Comprehensive diagnostics
Establishing an accurate diagnosis relies on Duke criteria. For verification, it is necessary to confirm the major criteria (documented bacteremia plus visualization of endocardial involvement) combined with multiple minor clinical and laboratory signs.
Laboratory markers:
- Blood: Acceleration of ESR up to 70–80 mm/h, anemia, thrombocytopenia. White blood count reacts with neutrophilic leukocytosis (in acute processes) or leukopenia (in subacute processes).
- Immunity and biochemistry: C-reactive protein (CRP) increases, rheumatoid factor (RF) and circulating immune complexes (CIC) appear. Dysproteinemia with an increase in the γ-globulin fraction is characteristic.
- Urine: Hematuria, proteinuria, and leukocyturia indicate kidney damage (immune complex nephritis or the result of embolism).
Instrumental visualization: EchoCG is the leading method, with transesophageal access (TOE) providing the best visualization. A direct sign of the disease is the presence of vegetations (most commonly on the mitral or aortic valve). Indirect signs include destruction of the valvular apparatus (chordal rupture, leaflet tears) and hemodynamic shifts leading to cavity dilation and a drop in ejection fraction.
Principles of therapy
Patients are subject to mandatory hospitalization with strict bed rest until the acute phase subsides.
Antibiotic therapy: Ideally, antibiotics are selected based on blood culture sensitivity results. If the pathogen is unknown, high doses are prescribed empirically:
- In acute course: combination of three drugs (Oxacillin + Ampicillin + Gentamicin).
- In subacute course: combination of two drugs (e.g., Ampicillin + Gentamicin).
Surgical treatment: If conservative tactics fail, heart failure worsens, or thromboembolic events recur, excision of the destroyed valve with replacement is indicated. Surgery saves lives, but the implanted prosthesis itself becomes a risk factor for recurrent infection.
Criteria for successful discharge from the hospital include persistent normalization of temperature, clean lab tests, sterile blood cultures, and complete resolution of symptoms.
Infective endocarditis in injection drug users
This form is classified into a separate category due to pathogenesis features: the pathogen massively enters the bloodstream directly during intravenous injections. Young men are predominantly affected (under 30 years old, 3:1 ratio).
Course features:
- Pathogen: Staphylococcus aureus dominates (60%), with streptococci, enterococci (20%), and gram-negative flora (10%) occurring less frequently.
- Localization: The infection hits the right side of the heart — the tricuspid valve is affected. Symptoms of its regurgitation appear rather late.
- Complications: Since emboli from the right ventricle travel into the pulmonary artery, almost 100% of patients develop septic pneumonia. Local thrombophlebitis (in the femoral or subclavian veins) and severe kidney damage are also characteristic.
Prevention in risk groups
Patients with congenital or rheumatic heart disease, as well as mitral valve prolapse, need special protection.
Transient bacteremia occurring during dental (tooth extraction) or urological procedures can trigger the development of endocarditis. The main method of prevention is premedication: administration of an adequate dose of an antibiotic 4 hours before the planned surgical procedure.
Briefly: answers to topical questions
What major Duke criteria are used to diagnose infective endocarditis?
The following major Duke criteria are used to diagnose infective endocarditis.
- Documented bacteremia — isolation of the pathogen from the blood. Officially recognized typical pathogens include, for example, Enterococcus faecalis.
- EchoCG signs of endocardial involvement — instrumental detection of vegetations on heart valves.
What are the absolute indications for surgical treatment of infective endocarditis?
The following indications exist for surgical treatment of infective endocarditis.
- Perforation or rupture of valve leaflets — upon the development of acute heart failure.
- Arterial thromboembolism — after the first episode due to a high risk of recurrences.
- Myocardial and valvular annular abscesses — conservative treatment is hopeless in these cases.
- Fungal endocarditis — inevitably leads to a fatal outcome without surgery.
- Prosthetic valve infective endocarditis — upon infection with particularly virulent flora.
- Inefficiency of etiotropic therapy — persistence of fever and progressive destruction for 3–4 weeks.
Which microorganisms are most frequently the causative agents of infective endocarditis in patients who are not injection drug users?
The main causative agents of infective endocarditis are the following microorganisms.
- Viridans streptococci (Streptococcus viridans) — the most frequent causative agent, causing over 50% of cases and typical for secondary endocarditis.
- Staphylococci (Staphylococcus aureus, Staphylococcus epidermidis) — account for 10–20% of cases, more frequently causing primary endocarditis.
Rare causative agents can include Enterococcus, gram-negative rods (Salmonella, Pseudomonas aeruginosa, Klebsiella), as well as fungi (Candida, Histoplasma capsulatum).
Duke criteria are based on two pillars (major criteria): Bacteremia (blood culture) + Vegetations (EchoCG).
Class and exam questions
Why is blood for sterility mandatory to draw multiple times in endocarditis?
Multiple blood cultures help avoid false-positive results due to accidental contamination with skin flora and increase the chance of "catching" the pathogen. The diagnosis is verified with at least two positive results.
What complication is most frequently encountered in injection drug users with endocarditis?
Septic pneumonia. Infection from the affected tricuspid valve (from the right side of the heart) is carried by the bloodstream directly into the pulmonary artery.
Can endocarditis be completely cured with antibiotics alone?
Yes, if therapy is selected correctly and initiated before irreversible valve destruction occurs. However, with chordal rupture, leaflet perforation, or drug refractoriness, surgical replacement is required.
What else to study on this topic
- Minor Duke criteria: detailed analysis of clinical manifestations
- Mechanisms of immune complex nephritis development in endocarditis
- Specifics of transesophageal EchoCG (TOE) in evaluating vegetations
- Mechanisms of hemodynamic disorders during leaflet perforation
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