Infective Endocarditis

1
2 Introduction
 Endocarditis is an inflammation of the endocardium,
the membrane lining the chambers of the heart and
covering the cusps of the heart valves.

 More commonly, endocarditis refers to infection of the

heart valves by various microorganisms

 Although it typically affects native valves, it also may

involve non-valvular areas or implanted material
 3 Cont.

IE could be
 Native Valve IE
 Community acquired

 Nosocomial IE

 Intravenous drug abuse (IVDA) IE

 Prosthetic Valve IE

 IE also classified as acute or subacute (old classification)

 Classification
Acute4  Subacute

 Affects normal heart valves  Often affects damaged

heart valves(VHD)
 Rapidly destructive

 Metastatic foci  Indolent nature

 Commonly Staph.  Caused by less virulent org

([Link])
 If not treated, usually fatal
within 6 weeks  If not treated, usually fatal

by one year
 5 Epidemiology and Etiology
 Infective endocarditis is uncommon, in US.

 Male-to-female ratio is approximately 2:1

 Most cases occur in those older than 50 years (>50%)

 Common bacteria

S. aureus, Streptococci (viridans),Enterococci

 Not so common
 Fungi, Pseudomonas,HACEK(Haemophilus,Actinobacillus,Cardiobacterium,
Eikenella, and Kingella)
 6 Cont.
The incidence of S. aureus, continues to increase
and it surpassed viridans streptococci

[Link] cause IE in patient with community

acquired disease and underlying cardiac
abnormalities (MVP, RHD)

[Link] are most common cause of prosthetic valve

endocarditis and intravenous drug abusers
 7 Cont.
Enterococcus more common in individual who
undergo genitourinary manipulation or obstetric
procedures

Subacute IE tend to involve mitral valve, whereas

acute often involve aortic valve
8 Risk factors
1. Presence of a prosthetic valve (highest risk)
2. Previous endocarditis (highest risk)
3. Healthcare-related exposure (high risk)
4. Congenital heart disease
5. Chronic intravenous access
6. Diabetes mellitus
7. Acquired valvular dysfunction (e.g, RHD)
8. Cardiac implantable device
9. Chronic heart failure
10. Mitral valve prolapse with regurgitation
11. IVDA
 9 Pathophysiology
 The most common route is via hematogenous spread

1. For IE to occur there must be alteration of endothelial

surfaces of heart valve to allow organism attachment

 These alterations may be produced by an inflammatory

process such as rheumatic heart disease or by injury from
turbulent blood flow

2. Platelets and fibrin now deposit on the damaged valves,

forming a nonbacterial thrombotic endocarditis (NBTE).
 10 Cont.
3. Bacteria through hematogenous spread (i.e., bacteremia) adhere
to and colonize the site of infection forming a vegetation

 Bacteremia is the result of trauma to a mucosal surface with a

high concentration of resident bacteria

 such as the oral cavity and GI tract

 Transient bacteremia commonly follow certain dental, GI,

urologic, and gynecologic procedures

 Further deposits of platelets and fibrin cover the bacteria,

providing a protective coating for organisms
11
Cont.
 staphylococci, [Link] and enterococci are most
likely to adhere to NBTE

because of production of specific adherence factors

such as dextran by some oral streptococci and
glycocalyx by staphylococci.

 Gram-negative bacteria rarely adhere to heart valves

and are uncommon causes of infective endocarditis
12
 13
Cont.
 Acquisition of PVE differs in early stages, where direct
inoculation may occur during surgery

 Causative organisms in early PVE are nosocomial, with

increased likelihood of being drug resistant

 However, in late PVE, the process of colonization and

vegetation is similar to that of native-valve IE

 The vegetations seen in IE may be single or multiple and vary in

size

 Bacteria within the vegetation grow slowly and are protected

from antibiotics and host defenses
 14
Complication of IE

 Effects of IE and the resulting lesions include

local peri-valvular damage,

e m b o l i z a t i o n o f s e p t i c f r a g m e n t s w i t h p o t e n t i a l
hematogenous seeding of remote sites, and

 Formation of antibody complexes

 15
Cont.
 Vegetations may destroy valvular tissue, & continued
destruction lead

Acute heart failure via perforation of the valve leaflet,

 Rupture of the chordae tendineae or papillary muscle,

For patients with PVE, valve dehiscence

V e g e t a t i o n s m a y b e f r i a b l e , a n d r e l e a s e d
downstream leading to septic emboli
 16 Cont…..
S e p t i c e m b o l i f r o m r i g h t - s i d e d I E ( t r i c u s p i d a n d
pulmonary)  pulmonary abscess

Left-sided IE (mitral and aortic valves)  embolus travel to

any organ system, especially the kidneys, spleen, and brain

 Circulating immune complexes consisting of antigen, antibody,

and complement may deposit in organs, producing local
inflammation, and organ damage.

