Infective Endocarditis

INFECTIVE ENDOCARDITIS

Infective endocarditis is a special form of sepsis which damages the endocardial surface of the heart including the heart valves (native, damaged or prosthetic), the rings of connective tissue surrounding the valves, as well as the inner lining of the heart chambers or a congenital anomalies

Classification of IE primary (affecting native valves)

secondary (developing on damaged valves)

Classification of IE Aetiology : •Streptococci (viridans, etc.) •Staphylococci (aureus, epidermidis) •Gram-negative bacteria (HACEK group: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella ) •Yeasts and fungi (Candida, Aspergillus) •Other agents •Negative blood culture

Current and clinical forms: •Acute infective endocarditis (AIE) •Subacute infective endocarditis (SIE) •Prosthetic valvular endocarditis (PVE) •Right-sided endocarditis •Nosocomial IE (NIE)

Aetiology of IE

Cardiovasc Rev Rep 24(7):375-380, 2003

Predisposal factors of IE •congenital bicuspid aortic valves, •mitral and aortic valves damaged by rheumatic fever, •calcific mitral and aortic valves in the elderly with arteriosclerosis, •mitral valve prolapse; •mechanical and bioprosthetic heart valves, •Marfan's syndrome, •idiopathic hypertrophic subaortic stenosis, •coarctation of the aorta, •arteriovenous shunt, •ventricular septal defect

Sources of bactetemia •Stomatologic procedures, cuts in an oral cavity •Operation on a nasopharynx •Diagnostic and surgical manipulations on colon, urinary tract, genitals . •Purulent process of any localization •Intravenous injections of unsterile solutions

Pathogenetic mechanisms of IE •Endocardial damages and sterile fibrin-platelet vegetation formation •Bacteremia and deposition of agents on the endothelium and sterile thrombi •Establishing of vegetations composed of organisms, fibrin and platelets •Breaking the vegetations away as emboli •cusp perforation or disruption of chordae, formation of valvular insufficiency • Extracardiac manifestations due to emboli or immune complex deposition

Location of microbe vegetations on valves of the heart

Vegetations on mitral leafletes

Destruction and rupture of mitral leaflet in the region of vegitation

Vegetations and destruction of aortal cups

Tricuspid IE due to Staph. aureus in drug addicted person

Tricuspid IE due to Candida

Prosthetic IE in aortal position

Principal clinical syndromes of IE •Septic condition •Damage of heart valves •Heart failure •Hemorrhagic syndrome •Thrombo-embolic syndrome •Immune damages (nephritis, vasculitis, sinovitis)

Symptoms of IE

Thromboembolic complications of IE

Thromboembolism of a.renalis in IE

CT data on thromboembolism of a.renalis in IE (wedge-shaped necrosis)

Two-sided thromboembolism of cerebral arteriae (MRT data)

Clinical symptoms of subacute IE • • • • •

symptoms usually begin insidiously; SIE is usually caused by streptococci; SIE typically affects abnormal valves; thrombo-embolic syndrome is characteristic; peripheral lesions are observed in only approximately 20% of patients; • manifestations of central nervous system involvement (in about 35% of patients)

Characteristic skin symptoms of IE

Clinical symptoms of acute IE • AIE can develop on normal valves and its course may be more rapid; • source of infection in AIE is usually obvious; • rapid valvular destruction, valve ring abscesses; • numerous petechiae and prominent embolic phenomena; • severe haemorrhagic syndrome and septic emboli forming abscesses in the inner organs

Specific manifestations of right-sided IE (RSIE) • RSIE involvs the tricuspid valve and less often the pulmonary valve and artery; • RSIE may result from intravenous use of illicit drugs or from central vascular lines; • cardiac murmurs are often absent; • prognosis of RSIE is more favourable than in leftsided; • drug-abusers often develop the recurrent RCIE with fatal outcome

Laboratory findings in IE •documentation of a continuous bacteremia •Leukocytosis, neutrophilia; •Monocytosis; •normocytic-normochromic anemia; •elevated ESR; •increased immunoglobulins, circulating immune complexes; •increased complement; •Positive reumatoid factor; •Proteinuria, microhematuria

EchoCG in IE: vegetations on mitral leaflets

EchoCG in IE: vegetations on aortal cups

EchoCG in IE: vegetations on tricuspid leaflets

Transesophageal EchoCG in IE: small vegetations on aortic cups

Diagnostic criteria of IE Major blood culture criteria: • Two blood cultures positive for organisms typically found in patients with IE (ie, S viridans, Streptococcus bovis, a HACEK group organism, S aureus, or enterococci in the absence of a primary focus); • Blood cultures persistently positive for one of the above organisms from cultures drawn more than 12 hours apart; • Three or more separate blood cultures drawn at least 1 hour apart

Diagnostic criteria of IE Major echocardiographic criteria: • Echocardiogram positive for IE, documented by an oscillating intracardiac mass on a valve or on supporting structures, in the path of regurgitant jets, or on implanted material in the absence of an alternative anatomical explanation; • Myocardial abscess; • Development of partial dehiscence of a prosthetic valve; • New-onset valvular regurgitation.

Diagnostic criteria of IE Minor criteria: • Predisposing heart condition or intravenous drug use; • Fever of 38°C or higher; • Vascular phenomenon, including major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhage, or Janeway lesions; • Immunological phenomenon such as glomerulonephritis, Osler nodes, Roth spots, and rheumatoid factor; • Positive blood culture results not meeting major criteria or serologic evidence of active infection with an organism consistent with IE (eg, Brucella, Coxiella, Legionella); • Echocardiogram results consistent with IE but not meeting major echocardiographic criteria.

Principles of IE treatment •antibiotics in high (bactericide) dozes during not less than 6 weeks; •until the reception of the bacteriological results the empirical treatment by two antibiotics (penicillin or cefalosporin + aminoglycoside) Oxacillini 1,5 x 6 times per day i/m or i/v Gentamycini 0,08 x 3 times per day i/m or i/v •at negative bacteriological results vankomicin + gentamycin during 6 weeks

Criteria of stopping the antibiotic therapy of IE • normalization of a body temperature; • normalization of laboratory parameters; • negative results of control blood bacteriological analysis; • disappearance of clinical displays of disease activity

Indications to surgical treatment: •Acute valvular insufficiency and heart failure; •Resistance to therapy during 2 weeks; •Fungal IE; •Abscesses of myocardium and valvular rings; •Prosthetic valve IE; •Recurring thromboembolisms