Infective Endocarditis Flashcards

1
Q

What are risk factors for infective endocarditis?

A
Prosthetic valves 
Valvular lesions (aortic >mitral) 
Congenital defects 
Invasive lines, pacemakers/ICDs
Recurrent bacteraemia (IVDU - tricuspid most affected; severe dental disease)
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2
Q

What causes infective endocarditis?

A

Acute forms

  • usually S.aureus
  • more often affecting healthy valves
  • most common in all groups (IVDU, prosthetic valves etc)

Subacute

  • usually Viridans streptococcal spp.
  • often following dental surgery involving infected gums, reproductive or genitourinary tract surgery or operations on the gastrointestinal tract
  • more often on previously damaged valves (often mitral)

(consider things like candida and aspergillus in the immunosuppressed, IVDU, cardiosurgical interventions/long term IV catheters)

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3
Q

What is the pathophysiology of infective endocarditis?

A

Localised infection - bacteraemia - colonisation on damaged valves - fibrin clot formation that encases the vegetation - valve destruction with loss of function

Mitral > aortic > tricuspid (thouhg common in IVDU) > pulmonary

Bacteria can also embolise - vessel occlusion with infarcts - to the brain is common (cerebral abscess formation)

Also formation of immune complexes against tissue antigens - glomerulonephritis

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4
Q

How does infective endocarditis present?

A
  • Fever* and chills
  • New murmur*, tachycardia or arrhythmias, signs of heart failure

General malaise, weakness, night sweats and weight loss

Dyspnoea, cough, pleuritic chest pain

Arthralgia, myalgia

Embolic phenomena

Splinter haemorrhages, Janeway lesions (painless palmar lesions), Osler’s nodes (painful, protruding, red points on palms and soles), Roth spots (on ophthalmoscopy)

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5
Q

How do you investigate infective endocarditis?

A

Bloods:

  • FBC
  • U+E
  • LFT
  • ESR/CRP
  • *Cultures = 3 sets from 3 sites at >1hr apart or during temp spikes, prior to commencing Abx EVEN IF patient is unwell

ECG:

  • Often non-specific
  • Monitor PR interval = prolonged by aortic disease

CXR:
- Pulmonary oedema

Echo:
- *Transoesophageal > transthoracic in terms of sensitivity at picking up valvular vegetations

CTPA:
- If septic PE suspected + ?aortic root abscess

Urine dip:
- Blood +/- protein

MRI head:
- Cerebral emboli

Dental/maxfax assessment:
- Regardless of initial source of bacteraemia

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6
Q

What is the modified Duke criteria for infective endocarditis?

A

Used to categorise diagnostic likelihood: - definite (2 Major/1M+3minor/5m)

  • possible (falling short of definite but not rejected)
  • rejected (alternative Dx made or resolution within <4d therapy)

Major/M:

1) Blood cultures
- +ve for typical organism on >2 separate occasions
- persistently +ve for organisms consistent with IE
- +ve for Coxiella burnetii or high antibody titre
2) Evidence of endocardial involvement = echo +ve

minor/m:

1) Predisposing heart condition or IVD use
2) Fever >38
3) Vascular signs (septic emboli, janeway, conjunctival haemorrhage)
4) Immunological signs (glomerulonephritis, oslers, roth spots, +ve rheumatoid factor)
5) Microbiological (bld culture +ve but not meeting Major)
6) Endocardiographic findings pointing to IE but not meeting Major

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7
Q

How do you manage infective endocarditis?

A

Early referral to cardiology and discussion with microbiology once cultures are back

Empirical Abx:

  • Consider risk factors, valve affected, local and individual flora and resistance patterns
  • Native valve = Vancomycin + ceftriaxone
  • Prosthetic = add gentamicin + rifampicin to the above

Antibiotics:
- Given long term - 2-6wks - therefore central line and long hospital stays are required

Supportive treatment:

  • Oxygen
  • Paracetamol
  • Antiemetics
  • Fluids
  • Diuretics (if CCF)

A significant portion of patients will require valve replacement:
- Heart failure, uncontrolled infection (debridement and replacement), prevention of embolism etc

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