Infective endocarditis
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Transcript of Infective endocarditis
INFECTIVE ENDOCARDITIS
DR. KALAIMANI
SENIOR RESIDENT
GENERAL MEDICINE
MGMCRI
Overview• Introduction
• Classification
• Etiology/Epidemiology
• Pathogenesis
• Clinical features
• Complications
• Diagnostic criteria
• Management
INTRODUCTION What is infective endocarditis?• infection of a native or prosthetic heart valve, the
endocardial surface, or an indwelling cardiac device
What is infective endarteritis?• arteriovenous shunts, arterio-arterial shunts (patent
ductus arteriosus), or a coarctation of the aorta
What is a vegetation?• is a mass of platelets, fibrin, microcolonies of
microorganisms, and scant inflammatory cells
CLASSIFICATION
Presentation
Acute(ABE)
Subacute
(SABE)
Valve characteristics
Native valve(NVE)
Prosthetic
valve(PVE)
Site involved
Rightsided
endocarditis
Left sided
endocarditis
Classification• Acute endocarditis:
– Toxic
– Develops within few days
– Valvular destruction and embolic manifestation
– Most commonly by Staph aureus
• Subacute endocarditis:
– Develops in weeks to months
– More associated with immunologic phenomena
– Mostly caused by streptococci and others
Etiology• Bacteria• Fungi
BacteriaOral cavitySkin
Upper resp tractStrep viridansStaphHACEK
GITStreptococcus gallolyticus
GUTEnterococci
Etiology/Epidemiology• Health care associated NVE S. aureus, CoNS,enterococci (
55% nosocomial onset, 45% community onset)
• PVE within 2 months of surgery nosocomial
• 68 – 85% of CoNS causing IE resistant to methicillin
• IVDU related IE most common S.aureus
• Polymicrobial endocarditis IVDU
• Negative culture 5 – 15% (1/3 to ½ due to prior antibiotics)
High velocity jet striking endotheliumFlow from high to low pressure chamber
Flow across a narrow orifice at high velocity
MalignancySLE
Antiphospholipid antibody syndromeDIC
Endothelial injury Hypercoagulable state
NBTE (sterile platelet fibrin )
+Bacteremia
Bacteria adhere to damaged endothelium and/or sterile platelet-fibrin nidus
Bacteria multiplyFurther platelet and fibrin binding
Local tissue destruction
Embolization Hematogenous spread
Antibody response
Growth of vegetation
PATHOGENESIS
• Marantic endocarditis - uninfected vegetations seen in patients with malignancy and chronic diseases
• Libman sacks endocarditis – bland vegetations in SLE
Organism enters bloodstream
Adherence
Infected vegetation
ADHESION MOLECULES
Clumping factorFss2Ace
Ebp pili
GlucansFim A
Staph aureus
Enterococcus fecalis Streptococci
Clinical manifestations
Clinical manifestations
Damage to intracardiac structures
Embolisation – Infection or infarction
Hematogenous infection – bacteremia
Circulating immune
complexes
Clinical presentation
Acute
• Βhemolytic streptococci
• S.aureus• Pneumococci
Subacute
• Viridans streptococci• Enterococci• CoNS• HACEK
Indolent• Bartonella• T. Whipplei• C.burnetti
ORGANISMS CAUSING ENDOCARDITIS
CLINICAL MANIFESTATIONSCardiac
• Heart murmurs• Congestive cardiac failure• Perivalvular abscess• Pericarditis• Heart block• Intracardiac fistulae• Myocardial infarction
Noncardiac
• Septic embolization - CNS - Skin
- Spleen - Kidneys
- Skeletal system• Immunological phenomenon -
Glomerulonephritis - Roth’s spots - Osler’s nodes
CLINICAL AND LAB FEATURES OF IE
EMBOLISATION
RIGHT LEFT
MODIFIED DUKE CRITERIA- MAJOR CRITERIA1. Positive blood culture
Typical microorganisms for IE from 2 separate blood cultures
Or Persistently positive blood culture,
defined as recovery of a microorganism consistent with infective endocarditis from:
Blood cultures drawn >12 h apart; or
All of 3 or a majority of ≥4 separate blood cultures, with first and last drawn at least 1 h apart
Or Single positive blood culture for Coxiella
burnetii or phase I IgG antibody titer of >1:800
2. Evidence of Endocardial involvement
Positive echocardiogram
Oscillating intracardiac mass on valve or supporting structures or in the path of regurgitant jets or in implanted material, in the absence of an alternative anatomic explanation, or
Abscess, or
New partial dehiscence of prosthetic valve,
Or New valvular regurgitation (increase
or change in preexisting murmur not sufficient)
MODIFIED DUKE CRITERIA- MINOR CRITERIA
1. Predisposition: predisposing heart conditions or injection drug use
2. Fever ≥38.0°C (≥100.4°F)
3. Vascular phenomena: – Major arterial emboli– Septic pulmonary infarcts– Mycotic aneurysm– Intracranial hemorrhage– Conjunctival hemorrhages– Janeway lesions
4. Immunologic phenomena:– Glomerulonephritis– Osler’s nodes– Roth’s spots– Rheumatoid factor
5. Microbiologic evidence: – positive blood culture but
not meeting major criterion– or serologic evidence of
active infection with an organism consistent with infective endocarditiS
DEFINITE INFECTIVE ENDOCARDITIS• Pathologic criteria Microorganisms demonstrated by
results of cultures or histologic
examination of a vegetation, a
vegetation that has embolized, or
an intracardiac abscess specimen;
or
Pathologic lesions; vegetation, or
intracardiac abscess confirmed by
results of histologic examination
showing active endocarditis
• Clinical criteria 2 major criteria, or
1 major criterion and 3 minor
criteria, or
5 minor criteria • Possible Infective
Endocarditis 1 major criterion and 1 minor
criterion, or
3 minor criteria
• Rejected Diagnosis of Infective Endocarditis Firm alternate diagnosis explaining evidence of suspected IE, or
Resolution of IE syndrome with antibiotic therapy for ≤4 days,
or
No evidence of IE at surgery or autopsy, on antibiotic therapy
for ≤4 days, or
Does not meet criteria for possible IE
INVESTIGATIONS• Blood cultures – 3 sets from different sites atleast 1 hour apart.
