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

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

The most dangerous and fast-flowing variant of endocarditis is septic. In the old classification, it was called acute endocarditis. Most often, the cause of its occurrence is surgical interventions on the heart, 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 causative agents are nosocomial strains. In the vast majority of cases, staphylococci, Pseudomonas aeruginosa and fungi are found in the sowing.

Subacute septic endocarditis

Subacute septic endocarditis is a protracted sluggish chronioseptic process with the localization of an infectious focus on valves disfigured by an old rheumatic, syphilitic, congenital, traumatic defect, or not previously changed.

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

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

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

For the onset of the disease, it is important to reduce the body's resistance due to previous sensitization. The incidence also increases during natural disasters, wars, etc. You can also get an experimental model of the disease - this is sepsis in a previously sensitized organism. Often the disease develops in patients with rheumatic heart disease, 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 a systemic involvement of the reticuloendothelial system, causing a generalized vascular lesion.
  • Other organs of the reticuloendothelial system (liver, spleen) are also involved.
  • When bacteria enter the bloodstream, they primarily settle on the heart valves, and more often on the aortic ones. In the future, the valves themselves become a source of infection, the mitral valve suffers less often, even the tricuspid one.

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, excessive sweating, subfebrile temperature), there is a periodic improvement in the general condition. The clinical picture consists of symptoms of a general septic nature (fever, chills, excessive sweating); symptoms of heart damage (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 pattern of heart disease, most often aortic); symptoms of vascular lesions (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 undulating and have a symmetrical arrangement. Sometimes Osler's nodules appear (reddish skin seals 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 has the character of warty-ulcerative with a predominance of decay. Bacteria are found in the thickness of the valves even with conventional microscopy. Most often, the aortic valves are affected, then the mitral, 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. With regard to the actual pathogenesis of the disease, neuroreflex and neurotrophic influences should be taken into account, which are discussed in the section on subacute septic endocarditis.

Symptoms of acute septic endocarditis

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

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, E. 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, embolism of the vessels of the brain, kidneys, and spleen occurs 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.

  1. Rheumatic endocarditis, or rheumatic valvulitis, with damage to the entire thickness of the valve, including its stroma, occurring simultaneously with the lesion, as a rule, of the myocardium and pericardium, why the broader term is more rational: rheumatic carditis, or rheumatic heart disease. Rheumatic heart disease, as is typical for other manifestations of rheumatism, often exacerbates many times and is more reliably diagnosed precisely with these exacerbations, relapses of the disease as recurrent endocarditis, or recurrent rheumatic carditis. This form is described in a separate chapter on rheumatic heart disease.
  2. Subacute septic endocarditis, the so-called lenta endocarditis, associated with chronic septic valvular disease, most often with green streptococcus-Streptococcus viridans.
  3. 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 have less clinical significance.
  4. Warty terminal, or cachectic, endocarditis resulting from the formation of thrombotic deposits on the valves (thromboendocarditis) in the last days of life with chronic cachectic diseases such as cancer, chronic nephritis, tuberculosis. Endocarditis is discovered incidentally at autopsy and is of only pathological interest, without showing any special signs during life.
  5. Parietal (mural) endocarditis in myocardial infarction, which is important as a possible source of embolism in various organs and, 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 rheumatic or indeterminate endocarditis; however, although there may be a combination of rheumatic and septic signs in the clinic, a characteristic clinical bias in one or another of the two directions is subsequently revealed, and, therefore, each case over time fits into one of the main forms of endocarditis. The term "indefinite endocarditis" was also applied to a special form of heart valve damage 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 borders of acute and subacute septic endocarditis in some infectious diseases are also not sharply outlined 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 the localization of an infectious focus on the valves, disfigured by an old rheumatic, syphilitic, congenital, traumatic defect, or not previously changed. The causative agent, 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 possible. The disease is characterized by a peculiar reaction on the part of the body, proceeding, as a rule, without purulent metastases, with a violation of the activity of the bone marrow and the reticuloendothelial apparatus. In recent decades, attention has been paid to the independence and relative frequency of this form of endocarditis.

