This document provides an overview of infective endocarditis. It defines infective endocarditis as a cardiac valve infection caused by platelet-fibrin vegetations containing bacteria and white blood cells. Risk factors include pre-existing heart conditions and procedures that cause bacteremia. Symptoms include fever, heart murmurs, heart failure, embolic events, and immunological findings. Diagnosis is based on modified Duke criteria using blood cultures, echocardiography, and clinical features. Treatment involves antibiotics targeted to the identified organism with consideration of surgery for complications or refractory infection. Prognosis depends on patient and infection factors with higher mortality for prosthetic valves and complications.

1. CVS lectures :
Infective
Endocarditis
Professor Ali A. Hadi Al-Saady
University of Al-Ameed / College of Medicine
Department of Medicine

2. Definition of Infective
Endocarditis ( IE )
• infection of cardiac endothelium, most
commonly the valves
• classifications: acute vs. subacute, native
valve vs. prosthetic valve, right sided vs. left
sided
• leaflet vegetations are made of platelet-
fibrin thrombi, WBCs, and bacteria.
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3. Risk Factors and Etiology
• Predisposing conditions:
high risk: prosthetic cardiac valve, previous IE, congenital heart
disease (unrepaired, repaired within 6 mo, repaired with
defects), cardiac transplant with valve disease (surgically
constructed systemic-to pulmonary shunts or conduits).
moderate risk: other congenital cardiac defects, acquired
valvular dysfunction, hypertrophic cardiomyopathy.
low/no risk: secundum ASD or surgically repaired ASD < VSD,
PDA, MV prolapse, ischemic heart disease, previous CABG.
Opportunity for bacteremia: IVDU, indwelling venous catheter,
hemodialysis, poor dentition, DM, HIV.
• frequency of valve involvement : MV >> AV > TV > PV
but in 50% of IVDU-related IE the tricuspid valve is involved
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5. Clinical Features
• systemic
fever (80-90%), chills, weakness, rigors, night
sweats, weight loss, anorexia
• cardiac
dyspnea, chest pain, clubbing (subacute)
regurgitant murmur (new onset or increased
intensity)
signs of CHF (secondary to acute MR, AR)
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6. Clinical Features
• embolic/vascular
petechiae over legs, splinter hemorrhages (linear, reddish-
brown lesion within nail bed)
Janeway lesions (painless, 5 mm, erythematous, hemorrhagic
pustular lesions on soles/palms)
focal neurological signs (CNS emboli), headache (mycotic
aneurysm)
splenomegaly (subacute)
microscopic hematuria, flank pain (renal emboli) ± active
sediment
• immune complex
Osler’s nodes (painful, raised, red/brown, 3-15 mm on digits)
glomerulonephritis, arthritis , Roth’s spots (retinal hemorrhage
with pale centre)
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8. Roth`s spots
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9. DiagnosisofIE:ModiedDukeCriteria
Definitivediagnosisif:2major,OR1major+3minor,OR5minor
Possiblediagnosisif:1major+1minor,OR3minor
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10. Investigations
• serial blood cultures: 3 sets (each containing one aerobic
and one anaerobic sample) collected from different sites
>1 h apart.
persistent bacteremia is the hallmark of endovascular
infection (such as IE).
• repeat blood cultures (at least 2 sets) after 48-72 h of
appropriate antibiotics to confirm clearance.
• blood work: CBC and differential (normochromic,
normocytic anemia), ESR (increased), RF (+), urea/Cr
• urinalysis (proteinuria, hematuria, red cell casts) and
urine C&S. 10

11. Investigations
ECG: prolonged PR interval may indicate perivalvular abscess
• echo findings: vegetations, regurgitation, abscess.
TTE (poor sensitivity) inadequate in 20% (obesity, COPD, chest
wall deformities).
TEE indicated if TTE is non-diagnostic in patients with at least
possible endocarditis or if suspect prosthetic valve endocarditis
or complicated endocarditis (e.g. paravalvular
abscess/perforation) (~90% sensitivity).
• TEE transesophageal echo
• TTE transthoracic echo
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12. Vegetations on echocardiography
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13. Treatment : Medical
• usually non-urgent and can wait for conformation of etiology
before initiating treatment unless patient is septic.
- empiric antibiotic therapy if patient is unstable; administer
ONLY after blood cultures have been taken. Generally, S. aureus,
coagulase-negative staphylococcus (CNST), and Gram-negative
coverage is important.
First line empiric treatment for native valve: vancomycin +
gentamicin OR ceftriaxone.
First line empiric treatment for prosthetic valve: vancomycin +
gentamicin + rifampin.
Targeted antibiotic therapy: antibiotic and duration (usually 4-6
wk) adjusted based on valve,organism, and susceptibilities. 13

14. Treatment : Medical
Monitor for complications of IE (e.g. HF, conduction block, new
emboli) and complications of antibiotics (e.g. renal disease.
Post treatment prophylaxis only recommended for high risk
individuals listed above with dental procedures that may lead to
bleeding OR invasive procedure of the respiratory tract that
involves incision or biopsy of the respiratory mucosa, such as
tonsillectomy and adenoidectomy OR procedures on infected
skin, skin structure, or musculoskeletal tissue
• dental/respiratory: amoxicillin single dose 30-60 min prior;
clindamycin if truly penicillin-allergic
• skin/soft tissue: cephalexin single dose 30-60 min prior;
clindamycin if truly penicillin-allergic (modify based on etiology
of skin/so tissue infection).
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15. Treatment : Surgical
• most common indication is refractory CHF.
• other indications include: valve ring
abscess, fungal etiology, valve perforation,
unstable prosthesis, 2 major emboli,
antimicrobial failure (persistently positive
blood cultures), mycotic aneurysm,
Staphylococci on a prosthetic valve.
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16. Prognosis
• adverse prognostic factors: CHF,
prosthetic valve infection,
valvular/myocardial abscess, embolization,
persistent bacteremia, altered mental status
• mortality: prosthetic valve IE (25-50%),
non-IVDU S. aureus IE (30-45%), IVDU S.
aureus or streptococcal IE (10-15%).
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