of the right heart chambers with localization of vegetations on the tricuspid valve (TC) leaflets in 84.1% and 80.9% of cases, respectively. The mean age of patients in group I was 29 ± 3.2 years, in group II - 31.9 ± 2.2 years. In the first and second groups of patients, males predominated - 38 (60.3%) and 29 people (61.7%), respectively. Of the surveyed drug addicted patients, damage to the left chambers of the heart was observed in 19 people (17.3%). The third group of patients was dominated by women (56.4%), whose mean age was 42.4 ± 6.9 years. Among the patients of the third group, 15 people had congenital and acquired heart defects, IE of artificial valves was detected in 25 patients, and damage to native heart valves was determined in 15 older patients.
In groups I and II of HIV-infected drug addicts, concomitant chronic hepatitis was diagnosed in 63 people (57.3%), of which hepatitis C occurred in 56 patients (88.9%), mixed hepatitis C and B - in 7 ( 11.1%) of patients.
All drug-addicted patients had damage to native (own) heart valves in the absence of congenital and acquired defects or other structural anomalies of the valves.
The distribution of patients with IE in groups I, II and III, depending on the presence of concomitant HIV infection and chronic hepatitis, is shown in Figure 1.
The work used general clinical, laboratory and instrumental studies.
Instrumental methods included transthoracic and transesophageal echocardiography (Logic 400 GE), computed tomography (Siemens, GE), ultrasound (Sonoline G60S).
Laboratory methods included immunoassays, enzyme-linked immunosorbent assay (ELISA), immune blotting (Western-blot) and PCR for the diagnosis of HIV infection, as well as the determination of DNA and RNA of hepatitis viruses using PCR.
Rice. 1. Distribution of patients depending on the presence of HIV infection and chronic hepatitis.
Data regarding the nature of heart valve damage in patients of group III are presented in Table 1.
Table 1
Distribution of patients with infective endocarditis of group III depending on the nature of the damage to the heart valves
Characteristics of the heart valves | Number of patients |
Mitral + aortic valve prostheses mitral valve prosthesis Aortic valve prosthesis | |
Congenital heart defects, including:
| |
Acquired heart defects, including:
| |
obstructive form | |
Microbiological methods included microscopy and cultures of venous blood, sectional material with the determination of sensitivity to antibiotics of isolated strains.
The morphological methods used included standard macro- and microscopic examinations with staining of paraffin sections with hematoxylin-eosin, azure-eosin, Gram and van Gieson. For the purpose of in-depth study of the morphological picture of infective endocarditis, we carried out a retrospective clinical and morphological analysis according to the protocols of postmortem autopsies of deceased patients for the period 1996-2008, as well as an analysis of the frequency of deaths and causes of death in IE using the data of the org.-method. Department of the pathoanatomical service of St. Petersburg.
In order to identify factors affecting the survival of patients with infective endocarditis, a statistical analysis was performed using the Cox proportional hazards model. Along with this, to assess the influence of individual factors on the outcome of the disease in drug addicted patients and patients without drug addiction, a regression analysis was performed with the determination of the conditional mathematical expectation of patient survival. For this purpose, a classical probabilistic model was used that determines the probability of an event A by the formula: P (A) \u003d m / n, where m is the number of outcomes that contribute to the occurrence of event A, and n is the total number of outcomes.
The statistical significance of differences in central hemodynamic parameters and other characteristics in patients of both groups was assessed using the Student's t-test, as well as using the multiple comparison method with the introduction of the Bonferroni correction. Mathematical processing of digital data was carried out using the Statistica-6 statistical software package.
RESULTS OF EXAMINATION OF PATIENTS WITH INFECTIOUS ENDOCARDITIS
Etiology of infective endocarditis in drug dependent and non-drug dependent patients
In accordance with the results of the studies, in most drug addicts of groups I and II, the causative agent of IE was Staphylococcus aureus (S. aureus), which was isolated in monoculture in 79 patients (71.8%). Along with this, in 8 patients (7.3%) the causative agent of the disease was Staphylococcus epidermidis, and in 3.6% of cases (4 people) the etiological factor of IE was enterococcus. Associations of microorganisms were determined only in 1.8% of observations (2 people).
When comparing the frequency and species composition of IE pathogens in patients of groups I and II, no significant differences were found. Staphylococcus aureus was detected in 71.4% (45 people) of cases in patients of group I and in 72.3% (34 people) of cases in patients of group II. Enterococcus was an etiological factor in 3.2% (2 people) of cases in group I patients and in 4.3% (2 people) in patients of group II.
In patients of groups I and II, negative results of venous blood cultures were obtained in 15.9% and 14.9%, respectively. Staphylococcus aureus, isolated from the blood of drug-addicted patients of groups I and II, was resistant to penicillin G, as well as ampicillin and methicillin, in 72% (57 people). At the same time, in 75 people (68.2%) of IE, this pathogen was sensitive to antibiotics of the III and IV generation cephalosporins, as well as vancomycin and imipinem. Polyresistance of Staphylococcus aureus to penicillin antibiotics, cephalosporins and aminoglycosides was detected in 22.7% of cases (25 patients).
Enterococcus, detected in 2 patients (3.2%) in group I and in 4.3% of cases (2 people) in patients of group II, was resistant to antibiotics of the penicillin series, aminoglycosides and cephalosporins of III and IV generations.
In patients with IE without drug addiction (group III), pathogens of IE were detected in 41.8% of cases (23 people). The etiological structure of IE in these patients was dominated by gram-positive cocci, of which Staphylococcus aureus accounted for 16.4%. Along with this, in 10.9% of cases, the causative agents of IE were gram-negative microorganisms, namely Pseudomonas aeruginosa, Klebsiella and Enterobacter. Gram-negative microbes were more often detected in patients with IE with lesions of native and artificial heart valves, and their pronounced in vitro resistance to penicillin antibiotics and cephalosporins was noted.