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

Subacute septic endocarditis develops on the basis of:

  1. most often rheumatic defects of the aortic and mitral valves, usually with a relatively unsharply affected myocardium in the compensation stage, without atrial fibrillation;
  2. congenital heart defects, especially non-closure of the interventricular septum, ductus arteriosus, pulmonary artery stenosis, congenital anomalies of the aortic valves;
  3. rarely on the basis of syphilitic aortic insufficiency and even less often on the basis of sclerotic defect of the aortic valves;
  4. as an exception on the basis of traumatic heart defects, generally extremely rare. It is possible to develop subacute septic endocarditis on previously unchanged valves (Chernogubov).

Rheumatic malformations numerically significantly predominate among other organic valvular malformations, therefore it is natural that rheumatism is more often found in the anamnesis of patients with subacute septic endocarditis. Some authors (Strazhesko) recognize a closer relationship between subacute septic endocarditis and rheumatism, believing that both diseases are based on the body's changing response to infection with the same low-virulence streptococcus. However, heart defects of a different etiology are complicated by subacute septic endocarditis in no lesser percentage of cases. The relationship of congenital heart defects with subsequent inflammatory endocarditis was established already 100 years ago, and the same relationship with traumatic heart defects was established more than 50 years ago.
The main pathogenetic mechanisms of development of subacute septic endocarditis, as well as other forms of endocarditis, are not well understood. It cannot be imagined that the pathological process is reduced to the settling of bacteria in certain places of slow or perverted blood flow (with heart defects) or to the engraftment of various microbes due to a violation of the conditions for the blood supply to the "perverse" valves themselves. Of leading importance, one must think, is the special reactivity of the valvular apparatus (or the parietal endocardium) as a result of neuroallergic or neurodystrophic effects, causing only under very specific conditions, difficult to reproduce in the experiment, a complex inflammatory process that progresses for a long 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 an inflammatory lesion of the arteries, which is observed in rare cases of subacute septic arteritis of the ductus arteriosus with its non-closure or with an artorio-venous aneurysm, may be facilitated by intravascular-cardiac reflex effects, and not only by the mechanical transfer of the infectious onset.

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

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 disease and a kind of intoxication.

Prolonged fever of indeterminate type is one of the most important signs of the disease. Often there are febrile waves lasting 1-2-3 weeks, or one-, two-day temperature jumps up to 39-40 °, provoked by various moments, or prolonged subfebrile condition. There is usually considerable variability in the febrile reaction, and for weeks and months the temperature may be almost normal. Prolonged fever most often leads the patient to the doctor.

The general appearance of the patient is characteristic: pale skin with a special dirty shade of "coffee with milk", however, 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, the tongue is not lined. Pain, due to embolism in various organs (in the spleen, kidneys, limbs, etc.), is 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 disturbances. Often heard diastolic murmur on the aorta or mitral melody at the apex. With the development of the process on unchanged (usually aortic) valves, a fresh defect (acute) is detected 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 to be significantly enlarged, and the complaints are not predominantly cardiac in nature. Patients, despite the frequent rise in temperature, at the beginning of the disease can move independently and outside the period of severe complications, they often come to an outpatient appointment with a doctor.

Examination reveals an enlarged spleen, sometimes to the extent of significant splenomegaly, along with an enlarged liver in 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 infarcts, which cause sharp pains radiating to the region of the left shoulder joint, muscular protection from the abdominal press, restriction of respiratory mobility of the lung on the left, sometimes peritoneal friction noise (perisplenitis) when auscultating 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. So, embolism in the kidneys often give acute paroxysmal or more dull pain in the lower back, sometimes with the release of bloody urine, soreness when tapping the kidney area from behind (positive symptom of Pasternatsky); embolism in the extremity causes petechiae, sometimes painful points or nodules on the fingers, especially on the terminal phalanges or on the elevations of the palm (thenar and hypo-thenar) in the form of red stripes, spots, sometimes with a white central dot - a bridge of vascular occlusion, which, along with tympanic fingers, represents changes in the limbs that are very characteristic of the disease. When examining the skin, petechiae are found due to the fragility of the vessels in other places of the body, and in the conjunctival sac, especially on the lower eyelid, petechiae 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, pain during stabbing.

