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Infective endocarditis
1. Dr.Azad A Haleem AL.Brefkani
University Of Duhok
Faculty of Medical Science
School Of Medicine
Pediatrics Department
azad82d@gmail.com
2015
2. Definition of Infective Endocarditis
• Infective endocarditis, a serious infection of
the endocardium of the heart, particularly the
heart valves,
• It generally occurs in patients with
• altered and abnormal heart architecture, in
combination with
• exposure to bacteria.
3. Etiology
• Infective endocarditis includes acute and
subacute bacterial endocarditis,
• as well as nonbacterial endocarditis caused by
viruses, fungi, and other microbiologic agents.
4. Etiology
• Viridans-type streptococci (α-hemolytic streptococci)
and Staphylococcus aureus remain the leading
causative agents for endocarditis in pediatric patients.
• Other organisms cause endocarditis less frequently
and, in ≈6% of cases, blood cultures are negative for
any organisms.
• Staphylococcal endocarditis is more common in
patients with no underlying heart disease;
• viridans group streptococcal infection is more common
after dental procedures;
• group D enterococci are seen more often after lower
bowel or genitourinary manipulation;
5. Distinction between Acute and
Subacute Bacterial Endocarditis
Feature Acute Subacute
Underlying Heart
Disease
Heart may be normal RHD,CHD, etc.
Presentation Toxic presentation
Progressive valve
destruction & metastatic
infection developing in
days to weeks
Mild toxicity
Presentation over weeks
to months
Organism S. aureus, Pneumococcus
S. pyogenes,
Enterococcus
viridans
Streptococci,
Entercoccus
6. Pathophysiology
• Turbulent blood flow due to a hole or stenotic orifice,
especially if there is a high pressure gradient across the
defect, are most susceptible to endocarditis.
• This 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) that is thought to be the initiating lesion
for infective endocarditis.
Bacteraemia – delivers organisms to the damaged (sticky)
endocardial surface resulting in adherence & colonisation
Eventual invasion of valve leaflets results in infected
vegetation (sheath of fibrin & platelets, ideal conditions for
further bacterial multiplications)
7. Epidemiology
• Infective endocarditis is often a complication
of congenital or rheumatic heart disease
• but can also occur in children without any
abnormal valves or cardiac malformations.
8. • Children at highest risk of adverse outcome
after infective endocarditis include those with:
• congenital heart disease.
• Repaired congenital heart disease.
• congenital or acquired valvular heart
disease.
• Immunocompromised patients with central
venous line.
9. Bacterial Endocarditis
Predisposing Factors
1. Dental manipulation & Dental disease (caries,
abscess)
3. Extra cardiac infection (lung, urinary
tract,skin, bone, abscess)
4. Instrumentation (urinary tract, GI tract, IV
infusions)
5. Cardiac surgery
6. Injection drug use
7. None apparent
10. Clinical Features
Fever (Prolonged fever without other manifestations that persists for as
long as several months may be the only symptom).
The symptoms are often nonspecific and consist of low-grade fever with
afternoon elevations, fatigue, myalgia, arthralgia, headache, and, at
times, chills, nausea, and vomiting.
Heart murmur (New or changing heart murmurs are common)
Nonspecific signs : Petechial and cutaneous manifestations, Conjunctival
and mucosal petechiae, splinter hemorrhages. petechiae,splinter
hemorrhages, clubbing.
Splenomegaly
More specific signs - Osler’s Nodes, Janeway lesions, and Roth Spots.
Splenomegaly
Embolism: CNS, spleen, lung, retinal vessels, coronary artery, large
vessels.
CHF
General. Weight loss, anorexia.
11. • Osler nodes (tender, pea-sized intradermal
nodules in the pads of the fingers and toes),
• Janeway lesions (painless small erythematous
or hemorrhagic lesions on the palms and
soles), and
• splinter hemorrhages (linear lesions beneath
the nails).
• These lesions may represent vasculitis
produced by circulating antigen-antibody
complexes.
12. Janeway Lesions
1. More specific
2. Erythematous, blanching macules
3. Nonpainful
4. Located on palms and soles
13. Splinter Hemorrhages
1. Nonspecific
2. Nonblanching
3. Linear reddish-brown lesions found under the nail bed
4. Usually do NOT extend the entire length of the nail
16. Osler’s Nodes
1. More specific
2. Painful and erythematous nodules
3. Located on pulp of fingers and toes
4. More common in subacute IE
17. Blood Cultures
Blood Cultures
– Minimum of three blood cultures ( start within 1 h prior to
commencement of empirical therapy)
– Three separate venipuncture sites ideally
– Obtain correct volume of blood for culture bottles
19. Imaging
Chest x-ray
– Look for multiple focal infiltrates and calcification
of heart valves
ECG
– Rarely diagnostic
– Look for evidence of ischemia, conduction delay,
and arrhythmias
Echocardiography
20. Diagnosis
• The Duke criteria help in the diagnosis of
endocarditis.
• Major criteria include
• (1) positive blood cultures; 2 separate cultures for
a usual pathogen, 2 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).
21. Minor criteria include
predisposing heart conditions, prior cardiac surgery, indwelling catheter.
Fever > 38c
embolic-vascular signs:
• Major arterial emboli.
• Septic pulmonary infarct.
• Mycotic aneurysm.
• Intracranial hemorrhage.
• Conjunectival hemorrhage.
• Janeway lesion.
immune complex phenomena:
• Glomerulonephritis
• arthritis, rheumatoid factor
• Osler nodes
• Roth spots.
positive blood culture not meeting the major criteria.
echocardiographic signs not meeting the major criteria.
22. • Two major criteria,
• one major and three minor, or
• five minor criteria suggest definite
endocarditis.
• A modification of the Duke criteria may
increase sensitivity while maintaining
specificity.
23. Prognosis and Complications
• Despite the use of antibiotic agents, mortality
is at 20-25%.
• Serious morbidity occurs in 50-60% of children
with documented infective endocarditis;
24. Complications
o Local cardiac complications:The most
common is heart failure, Myocardial abscesses, toxic
myocarditis, life-threatening arrhythmias and heart
block.
o Embolic like Stroke & Ischemic limbs
o Metastatic spread of infection like
Meningitis
o Formation of immune complexes –
glomerulonephritis and arthritis.
25. Treatment
• Antibiotic therapy should be instituted immediately
once a definitive diagnosis is made.
• Empirical therapy before the identifiable agent is
recovered may be initiated with vancomycin plus
gentamicin in patients without a prosthetic valve and
when there is a high risk of S. aureus enterococcus or
viridans streptococci (the 3 most common organisms).
• A total of 4-6 wk of treatment is usually recommended.
• Depending on the clinical and laboratory responses,
antibiotic therapy may require modification and, in
some instances, more prolonged treatment is required.
26. • If symptoms and signs of heart failure,
appropriate therapy should be instituted,
including diuretics, afterload reducing agents,
and in some cases, digitalis.
• Surgical intervention for infective endocarditis
is indicated for severe aortic or mitral valve
involvement with intractable heart failure.
• Other surgical indications include failure to
sterilize the blood despite adequate antibiotic
levels, myocardial abscess.
29. Antibiotics Guidelines IE prophylaxis
• Standard general prophylaxis:
• Oral Amoxicillin 50 mg/kg or IV/IM Ampicillin
50 mg/kg .
• Penicillin Allergy: Erythromycin 20 mg/kg
• Note: give oral therapy one hour before
procedur; IV therapy 30 min before procedure