INFECTIVE ENDOCARDITIS
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Transcript of INFECTIVE ENDOCARDITIS
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INFECTIVE ENDOCARDITIS
Michael Sales20/02/13
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Infective Endocarditis• 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
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Acute IE• 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
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Subcute IE• 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
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Aetiology & Pathogenesis• 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
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Aetiology & Pathogenesis• More common causes now:
• Mitral valve prolapse
• Degenerative calcific valvular stenosis
• Bicuspid aortic valve
• Prosthetic valves
• Congenital defects
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Aetiology & Pathogenesis• 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
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Aetiology & Pathogenesis• 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
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Aetiology & Pathogenesis• Enterococci
• HACEK group:
• Haemophilus group
• Actinobacillus group
• Cardiobacterium hominis• Eikenella corrodens• Kingella kingae
• All commensals in the oral cavity
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Other Causes• 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)
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Other Causes• Whenever BC -ve IE is suspected other organisms such as
Coxiella burnetti, Legionella spp, Brucella spp, Bartonella spp &, Chlamydiae spp, must be considered
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Aetiology & Pathogenesis• The most common factors predisposing to IE are those that cause
bacteraemia:
• 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)
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Morphology• 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)
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Morphology• 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
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Morphology• 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
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Diagnosis• 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
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Modified Duke CriteriaMajor 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
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Diagnosis• 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
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Clinical Features & Diagnosis
• 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
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Clinical Features• 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
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Splinter Haemorrhages
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Janeway Lesions
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Osler Nodes
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Roth Spots
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Clinical Features• 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:
• Pulmonary infarction
• Pulmonary abscess
• Bilateral pneumothoraces
• Pleural effusion
• Empyema
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Clinical Features• The severity of valvular destruction depends on virulence of
infecting organism & infection duration
• Heart failure can be the initial presentation
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Micro• +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%
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Micro• 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)
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Echo• 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
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Echo• Findings:
• 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
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Echo Findings• ~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
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Echo Findings• 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%)
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Echo Findings• 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
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Echo• 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
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Prophylaxis• 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
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Prophylaxis• However in the case of infection at the operative site, Abx
prophylaxis is still recommended in high-risk patients eg:
• Acquired valvular HD
• Previous valve replacement
• Structural congenital HD (excluding repaired ASD, VSD or PDA)
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Antibiotics• 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
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Fungal IE• 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
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Treatment Course• IV Abx is normally continued for 4-6 weeks, with the aim of
sterilising the vegetations
• ID should be involved in BC -ve IE
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Surgery• 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
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Surgery• 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
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Surgery• 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
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Surgery• Most common complications:
• 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
• 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
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References• 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: 384-386
• 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
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References• Wikipedia (images)
• Dermnet.nz (images)
• Beaulieu, A., Rehman, H., Janeway Lesions, Canadian Medical Association Journal, 2010; 182:10 (images)