Infective Endocarditis

P.Pujowaskito
Blok 10 FK Unjani

Is an uncommon but life-threatening disease

- By many species of bacteria and fungi; mycobacteria; rickettsiae; chlamydiae; and mycoplasma. (mostly by streptococci, staphylococci, and fastidious gram negative coccobacilli)

THE CHANGING FACE OF INFECTIVE ENDOCARDITIS

Insidence ~ 2-4%
1970 2006

IV drug use, valve prostheses, degenerative valve sclerosis, and invasive procedures

Rheumatic & Congenital

(1) the absence of a reduction in the incidence of IE; and (2) major changes in the microbiological profile of IE
Hoen B. Epidemiology and antibiotic treatment of infective endocarditis: an update. Heart 2006;92:1694-700

Anti-aggregatory via prostacycline

Intact endothelium
A single cell lining covering the internal surface blood vessels cardiac valves body cavities

Vasodilatory via nitric oxide Fibrinolytic via tPA Antithrombotic via thrombomodulin

Venturi effect
Valvular and congenital abnormalities, especially those associated with high-velocity jets, can result in endothelial damage, plateletfibrin deposition, and a predisposition to bacterial colonization.

PATHOPHYSIOLOGY OF INFECTIVE ENDOCARDITIS

PATHOGENESIS OF INFECTIVE ENDOCARDITIS

Vascular endothelium

Infection

hemostatic mechanism

SELECTED
MICROORGANISM

Immune system

HUMAN HOST

Heart abnormalities

Toxin production

INFECTIVE ENDOCARDITIS

NONBACTERIAL THROMBOTIC ENDOCARDITIS

- Progress over days to several weeks ACUTE - Valvular destruction - Metastatic infection INFECTIVE ENDOCARDITIS

Caused typically by Staphylococcus aureus

Caused by

- Evolves over weeks to several months SUBACUTE - Rarely causes metastatic infection

- viridans streptococci - enterococci - Gram negative coccobacilli - coagulase-negative staphylococci

VEGETATION

A amorphous mass of platelets, microorganism, and inflamatory cells

fibrin,

Venkatesan, S. Expressions in cardiology: vegetation ? Indian Heart Journal 2005

Can we diagnose Infective endocarditis without

CLINICAL FEATURES
SYMPTOMS Fever Chills Sweats Anorexia Weight loss Dyspnea Headache Nausea/vomiting Myalgia/arthralgia Chest pain in iv drug abuser Abdominal pain Back pain

Cough
Stroke

confusion
Malaise

CLINICAL FEATURES
SIGNS Fever Murmur Peripheral manifestation - Osler nodes

Changing/new murmur
Neurological abnormalities Embolic events Splenomegaly Clubbing

- Ptechiae
- Splinter hemorrhage - Retinal lesion/Roth spot - Janeway lesion

Few theories: 1. Deposit of the septic microemboli from the endocardium 2. Nodes due to immunologically-mediated vasculitis caused by the circulating immune complexes.

Janeway lesion

Theories: 1. Necrotic microabscesses with an inflammatory infiltrate that involve the dermis but not the epidermis 2. Deposit of the septic microemboli from the endocardium

Is caused by the engorgement of the capillaries, resulting in hemorrhage. But what causes the engorgement and hemorrhage is not known

Roth's spot:

Severe potential mechanisms: a. embolization of bacterial infiltrates from endocardium causing localized retinal abscesses b. embolized bacterail infiltrates to retinal causing anoxia resulting in sudden increase in venous pressure, thus capillary rupture in the inner retinal layers

Petechiae

Tiny purple or red spots on the skin associated with endocarditis, resulting from hemorrhages under the skin's surface.

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

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

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

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

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

A Guideline from the American Heart Association Rheumatic 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.

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

Endocarditis Prophylaxis:Does It Make Sense?

Cumulative risk of endocarditis resulting from bacteremia caused by daily activities is far greater than the risk of endocarditis resulting from a single dental procedure
Scientists also found no compelling evidence that taking antibiotics before a dental procedure prevents IE in patients who are at risk of developing a heart infection. Their hearts already often are exposed to bacteria from the mouth that can enter their bloodstreams during basic daily activities such as brushing or flossing.