Laboratory studies reveal characteristic data. First of all, in the urine, as usual with septic processes, changes are found that are characteristic of focal nephritis: erythrocytes in the sediment, a small amount of protein with a normal specific gravity of urine, intact kidney function and normal blood pressure (with aortic defects, there is naturally a high systolic and low diastolic pressure). Occasionally there is massive hematuria. However, it is not uncommon to find more 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, severe anemia with a drop in hemoglobin to 40-30%, leukopenia (about 4,000 leukocytes), thrombopenin with thrombopenic phenomena: a sharply prolonged bleeding time, the appearance of petechiae after applying a tourniquet to the shoulder. Among the erythrocytes, there may be nuclear forms, among the leukocytes, monocytes and histiocytes as an indicator of a peculiar reaction of the reticuloendothelial system to a septic infection. Blood serum with a high content, apparently due to the same irritation of the reticulo-endothelial system, globulins, in particular, eiglobulins, also presents peculiar changes, which is why the serum, when formalin is added, jelly-like 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 more activity of the process.

Course, clinical forms and complications of subacute septic endocarditis

The onset of the disease is difficult to pinpoint. It begins gradually with general symptoms of weakness, decreased ability to work, which are often incorrectly interpreted by an inexperienced doctor as dependent on overwork, exhaustion of the nervous system.
Clinically, it is possible to distinguish various types, variants of the course of the disease, depending on the virulence of the infectious onset or the predominant clinical syndrome due to the predominant lesion of one or another organ. So, it is possible to distinguish more malignant forms with high fever, with an abundance of embolism, which lead to death already in the first months of the disease, as well as the so-called outpatient forms with an almost normal temperature. According to the leading clinical syndrome, 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.
Peculiar 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 found more often only at the opening of an aneurysm a. lienalis, a. fossae Sylvii, etc. Spontaneous rupture (perforation) of the valves or septum can cause a sudden change in heart murmurs. Occasionally observed embolic ulcers of the spleen, liver.

Diagnosis and differential diagnosis of subacute septic endocarditis

It is necessary to carefully evaluate each symptom suspicious for the disease in order to make the correct diagnosis in a timely manner. The relatively good state of health of the patient, even the preservation of working capacity within certain limits, the absence of severe shortness of breath, periods of normal temperature, the scarcity of complaints should not, if there are good reasons, prevent the doctor from diagnosing subacute septic endocarditis. The most significant signs, in addition to fever, 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 serum formol gelatinization. The last reaction is very simple: when blood serum is added to 1-2 ml of it in a test tube, 1-2 drops of formalin quickly, after 15-30 minutes, turns into a jelly-like mass that does not pour out when the tube is overturned; the mass can take the form and color of a curdled egg white; normal serum does not change from the addition of formalin and a day later. Very rarely, formol gelatinization is obtained in other diseases, when it is also associated with severe hyperglobulinemia: with multiple myeloma, visceral leishmaniasis; in rheumatic endocarditis, the reaction is usually negative.

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

Syphilitic aortitis, accompanied by aortic insufficiency, is also 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, brain phenomena, can be with syphilitic aortitis, with active syphilitic infection and without complications of septic infection. It should be borne in mind that with subacute septic endocarditis, there is often a nonspecific positive Wasserman reaction due to significant colloidal shifts in 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 anti-syphilitic 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.

Often subacute septic endocarditis is mistaken for influenza, typhoid fever, brucellosis, tuberculosis, especially for malaria, i.e., 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 with baths, physical overwork, etc. However, in subacute septic endocarditis, there are signs that are not characteristic of malaria: persistent persistent hematuria, "drum fingers", pain in the joints, sternum, petechiae, conjunctival symptom, etc. The main significance for the recognition of malaria is the detection of plasmodia, all the more mandatory, that in case of heart disease, in case of doubt, it is always more correct to think of endocarditis than of 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 this decrease can only be a coincidence. Similar considerations should be followed when deciding whether a heart patient has brucellosis, typhoid fever, etc. (hemoculture, 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 neurogenic subfebrile condition.

If there is one or another pronounced local lesion, the question arises of excluding the independent suffering of this organ. So, significant hematuria and pain in the kidney area can cause suspicion of nephrolithiasis, which, however, is characterized by irradiation of pain in the groin, etc., the absence of general symptoms; in diffuse nephritis with generalized edema or azotemia occurring during subacute septic endocarditis, it is possible to erroneously establish the primary form of Bright kidney disease. With severe anemia, splenomegaly, hemorrhagic diathesis, one can think of 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 generally not diagnosed.

