Infective endocarditis Flashcards
Definition
- which side of the heart is affected?
Infection of heart valves (native/prosthetic) or other endocardial lined structures e.g. pacemaker leads, ventricular septal defect. Infected vegetations can form on:
- native valves with congenital defects or acquired defects (IVDU)
- prosthetic valves & pacemakers
- normal native valves due to virulent organisms e.g. Viridans group streptococci, S. epidermidis
Left sided endocarditis affecting mitral valve is most common; R sided endocarditis is seen in IVDU - typically tricpusid valve in IVDU
Epidemiology- 4 groups affected?
- young IVDU (MC cause = S. aureus, skin commensal)
- male, elderly w/ prosthetic valves
- young with congenital heart defects
- those with rheumatic heart disease (2-4 weeks after streptococcal pharyngitis or Scarlet fever due to Group A beta haemolytic S. pyogenes, some ppl develop rheumatic fever due to molecular mimicry)- decreasing incidence now
Risk factors (6)
- poor dental hygiene + dental surgery (Viridans group streptococci)
- IVDU (S. aureus)
- prosthetic valves/pacemaker
- recent cardiac surgery
- indwelling line/catheter/ IV cannulae (S. epidermidis forms biofilms, nosocomial infections)
- previous IE
Pathophysiology + complications
Abnormal/damaged cardiac endothelium + presence of abnormal microoganisms in bloodstream (BACTERAEMIA)
- Platelets & fibrin deposit on valves, allowing bacteria to adhere & form infective vegetations
- Virulent organisms destroy the valve they are on causing valve regurgitation & worsening heart failure (mitral regurgitation -> CHF)
- Septic microemboli can travel to: lungs & cause staphylococcal cavitating pneumonia (complication of R. sided endocarditis in IVDU) & travel to kidneys causing renal infarcts & other places causing infarcts e.g. splinter haemorrhages (septic microemboli cause infarcts in nailbeds), Janeway lesions (septic microemboli cause infarcts in palms & soles)
Causative microorganisms (7) + how they enter bloodstream + which patient groups you’d see them in
- **Staphylococcus aureus **= MC in IVDU. Skin commensal
- Viridans group streptococci= MC in non-IVDU; associated with poor dental hygiene + recent dental surgery
- Staphylococcus epidermidis- can form biofilms in indwelling lines, catheters & IV cannulae, associated with nosocomial infection. Coagulase -ve staph
- Enterococcus faecalis & Streptococcus bovis- gut commensals, associated w/ colon cancer & ulcerative colitis
- HACEK microbes (gram -ve bacilli)- Hameophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella
- Fungal sources e.g. Candida albicans - usually immunocompromised patients e.g. chemo
Microbio properties- Viridans group streptococci
Catalase -ve (add H202, no bubbling therefore strep), alpha hameolysis on blood agar (green/brown discoloration due to partial RBC breakdown), Optochin resistant (no zone of inhibition around optochin disc)
- Gram +ve - purple chains of cocci
ID- Staphylococcus aureus
Gram +ve, catalase +ve & coagulase +ve (add rabbit plasma & clumping observed as fibrinogen converted to insoluble fibrin)
- golden colonies on blood agar
ID- Staphylococcus epidermidis
- catalase +ve, coagulase -ve staph
- white colour colonies on blood agar
ID- Candida albicans
- appearance on different agars
cream colour colonies on Sabourard agar.
Can grow on blood agar- appears as large gram +ve cocci undergoing budding
Sx & signs (+ include immunological phenommena)
Sx = nonspecific & variable e.g. fever, malaise, headache, night sweats, sepsis/emboli of unknown origin
Fever & new regurgitant murmur-> consider IE as DDx
Signs (develop later) = pathognomonic
- **Roth spots **= retinal hameorrhages with clear centres on fundoscopy
- Osler’s nodes = tender nodules in fingers due to immune complex deposition
- Splinter haemorrhages = due to septic emboli causing infarcts in nailbeds
- Janeway lesions= painless plaques in palms & digits due to septic emboli causing infarcts
- *Glomerulonephritis (T3 hypersensitivity reaction- deposition of immune complexes in kidneys)- causing haematuria
+ peetchia + ** septic emboli** - kidney function can be affected
immunological phenomena = glomerulonephritis, Osler’s nodes, Roth spots
What are the immunological phenomena in IE? (3)
*Glomerulonephritis (T3 hypersensitivity reaction- deposition of A-A complexes in kidneys)- causing haematuria
*Roth spots = retinal hameorrhages with clear centres on fundoscopy
- *Osler’s nodes = tender nodules in digits due to immune complex deposition
6 investigations you would do?
- FBC- shows neutrophilia
- ESR & CRP- raised, inflammatory markers
- Blood cultures- take 3 from different sites over 24 hrs. Can be negative, especially if ABx therapy has been commenced BEFORE.
- GS - transoeosphageal echocardiogram (more invasive than transthoracic but better sensitivity)- may show infected vegetations & regurgitant valves
- ECG- check for aortic root abscess indicated by prolonged PR interval >200ms
- Urinalysis- check for kidney damage due to septic emboli causing renal infarcts or glomerulonephritis causing haematuria
Wha would you look for on an ECG?
ECG- check for aortic root abscess indicated by prolonged PR interval >200ms
How would you diagnose IE?
Duke’s criteria- use 2 major criteria OR 1 major + 3 minor criteria OR 5 minor criteria
Major Duke’s criteria?
- 2 or more positive blood cultures
- Transoeosophageal echocardiogram showing endocardial involvement- infected vegetations or regurgitant valves