Among the pathogens related to gram-positive cocci, enterococcus was distinguished by a high degree of resistance to most antibiotics, which was detected in 2 patients with IEIC. The high frequency of negative results of blood cultures in patients with IE group III, which amounted to 58.2% (32 people), was determined by the long-term use of antibiotics in the prehospital period.
In the diagnosis of IE in the examined groups of patients, a system of criteria proposed by D. T. Durack et al. was used, called the Duke criteria (Durack D. T., Lukes A. S., Bright D. K., 1994), taking into account their modified version according to L. M. Baddour, W. R. Wilson, A. S. Bayer (2005 ).
A reliable diagnosis of IE was established in the presence of two main criteria or one main and three or five auxiliary criteria.
In accordance with this system of criteria, the diagnosis of IE was regarded as reliable in all examined patients.
The results of ultrasound examination of the heart
in drug addicted patients with infective endocarditis
According to the TTE, 100% of patients in groups I and II had mobile vegetations localized on the leaflets of the heart valves. In the surveyed group of drug addicted patients, there was a lesion of native heart valves.
Data regarding the size of the vegetation on the TC are presented in table 2.
table 2
Dimensions of microbial vegetations on the tricuspid valve
in drug addicted patients with infective endocarditis
| Vegetation dimensions (cm) | The number of patients with TC lesions in groups I and II |
|
The vegetations on the valve cusps were mobile, had uneven contours and a heterogeneous echostructure. Their sizes ranged from 0.5 cm in diameter to 3 cm or more. The formation of vegetations was accompanied by insufficiency of valves of I–III degrees and the formation of regurgitation flows.
The conducted Doppler echocardiographic study made it possible to determine the main indicators of central hemodynamics in drug-addicted patients with IE.
In patients with damage to the left chambers of the heart, in contrast to the group of patients with isolated TC insufficiency, a significant decrease in the LV ejection fraction was determined, the average values of which were 56.1 ± 9.8%, expansion of the right and left cavities of the heart, as well as a significantly increased TC -pressure gradient and systolic pressure in the pulmonary artery (P< 0,05). У больных с сочетанным поражением клапанов средние значения АД были ниже, чем в группе больных с изолированной ТК-недостаточностью (разница статистически значимая).
The average values of individual indicators are shown in Table 3.
Table 3
Baseline hemodynamic parameters in drug addicted patients with infective endocarditis
Hemodynamic parameters | Number of patients with IE (n = 110) | Values |
||
Isolated lesion of TC | The defeat of the MK, AK and combined valvular lesions |
|||
Systolic TC pressure gradient (mm | 39.85 ± 21.83 | |||
CDR PP (cm) | ||||
EDD RV (cm) | ||||
KDR LP (cm) | ||||
EDR LV (cm) | ||||
| (mm water column) | ||||
Note: - the difference in indicators is statistically significant (P< 0,05)
According to the results of echocardiography, in 100% of cases, patients of group III showed signs of damage to the valvular apparatus of the heart.
According to the EchoCG study, patients of group III with lesions of native valves showed more severe disorders of central hemodynamics compared with patients with valve prostheses and patients with IE with heart defects. Most patients showed a significant decrease in ejection fraction along with the expansion of the right and left chambers of the heart and the formation of pulmonary hypertension.
The main indicators of central hemodynamics in patients with IE without drug dependence are presented in Table 4.
Table 4
Comparative characteristics of indicators of the central
hemodynamics in patients with infective endocarditis
without drug addiction
Hemodynamic parameters | Patients with IE with heart defects | Patients with IE with native valve disease | Patients with IEIK |
Systolic pressure in LA mm Hg. Art. | |||
CDRLP (cm) | |||
LV CR (cm) | |||
KDRPP (cm) | |||
CRWP (cm) | |||
LV ejection fraction (%) |
Note: * - statistically significant difference (P< 0,05).
IE in patients with valve prostheses (25 people) was characterized by the formation of both single and multiple mobile vegetations on the elements of the prosthesis. Violation of the contractility of the left ventricle with a decrease in ejection fraction up to 44% and below was recorded in 22 patients with IEIK (89%). Hypertrophy and dilatation of the left ventricle in patients with IEIK were detected in 84% of cases (21 people).
in drug addicts
Infective endocarditis in people with drug addiction was characterized by an acute course and polysyndromicity.
The reason for hospitalization of most patients was acute complications of the underlying disease. A significant part of the patients were admitted to the intensive care unit of the hospital with a clinic of unilateral or bilateral multifocal pneumonia, the cause of which was septic thromboembolism of the branches of the pulmonary artery. Secondary nephropathy with the development of acute renal failure (ARF) was the reason for hospitalization in 7 patients, and in most cases this complication was mistakenly interpreted as an exacerbation of chronic glomerulo- or pyelonephritis, as well as urolithiasis. Acute thrombophlebitis of peripheral veins, accompanied by fever and pain syndrome, was the reason for admission of patients to the hospital in 5.5% of cases. Relatively rare causes of hospitalization of drug addicted patients were arthritis of the joints of the lower extremities, as well as complications of IE associated with erosive and ulcerative lesions of the gastrointestinal tract (2.7 and 0.9%, respectively).
The clinical picture of the disease consisted of a number of syndromes and symptoms caused by the course of a generalized bacterial infection along with clinical manifestations of heart damage and the presence of complications of a thromboembolic nature. In most cases, the condition of patients upon admission to the hospital was assessed as severe or moderate. Infectious-toxic syndrome (ITS) was observed in 100% of cases in drug-addicted patients of groups I and II. The main manifestations of ITS included general weakness, fever over 38C hectic type, sweating, arthralgia and myalgia, weight loss. At the same time, the severity of ITS in patients of this group was different - from moderately pronounced clinical manifestations of intoxication to an extremely severe general condition.
Thromboembolism of the branches of the pulmonary artery with the development of multiple foci of infiltration in the lungs was detected in 69.2% of cases in patients with isolated lesions of the TC. Acute left ventricular failure was determined in more rare cases in patients with isolated lesions of the TC (27.5%) than in patients with combined lesions of the right and left chambers of the heart, in which the incidence of this complication was 73.7%.
