Transcript INFECTIVE ENDOCARDITIS

INFECTIVE
ENDOCARDITIS
Michael Sales
20/02/13
Infective Endocarditis
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Colonisation or invasion of heart valves or mural endocardium
by microbes
Formation of vegetations composed of thrombotic debris &
organisms
Often associated with destruction of underlying cardiac tissue
Aorta, aneurysmal sacs, other blood vessels & prosthetic
devices can be involved
Most cases bacterial
Acute IE
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Infection of previously normal heart valve by a highly virulent
organism that produces necrotising, ulcerative, destructive
lesions
Difficult to cure with Abx & usually require Sx
Death can occur within days to weeks despite Rx
Subcute IE
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Organisms are usually of lower virulence
Cause insidious infections of deformed (native) valves that are
less destructive
Can take prolonged course: weeks to months
More amenable to treatment with antibiotics
Aetiology & Pathogenesis
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Incidence 1.7-7.2 cases per 100 000
Female to male 1:2
Median age has increased from 30-40 to 47-69 yrs
Rheumatic HD is no longer the major risk factor in Western
countries
Aetiology & Pathogenesis
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More common causes now:
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Mitral valve prolapse
Degenerative calcific valvular stenosis
Bicuspid aortic valve
Prosthetic valves
Congenital defects
Aetiology & Pathogenesis
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Majority of cases of IE are caused by gram +ve bacteria
Staphylococcus aureus is now more common (31-54%) than
oral Streptococci
MSSA is more frequent in community-acquired IE, infects
mainly native valves & is associated with bacteraemia of
unknown origin
MRSA is more related to nosocomial infection, wound
infection, permanent IV catheters or surgery in previous 6/12
Aetiology & Pathogenesis
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Strep viridans is now less common (12-26%) but difficult to
isolate & confers partial resistance to ABx
Coag -ve Staph were main cause of prosthetic valve
endocarditits in the past, esp within first 6-12/12 after valve
surgery, MRSA is now more common
Aetiology & Pathogenesis
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Enterococci
HACEK group:
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Haemophilus group
Actinobacillus group
Cardiobacterium hominis
Eikenella corrodens
Kingella kingae
All commensals in the oral cavity
Other Causes
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Candida & Aspergillus species cause the majority of fungal IE
(1-3% of IE)
Patients with IVDU, prosthetic valve & long-term CVC are
more likely to have fungal IE: needs to be considered in
presence of bulky vegetations, metastatic infection, perivalvular
invasion, or embolisation to large blood vessels despite -ve BC
In 10-15% of all cases of endocarditis no organism can be
isolated from BC (“culture-negative” endocarditis)
Other Causes
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Whenever BC -ve IE is suspected other organisms such as
Coxiella burnetti, Legionella spp, Brucella spp, Bartonella spp
&, Chlamydiae spp, must be considered
Aetiology & Pathogenesis
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The most common factors predisposing to IE are those that cause
bacteraemia:
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Dental/surgical procedures
Needle sharing amongst IVDU
Breaks in skin
The risk in those with predisposing factors (eg valve
abnormalities) can be lowered by using prophylactic Abx
however the use of prophylactic Abx is no longer recommended
(discussed further later)
Morphology
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Presence of friable, bulky, potentially destructive vegetations
containing fibrin, inflammatory cells & infective organism (ie
bacteria, fungi) on heart valves
Aortic & mitral most common sites
Right heart more common in IVDU
Vegetations can be single or multiple & may involve more than
one valve
Vegetations can erode into underlying myocardium producing
abscesses (ring abscess)
Morphology
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Emboli can break off vegetations causing abscesses at distant
sites where they lodge leading to sequelae such as septic
infarcts or mycotic aneurysms
Vegetations of subacute endocarditis are associated with less
valvular destruction than acute endocarditis
Gram +ve bacteria are particularly resistant to pts innate
antibacterial activity (eg complement) which facilitates the
adhesion & formation of vegetations
Morphology
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When the left heart is involved vegetations most often develop
