What congenital defects are complicated by septic endocarditis. Septic endocarditis and its treatment

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

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

Subacute septic endocarditis

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

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

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

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

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

Features of the disease

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

Symptoms of subacute septic endocarditis

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

Acute septic endocarditis

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

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

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

Symptoms of acute septic endocarditis

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

Endocarditis

General information

Endocarditis– inflammation of the connective tissue (inner) lining 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 with endocarditis reaches 30%.

Infectious endocarditis occurs in the presence of the following conditions: transient bacteremia, damage to the endocardium and vascular endothelium, changes in hemostasis and hemodynamics, and impaired immunity. Bacteremia can develop due to existing foci of chronic infection or invasive medical procedures.

The leading role in the development of subacute infective endocarditis belongs to viridans streptococcus, in acute cases (for example, after open heart surgery) - Staphylococcus aureus, less often enterococcus, pneumococcus, and Escherichia coli. In recent years, the composition of infectious agents of endocarditis has changed: the number of primary acute endocarditis of staphylococcal nature has increased. With Staphylococcus aureus bacteremia, infective endocarditis develops in almost 100% of cases.

Endocarditis caused by gram-negative and anaerobic microorganisms and fungal infection has a severe course and is difficult to respond to antibacterial therapy. Fungal endocarditis occurs more often with long-term treatment with antibiotics in the postoperative period, with long-standing venous catheters.

Adhesion (sticking) of microorganisms to the endocardium is promoted by certain general and local factors. Common factors include severe immune disorders observed in patients undergoing 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 defects or rheumatic lesions of the heart valves. Hemodynamic disturbances caused by heart defects contribute to microtrauma of the valves (mainly mitral and aortic) and changes in the endocardium. On the heart valves, characteristic ulcerative-warty changes develop that look like cauliflower (polypous deposits of thrombotic masses on the surface of the ulcers). Microbial colonies contribute to the rapid destruction of the valves; their sclerosis, deformation and rupture can occur. A damaged valve cannot function normally - heart failure develops, which progresses very quickly. There is immune damage to the endothelium of small vessels of the skin and mucous membranes, leading to the development of vasculitis (thrombovasculitis, hemorrhagic capillary toxicosis). Characterized by impaired permeability of the walls of blood vessels and the appearance of small hemorrhages. Often there are lesions in larger arteries: coronary and renal. Often an infection develops on a prosthetic valve, in which case the causative agent is most often streptococcus.

The development of infective endocarditis is facilitated by factors that weaken the body’s immunological reactivity. The incidence of infective endocarditis is constantly increasing throughout the world. The risk group includes people with atherosclerotic, traumatic and rheumatic damage to the heart valves. Patients with ventricular septal defect and coarctation of the aorta have a high risk of infective endocarditis. Currently, the number of patients with prosthetic valves (mechanical or biological) and 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 is distinguished. Primary usually occurs in septic conditions of various etiologies against the background of unchanged heart valves. Secondary - develops against the background of an existing pathology of blood vessels or valves due to congenital defects, rheumatism, syphilis, after valve replacement surgery or commissurotomy.

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

acute - duration up to 2 months, develops as a complication of an acute septic condition, severe injuries or medical manipulations on blood vessels, heart cavities: nosocomial (in-hospital) angiogenic (catheter) sepsis. It is characterized by a highly pathogenic pathogen and severe septic symptoms.
subacute – duration 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 heart valves or with damage extending 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, formation of microbial vegetations;
infectious-allergic or immuno-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 damage to 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, as well as on previously administered antibacterial 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.

Clinical manifestations of infective endocarditis are mainly caused by bacteremia and toxinemia. Patients complain of general weakness, shortness of breath, fatigue, lack of appetite, and weight loss. A characteristic symptom of infective endocarditis is fever - a rise in temperature from subfebrile to hectic (debilitating), with chills and profuse sweating (sometimes, heavy sweats). Anemia develops, manifested by pallor of the skin and mucous membranes, sometimes acquiring an “earthy”, yellowish-gray color. Small hemorrhages (petechiae) are observed on the skin, mucous membrane of the oral cavity, palate, on the conjunctiva of the eyes and folds of the eyelids, at the base of the nail bed, in the area of the collarbones, arising due to the fragility of the blood vessels. Capillary damage is detected by mild trauma to the skin (pinch symptom). Fingers take the shape 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. When the cusps of the mitral and aortic valves are damaged, signs of their insufficiency develop. Sometimes angina is observed, and occasionally a pericardial friction rub is noted. Acquired valve defects and myocardial damage lead to heart failure.

In the subacute form of infective endocarditis, embolism of the vessels of the brain, kidneys, and spleen occurs due to thrombotic deposits torn off from the heart valves, accompanied by the formation of infarctions in the affected organs. Hepato- and splenomegaly are detected, from the kidneys - the development of diffuse and extracapillary glomerulonephritis, less often - focal nephritis, arthralgia and polyarthritis are possible.

Complications of infective endocarditis

Complications of infective endocarditis with a fatal outcome are septic shock, embolism in the brain, heart, respiratory distress syndrome, acute heart failure, multiple organ failure.

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

Diagnosis of infective endocarditis

When collecting anamnesis from the patient, the presence of chronic infections and past medical interventions is determined. The final diagnosis of infective endocarditis is confirmed by data from instrumental and laboratory studies. A clinical blood test reveals large leukocytosis and a sharp increase in ESR. Repeated blood cultures to identify the causative agent of infection have important diagnostic value. It is recommended to collect blood for bacteriological culture at the height of fever.

Biochemical blood test data can vary widely for a particular organ pathology. With infective endocarditis, changes are noted in the protein spectrum of the blood: (α-1 and α-2-globulins increase, later - γ-globulins), in the immune status (CEC, immunoglobulin M increases, the overall hemolytic activity of complement decreases, the level of anti-tissue antibodies increases) .

A valuable instrumental study for infective endocarditis is echocardiography, which makes it possible 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

For infective endocarditis, treatment must be inpatient; bed rest and diet are prescribed until the patient’s general condition improves. The main role in the treatment of infective endocarditis is given to drug therapy, mainly antibacterial, which begins 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 the drug amphotericin B is prescribed for a long time (several weeks or months). They also use other agents with antimicrobial properties (dioxidine, antistaphylococcal globulin, etc.) and non-drug treatment methods - autotransfusion of ultraviolet irradiated blood.

