Endocarditis: DR Mumba

endocarditis
Dr Mumba
Outline
• Definition
• Classification
• Pathogenesis
• Diagnosis
• Treatment
• Prevention
Definitions
• Endocarditis refers to microbial infection of the endocardium
• 30% mortality with staphylococci, 14% with enterococci, 6% with
streptococci
Pathogenesis
• IE is characterized by microbial proliferation on the endothelium of
the heart
• IE typically occurs at sites of pre-existing endocardial damage
• Damaged heart valves are particularly susceptible
• Sterile sites of insult become the foci of fibrin and platelet
aggregations [thrombi] that are subsequently seeded by organisms in
the bloodstream
Pathogenesis
• Damage to the endothelial lining of the myocardium activates primary
and secondary hemostasis – in particular platelets become activated
and begin to aggregate
• Sites of endothelial damage attract these deposits of platelets and
fibrin that are vulnerable to colonization by blood-borne organisms
Pathogenesis
• The micro-organisms that attach to the fibrin/platelet aggregate
divide and form vegetations
• Vegetations are infected thrombi
Pathogenesis
• The avascular valve tissue along with fibrin and platelet aggregates
help to protect the proliferating organisms from host defense
mechanisms
• The avascular tissue and clot also impede antibiotic penetration of the
infected tissue
Pathogenesis
• However particularly virulent and/or aggressive organisms can cause
infection in previously normal heart tissue
• Staphylococcus aureus is one such organism
Organisms
• The causative organism is usually a bacterium, but may be a
rickettsial, chlamydial or fungal
• 80% gram positive cocci [mostly staphylococcus aureus/epidermidis
& streptococcus viridans]
• 10% enterococcus – cell wall agents are not bactericidal against
enterococci
• Toxic aminoglycosides must be added to the regimen throughout the
duration of therapy
Organisms
• 50% of all IE occurs on normal valves and is mostly caused by
staphylococcus
• Acute IE tends to follows an acute course [ADHF]
• IE afflicting abnormal valves tends to follow a sub acute course and is
most often due to streptococcus viridans [30 – 50%]
• Diphtheroids, microaerophilic streptococcus
Risk factors
• Intravenous drug users [IVDA] – right sided endocarditis
• Valvular heart disease [RHD]
• Health-care associated endocarditis- Indwelling catheters [dialysis
lines, PICC lines, Swan Ganz catheters etc.] pacemaker leads, CRT
devices, ICD leads, prosthetic valves [TAVR/TAVI]
Organisms
• IVDA associated endocarditis affects mostly normal tricuspid valve but
the left side may be affected as well
• IVDA- related endocarditis tends to be polymicrobial
• Typical organisms include Pseudomonas aeruginosa, candida species
Gram negative organisms
• Most common is pseudomonas aeruginosa
• HACEK group of Gram–negative organisms
• Slow growing fastidious [may take > 3 weeks to grow in culture]
• Haemophilus species
• Actinobacillus
• Cardiobacterium
• Eikenella
• Kingella kingae
Q fever endocarditis
• Coxiella burnetii
• Positive serology for coxiella is now considered a major criterion for
endocarditis
• Chlamydia
• Bartonella
• Candida, aspergillus, histoplasma
Risk factors
• Patent ductus arteriosus [PDA]
• Coarctation of the aorta [CoA]
• Ventricular septal defect [VSD]
• Rheumatic heart disease [RHD]
• Bicuspid aortic valve [BAV]
• Mitral valve prolapse [MVP]
• Prosthetic heart valves
Prosthetic valve endocarditis [PVE]
• PVE may be ‘early’ – acquired at the time of surgery or ‘late’ –
acquired subsequently haematogenously
• Early PVE carries a poor prognosis
Clinical features
• Signs of infection
• Cardiac lesions
• Immune complex deposition [Oslerian features]
• Thromboembolism
Oslerian features
Oslerian features
Osler’s node Janeway lesion
Diagnosis
• Modified Duke criteria for definitive diagnosis
• 2 major criteria
• 1 major + 3 minor criteria
• All 5 minor criteria
Major criteria
• Positive echo findings
• Vegetations
• Abscess / conduction abnormalities
• Prosthetic Valve dehiscence/ paravalvular leak
• Valve perforation / fistula formation
• Valve destruction / chordal rupture / new regurgitation
• Valve obstruction
• Pseudo aneurysm formation
Major criteria
• Microbiology
• Positive blood culture of typical organism in 2 separate cultures
• Persistently positive cultures >/= 3 >12 hours apart [or majority of 4
or more collected]
• Positive coxiella serology
• IgG titer >1:800
Minor criteria
• Echocardiography findings not meeting major criteria
• Microbiological criteria [Positive blood culture] not meeting major
criteria
• Fever - Temperature >38 C
• Vascular
• (Janeway’s lesions, emboli, Mycotic aneurysm)
Minor criteria
• Immunologic
• (Osler’s nodes, Roth’s spots, glomerulonephritis, positive rheumatoid
factor)
• Serological data supporting infection with an organism known to
cause endocarditis
• Predisposing heart condition or IVDU
Investigations
• Blood cultures
• Echocardiography
• CXR
• ECG – aortic root abscess may cause P-R prolongation, complete AVB
• Coxiella serology
• C- reactive protein
• FBC + DC
• U/E + creatinine, LFTs
Ancilliary tests
• Urinalysis
• Procalcitonin
• NT-pro BNP
echocardiography
• 65% of vegetation
• TTE picks vegetation > 2mm
• TEE pick 90%, Vegetation size up to 1.2mm
investigations
• Echocardiography
• TTE starting point for suspected native valve endocarditis
• Sensitivity 32% - 63%
• Specificity 98% - 100%
• TEE
• next step where TTE is nondiagnostic and endocarditis is still suspected
• First step in prosthetic valve evaluation
• Sensitivity 94 – 100%, specificity same as TTE
• Also enhanced detection of myocardial abscess, aneurysm and fistula
Blood cultures
• Positive culture for a typical organism from 2 or more samples taken
from separate sites > 1 hour apart
Principles of treatment
• The treatment of IE relies on the combination of prolonged
antimicrobial therapy and - in about half patients - surgical
eradication of the infected tissues
• Prolonged therapy with a combination of bactericidal drugs is
the basis of IE treatment
• Drug treatment of PVE should last longer (at least 6 weeks) than
that of native valve endocarditis (NVE) (2– 6 weeks).
Penicillin-sensitive Penicillin-resistant
Streptococcus Pen G or ceftriaxone x Pen G or ceftriaxone x 4 weeks