on the ventricular aspect of the aortic valve & atrial surface of
mitral valve, usually along the valve leaflets
Septic embolism has usually occurred before diagnosis
Up to 30% of patients have renal or splenic infarcts at the time
of diagnosis
Septic emboli can also occur in the heart, brain, intestine &
other large organs
Diagnosis
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The modified Duke criteria based on clinical, microbiological
& echo findings providing high sensitivity & specificity
(~80%) for diagnosis of IE when applied to patients with native
valve IE with +ve BC
Modified Duke Criteria
Major Criteria:
Posititive blood cultures
 Positive echocardiogram for IE defined as
 Oscillating intracardiac mass
 Intracardiac abscess
 New partial dehiscence of prosthetic valve
Minor Criteria:
Predisposition such as a heart condition or IV drug use
Fever
Vascular phenomena or immunological phenomena such as major arterial emboli,
septic pulmonary infarcts, mycotic aneurysm, intracranial haemorrhage, conjunctival
haemorrhage, & Janeway lesions
Other microbial evidence such as PCR, serological tests, or a positive blood cuture but
does not meet a major criterion
Diagnosis
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The dx is confirmed in presence of 2 major criteria, 1 major + 2
minor or 5 minor criteria
IE considered in presence of 1 major + 1 minor or 3 minor
Clinical Features &
Diagnosis
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The modified Duke criteria have low sensitivity when BC -ve,
infection affecting prosthetic valve/pacing system & when IE
effects right heart
It’s not always useful for rapid diagnosis: one of its major
criteria includes +ve blood cultures
Clinical Features
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Fever, chills, weakness, lethargy, weight loss, flu-like illness
(not always present)
Longstanding IE (rarely seen now with earlier diagnosis):
splinter haemorrhages, Janeway lesions, Osler nodes, Roth
spots
Murmurs are present in 90% of patients with left sided IE
Splinter Haemorrhages
Janeway Lesions
Osler Nodes
Roth Spots
Clinical Features
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In IVDU right sided IE usually affect the tricuspid valve &
occasionally the pulmonary valve, instead of systemic issues
pulmonary embolism is the most important complication which
can evolve into:
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Pulmonary infarction
Pulmonary abscess
Bilateral pneumothoraces
Pleural effusion
Empyema
Clinical Features
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The severity of valvular destruction depends on virulence of
infecting organism & infection duration
Heart failure can be the initial presentation
Micro
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+ve BC still the best method for identifying the causative agent:
considered a major diagnostic criteria
BC are +ve in ~80% of cases
BC -ve in cases of intracellular or fastidious pathogens or after
prior Abx treatment
BC are important in suspected IE (eg T > 38, new regurgative
murmur, hx of valvular disease, IVDU): in cases where Abx
have been commenced prior to BC the recovery rate is only ~
35-40%
Micro
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It is recommended to draw 3 sets of cultures
Culture -ve IE delays diagnosis + initiation of treatment/correct
treatment
Using PCR has been proposed in these cases
PCR of excised valve tissue or embolic material should be
performed in culture -ve IE (in cases of valve surgery or
embolectomy)
Echo
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Important non-invasive technique for diagnosis & management
Sensitivity of TTE ranges from 45-60%
TOE offers better quality & sensitivity ranges from 90-100%, it
is necessary whenever perivalvular complications or mitral
valve involvement is suspected
Echo
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Findings:
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Vegetation (hallmark lesion of IE): mobile echodense
mass attached to valvular leaflets or mural endocardium.
Sensitivity TTE 75% TOE 90%
Periannular abscess
New dehiscence of valvular prosthesis
Echo Findings
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~10% of IE involves right side of heart: most commonly the
triscupid valve alone (98%), although the pulmonary valve &
Eustachian valve (junction of IVC & RA) can be involved
Isolated right sided involvement is well detected by TTE & in
those cases a TOE isn’t necessary
However ~15% IVDU associated IE affects left-sided valves &
a TOE should be considered
Echo Findings
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An abscess usually affects the aortic root & presents as a
perivalvular zone of reduced echo density without blood flow.
