Infectious endocarditis

Infectious endocarditis (IE) is an inflammation of the endocardium characterized by the presence of infectious vegetations ( thrombus with microorganisms) on the valve and / or wall endocardium.

Etiology
IE most often occurs on a primarily damaged valve or in immunocompromised patients. The causative agents may be:

Predispositions are bicuspid aortic valve, pulmonary stenosis, open arterial ductus, ventricular septal defect (separate / part of Fallot's tetralogy).
 * bacteria (viridizing streptococci, coagulase-negative staphylococci, Staphylococcus aureus, enterococci, gram-negative bacteria…, HACEK group bacteria - Haemophilus, Actiobacillus, Cardiobacterium, Eikenella, Kingella);
 * fungi (Candida, Aspergillus);
 * rarely chlamydia.

The condition for the development of infectious endocarditis is: First, an endothelial defect develops, which is then colonized by bacteria and covered with platelets and fibrin fibers. Infectious vegetation is created by the multiplication of bacteria.
 * receptive terrain,
 * the presence of bacteria in the blood (bacteremia), the source of which may be:
 * local purulent infection,
 * instrumental examination,
 * operation,
 * implantation of an artificial heart valve,
 * drug addiction with i.v. drug application, etc.

Types of infective endocarditis
Clinically, infectious endocarditis is divided according to pathogenesis; to into infectious endocarditis :


 * on native valves - most often in mitral valve prolapse and degenerative aortic or mitral valve defects, less often the cause is rheumatic fever and congenital heart defects,
 * in intravenous drug users - the right valves (mainly tricuspid) are affected, similarly IE can occur in the case of poorly treated central venous catheters,
 * in valve replacements - similarly in pacemaker electrodes.

Dividing by the course of infectious endocarditis
According to the course, infectious endocarditis is divided into two types:

Note: The division into acute and subacute is no longer used. The newer classifications of infectious endocarditis reflects the nature of the disease better. The newer division according to pathogenesis is as follows: Infectious endocarditis on native valves, infectious endocarditis in iv addicts, infectious endocarditis in valve replacements .
 * 1) subacute - primarily affects pre-degeneratively changed (after rheumatism) or malformed (bicuspid aortalis) valve or wall of the endocardium (atrial septal defect, tetralogy of Fallot, etc.), caused by less virulent strains (in particular streptococci, Streptococcus viridans, Streptococcus bovis, Enterococcus faecalis),
 * 2) acute - affects pathologically unchanged valves, caused by highly virulent strains (mainly staphylococci).

According to morphology and course we distinguish:

1. acute malignant endocarditis (ulcerosa);

2. endocarditis lenta maligna (polyposis).

Endocarditis maligna acuta (ulcerosa)
Vegetation - irregularly lobed, reddish, yellowish to greenish, soft consistency, found mainly on the aortic (free edge or ventricular surface) and mitral (atrial surface) valve, rarely on the pulmonary, exceptionally tricuspid - in the right heart, especially in drug addicts and with a long-term catheter inserted into the right heart. It forms mainly in the place of large pressure gradients, either just before the narrowing or directly in the place where the pathological blood flow falls.
 * Infectious vegetation consists of a thrombus of platelets and fibrin with bacteria, under the thrombus is necrotic tissue with leukocyte infiltration, purulent coccal necrotic tissue, ulceration occurs.
 * Infectious vegetation, necrosis and ulceration are visible with macroscope.Streptococcus viridans PHIL 2897 lores.jpg

Necrosis and ulceration - they can be on the periphery of the valve (they form a "bite" of the free edge) or in its center (valve aneurysm to its perforation), on the wall endocardium we talk about ulcus cordis acutum, located on the tendons leading to their rupture.

Healing (eg in antibiotic therapy) occurs by organisation of the the vegetation of granulation tissue, and the fibrous growth remains on the valve, often calcified.

Endocarditis lenta maligna (polyposis)

 * Infectious vegetation, as in acute infectious endocarditis, consists of thrombi from platelets and fibrin with bacteria, below which is necrosis with mild leukocyte infiltration - there is no purulent cocculation.
 * Macroscopically, ulcerations are less marked, vegetation may have a polyposis shape, but there may be valve aneurysms and tendon ruptures, the mitral valve is more often affected than the aortic valve.

Complications

 * 1) Cardiac (resulting in heart failure):
 * 2) valve damage - insufficiency (ulceration or perforation) or stenosis (bulky vegetation),
 * 3) myocardial involvement -by self- agent (transition of infection from vegetation or embolization of septic thrombi to coronary arteries - septic abscessing myocarditis ) or by its toxins.
 * 4) Extracardiac (resulting in mainly brain (neurological symptoms) and kidney damage (renal insufficiency)):
 * 5) embolization of parts of vegetation - leads to septic pyemia (establishment of metastatic abscesses in large (brain, spleen, kidney…) or small (lungs) circulation), in the case of bland emboli, infarcts occur (brain, kidneys, spleen, limbs, Osler's nodes in the skin),
 * 6) formation of immunocomplexes - their deposition into the walls of blood vessels, where they cause fibrinoid necrosis (vasculitis, glomerulonephritis, etc.).

Screening and diagnosis
We use Durack's IE criteria to clarify the diagnosis.
 * Anamnesis.
 * Objective finding.
 * Laboratory examination.
 * Repeated blood culture.
 * Echocardiography, (Transesophageal echocardiography, TEE ).

Main criteria :

 * positive blood cultures - at least 2;
 * echocardiographic visualization of vegetation or abscess.

Secondary criteria :

 * predisposition (valve or short-circuit defects) or i.v. drug addiction;
 * fevers above 38.0 ° C;
 * vascular symptoms (embolization, hemorrhage, splinter hemorrhage under the nails);
 * immunological symptoms (glomerulonephritis, Osler's nodes, positive rheumatoid factor);
 * one positive blood culture, or serological evidence of microorganisms.

Proven IE must meet 2 main, or 1 main and 3 secondary, or 5 secondary criteria.

Possible IE : 1 main and one secondary, or 3 secondary criteria.

Pharmacological
It is difficult fot ATBs to penetrate into vegetation (ATB therapy should be consulted with a microbiologist and adapted to the patient's clinical condition). Treatment usually lasts 4-6 weeks. Antibiotic therapy is terminated in patients who are afebrile for at least one week, have normal CRP levels, no new signs of embolization or new vegetation appear, and no foci are known in the body that could cause bacteremia.

CAVE !!'''Accurate identification of the microbial agent is more important than in other common infections. When IE is suspected, it is a big mistake to start ATB treatment blindly, unless it is a very critical condition. If IE is suspected after the start of treatment, it is recommended to stop ATB treatment and recruit additional blood cultures. ATB treatment must be targeted!'''

Cardiac
As medical prophylaxis are used amoxicillin + gentamicin (erythromycin).

Despite adequate treatment, mortality reaches tens of percent. It is always desirable to be hospitalized in a specialized workplace.