 Petechiae, Osler nodes, and Janeway lesions, Roth spots

(within the eye ) and glomerulonephritis
17 Cont.
18
Clinical presentation and
Diagnosis
General

Patients typically present with nonspecific and

variable sign or symptoms

Symptoms:

Fever, chills, weakness, dyspnea, night sweats,

weight loss, and/or malaise.
19
Cont.
 Signs

 Fever is the most common sign of IE.

 New or changing heart murmur

 Embolic phenomena (emboli affect the heart, lungs,

abdomen, or extremities)

 Vascular phenomena(e.g., petechiae, splinter hemorrhages,

Janeway lesions)

 Immunologic phen om e n a ( O sle r n ode s, Roth sp ot,

glomerulonephritis, +RF)
 Petechiae

1. Nonspecific
2. are very small(<3mm
3. often located on extremities,
mucous membranes or
conjunctiva
 Splinter Hemorrhages

[Link]
[Link] dark streaks beneath the fingernails or toenails
[Link] due to local vasculitis or microemboli
[Link] do NOT extend the entire length of the nail
 Osler’s Nodes

[Link]
[Link] and erythematous nodules
[Link] on pads of fingers and toes
[Link] common in subacute IE
 Janeway Lesions

[Link], painless, hemorrhagic macular Plaque

2. Located on palms and soles
3. More common in acute IE
24
Diagnosis

Laboratory test
 Blood cultures are important for persistent bacteremia,
which occurs commonly in IE.

 Three blood culture sets should be drawn within the initial

24 hours

 approximately 90% of the first two cultures will yield a

positive result.

 WBC may be elevated in acute disease but could be normal

in subacute IE
 25 Cont.
 Nonspecific findings include

H e m a t o l o g i c t e s t s f o r a n e m i a ( n o r m o c h r o m i c ,
normocytic), Thrombocytopenia, elevated ESR or CRP,
proteinuria/microscopic hematuria

 Another diagnostic test

 An echocardiogram (TTE with 60% sensitivity or TEE with

95% sensitivity) should be performed on any patient with
suspected IE to detect the presence of vegetations.
 26
Diagnosis criteria for IE (Duke’s Criteria)

Major criteria

Blood culture positive for IE:

üTypical microorganisms consistent with IE

Evidence of endocardial involvement: Echo

27
Cont.
 Minor Criteria
 Predisposition: predisposing heart condition or injection
drug use

 Fever: temperature greater than 38°C (100.4°F)

 Vascular phenomena: major arterial emboli, septic

pulmonary infarcts, mycotic aneurysm, intracranial
hemorrhage, conjunctival hemorrhages, and Janeway’s
lesions

 Immunologic phenomena: glomerulonephritis, Osler’s nodes,

Roth’s spots, and rheumatoid factor
 28 Cont.
 Definitive : 2 major criteria or
: 1 major and 3 minor criteria or
: 5 minor criteria
Possible : 1 major and 1 minor criteria
: 3 minor criteria

 Rejected : firm alternate diagnosis

R e s o l u t i o n o f m a n i f e s t a t i o n s o f I E w i t h
antimicrobial therapy for ≤ 4 days
 29 Treatment
Desired outcome

Relieve the signs and symptoms of the disease

Decrease morbidity and mortality

Eradicate the causative organism with minimal drug

exposure

Provide cost-effective antimicrobial therapy

 Indicate appropriate prophylactic antimicrobials for

those with high risk
 30 Cont.
General approach to treatment
 Empirical therapy

 Should cover MRSA and gram-negative bacilli

vancomycin plus gentamicin

 Then;

 Isolation of the infecting pathogen and determination of

antimicrobial susceptibilities,

 High-dose, parenteral, bactericidal antibiotics for an extended

period.
 31 Cont.
Nonpharmacologic therapy
 Surgery

 Vulvectomy and Valve replacement

 Echocardiographic features that suggest the need for surgery

include:

 Persistent vegetation or an increase in vegetation size after

prolonged antibiotic treatment,

 Valve dysfunction, or

 Para-valvular extension (e.g., abscess).