Secondary nephropathy with the development of acute renal failure was more often observed in patients with combined heart valve disease (31.6%) than in the group of patients with isolated lesion of the TC (15.4%).
The frequency of development about. DIC was 71.4% in patients with isolated lesions of the TC. In the group of patients with combined lesions of the right and left chambers of the heart, Fr. DIC was detected in 57.9% of cases.
One of the characteristic syndromes in drug-addicted patients with IE was anemia of severe and moderate severity, as well as hepato-splenomegaly, which were determined in 100% of cases in these patients.
Clinical picture of heart damage in drug addicted patients with infective endocarditis
Clinical manifestations of heart damage in the group of patients with drug dependence varied depending on the degree of valve dysfunction, localization of microbial vegetations in the right or left chambers of the heart and the presence of heart failure, while significant differences in the frequency of major syndromes in HIV-infected patients with chronic hepatitis (group I ) and in HIV-seropositive patients without chronic hepatitis (group II) was not detected.
In people with drug addiction, isolated damage to the right chambers of the heart was determined in 82.7% of cases (91 people). At the same time, the incidence of TC damage in groups I and II of patients with IE did not differ significantly and amounted to 84.1% and 80.9%, respectively.
Among the characteristic clinical features of IE in these patients was an asymptomatic course of tricuspid valve damage. Thus, the formation of tricuspid insufficiency in most patients was characterized by moderate signs of "overload" of the right chambers of the heart, swelling of the jugular veins, the appearance of hepato-jugular reflux in the absence of peripheral edema and other signs of acute right ventricular decompensation.
Of the surveyed drug addicted patients, clinical signs of right ventricular failure were determined in only 18 people (16.4%) with relapses of IE, as well as with combined lesions of the TC, mitral and aortic valves. Involvement of the left heart chambers in drug-addicted patients with IE in the early stages was accompanied by signs of heart failure, which were manifested by increased dyspnea, cardiomegaly and the development of edematous syndrome.
Along with the clinical picture of endocardial damage, the acute course of IE in drug addicted patients was accompanied by the development of acute diffuse myocarditis, the clinical manifestations of which were pain in the precordial region, palpitations, shortness of breath, and characteristic ECG changes. Severe myocarditis, complicated by the development of acute circulatory failure with dilatation of the heart cavities, peripheral edema, was observed in 25 patients with IE (27.5%) with isolated lesions of the TC.
Cardiac arrhythmias and conduction disturbances were determined in all patients of this group. So, sinus tachycardia was observed in 100% of patients, atrial and ventricular extrasystole - in 38% of cases, bundle branch block - in 58% of cases, atrioventricular block I degree was detected in 18% of patients. In most cases, there were combined forms of arrhythmias.
Clinical characteristics of complications of infective endocarditis in people with drug dependence
When comparing the clinical course of IE in HIV-infected patients of groups I and II, no significant differences were found regarding the frequency of individual clinical syndromes and the nature of complications of the underlying disease. Thus, thromboembolic syndrome was one of the most frequent complications of IE in drug addicts. Of the examined patients of both groups, acute pulmonary embolism (PE) was observed in 74 people (67.3%), and in 87.8% of cases (65 people) it served as the main reason for their hospitalization. The frequency of septic pulmonary embolism in the group of patients with isolated lesions of the TC was 69.2% (63 people), and in patients with combined lesions of the right and left heart chambers - 57.9% (11 people).
Clinical manifestations of septic pulmonary embolism at the prehospital stage were characterized by the appearance of acute pain in the chest, severe inspiratory dyspnea and arterial hypotension. Patients were admitted to the intensive care unit of the hospital with a clinical picture of unilateral or bilateral infarction pneumonia, which was accompanied by respiratory failure of II–III degrees, sinus tachycardia with a pulse rate of up to 160–200 beats per minute. In a number of patients, the clinical picture of pulmonary embolism was accompanied by characteristic ECG changes in the form of the appearance of signs of QIII SI, as well as the rise of the ST segment in the right chest leads, the formation of P-pulmonale, which were observed in 14.9% of cases (11 people) in patients with isolated lesion of the TC, as well as with combined valvular lesions
In 13.5% of cases (10 people), patients with developed PE developed acute respiratory distress syndrome (ARDS), which was accompanied by progressive respiratory failure, hypoxemia with a decrease in PaO2 to 55 mm Hg. Art., X-ray signs of pulmonary edema. Increasing metabolic acidosis (pH 7.1), hypocapnia were determined. These patients, along with other measures aimed at maintaining the homeostasis system, were artificially ventilated.
During clinical observation, 29 patients (39.2%) had relapses of septic pulmonary embolism. Relapses of pulmonary embolism developed against the background of the ongoing complex therapy for IE and were characterized by the appearance of new foci of infiltration in the lungs, as well as the formation of multiple destructions of the lung tissue.
The recurrent course of septic PE in patients with IE with lesions of the TC often led to the formation of acute destruction and abscesses in the lung tissue. A number of patients had an abscess breakthrough into the pleural cavity, followed by the development of pneumothorax and exudative purulent pleurisy.
The formation of lung abscesses with the development of pleural empyema was observed in 3 patients with IE with an isolated lesion of the TC and was accompanied by an unfavorable prognosis. In drug-addicted patients with damage to the valves of the left chambers of the heart, embologenic infarctions of the kidneys and spleen were formed, and in some cases, thromboembolism of the cerebral and coronary vessels with a fatal outcome occurred. Heart failure was not among the frequent complications of IE in drug addicts. At the same time, in patients with MV and AC lesions, as well as combined lesions of the right and left heart chambers, the incidence of heart failure was significantly higher (73.7%) than in the group of patients with isolated MC lesions (27.5%).