ACC/AHA Recommendations for Endocarditis Prophylaxis

Class I recommendation Class III recommendation

High-risk
Prosthetic valves

Moderate-risk

Negligible-risk

Other than already listed Isolated ASD II CHD Acquired valvular dysfunction (e.g., RHD) Hypertrophic cardiomyopathy MVP with auscultatory regurgitation or thickened leaflet Repair of ASD, VSD, or PDA (without residual 6 mo) Previous CABG

Previous endocarditis

Complex congenital HD (TGA, ToF, singleventricle) Systemic-pulmonary shunt or conduits

MVP without regurgitation

AR/AS/MR/MS + MR/VSD Dajani AS et al.. Circulation 1997;96:358-66

Cardiac pacemakers

PREVENTION OF INFECTIVE ENDOCARDITIS-WALLET CARD Name: _______________________________________ needs protection from INFECTIVE (BACTERIAL) ENDOCARDITIS because of an existing heart condition. Diagnosis: ______________________________________ Prescribed by: __________________________________ Date: __________________________________________

Treatment for native valve endocarditis caused by penicillin-

susceptible viridans streptococci and staphylococcis bovis

Antibiotic Aqueous penicillin G Dosage and route* 12-18 million units/24 hr IV either continuously or every 4 hr in six equally divided doses Aqueous penicillin G plus Gentamycin Ceftriaxone Vancomycin 12-18 million units/24 hr IV either continuously or every 4 hr in six equally divided dose 1 mg/kg IM or IV every 8 hr 2 gm once daily IM or IV 30 mg/kg/24 hr IV in two equally divided doses, not to exceed 2 gm/24 hr unless serum levels are monitored 2 4 4 2 Duration (wk) 4

* Dosages are for patients with normal renal function

Wilson WR, et al. JAMA 1995;274:1706

Treatment for native valve endocarditis caused by viridans strepto-

cocci and staphylococcis bovis relatively resistance to penicillin G

Antibiotic Aqueous penicillin G Dosage and route* 18 million units/24 hr IV either Duration (wk) 4

plus

continuously or every 4 hr in six

equally divided doses

Gentamycin

1 mg/kg IM or IV every 8 hr

Vancomycin

30 mg/kg/24 hr IV in two equally divided doses, not to exceed 2 gm/24 hr unless serum levels are monitored

* Dosages are for patients with normal renal function

Wilson WR, et al. JAMA 1995;274:1706

Standard therapy for endocarditis caused by enterococci

Antibiotic Aqueous penicillin G plus Dosage and route* 18-30 million units/24 hr IV given continuously or every 4 hr in six equally divided doses Gentamicin Ampicillin plus 1 mg/kg IM or IV every 8 hr 12 gm/24 hr IV given continuously or every 4 hr in six divided doses 4-6 4-6 Duration (wk) 4-6

Gentamicin
Vancomycin plus

1 mg/kg IM or IV every 8 hr
30 mg/kg/24 hr IV in two equally divided doses not to exceed 2 gm/24 hr unless serum levels are monitored

4-6

Gentamicin

1 mg/kg IM or IV every 8 hr

4-6
Wilson WR, et al. JAMA 1995;274:1706

* Dosages are for patients with normal renal function

Treatment for staphylococcus endocarditis in the absence of prosthetic material

Antibiotic
Methicillin-susceptible Nafcillin or oxacillin With optional addition of gentamicin Cefazolin (or other first generation cephalosporin in equivalent doses) With optional addition of gentamicin Vancomycin 2 gm IV every 4 hr 1mg/kg IM or IV every 8 hr 2 gm IV every 8 hr 4-6 wk 3-5 d 4-6 wk

Dosage and route*

Duration

1mg/kg IM or IV every 8 hr 30 mg/kg/24 hr in two equally divided doses, not to exceed 2 gm/24 hr unless serum level are monitored

3-5 d 4-6

Methicillin-resistent Vancomycin As noted previously 4-6

* 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 oxacillin Wilson WR, et al. JAMA 1995;274:1706