It should be remembered that fingers in the form of drumsticks, together with a sharp cyanosis, may be a sign of congenital heart disease as such, and then they should not be decisive for the recognition of subacute septic endocarditis.

Forecast. The forecast until recently 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. The death of patients treated with penicillin can also occur when the infectious process is suppressed from the consequences of far-reaching organ damage, such as uremia or heart failure, embolism of the brain, coronary arteries of the heart.

Prevention and treatment of subacute septic endocarditis

As measures for the prevention of subacute septic endocarditis, one should name the fight against rheumatism and other infections that cause organic heart valve defects. With already existing heart disease of any nature, patients must be especially protected from septic infection by, for example, prophylactic penicillin therapy during tooth extraction operations, tonsillectomy and similar interventions. In patients with congenital malformations, in particular, with non-closure of the ductus arteriosus, it is advisable to use surgery that restores normal hemodynamic conditions and, 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, clean air, calm environment, good nutrition, protection from infection.

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

Additionally, drugs are used that enhance the effect of penicillin and increase the body's resistance, its immune strength, as well as symptomatic drugs. They try to increase the effect of penicillin on streptococci by creating special conditions that delay its release from the body and, consequently, increase 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 raising the patient's body temperature to increase action of penicillin. However, anticoagulants and artificial fever are not indifferent to the patient and, while seemingly justified from the theoretical side, do not provide undoubted and significant advantages over conventional therapy with penicillin alone. The appointment of drugs simultaneously with penicillin, even if with a weaker clotting-retarding effect, like salicylates, quinine, could be justified already 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 in the form of heart failure or frequent embolism. Pyramidone is also prescribed from medicines, often definitely lowering the temperature, soothing 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 botallian duct, which reduces fever and leads to more successful blood sterilization and cure valve infections.

When sowing penicillin-resistant microbes from the blood, large doses of sulfonamide preparations (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 the usual cases of subacute septic endocarditis gives, of course, more modest results compared with penicillin, while one should be aware of the possible side effects of these drugs. Previously used antibacterial therapy - rivanol, flavacridine (tripaflavin, acriflavin), silver preparations, vaccination, immunotransfusion - is often poorly tolerated and, as it were, suppresses the body's defenses. The altered reactivity of patients with subacute septic endocarditis is probably of great importance in the outcome of this chronic septic process caused by a low-virulence pathogen, however, it is usually not possible to significantly change this reactivity. It should be limited to mildly acting disinfectants (urotropin, salitropin in a vein or per rectum) and especially recommend, as already mentioned, a general strengthening regimen (physical and mental rest, a complete easily digestible diet, multivitamin mixtures, light sedatives, liver preparations, 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 a long-term remission occurs. If treatment is started already with the development of a complete clinical picture or in a late period, it is also almost always possible to cause remission - an improvement in well-being, a decrease in temperature, often to normal, an improvement in blood composition, a decrease in embolism; less often there is a significant contraction of the enlarged spleen, etc. Moreover, as mentioned above, and after the cessation of fever, heart and kidney failure 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 disease with sepsis is possible, sometimes already caused by a different pathogen.

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 has the character of warty-ulcerative with a predominance of decay. Bacteria are found in the thickness of the valves even with conventional microscopy. Most often, the aortic valves are affected, then the mitral, 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.

With regard to the actual pathogenesis of the disease, one should take into account 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 severe. Often there is weakness, prostration, hectic fever, sweats, septic diarrhea, etc.

Complaints about palpitations, pains in the heart are not very pronounced and usually do not attract the doctor's attention to this organ. In the study, signs of heart disease are found, if there was one before, and with a previously healthy heart, only doubtful signs of damage to it. There is a soft systolic murmur at the apex or aorta, or a faint diastolic murmur at the aorta, which is usually mistaken for the anemic or muscular murmur so common in severe infections in general. A pronounced jumping pulse, characteristic of the formed aortic defect, is also usually not noted. Significant expansion of the heart, as well as obvious signs of its insufficiency, is usually not observed. More characteristic is a sharp tachycardia, arrhythmia, and especially the variability of noise.
The spleen is palpable indistinctly due to its soft consistency and the general severe condition of the patients, although an autopsy naturally reveals its enlargement. Embolic and pyemic phenomena from various organs are characteristic: from the side of the nights, focal nephritis, which affects hematuria, as well as degeneration of the tubules, purulent pericarditis, pleurisy, arthritis, embolism in the spleen, brain, etc., petechial rash.

