Infective endocarditis Flashcards

1
Q

List some DDx for a presentation of:

  • fever
  • new onset murmur at L sternal edge
  • pleuritic chest pain
  • haemoptysis
  • risk factor: IVDU or dental procedure
A
PDx. Infective endocarditis
DDx.
Respiratory
o Embolism- thrombotic, septic
o Pneumothorax 
o Infection- pneumonia, TB, abscess
o Neoplastic- lung ca, mets
Cardiac
o Pericarditis
o Endocarditis (50% tricuspid, 20% aortic, 20% mitral)
- Infective- streptococci or staphylococci
- Non-infective- hypercoagulable state, Libman-Sacks (SLE, immune comlpex deposition) 
o MI, angina 
o Rheumatic fever
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2
Q

What investigations would you order for endocarditis?

A
Diagnostic:
- TOE
- Blood cultures
Bedside
- ECG
- ABG
- Sputum MCS
Bloods
- FBC
- CRP/ESR
- Troponins
- Coag panel
- EUC (renal septic emboli)
- LFT
- Rheumatoid factor
- Iron studies
Imaging:
- CXR
- Venous Doppler US
- CT pulmonary angiogram
- VQ scan
- CT
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3
Q

What abnormalities do you expect to see on CXR and why?

A

• Cardiomegaly- valvular dysfunction -> increased work of heart muscle -> hypertropy
• Calcified valves
• Infectious spread to lung- consolidation
• PE signs- valvular vegetation embolised (tricuspid valve in IVDU) -> lung infarction
- Fleisher’s signs (20%)- enlarged pulmonary a proximal to thrombus (HTN from distal emboli)
- Hampton’s hump (20%)- peripheral wedge of airspace opacity distal to thrombus
- Westermark’s signs (10%)- regional hypovolaemia (due to segmental artery occlussion)
- Pleural effusion (35%)- visible pleural edge
- Knuckle sign- abrupt tapering pulmonary a (due to distal embolus)
- Atelectasis

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4
Q

Describe the process of taking blood cultures?

A
  • Blood is collected from 3 different sites at differing times (>10 mins apart, infective endocarditis samples taken over 24hrs)
  • Collection ideally prior to abx
  • Aseptic venepuncture technique
  • Aerobic (first) and anaerobic bottles filled 10mL each
  • Incubated at body temperature for 5 days
  • If bacteria present -> metabolise nutrients -> CO2 released will cause pH change -> flourescent disc colour change
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5
Q

What is the likely causative organism of infective endocarditis?

A
  • Strep viridans (most common, low virulence requires damaged valve)
  • Strep sanguinis
  • Strep oralis
  • Staph aureus- IVDU, acute/severe illness, MRSA potential, metastatic infection risk

Prosthetic valve- staph aureus, staph epidermis, haemophilus

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6
Q

What are some causes of non-infective endocarditis?

A
  • hypercoagulable state

- Libman-Sacks (SLE, immune comlpex deposition)

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7
Q

Which valve is it most likely to be affected in an IVDU?

A
  • Tricuspid valve (50% all IE)
  • IVUD: pathogens enter venous system and encounter tricuspid valve first
  • Likely causative organism: staph aureus
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8
Q

What is the pathophysiology of infective endocarditis? 


A

⇒ Risk factor (IVUD, dental surgery)
⇒ Virulent organism (e.g. staph aureus) directly injures endocardium -> endothelial erosion
⇒ Platelet and fibrin adhere to injured site
⇒ Bacteria protected from host defences by overlying fibrin and avascularity of valve leaflet -> vegetations form
⇒ Bacterial proliferates -> colonies
⇒ Leukocytosis -> vegetation growth
⇒ Neutrophils release protelolytic enzymes -> friable vegetation (prone to embolisation)

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9
Q

What are the virulence factors of Staph aureus? 


A

Enzymes:
o Coagulase -> clots plasma, coats bacterial cell (avoid phagocytosis)
o Hyaluronidase -> breaks down hyaluronic acid (in plasma membrane)-> allow bacterial spread
o Deoxyribonuclease -> breaks down DNA
o Staphylokinase -> dissolves fibrin -> aids spread
o B-lactamase -> drug resistance
Toxins:
o Super antigens (e.g. Toxic Shock Syndrome Toxin 1 (TSST 1) -> toxic shock syndrome
o Exfoliative toxins -> skin peeling
Other:
o Protein A -> binds to Fc regions of Ab -> impairs phagocytosis -> cripples antibody-mediated response
o Staphyloxanthin (gold pigment) -> antioxidant allowing avoidance of ROS

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10
Q

Compare community vs hospital acquired MRSA?

A

Community acquired MRSA
o Risk: IVDU, young people, indigenous, aged care residents
o Resistance: B-lactam resistance only -> usually susceptible to Flouroquinolone (Ciprafloxacin) and Sulfonamide (sulfamethoxazole)
o Clincial: skin infection

Hospital acquired MRSA:
o Risk: elderly, DM, dialysis, prolonged hopsitalisation, ICU, IV lins
o Resistance: multi-drug resistance common -> usually susceptible to Sulfonamide (sulfamethoxazole), NOT Flouroquinolone (Ciprafloxacin)
o Clinical: pneumonia, UTI, blood stream

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11
Q

What is the diagnostic criteria for infective endocarditis?

A

Clinically modified Dukes Criteria:
(needs 2 major criteria OR 1 major and 3 minor OR 5 minor)
Major criteria:
o Blood culture- positive typical organisms on 2 cultures, single culture Coxiella Burnetti
o Endocardial involvement on Echo (e.g. mass, abscess, new valve regurg)
Minor criteria:
o Fever >38
o Immunological phenomena (e.g. peripheral stigmata, Rheumatoid factor, glomerulonephritis)
o Vascular findings (e.g. Janeway lesions, major embolic infarct, intracranial haemorrhage)
o Microbio evidence not fulfilling major criteria
o Risk factors (e.g. IVDU, RHD, congenital heart disease)

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12
Q

List some risk factors for infective endocarditis?

A
  • IVDU
  • Dental surgery
  • Immunocompromised- HIV, malignancy/chemo
  • Prosthetic valve
  • Rheumatic heart disease
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13
Q

How would you treat infective endocarditis?

A

Empirical Rx:

1) Benzylpenicillin (1.8g IV QD) –cover strep
2) Flucloxacilin (2g IV QD)- cover staph
3) Gentamicin (4-6mg/kg, based on renal function)- cover gram neg bacilli

  • If MRSA risk (IVDU, prosthetic valve, pacemaker): Vancomycin and Gentamicin
  • If penicillin allergy: Cephazolin (cephalosporin class)
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14
Q

List some possible complications of infective endocarditis?

A
Cardiac:
- valve dysfunction 
- conduction defects (damage AV node fibers or Bundle of HIS)
- myocotic aneurysm
- suppurative pericarditis
- HF
Septic emboli:
- neuro (embolic stroke, intracerebral haemorrhage, metastatic abscess)
- lung (septic PE)
- kidney (infarction, metastatic abscess)
- spleen (infarction, metastatic abscess)
Immune response:
- glomerulonephritis (Ig GMB deposition)
- AKI
- CKD (immune-complex mediated GN)
Metastatic infection
- vertebral osteomyelitis
- septic arthritis
- psoas abscess
Sepsis
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