Clinical features of infective endocarditis
in patients without drug dependence
Most patients with IE without drug dependence had a subacute course of the disease (69.1%).
The main reasons for hospitalization of patients in this group included prolonged febrile syndrome and progressive congestive heart failure. The development of anemia in combination with febrile syndrome was the reason for hospitalization in 14.5% of cases (8 people). At the same time, in 4 (7.3%) patients with IE with artificial valves, the reason for hospitalization was the development of acute cerebrovascular accident.
IEIK in the observed group of patients was characterized by a significant number of thromboembolic complications, among which cerebral vascular embolism was observed with the highest frequency. Along with this, heart failure was one of the leading syndromes in IE in patients with heart valve prostheses. The formation of CHF III-IV functional classes according to the NYHA classification was observed in 48% of patients with IEIK. The leading syndrome in the clinical picture of IE in patients with congenital heart defects was progressive heart failure. Formation of aortic insufficiency II-III degrees in 2 patients with congenital aortic valve disease (bicuspid valve) and the development of destruction of its valves was accompanied by significant cardiomegaly, the presence of diastolic murmur in the projection of the aortic valve, combined with signs of congestion in the pulmonary circulation and edematous syndrome. In the group of patients with IE with heart defects, among which elderly and senile persons predominated, along with signs of stagnation in the small and large circles of blood circulation, the clinical picture of the disease was characterized by a severe course of a generalized infection with a pronounced infectious-toxic syndrome, the formation of embologenic infarcts of the kidneys, lungs and brain, as well as the formation of foci of purulent inflammation in the kidneys, liver, lower lobes of both lungs.
The clinical feature of the subacute course of IE in patients with rheumatic heart disease was a long febrile period at the prehospital stage. In this group of patients, one of the main reasons for hospitalization was the progression of heart failure as a result of destruction of the cusps of the heart valves. Deterioration of the condition of patients associated with the progression of heart failure was formed in the period from 2 weeks to 1-1.5 months before their admission to the hospital. In this group of patients with IE, heart rhythm disturbances were determined with a high frequency, of which tachysystolic atrial fibrillation occurred in 80% of cases.
Outcomes of infective endocarditis in drug addictspatients and patients without drug addiction
In drug-addicted patients with IE of groups I and II, hospital mortality was 35.5% (39 people), of which the number of patients who died in group I was 22 people (30.2%), and in group II - 17 people (36.2 %).
According to autopsy data, the main causes of death in patients were:
1. Septicopyemia with the formation of purulent foci in the myocardium, liver, kidneys, spleen, brain with the development of multiple organ failure - 16 people (41%).
2. Heart failure against the background of polyposis-ulcerative endocarditis, as well as acute myocarditis with dilatation of the heart cavities - 14 people (35.9%).
3. Secondary nephropathy with the development of renal failure, pulmonary edema, cerebral edema - 9 people (23.1%).
According to our data, among the most common causes of death in drug-addicted patients with IE was the generalization of infection with the development of multiple organ failure. In this group of patients, an acute course of the disease was observed, caused by highly virulent Staphylococcus aureus, and in 28.2% of cases (11 patients), this pathogen was resistant to most antibiotics.
Of the deceased drug addicts, high mortality was observed in patients with combined lesions of the right and left chambers of the heart (9 people), as well as in cases of severe acute myocarditis (5 people), which was accompanied by early development of acute heart failure (35.9 %). A high frequency of deaths was noted in patients with vegetation sizes from 1.0 to 2.0 cm in diameter and the presence of high-grade tricuspid valve insufficiency. In the overall structure of deaths in the observed group of patients with IE, acute renal failure was 23.1% (9 people), and in two cases it was due to the development of acute glomerulonephritis.
A pathoanatomical study of deceased patients with IE without drug addiction (group III) made it possible to establish that in these patients the main cause of death was progressive heart failure, which was determined in 74% (23 people) of cases. Along with this, in 26% of cases (8 people) in patients of this group, complications of a purulent-septic nature and multiple systemic thromboembolism were the cause of death.
Factors affecting the outcome of infective endocarditis in drug-dependent and non-drug dependent patients
In order to identify factors affecting the outcome of IE in drug addicted patients of groups I and II, as well as in patients without drug addiction (group III), a statistical analysis of survival was performed using a Cox regression model. In the group of drug addicted patients (110 people), factors such as the presence of high-grade tricuspid insufficiency, the size of vegetations on the tricuspid valve, as well as the formation of foci of destruction in the lungs, DIC, acute renal failure, congestive heart failure, the presence of HIV infection, chronic hepatitis C, mixed hepatitis B and C, as well as the type of IE pathogen.
The graph shows the dynamics of survival of drug addicted patients depending on the influence of risk factors for death in the range from 1 to 8 weeks of their stay in the hospital (Fig. 2).
Rice. Fig. 2. Graph of survival of drug addicted patients with infective endocarditis using the Cox proportional hazards model of death.
In patients with IE without drug addiction (group III), the main factors affecting the outcome of the disease included such complications as thromboembolism of cerebral, renal and coronary vessels, DIC, acute renal failure, ITN, complications of immunocomplex genesis, as well as the size of vegetations on the valves hearts.
According to the data obtained, a high risk of death in drug-addicted patients with IE was observed in the range from 1 to 4 weeks of their stay in the hospital and was due to the influence of multiple factors, the main of which were the size of microbial vegetations (Beta = 1.668477), the presence of left ventricular failure (Beta = 1.261233), DIC (Beta = 1.002212), lung tissue destruction (Beta = 0.141461), and high-grade tricuspid valve insufficiency (Beta = 0.947014).
Statistical analysis of Cox survival in 55 patients without drug dependence (group III) allowed us to establish a number of leading factors influencing the outcome of IE.
The graph illustrates the proportional effect of risk factors for death in the range from 1 to 6 weeks of hospital stay of patients in this group (Fig. 3).
