L22: Fever and new murmur - endocarditis Flashcards
Endocarditis features
- Signs and symptoms of infections (fever, lethargy)
- Embolic phenomena (clots blocking arteries causing splinter haemorrhages in nail bed, lower eyelid, soles of feet, hands)
- Abnormal heart valve (mostly aortic and mitral)
- Murmur in endocarditis usually due to regurg not stenosis
- May see vegetations on mitral/aortic valve cusps, renal/splenic embolic infarcts, cerebral embolic infarct, perforation of aortic valve
Valve abnormalities and murmurs
Mitral stenosis:
- Diastolic
- Soft, long
Aortic stenosis:
- Systolic
- High-pitched crescendo-decrescendo
Aortic regurg:
- Diastolic
- Soft, early diastolic
Endocarditis pathogenesis
- Turbulent flow through abnormal valve (.e.g congenital, nodules from RHD)
- Platelets and fibrin attach to damaged valvular epithelium forming sterile vegetations
- Transient bacteraemia from skin, mouth, gut, urinary tract etc seeds bacteria on sterile vegetations
- Infected vegetation enlarges and sheds infected emboli leads to valvular destruction
Consequences of endocarditis
Emboli can break off and lodge –> infarcts or stroke
Impaired valve function –> heart failure (leaky valve causing backflow putting pressure on ventricles, then atrium, then pulmonary circulation –> pulmonary oedema)
0% chance of cure by host defences
Causative bacteria
Viridans streptococci (MOST): from mouth (alpha/green-haemolysis)
Staph aureus: from nose/skin
Enterococcus faecalis: from gut/urinary tract
Why do host defences not work?
- Valves are avascular = no capillaries to deliver neutrophils
- Flow across valve is too fast to allow neutrophil adhesion = minimal neutrophil infiltration
- Thus infection cannot be eradicated without antimicrobials
Diagnostic methods
Continuous bacteria:
- High conc of bacteria in and on vegetations, with bacteria continually shed into blood
- Constant bacteraemia: expect all blood cultures to be positive
- Culture blood on 3-4 occasions at least 20mins apart (90-100% positive)
- Culture excised valve
- Organism identified in 95% of cases
Then listen for murmur, perform echocardiogram and look for evidence of emboli (+ask about episodes of transient ischaemic attacks)
Bacteraemia
True bacteraemia: pathogen cultured, sometimes more than one set of cultures positive, clinically compatible infective source identified
Contaminant bacteraemia: skin commensal cultured, only one set of cultures positive (e.g. staph epidermidis), no apparent infective source
Transient bacteraemia: gut or mouth organism cultured, only positive briefly, no apparent infective source
Treatment
(all high dose and IV)
Initially (before knowing cause): penicillin + gentamicin + flucloxacillin
Viridans streptococcus: penicillin + gentamicin
S. aureus: flucloxacillin
Enterococcus faecalis: amoxicillin + gentamicin
For 2 weeks (sometimes 4)
Cure rate 70-90%
Rheumatic fever pathogenesis
Not the same as endocarditis
Rheumatic fever: pharyngitis due to S. pyogenes -> immune response to GAS throat infection -> inflammation of joints, heart valves, skin, brain
Comparison of rheumatic fever and endocarditis
RF:
- S. pyogenes only
- Immunological damage to valves, nodules
- Treatment w oral penicillin for 10 days
- Prophylaxis w IM penicillin for many yrs
Endocarditis:
- Viridans streptococci + others
- Mouth commensals
- Infection of valves, vegetations on valves
- Treatment w IV penicillin for one month
- Prophylaxis w oral penicillin when dental work