Infective endocarditis Flashcards

1
Q

What are symptoms of acute infective endocarditis?

A

1) spiking fevers
2) tachycardia
3) fatigue
4) progressive damage to cardiac structures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What valves are usually affected?

A
Aortic	5-36%
Mitral	28-45%
Aortic and mitral	0-35%
Tricuspid	0-6%
Pulmonary	<1%

Reduction in rheumatic heart disease → less mitral valve endocarditis seen

Increase in IV drug use → more tricuspid valve endocarditis seen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Who is at risk of infective endocarditis?

  • high risk
  • moderate risk
  • low risk
A

High risk

  • Prosthetic valves (s aureus, coagulase –ve S)
  • Cyanotic congenital heart disease
  • Intravenous drug use (s. aureus)
  • Previous infective endocarditis

Moderate risk

  • Valvular heart disease - Aortic disease; Mitral regurgitation
  • Congenital heart disease - VSD; Bicuspid aortic valve; PDA, coarctation
  • HOCM

Low risk

  • Atrial septal defect
  • Mitral calcification
  • Intra-cardiac electronic devices ICED – e.g. pacemakers
  • (CABG = no risk)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What may happen to structures in the heart?

A

valve leaflet may be destroyed / may have hole in valve

chordae tendineae may rupture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What organisms causes endocarditis?

A

40% Staphylococci – grape like clusters

30% Streptococci – cocci chain

11% Enterococci

2% Fungi

2% polymicrobial

10% culture negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What organisms should you suspect in native valve endocarditis?

A

enterococci
viridans group streptococci
staph aureus

Rarely HACEK - haemophilus actinobacillus, cardiobacterium, eikenella, kingella

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What organisms should you suspect in IVDU?

A

Fungi - candid, aspergillus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What organism should you suspect in SLE?

A

Libman-Sacks endocarditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

When should you suspect endocarditis?

A

Fever + new murmur = endocarditis until proven otherwise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How would sub-acute and acute presentation of infective endocarditis differ?

A

Sub-acute
• Gradual onset fever, fatigue, sweats, weight loss
•Usually with known congenital or valve disease
•May have clubbing, splenomegaly, haematuria
•May have stigmata of chronic endocarditis
•Classically caused by streptococci

Acute
•Rapid onset, severe febrile illness
•Cardiac murmur
•Stigmata of chronic endocarditis absent
•May present with emboli, cardiac failure, and/or renal failure
•Stroke, septic joint, splenic infarct
•Highly pathogenic organisms e.g. Staph aureus

Common features:
Non-specific
•Malaise
•Fever - 96% of cases
•Sweating
•Anorexia
•Weight loss (malignancy is often  suspected)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What classical signs would you expect to find on examination

A

Splinter haemorrhages

  • Linear haemorrhages
  • Similar to peripheral petechiae
  • Distal nail bed
  • Nonspecific – may be due to trauma

Osler’s nodes

  • Painful, peripheral nodulae haemorrhagic or erythematous lesions of distal phalanges
  • Due to immune complex deposition
  • May be seen in systemic vasculitis

Janeway lesions

  • Similar appearance and pathogenesis to Osler nodes
  • Located on palms and soles
  • NOT painful
  • Can be transient
  • May ulcerate or become haemorrhagic

Mucosal petichieae - Can be seen when pull eyelid down

Roth’s spots

  • Small haemorhaggic lesion with central pallor
  • May be seen in conditions associated with vasculitis (e.g. SLE)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Splinter haemorrhages

A
  • Linear haemorrhages
  • Similar to peripheral petechiae
  • Distal nail bed
  • Nonspecific – may be due to trauma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Osler’s nodes

A
  • Painful, peripheral nodulae haemorrhagic or erythematous lesions of distal phalanges
  • Due to immune complex deposition
  • May be seen in systemic vasculitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Janeway lesions

A
  • Similar appearance and pathogenesis to Osler nodes
  • Located on palms and soles
  • NOT painful
  • Can be transient
  • May ulcerate or become haemorrhagic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Mucosal petichieae

A
  • Can be seen when pull eyelid down
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Roth’s spots

A
  • Small haemorhaggic lesion with central pallor

- May be seen in conditions associated with vasculitis (e.g. SLE)

17
Q

How would you diagnose infective endocarditis?