Rice. Fig. 3. Graph of survival of patients with infective endocarditis without drug dependence using Cox regression analysis
Based on the study, it was found that in the group of patients with IE without drug addiction, one of the main factors affecting the outcome of IE was progressive heart failure, which was detected in 83.6% of cases (Beta = 1.534146). Along with this, the development of thromboembolism of cerebral vessels (Beta = 0.972088), embologenic myocardial infarctions (Beta = 0.681587), as well as acute renal failure and DIC are associated with an increased risk of death in patients of this group (Beta = 0 .500103 and 1.340218, respectively).
Thus, in patients with IE without drug addiction (group III), the development of multiple systemic thromboembolism in combination with progressive heart failure led to a high risk of death in the interval from 1 to 2 weeks of their stay in the hospital.
Influence of Vegetation Sizes on the Tricuspid Valve Leaflets on the Prognosis of Infective Endocarditis in Drug Addicts
In order to identify the relationship between the size of the vegetation and the frequency of deaths in drug-addicted patients with IE with an isolated lesion of the MC, a quantitative assessment of the effect of the size of the vegetation on the survival rate of patients in groups I and II was made. Data regarding vegetation size and IE outcomes are presented in Table 5.
Table 5
Sizes of vegetations on the leaflets of the tricuspid valve
and outcomes of infective endocarditis in drug addicted patients
Vegetation sizes on TC (cm) | ||
Number of survivors | Number of deaths |
|
In this case, (X = X1) corresponds to a random event, in which the size of the vegetation on the TC in the patient is on the interval .
Then, (X = X2) corresponds to the size of vegetations ,
(X=X3) « « « « ,
(X=X4)
(X=X5) « « « «
Rice. Fig. 4. Graph of the dependence of the degree of survival and the size of vegetations on the tricuspid valve in drug addicted patients with infective endocarditis
The conditional mathematical expectation of a random variable Y as a function of the possible values of a random variable X was taken as a numerical characteristic of the survival of patients depending on the size of vegetations in the TC, that is, the regression function of Y on X was determined. x).
Thus, we have determined the dependence of the decrease in the degree of survival of drug addicted patients, expressed through conditional mathematical expectation, with an increase in the size of vegetations on the tricuspid valve.
endocarditis
We have analyzed the lethal outcomes based on the results of post-mortem autopsies for the period 1993–2008. The material of the database of the organizational and methodological department of the pathoanatomical service of St. Petersburg was taken as the basis. As a result of the analysis of these data, an increase in the frequency of deaths associated with infective endocarditis was revealed in the overall structure of deaths (Fig. 5). During the period 1993–1999, out of the total number of deaths, the proportion of deaths due to IE was 0.12% (74 people out of 63,173 who died), while in 2000–2001 this figure increased to 0.22% (53 people). of 24,289 deaths). For the period 1993-2008, in the overall structure of mortality in IE, the predominance of deceased patients without drug dependence was determined, which amounted to 82.9% (213 people).
Rice. Fig. 5. Dynamics of mortality rates from infective endocarditis in the overall structure of deaths according to postmortem autopsy data for the period 1993–2008
Along with this, in recent years there has been an increase in mortality rates among drug-addicted patients with IE. During the period 1993-2008, the proportion of deaths of drug-dependent patients with IE increased from 11.5% to 30% of the total number of deaths associated with IE.
At the same time, the largest number of drug addicts who died was registered in 1999, 2001 and 2005. During this period, the proportion of drug addicts who died was 30%, 21% and 32.1%, respectively. Among the deceased drug addicts with IE, males predominated - 75.7% (35 people). The mean age in this group of patients was 28.9 ± 5.8 years.
Analysis of the results of microbiological examination of sectional material of deceased drug addicts with IE for the period 1996-2008 showed that the etiological factor of the disease in 86.5% of cases (32 people) was Staphylococcus aureus.
According to the results of autopsy, in 65.6% of cases (37 people) in drug addicted patients, primary IE was detected with a predominant lesion of the tricuspid valve. Concomitant HIV infection was found in 74% of cases (37 people), and patients with IE at the AIDS stage were not identified. According to autopsy results, concomitant chronic hepatitis was found in 34 people (68.2%), of which hepatitis C was detected in 27 patients (79.4%), mixed hepatitis B and C - in 4 people (11.8%), and two cases had chronic hepatitis B (8.8%).
For the period 1993–2002, as well as in 2004–2008, in the overall structure of mortality in IE, 80.7% (213 people) were patients without drug dependence. Among the deceased patients, men accounted for 70.1%, women - 29.9% aged 47 to 92 years (mean age 63.6 ± 15.2 years). Of the deceased patients with IE without drug addiction, in 42.7% of cases, primary IE with damage to the aortic valve was detected. Secondary forms of IE accounted for 57.3%, of which rheumatic heart disease was determined in 19.3% of cases, congenital heart disease - in 7.4% of cases, atherosclerotic aortic valve stenosis - in 12.1% and IE of artificial valves in 11 cases. .2% of cases. Among the deceased patients with the primary form of IE, concomitant pathology was detected with a high frequency. According to autopsies, the main comorbidities were: chronic alcoholism (57.9%), type II diabetes mellitus (24.8%), chronic pyelonephritis, including apostematous forms (7.3%), chronic pancreatitis and cholelithiasis (6.9%), as well as oncopathology - colon cancer (1.8%), lung cancer (1.3%).
When comparing clinical data and the results of a pathoanatomical study of patients with IE, the absence of discrepancies in the diagnosis in the group of drug addicted patients attracts attention, while in patients without drug dependence in 39.4% (61 people) of cases, the diagnosis of IE was established posthumously.
Of the cases of IE not diagnosed during lifetime, the discrepancy between diagnoses of category I was registered in 27.6%, category II - in 58.6% and category III - in 13.8%. The main reason for the underdiagnosis of IE in patients without drug dependence was the presence of concomitant pathology, masking the course of the underlying disease, as well as late hospitalization of patients in this group.
