IE/AS Flashcards
What is infective endocarditis?
Inflammation of the endothelial surfaces of the heart including heart valves caused by certain micro-organisms
What are the types of endocarditis?
Infective endocarditis
–> micro-organisms colonise the heart valves and form friable vegetations
–> The two types are acute and subacute
–> Diagnosis is via duke’s criteria
Non bacterial thrombotic endocarditis (marantic endocarditis)
–> Typically occurs in advanced malignancy
–> sterile vegetations on heart valves
Libman sacs endocarditis
–> Same as NBTE
–> occurs in malignancy
Why are patients with rheumatic heart disease or valve replacements more susceptible to endocarditis?
-In normal heart blood flows smoothly over the valves
-This is not the case in damaged tissues e.g. due to RHD or valve replacement, which are susceptible to bacterial colonisation
What is the pathophysiology of rheumatic heart disease?
-Acute rheumatic fever results from host response to strep A antigens which cross-react with host proteins
-In particular CD4+ T cells directed against Streptococcal M proteins recognise cardiac self antigens
-Cytokines subsequently produced by CD4+ T cells attract neutrophils and macrophages
-These are additionally attracted by antibody binding and complement activation
-Damage to heart tissue is therefore caused by combination of antibody and t cell mediated reactions
Recurrent inflammation leads to:
–> commissural fibrosis
–> valve thickening and calcification
–> Shortened and fused chordae tendinae (fish mouth shape)
What are the gross findings in endocarditis?
Acute phase: vegetations along line of closure with minimal impact on function
Chronic phase: commissure fibrosis, valve thickening and calcification, shortened and fused chordae tendinae (fish mouth shape)
Microscopic findings
Aschoff bodies
–> form of granulomatous inflammation
–> consists of central zone of degenerating extracellular matrix infiltrated by lymphocytes, plasma cells and anitschkow cells (activated macrophages also known as caterpillar cells due to wavy nuclear outlines)
–> Can be found in all 3 layers of heart (endocardium, myocardium, pericardium
What is seen macroscopically?
Aschoff nodules
Fibrinoid necrosis
What investigation is used to identify valvular vegetations?
-2D echocardiogram
What to look for on 2D echocardiogram
1) Regurgitation
2) Leaflet: thickening, coaptation failure, prolapse, reduced mobility, nodules
3) Pericardial effusion
4) mobile mass (vegetations)
Coaptation failure: coaptation is the distance of apposition of the two valve leafelets
What micro-organisms are commonly implicated?
-Strep viridans
-Coagulase negative staph (staph aureus, staph epidermidis)
-Enterococci
-Hacek group of micro-organisms (oral commensals)
How is endocarditis diagnosed?
Dukes criteria
2 major criteria and 0 minor criteria
1 major criteria and 3 minor criteria
5 minor criteria and 0 major criteria
What are the major criteria for diagnosis of infective endocarditis?
+ve blood culture suggestive of endocarditis
-2x separate positive blood cultures with suggestive organisms, 1x blood culture with coxiella burnetii, antiphase 1 antibody titre >1:800
Evidence of endocardial involvement
-Endocardium +ve for vegetations, abscess, prosthetic valvular dehiscence, new valvular regurgitation (not changing of existing murmur)
What are the minor criteria for diagnosis of infective endocarditis?
Predisposition
-IV drug use
-Heart condition
Vascular phenomena
-Major arterial emboli
-Septic pulmonary infarcts
-Mycotic aneurysm*
-Janeway lesions*
-Intracranial haemorrhage
-Conjunctival haemorrhage
Immunologic phenomena
-Glomerulonephritis
-Roth spots
-Osler’s nodes
-Rheumatoid factor
Fever
- >38 degrees
Microbiological evidence
- +ve blood culture consistent with IE but doesn’t fit major criteria
Echocardiogram
-Evidence on echocardium but does not fit major criteria
*Janeway lesion: haemorrhagic lesion on palms or soles
*mycotic aneusysm: aneurysm due to infection
-Roth spots: retinal haemorrhages
What are the risk factors for infective endocarditis?
-Valvular heart disease (stenosis/regurg)
-Structural congenital heart disease
-prostheticvalve
-Tooth extraction
-Immunosuppression (HIV)
-Rheumatic heart disease
-IVDU
What are the complications of endocarditis?
Cardiac
-AMI
-Arrythmia
-Intracardiac abscess
-pericarditis
-valvular inssuficciency
-CCF
Non cardiac
-Glomerulonephritis
-AKI
-stroke
-Mesenteric/splenic infarct
What are the signs of infective endocarditis in the hand?