An infectious agent is constantly easily sown from the blood; find also a sharp neutrophilic leukocytosis and anemia.

Flow. Acute septic endocarditis begins gradually, lasts a few weeks, rarely drags on for up to 2-3 months. Perhaps a longer course or development of endocarditis only months later 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. One should think about this disease in severe septic course of acute infections, in surgical and gynecological patients, and evaluate in this direction even minor signs of the heart, embolic phenomena, kidney damage. Progressive metastasis of the infection involving the meninges and serous membranes, with phlebitis with persistent positive blood culture is highly suspicious of endocarditis. Complaints to the heart may not be, or they are not very typical. The appearance of noises, especially diastolic, during observation or changes in the nature or intensity of the old (pre-existing) noise is more convincing.

Treatment of acute septic endocarditis

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

In surgical (wound) and obstetric sepsis, elimination of the primary focus of infection is of great importance. Basically, treatment is reduced to the persistent use of antibiotics and chemotherapeutic agents, according to the compliance of the causative agent of this case of endocarditis with one or another drug, along with blood transfusions and other general measures of influence on the body. Usually treatment is carried out with penicillin, sometimes together with sulfonamides. In some cases, it is advisable to use other antibiotics (streptomycin, synthomycin, etc.).

Penicillin is administered intramuscularly in large doses, 400,000 - 800,000 or more units per day (at intervals of 3 hours). The treatment is usually long, and the course requires several tens of millions of units of penicillin, as in subacute septic endocarditis. Of the sulfonamide preparations, preferably those are used 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, 0 drug or more per course of treatment. Neurovascular agents, tonics, vitamins, etc. are also widely used.

Septic endocarditis is an inflammatory reaction of the body to a passing 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 valves of the heart, the cardio-vascular system is exposed to the greatest damage.

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

  1. By the nature of the flow:
  • Acute bacterial endocarditis. Its duration is 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. It develops due to insufficient treatment.
  • Chronic (protracted) stage. Runs for years.
  1. Depending on the pathogenesis:
  • Primary. Healthy heart valves become infected.
  • Secondary. It takes its development from other heart diseases.
  1. According to the degree of damage:
  • Passes with limited damage to the cusps of the heart valves.
  • Extends beyond the heart valves.

The reasons

Provoke the appearance of septic endocarditis bacteria. 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, into the bloodstream, the heart and begin to multiply there.

People can easily get sick:

  • Suffering from infections such as tonsillitis, sinusitis and others.
  • The organism that is affected: staphylococcus, streptococcus, enterococcus.
  • Having undergone surgery.

At risk are patients with:

  • scars on the valves of the heart;
  • with disease;
  • artificial heart valve;
  • sagging of the valve leaflets;
  • heart anomalies.

Predisposed to the disease:

  • Patients who use invasive research methods (with penetration into the body).
  • Intravenous drug addicts.
  • People who have a weakened immune system. The reason for this is the intake of a large number of antibiotics or an unfavorable environmental situation.
  • Patients who have undergone surgery with exposure to the mucous membrane of the respiratory and urinary tract, gastrointestinal tract, in the presence of infection of these organs.

Symptoms of septic endocarditis

What affects the symptoms of the disease?

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

The disease progresses differently for everyone. It can start abruptly and be pronounced, or, on the contrary, develop gradually, the signs are mild. The second case is the most dangerous. A person does not turn to a specialist in time.

  1. Acute endocarditis is accompanied by the following symptoms:
  • Sudden rise in temperature.
  • The number of strokes of the heart muscle increases, which leads to rapid damage to the valve.
  • Emboli can come off, they are transferred with 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.
  • The walls of the arteries become weak and can rupture, leading to death if the vessel is located in the brain or near the heart.
  1. Endocarditis of the subacute stage, which can last several months, has the following symptoms:

The most pronounced common signs of septic endocarditis are:

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

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

Diagnostics

  • The first stage - it turns out whether there were surgical interventions and whether there are chronic infections.
  • The second stage is the use of laboratory and clinical studies.

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 the presence of changes in the blood protein, a change in the 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 used diagnostics is 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 he will be monitored every minute and receive high-quality treatment.

