Infective endocarditis (IE) is an infection of the endocardium

and/or heart valves that involves thrombus formation (vegetation),

which may damage the endocardial tissue and/or valves.
Pediatric patients are rarely diagnosed as having infective
endocarditis (IE); however, IE is a significant cause of morbidity and
mortality in children.

Most often IE is a complication of CHD, but it can occur in children

who do not have a cardiac abnormality.
• Congenital heart disease
• Central venous catheters
• Rheumatic heart disease
• Other risk factors: Intravenous drug abuse (associated with
right-sided IE) and degenerative heart disease, which are
important predisposing factors in the adult population, are less
commonly seen in children
The most common organisms responsible for IE in pediatric
patients with or without CHD are viridans streptococci and
Staphylococcus aureus.

Fungi, most commonly Candida and Aspergillus, can also be

responsible for IE, especially in hospitalized patients who have
prosthetic valves or indwelling CVCs.
 The clinical presentation of pediatric IE can be classified as either
a subacute or acute process.
Common Manifestations of Pediatric Infective Endocarditis
Manifestation Frequency, % Manifestation Frequency, %
Fever 75–100 Splenomegaly 50–75
Symptoms

Malaise 50–75 Embolic phenomenon 25–50

Signs
Anorexia 25–50 Murmur (new or changing) 21–50
Heart failure 25–50 Petechiae 21–50
Arthralgia 17–50
Children rarely have the classic signs of IE that
develop late in disease, such as:

Roth spots (small retinal hemorrhages),

Janeway lesions (small, painless, hemorrhagic lesions on the
palms and soles),
Osler nodes (small, tender, intradermal nodules on the
fingers and toes),
Splinter hemorrhages (linear streaks beneath the nail beds).
IE is a complex syndrome that requires the presence of multiple
findings to establish the diagnosis.

The Duke criteria serve as a clinical guide to aid in the diagnosis of

IE and have been validated and modified to increase sensitivity.
 Modified Duke Criteria for the Diagnosis of IE
Definite IE:
Pathologic Criteria:
1. Microorganisms demonstrated by culture or histologic testing in
a vegetation, embolized vegetation, or intracardiac abscess; or
2. Pathologic lesions (vegetation or intracardiac abscess) with
active endocarditis confirmed by histologic testing.

Clinical Criteria:
2 major criteria,
1 major and 3 minor criteria, or
5 minor criteria
 Modified Duke Criteria for the Diagnosis of IE
Major Criteria
1. Positive blood culture result for IE:
a. Typical microorganism consistent with IE from 2 separate blood
cultures:
i. Viridans streptococci, ii. Streptococcus bovis, iii. AAECK group
iv. Staphylococcus aureus, v. Community-acquired enterococci (without a primary focus)
b. Microorganism consistent with IE from blood cultures with
persistently positive results if:
i. At least 2 positive results of blood cultures sampled > 12 hours apart
ii. All 3 or a majority of more than 4 blood cultures
c. Single positive blood culture for Coxiella burnetii or IgG antibody titer
>1:800
2. Evidence of endocardial involvement by echocardiogram result
positive for IE,
 Modified Duke Criteria for the Diagnosis of IE
Major Criteria
1. Positive blood culture result for IE:
2. Evidence of endocardial involvement by echocardiogram result
positive for IE, defined as:
a. Oscillating intracardiac mass on valve or supporting structures
in the path of regurgitant jets or on implanted material
b. Abscess
c. New partial dehiscence of prosthetic valve
d. New valvular regurgitation (worsening or changing of
preexisting murmur not sufficient).
Modified Duke Criteria for the Diagnosis of IE
Major Criteria.
Minor Criteria:
1. Predisposing heart condition or intravenous drug abuse.
2. Fever: temperature 100.4oF (≥38oC).
3. Vascular phenomena:
major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial
hemorrhage, conjunctival hemorrhages, Janeway lesions.
4. Immunologic phenomena:
glomerulonephritis, Osler nodes, Roth spots, rheumatoid factor
5. Microbiologic evidence:
positive blood culture result but does not meet major criteria or serologic evidence
of active infection with organism consistent with IE.
 Modified Duke Criteria for the Diagnosis of IE
Possible IE:
1. 1 Major criterion and 1 minor criterion
2. 3 Minor criteria

Rejected
1. Firm alternative diagnosis for manifestations of endocarditis.
2. Resolution of endocarditis manifestations with antibiotic ≤ 4 days.
3. No pathologic evidence of IE at surgery or autopsy with antibiotic
therapy for ≤ 4 days
4. Does not fulfill criteria above
Blood cultures are the most important laboratory test for the diagnosis of IE
Because IE can be caused by organisms found on the skin, it is important to
obtain 3 or more cultures on separate occasions to reduce the likelihood of
contamination.
Other nonspecific laboratory findings can be present, including:
Increased erythrocyte sedimentation rate,
Anemia,
Positive rheumatoid factor,
Hematuria, and
Low complement.

