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 secondary (developing
native valves) 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 Tricuspid IE due to
Staph. aureus Candida
in drug addicted person
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 left-
sided;
• 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