TTE (45-50%) TOE (>90%)
Important because the diagnosis of an abscess is an indication
for early surgery
Aortic/mitral regurg is secondary to valvular necrosis,
perforation or prolapse
~50-60% of pts with IE develop HF secondary to valvular
destruction & require early surgery (mortality without surgery
~80%)
Echo Findings
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Vegetation size & mobility is important
Stroke complicates 20-40% of left-sided IE & is the second
most common cause of death
*Vegetation > 10mm &/or high vegetation mobility are
associated with increased embolic risk, & early surgery
(within 1/52 of dx) is associated with improved long-term
outcomes through reduction in systemic embolic events*
If vegetations are small or have already embolised, echo can
provide false -ve results in ~15%. When suspicion is high a
TOE can be repeated in 7-10 days
Echo
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In the emergency department bedside USS is starting to be used
in patients suspected of IE to help speed up diagnosis: it has its
limitations (should be used to rule in IE not rule out) & must be
followed up with a formal USS
Prophylaxis
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2008 National Institute of Clinical Excellence (NICE) produced
guidelines re: antimicrobial prophylaxis for IE in pts
undergoing interventional procedures
The guidelines suggest there is weak evidence to support
routine preop Abx for pts at risk of IE
They state risk of allergic reaction, cost & resistance
implications from Abx overuse
Therefore the routine use of Abx prophylaxis is no longer
recommended
Prophylaxis
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However in the case of infection at the operative site, Abx
prophylaxis is still recommended in high-risk patients eg:
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Acquired valvular HD
Previous valve replacement
Structural congenital HD (excluding repaired ASD, VSD
or PDA)
Antibiotics
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Empirical treatment; flucloxacillin & gentamicin are the usual
first line
Adjusted according to MCS
Vancomycin is used in pts with intracardiac prosthetic material
or suspected MRSA
Benzylpenicillin is the first choice for Streptococcus or
Enterococcus penicillin-susceptible strains
For vanc-resistant MRSA: teicoplanin, lipopeptide daptomycin
or oxazilidones (linezolid) is recommended
Fungal IE
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Usually requires surgery
Amphotericin B doesn’t penetrate well into vegetations
however is used successfully against Candida endocarditis
Fluconazole is a fungistatic & only active against Candida spp
Caspofungin is usually fungicidal for Candida spp but its
penetration into vegetations is unknown
Treatment Course
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IV Abx is normally continued for 4-6 weeks, with the aim of
sterilising the vegetations
ID should be involved in BC -ve IE
Surgery
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Antimicrobial therapy can only offer curative treatment in
~50%
The other 50% require surgery
The surgical goal is valve repair but most require valve
replacement
Pts with IE + large vegetations, intracardiac abscess (9-14%) or
persisting infection (9-11%) almost always require surgery
Surgery
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Anaesthetic can be complicated secondary to haemodynamic
instability
Mitral or aortic regurg particularly challenging
Induction often complicated by hypotension despite
hyerdynamic left ventricle & hypoxaemia secondary to severe
pulmonary oedema
Some pts may develop acute RV dysfunction & severe
tricuspid regurg
These pts require arterial pressure & CVP monitoring & may
require inotropes/vasopressors
Surgery
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Pts with peri-annular abscess have higher risk of para-valvular
regurgitation & valve dehiscence after OT
Current IE perioperative mortality is 5-15%
If sepsis is under control the mortality is similar to non-infected
valve replacement
Surgery
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Most common complications:
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Persistent septic shock
Coagulopathy
Acute renal failure
Stroke
Refractory heart failure
Conduction abnormalities
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Summary
Challenging diagnosis therefore diagnosis often delayed
Need to have a high index of suspicion: esp high risk pts
Clinical examination is still very important
Cultures are extremely important for diagnosis/treatment
The use of TTE/TOE is vital for Dx & Tx planning
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Bedside USS is now being used for rapid assessment in ED
Treatment needs to be started early to reduce morbidity/mortality
Many pts require surgical intervention
Pts can be haemodynamically unstable peri-operatively
ID involvement is useful esp in BC -ve IE
References
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Martinez, G., Valchanov, K., Infective Endocarditis, Continuing Education in
Anaesthesia, Critical Care & Pain, 2012; 12:3
Kumar., Abbas., Fausto., Aster., Robbins and Cotran Pathological Basis of Disease,
8th Edition, 2010
Deng, H., Ma, Y., Zhia, H., Miao, Q., Surgical valve repair of isolated pulmonary
valve endocarditis, Interactive Cardiovascular and Thoracic Surgery, 2013; 16: 384386
Seif, D., Meeks, A., Mailhot, T., Perera, P., Emergency department diagnosis of
infective endocarditis using bedside emergency ultrasound, Clinical Ultrasound
Journal, 2013; 5:1
Kang, D., Kim, s., Yun, S., Choo, S., Song, J., Sohn, D., Early Surgery versus
conventional treatment for infective endocarditis, The New England Journal of
Medicine, 2012; 366: 2466-73
References
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Wikipedia (images)
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Dermnet.nz (images)
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Beaulieu, A., Rehman, H., Janeway Lesions, Canadian Medical Association Journal,
2010; 182:10 (images)