A

Definite IE
Pathological criteria
Microorganisms demonstrated by culture or histological examination of vegetation, a vegetation that has embolized, or an intracardiac abscess specimen; or pathological lesions; vegetation or intracardiac abscess confirmed by histological examination showing active endocarditis

Clinical criteria
2 Major criteria, 1 major criterion and 3 minor criteria, or 5 minor criteria

Possible IE
-1 Major criterion and 1 minor criterion, or 3 minor criteria

MAJOR

  • Blood Cultures with typical organisms
  • Evidence of endocardial involvement – abnormal Echo or new valvular regurgitation

MINOR

  • Predisposing condition (e.g. valvular abnormality, CHD) or IVDU
  • Fever (common and non specific)
  • Immunological phenomena e.g. vasculitis, rash, splinters, Roth spots
  • Vascular phenomena e.g. Embolism; Janeway lesions
  • Other microbiological criteria
18
Q

What investigations should you do in infective endocarditis?

A

History, clinical exam, haematuria

FBC→ normochromic, normocytic anaemia, neutrophilia, high ESR/ CRP, positive rheumatoid factor
- Blood cultures → 3 sets at different times from different sites at peak of fever (1 hour apart)

ECG→ prolonged PR interval/ AV block if aortic root abscess

ECHO → valvular, mobile vegetations.
- TOE more sensitive for mitral lesions/aortic root abscess

CXR→ pulmonary oedema, cardiomegaly

Sometimes specific microbial tests
- E.g. suspected Q fever

Urinalysis→ RBC/WBC casts, proteinuria from septic emboli

19
Q

When should you suspect infective endocarditis?

A
  1. A febrile illness and a murmur of new valvular regurgitation;
  2. A febrile illness, a pre-existing at-risk cardiac lesion (see Figure 2) and no clinically obvious site of infection;
  3. A febrile illness associated with any of:
    - Predisposition and recent intervention with associated bacteraemia,
    - Evidence of congestive heart failure,
    - New conduction disturbance
    - Vascular or immunological phenomena: embolic event, Roth spots, splinter haemorrhages, Janeway lesions, Osler’s nodes,
    - A new stroke,
    - Peripheral abscesses (renal, splenic, cerebral, vertebral) of unknown cause;
  4. A protracted history of sweats, weight loss, anorexia or malaise and an at-risk cardiac lesion;
  5. Any new unexplained embolic event (e.g. cerebral or limb ischaemia);
  6. Unexplained, persistently positive blood cultures;
  7. Intravascular catheter-related bloodstream infection with persistently positive blood cultures 72 h after catheter removal
20
Q

What conditions places someone at risk of infective endocarditis?

A
  • Valvular heart disease with stenosis or regurgitation
  • Valve replacement
  • Structural congenital heart disease, (even if surgically corrected or palliated)
  • Structural conditions, but excluding isolated atrial septal defect, fully repaired ventricular septal defect or fully repaired patent ductus arteriosus, and closure devices that are judged to be endothelialized
  • Previous infective endocarditis
  • Hypertrophic cardiomyopathy
  • Intravenous drug users
  • Patients with implantable cardiac electronic devices e.g. pacemakers
21
Q

What is the guidelines on blood cultures in infective endocarditis?

A
  • Blood cultures should be taken prior to starting treatment in all cases.
  • Aseptic technique - reduce risk of contamination with skin commensals
  • In patients with chronic or subacute presentation, 3 sets of blood cultures should be taken from peripheral sites with ≥6 h between them prior to commencing antimicrobial therapy.
  • In patients with suspected IE and severe sepsis or septic shock at time of presentation, 2 sets of optimally filled blood cultures should be taken at different times within 1 h prior to commencement of empirical therapy
  • Once on antibiotics - antibiotic therapy may need to be stopped for 7–10 days before blood cultures will become positive again. Patients often too ill to do this.
  • Include risk factors for endocarditis with clinical details on request - prosthetic valves; ICEDs as alter interpretation of results for possible skin contaminants.
22
Q

What should you do if you suspect infective endocarditis in a patient?

A

Ask for cardiology opinion

  • do not request an ECHO
23
Q

How long does antibiotic treatment usually last?

