Infetive endocarditis Flashcards

1
Q

what is infective endocardittis?

A

Infection of the
endocardium
(endothelial lining) of
the heart
 Usually occurs on the
heart valves
 Can involve septal
defects and mural
surfaces and prosthetic
devices(pacemaker
wires)

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2
Q

pathogenissi?

A

 Endothelium becomes damaged by
- Trauma
- Congenital defects
- Previous disease
 microorganisms adhere to the
endothelial surface
 Triggers an inflammatory and immune
response

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3
Q

vegegation path

A
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4
Q

predisposing factors

A

 Heart defects
- Congenital
(VSD, biscupid AV, prolapsed MV, (ASD))

 Acquired

  • Rheumatic heart disease
  • Atherosclerotic degeneration
  • Valve replacement (prosthetic, homograft)

 Prosthetic devices

  • Intravenous long lines
  • Pacemaker wires

 Others
- Intravenous drug abuse

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5
Q

site

A

 Maximum deposition of thrombus bacteria
occurs at sites of turbulent flow
- eg when blood is driven from a high to a low
pressure area
AV > MV > TV > PV
 Exceptions
- Rheumatic heart disease predisposes infection of
the MV
- IV drug abuse (mainlining) and intravenous lines
predispose the right side of the heart

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6
Q

causative organisms

A
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7
Q

endocarditis

A

 Sometimes referred to as
- Acute
(Rapidly fulminant course with death occurring within
days – weeks)
- Subacute (SBE)
(Indolent and prolonged course)
 Based on progression of untreated disease as
determined by the virulence of the organism
 Ignores frequent overlap of syndromes
 Classification based on aetiology more
appropriate beacause it has implications for
management and treatment

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8
Q

clinical findings

A

 Fever

 Heart murmur (new or changing)

 Peripheral signs

  • splinter haemorrhages
  • petechiae
  • Osler’s nodes
  • Janeway lesions
  • Roth spots

 Systemic emboli

 Splenomegaly

 Haematuria

 Anaemia

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9
Q

lab findings

A

 Blood cultures
- Positive in 90% of cases

 Non-specific
- Evidence of infective process
( Raised WBC, anaemia, raised CRP/ESR)
- Evidence of immune complex disease
( Low complement levels, haematuria)

 Cardiological

  • Echocardiography
  • ECG
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10
Q

culture negative endocaritis

A

 Causes

  • Previous antibiotics
  • Non-culturable
    (Rickettsiae, Chlamydiae)
  • Fastidious organisms
    (Nutritionally dependent, Slow-growing)
  • Right-sided disease
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11
Q

duke criteria major

A

major

 Positive blood cultures
- Typical organism (eg staph/strep) from 2 sets in
absence of a focus
- Persistent bacteraemia with organism from
( 2 sets drawn >12 hours apart, 3 out of 4 sets drawn one hour apart)

 Evidence of endocardial involvement
- New valvular regurgitation
- Positive echocardiogram
(Oscillating intracardiac mass, Abscess)

  • New or partial dehiscence of prosthetic valve
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12
Q

duke criterai minor

A

 Predisposition
- Heart defect, prosthetic valve, drug abuse

 Fever

 Vascular phenomena
- Haemorrhage, emboli, infarcts

 Immunological phenomena
- Splinters, Osler’s nodes, Roth spots

 Blood cultures not meeting major criteria

 Echo abnormality not meeting major criteria

 Serological evidence of infection

 (Raised CRP)

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13
Q

duiagnsis

A

 Definite histological
- Pathologically confirmed by culture and
histology of specimen

 Definite clinical

  • 2 major criteria
  • 1 major and 3 minor criteria
  • 5 minor criteria
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14
Q

marantic vegetation

A

Marantic endocarditis, also known as non-bacterial thrombotic endocarditis (NBTE), is the deposition of small sterile vegetations on valve leaflets.
The previous term for nonbacterial thrombotic endocarditis (NBTE) was marantic endocarditis, from the Greek marantikos, meaning “wasting away.”[1]
The term “Marantic endocarditis” is still sometimes used to emphasize the association with a wasting state[2] such as cancer.[3]

Marantic vegetations are often associated with previous rheumatic fever.
Other risk factors include:
hypercoagulable states,
mucin-producing adenocarcinomas, (most commonly associated with pancreatic adenocarcinomas)
lupus and
trauma (e.g., catheters).

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15
Q

treatemtn

A

 Use cidal antibiotics in synergic combinations
 Use parenteral antibiotics for a minimum of 2
weeks (often 4 weeks required) before
switching to oral regimens for total of 6 weeks
 Identify the organism wherever possible and
determine MICs
Synergic: the activity of the combination of antibiotics is greater
than the sum of the individual activities
MIC: minimum inhibitory concentration. The lowest
concentration of antibiotic required to inhibit growth of the
organism in vitro

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16
Q

antibiotic regime

A
17
Q

aminoglycoside toxicity

A

 50% cases associated with endocarditis

 Ototoxicity (vestibular followed by cochlear)
is irreversible

 Nephrotoxicity is usually reversible

 Predisposing factors

  • Long course, total cumulative dose
  • Age, pre-existing renal damage
  • Other drugs: cephalosporins, loop dieretics

 Must monitor drug levels, creatinine and
audiovestibular function

18
Q

when to perfrom surgery

A

 Refractory failure
 Acute heart failure
 Aortic root abscess
 Major emboli
 Fungal aetiology
 Heart block
 Large vegetations
Indication for surgery

19
Q

structural conditions that make you at risk

A

• acquired valvular heart disease with
stenosis or regurgitation
• valve replacement
• structural congenital heart disease
• hypertrophic cardiomyopathy
• previous infective endocarditis

20
Q

do not offerf

A

Do not offer antibiotic prophylaxis against infective endocarditis:
 to people undergoing dental procedures
 to people undergoing non-dental procedures at the following
sites:
 – upper and lower gastrointestinal tract
 – genitourinary tract; this includes urological, gynaecological
and obstetric procedures, and childbirth
 – upper and lower respiratory tract; this includes ear, nose
and throat procedures and bronchoscopy.

 Chlorhexidine mouthwash as
prophylaxis against infective
endocarditis to people at risk of
infective endocarditis undergoing dental
procedures.

21
Q
A