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