B4.013 Prework 1 Infectious Cardiac Valve Disease Flashcards
what are valve vegetations made up of?
platelets, fibrin, microbes, collagen
what are 4 different ways to classify infective endocarditis
temporal evolution
cause of infection
site of infection
predisposing risk factor
what is acute endocarditis
febrile illness that rapidly damages cardiac structures, seeds extracardiac sites via bloodstream, and, if untreated progresses to death within weeks
typical picture of acute endocarditis
caused by high virulence organisms involving a normal valve
large vegetations more prone to embolize
higher mortality, harder to cure with antibiotics
higher incidence of surgical treatment
s.aureus most common causative organism
what is subacute endocarditis (SBE)
an indolent, febrile illness developing over weeks to months
new or changing cardiac murmur and embolic phenomena on exam
typical picture of SBE
usually lower virulence organisms
strep viridans, enterococci, HACEK most common
smaller vegetations usually on abnormal or diseases valves
less likely to cause tissue/structural damage
higher cure rate w antibiotics
how can partially treated acute endocarditis present?
as SBE
most common cause of infective endocarditis
strep viridans (50-60%)
most common cause of IE in IV drug users
s. aureus (20-30%)
most common cause of acute IE
s.aureus
most common cause of prosthetic valve endocarditis
staph epidermidis
IE causative organism with underlying colon polyps/cancer
strep gallolyticus (bovus)
IE causative organisms commonly associated with neg blood cultures
Hemophilus Actinobacillus Cardiobacterium Ekinella Kingella
IE causative organism in immunocompromised patients
fungi (candida)
what % of IE cases are culture neg
10%
common organisms w oral, skin, resp portals of entry
strep viridans
staph
HACEK
GI portal of entry
strep gallolyticus (bovus)
GU portal of entry
enterococci
most common cause of community acquired endocarditis
strep viridans from dental procedures or poor dental hygiene
characterize nosocomial endocarditis
> 72 hours post admission or within 6-8 weeks after hospital procedure
3x increase in mortality over community acquires
6-25% of IV catheter related bacteremia results in endocarditis
most common organisms in nosocomial endocarditis
staph aureus
coag neg staph
enterococci
characterize prosthetic valve endocarditis
within 2 months of surgery
s. aureus, coag neg staph, fungi
characterize pacemaker/ICD associated endocarditis
within weeks of procedure
s. aureus, coag neg staph
what is a common virulence factor of organisms that cause endocarditis
surface adhesion molecules
fibronectin binding proteins - gram +
clumping factor- staph aureus
glucans/FimA- strep
how do microcolonies form?
organisms enmesh into growing platelet/fibrin vegetations and proliferate
why are microcolonies hard to treat?
organisms deep within vegetation are metabolically inactive and resistant to killing by antimicrobial agents
proliferating surface organisms are shed into blood continuously
what allows for infection of the typically resistant endothelium in the heart?
endothelial injury (at site of impact of high velocity blood jets or on low P side of cardiac structural lesion)
what is NBTE
non bacterial thrombotic endocarditis
uninfected platelet-fibrin thrombus on valve
subsequently serves as a site of bacterial attachment during transient bacteremia
which organism can adhere directly to intact endothelium? i.e. doesn’t require a site of NBTE
staph aureus
how do organisms induce platelet deposition and a procoagulant state?
elicit TF from endothelium
describe the morphology of IE
friable, bulky, potentially destructive lesions on valves
contain fibrin, inflamm cells, bacteria, and other organisms
can be single or multiple
occasionally erode into underlying myocardium and produce abscess or fistula
what can happens if a IE vegetation embolizes?
embolic fragments often contain virulent organisms
can develop abscesses where they lodge
septic infarcts or mycotic aneurysms can develop
how do vegetations of SBE differ from those of acute endocarditis?
SBE are associated w less destruction
exhibit granulation tissue at their bases indicative of healing
fibrosis, calcification, chronic inflamm infiltrate can develop
structural risk factors for IE
prior endocarditis rheumatic heart disease degenerative mitral valve (prolapse) bicuspid aortic valve prosthetic valve intravascular device atrial septal defect ventricular septal defect tetralogy of Fallot
risk factors for bacteremia
IV drug use indwelling venous catheters poor dentition hemodialysis DM
common clinical manifestations of infective endocarditis
fever elevated ESR chills and sweats murmur anemia
remote embolic effects of IE
brain infarcts retinal infarction petechiae of skin and finger clubbing mycotic aneurysms of splenic arteries and/or infarct of spleen (splenomegaly) petechiae and gross infarcts of kidney petechiae of mucous membranes
classic IE physical findings
Roth’s spots
Osler’s nodes
Splinter hemorrhages
Janeway lesions
Roths spots
retinal hemorrhages with white or pale centers
osler nodes
painful, red, raised lesions on hands and feet
janeway lesions
nontender, small erythematous or hemorrhagic macular or nodular lesions on the palms or soles
clinical presentation of fungal endocarditis
extremely debilitating present w constitutional symptoms candida most common immunocompromised or IV drug user low rate of pos blood cultures
diagnosis of IE
modified Duke criteria
pos blood cultures
echocardiography
blood culture technique for IE
2-3 bottles from different sites
drawn >30 min apart
aseptic technique to avoid false pos
don’t draw from IV lines
what is a reason for false neg results?
prior antibiotic use (draw >48 h after antibiotics)
fungal
HACEK
-if culture is neg, repeat in 7 days
accepted blood culture contam rate
< 3%
what are some important findings of echocardiography
anatomic confirmation of endocarditis
vegetation size
intracardiac complications
assessment of cardiac function
TTE
trans thoracic echo
non invasive, but difficult in 20% of pts
65% sense, high spec
TEE
trans esophageal echo 90% sense needed for: prosthetic valve endocarditis myocardial abscesses, valve perf, intracardiac fistula
complications of IE
valvular regurg CHF (severe regurg) (aortic or mitral) cerebrovascular emboli or stroke peripheral arterial emboli mycotic aneurysm splenic abscess/infarct para-prosthetic valve abscess/dehiscence intracardiac fistula cardiac conduction system abnormalities (myocardial abscess)
what is a mycotic aneurysm
focal dilation of an artery caused by growth of microorganisms within the vascular wall, usually after the impact of a septic embolus
monitoring anti microbial therapy in IE
antibiotic toxicities occur in 25-40% of patients, commonly in 3rd week
blood tests to detect renal, hepatic, hematologic toxicity should be performed periodically
cultures repeated daily until sterile, recheck is there is a recurring fever and performed 4-6 weeks post therapy to document cure
when is surgery required for optimal outcome?
heart failure due to valve damage
failure of antibiotic therapy
partially dehisced prosthetic valve
s.auerus prosthetic valve endocarditis w intracardiac complication
when should surgery be strongly considered
perivalvular extension persistent unexplained fever in culture neg large vegetations on left heart recurrent emboli when on antibiotics abscess formation fungal large, hypermobile vegetations
when is endocarditis prophylaxis recommended
for people w prosthetic valves, previous endocarditis, cardiac transplant, or congenital cyanotic heart disease
when they get dental or resp procedures
most important way to avoid endocarditis
routine maintenance of good oral hygiene