Elevated b-natriuretic peptide and troponin I levels can indicate cardiac

injury.
ECHO is the primary imaging modality used in the diagnosis and
treatment of IE.

It allows visualization of the abnormalities listed in the Duke criteria:

vegetations, abscesses, or prosthetic valve dehiscence
Figure. Echocardiogram of a 21-month-old girl with Staphylococcus
aureus bacteremia. A vegetation is present on the anterior mitral
valve.
Antibiotic regimens for IE are based on the patient’s age, clinical
presentation, cardiac status, and organisms most commonly
isolated in infections.
Intravenous bactericidal antibiotics are necessary for the
treatment of IE, and high serum levels are required to eliminate
bacterial growth at the site of infection.
Before identification of a pathogen and after appropriate volume
blood cultures are obtained, empiric vancomycin and gentamicin
therapy is recommended because this regimen provides coverage
against the most common pathogens of IE, S aureus and viridans
streptococci.
If a specific pathogen is identified in culture, the antibiotic
regimen can be tailored based on susceptibility profiles.

Typically, 4 to 6 weeks of therapy is recommended in

uncomplicated cases of IE; however, longer courses are
required in patients who have prosthetic valves.

Clinical response to therapy should be monitored closely to

determine whether antibiotic modification or surgical
intervention is necessary.
Surgical interventions to remove vegetations or replace valves can
be life-saving in the management of certain cases of IE.

Surgery should be considered in patients with intractable heart

failure, prosthetic valve endocarditis, and uncontrolled infection
(persistent fever and positive blood culture results for more than 5-7
days) and for those at high risk of embolic events.
Conditions for Which Prophylaxis for IE Is Recommended:

Prosthetic cardiac valve or prosthetic material used for

cardiac valve repair.
Previous IE
CHD:
Unrepaired cyanotic CHD, including palliative shunts and
conduits
Completely repaired defect with prosthetic material or device
during the first 6 months after the procedure
Repaired CHD with residual defects at the site or adjacent to
the site of a prosthetic patch or prosthetic device
Cardiac transplantation recipients who develop cardiac
valvulopathy
 Definition:
Immunologic disease affecting connective tissue of the
heart, joints & skin as a consequence of infection with group
A beta hemolytic streptocci

Risk factors:
1- Onset between 5-15 year (rare before 5 years).
2- Low socioeconomic status ,poverty ,poor sanitation.
3- Genetic predisposition (Associated with certain
HLA).
4- Group A -hemolytic strept pharyngitis (with M
serotypes 1, 3, 5, 6,18, 24)
 Pathogenesis:
1- Following strept infection antibodies is formed against
strept cross react against host connective tissue.
2- Inflammation is either
 Exudative (as in joints) → resolve without residual
damage
 Aschoff nodules (in the heart) → heal by fibrosis.

Clinical Picture:
(latent period of 1-3 weeks usually lapse between
pharyngitis & acute rheumatic fever)
 Major criteria of Rheumatic fever
i- Arthritis (75%)
 Usually affect big joints (e.g. knee, ankles, wrist,
elbow).
 Polyarticular, either simultaneous or successive.
 Migratory (fleeting) form one joint to another.
 Affected joint is:
➢ red - hot – swollen
➢ with absolute limitation of movement (severely tender)
 Dramatic response to salicylates.
 Resolve without residuals, even without treatment, over
days to few weeks.
ii- Carditis (50%)
Endocarditis:
Valvulitis affecting commonly mitral valve with or without
aortic valve:
1- Mitral valve:
 Leaflets oedema → transient mitral stenosis (Carey
Combs murmur)
 Leaflets destruction → mitral regurgitaion.
2- Aortic valve → aortic regurgitaion.
Myocarditis:
1- Tachycardia → out of proportion to age & fever.
2- Heart failure (with gallop rhythm, muffled heart sounds
& cardiomegaly) indicates severe carditis
 Pericarditis:
1- Dry pericarditis:
 Stitching chest pain.
 Pericardial rub (unrelated to respiration).
2- Pericardial effusion:
 uncommon.
 dull aching pain.
 distant heart sounds.
 Low voltage ECG.

N.B: Carditis may be silent or late onset (appear after

6 week – 6 months of onset)
iii- Rheumatic chorea “Sydenham chorea” (10%)

 Incidence
➢ more in girls 8-12 years (school age).
➢ occur weeks or months after strept. pharyngitis so,
other criteria are usually lacking.

A/E:
Dysfunction of the basal ganglia due to antineuronal
antibodies.
 Manifestations:
1- Emotional lability and personality changes.
2- Involuntary movements:
➢ Spontaneous purposeless movements of limbs and
facial grimace.
➢ increase with emotional stress and decrease by sleep.
➢ Last for months.
3- Hypotonia.
 Tests for chorea:

➢ Milk maid’s grip: irregular contraction & relaxations

while sequeezing examiner fingers (choreic hand).
➢ Extension of arm → spooning & pronation of hands.
➢ Wormian movements of tongue upon protrusion.
➢ Evaluate hand writing.
iv- Erythema marginatum (< 5%)

 Site
➢ on the trunk & proximal parts of the limbs.

