Flashcards in Infective Endocarditis Deck (35)
Infective Endocarditis (IE)
-an infections of the hearts endocardial surface
-typically involves the valves, but may involve any structure of the heart
-Strep (most common)
--Strep Viridans is 40-50% of Strep IE
-fastidious gram negative cocco-bacillary forms
-Native valve IE
-Prosthetic Valve IE
-Intravenous drug abuse (IVDA) IE
Why are Staph, Strep, and Enterococcus such a problem?
-they contain adhesins that attach to the fibrin platelet matrix of non-bacterial thrombotic endocarditis (NBTE)
-Adhesins also attach to the matrix proteins that coat implanted medical devices
-bacterial extracellular structures form biofilm on surface of implanted devices
What is HACEK?
-gram negative, slow growing, fastidious organisms that may need 3 weeks to grow out of culture
-normal oral flora... leading cause of culture negative endocarditis
What is the most common gram negative bug that causes IE?
What is vegitation?
An amorphous mass of fibrin and platelets, abundant organisms, few inflammatory cells, variable in size
Describe acute IE.
-may affect normal heart valves
-if not treated, usually fatal within 6 weeks
-Usually affects damaged heart valves
-if not treated, usually fatal by one year
NVE (native) vs PVE (prosthetic) infection sites
-infection is largely confined to leaflets
-infection commonly extends beyond valve ring into annulus/periannular tissue
1. Turbulent blood flow (from congenital or acquired heart disease) disrupts the endocardium making it "sticky" (platelets and fibrin deposit on damaged endothelium)...this would be Nonbacterial thrombotic endocarditis (NBTE)
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 (bacterial vegetation)
Where are the lesions usually seen with Nonbacterial thrombotic endocarditis (NBTE)?
What is the Venturi Effect?
Usually at the coaptation (the drawing together of the separated tissue in a wound or fracture) points
-atrial surface of the mitral/tricuspid
-ventricular surface of aortic/pulmonic
-The Venturi effect is the reduction in fluid pressure that results when a fluid flows through a constricted section (or choke) of a pipe. (this is where bacteria are deposited)
clinical manifestations (direct and indirect)
-constitutional sx of infection
-local destructive effects of infection (valvular distortion/destruction, chordal rupture, perforation/fistula formation, conduction abnormalities)
-Embolization (clinically evident in 11-43%)
-Hematogenous seeding of infection (may present as local infection or persistent fever,metastatic abscesses may be small)
Factors that influence the conversion of NBTE to IE
-density of colonizing bacteria (oral over GU over GI)
-disease state of surface
-extent of trauma
-resistance of organism to host defenses
Predisposing/risk factors of IE
-rheumatic heart disease
-congenital heart disease
-the majority for cases after the neonatal period are associated with an underlying congenital abnormality
-IV drug abuse (staph aureus is predominant organism)
-Prosthetic Valve Endocarditis
-accquired heart defects
-high grade fever, chills
-pleuritic chest pain
-low grade fever
*onset of sx is usually about 2 weeks or less from the initiating bacteremia
-fever (most common)
-heart murmur (new or change in existing one)
-nonspecific signs (petechiae, subungal hemorrhages, clubbing, splenomegaly, neuro changes)
-Osler's nodes: painful, red, raised lesions on hands and feet (pads of fingers and toes)
-Janeway lesions: nontender, red, macular (flat) or nodular (raised) lesions on palms and soles
-Roth spots: white spot surrounded by red hemorrhage in the retina
Acute vs subacute presentation
-progressive valve destruction and metastatic infection developing in days to weeks
-most commonly caused by S. aureus
-presentation over weeks to months
-rarely leads to metastatic infection
-most commonly S. viridans or entercoccus
Manifestations of IE
-neurological sequelae (embolic stroke, mycotic aneruysm, cerebritis)
-CHF (d/t mechanical disruption)
-Renal insufficiency (Immune complex mediated, impaired hemodynamics, drug toxcitity)
What are some of the classical peripheral manifestations of IE?
-Petechiae (most common) (often located on extremities or mucous membranes)
-Splinter Hemorrhages (nonblanching, linear red/brown lesions under the nail bed, do not extend the length of the nail)
-Osler's nodes (painful, red nodules on fingers and toes)
-Janeway lesions (red, blanching macules, nonpainful, on palms and soles)
-Roth spots (pale retinal lesions surrounded by hemorrhage)
Work up for IE (labs, imaging)
-ESR and CRP
-Complement levels (C3, C4, and CH50)
-baseline chemistries and coags
-CXR (multiple focal infiltrates and calcification of heart valves)
-EKG (rarely diagnostic)
-echocardiography (TEE is more sensitive than TTE, although TTE is first line in suspected native valve IE, TEE for other complications such as prosthetic valves)
What is the ESSENTIAL blood test for IE?
-minimum of 3 sets
-3 separate venipuncture sites
-obtain 10-20 mL in adults and 0.5-5mL in children
A positive result= typical organisms present in at least 2 separate samples
What is Duke's Critera used for?
determining Definite, Possible, or Rejected IE
What are the four major complications of IE?
-Local spread of infection
-Metastatic spread of infection
-Formation of immune complexes: glomerulonephritis and arthritis
Predictors of embolization in IE? Possible outcomes with embolization during IE?
-Size of vegetation
-left sided vegetation
-fungal pathogens, S. aureus, and Strep bovis
-hypoxia from pulmonary emboli
Possible outcomes with metastatic spread of infection during IE?
-Metastatic abscess (Kidney, spleen, brain, soft tissues)
-meningitis and/or encephalitis
-pulmonary abscess (right sided endocarditis)
Possible outcomes with local spread of infection during IE?
-Heart Failure (d/t extensive valvular damage)
--most common in aortic valve, IVDA, and s. aureus
--may cause arrythmias
--higher rates of embolization and mortality
-Fistulous intracardiac connections
Poor Prognostic factors for IE
-low serum albumin
Treatment of IE
--high serum concentrations to penetrate vegetations
--prolonged tx to kill dominant bacteria clustered in vegetations
-surveillance blood cultures
If you suspect acute bacterial endocarditis, should you begin abx therapy before or after the blood cultures turn positive?
-start with broad spectrum and narrow from there. don't wait to give abx, you can always withdraw them
If there is a persistent fever in IE, you might suspect the cause to be...
a drug reaction
How long are abx typically administered after IE? what route?
administered IV for 4-6 weeks (duration depends on pathogen)
What is the drug of choice for most cases of viridians streptococcal endocarditis?
-cure rate is above 90%
-without tx, VSE is fatal within 6 months
-quinolones or IV Vancomycin not recommended for prophylaxis d/t concern of creating new drug resistance