Why?
• Complete blood count – Leucocytosis– Thrombocytosis– Thrombocytopenia– Anemia
• ESR, CRP• Serology
Electrocardiography
– to assess for conduction abnormalities (such as varying and
progressive degrees of atrioventricular [AV] block) suggestive of
abscess formation, which are particularly associated with aortic
valve endocarditis
– Ischemic/infarct changes suggestive of coronary emboli
CXR
– Evidence of HF (pulmonary edema)
– Septic emboli, particularly in IV drug users with suspected right-
sided endocarditis
Transthoracic Echo (tte)
• TTE may detect valvular vegetations with or without positive blood
cultures
• It is used to characterize the hemodynamic severity of valvular
lesions in known IE
• It can also assess for complications of IE (e.g. abscesses, perforation,
and shunts)
• TTE can be used to reassess high-risk patients (e.g., those with a
virulent organism, clinical deterioration, persistent or recurrent
fever, new murmur, or persistent bacteremia)
ECHO
Vegetations attached to Aortic valve
Aortic regurgitation ( Colour doppler)
Transesophageal Echo(TEE)
• Assess the severity of valvular lesions in symptomatic patients with
IE if TTE is nondiagnostic
• Diagnose IE in patients with valvular heart disease and positive
blood cultures if TTE is nondiagnostic
• Diagnose complications of IE with potential impact on prognosis and
management (e.g. abscesses, perforation, and shunts)
• First-line diagnostic study to diagnose PVE and to assess for
complications
TREATMENTORGANISM• Streptococi• Penicillin sensitive
• Relatively penicillin resistant
• Moderately penicillin resistant
DRUG ( DURATION)
• Penicillin G x 4 weeks• Ceftriaxone x 4 weeks• Vancomycin x 4 weeks• Penicillin G + Gentamicin x 2 weeks
• Penicillin G or Ceftriaxone x 4 weeksplus Gentamicin x 2 weeks
• Vancomycin x 4 weeks
• Penicillin or Ceftriaxone x 6 weeksplus gentamicin x 6 weeks
• Vancomycin x 4 weeks
TREATMENTORGANISM• Enterococci
DRUG ( DURATION)
• Penicillin G + Gentamicin x 4 - 6 weeks• Ampicillin + gentamicin x 4 - 6 weeks
• Vancomycin + gentamicin x 4 - 6 weeks
• Ampicillin + ceftriaxone x 6 weeks
TREATMENTORGANISM DRUG ( DURATION)• Staphylococi• Native valve
MSSA Nafcillin, Oxacillin or Flucloxacillin x 4 – 6 weeks Or Cefazolin x 4 – 6 weeks
Or Vancomycin x 4 – 6 weeks
MRSA Vancomycin x 4 – 6 weeks
• Prosthetic valve MSSA Nafcillin, Oxacillin or Flucloxacillin x 6 – 8 weeks plus Gentamicin x
2 weeksplus Rifampicin x 6 – 8 weeks
MRSA Vancomycin x 6 – 8 weeksplus Gentamicin x 2 weeksplus Rifampicin x 6 – 8 weeks
TreatmentORGANISM• Coxiella burnetii
• Bartonella spp.
DRUG ( DURATION)
• Doxycycline + x 18 months (NVE)Hydroxychloroquine x 24 months (PVE)
• Ceftriaxone or Ampicillin x 6 weeksor doxycycline plus Gentamicin x 3 weeks
DRUG DOSAGE Penicillin G 4 mU iv q4h
Ceftriaxone 2 g iv qd
Vancomycin 15mg/kg iv q12h
Gentamycin 3 mg/kg iv or im single dose Or 1 mg/kg iv q8h
Ampicillin 2 g iv q4h
Nafcillin/Oxacillin 2 g iv q4h /Flucloxacillin
Cefazolin 2 g iv q8h
Rifampicin 300 mg PO q8h
INDICATIONS FOR SURGERY
TIMING OF SURGICAL INTERVENTION
REFERENCES
1. Harrison’s Principles of Internal Medicine 19th edition
2. Braunwald’s Heart disease 10th edition