Criteria
➢ large erythematous macules.
➢with pale centers & serpiginous borders.
➢evanescent.
➢not pruritic
iv- Erythema marginatum (< 5%)
v- Subcutaneous nodules (< 1%)

 Site
➢ over the extensor surfaces of tendons near bony
prominence.

 Criteria
➢ size about 1 cm.
➢ firm, mobile, painless.
➢ usually associated with severe carditis.
v- Subcutaneous nodules (< 1%)
 Minor criteria of Rheumatic fever
A- Clinical:
1- Fever → usually between 38.4 – 40 C
2- Arthralgia
3- Prolonged P-R interval in ECG.
Arthralgia & prolonged P-R interval can’t be used as
minor manifestation in presence of arthritis or carditis
respectively.
B- Laboratory:
→  ESR 4-  acute phase reactants
→  C-reactive protein.
→ Leukocytosis.
 Modified Jones criteria for Rheumatic Fever
diagnosis (1992)
I- 2 major criteria or 1 major & 2 minor criteria.
Plus.
II- Evidence of recent streptococcal infection.
•. +ve throat swab.
•  ASO titer.
•  Anti Deoxyribonuclase (DNase)  titer.
 Prognosis:
1- Arthritis subside within days to weeks even without
treatment.
2- Chorea subside within few months without residuals.
3- Only carditis can cause permanent damage especially in
recurrences which may Result in organic valve lesions
e.g. → MS, AS, combined valve lesions.
4- Recurrences is suggested by:
 Appearance of new murmurs.
 Change in character of the murmur.
 Carditis.
 Fever with arthritis or arthralgia.
Differential diagnosis:
1- Other causes of arthritis
 Rheumatoid arthritis:
➢ Involve small peripheral joints.
➢ Non migratory
➢ No evidence of recent strept. Infection.
➢ No response to salicylates within 48 hours.
➢ Deformities are common.
 Infections → viral, bacterial, T.B.
 Hematologic → hemophilia, leukemia
 Immunologic → SLE & HSP
 2- Other causes of carditis e.g.:
 Vial carditis.
 Infective endocarditis.
 Drug induced.

3- Other causes of chorea e.g.:

 Wilson disease.
 Huntington chorea
 Cerebral palsy.
Treatment of acute Rheumatic fever:
1- Prophylactic:
1ry prevention:
 Hygienic housing.
 Proper treatment of strept. infection: penicillin or
erythromycin for 10 days.
2ry prevention:
 Prevent recurrence of Rheumatic fever by:
➢ Long acting penicillin (Benzathine penicillin)
➢ Dose → 0.6 – 1.2 million unit single injection, I.M
every 3-4 weeks.
➢ For at least 5 years after last acute attack (for life if
patient had carditis).
➢ Alternatives: daily oral penicillin V or erythromycin
(250 mg twice daily)
 Prophylaxis against infective endocarditis for cases with
valvular lesions.
2-Treatment of acute attack:

1- Bed rest: needed mainly for cases with carditis & heart
failure till heart failure is controlled & ESR is
normalized
2- Diet: light, low salt in cases with heart failure.
3- Eradicate strept. infection by: Oral penicillin V or
Erythromycin (for penicillin sensitive) for 10 days.
 4- Anti inflammatory drugs.
a- Salicylates
 Indications:
➢ Rheumatic arthritis
➢ Mild rheumatic carditis without heart failure.
➢ During steroid withdrawal
 Dose: 100 mg/kg/day (max = 6 gram /day); in four
devided doses.
➢ For 3-5 days then 75 mg/kg/d for 4 weeks .then
➢ Gradual withdrawal monitored by decline in ESR &
CRP
 Side effect:
➢ Toxicity (early symptoms are tinnitus,
hyperventilation)
➢ Gastritis → GIT bleeding
➢ Reye’s syndrome
 b- Corticosteroids (Prednisone)
 Indications:
➢ Moderate to severe carditis
➢ Heart failure.
 Dose: 2 mg/kg/d (max = 60 mg/day); in devided
doses
for 2-3 weeks Then
➢ Taper the dose by reducing 5 mg (one tablet) every
2-3 days.
➢ At beginning of tapering aspirin is started with dose
75 mg/kg/d for 6 weeks.
Treatment of rheumatic chorea: 5-
i- Avoid emotional stress.
ii- Control abnormal movements:
 Phenobarbitone 15-30 mg / 8 hours oral.
 Or Haloperidole (Safinase tablet) 0.01-0.03 mg/kg.
 Or chlorpromazine 0.5 mg/kg.
iii- Long acting penicillin prophylaxis
6- Treatment of:
 heart failure (diuretics-vasodilators–Digoxin used
cautiously).
 Infective endocarditis.