The absence of discrepancies in the diagnosis of injecting drug users is explained by the characteristic clinical symptoms in most drug dependent patients and the presence of a risk factor for the development of IE associated with intravenous drug use.
Pathological characteristics of infectious
endocarditis in drug addicts and patients without drug addiction
Conducted pathoanatomical studies have shown that the most common cause of death in drug-addicted HIV-infected patients with IE was the generalization of a bacterial infection with the development of multiple organ failure. In this group of the deceased, the morphological picture of IE was represented by the formation of foci of purulent fusion with abundant leukocyte infiltration, secondary septic endovasculitis, edema of the interstitial tissue, and severe dystrophic changes in organs and tissues. When sowing sectional material in most patients in this group, the growth of Staphylococcus aureus (75%) was obtained. According to the pathoanatomical study, heart damage in drug addicted patients was characterized by the imposition of thrombotic masses on the valve leaflets, as well as abundant leukocyte infiltration and purulent fusion of the valve tissue and subvalvular structures, and in most cases there was an isolated lesion of the tricuspid valve.
A characteristic feature of IE in drug addicts was lung damage with the formation of infarction foci of different periods of prescription due to repeated embolism of the branches of the pulmonary artery, as well as the presence of multiple foci of pneumonic infiltration as a manifestation of a generalized infection.
However, in the group of drug-addicted HIV-infected IE patients, according to our data, a high activity of systemic inflammation with the development of exudative reactions and immunocomplex pathology was rarely observed. According to the results of the study of the organs of the immune system in HIV-infected deceased of this group, lymphoid devastation of the spleen tissue was determined along with widespread myeloid hyperplasia of the red pulp, as well as involutive changes in the tissue of the lymph nodes. Along with this characteristic morphological manifestation of HIV infection in the early stages, drug addicted patients had a mild HIV encephalitis, which in most cases had no significant significance in the thanatogenesis of these patients. In a significant part of the deceased patients of this group, widespread septic vasculitis with surrounding leukocyte infiltration, perivascular and pericellular edema of the brain tissue, as well as secondary circulatory disorders were observed.
The presence of a moderately pronounced inflammatory activity of chronic hepatitis C without a pronounced structural reorganization of the liver tissue in drug-addicted patients with IE did not significantly affect the outcome of the underlying disease. In the group of patients with IE without drug addiction, the main causes of death were thromboembolic complications in the systemic circulation (48.1%) and progressive congestive heart failure (31.3%). According to autopsy data, a characteristic feature in this group of patients was a high frequency of septic embolism of cerebral vessels with the development of secondary purulent meningoencephalitis. Along with the defeat of the endocardium, multiple foci of necrosis in the myocardium were often determined as a result of septic embolism of the coronary arteries, as well as serous-purulent effusion in the pericardial cavity and pleural cavity.
In the organs of immunogenesis in patients with IE in the absence of HIV infection, both destructive and hyperplastic processes were observed. When comparing the two groups, myeloid hyperplasia of the spleen, as well as hyperplasia of the lymphoid tissue, was more pronounced in patients with IE in the absence of drug addiction and HIV infection.
Complex treatment of drug addicted patientsinfective endocarditis
As part of antibiotic therapy, drug-dependent patients with IE received III-IV generation cephalosporins 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 at a daily dose of 1.5 g IV) and metronidazole 1.5–2 g per day IV. In case of ineffectiveness or contraindications, antibiotics of the lincosamine group were used for the above drugs: clindamycin 1.2 g per day i.v. or lincomycin 3 g per day i.v. in combination with fluoroquinolones (ciprofloxacin 400 mg per day i.v.). Imipinem (Tienam) at a dose of 2–4 g per day IV or rifampicin at a daily dose of 0.45–0.6 g IV was administered for 5–7 days in the intensive care unit. The average duration of antibiotic therapy in the examined group of patients was 28 ± 3.5 days.
Detoxification therapy included intravenous infusions of rheopolyglucin, gemodez, polarizing mixtures in combination with loop diuretics. The volume of fluid administered averaged 2–2.5 liters per day. In the conditions of the intensive care unit, all patients underwent CVP monitoring. The average course duration was 22 ± 4.5 days.
The development of pulmonary embolism, especially in combination with signs of acute DIC in the stage of hypercoagulability, served as the basis for prescribing anticoagulant therapy. The initial dose of heparin was 10 thousand IU intravenously, bolus, then - 1000 IU per hour intravenously, with a transition to subcutaneous administration up to 30,000 IU per day. The introduction of heparin was carried out under the control of coagulogram parameters and blood clotting time. At the same time, intravenous transfusions of fresh frozen plasma were carried out at 300-600 ml per day with the addition of 2500-5000 IU of heparin. Severe anemia (Hb less than 80 g/l, Ht 25) was corrected by red blood cell transfusions (5–7 doses). Therapy with direct-acting anticoagulants in combination with cryoplasma transfusions was carried out until a stable improvement in hemostasis. According to our data, relief of the manifestations of acute DIC at the stage of hypercoagulability was observed on the 7th–10th day from the start of complex therapy. Long-term use of broad-spectrum antibiotics in 63 patients (57.3%) was accompanied by the development of side effects of antibiotic therapy. Candidiasis of the oral cavity, pharynx, esophagus, as well as intestinal dysbacteriosis stages III-IV were detected in 32.7% of cases (36 people). The use of antibiotics with hepatotoxic properties (cephalosporins, lincosamines, metronidazole) in 2 patients with chronic hepatitis C and B contributed to the progression of liver failure, which was accompanied by high fermentemia and jaundice.
