Infective Endocarditis Flashcards
What is the classic presentation of infective endocarditis?
Fever and new murmur
What is the difference between acute and subacute endocarditis?
Acute:
- occurs on normal heart valves
- sudden= can present with acute HF and emboli
- rapid progression
- high mortality
- staphlycoccus aureus
- RF= skin breaches/renal failure/ immunosuppression/diabetes
Subacute:
- occurs on abnormal valves
- indolent
- slowly progressive i.e. patient unwell over few weeks
- high mortality
- streptococci/coagulase negative staph
- RF= aortic or mitral valve disease/coarctation/patent ductus arteriosus/IVDU/prosthetic valves
What are the most common causes?
Bacteria
- staph viridans= subacute
- staph aureus= acute
Fungal
-tends to be in IVDU or immunocompromised patients or people with prosthetic valves
How might someone with IE present? What should you also be looking for?
Subacute: (5 weeks of symptoms)
- low grade fever
- rigours
- night sweats
- fatigue
- weight loss
Acute
- very high fever (40 degrees)
- acutely ill
NOTE:
Can present with symptoms due to embolic phenomena i.e. CP/SOB/Back pain/facial drop etc
How is IE diagnosed?
ECG= arrhythmia
Urine dip= haematuria
Blood cultures:
-3 at different sites, at least 6 hrs apart= bacteraemia not associated with fever and should remain constant i.e. differentiates from abscess= varying levels of bacteria depending on when levels taken in relation to fever
FBC:
- Normochromic, normocytic anaemia
- neutrophilia
- raised CRP
- Rheumatic factors positive
CXR:
- cardiomegaly
- pulmonary oedema
Echocardiogram
-might be able to identify vegetations on valves
What organisms are associated with the following forms of IE?
- Native valve endocarditis
- Prosthetic valve endocarditis
1. Staph aureus Streptococci Enterococcus HÁČEK group
2. <2 months post op -nosocomial pathogens -staph aureus -coagulase negative strep >2 months post op -mouth and skin flora s viridans -coagulase negative staph
What are the most common causes of IE in IVDU and why?
S.Aureus
-injecting leads to introduction of S.aureus from skin into vein which travels via IVC to RA i.e. leads to tricuspid valve preferentially effected
- mixed flora
- fungi= injecting in groin can introduce thrush
What malignancy can be associated with IE?
Colon malginancy
-leads to IE caused by streptococcus bovis
IE can be associated with the formation of emboli. Where will these emboli be found and why?
Multiple organs i.e. brain/liver/spleen
-when L sided valve (aortic) affected i.e. emboli travel in blood travelling to systemic circulation
Lungs
-when R sided valve (tricuspid valve) i.e. emboli travel via pulmonary artery to lungs
What is the pathogenic of IE?
Alteration to valvular endothelium leading to deposition of platelets and fibrin
Alternating layers of deposition leads to formation of vegetation
Bacteraemia occurs with seeding of thrombotic vegetation
Seeds adhere and grow leading to further platelet and fibrin deposition
Leads to extension into adjacent structures i.e. papillary muscles/valvular rings/cardiac conduction tissue
What are the complications associated with local spread of endocarditis infection?
Heart failure due to extensive valve damage
Valvular abscess= AV most commonly
-associated with IVDU + s. Aureus
Arrhythmias= due to extension into conduction tissue
Pericarditis
Fistulous intracardiac connections
What are the consequences of emboli formation in IE?
LEFT SIDED: MI Stroke Splenic/renal infarct Discitis (spinal tenderness) Septic arthritis
RIGHT SIDED:
PE
What signs would you look for on examination which might suggest IE?
Look for evidence of IVDU, new tattoos and assess dental hygiene
- Jane way lesions= emboli which cause abscesses to form (disappear very quickly)
- Oslers nodes = due to immune complex deposition
- Splinter haemorrhages
- Conjunctival petechiae
- Roth spots= retinal haemorrhages with pale spots
- Splenomegaly (splenic infarct)
- haematuria
What are the major and minor criteria for the Modified Duke Criteria for IE?
2 Major:
- +ve blood cultures (in 2 separate blood cultures)
- Evidence of endocardial involvement
7 minor:
- Predisposing factor
- temp >38 degrees
- vascular phenomena
- immunologic phenomena (glomerular nephritis/oslers nodes/Jane way lesions/rheumatic factor)
- microbiological evidence
- PCR
- Echo no meeting major criteria
Why is microscopic haematuria associated with IE?
Antigen-Antibody deposition in kidney leading to glomerulonephritis
-induces microscopic haematuria
