donot use for patient management

1. Infective endocarditis
Dr. Birhanu Abie ( pediatrician)
University of Gondar March,2020
8/28/2020 1IE

2. outline
 Introduction
 Epidemiology
 Etiologies
 Pathogenesis
 Clinical manifestation
 diagnosis
 Complication
 Treatment
 References
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3. Introduction
 Is an infection of the
endocardium and/or heart valves that
involves thrombus formation
(vegetation), which may damage the
endocardial tissue and/or valves.
 Bacteria are the predominant
microbial pathogens
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4.  Nonbacterial endocarditis can be
caused by viruses, fungi, and other
microbiologic agents.
 It is a significant cause of morbidity
and mortality in children and
adolescents despite advances in the
management and prophylaxis of the
disease with antimicrobial agents.
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5.  Native or prosthetic heart valves are
the most frequently involved sites.
 Endocarditis also can involve septal
defects, the mural endocardium, or
intravascular foreign devices such as
intracardiac patches, surgically
constructed shunts, and intravenous
catheters.
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6.  Infective endarteritis is a similar
clinical illness involving arteries,
including the ductus arteriosus, the
great vessels, aneurysms, or
arteriovenous shunts.
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7. EPIDEMIOLOGY
 The prevalence of definite IE was
approximately 12%, and definite or
possible IE was 20%.
 About 35-50% of children with IE have
CHD.
 The risk of IE is increased in patients
with complex cyanotic heart disease,
especially in those who undergo
surgical procedures
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8.  The cumulative incidence of IE over
25 years following surgery was
determined for the following CHD
defects.
 Valvular aortic stenosis — 13.3%
 Coarctation of the aorta — 3.5%
 Primum atrial septal defect — 2.8%
 Ventricular septal defect (VSD) — 2.7%
 Tetralogy of Fallot (TOF) — 1.7%
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9. ETIOLOGIES
 Gram-positive cocci account for about
90% of recoverable bacteria( Adult
studies)
 Viridans-type streptococci (α-hemolytic
streptococci) and S.aureus remain the
leading causative agents.
 Staphylococcal endocarditis is more
common in patients with no underlying
heart disease.
 viridans group streptococcal infection is
more common after dental procedures.
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10.  Group D enterococci are seen more
often after lower bowel or
genitourinary manipulation.
 P.aeruginosa or S.marcescens is seen
more frequently in intravenous drug
users.
 Fungal endocarditis – one of the most
feared forms (complications, like
embolization are common)
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11.  Fungal organisms are encountered
after open heart surgery.
 Coagulase-negative staphylococci are
common in the presence of an
indwelling central venous catheter.
 Gram-negative organisms cause
<10% of the endocarditis in children.
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12.  Approximately 5% -10% of patients
with endocarditis have negative blood
cultures.
 The most common cause of culture-
negative IE is current or recent
antibiotic therapy or infection caused
by a fastidious organism that grows
poorly in vitro.
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13. Pathogenesis
 Turbulent flow traumatizes the
vascular endothelium, creating a
substrate for deposition of fibrin and
platelets, leading to the formation of a
nonbacterial thrombotic embolus
(NBTE).
 Biofilms form on the surface of
implanted mechanical devices such as
valves, catheters, or pacemaker wires
that also serve as the adhesive
substrate for infection.
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14.  The development of transient
bacteremia then colonizes this NBTE
or biofilm, leading to proliferation of
bacteria within the lesion.
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15. Occurrence of transient bacteremia
Adherence of bacteria to the NBTE
Proliferation of bacteria with in the
vegetation
 Large fibrin deposit encase the bacteria
inside
 Prevent phagocytosis and anti-microbial
penetration
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16.  Virtually all vegetations occur in areas
where there is a pressure gradient with
resulting turbulence of blood flow.
 The sites of high-velocity jets where
most IE vegetations occur are on the
atrial side of the atrioventricular valves
and the ventricular side of the semilunar
valves.
 In ≈30% of patients with infective
endocarditis, a predisposing factor is
presumably recognized.