Positive results of conservative therapy were obtained in 63 patients (69.2%) with isolated lesions of the TC (Table 6). Table 6
Indicators of central hemodynamics in drug addicted patients with infective endocarditis with isolated lesion of the TC before and after treatment
Hemodynamic parameters | The number of patients with IE with an isolated lesion of the TC (n = 91) | Values |
||
before treatment | after treatment |
|||
Systolic TC pressure gradient (mmHg) | 39.85 ± 21.83 | |||
Systol. pressure in the LA (mm Hg) | ||||
CDR PP (cm) | ||||
EDD RV (cm) | ||||
KDR LP (cm) | ||||
EDR LV (cm) | ||||
CVP (mm water column) | ||||
According to the results of an echocardiographic study conducted after the completion of the course of complex therapy for IE, in this group of patients, a decrease in the size of vegetations on the valves of the TC, a decrease in the size of the right chambers of the heart, and a decrease in systolic pressure in the pulmonary artery were determined.
The outcome of IE in the group of patients with damage to the right heart chambers was tricuspid valve insufficiency of I–II degree with a moderate increase in the size of the right heart chambers. In this group of patients, there was no significant increase in the level of CVP in comparison with the baseline: 8.11 ± 3.1 mm of water. Art. - before treatment and 7.8 ± 2.2 mm of water. Art. after completion of therapy (P > 0.05).
In the group of drug-addicted patients with IE with isolated lesions of the MV and AC (8 people), as well as with combined damage to the right and left chambers of the heart (11 people), clinical improvement on the background of conservative therapy was achieved in 10 patients (52.6%).
The effect of systemic enzyme therapy (SET) drugs on the course of infective endocarditis in people with drug dependence
In order to study the effect of systemic enzyme therapy drugs on the course of IE and the recurrence rate of septic PE, Wobenzym was used in the complex treatment of patients.
Drug-dependent patients with IE were divided into two groups. The first group (control) in the amount of 30 people (23 men and 7 women, mean age 22.3 ± 4.1 years) received traditional complex treatment, which included the combined use of broad-spectrum antibiotics in combination with detoxification, anticoagulant therapy transfusion of plasma and blood products.
The second group of patients in the amount of 30 people (20 men and 10 women, mean age 24.1 ± 3.5 years) received complex therapy in combination with Wobenzym in the following doses: 10 tablets 3 times a day in severe IE and in moderate severity of IE - 7 tablets 3 times a day. Wobenzym was administered orally 30-40 minutes before a meal. The duration of the course was 4 weeks.
Comparison of the results of treatment in the two groups of patients was carried out taking into account clinical and laboratory data, such as the duration of the period of febrile fever, the timing of relief of the intoxication syndrome, the duration of the period of bacteremia, the timing of normalization of laboratory parameters, relief of o. DIC, as well as the frequency of recurrence of septic pulmonary embolism.
In the group of patients treated with Wobenzym, regression of the systemic inflammatory syndrome was observed earlier than in the control group. After a 30-day course of treatment, there was a significant decrease in the content of circulating immune complexes and immunoglobulins G in the blood serum of patients who received Wobenzym as part of the complex therapy for IE.
Comparative analysis of some indicators of hemostasis in patients treated with SET preparations revealed a statistically significant decrease in the content of soluble fibrin-monomer complex (SFMC) and D-dimer, as well as an improvement in the rheological properties of blood, normalization of fibrinogen, prothrombin, thrombin time levels in comparison with the same indicators in patients of the control group
In patients with IE on the background of taking Wobenzym, it was possible to stop the manifestations of acute DIC in the stage of hypercoagulation in a shorter time than in the control group, which made it possible to reduce the administered dose of heparin by 1.5–2 times. At the same time, the normalization of blood rheological parameters occurred on average in 7.7 ± 0.33 days, while in the control group these terms were 11.6 ± 0.32 days (P< 0,05).
Relapses of septic pulmonary embolism with the appearance of new infiltrates in the lungs were detected only in 6 out of 30 (20%) patients who received SET preparations as part of complex therapy, while in the control group they were diagnosed in 13 people (43.3%), 2 > 3.84.
In the control group of patients, 7 people (23.3%) showed resistance to antibiotic therapy. In the group of patients treated with Wobenzym, we did not observe the development of resistance to antibiotic therapy.
In patients with IE treated with Wobenzym, elimination of the pathogen from the blood, along with relief of manifestations of systemic inflammation, occurred in a shorter time than in the control group. The duration of the period of bacteremia in patients of the second group was 6.67 ± 0.37 days, while in the first group it was 9.97 ± 0.38 days (P< 0,05).
The duration of the period of febrile fever in patients taking SET preparations was 14.47 ± 5.78 days, while in the control group, febrile fever lasted for 18.93 ± 3.13 days (P< 0,05).
Thus, an adequate response to ongoing complex therapy for IE was obtained in 73 (66.4%) drug-dependent patients with IE. At the same time, the progression of heart failure, as well as resistance to ongoing antibiotic therapy, was observed in 25 (22.7%) patients of this group.
Antibacterial therapy for IE patients without drug dependence included III-IV generation cephalosporins in combination with aminoglycosides, as well as lincosamines and vancomycin. The average duration of the course was 24 ± 2.9 days. Along with etiotropic therapy, the main syndromes were corrected, as well as the treatment of concomitant pathologies - progressive CHF, decompensated type II diabetes mellitus, coronary artery disease, arterial hypertension, anemic syndrome, etc. Positive results of conservative therapy were noted in 24 patients (43.6%), of they were in 10 patients with IEIK, of which 3 patients had mechanical prostheses of the MV and AV, in 2 cases - an AV prosthesis, and in 5 patients - a MV prosthesis. Of the patients with congenital and acquired heart defects, an adequate response to ongoing complex therapy was obtained in 2 patients with congenital AV disease, in 3 patients with MV stenosis of rheumatic origin, and also in 2 cases of syphilitic mesoaortitis with aortic valve damage and in 1 patient with an obstructive form of HCM and MV damage. Against the background of intensive antibacterial and detoxification therapy, these patients showed clinical improvement, regression of the intoxication syndrome, and a decrease in body temperature to subfebrile numbers. Along with this, in patients of this group, clinical manifestations of congestive heart failure II–III functional classes according to NYHA persisted, which was the basis for consultation of these patients by a cardiac surgeon in order to determine indications for surgical treatment.