For concomitant diseases (myocarditis, polyarthritis, nephritis), non-hormonal anti-inflammatory drugs are added to treatment: diclofenac, indomethacin. If there is no effect from drug treatment, surgical intervention is indicated. Heart valve replacement is performed with excision of damaged areas (after the severity of the process subsides). Surgical interventions should be performed by a cardiac surgeon only when indicated and accompanied by antibiotics.

Prognosis for infective endocarditis

Infective endocarditis is one of the most severe cardiovascular diseases. The prognosis for infective endocarditis depends on many factors: existing valve lesions, 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 antibacterial therapy, mortality is 30%, and for infection of prosthetic valves - 50%. In elderly patients, infective endocarditis is more indolent, often not immediately diagnosed and has a worse prognosis. In 10-15% of patients, the disease transitions into a chronic form with recurrent exacerbations.

Prevention of infective endocarditis

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

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

Rheumatic endocarditis, or rheumatic valvulitis, with damage to the entire thickness of the valve, including its stroma, occurring simultaneously with damage, as a rule, to the myo- and pericardium, which is why a broader term is more rational: rheumatic carditis, or rheumatic carditis. Rheumatic carditis, as is typical for other manifestations of rheumatism, often worsens many times and is more reliably diagnosed precisely during these exacerbations, recurrences of the disease as recurrent endocarditis, or recurrent rheumatic carditis. This form is described in a separate chapter on rheumatic heart disease.
Subacute septic endocarditis, the so-called endocarditis lenta, associated with chronioseptic damage to the valves, most often by viridans streptococcus - Streptococcus viridans.
Acute septic endocarditis, caused by various pathogens, usually as a complication of various acute infectious diseases, surgical or birth sepsis, etc.
Other forms of endocardial damage are of less clinical significance.
Warty terminal, or cachectic, endocarditis, resulting from the formation of thrombotic deposits on the valves (thromboendocarditis) in the last days of life in such chronic cachectic diseases as cancer, chronic nephritis, tuberculosis. Endocarditis is discovered accidentally at autopsy and is only of pathoanatomical interest, without showing any special signs during life.
Parietal (mural) endocarditis during myocardial infarction, which is important as a possible source of embolism in various organs and thereby, by the way, confirms the diagnosis of the underlying disease - myocardial infarction.

In addition, there are intermediate forms between rheumatic and subacute septic endocarditis called rheumoseptic or indeterminate endocarditis; however, although in the clinic there may be a combination of rheumatic and septic symptoms, a characteristic clinical bias in one or the other of the two directions is subsequently revealed, and, therefore, each case over time fits into one of the main forms of endocarditis. The term “indeterminate endocarditis” was also applied to a special form of damage to the heart valves in acute disseminated lupus erythematosus, a disease that occurs with widespread vascular changes close to periarteritis nodosa, not only in the vessels of the skin, but also in the internal organs.
The boundaries of acute and subacute septic endocarditis in some infectious diseases are also not clearly defined clinically.

Inflammation of the endocardium - syphilitic valvulitis - is often present in specific aortitis.

Causes of subacute septic endocarditis

The disease was described by Tsangov (1884), Lukin (1903) and only later by foreign authors.

Etiology and pathogenesis. Subacute septic endocarditis is a protracted sluggish chronioseptic process with localization of the infectious focus on valves disfigured by an old rheumatic, syphilitic, congenital, traumatic defect, or previously unchanged. The causative agent, the non-hemolytic Streptococcus viridans, a common inhabitant of the oral cavity and pharynx, is found on the valves and in the blood of patients; however, a clinical association with tonsillitis is usually not established. The disease is characterized by a peculiar reaction on the part of the body, occurring, as a rule, without purulent metastases, with disruption of the activity of the bone marrow and reticuloendothelial apparatus. In recent decades, attention has been paid to the independence and relative frequency of this form of endocarditis.

Subacute septic endocarditis develops due to:

most often rheumatic defects of the aortic and mitral valves, usually with relatively mildly affected myocardium in the compensation stage, without atrial fibrillation;
congenital heart defects, especially patent ventricular septum, ductus botanus, pulmonary stenosis, congenital anomaly of the aortic valves;
rarely due to syphilitic aortic insufficiency and even less often due to sclerotic defect of the aortic valves;
as an exception due to traumatic heart defects, which are generally extremely rare. It is possible to develop subacute septic endocarditis on previously unchanged valves (Chernogubov).

Rheumatic defects numerically significantly predominate among other organic valve defects, so it is natural that rheumatism is more often found in the anamnesis of patients with subacute septic endocarditis. Some authors (Strazhesko) recognize a closer connection between subacute septic endocarditis and rheumatism, believing that the basis of both diseases is the body’s changing response to infection with the same low-virulent streptococcus. However, heart defects of other etiologies are complicated by subacute septic endocarditis in no less percentage of cases. The connection between congenital heart defects and subsequent inflammatory endocarditis was established already 100 years ago, and the same connection with traumatic defects over 50 years ago.
The main pathogenetic mechanisms of the development of subacute septic endocarditis, as well as other forms of endocarditis, have not been sufficiently studied. It cannot be imagined that the pathological process is reduced to the settling of bacteria on certain places of slow or perverted blood flow (with heart defects) or to the engraftment of various microbes due to a violation of the blood supply conditions of the “vicious” valves themselves. Of leading importance, one must think, is the special reactivity of the valve apparatus (or parietal endocardium) as a result of a neuroallergic or neurodystrophic effect, which causes only under very specific conditions, difficult to reproduce in experiment, a complex inflammatory process that progresses over a long period of time towards the development of a pronounced clinical and anatomical disease of the endocardium .

It is characteristic that the development of especially typical protracted forms of endocarditis is more often observed with low virulent pathogens that do not cause suppuration in the organs, just as recurrent vascular lesions are often observed with a weakened infection.
The development of endocarditis of the heart valves following inflammatory damage to the arteries, which is observed in rare cases of subacute septic arteritis of the ductus arteriosus when it is not closed or with an artoriovenous aneurysm, may be facilitated by intravascular-cardiac reflex effects, and not just the mechanical transfer of the infectious origin.

