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Infective Endocarditis

P.Pujowaskito

Blok 10 FK Unjani

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- By many species of bacteria and fungi;mycobacteria; rickettsiae; chlamydiae; and

mycoplasma. (mostly by streptococci, staphylococci,and fastidious gram negative coccobacilli)

Is an uncommon but

life-threatening disease

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Insidence ~ 2-4%1970 2006

THE CHANGING FACE OF INFECTIVE ENDOCARDITIS

Rheumatic &Congenital

IV drug use, valve prostheses,degenerative valve sclerosis,

and invasive procedures

Hoen B. Epidemiology and antibiotic treatment of infective endocarditis: an update. Heart 2006;92:1694-700

(1) the absence of a reduction in the incidence of IE; and(2) major changes in the microbiological profile of IE

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Intactendothelium

Anti-aggregatory

via prostacycline

Vasodilatory

via nitric oxide

Fibrinolytic

via tPA

Antithromboticvia thrombomodulin

A single cell lining covering

the internal surface

blood vessels

cardiac valves

body cavities

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Valvular and

congenitalabnormalities,especially thoseassociated with

high-velocity jets,can resultin endothelialdamage, platelet-fibrin deposition,and a predispositionto bacterialcolonization.

Venturi effect

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PATHOPHYSIOLOGY OF INFECTIVE ENDOCARDITIS

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PATHOGENESIS OF INFECTIVE ENDOCARDITIS

SELECTED

MICROORGANISM HUMAN HOST

Vascular endothelium

hemostatic mechanism

Immune system

Heart abnormalities

Toxin production

NONBACTERIAL

THROMBOTIC

ENDOCARDITIS

INFECTIVE

ENDOCARDITIS

Infection

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INFECTIVEENDOCARDITIS

ACUTE

SUBACUTE

- Progress over

days to several

weeks

- Valvulardestruction

- Metastatic

infection

- Evolves over

weeks to

several months

- Rarely causes

metastatic

infection

Caused typically by

Staphylococcus aureus

Caused by

- viridans streptococci

- enterococci

- Gram negative cocco-

bacilli

- coagulase-negative

staphylococci

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VEGETATION

A amorphous mass of platelets, fibrin,microorganism, and inflamatory cells

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Venkatesan, S. Expressions in cardiology: Can we diagnose Infective endocarditis withoutvegetation ? Indian Heart Journal 2005

http://drsvenkatesan.wordpress.com/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/http://drsvenkatesan.wordpress.com/http://drsvenkatesan.wordpress.com/

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CLINICAL FEATURES

SYMPTOMS

Fever Headache

Chills Nausea/vomiting

Sweats Myalgia/arthralgia

Anorexia Chest pain in iv drug abuser

Weight loss Abdominal pain

Dyspnea Back pain

Cough confusion

Stroke Malaise

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CLINICAL FEATURES

SIGNS

Fever Peripheral manifestation

Murmur - Osler nodes

Changing/new murmur - Ptechiae

Neurological abnormalities - Splinter hemorrhage

Embolic events - Retinal lesion/Roth spot

Splenomegaly - Janeway lesion

Clubbing

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Few theories:1. Deposit of the septic microemboli from the endocardium2. Nodes due to immunologically-mediated vasculitis caused bythe circulating immune complexes.

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Janeway lesion

Theories:1. Necrotic microabscesses with an inflammatory infiltrate thatinvolve the dermis but not the epidermis

2. Deposit of the septic microemboli from the endocardium

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Is caused by the engorgement of the capillaries, resulting inhemorrhage. But what causes the engorgement and hemorrhageis not known

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Severe potential mechanisms:a. embolization of bacterial infiltrates from endocardium causinglocalized retinal abscessesb. embolized bacterail infiltrates to retinal causing anoxiaresulting in sudden increase in venous pressure, thus capillary

rupture in the inner retinal layers

Roth's spot:

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Petechiae

Tiny purple or red spots on the skin associated withendocarditis, resulting from hemorrhages under the skin'ssurface.