viridans 4/52, + gentamicin 80mg q 12h IV x
Then oral amoxicillin x 2 2 weeks
weeks [monitor gentamicin
levels/renal function]
Streptococcus Pen G or ceftriaxone x Pen G or ceftriaxone x 4 weeks

bovis 4/52, + gentamicin 80mg q12h IV x 2
Then oral amoxicillin x 2 weeks
weeks [monitor gentamicin levels &
renal function]
Penicillin allergy Vancomycin x 4 weeks

Treatment
Penicillin-sensitive Ampicillin x 4 – 6 weeks
Enterococcus [or amoxicillin 1g/6h] +
Gentamicin 80mg/12h IV x
4 – 6 weeks
Pen G 4-6 weeks +
Gentamicin 80mg/12h IV 4
-6 weeks
Penicillin allergy Vancomycin + gentamicin x
6 weeks
Treatment
Oxacillin –sensitive staphylococcus Nafcillin or Oxacillin x 6 weeks +/- 3 –
[MSSA] 5 days of gentamicin;
Acute endocarditis Flucloxacillin 2g q 6h for 6 – 8 weeks
+ gentamicin 80mg/12h IV for 5 days
Penicillin allergy Cefazolin x 6 weeks (Not anaphylaxis)
Oxacillin-resistant Vancomycin x 6 weeks

staphylococcus [MRSA]
HACEK endocarditis Cetfriaxone or ampicillin/sulbactam

or ciprofloxacin (ampicillin or
ceftriaxone allergy) x 6 weeks
ESC 2015 essential messgaes
• The indications and pattern of use of aminoglycosides have
changed
• They are no longer recommended in staphylococcal NVE
because their clinical benefits have not been demonstrated but
they can increase renal toxicity; and, when they are indicated in other
conditions, aminoglycosides should be given in a single daily dose
in order to reduce nephrotoxicity
Q fever endocarditis
• Coxiella burnetii -Doxycycline 100mg/12h PO indefinitely + CTX,
Rifampicin, or ciprofloxacin
Indications for surgery
• Persistent bacteremia despite optimal antimicrobial therapy
• Large [10mm] diameter hypermobile vegetations with increased risk of
embolism
• Heart failure due to valvular damage at any stage of the disease
• Abscess formation
• Repeated emboli
• Fungal endocarditis
• Unstable infected prosthetic valve
Complications
• Thromboembolism
• Stroke
• Arterial occlusions [gangrene]
• Sepsis
• Heart failure
• Valve regurgitation
• Valve destruction/ perforation
• Fistula formation
Septic pulmonary emboli
Complications
Prophylaxis
• Tooth extraction
• Bronchoscopy
• Endoscopy
• Urinary catheterization
• Bladder cystoscopy
• GIT e.g. Sclerotherapy of varices
pearls
• In 50% of cases the organism arises from the oropharynx
• A bicuspid aortic valve (BAV) is associated with an increased risk of
endocarditis, 20 – 25% of cases of AV endocarditis
• NB 50% of coarctations are associated with BAV
• Renal failure reverses with treatment of the endocarditis
• Valve replacement is indicated at all stages of treatment if LVF
develops
• Timing of blood cultures does not increase the yield of positive
cultures; 6 – 8 samples should be collected in the first 24 hours
Practice questions
• In congenital VSD if endocarditis develops, the left ventricular cavity is
usually involved T or F?

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endocarditis

Streptococcus Pen G or ceftriaxone x Pen G or ceftriaxone x 4 weeks

Streptococcus Pen G or ceftriaxone x Pen G or ceftriaxone x 4 weeks

Penicillin allergy Vancomycin x 4 weeks

Penicillin allergy Cefazolin x 6 weeks (Not anaphylaxis)

Oxacillin-resistant Vancomycin x 6 weeks

HACEK endocarditis Cetfriaxone or ampicillin/sulbactam

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