Internal illnesses. Infective endocarditis (lecture notes)

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Internal illnesses. Infective endocarditis (lecture notes)

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LECTURE № 5. Infective endocarditis

It is a peculiar form of sepsis, characterized by the localization of the pathogen on the heart valves or parietal endocardium, followed by damage to many organs and systems.

Etiology. The causative agents of the disease include microbial flora: cocci (Staphylococcus aureus, viridescent streptococcus, S. Epidermidis, enterococci), gram-negative bacteria (E. coli, Proteus, Pseudomonas aeruginosa, Klebsiella), fungi such as Candida, rickettsia, viruses, Brucella.

Pathogenesis. Of great importance in the development of the disease are risk factors that reduce the immunobiological resistance of the body. These include: acquired and congenital heart defects (ventricular septal defect, open aortic disease), minor surgical and dental operations, parenteral drug administration, heart valve replacement, urinary tract infection, prolonged use of catheters, abortions, program hemodialysis.

Damage to the valvular apparatus of the heart occurs with malformations of the heart muscle, microtrauma, impaired hemodynamics and microcirculation. Interstitial valvulitis and thrombotic vegetations develop. The reactivity of the endocardium changes, the pathogenic flora is activated. Thromboembolic complications (heart attacks and abscesses of the myocardium, brain, lungs, and other organs), bacterial damage to the valves (endocarditis) with bacteremia, and focal nephritis are formed. Immune generalization of the process is accompanied by the development of immunocomplex nephritis, vasculitis, myocarditis, hepatitis, splenomegaly. At the final stage, dystrophic changes in internal organs are formed: the heart, blood vessels, kidneys, liver, and other organs (dystrophic phase).

Pathological anatomy. With this pathology, the aortic valve is most often affected, less often the mitral valve. On the affected valves, tendon chords, sometimes parietal endocardium, ulcerative defects are formed, covered with massive polyp-like thrombotic deposits. There may be perforations or aneurysms of the leaflets. Inflammatory infiltrates consist of lymphoid cells and histiocytes. In the future, wrinkling of the maturing granulation tissue occurs, deformation of the valve leaflets.

Classification. When making a diagnosis, the following points should be considered:

1) clinical and morphological form: primary (on unchanged valves) and secondary (against the background of rheumatic, syphilitic, atherosclerotic, lupus, traumatic defects, arteriovenous aneurysms, prosthetic valves);

2) the nature of the course (acute, subacute, chronic (recurrent));

3) the degree of activity of the process: I degree - minimal (ESR up to 20 mm/h), II degree - moderate (ESR 20-40 mm/h), III degree - high (ESR more than 40 mm/h).

Clinic. The main manifestations of the disease include:

fever (from subfebrile to high), which persists for a long time, is accompanied by chills, profuse sweating. Muscle weakness, pain in muscles and joints appear, appetite decreases.

At the onset of the disease, chills, profuse cold sweats, high fever, severe intoxication may occur, which is typical for primary endocarditis. The onset of the disease may be imperceptible with the development of malaise, weakness, weight loss, subfebrile condition.

The skin is pale with an icteric tint, petechial rashes appear, especially on the skin of the lower eyelid (Lukin-Libman symptom), painful nodules on the palms and soles (Osler's nodules). The fingers are like drumsticks, the nails are like watch glasses.

Valve damage begins with the appearance of a systolic murmur over the aorta due to narrowing of the aortic orifice. This occurs a few weeks after the onset of the disease. Less often, the presence of systolic murmur over the apex of the heart can be determined; later, with the development of aortic insufficiency, diastolic murmur appears over the aorta. There are: tachycardia, muffled heart sounds, rhythm and conduction disturbances, which is typical for developing myocarditis. From the side of the vessels, the development of thrombosis, aneurysms, vasculitis, developing in the internal organs, can be observed. Diffuse glomerulonephritis may develop in the kidneys.

The criteria for remission of the disease are repeated negative blood cultures, the disappearance of clinical manifestations, the disappearance of vegetations with repeated echocardiography.

Additional diagnostic study. A general blood test is performed, in which anemia, leukopenia, thrombocytopenia, and an increase in ESR can be detected. A biochemical blood test can determine the presence of dysproteinemia, hypergammaglobulinemia, and a positive formol test.

Immunological study determines the inhibition of the non-specific link of the immune response, the activation of its humoral link (increased IgA, IgM, CEC).

Bacteriological examination of blood is carried out with three blood cultures. In this case, the pathogen must be detected in two crops.

An ECG study reveals a rhythm and conduction disturbance, a decrease in the voltage of the teeth. An echocardiographic study reveals the presence of vegetations on the cusps of the affected valve, signs of a formed heart disease in the form of insufficiency, ruptures of the chords, perforation of the cusps can be established.

Complications. Complications include pulmonary infarction, pulmonary edema, myocardial infarction, heart failure, kidney infarction, cerebrovascular accidents, splenic infarction, and retinal embolism.

Differential diagnostics. Should be carried out with rheumatic heart disease, acute and subacute SLE, brucellosis, patent ductus arteriosus, aortic lesions of syphilitic or atherosclerotic origin, myeloma, visceral form of lymphogranulomatosis, some tumors, serum sickness.

Treatment. Treatment should be as early as possible, it must be carried out in a hospital. It is necessary to introduce an anti-staphylococcal penicillinase-resistant antibiotic oxacillin, 2 g every 4 hours (12 g / day). After clarifying the type of pathogen, further selection of antibiotics is carried out. Antistaphylococcal plasma is administered intravenously (5 infusions per course).

The duration of the first course of antibiotic therapy is at least 4-6 weeks; with a late start of treatment - up to 8-10 weeks. Antibiotics should be changed every 2-4 weeks, their administration can be both intravenous and intramuscular.

After discharge from the hospital, further prophylactic antibacterial courses are carried out for 2-3 weeks, then after 1, 3 and 6 months with an antibacterial drug that produced the greatest effect.

With pronounced immunological manifestations, the following are used: prednisolone (40-60 mg / day), non-steroidal anti-inflammatory drugs.

In the dystrophic phase, cardiac glycosides, potassium preparations, diuretics are prescribed, for anemia - iron preparations in combination with vitamins of groups B and C.

Perhaps a blood transfusion or red blood cells.

Indications for surgical treatment are: progressive heart failure, lack of effect from conservative therapy, repeated embolism, fungal endocarditis.

Flow. In the acute form, the course can be rapidly progressive, in the subacute form - protracted, in the chronic form - recurrent.

Forecast. In the acute form, the prognosis is unfavorable, life expectancy is not more than 2 months. In subacute and chronic forms, the prognosis is relatively favorable, up to 60% of patients are cured.

Prevention. It consists in preventing the development of bacterial infections, active treatment of acute infections, rehabilitation of foci of chronic infection, hardening of the body, and secondary prevention in people who have had infective endocarditis.

Author: Myshkina A.A.

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