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Modified Duke Criteria: Major criteria

BLOOD CULTURE

Positive blood culture for IE from two separate blood cultures, or

Persistently positive blood culture, defined as recovery of microorganism

consistent with IE from blood cultures (2) drawn more than 12 hr apart, or

Three or a majority of four or more separate blood cultures, with first

and last drawn at least 1 hr apart, or

Single positive blood culture for coxiella burnetti or antiphase I IgG

antibody titer >1:800

EVIDENCE OF ENDOCARDIAL INVOLVEMENT

Positive echocardiogram

- Oscilating intracardiac mass, on valve or supporting structures, or

- Abscess, or

- New partial dehiscence of prosthetic valve, or

New valvular regurgitation Li JS, et al. Clin Infect Dis 2000;30:633

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Modified Duke Criteria: Minor criteria

Predisposition: predisposing heart condition or intravenous drug use

Fever 38.00C

Vascular phenomena: major arterial emboli, septic pulmonary infarcts,

mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhage,

Janeway lession

Immunological phenomena: glomerulonephritis, Osler nodes, Roth spots,

rheumatoid factor

Microbiological evidence: positive blood culture but not meeting major

criterion as noted previously or serologic evidence of active infection

with organism consistent with IE

Li JS, et al. Clin Infect Dis 2000;30:633

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Diagnosis of infective endocarditis (Modified Duke Criteria)

1. DEFINITIVE

Pathological criteria

- Microorganism: demonstrated by culture or histology in a

vegetation, or in vegetation that has embolized, or in

intracardiac abscess, or

- Pathological lesions: vegetation or intracardiac abscess

confirm by histology

Clinical criteria

- Two major criteria, or

- One major criteria and three minor, or

- Five minor criteria

Li JS, et al. Clin Infect Dis 2000;30:633

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Diagnosis of infective endocarditis (Modified Duke Criteria)

2. POSSIBLE

One major criterion and one minor criterion or three minor criteria

3. REJECTED

- Firm alternative diagnosis of manifestation of endocarditis, or

- Sustained resolution of manifestation of endocarditis, with

antibiotic therapy for 4 days or less, or

- No pathological evidence of IE at surgery or autopsy, after

antibiotic therapy for 4 days or less

Li JS, et al. Clin Infect Dis 2000;30:633

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Wilson W, Taubert KA, Gewitz M, et al.

Prevention of infective endocarditis.Guidelines from the American Heart Association.

A Guideline from the American Heart AssociationRheumatic Fever, Endocarditis, and Kawasaki Disease Committee,Council on Cardiovascular Disease in the Young, and

the Council on Clinical Cardiology,Council on Cardiovascular Surgery and Anesthesia, and

the Quality of Care and Outcomes Research Interdisciplinary Working Group.

Circulation 2007;115:1656-8.

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Scientists also found no compelling evidence that takingantibiotics before a dental procedure prevents IE in patientswho are at risk of developing a heart infection. Their heartsalready often are exposed to bacteria from the mouth that canenter their bloodstreams during basic daily activities such asbrushing or flossing.

Endocarditis Prophylaxis:Does It Make Sense?

Cumulative risk of endocarditis resulting frombacteremia caused by daily activities is far greaterthan the risk of endocarditis resulting from asingle dental procedure

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ACC/AHA Recommendations for Endocarditis Prophylaxis

Class IIIrecommendation

Class I recommendation

Cardiac pacemakersAR/AS/MR/MS + MR/VSD

MVP without

regurgitation

MVP with auscultatory

regurgitation or

thickened leaflet

Systemic-pulmonary

shunt or conduits

Previous CABGHypertrophic

cardiomyopathy

Complex congenital HD

(TGA, ToF, single-

ventricle)

Repair of ASD, VSD, or

PDA (without residual 6 mo)

Acquired valvular

dysfunction (e.g., RHD)Previous endocarditis

Isolated ASD IIOther than already listed

CHDProsthetic valves

Negligible-riskModerate-riskHigh-risk

Dajani AS et al.. Circulation 1997;96:358-66

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Name: _______________________________________needs protection from

INFECTIVE (BACTERIAL) ENDOCARDITISbecause of an existing heart condition.Diagnosis: ______________________________________Prescribed by: __________________________________Date: __________________________________________

PREVENTION OF INFECTIVE ENDOCARDITIS-WALLET CARD

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Treatment for native valve endocarditis caused by penicillin-

susceptible viridans streptococci and staphylococcis bovis

Antibiotic Dosage and route* Duration (wk)

Aqueous penicillin G 12-18 million units/24 hr IV

either continuously or every 4 hr

in six equally divided doses

4

Aqueous penicillin G

plus

12-18 million units/24 hr IV

either continuously or every 4 hr

in six equally divided dose

2

Gentamycin 1 mg/kg IM or IV every 8 hr 2

Ceftriaxone 2 gm once daily IM or IV 4

Vancomycin 30 mg/kg/24 hr IV in two equally

divided doses, not to exceed 2

gm/24 hr unless serum levels are

monitored

4

Wilson WR, et al. JAMA 1995;274:1706* Dosages are for patients with normal renal function