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17. Relative risk of IE for underlying
cardiac lesions & conditions
High risk:
prosthetic valves
Previous episode of endocarditis
Complex cyanotic congenital heart
diseases (e.g. single ventricle states,
TGA, TOF)
Surgically corrected systemic artery to
pulmonary artery shunts
Injection drug use
Indwelling central venous catheters
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18. Moderate risk
uncorrected PDA
Uncorrected VSD
Bicuspid Aortic valve
Mitral valve prolapse with regurgitation
Rheumatic mitral or aortic valve
diseases
Hypertrophic cardiomyopathy
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19. Negligible risk
 Isolated secundum atrial septal defect
 Surgical repair of ASD, VSD, or PDA
(without residual beyond 6 mo)
 Previous coronary artery bypass graft
surgery
 Mitral valve prolapse without valvar
regurgitation
 Previous rheumatic fever without valvar
dysfunction
 Cardiac pacemakers (intracardiac and
epicardial) and implanted defibrillators
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20. Clinical manifestations
Result from:
Hemodynamic and structural changes
caused by the local infection
Embolization from vegetations, or
Immunologic reactions by the host
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21. Conti……
HISTORY
 Prior congenital or rheumatic heart
disease
 Preceding dental, urinary tract, or
intestinal procedure
 Intravenous drug use
 Central venous catheter
 Prosthetic heart valve
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22. SYMPTOMS
 Non specific symptoms(Fever,Chills,
Arthralgia, myalgia, Malaise,
weakness)
 Chest and abdominal pain
 Dyspnea
 Night sweats
 Weight loss
 CNS manifestations (stroke, seizures,
headache
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23. SIGNS
 Elevated temperature
 Tachycardia
 Vascular- Embolic phenomena (Roth spots,
petechiae, splinter nail bed hemorrhages,
CNS or ocular lesions)
 Immune complex phenomena
(glomerulonephritis, arthritis,Osler nodes,
Roth spot, )
 Janeway lesions
 New or changing murmur
 Splenomegaly
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24.  Heart failure
 Arrhythmias
 Metastatic infection (arthritis,
meningitis, mycotic arterial aneurysm,
pericarditis, abscesses, septic
pulmonary emboli)
 Clubbing
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29. DIAGNOSIS
Blood culture
 Three to 5 separate blood collections
should be obtained.
 The timing of collections is not
important because bacteremia can be
expected to be relatively constant.
 In 90% of cases of endocarditis, the
causative agent is recovered from the
first 2 blood cultures
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30.  Usually 20 to 30 mL of blood is collected
from an adult patient, but this is not
possible in a small child.
 Thus 1 to 3 mL in infants and young
children and 5 to 7 mL in older children
are optimal.
 Usually, three blood cultures are
obtained by separate venipunctures on
the first day, and if there is no growth by
the second day of incubation, two more
may be obtained. 8/28/2020 30IE

31.  Antimicrobial pretreatment of the patient
reduces the yield of blood cultures to 50-
60%
 Echocardiography
◦ evidence of valve vegetations,
◦ prosthetic valve dysfunction or leak,
◦ myocardial abscess,
◦ new-onset valve insufficiency
◦ predicting embolic complications( fungating
mass >1cm in size)
◦ sensitivities in children reported to be >80%
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32. Other laboratory findings
 Elevated erythrocyte sedimentation rate; may be low
with heart or renal failure
 Elevated C-reactive protein
 Anemia
 Leukocytosis
 Immune complexes
 Hypergammaglobulinemia
 Hypocomplementemia
 Rheumatoid factor
 Hematuria
 Renal failure: azotemia, high creatinine
(glomerulonephritis)
 Chest radiograph: bilateral infiltrates, nodules, pleural
effusions
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33. Duke crteria
Major criteria
1) positive blood cultures (2 separate
cultures for a usual pathogen, 1 or more
for less-typical pathogens), and
2) evidence of endocarditis on
echocardiography
-intracardiac mass on a valve or other site
-regurgitant flow near a prosthesis
-abscess
-partial dehiscence of prosthetic valves, or
- new valve regurgitant flow
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34. Minor criteria
 Predisposing conditions,
 fever,
 Embolic-vascular signs,
 Emmune complex phenomena
(glomerulonephritis, arthritis, rheumatoid
factor, Osler nodes, Roth spots),
 A single, positive blood culture or
 Serologic evidence of infection, and
 Echocardiographic signs not meeting the
major criteria.