Pathoanatomically An ulcerative, destructive process predominates, sometimes with valve perforation; sometimes warty growths are found, often with damage to the parietal endocardium. In the thickness of wart-ulcerative changes, bacterial masses are found in large quantities even at low microscope magnification. Embolic processes in various organs are characteristic, but purulent melting in them is observed only as an exception; Usually they find focal embolic, and often diffuse nephritis, splenomegaly with multiple infarctions, etc. Constant participation of the spleen in the process with a possible increase in its function can contribute to anemia, leukopenia, thrombopenia by inhibiting bone marrow function.

Symptoms and signs of subacute septic endocarditis

The clinical picture is associated primarily with the infectious nature of the disease and embolic processes in the presence of an old heart defect and a kind of intoxication.

Prolonged fever of unknown type is one of the most important signs of the disease. Fever waves lasting 1-2-3 weeks, or one- or two-day temperature rises to 39-40°, provoked by various moments, or prolonged low-grade fever are often observed. There is usually considerable variability in the febrile response and the temperature may be near normal for weeks and months. Prolonged fever most often brings the patient to the doctor.

The general appearance of the patient is characteristic: pale skin with a special dirty “café au lait” hue, although rarely clearly expressed; “drum fingers” as a manifestation of a kind of intoxication, pathogenetically not entirely clear. Patients complain of weakness, decreased appetite; As a rule, there is no severe intoxication, delirium, headaches, and the tongue is not blocked. Painful phenomena due to embolism in various organs (spleen, kidneys, limbs, etc.) are often the main complaint of the patient.
On the part of the heart, signs of an old defect are found - rheumatic, congenital or syphilitic, usually compensated, without severe rhythm disorders. Often a diastolic murmur is heard at the aorta or a mitral melody at the apex. As the process develops, a fresh defect (acute) is detected on unchanged (usually aortic) valves due to septic damage to the valves, which, however, does not give obvious local signs for a long time. The heart usually does not appear significantly enlarged, and complaints are not predominantly cardiac in nature. Patients, despite frequent increases in temperature, at the onset of the disease can move independently and, outside the period of severe complications, often come to an outpatient appointment with a doctor.

The examination reveals an enlarged spleen, sometimes to the extent of significant splenomegaly, simultaneously with an enlarged liver of the nature of an infectious rather than congestive liver. The contours of the spleen are easily determined by palpation, with the exception of periods of fresh splenic infarctions, causing sharp pain radiating to the area of the left shoulder joint, muscular protection from the abdominal press, restriction of respiratory mobility of the lung on the left, sometimes friction noise of the peritoneum (perisplenitis) when listening to the area of the lower ribs on the left or the spleen itself below the costal margin.

Similar embolic manifestations from other organs cause complaints primarily of pain or are detected during a thorough examination of the patient. Thus, embolisms in the kidneys often result in acute paroxysmal or more dull pain in the lower back, sometimes with the release of bloody urine, pain when tapping the kidney area from behind (positive Pasternatsky’s symptom); emboli in the extremity cause petechiae, sometimes painful spots or nodules on the fingers, especially on the terminal phalanges or on the palm elevations (thenar and hypo-thenar) in the form of red stripes, spots, sometimes with a white central point - a bridge of vascular occlusion, which, along with drum fingers, presents changes in the extremities that are very characteristic of the disease. When examining the skin, petechiae are found, due to the fragility of blood vessels, in other places of the body, and in the conjunctival sac, especially in the lower eyelid, petechiae are found due to hemorrhages, embolism and vasculitis (Lukin's symptom). On the part of the joints, mild arthralgic phenomena are noted; on the part of the bones, especially the sternum, there is pain when beating.

Laboratory studies reveal characteristic data. First of all, in the urine, as usual in septic processes, changes characteristic of focal nephritis are found: red blood cells in the sediment, a small amount of protein with a normal specific gravity of urine, unimpaired renal function and normal blood pressure (with aortic defects there is, naturally, high systolic and low diastolic pressure). Rarely, massive hematuria occurs. However, it is not so rare to find a larger amount of protein in the urine as a sign of diffuse nephritis or amyloid nephrosis with general edema, increased blood pressure and even azotemia.

In the blood there is severe anemia with a drop in hemoglobin content to 40-30%, leukopenia (about 4,000 leukocytes), thrombopenine with thrombopenic phenomena: sharply prolonged bleeding time, the appearance of petechiae after applying a tourniquet to the shoulder. Among erythrocytes there may be nuclear forms, among leukocytes there may be monocytes and histiocytes as an indicator of a peculiar reaction of the reticuloendothelial system to a septic infection. Blood serum also presents peculiar changes with a high content, apparently due to the same irritation of the reticuloendothelial system, of globulins, in particular eiglobulins, which is why the serum, when formalin is added, coagulates and becomes cloudy (positive formol reaction).

The most direct evidence of the septic nature of the disease is a positive blood culture, which is obtained by following the appropriate technique during periods of higher temperature and generally greater activity of the process.

Course, clinical forms and complications of subacute septic endocarditis

The onset of the disease is difficult to determine precisely. It begins gradually with general symptoms of weakness and decreased ability to work, which are often incorrectly interpreted by an inexperienced doctor as depending on overwork and exhaustion of the nervous system.
Clinically, different types and variants of the course of the disease can be distinguished, depending on the virulence of the infectious onset or the prevailing clinical syndrome due to the predominant damage to one or another organ. Thus, we can distinguish more malignant forms with high fever, with an abundance of embolism, which lead to death in the first months of the disease, as well as the so-called outpatient forms with almost normal temperature. According to the leading clinical syndrome, the following types are distinguished: anemic, splenomegalic, hepato-splenomegalic, nephritic (with kidney damage by diffuse nephritis with hypertension and azotemia or with kidney damage by amyloid with anasarca, hypercholesterolemia, etc.), cerebral, psychotic, etc.
Some of the unique and severe complications include embolism of the cerebral arteries with hemiplegia, retinal embolism, pulmonary embolism (from the right heart), embolism of the coronary arteries of the heart with myocardial infarction, the development of multiple aneurysms of various organs of an embolic-bacterial (“mycotic”) nature, for example, aneurysms a. gluleae, or more often found only at the opening of the aneurysm a. Lienalis, a. fossae Sylvii, etc. Spontaneous rupture (perforation) of the valves or septum can cause a sudden sharp change in heart murmurs. Occasionally, embolic ulcers of the spleen and liver are observed.