Osler’s nodes:
-Raised painful lesions in fingers caused by deposition of immune complexes
Janeway lesions
-non painful macular or nodular lesions in palms and soles of foot caused by septic emboli depositing bacteria, causing microabscesses
Splinter haemorrhages
-Tiny blood clots under finger nails
What are the indications for surgery in IE?
-Abscess
-Valvular destruction/obstruction
-Haemodynamic compromise
-CCF
-Septic emboli
-Fungal infective endocarditis
-Failureof medical therapy
Signs and symptoms of IE FROM JANE
Fever
Roth spots
Osler’s nodes
Murmur
Janeway lesions
Anaemia
Nail (splinter) haemorrhage
Emboli
What is the treatment of infective endocarditis? Why is treatment challenging?
IV antibiotics for 6 weeks
Restictions
-Valves do not have specific blood supply so antibiotics struggle to reach the micro-organisms
-Micro-organisms live within vegetations
-Micro-organisms form a bio-film
What happens if endocarditis occurs in tricuspid valve?
Right sided heart failure
What is the management if there is poor response to medical therapy?
-Valve replacement
-Heart transplant
What matching is required prior to heart transplantation?
HLA matching
How can you prevent organ rejection in heart transplant patient?
Immunosuppressant therapies
-Tacrolimus
-Mycophenolate
-Steroids
What are the side effects of long term steroid use?
-Opportunistic bacterial and viral infections such as EBV, CMV, leukaemia, lymphoma
-Cushingoid: hirsutism, striae, obesity, muscle weakness
-Cardiovascular: Fluid retention, hypertension
-Endocrine: DM
-MSK: proximal myopathy, AVN, osteoporosis
What are the classes of immunoruppressive drugs? what is their mechanism of action?
What is the mechanism of action of warfarin/
Vitamin K antagonist: inhibits 2,7,9,10`
What are the options to reverse warfarin?
Vitamin K
FFP
PCC
What is the likely aetiology of tricuspid valve vegetations?
Right heart: IV drug user
Describe prophylaxis for endocarditis
Prophylactic antibiotics/chlorhexidine mouthwash not routinely recommended
What are the symptoms and signs of aortic stenosis?
Symptoms
-Syncope
-Angina
-Dyspnoea
-PND
-Orthopnoea
Signs
-Pulsus alternans (alternating strong and weak beats)
-Narrow pulse pressure/slowrising pulse
-Paradoxical splitting S2
-Ejection systolic murmur (right 2nd intercostal space on right sternal border)
What is split S2/paradoxical split s2?
-Caused when closure of aortic valve (A2) and closure of pulmonary valve (P2) are not syncronised during inspiration
-A2 followed by P2 in healthy person
Paradoxical splitting
-Reversal of normal physiology, splitting of second heart sounds during expiration, singular during inspiration
What are the complications of AS?
-LVH,
-HTN
-CHF
-VT, VF
-Angina
What are the causes of aortic stenosis?
-Senile calcific aortic stenosis
-Calcification of congenitally deformed heart valve (bicuspid valve)
-Scarring post rheumatic heart disease
What is the cause of sudden cardiac death in aortic stenosis?
MI
Dissection
How does aortic stenosis occur?
Bicuspid or degenerative valve –> endothelial injury from mechanical stress –> inflammation –> lipid accumulation –> fibroblasts cause ECM/calcium deposition
Lipid accumulation, inflammation, calcification -> stenosis
What is the pathophysiology of aortic stenosis?
Bicuspid or degenerative valve –> endothelial injury from mechanical stress –> inflammation –> lipid accumulation –> fibroblasts cause ECM/calcium deposition
-Stenosis –> increased afterload –> thickening of left ventricular wall (hypertrophy)
-Effects of increased afterload: increased workload, increased oxygen consumption and reduced coronary blood flow and myocardial elasticity.
Late manifestations:
–> Reduced left chamber size: reduced preload/systolic dysfunction
–> Insufficient CO/EF
–>Pulmonary hypertension
Aortic valve endocarditis, after a while weakness in left arm, why?
Embolism and CVA
Which coagulation pathway does warfarin affect?
Extrinsic pathway
Define a thrombus
A thrombus is solid material formed from the constituents of blood in flowing blood
What are the surgical options for managing a diseased aortic valve?
-Mechanical valve: long lasting valve made of durable materials
-Tissue valve: animal or human donor
-Ross procedure: Diseased aortic valve is replaced with pulmonary valve, pulmonary valve is replaced with allograft
-TAVI: transcatheter aortic valve replacement
If metallic valve is inserted and pt develops endocarditis, why should the valve be removed?
-Valve will be septic focus
-valve will be dehiscent
If microscopic branching hyphae were found on metallic heart valve, what would be the cause?
Fungal infection:
-Aspergillus
-Candida
-microsporum
What are the benefits/drawbacks of mechanical/tissue valve?
