endocarditis Flashcards
what is transient and continuous bacteremia?
- Transient bacteremia
Common
Usually asymptomatic
Triggered by daily activities - flossing, tooth brushing, chewing hard candy, medical procedures et.c - Continuous bacteremia
Bacteremia lasting longer than 30 minutes duration
In Endocarditis, bacteremia persists over long periods – until sterilization of the vegetations due to continuous release of bacteria from vegetations
What is the classification of endocarditis based on?
Older classification based on presentation
Acuity related to organism
Acute - S. aureus, Strep pneumoniae, GAS
Subacute - viridans group strep
Currently classification is more commonly based on risk factors Nosocomial – often line associated Native valve Prosthetic valve Injection drug use associated
what is the pathogenesis of endocarditis?
transient bacteremia + turbulent flow across a valve –> bacterial adherence and colonization –> local tissue damage, platelet adherence, fibrin deposition –> vegetation this can lead to one of two things. Release of bacteria from vegetation –> circulating immune complexes –> golmerulonephritis, positive rheumatoid factor, vasculitis, osler’s nodes/roth spots OR release of tissue from vegetation –> emboli –> stroke, septic pulmonary emboli, splinter hemorrhages, metastatic abscesses, janeway lesions
what is bacterial pathogenesis for endocarditis?
- Serum resistance (complement resistance) – allows for persistence of viable bacteria in blood.
Gram positives > gram negatives - Bacterial adhesins – promote binding to endothelial cells and nonbacterial thrombus (nonbacterial thrombus forms on damaged valve surfaces)
- Invasiveness
Elaboration of extracellular proteases
Metastatic seeding
What is a roth spot?
1 – Roth spots are ring shaped retinal hemorrhages with a white center of coagulated fibrin.
Immune complex mediated vasculitis.
May also be found in HIV retinopathy, diabetes, leukemia
what are janeway lesions?
Janeway lesions are irregular, nontender hemorrhagic macules located on the palms, soles, thenar and hypothenar eminences of the hands, and plantar surfaces of the toes. They typically last for days to weeks. They are usually seen with the acute form of bacterial endocarditis.
The lesions are believed to be caused by septic microemboli from the valvular lesion. Cultures of specimen are usually positive. Histologically, Janeway lesions consist of microabscesses in the dermis with thrombosis of small vessels without vasculitis.
How do Janeway lesions and Osler’s nodes differ?
Pathogenesis- Pathogenesis, one is embolic and the other is related to immune complex
Presence or absence of tenderness
Janeway - Painless, hemorrhagic lesions
Embolic in origin
Typical locations: palms and soles
Osler’s nodes - Painful
Immune complex mediated - ?
Typical locations: finger pulp, thenar eminence
what lab features might be present in endocarditis?
anemia - usually normochromic normocytic
thrombocytopenia
hematuria
increased ESC/CRP
Indicators of immune activiation - increased rheumatoid factor, cryoglobulins, hypergammaglobulinemia, circulating immune complexes, decreased complement levels
what do you need for blood culture?
When you order a blood culture…you get:
Two bottles from one site (aerobic and anaerobic) PLUS one aerobic bottle from a second site.
Why the second site?
do help detect any contamination upon retrieval of specimen
Does this allow you to make a diagnosis of endocarditis?
No, because you need to test over time to prove it is a continual bacteremia.
What do you need to guide antibiotic choices in the blood culture? and what do you need to do in terms of documentation?
The organism – to guide antibiotic choices
A single blood culture will yield this information
Documentation of continuous bacteremia – to make diagnosis and guide duration of therapy
Requires multiple cultures over time
How can we get the information we need to make an accurate Dx?
Order one “set” of blood cultures = 3 bottles PLUS one aerobic bottle x 2 at specified times
If patient is unstable, use short intervals for multiple draws – 45-60 minutes
If patient is stable and no need to initiate antibiotics immediately, can use longer intervals such as 12 hours
Anaerobic endocarditis is rare – no need for anaerobic bottle
We are looking for a specific species to be present continuously so do not need extra vial to rule out contamination
what if someone has already started antibiotics, will this effect the blood tests?
Because it takes time for vegetations to be sterilized, we can often recover organisms even after initiation of antibiotics.
Simple Staph bacteremia should clear within 2-3 days
Staph endocarditis bacteremia typically persists 5+ days
Draw more cultures
Towards the end of the dosing interval
Use ‘resin’ bottles to enhance growth
Does he need an echo to diagnose endocarditis?
Blood cultures are positive for Staphylococcus aureus in all vials and 3 out of 3 sets taken over 4 hours.
he doesn’t need this.
what’s the role of echocardiography?