Diagnosis and differential diagnosis of subacute septic endocarditis

It is necessary to carefully evaluate each symptom suspicious for the disease in order to make a correct diagnosis in a timely manner. The patient’s relatively good health, even maintaining working capacity within certain limits, the absence of severe shortness of breath, periods of normal temperature, and the paucity of complaints should not, if there are compelling reasons, deter the doctor from diagnosing subacute septic endocarditis. The most significant signs, besides elevated temperature, in such patients should be considered a painful enlarged spleen, “drum fingers”, pallor; from laboratory confirmations - microhematuria, anemia with leukopenia, positive blood culture, as well as formol gelatinization of serum. The last reaction is very simple: blood serum, when added to 1-2 ml of it in a test tube, quickly, after 15-30 minutes, turns into a jelly-like mass that does not pour out when the test tube is overturned; the mass can take on the appearance and color of coagulated egg white; normal serum does not change with the addition of formalin even after 24 hours. It is extremely rare that formol gelatinization occurs in other diseases, when it is also associated with severe hyperglobulinemia: with multiple myeloma, visceral leishmaniasis; with rheumatic endocarditis, the reaction is usually negative.

Severe rheumatic carditis in the presence of heart disease, prolonged fever, sometimes it is only difficult to differentiate from subacute septic endocarditis; rheumatic carditis is especially prone to give a continuously relapsing severe course with anemia, etc. in adolescents; on the contrary, subacute septic endocarditis is rare in them. Rheumatic carditis affects more often women, and subacute septic endocarditis affects men, perhaps because aortic defects, which are more often accompanied by a septic process, occur predominantly in men, like some other arterial diseases. The rheumatic nature of heart damage is indicated by: the presence of severe congestive decompensation, congestive liver, atrial fibrillation, polyserositis, in particular, pericarditis (in septic endocarditis only purulent pericarditis occurs as a rare complication), polyarthritis (and not polyarthralgia, which is observed in subacute septic endocarditis) , the connection of acute manifestations with previous tonsillitis (usually not pronounced in subacute septic endocarditis), attenuation of exacerbation without special treatment even after a course of many months, negative blood culture results, negative formol reaction, tendency to leukocytosis, changes in the type of congestive kidney in the urine more often than persistent hematuria.

Syphilitic aortitis, accompanied by aortic insufficiency, can also be easily confused with subacute septic endocarditis. An increase in temperature, pallor of the integument, a progressive course, an enlarged spleen or the presence of hepatolienal syndrome, vascular lesions, in particular cerebral phenomena, can occur with syphilitic aortitis, with an active syphilitic infection and without complications of septic infection. It should be borne in mind that in subacute septic endocarditis there is often a nonspecific positive Wassermann reaction due to significant colloidal shifts in the serum characteristic of this disease. The presence of subacute septic endocarditis is indicated by significant anemia, splenomegaly, embolic phenomena, a positive formol reaction, and a positive blood culture. It is difficult to use antisyphilitic treatment for differential diagnosis, since even with advanced syphilitic aortitis, the effect of treatment is not particularly striking and, at best, is expressed in a delay in the progression of the process.

Subacute septic endocarditis is often mistaken for influenza, typhoid fever, brucellosis, tuberculosis, especially malaria, i.e., a febrile illness is interpreted as an accidental infectious disease in a patient with heart disease, or heart disease is generally visible. Indeed, there is a superficial similarity of subacute septic endocarditis with malaria (and partly with brucellosis): individual jumps or waves of temperature, painful enlarged spleen, leukopenia, anemia, often monocytosis, significant changes in red blood cells, provocation of febrile attacks by baths, physical fatigue, etc. However, with subacute septic endocarditis there are signs that are not characteristic of malaria: persistent constant hematuria, “tympanic fingers”, pain in the joints, sternum, petechiae, conjunctival symptom, etc. The detection of plasmodia is of primary importance for the recognition of malaria, especially mandatory, that in case of heart disease, in case of doubt, it is always more correct to think about endocarditis than about malaria; persistent antimalarial treatment leads to persistent progressive improvement. It is completely wrong to consider a temporary decrease in temperature after quinine or quinine as proof of the presence of malaria, since subacute septic endocarditis is generally characterized by an undulating course of fever and the indicated decrease can only be a coincidence. Similar reasoning should be used when deciding whether a heart patient has brucellosis, typhoid fever, etc. (blood culture, immune reactions, etc.). With a satisfactory general condition of patients in the initial stages and a slight increase in temperature, subacute septic endocarditis can be mistaken for a neurogenic subfebrile condition.

If there is one or another pronounced local lesion, the question arises of excluding independent suffering of this organ. Thus, significant hematuria and pain in the kidney area may raise suspicion of kidney stones, which, however, is characterized by irradiation of pain in the groin, etc., and the absence of general symptoms; with diffuse nephritis with general edema or azotemia that occurs during subacute septic endocarditis, the primary form of Bright's kidney disease can be mistakenly established. With severe anemia, splenomegaly, hemorrhagic diathesis, one can think about independent anemia, splenomegaly, thrombopenia, etc. Murmurs, especially systolic, with significant anemia in a patient with subacute septic endocarditis can be mistakenly recognized only as anemic, and at the same time organic heart disease is not diagnosed at all.

It should be remembered that drumstick fingers together with severe cyanosis may be a sign of congenital heart disease itself, and then they should not be decisive for the recognition of subacute septic endocarditis.

Forecast. Until recently, the prognosis was considered hopeless. Treatment with penicillin improves the prognosis, causing a more protracted course of the disease, and in some cases even complete recovery. Nevertheless, in these cases there remains the danger of a new septic lesion of the altered valves. To improve prognosis, early recognition and vigorous treatment of the disease are essential. Death of patients treated with penicillin can also occur when the infectious process is suppressed from the consequences of advanced organ damage, such as uremia or heart failure, embolism of the brain, coronary arteries of the heart.

Prevention and treatment of subacute septic endocarditis

Measures to prevent subacute septic endocarditis include the fight against rheumatism and other infections that cause organic heart valve defects. If there is already a heart defect of any nature, patients must be especially protected from septic infection by, for example, preventive penicillin therapy during tooth extraction operations, tonsillectomy and similar interventions. In patients with congenital defects, in particular, with patent ductus arteriosus, it is advisable to use surgical intervention that restores normal hemodynamic conditions and thus, apparently, eliminates the predisposition to septic infection.

Treatment of subacute septic endocarditis consists of general measures and specific treatment. Patients need bed support already in the early period of the disease, regardless of their sometimes good health, in clean air, a quiet environment, good nutrition, and protection from infection.