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

Treatment for native valve endocarditis caused by penicillin-

susceptible viridans streptococci and staphylococcis bovis

Antibiotic Aqueous penicillin G Dosage and route* 12-18 million units/24 hr IV either continuously or every 4 hr in six equally divided doses Aqueous penicillin G plus Gentamycin Ceftriaxone Vancomycin 12-18 million units/24 hr IV either continuously or every 4 hr in six equally divided dose 1 mg/kg IM or IV every 8 hr 2 gm once daily IM or IV 30 mg/kg/24 hr IV in two equally divided doses, not to exceed 2 gm/24 hr unless serum levels are monitored 2 4 4 2 Duration (wk) 4

* Dosages are for patients with normal renal function

Wilson WR, et al. JAMA 1995;274:1706

Treatment for native valve endocarditis caused by viridans strepto-

cocci and staphylococcis bovis relatively resistance to penicillin G

Antibiotic Aqueous penicillin G Dosage and route* 18 million units/24 hr IV either Duration (wk) 4

plus

continuously or every 4 hr in six

equally divided doses

Gentamycin

1 mg/kg IM or IV every 8 hr

Vancomycin

30 mg/kg/24 hr IV in two equally divided doses, not to exceed 2 gm/24 hr unless serum levels are monitored

* Dosages are for patients with normal renal function

Wilson WR, et al. JAMA 1995;274:1706

Standard therapy for endocarditis caused by enterococci

Antibiotic Aqueous penicillin G plus Dosage and route* 18-30 million units/24 hr IV given continuously or every 4 hr in six equally divided doses Gentamicin Ampicillin plus 1 mg/kg IM or IV every 8 hr 12 gm/24 hr IV given continuously or every 4 hr in six divided doses 4-6 4-6 Duration (wk) 4-6

Gentamicin
Vancomycin plus

1 mg/kg IM or IV every 8 hr
30 mg/kg/24 hr IV in two equally divided doses not to exceed 2 gm/24 hr unless serum levels are monitored

4-6

Gentamicin

1 mg/kg IM or IV every 8 hr

4-6
Wilson WR, et al. JAMA 1995;274:1706

* Dosages are for patients with normal renal function

Treatment for staphylococcus endocarditis in the absence of prosthetic material

Antibiotic
Methicillin-susceptible Nafcillin or oxacillin With optional addition of gentamicin Cefazolin (or other first generation cephalosporin in equivalent doses) With optional addition of gentamicin Vancomycin 2 gm IV every 4 hr 1mg/kg IM or IV every 8 hr 2 gm IV every 8 hr 4-6 wk 3-5 d 4-6 wk

Dosage and route*

Duration

1mg/kg IM or IV every 8 hr 30 mg/kg/24 hr in two equally divided doses, not to exceed 2 gm/24 hr unless serum level are monitored

3-5 d 4-6

Methicillin-resistent Vancomycin As noted previously 4-6

* 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 oxacillin Wilson WR, et al. JAMA 1995;274:1706

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

PREVENTIVE ASPECT: Healthy Dental Practices can Help to Prevent Heart Diseases Dentist detects heart problems

Antibiotics before a dental visit are now recommended only for those heart Patients with artificial heart valves, heart transplant patients who develop cardiac valve problems, certain congenital heart disease, recipients of an artificial patch to repair a congenital defect within the past six months or patients with a history of IE.
HIGH RISK: CLASS I Prosthetic heart valves Previous infective endocarditis Complex cyanotic congenital heart disease Transposition of great arteries Fallots tetralogy Gerbodes defect Surgically constructed systemic pulmonary shunts or conduits Mitral valve prolapse with mitral regurgitation or thickened valve leaflets MODERATE RISK: CLASS II Acquired valvular heart disease eg: rheumatic heart disease Aortic stenosis Aortic regurgitation Mitral regurgitation Other structural cardiac defects eg: ventricular septal defect Bicuspid aortic valve Primum atrial sepal defect Patent Ductus Arteriosus Aortic root replacement Coarctation of aorta Atrial septal aneurysm/patent foramen ovale Ventricular septal defect Hypertrophic obstructive cardiomyopathy Subaortic membrane

Venkatesan, S. Expressions in cardiology: vegetation ? Indian Heart Journal 2005

Can we diagnose Infective endocarditis without