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Treatment for native valve endocarditis caused by viridans strepto-

cocci and staphylococcis bovis relatively resistance to penicillin G

Antibiotic Dosage and route* Duration (wk)

Aqueous penicillin G

plus

18 million units/24 hr IV either

continuously or every 4 hr in six

equally divided doses

4

Gentamycin 1 mg/kg IM or IV every 8 hr 2

Vancomycin 30 mg/kg/24 hr IV in two equally

divided doses, not to exceed 2

gm/24 hr unless serum levels are

monitored

4

Wilson WR, et al. JAMA 1995;274:1706* Dosages are for patients with normal renal function

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Antibiotic Dosage and route* Duration (wk)

Aqueous penicillin G

plus

18-30 million units/24 hr IV given

continuously or every 4 hr in six equally

divided doses

4-6

Gentamicin 1 mg/kg IM or IV every 8 hr 4-6

Ampicillin

plus

12 gm/24 hr IV given continuously or

every 4 hr in six divided doses

4-6

Gentamicin 1 mg/kg IM or IV every 8 hr 4-6

Vancomycin

plus

30 mg/kg/24 hr IV in two equallydivided doses not to exceed 2 gm/24 hr

unless serum levels are monitored

Gentamicin 1 mg/kg IM or IV every 8 hr 4-6

Standard therapy for endocarditis caused by enterococci

* Dosages are for patients with normal renal functionWilson WR, et al. JAMA 1995;274:1706

Treatment for staphylococcus endocarditis in the absence of prosthetic material

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Antibiotic Dosage and route* Duration

Methicillin-susceptible

Nafcillin or oxacillin 2 gm IV every 4 hr 4-6 wk

With optional addition of

gentamicin

1mg/kg IM or IV every 8 hr 3-5 d

Cefazolin (or other first

generation cephalosporin in

equivalent doses)

2 gm IV every 8 hr 4-6 wk

With optional addition of

gentamicin

1mg/kg IM or IV every 8 hr 3-5 d

Vancomycin 30 mg/kg/24 hr in two equally divided

doses, not to exceed 2 gm/24 hr unless

serum level are monitored

4-6

Methicillin-resistent

Vancomycin As noted previously 4-6

Treatment for staphylococcus endocarditis in the absence of prosthetic material

* Dosage are for patients with normal renal function

For penicillin-susceptible staphylococci use aqueous penicillin G 18-24 million units/24 hr for 4-6 wk instead of nafcillin or oxacillinWilson WR, et al. JAMA 1995;274:1706

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Cardiac surgery for patients with infective endocarditis

INDICATIONS

Moderate to severe congestive heart failure cause by valve dysfunction

Uncontrolled infection despite optimal antimicrobial therapy

Unstable prosthesis, prosthesis orifice obstructed

Unavailable effective antimicrobial therapy: endocarditis caused by

fungi, Brucellae, Pseudomonas aeroginosa (aortic or mitral valves)

Staphylococcus aureus prostetic valve endocarditis with an intracardiac

complication

Relaps of prosthetic valve endocarditis despite of optimal therapy

Fistula to pericardiac sac

Cited from Karchmer AW. In Zipes DP, et al (eds). Heart Disease 2005

T f i l d di i d b i illi

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Treatment for native valve endocarditis caused by penicillin-

susceptible viridans streptococci and staphylococcis bovis

Antibiotic Dosage and route* Duration (wk)

Aqueous penicillin G 12-18 million units/24 hr IV

either continuously or every 4 hr

in six equally divided doses

4

Aqueous penicillin G

plus

12-18 million units/24 hr IV

either continuously or every 4 hr

in six equally divided dose

2

Gentamycin 1 mg/kg IM or IV every 8 hr 2

Ceftriaxone 2 gm once daily IM or IV 4

Vancomycin 30 mg/kg/24 hr IV in two equally

divided doses, not to exceed 2

gm/24 hr unless serum levels are

monitored

4

Wilson WR, et al. JAMA 1995;274:1706* Dosages are for patients with normal renal function

T t t f ti l d diti d b i id t t

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Treatment for native valve endocarditis caused by viridans strepto-

cocci and staphylococcis bovis relatively resistance to penicillin G

Antibiotic Dosage and route* Duration (wk)