- To help confirm a clinical suspicion of endocarditis when blood cultures:
When blood cultures are negative but suspicion is high
Blood cultures not obtained early enough
Fastidious pathogens - “culture negative” endocarditis
- To assess for complications and need for surgery Size of vegetation Location of vegetations – which valve? Paravalvular abscesses Leaflet damage CHF
What is the most common bacterial cause of native valve endocarditis?
viridians group streptococcus
which organism is the most common cause of prostheticvalve endocarditis?
coagulase negative staph
what about prosthetic valve endocarditis?
- Early – less than 12 months post op
Nosocomial pathogens: Staph aureus, CoNS, Gram Negative bacilli - Late – more than 12 months post op
Skin and oral flora: CoNS, Staph aureus, viridans group streptococci - Gram negative and Fungi are infrequent causes of early and late PVE
What are important points about microbial etiology?
- ***Gram positive cocci cause the majority of cases of endocarditis
- Staphylococcus aureus is important in all patient groups
Native valve endocarditis – 10-27%
Nosocomial endocarditis – most important pathogen
Injection drug use related IE – 50%
Prosthetic valve endocarditis - Early – 20% / Late – 10% - Uncommon causes of endocarditis
Gram negative bacilli <1% (more common in IDU) - Culture negative endocarditis - ~5%
what are the complications of endocarditis?
- 100% of patients with untreated endocarditis will die
- Even with treatment, complications are common with over half of all patients experiencing one or more complications.
- Complications occur due to:
Local tissue destruction and invasion
Embolic events
Immunologic events
Cardiac complications
Neurologic complications
Renal complications
what are the cardiac complications of endocarditis?
Destruction of the valve leading to free regurgitation
Congestive heart failure
Large vegetations can obstruct outflow
Heart block - perivalvular abscesses / invasion around aortic valve
Pericarditis
Myocardial infarction
What are neurologic complications of endocarditis?
Stroke Retinal emboli Encephalopathy Brain abscess Meningitis Mycotic cerebral aneurysm Intracranial hemorrhage
what are renal complications of endocarditis?
Renal failure develops in about 1/3 of patients
Glomerulonephritis from circulating immune complexes
Renal emboli
- Drug toxicity
Treatment of endocarditis requires high doses and long duration to sterilize vegetations which form a protected environment for organisms
High dose cloxacillin – interstitial nephritis
what are embolic complications of endocarditis?
Small pieces of the vegetations can break off and become lodged in arteries or arterioles
Obstruction
Abscess formation
Left sided emboli – 2/3 go to brain
Kidney, spleen, liver, extremities
Mycotic aneurysms – emboli lodge at bifurcation of arteries, occlude vasa vasorum damage to vessel wall aneurysm formation (S. aureus)
Right sided emboli – septic pulmonary emboli
what treatment is indicated for endocarditis/
Bactericidal therapy is necessary
Treatment must be prolonged
Beta lactams are superior to vancomycin when the organism is susceptible
Cloxacillin Vancomycin
Synergy with aminoglycosides has not been shown to be of benefit and increases risk of renal failure
Short course therapy (2 weeks) may be used in non HIV infected patients with S. aureus Tricuspid valve endocarditis, all others require protracted therapy – 6-8 weeks.
Vancomycin does not get in to vegetation very well because of its size. It is also polar so won’t penetrate tissues as much.
What about nosocomial endocarditis?
Risk of endocarditis associated with hospitalization is 27 times that of non hospitalized persons.
Accounts for up to 30% of cases of endocarditis.
Increasing risk associated with increased invasive monitoring and therapeutic interventions
Diagnosis may be challenging due to underlying disease
Increased mortality compared to community acquired endocarditis.
Microbial etiology
Staphylococcus is the most common pathogen - ~77%
Coagulase negative staph – much less common (1-30%)
Viridans group streptococci rarely cause nosocomial endocarditis
23% of patients with S. aureus bacteremia associated with intravascular devices will have endocarditis
When a hospitalized patient has Staphyloccocus aureus bacteremia, they must be carefully assessed to rule out endocarditis, which may not be evident clinically or on TTE.
Who needs TEE? Selective vs. Broad use?
Valvulopathy
Metastatic foci
Persistent bacteremia (>2-3 days)
Persistent fever
TEE is transesophegeal echo
TTE is transthoracic echo
what are the key take home points about endocarditis?
Presentation of endocarditis can be non-specific
Low grade fever, malaise, anorexia, night sweats
Myalgias, arthralgias – may be mistaken for connective tissue disease
Low back pain – may be mistaken for orthopedic conditions
Continuous bacteremia is the hallmark of endovascular infection
Get appropriate cultures before antibiotics
Rational use of echocardiography
Gram positive cocci are the most common pathogens in all forms of endocarditis.
Nosocomial S. aureus bacteremia is associated with endocarditis in up to 25% of cases.