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35.  clubbing,
 splenomegaly,
 splinter hemorrhages,
 petechiae
 a high erythrocyte sedimentation rate
 a high C-reactive protein level
 the presence of central nonfeeding
lines, peripheral lines,
 microscopic hematuria
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36. Definite infective endocarditis (IE):
 Pathologic criteria:
◦ Micro-organisms demonstrated by culture or
histologic examination of a vegetation, a
vegetation that has embolized, or an intracardiac
abscess specimen; or
◦ Pathological lesions; vegetation or intracardiac
abscess confirmed by histologic examination
showing active endocarditis
 Clinical criteria :
◦ 2 major criteria; or
◦ 1 major criterion and 3 minor criteria; or
◦ 5 minor criteria
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37. Possible IE:
◦ 1 major criterion and 1 minor criterion; or
3 minor criteria
Rejected IE:
◦ Firm alternative diagnosis explaining
evidence of IE; or
◦ Resolution of IE syndrome with antibiotic
therapy for 4 days; or
◦ No pathologic evidence of IE at surgery or
autopsy, with antibiotic therapy for 4 days; or
◦ Does not meet criteria for possible IE as
above
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38. COMPLICATIONS
 PREDISPOSING FACTORS
◦ Prosthetic cardiac valves
◦ Left-sided involvement
◦ Staphylococcus aureus or fungal IE
◦ Previous IE
◦ Prolonged symptoms ≥3 months
◦ Cyanotic congenital heart disease
◦ Systemic-to-pulmonary shunts
◦ Poor clinical response to antimicrobial
therapy
◦ Vegetation size >10mm
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39.  Heart failure
 Myocardial abscess
 Toxic myocarditis
 Arrhythemia
 mycotic aneurysms,
 rupture of a sinus of Valsalva,
 obstruction of a valve secondary to large
vegetations
 Thromboembolic phenomenon
 Heart block
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40.  meningitis,
 osteomyelitis,
 arthritis,
 renal abscess,
 purulent pericarditis, and
 immune complex-mediated
glomerulonephritis
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41. treatment
Antimicrobial
 General principles
◦ Prolonged periods of treatment(4 to 6
weeks)
◦ Bacteriocidal rather than bacteriostatic
◦ Parentral antibiotic
◦ High dose
◦ Combination of antibiotic which have
synergistic effect
◦ Managed in hospital initialy
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42.  Antibiotic therapy should be instituted
immediately once a definitive
diagnosis is made.
 outpatient therapy can be undertaken
if the patient is afebrile, has negative
blood cultures, and is at negligible
risk for complications.
 Empiric therapy should cover
staphylococci, streptococci, and
enterococci.
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43.  Most patients with IE become afebrile
5-6 days after treatment is begun with
an appropriate antibiotic.
 Patients with S. aureus endocarditis
may respond somewhat more slowly,
remaining febrile for 5-7 days after the
institution of therapy
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44.  The initial microbiologic response to
therapy should be assessed by
obtaining repeat blood cultures 48 -72
hours after antibiotics are begun.
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45. Surgical management
 INDICATIONS
◦ Severe aortic, mitral or prosthetic valve
involvement with intractable heart failure.
◦ Mycotic aneurysm
◦ Rupture of an aortic sinus
◦ Intraseptal abscess causing complete
heart block
◦ Dehiscence of an intracardiac patch
◦ Fungal endocarditis
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46. ◦ Failure to sterilize the blood despite
adequate antibiotic levels in 7-10 days
◦ Increasing size of vegetations while
receiving therapy.
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47. PROPHYLAXIS
 Prosthetic cardiac valve
 Previous infective endocarditis
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48. CONGENITAL HEART DISEASE
(CHD)
 Unrepaired cyanotic CHD
 Completely repaired CHD with
prosthetic material or device during
the 1st 6 mo after the procedure
 Repaired CHD with residual defects
 Cardiac transplantation recipients who
develop cardiac valvulopathy.
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49. reference
 Nelson 20th edition
 Moss and Adams cardiology 7th edition
 Uptodate 20.2
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