CONCLUSIONS
1. Infective endocarditis in HIV-infected drug addicts is characterized by an acute course, the development of thromboembolic and infectious-toxic syndromes, as well as acute DIC, hepato-splenomegaly, anemia and secondary nephropathy. In patients without drug addiction and HIV infection, the most common syndromes of the disease include congestive heart failure along with the formation of foci of purulent inflammation in parenchymal organs and the brain.
2. A feature of infective endocarditis in HIV-infected drug addicts is the predominant lesion of the tricuspid valve (82.7%), and in people without drug dependence, isolated lesions of the aortic valve (40%) and combined lesions of the mitral and aortic valves (36.4%) prevail ). The development of diffuse myocarditis, as well as the formation of purulent pericarditis, pleurisy, meningitis in drug addicted patients with infective endocarditis are much less common than in patients without drug dependence due to the immunosuppression present in HIV-infected drug addicts.
3. The most common causative agent of infective endocarditis in people with drug addiction is Staphylococcus aureus, resistant to beta-lactam antibiotics, and in patients without drug addiction, opportunistic microflora, including gram-negative microorganisms, predominates in the etiological structure of the disease.
4. Septic thromboembolism of the branches of the pulmonary artery with the formation of multiple foci of myocardial pneumonia in the lungs is the most common complication of infective endocarditis in people with drug addiction, and in patients without drug addiction, embolism of cerebral, renal and coronary vessels is more often observed.
5. The appointment of systemic enzyme therapy drugs as part of the complex therapy of infective endocarditis leads to a reduction in the duration of bacteremia due to the potentiation of the action of antibacterial agents, as well as a decrease in the frequency of relapses of septic thromboembolism of the pulmonary artery branches due to the fibrinolytic and antiaggregation effects of polyenzymatic therapy.
6. In patients with primary and secondary forms of infective endocarditis, lethal outcomes were due to the development of thromboembolic complications in the systemic circulatory system (48.1%) and progressive congestive heart failure (31.3%), and in the group of drug addicted patients with infective endocarditis, the main cause of death was septicopyemia with the development of multiple organ failure (66.7%).
7. The most significant prognostic criteria in drug-addicted patients with infective endocarditis are the size of microbial vegetations, severe destructive lung lesions, high-grade tricuspid valve insufficiency, as well as the presence of DIC and left ventricular failure. In patients with infective endocarditis without drug dependence, the main factors that determine the lethal outcome of the disease include heart failure, cerebral embolism, myocardial infarction, and acute renal failure.
8. The morphological picture of infective endocarditis in HIV-infected drug addicts with secondary immunodeficiency is characterized by pronounced alterative and degenerative changes in organs and tissues, as well as microcirculation disorders with a mild exudative component of the inflammatory response. In patients without HIV infection and drug dependence in the morphogenesis of the inflammatory response in IE, complications of a purulent-exudative nature occupy a significant place.
1. In order to improve the diagnosis of infective endocarditis in people with drug addiction, as well as in patients with heart defects, valve prostheses and in patients with intravenous catheters, it is necessary to conduct targeted diagnostic studies using the Duke criteria system, which includes 2 main criteria - blood cultures and echocardiographic data, as well as 6 auxiliary criteria, which include predisposing conditions and diseases of the heart or intravenous drug use, fever of 38 C or more, embolism of large arteries, septic pulmonary infarcts, cerebral septic thromboembolism, conjunctival hemorrhages , acute glomerulonephritis, Osler's nodules, Roth's spots, as well as microbiological findings and echocardiographic findings that are characteristic of infective endocarditis but do not meet the main criteria. The diagnosis of infective endocarditis is established by the presence of two main criteria or one main and three or five auxiliary criteria.
2. Identification of factors associated with an unfavorable outcome of infective endocarditis in people with drug dependence, which include the size of microbial vegetations on the tricuspid valve more than 2.0 cm in diameter, the presence of left ventricular failure, as well as high-grade tricuspid valve insufficiency, are indications for surgical treatment of this disease.
3. The appointment of Wobenzym significantly improves the clinical course of infective endocarditis due to the fact that it has immunoregulatory, anti-inflammatory, antiplatelet and fibrinolytic effects. In severe cases of infective endocarditis, it should be prescribed at a dose of 10 tablets 3 times a day before meals and 5 tablets 3 times a day with moderate severity of the disease. The duration of the course is 4-6 weeks.
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LIST OF ABBREVIATIONS
APTT activated partial prothrombin time
HIV (HIV) human immunodeficiency virus
DIC disseminated intravascular coagulation
PSLV posterior wall of the left ventricle
IEIK infective endocarditis of artificial valves
CPP end-diastolic pressure
LVCD end-diastolic size of the left ventricle
RLVC end-systolic size of the left ventricle
CDRLP end-diastolic size of the left atrium
KDRPP end-diastolic size of the right atrium
CRPC end-diastolic size of the right ventricle
KOS acid-base state
IVS interventricular septum
MK mitral valve
IOC minute volume of blood circulation
ALI acute lung injury
acute renal failure
ARDS acute respiratory distress syndrome
PP right atrium
PCR polymerase chain reaction
RFMK soluble fibrin-monomer complex
MODS multiple organ failure syndrome
SET systemic enzyme therapy
TK tricuspid valve
TTE transthoracic echocardiography
TEE transesophageal echocardiography
SV stroke volume
EF ejection fraction
CHF, chronic congestive heart failure
CVP central venous pressure
CEC circulating immune complexes
CD differentiation antigen on the membrane
immunocompetent cells
CD4 marker of T-lymphocytes with a helper phenotype
CD8 marker of T-lymphocytes with a suppressor phenotype
NASEC-group Haemophilus, Actinobacillus, Cardiobacterium,
Eikenella, Kingella
HBV hepatitis B virus
HCV hepatitis C virus
IL-2 interleukin-2
MRSA......................methicillin-resistant strains of aureus
staphylococcus