Aqueous penicillin G

plus

18 million units/24 hr IV either

continuously or every 4 hr in six

equally divided doses

4

Gentamycin 1 mg/kg IM or IV every 8 hr 2

Vancomycin 30 mg/kg/24 hr IV in two equally

divided doses, not to exceed 2

gm/24 hr unless serum levels are

monitored

4

Wilson WR, et al. JAMA 1995;274:1706* Dosages are for patients with normal renal function

S d d h f d di i d b i

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Antibiotic Dosage and route* Duration (wk)

Aqueous penicillin G

plus

18-30 million units/24 hr IV given

continuously or every 4 hr in six equally

divided doses

4-6

Gentamicin 1 mg/kg IM or IV every 8 hr 4-6

Ampicillin

plus

12 gm/24 hr IV given continuously or

every 4 hr in six divided doses

4-6

Gentamicin 1 mg/kg IM or IV every 8 hr 4-6

Vancomycin

plus

30 mg/kg/24 hr IV in two equallydivided doses not to exceed 2 gm/24 hr

unless serum levels are monitored

Gentamicin 1 mg/kg IM or IV every 8 hr 4-6

Standard therapy for endocarditis caused by enterococci

* Dosages are for patients with normal renal functionWilson WR, et al. JAMA 1995;274:1706

Treatment for staphylococcus endocarditis in the absence of prosthetic material

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Antibiotic Dosage and route* Duration

Methicillin-susceptible

Nafcillin or oxacillin 2 gm IV every 4 hr 4-6 wk

With optional addition of

gentamicin

1mg/kg IM or IV every 8 hr 3-5 d

Cefazolin (or other first

generation cephalosporin in

equivalent doses)

2 gm IV every 8 hr 4-6 wk

With optional addition of

gentamicin

1mg/kg IM or IV every 8 hr 3-5 d

Vancomycin 30 mg/kg/24 hr in two equally divided

doses, not to exceed 2 gm/24 hr unless

serum level are monitored

4-6

Methicillin-resistent

Vancomycin As noted previously 4-6

p y p

* Dosage are for patients with normal renal function

For penicillin-susceptible staphylococci use aqueous penicillin G 18-24 million units/24 hr for 4-6 wk instead of nafcillin or oxacillinWilson WR, et al. JAMA 1995;274:1706

C di f ti t ith i f ti d diti

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Cardiac surgery for patients with infective endocarditis

INDICATIONS

Moderate to severe congestive heart failure cause by valve dysfunction

Uncontrolled infection despite optimal antimicrobial therapy

Unstable prosthesis, prosthesis orifice obstructed

Unavailable effective antimicrobial therapy: endocarditis caused by

fungi, Brucellae, Pseudomonas aeroginosa (aortic or mitral valves)

Staphylococcus aureus prostetic valve endocarditis with an intracardiac

complication

Relaps of prosthetic valve endocarditis despite of optimal therapy

Fistula to pericardiac sac

Cited from Karchmer AW. In Zipes DP, et al (eds). Heart Disease 2005

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PREVENTIVE ASPECT: Healthy DentalPractices can Help to Prevent Heart Diseases

Dentist detects heart problems

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HIGH RISK: CLASS I Prosthetic heart valves Previous infectiveendocarditis Complex cyanotic congenital heart disease Transposition ofgreat arteries Fallots tetralogy Gerbodes defect Surgically constructedsystemic pulmonary shunts or conduits Mitral valve prolapse with mitralregurgitation or thickened valve leafletsMODERATE RISK: CLASS II Acquired valvular heart disease eg: rheumaticheart disease Aortic stenosis Aortic regurgitation Mitral regurgitation Other

structural cardiac defects eg: ventricular septal defect Bicuspid aortic valvePrimum atrial sepal defect Patent Ductus Arteriosus Aortic rootreplacement Coarctation of aorta Atrial septal aneurysm/patent foramenovale Ventricular septal defect Hypertrophic obstructive cardiomyopathySubaortic membrane

Antibiotics before a dental visit are now recommended only for thoseheart Patients with artificial heart valves, heart transplant patients whodevelop cardiac valve problems, certain congenital heart disease,

recipients of an artificial patch to repair a congenital defect within thepast six months or patients with a history of IE.

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Venkatesan, S. Expressions in cardiology: Can we diagnose Infective endocarditis withoutvegetation ? Indian Heart Journal 2005

http://drsvenkatesan.wordpress.com/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/2009/04/10/can-we-diagnose-infective-endocarditis-without-vegetation/http://drsvenkatesan.wordpress.com/http://drsvenkatesan.wordpress.com/http://drsvenkatesan.wordpress.com/