At present, the most effective remedy should be considered penicillin, which, as experience shows, has a detrimental effect on most strains of viridans streptococcus sown from the blood of patients with subacute septic endocarditis, as well as penicillin together with streptomycin. Treatment with penicillin is carried out according to general rules in large doses of 500,000-1,500,000 units per day for 4-6 weeks in a row, with such courses repeated several times after short breaks. It is especially important to begin treatment with penicillin in the very first months of the disease.

Additionally, agents are used that enhance the effect of penicillin and increase the body's resistance and immune strength, as well as symptomatic medications. They try to increase the effect of penicillin on streptococci by creating special conditions that delay its release from the body and, therefore, increasing its concentration in the blood, as well as by preventing the formation of blood clots on the affected valves, blocking the access of the antibiotic to microbes, or by artificially increasing the patient’s body temperature to enhance action of penicillin. However, anticoagulants and artificial fever are not indifferent to the patient and, while seemingly justified from a theoretical point of view, do not provide undoubted and significant advantages over conventional therapy with penicillin alone. Prescribing drugs simultaneously with penicillin, even if they have a weaker clotting-inhibiting effect, such as salicylates and quinine, could be justified from the point of view that blood clotting under the influence of penicillin itself is somewhat accelerated; however, these provisions cannot yet be considered sufficiently firmly established. To increase the overall resistance of the body, treatment with liver preparations, vitamins, as well as blood transfusions of 100-150 ml can be used in the absence of contraindications such as heart failure or frequent embolism. Among the medications, pyramidon is also prescribed, which often definitely reduces the temperature, sedative bromides, luminal, etc.

In order to sanitize various infectious foci, for example, in the oral cavity, nasopharynx, as well as to change abnormal conditions, blood circulation, surgical interventions should be used - tonsillectomy, etc., ligation of the open botal duct, which reduces fever and leads to more successful blood sterilization and cure valve infections.

When culturing penicillin-resistant microbes from the blood, large doses of sulfonamide drugs (up to 100.0 or more per course), streptomycin and other antimicrobial agents are used, depending on the properties of the pathogen. Treatment with sulfonamides in ordinary cases of subacute septic endocarditis undoubtedly gives more modest results compared with penicillin, but one should remember the possible side effects of these drugs. Previously used antibacterial therapy - rivanol, flavacridine (trypaflavin, acriflavine), silver preparations, vaccination, immunotransfusion - is often poorly tolerated and seems to suppress the body's defenses. The altered reactivity of patients with subacute septic endocarditis is likely to be of great importance in the outcome of this chronioseptic process caused by a low-virulent pathogen, but it is usually not possible to significantly change this reactivity. You should limit yourself to mildly acting disinfectants (urotropine, salitropin in a vein or per rectum) and especially recommend, as already mentioned, a general restorative regimen (physical and mental rest, nutritious, easily digestible nutrition, multivitamin mixtures, mild sedatives, liver medications, etc. .).

Under the influence of early treatment with large doses of penicillin, fever decreases, severe organ damage does not develop, and recovery or at least long-term remission occurs. If treatment is started already when the full clinical picture has developed or in a late period, it is also almost always possible to induce remission - improvement in well-being, decrease in temperature, often to normal, improvement in blood composition, reduction in embolism; less often, a significant contraction of the enlarged spleen occurs, etc. Moreover, as stated above, even after the cessation of fever, failure of the heart and kidneys may increase, leading the patient to death; It should be remembered that even after a long remission or apparently complete recovery, a new exacerbation or a new sepsis disease, sometimes already caused by a different pathogen, is possible.

Acute septic endocarditis

The disease occurs at any age, somewhat more often in men.

In relation to the actual pathogenesis of the disease, one should take into account the neuroreflex and neurotrophic influences, which are discussed in the section on subacute septic endocarditis.

Clinical picture of acute septic endocarditis

The general condition of the patients is serious. Adynamia, prostration, hectic fever, sweats, septic diarrhea, etc. are often observed.

Complaints about palpitations and pain in the heart are mild and do not usually attract the doctor’s attention to this organ. During the examination, signs of a heart defect are found, if there was one before, but with a previously healthy heart, only doubtful signs of damage to it are found. A soft systolic murmur is heard at the apex or on the aorta or a weak diastolic murmur on the aorta, which are usually mistaken for an anemic or muscle murmur, so common in severe infections in general. A pronounced jumping pulse, characteristic of a mature aortic defect, is also usually not observed. Significant enlargement of the heart, as well as obvious signs of its failure, are usually not observed. More typical are sharp tachycardia, arrhythmia, and especially murmur variability.
The spleen cannot be palpated clearly due to its soft consistency and the general serious condition of the patients, although at autopsy it is naturally found to be enlarged. Embolic and pyemic phenomena from various organs are characteristic: from the nocturnal side - focal nephritis, which results in hematuria, as well as degeneration of the tubules, purulent pericarditis, pleurisy, arthritis, embolism in the spleen, brain, etc., petechial rash.

An infectious pathogen is constantly easily cultured from the blood; Severe neutrophilic leukocytosis and anemia are also found.

Flow. Acute septic endocarditis begins gradually, lasts a few weeks, and rarely lasts up to 2-3 months. A longer course or the development of endocarditis only after months is possible with a milder course of sepsis, for example, with chronic meningococcal sepsis. The prognosis is serious. Before the introduction of penicillin, all cases ended in death.

Diagnosis. You should think about this disease in severe septic conditions of acute infections, in surgical and gynecological patients, and evaluate even minor signs of the heart, embolic phenomena, and kidney damage in this direction. Progressive metastasis of infection involving the meninges and serous membranes, with phlebitis with persistent positive blood culture is highly suspicious for endocarditis. There may not be any complaints about the heart, or they may be of little character. More conclusive is the appearance of murmurs, especially diastolic ones, during observation or changes in the nature or intensity of an old (pre-existing) murmur.

Treatment of acute septic endocarditis

Treatment comes down to good care, good nutrition, and increasing the overall resistance of the body. Prevention of bedsores, etc. is necessary.

In surgical (wound) and obstetric sepsis, elimination of the primary source of infection is of great importance. Basically, treatment comes down to the persistent use of antibiotics and chemotherapeutic agents, depending on the susceptibility of the causative agent of a given case of endocarditis to one or another drug, along with blood transfusions and other general measures of influence on the body. Treatment is usually carried out with penicillin, sometimes together with sulfonamides. In some cases, it is advisable to use other antibiotics (streptomycin, syntomycin, etc.).