  1. Medication (therapeutic).

Its essence lies in taking antibiotics. They are administered through a drip. Thanks to them, harmful bacteria are destroyed.
Before prescribing the drug, it turns out which pathogen is the cause of the disease. An 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, the antibiotic is prescribed immediately, based on empirical therapy. Such an action is carried out until the results of the analysis are received, and then it is adjusted.
The maximum dose of the drug is usually prescribed, the duration of their use is about eight weeks.

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

  1. Immunocorrection

In order to neutralize the toxins moving with the bloodstream, passive immunization using antitoxic sera is used. They are administered daily for five days.

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

It is used if medical treatment has not yielded 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 when 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.
  • Restoration of heart valves. This goal is achieved by the placement of implants or if the patient's valves can be reconstructed.

Treatment using traditional medicine

In bacterial endocarditis, the same plants can be used as in 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 the muscles. The strongest of them is rhododendron, it, like foxglove, does not affect blood pressure. But at the same time, it should not be used by people with problems of the urinary system and tissue necrosis.

Digitalis and rhododendron should not be given to people with bradycardia and atrial fibrillation. Since they constantly accumulate in the body and eventually lead to toxicosis, they are recommended to be used 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 the treatment of disease, but its actions are not so pronounced. Plus - it has no contraindications, and it can be used for quite a long time.

Remedies 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 strenuous exercise.
  • Strengthen immunity.
  • Immediately consult a doctor 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.
  • In the presence of chronic heart disease and artificial valves, it is necessary to be observed by a specialist. People in this category are at risk.
  • Antibiotics are prescribed for people at risk after surgical medical intervention, where there is a violation of body tissues.
  • Proper nutrition.
  • Rejection of bad habits.

Complications

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

  • In the lungs: edema, hypertension, abscess, infarction.
  • 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, aneurysms and thrombosis.

Forecast

Previously, septic endocarditis could not be cured. After three years of the course of the disease, the patient died. Everything has changed these days. The use of antibiotics helps to 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 be started and the prognosis will be only positive. But it is better to prevent the disease than to treat it later.

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

Acute septic endocarditis (endocarditis septica acuta) is less than 1% of all endocarditis [V. Jonas]. Usually this endocarditis is a manifestation of sepsis after childbirth, abortion, wound infection, thrombophlebitis, otitis media, osteomyelitis, meningitis, pneumonia, lung 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 has remained untreated or healed by 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 fever (2° to 39-40°) of the wrong type with chills and profuse sweat during the fall of temperature. Fever is accompanied by a sharp general weakness, headache, loss of appetite, often shortness of breath, pain in the heart. The patient is pale, small hemorrhages are frequent on the skin. The pulse is frequent, small, often arrhythmic. Myocarditis is a constant companion of endocarditis, so the size of the heart is always increased, the apex beat is shifted to the left. When listening, significant variability of sound phenomena is detected: heart sounds, especially the first one, weaken, sometimes a gallop rhythm is noted, noises appear - systolic at the apex and in the region of the tricuspid valve, systolic and diastolic on 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 polyposis overlays on the valves. Sometimes 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 severe neutrophilia and a shift of the leukocyte formula to the left; eosinopenia; large epithelioid cells (typical and atypical histiocytes) may be found. A tendency to embolism is expressed, repeated embolisms are often observed in the skin with the formation of petechial spots, in the brain, the central retinal artery, spleen, kidneys, sometimes in large arteries of the extremities, etc. Symptoms of phlebitis, septic arteritis can 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 septic-pyemic. At the first onset of the disease is relatively gradual, there are vomiting, diarrhea, abdominal pain, darkening of consciousness, fever with large fluctuations, chills. The septic-pyemic form is distinguished by a more sudden onset, high fever, numerous metastatic abscesses, acute glomerulonephritis, skin embolism, 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 the general condition, an increase in signs of heart damage, the manifestation of new symptoms due to embolism of various organs or intoxication. Death occurs from a complication (embolism in the brain, 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 beginning of the disease is difficult. A positive blood culture confirms the presence of sepsis. The main diagnostic value are changing loud heart murmurs and the appearance of signs of embolism. Endocarditis is often overlooked in older people, where it is accompanied by extreme weakness and usually ends in death in 4-5 days.