 32 Cont.

Pharmacologic therapy
A. Streptococci

1. Penicillin-susceptible streptococci, S. bovis

• Penicillin G (12-18mU /day IV q4/6hr for 4 weeks)

• Ceftriaxone (2 g/d IV as a single dose for 4 weeks)

In beta-lactam allergic patients

• Vancomycin (30 mg/kg/day i.v. in 2 doses for 4weeks)

 33
Cont.
2. Penicillin-resistant streptococci

Penicillin G (4 mU IV q4h) or ceftriaxone (2 g IV qd) for

4 weeks plus gentamicin (3 mg/kg qd IV or IM, as a
single dose for 2 weeks)

Vancomycin as noted above for 4 weeks

2-week regimens are not intended for the following

patients
 Most patients >65 years of age, Children, Impairment of the eighth cranial nerve function, Renal function with a
creatinine clearance <20 mL/min(<0.33 mL/s, Known cardiac or extracardiac abscess, Infection with Abiotrophia,
Granulicatella, or Gemalla species
 34 Cont.
B. Enterococci

Penicillin G (4–5 mU IV q4h) plus gentamicin (3

mg/kg/d IV/IM in 1 dose), both for 4–6 weeks

Ampicillin (2 g IV q4h) plus gentamicin (3

mg/kg/d IV/IM in 1 dose), both for 4–6 weeks

Vancomycin (15 mg/kg IVq12h) plus gentamicin

(3 mg/kg/d IV/IM in 1 dose), both for 4–6 weeks
 35 Cont.

C. Staphylococci

1. Methicillin-susceptible, infecting native valves

 Nafcillin or oxacillin (2 g IV q4h for 4–6 weeks)

For penicillin-allergic (non-anaphylactoid type)

 Cefazolin (2 g IV q8h for 4–6 weeks)

2. Methicillin-resistant, infecting native valves

• Vancomycin (15 mg/kg IV q12h for 4–6 weeks)

 36 Cont..
3. Methicillin-susceptible, infecting prosthetic valves

• Nafcillin or Oxacillin (2 g IV q4h for 6–8 weeks) plus

Gentamicin (3 mg/kg/d IM or IV for 2 weeks) plus
Rifampicin (300 mg i.v/ PO q8h for 6–8 weeks)

4. Methicillin-resistant, infecting prosthetic valves

Vancomycin (15 mg/kg IV q12h for 6–8 weeks) plus

Gentamicin (3 mg/kg/sd IM or IV for 2 weeks) plus
Rifampicin (300 mg i.v/PO q8h for 6–8 weeks)
37 Cont.

D. HACEK Organisms

Ceftriaxone (2 g/d IV as a single dose for 4

weeks)

Ampicillin/sulbactam (3 g IV q6h for 4 weeks)

 38 Prevention

For dental procedures

But not for:

Gastrointestinal or

Genitourinary tract procedures

 High-Risk Cardiac Lesions for Which Endocarditis Prophylaxis Is
Advised before Dental Procedures

Patients with prosthetic heart valves

Patients with prior endocarditis

Unrepaired cyanotic congenital heart disease, including palliative shunts or

conduits

congenital heart disease repaired with prosthetic valve, up to 6 month after

the procedure

Incompletely repaired congenital heart disease with residual defects adjacent to

prosthetic material

Valvulopathy developing after cardiac transplantation

 40 Empiric antibiotic regimen for prophylaxis

 Standard oral regimen

Amoxicillin 2 g PO 1 h before procedure

 Inability to take oral medication

Ampicillin 2 g IV or IM within 1 h before procedure

 41 Cont.
 Penicillin allergy

 Clarithromycin or azithromycin 500 mg PO 1 h before procedure

 Cephalexin 2 g PO 1 h before procedure

 Clindamycin 600 mg PO 1 h before procedure

 Penicillin allergy, inability to take oral medication

 Cefazolin or ceftriaxone 1 g IV or IM 30 min before procedure

 Clindamycin 600 mg IV or IM 1 h before procedure