Penicillin is prescribed intramuscularly in large doses, 400,000 - 800,000 or more units per day (at intervals of 3 hours). Treatment is usually long-term, and a course requires several tens of millions of units of penicillin, as in subacute septic endocarditis. Of the sulfonamide drugs, preferably those that are well absorbed and create a high concentration in the blood (sulfazine, sulfathiazole), usually 4.0-6.0 per day, provided that these drugs are well tolerated and a sufficient amount of fluid is administered - up to 100 in total, 0 drug or more per course of treatment. Neurovascular drugs, tonics, vitamins, etc. are also widely used.

Septic endocarditis is an inflammatory reaction of the body to an ongoing infectious process, accompanied by damage to the heart valves.

With this disease, there is an increased reactivity of the body, which is why it can be considered as a bacterial infection of the blood. And since it develops on the heart valves, the cardiovascular system is most damaged.

Let's move on to the types of septic endocarditis.

According to the nature of the flow:

Acute stage bacterial endocarditis. Its duration ranges from one to two weeks. It can develop as a complication after injuries or operations on the vessels and cavities of the heart.
Subacute stage of the disease. Duration up to three months. Develops due to insufficient treatment.
Chronic (protracted) stage. It lasts for years.

Depending on the pathogenesis:

Primary. Healthy heart valves become infected.
Secondary. It develops from other heart diseases.

By degree of damage:

It occurs with limited damage to the heart valves.
Extends beyond the heart valves.

Causes

Bacteria provoke the appearance of septic endocarditis. These include: staphylococcus, streptococcus, enterococcus. Less commonly, the cause of the disease may be a fungal infection.

Through the mouth, microorganisms enter the human body, the bloodstream, the heart and begin to multiply there.

People can easily get sick:

Suffering from infections such as tonsillitis, sinusitis and others.
Organism affected by: staphylococcus, streptococcus, enterococcus.
Having undergone surgery.

At risk are patients with:

scars on the heart valves;
with illness;
artificial heart valve;
sagging valve flaps;
heart abnormalities.

Predisposed to the disease:

Patients who undergo invasive research methods (with penetration into the body).
Drug addicts who use drugs intravenously.
People who have a weakened immune system. The reason for this is taking a large number of antibiotics or unfavorable environmental conditions.
Patients who have undergone operations affecting the mucous membrane of the respiratory and urinary tracts, gastrointestinal tract, and in the presence of infection of these organs.

Symptoms of septic endocarditis

What affects the symptoms of the disease?

Statute of limitation of the disease;
flow stage;
the cause of the disease;
state of the human immune system;
patient's well-being;
the number of bacteria in the blood;
age of the patient.

The disease progresses differently for everyone. It can begin abruptly and be pronounced, or, on the contrary, it can develop gradually, the signs are weakly expressed. The second case is the most dangerous. A person turns to a specialist at the wrong time.

Acute endocarditis is accompanied by the following symptoms:

Sudden rise in temperature.
The number of heart muscle beats increases, which leads to rapid valve damage.
Emboli can break off and are transported with the blood to other organs, thereby creating new foci of inflammatory processes and abscesses.
Heart failure develops very quickly, even shock is possible.
The kidneys, as well as other organs of the body, may stop working.
Artery walls become weak and can rupture, leading to death if the vessel is located in the brain or near the heart.

Subacute stage endocarditis, which can last several months, has the following symptoms:

The most pronounced general signs of septic endocarditis are:

Stomach upset;
nausea and vomiting;
dizziness;
fever;
fingers and toes become deformed;
shortness of breath and cough appear:
pain is felt in the joints and muscles.

In young children, bacterial endocarditis is accompanied by a change in skin color, it becomes sallow.

Diagnostics

The first stage is to find out whether there have been surgical interventions and whether there are chronic infections.
The second stage is the use of laboratory and clinical research.

A blood test shows an increased ESR and an increase in leukocytes.

Blood cultures performed several times indicate the causative agent of the infection.

A biochemical blood test shows changes in blood protein and changes in immune status.

EchoCG - helps to see changes that are more than five millimeters in size on the heart valves and the reasons for their appearance.

A more accurate and complete diagnosis is obtained using MSCT of the heart and MRI.

All diagnostics used are aimed at identifying the inflammatory process occurring in the body.

Treatment

If septic endocarditis is detected, the patient is immediately admitted to the hospital. Only there will he be monitored every minute and receive quality treatment.

Medication (therapeutic).

The essence of it is to take antibiotics. They are administered through an IV. Thanks to them, harmful bacteria are destroyed.
Before prescribing a drug, it is determined which pathogen is the cause of the disease. The infectious agent is isolated from the blood and the blood is cultured for sterility. But since the result of this analysis must wait a week, an antibiotic is prescribed immediately, relying on empirical therapy. This action is carried out until the results of the analysis are obtained, and then it is adjusted.
Usually the maximum dose of the drug is prescribed, the duration of their use is about eight weeks.

Remember, antibacterial therapy is only effective in twenty percent of cases.

Immunocorrection

In order to neutralize toxins traveling in the bloodstream, passive immunization using antitoxic serums is used. They are administered daily for five days.

Surgical intervention is the mechanical removal of infected lesions located in the heart, followed by their reconstruction and implantation.

It is used if drug treatment has not produced results or there are direct indications for surgery. The patient is diagnosed with heart failure or the infection progresses over two weeks. Surgical intervention is also necessary if an abscess appears in the myocardial cavity.

The essence of the procedure has two goals:

Removal of dead and infected tissue, which leads to the destruction of infection in distant areas of the heart.
Restoring the functioning of heart valves. This goal is achieved by installing implants or, if possible, reconstructing the patient's valves.

Treatment using traditional medicine

For bacterial endocarditis, you can use the same plants as for heart failure: spring adonis and golden rhododendron, as well as rusty foxglove. All these plants have one property that applies to all - they reduce the number of heart contractions and improve the contractile properties of muscles. The strongest of them is rhododendron; like foxglove, it has no effect on blood pressure. But at the same time, it should not be used by people with problems with the urinary system and tissue necrosis.