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

Acute septic endocarditis

It happens infrequently in childhood. According to the anatomical characteristic, it is ulcerative. Heart symptoms usually fade into the background compared to other symptoms of generalized sepsis. The clinic of the disease in childhood is little studied. The development of embolic processes will undoubtedly speak in favor of heart damage. Its etiology is different. The forecast is heavy. Treatment is primarily to treat the septic condition; cardiac symptoms usually require symptomatic treatment.

More common in children chronic septic endocarditis. According to the clinical picture, chronic septic endocarditis has much in common with rheumatic endocarditis: periodic longer periods of fever of an irregular relapsing or intermittent type, the same connection with chronic tonsillitis and tonsillitis. skin manifestations in the form of polymorphic erythema. hives. annular Leiner's erythema, polyarthritic manifestations without reaction from the regional glands in relation 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. In contrast to typical rheumatism, there is an enlargement of the spleen, often the liver, chronic focal glomerulonephritis, and especially a tendency to embolism. For this disease, the presence of chills is considered characteristic. However, this symptom in childhood is not entirely reliable: some rheumatic patients without other signs of a septic process complain of chills and vice versa - sometimes there are no chills in chronic sepsis. The same can be said for pots.

It is also generally accepted that with chronic sepsis, 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 chronic septic 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 another. The final diagnosis can be obtained by bacteriological examination during blood culture. Often, but not always, it is possible to sow a green streptococcus. A negative culture result does not rule out a septic process, even with repeated cultures. Especially often negative results are obtained in connection with antibiotics used for treatment - penicillin, streptomycin, etc.

Nevertheless, the clinical symptom complex is quite characteristic. Severe weakness, intermittent fever, noise, rapidly progressive anemia, skin manifestations, enlargement and sometimes tenderness of the spleen, hemorrhagic nephritis or prolonged hematuria, chills, sweats in a child who has previously had rheumatism make the diagnosis of chronic sepsis very likely.

Treatment of septic endocarditis should 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 at a dose of at least 500,000 - 1,000,000 IU per day and for at least 2-4 weeks; some authors require continuous treatment for 2 months.

Penicillin is well combined with streptomycin, especially in cases where the microbe is resistant to penicillin. Biomycin and synthomycin 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 as well.

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

Acute septic endocarditis

Acute septic endocarditis- This is a severe septic disease that develops with complications of various bacterial infections, with a secondary lesion of the endocardium.

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

The causative agents of the considered endocarditis are highly virulent pyogenic bacteria - hemolytic streptococcus, Staphylococcus aureus, pneumococcus, and also Escherichia coli. Recently, cases of acute septic endocarditis with actinomycosis and fungal sepsis have been described. Primary foci can be easily detected with their external localization, for example, panaritiums, carbuncles, wounds, or with appropriate anamnestic data (past abortion, gonorrhea). There are frequent cases when the primary focus cannot be recognized.

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

As in subacute septic endocarditis, altered immunobiological reactivity plays a significant role in the development of the disease.

Pathological anatomy The valves are pronounced, loose thrombotic masses are deposited on the bottom and along the edges of the ulcers, which are not associated with the underlying tissues and contain 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 heart attacks. or loss of function of these organs.

The septic process in the endocardium leads to rupture of the tendon filaments, destruction of the valve leaflets and their perforation. Insufficiency of aortic valves is more often formed, less often - mitral; with pneumonia. puerperal sepsis is the defeat of the tricuspid valve.

Clinical picture of acute septic endocarditis

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

Characterized by septic embolism in the spleen, accompanied by severe pain in the left hypochondrium, sometimes the friction noise of the capsule (perisplenitis), as well as in the kidney, causing sharp pain in the lumbar region, followed by hematuria. There are multiple embolic petechiae in the skin. Sometimes there is a development of purulent pleurisy, pericarditis. joint damage occurs. In the peripheral blood, neutrophilic leukocytosis with a stab shift, progressive anemia, and accelerated ESR are detected. With blood cultures, sometimes multiple, it is possible to sow the causative agent of the disease (green streptococcus, less often pneumococcus).

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

Prevention and treatment

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

The elimination of the main septic process is achieved by the use of massive doses of antibiotics in combination with sulfonamides, with the mandatory determination of the sensitivity of the microbial flora to them. Doses and preparations are the same as in the treatment of subacute septic endocarditis.

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

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