Infective Endocarditis

DR Mohamad Jarrah Assistatnt Professor Cardiologist JUST

Definition
Infectious Endocarditis (IE): an infection of the hearts endocardial surface Classified into four groups:
Native Valve IE Prosthetic Valve IE Intravenous drug abuse (IVDA) IE Nosocomial IE

Further Classification
Acute
Affects normal heart valves Rapidly destructive Metastatic foci Commonly Staph. If not treated, usually fatal within 6 weeks

Subacute
Often affects damaged heart valves Indolent nature If not treated, usually fatal by one year

Etiology
Native valve Endocarditis- Streptococcus viridans, Staphylococci,
HACEK - Oral cavity, skin, upper respiratory tract Streptococcus bovis (GIT), Enterococci Intravascular catheters, UTI, Nosocomial wound infections, HD- transient bacteremia

Prosthetic Valve Endocarditis- Coagulase negative Staphylococci,

S.Aureus, GNB, diptheroids, fungii
Within 2 months- intra-operative contamination

IV Drug abuse endocarditis:- Tricuspid valve

MRSA More varies Etiology if left sided heart valves are involved Polymicrobial Unusual organisms- Pseudomonas Aeruginosa, Candida, Bacillus, Lactobacillus, Corynebacterium

Nosocomial- Transvenous pacemaker lead- and/or implanted

defibrillator associated endocarditis

5-15% may be culture negative (?prior antibiotic exposure)

Or fastidious organisms- Coxiella burnetti in Europe, Brucella in the Middle East

Tropheryma whipplei- indolent afebrile culture negative endocarditis

Pathophysiology
1. Turbulent blood flow disrupts the endocardium making it sticky 2. Bacteremia delivers the organisms to the endocardial surface 3. Adherence of the organisms to the endocardial surface 4. Eventual invasion of the valvular leaflets

Inherently endothelium is resistant to infection Turbulent blood flow causes endothelial injury- direct infection OR Nonbacterial thrombotic endocarditisplatelet fibrin thrombus- site of infection

Epidemiology
Incidence difficult to ascertain and varies according to location Much more common in males than in females May occur in persons of any age and increasingly common in elderly Mortality ranges from 20-30%

Risk Factors
Intravenous drug abuse Artificial heart valves and pacemakers Acquired heart defects
Calcific aortic stenosis Mitral valve prolapse with regurgitation

Congenital heart defects Intravascular catheters

Symptoms
Acute
High grade fever and chills SOB Arthralgias/ myalgias Abdominal pain Pleuritic chest pain Back pain

Subacute
Low grade fever Anorexia Weight loss Fatigue Arthralgias/ myalgias Abdominal pain N/V

The onset of symptoms is usually ~2 weeks or less from the initiating bacteremia

Signs
Fever Clubbing Splenomegaly Neurological manifestations Heart murmur Peripheral manifestations- Oslers nodes, Subungual hemorrhage, Janeway lesions,

Anemia Leukocytosis Microscopic hematuria Elevated ESR, CRP Decreased serum complement Immune complexes Rheumatoid factor

Cardiac Manifestations
New regurgitant murmurs- 30-35% then 85% CHF- 30 to 40%- valvular damage (aortic), myocarditis, intracardiac fistula Perivalvular abscess Fistulae (Root of aorta to chambers/ between cardiac chambers) Pericarditis Heart block/ MI due to embolic phenomena

Septic Pulmonary Emboli

http://www.emedicine.com/emerg/topic164.htm

Non cardiac
Septic embolization- subungual hemorrhage, Oslers nodes Musculoskeletal Skin, spleen, kidney, meninges, skeletal systeminfarcts Embolic strokes Mycotic aneurysms (infection in vasa vasorum) Brain microabscesses Glomerulonephritis (reduced complement)

Petechiae
1. Nonspecific 2. Often located on extremities or mucous membranes

Splinter Hemorrhages

1. 2. 3. 4. 5.

Nonspecific Nonblanching Linear reddish-brown lesions found under the nail bed Usually do NOT extend the entire length of the nail vessel damage from swelling of the blood vessels (vasculitis) or tiny clots that damage the small capillaries (microemboli).

Oslers Nodes- immune

American College of Rheumatology webrheum.bham.ac.uk/.../ default/pages/3b5.htm www.meddean.luc.edu/.../ Hand10/Hand10dx.html

1. More specific 2. Painful and erythematous nodules 3. Located on pulp of fingers and toes 4. More common in subacute IE

Janeway Lesions

1. More specific 2. Erythematous, blanching macules 3. Nonpainful 4. Located on palms and soles 5. Microabscess of the dermis with marked necrosis and inflammatory infiltrate not involving the epidermis.

Roth Spots

septic embolization, leukemia, lupus erythematosus, or pernicious anemia.

The Essential Blood Test

Blood Cultures
Minimum of three blood cultures Three separate venipuncture sites atleast 1 hour apart- over 24 hrs
SerologyBrucella, bartonella, Legionella, C. Burnetti Schiff stain for T. whippeli

Imaging
Chest x-ray
Look for multiple focal infiltrates and calcification of heart valves

EKG
Rarely diagnostic Look for evidence of ischemia, conduction delay, and arrhythmias

Echocardiography

Indications for Echocardiography

Transthoracic echocardiography (TTE)
First line if suspected IE Native valves

Transesophageal echocardiography (TEE)

Prosthetic valves High risk patients Intracardiac complications Inadequate TTE Fungal or S. aureus or bacteremia

Major Criteria
1. Positive blood culture
Typical organism from 2 separate culturesViridans streptococci, Strptococcus bovis, HACEK, S. aureus, enterococci

OR
Persistently + blood culture- all of three/ majority 4 blood cultures

OR
Single +ve blood culture for Coxiella or phase IgG > 1:800

2. Evidence of endocardial involvement ECHO- oscillating intracardiac mass OR Abscess OR New partial deheiscence of prosthetic valve/ new regurgitation

Minor criteria
Predisposing heart condition Fever > 100.4F Vascular- Emboli, pulmonary infarct, mycotic aneurysm, Janeway lesions Immune- Oslers nodes, Roth spots, glomerulonephritis Microbiological evidence

Modified Duke Criteria

Definite IE
Microorganism (via culture or histology) in a valvular vegetation, embolized vegetation, or intracardiac abscess Histologic evidence of vegetation or intracardiac abscess 2 Major 1 Major + 3 minor 5 Minor

Possible IE
1 major and 1 minor 3 minor

Treatment
Parenteral antibiotics
High serum concentrations to penetrate vegetations Prolonged treatment to kill dormant bacteria clustered in vegetations

Surgery
Intracardiac complications

Surveillance blood cultures

Monitor for side effects Improvement in 5-7 days Repeat blood cultures till sterile Again 4-6 weeks after therapy

Prophylaxis
Amoxicillin 2 g PO I hour before procedure Ampicillin 2 g iv within 1 hr

Clarithromycin/ Azithromycin 500 mg Cephalexin 2 g Clindamycin 600 mg

Cefazolin/ceftriaxone 1 g iv 30 min before procedure Clindamycin 600 mg iv

WHO prophylaxis
Prosthetic heart valves Prior history Unrepaired cyanotic congenital heart disease Completely repaired congenital heart disease within 6 months of repair

Incompletely repaired CHD

Valvulopathy after cardiac transplantation

Poor Prognostic Factors

Female S. aureus Vegetation size Aortic valve Prosthetic valve Older age Diabetes mellitus Low serum albumen Heart failure Paravalvular abscess Embolic events