Digitalis and rhododendron should not be prescribed to people with bradycardia and atrial fibrillation. Since they constantly accumulate in the body and eventually lead to toxicosis, it is recommended to use them for no more than two months. Then be sure to take a break for two months. You can replace these plants with adonis or hawthorn.

Adonis is also effective in treating the disease, but its effects are not as pronounced. Plus, it has no contraindications and can be used for quite a long time.

Treatments from all herbs are prepared in the same way; the raw materials are dry leaves and herbs. In the pharmacy you can buy infusions and tinctures of these plants.

Prevention

Try to avoid heavy physical activity.
Strengthen immunity.
Contact your doctor immediately at the first symptoms of a chronic infection.
Do not delay treatment: caries, laryngitis, tracheitis, tonsillitis. This is especially true for people with heart disease.
If you have chronic heart disease and artificial valves, you should definitely see a specialist. People in this category are at risk.
People at risk after surgical medical intervention where tissue damage occurs in the body are prescribed antibiotics.
Proper nutrition.
Rejection of bad habits.

Complications

Bacterial endocarditis is a very dangerous disease if you do not consult a doctor in time. It can cause serious complications that are almost untreatable. The explanation for this situation is that bacteria, having reached the heart, concentrate cells around themselves that settle on them. Scabs form, over time they separate and penetrate into other organs. Where they end up is where the pathology begins.

In the lungs: edema, hypertension, abscess, heart attack.
In the spleen: splenomegaly, infarction.
The liver is affected by hepatitis.
Meningitis and cyst, as well as circulatory disorders in the brain.
The heart becomes enlarged, myocardial infarction and abscess are observed, as well as autonomic damage to the heart valves.
Thrombophlebitis and vasculitis, aneurysm and thrombosis.

Forecast

Previously, septic endocarditis could not be cured. After three years of the disease, the patient died. Nowadays everything has changed. The use of antibiotics helps correct the situation and achieve clinical recovery in a large number of patients.
Your health is only in your hands. The sooner you contact a specialist, the sooner treatment will begin and the prognosis will be only positive. But it is best to prevent a disease than to treat it later.

A video presentation of septic endocarditis is provided. After looking at it, you will find out what kind of disease this is, the causes that cause it. How to escape from the disease, and what prognosis can be expected.

Acute septic endocarditis (endocarditis septica acuta) accounts for less than 1% of all endocarditis [V. Jonas]. Typically, this endocarditis is a manifestation of sepsis after childbirth, abortion, wound infection, thrombophlebitis, otitis, osteomyelitis, meningitis, pneumonia, pulmonary abscesses and other diseases caused by virulent strains of strepto- and staphylococci and other bacteria with the formation of a secondary septic focus on the endocardium. In some cases of septic endocarditis, endocardial damage may have the character of a primary septic focus as a result of the penetration of bacteria into the blood from an infectious focus that remained untreated or healed at the time of the study (tonsils, skin lesions, etc.).

Clinical picture and course acute septic endocarditis correspond to the picture of acute sepsis. As a rule, there is a fever (2° to 39-40°) of the wrong type with chills and profuse sweats when the temperature drops. Fever is accompanied by severe general weakness, headache, loss of appetite, often shortness of breath, and pain in the heart. The patient is pale, and there are frequent small hemorrhages on the skin. The pulse is frequent, small, often arrhythmic. Myocarditis is a constant companion of endocarditis, therefore the size of the heart is always increased, the apical impulse is shifted to the left. When listening, significant variability of sound phenomena is revealed: heart sounds, especially the first, weaken, sometimes a gallop rhythm is noted, noises appear - systolic at the apex and in the area of the tricuspid valve, systolic and diastolic in the aorta and pulmonary artery. Heart murmurs, sometimes soft, sometimes hard, can vary significantly in strength and duration during the day due to the layering or destruction of thrombotic polypous deposits on the valves. Sometimes a musical noise occurs due to a ruptured valve or chord.

At the end of the disease, circulatory failure may occur. Usually the spleen and liver are enlarged. Anemia of the hypochromic type appears and rapidly progresses. Leukocytosis increases (up to 20,000 or more) with pronounced neutrophilia and a shift in the leukocyte formula to the left; eosinopenia; large epithelioid cells (typical and atypical histiocytes) may be detected. There is a pronounced tendency to embolism, repeated embolisms are often observed in the skin with the formation of petechial spots, in the brain, central retinal artery, spleen, kidneys, sometimes in large arteries of the extremities, etc. Symptoms of phlebitis and septic arteritis may be associated with damage to the entire vascular system , phenomena of hemorrhagic diathesis (petechial rashes, nosebleeds, hematuria).

There are two clinical forms of acute septic endocarditis - pseudotyphoid and septicopyemic. With the first, the onset of the disease is relatively gradual, there is vomiting, diarrhea, abdominal pain, blackouts, fever with large fluctuations, and chills. The septicopyemic form is characterized by a more sudden onset, high fever, numerous metastatic abscesses, acute glomerulonephritis, skin emboli, petechiae, sometimes meningeal symptoms, as well as cardiac enlargement and the auscultatory signs described above.

The course of the disease is characterized by a progressive deterioration in general condition, increasing signs of heart damage, and the appearance of new symptoms due to embolism of various organs or intoxication. Death occurs from complications (cerebral embolism, pneumonia) or due to exhaustion and intoxication. The duration of the disease is from several days to two months.

Diagnosis Acute septic endocarditis at the onset of the disease is difficult. A positive blood culture confirms the presence of sepsis. The main diagnostic significance is changing loud heart murmurs and the appearance of signs of embolism. Endocarditis is often unrecognized in older people, in whom it is accompanied by extreme weakness and usually ends in death after 4-5 days.

Forecast. exceptionally bad before, now improving due to the possibilities of chemotherapy and antibiotic therapy.

Acute septic endocarditis

It happens rarely in childhood. According to its anatomical characteristics, it is ulcerative. Heart symptoms usually fade into the background compared to other symptoms of general sepsis. The clinical picture of the disease in childhood has been little studied. The development of embolic processes will undoubtedly speak in favor of heart damage. Its etiology is different. The prognosis is difficult. Treatment primarily focuses on treating the septic condition; cardiac symptoms usually require symptomatic treatment.