A

4-6 weeks of IV antibiotics

24
Q

Blind therapy: native/prosthetic implanted

A

Blind therapy: native/prosthetic implanted >1yr→ ampicillin, flucloxacillin, gentamicin (if Gram -ve, meropenem and vancomycin)

25
Q

Blind therapy: prosthetic

A

Blind therapy: prosthetic→ vancomycin, gentamicin, rifampicin

26
Q

Treatment for Staph native

A

flucloxacillin > 4 weeks

27
Q

Treatment for Staph (prosthetic)

A

Staph (prosthetic)→ flucloxacillin, gentamicin, rifampicin >6weeks

28
Q

Treatment for Strep (+ alpha haem)

A

Strep (+ alpha haem) → benzylpenicillin 1.2g/4h IV 4-6weeks/ if less sensitive→ benzylpenicillin+gentamicin, then penicillin alone 2 weeks or vancomycin

29
Q

Treatment for Enterococci

A

Enterococci→ amoxicillin+gentamicin or vancomycin+gentamicin (4-6 weeks)

30
Q

Treatment for HACEK

haemophilus actinobacillus, cardiobacterium, eikenella, kingella

A

HACEK→ ceftriaxone 4 weeks (native), 6 weeks (prosthetic)

31
Q

Treatment for Fungal

A

Fungal → candida (amphotericin), aspergillus (voriconazole)

32
Q

Possible complications of infective endocarditis

A

Cardiac
Heart failure
• Valvular destruction causing AR, MR, fistulae occurs in both acute or subacute endocarditis
• Fistula
• Staph aureus aortic & tricuspid valve endocarditis in end-stage renal disease
• Fistula may extend from base of coronary cusp to ventricle just below septal cusp of tricuspid valve
Cardiac abscesses
• TOE best Investigation
• Most require surgery
• Aortic root abscess can cause heart block

Extra-cardiac
Systemic arterial embolism
• In over 20 %, usually CNS
• Right sided endocarditis → emboli go to lungs (PE)
• Caution – patient with ICED and ‘recurrent chest infections’ – may be recurrent pulmonary emboli from right sided endocarditis
Extra-cardiac abscesses
• Septic infarction or bacterial seeding
• Vertebral Osteomyelitis and disciitis are common
Mycotic aneurysms
Renal complications
• Glomerulonephritis, emboli, low Cardiac output, medication
• Renal infarction
• Area of low attenuation of kidney extending to renal cortex → indicate renal infarction due to septic embolization of kidney.
• Embolization of renal arteries very common due to large volume of renal blood flow, but asymptomatic unless emboli are large and renal infarction is present.
• Flank pain, hematuria, pyuria, and bacteriuria
• Renal insufficiency due to embolization is uncommon.
Neurological complications → Emboli, haemorrhage, vasculitis, abscess
Splenic infarction → Splenic emboli common due to high blood flow

33
Q

Indications for surgery in infective endocarditis

A

• Emergency = same day / urgent within 1-3 days
• Heart failure
• Aortic or mitral IE with:
o Severe acute regurgitation or valve obstruction causing refractory pulmonary oedema/shock (emergency)
o Fistula into a cardiac chamber or pericardium causing refractory pulmonary oedema/shock (emergency).
o Severe acute regurgitation or valve obstruction & persisting heart failure or ECHO signs of poor haemodynamic tolerance (urgent).
o Severe regurgitation and no heart failure (elective).
• Uncontrolled infection
o Locally uncontrolled infection - abscess, false aneurysm, enlarging vegetation (urgent).
o Persisting fever & +ve blood culture for ≥10 days after commencing appropriate antimicrobial therapy (urgent).
o Infection caused by fungi or multiresistant micro organisms (urgent/elective).
• Prevention of embolism
o Aortic or mitral IE with large vegetations (>10 mm) resulting in ≥1 embolic episodes despite appropriate antibiotic therapy (urgent).
o Aortic or mitral IE with large vegetations (>10 mm) and other predictors of complicated course like heart failure, persistent infection or abscess (urgent).
o Isolated very large vegetations >15 mm (urgent).

34
Q

When should you consider removing ICED in infective endocarditis?

A

• Complete and early (ASAP, but not > 2 weeks after diagnosis) removal of an infected ICED system (generator and all leads) combined with appropriate antimicrobial therapy =most effective, safe and efficient treatment option.

35
Q

Is prosthetic valve or native valve endocarditis associated with a worse prognosis?

A

prosthetic valve

36
Q

What is the guidance on antibiotic prophylaxis for procedures on patients at risk of endocarditis?

A
  • UK - Antibiotic Prophylaxis not recommended for procedures on patients at risk of endocarditis BUT may need to adjust usual antibiotics for some procedures. E.g. (If risk of infective endocarditis & receiving antimicrobial therapy as undergoing a GI procedure at a site where suspected infection → should receive antibiotic that covers organisms causing infective endocarditis.)
  • Antibiotic prophylaxis is controversial: European and American guidelines are: “May still be considered for those at highest risk e.g. Prosthetic valves, Previous endocarditis, Cyanotic congenital heart disease”