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CR - path of valvular heart disease (ii) Valvular Vegetations (rheumatic…
CR - path of valvular heart disease (ii) Valvular Vegetations
rheumatic fever
systemic immune-mediated response
precipitated by b-haemolytic GAS pharyngitis (occurs 10 days - a few wks later)
multisystem inflamm disease
acute rheumatic carditis manifests during acute phase
may progress to chronic rheumatic heart disease with valvular abnormalities
clinical features
migratory polyarthritis of large joints
pancarditis
subcut nodules
growth of abnormal tissue just under skin (primarily on extensor surfaces)
erythema marginatum
pink rings on torso + inner surfaces of limbs (primarily on extensor surfaces)
sydenham chorea
rapid irregular purposeless involuntary movements of arms, legs, trunk, facial muscles
Dx = Jones criteria
@ least 2 major (carditis, polyarthritis, chorea, erythema marginatum, subcut nodules) + 1 minor (fever, arthralgia, high ESR/CRP, prolonged PR interval)
supporting evidence of GAS aids Dx (ASOT or +ve throat culture)
microscopic features
immune-mediated inflamm lesions in various tissues
Aschoff bodies in endo/myo/pericardium
foci of lymphocytes, occasional plasma cells + activated macrophages called Anitschkow cells
causes pancarditis
inflamm most commonly of endocardium + esp left valves
fibrinoid necrosis within cusps or along the tendinous cords
poor valve function (usually regurg)
these vegetations are only clumps of dead cells + polymorphs (no microorganisms, sterile, rarely embolise)
infective endocarditis
serious infection
microbe colonises/invades valves or mural endocardium
infective vegetations
composed of thrombotic debris, fibrin, inflamm cells + ORGANISMS
cause further damage + even destroy valve (necrosis), subsequent healing by fibrosis
septic emboli may shed
3 different mechanisms
acute
native valves usually
highly virulent organism
S Aureus in 20-30% of cases
enterococcus faecalis
immunocompetent host
necrotising, ulcerative, destructive lesions
difficult to Tx
subacute
insidious infection
deformed valves
lower virulence organisms (e.g. strep viridian's)
less destructive
longer course
txed with antibiotics
prosthetic valve infection (e.g. by S epidermidis)
2 main aetiologies
abnormal/prosthetic valve + low virulence organism (50-60% of cases)
normal valve + high virulence organism (esp common in IVDUs)
other organisms
enterococci
HACEK (culture -ve endocarditis)
fungi
clinical presentation
fever
weightloss
night sweats
rigors
signs of ICD
roth spots
Osler's nodes
glomerulonephritis
murmur
complications of valve destruction (e.g. LVF)
effects of emboli
stroke
coronary/splenic infarcts
Janeway lesions
Dx
blood cultures
TOE
Tx
aggressive prolonged antimicrobial Tx
surgery may be required if very poor valve function
chronic rheumatic heart disease
cumulative damage, ongoing deformity, turbulence, more fibrosis (post inflamm repair)
manifests yrs laters
mitral valve almost always involved
fish mouth deformity if fibrosis is across commissures (only v narrow slit for blood to pass through)
Libmann Sacks endocarditis
aka endocarditis of SLE
non-infective vegetations
Non-bacterial thrombotic endocarditis (NBTE)
non-infective vegetations
deposition of small sterile thrombi on valve cusps along line of closure
source of emboli
common in debilitated patients (e.g. cancer, sepsis)