More common in children chronic septic endocarditis. According to the clinical picture, chronioseptic endocarditis has much in common with rheumatic endocarditis: periodic longer periods of fever of an irregular remitting or intermittent type, the same connection with chronic tonsillitis and tonsillitis. skin manifestations in the form of polymorphic erythema. hives. Leiner's erythema annulare, polyarthritic manifestations without reaction from the glands regional to the affected joints, the same manifestations of heart damage. Often endocarditis lenta develops in a heart affected by a rheumatic process or with congenital heart defects. Unlike typical rheumatism, it causes enlargement of the spleen, often the liver, chronic focal glomerulonephritis, and especially a tendency to embolism. This disease is characterized by the presence of chills. However, this sign in childhood is not entirely reliable: some rheumatic patients without other signs of the septic process complain of chills and vice versa - with chroniosepsis sometimes there are no chills. The same can be said in relation to sweats.

It is also generally accepted that with chroniosepsis anemia develops to a greater extent than with rheumatism. But this is not a reliable sign either. According to E.V. Kovaleva, in severe cases of rheumatism, especially with polyserositis and pericarditis, in 60% of cases the hemoglobin content drops to 40-30%.

Thus, the difference between chronioseptic endocarditis and rheumatic endocarditis in a child is not always easy, and dynamic observation is often required to finally resolve the issue in one direction or the other. A definitive diagnosis can be made by bacteriological examination using blood culture. Often, but not always, it is possible to culture viridans streptococcus. A negative culture result does not yet exclude a septic process, even with repeated cultures. Negative results are especially often obtained in connection with the antibiotics used for treatment - penicillin, streptomycin, etc.

But still, the clinical symptom complex is quite characteristic. Sharp weakness, periodic increases in temperature, the presence of noise, rapidly progressing anemia, skin manifestations, enlarged and sometimes painful spleen, hemorrhagic nephritis or prolonged hematuria, chills, sweats in a child who has previously had rheumatism, make the diagnosis of chroniosepsis very likely.

Treatment of septic endocarditis must be not only symptomatic, but also etiological. The use of antibiotics in large doses and for a long time gives hope for success.

Penicillin should be used in a dose of at least 500,000 - 1,000,000 units per day and for at least 2-4 weeks; some authors require continuous treatment for 2 months.

Penicillin is good to combine with streptomycin, especially in cases where the microbe is resistant to penicillin. Biomycin and syntomycin can also be used. At the same time, to increase immunity, especially in the presence of anemia, repeated blood transfusions (50-100 cm3 each) should be carried out. If there is a focal infection (teeth, tonsils, paranasal cavity, ears, gallbladder, appendix, etc.), it is necessary to sanitize them too.

Anatomically, chronioseptic endocarditis is characterized by the development of warty endocarditis on the valves (as in rheumatism) with ulcerations (which does not happen in pure forms of rheumatism). The overlays on the valves are more loose than in rheumatism, so they come off more easily and more easily give rise to the development of embolism.

Acute septic endocarditis

Acute septic endocarditis is a severe septic disease that develops as complications of various bacterial infections, with secondary damage to the endocardium.

Etiology and pathogenesis Acute septic endocarditis is more often observed after abortion, childbirth and as a complication of various surgical interventions, but it can develop with erysipelas, osteomyelitis, etc.

The causative agents of the endocarditis in question are highly virulent pyogenic bacteria - hemolytic streptococcus, Staphylococcus aureus, pneumococcus, and Escherichia coli. Recently, cases of the development of acute septic endocarditis with actinomycosis and fungal sepsis have been described. Primary lesions can be easily detected when they are externally localized, for example felon, carbuncles, wounds, or with appropriate anamnestic data (previous abortion, gonorrhea). There are often cases when the primary focus cannot be recognized.

Microorganisms from primary septic foci enter the blood and initially settle in significant quantities on the surface of the valves. Thus, a secondary (daughter) septic focus is formed in the endocardium. Subsequently, pathogens penetrate from the surface of the valves into their thickness, causing extensive destruction in them.

As with subacute septic endocarditis, altered immunobiological reactivity plays an important role in the development of the disease.

Pathological anatomy The valves are ulcerated, loose thrombotic masses are deposited at the bottom and along the edges of the ulcers, not associated with the underlying tissues and containing a large number of bacteria. Thrombotic masses begin to become a source of embolism in some organs - the spleen, kidneys, brain - with the development of infarctions. or loss of function of these organs.

The septic process in the endocardium leads to rupture of tendon threads, destruction of valve leaflets and their perforation. Insufficiency of the aortic valves is more often formed, less often - of the mitral valves; for pneumonia. Postpartum sepsis causes damage to the tricuspid valve.

Clinical picture of acute septic endocarditis

Patients complain of pain in the head, pain in the heart, weakness, general malaise, and chills. Fever (temperature) is of a laxative type, accompanied by severe chills with further profuse sweating. Enlarged heart; with long-term endocarditis, murmurs occur; on the aorta it is diastolic, at the apex, also above the tricuspid valve - systolic. The cause of the appearance of murmurs is the manifestation and development of insufficiency of the mitral, aortic and tricuspid valves. Tachycardia and arrhythmia are observed. The soft (septic) spleen is palpable.

Characteristic are septic emboli in the spleen, accompanied by severe pain in the left hypochondrium, sometimes a capsule friction noise (perisplenitis), as well as in the kidney, causing sharp pain in the lumbar region followed by hematuria. Multiple embolic petechiae are noted in the skin. Sometimes purulent pleurisy and pericarditis develop. joint damage occurs. In the peripheral blood, neutrophilic leukocytosis with a band shift, progressive anemia, and accelerated ROE are detected. With blood cultures, sometimes multiple ones, it is possible to culture the causative agent of the disease (viridans streptococcus, less commonly pneumococcus).

Prognosis The disease is curable, but defects in the valves persist and cause progressive deterioration of blood circulation, which requires further monitoring and treatment.

Prevention and treatment

Prevention of septic endocarditis consists of the active and timely elimination of infectious foci in the tonsils, nasopharynx, middle ear, female genital organs, the fight against out-of-hospital abortions, the use of antibiotics for premature birth, and early rupture of water.

Elimination of the main septic process is achieved by using massive doses of antibiotics in combination with sulfonamides with the mandatory determination of the sensitivity of the microbial flora to them. Doses and medications are the same as for the treatment of subacute septic endocarditis.

Treatment should also be long-term and combined with restorative therapy, blood and plasma transfusions. A nutritious diet rich in vitamins is necessary. If the main focus is accessible to local treatment, it is carried out in full, including surgical intervention.