Infective endocarditis

infection of endocardium

1. Infective Endocarditis
Most important acquired
cardiovascular disease
Significant cause of morbidity in
pediatric age group
Includes acute and subacute bacterial
endocarditis
Nonbacterial endocarditis
JERIN.T.S, 3RD YEAR BSC
NURSING, KRSMCON
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2. Infective endocarditis is a form of
endocarditis, or inflammation, of
the inner tissue of the heart, such
as its valves, caused by infectious
agents. The agents are usually
bacterial, but other organisms can
also be responsible like fungi or
Rickettsia.
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3. The valves of the heart do not receive any
dedicated blood supply. As a result,
defensive immune mechanisms (such as
white blood cells) cannot directly reach the
valves via the bloodstream. If an organism
(bacteria) attaches to a valve surface and
forms a vegetation, the host immune
response is blunted. The lack of blood
supply to the valves also has implications
on treatment, since drugs also have
difficulty reaching the infected valve.
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4. Vegetations in the Heart
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5. Definition
Infective endocarditis/ subacute bacterial
endocarditis is an infection of the valves
and inner lining of the heart.
It develops most often as a complication
of congenital or rheumatic heart disease
but can occur without an underlying heart
disease.
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6. Incidence
Commonly seen in children of 10 or
above 10 yrs
Occasionally seen in infants and young
children rare below 2yrs.
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7. Etiology
Causative organisms
Streptococcus viridans
Staphylococcus aureus
Enterococci
Pseudomonas aeruginousa
Candida albicans
Rickettsia
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8. Classification
By duration :
Clinically divided into acute and subacute:
Subacute bacterial endocarditis (SBE) is often
due to streptococci of low virulence and mild to
moderate illness which progresses slowly over
weeks and months.
Acute bacterial endocarditis (ABE) is a fulminant
illness over days to weeks, and is more likely
due to Staphylococcus aureus which has much
greater virulence, or disease-producing capacity
and frequently causes metastatic infection.
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9. By Side of the heart
Endocarditis can also be classified by
the side of the heart affected:
Patients who inject narcotics or other drugs
intravenously may introduce infection which will
travel to the right side of the heart classically
affecting the tricuspid valve.
In other patients without a history of intravenous
exposure, endocarditis is more frequently left-
sided.
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10. By culture media
Infective endocarditis may also be classified as
culture-positive or culture-negative. The most
common cause of a "culture-negative"
endocarditis is prior administration of antibiotics.
Some times the organism may take a long time
to grow in the culture media which may also
cause culture-negative endocarditis

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11. By valve type
Native valve endocarditis
Prostatic valve endocarditis

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12. Predisposing factors
1.Bacteremia in child with congenital
anomalies of the heart
2.Children with vascular abnormalities
3.Recent cardiac surgery with invasive
lines
4.Prostatic valves
5.Rheumatic heat disease with valvular
involvement
6.Drug abuse
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13. 7. Dental procedures without aseptic
precautions
8. Tonsillectomy/ adenoidectomy
9. Bronchoscopy
10 .Esophageal stricture dilatation
11. Manipulation of urinary tract
12. Long term I.V lines and central lines
13. Lymphatic spread from a wound site
14. Infected thrombi which attain direct
access into the general circulation
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14. Pathophysiology
Organisms enter the blood stream from
any site of localized infections like
-Dental procedure (S.viridans)
-Urinary tract catheterization (Gram -ve
bacilli)
-Cardiac surgeries, valves, patches etc
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15. Because of the congenital lesions:
High velocity turbulent flow
¯
Erosion of intima of vessels & endocardium
¯
Growth of microorganisms on the endocardium
¯
Formation of vegetations
¯
Formation of fibrin & platelet thrombi
¯
Invasion of adjacent tissues like myocardium, aortic and
mitral valve
¯
Breaking of thrombi & formation of emboli
¯
Travel to lungs, kidneys, spleen, brain, skin and mucus
membrane
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16. Clinical features may be grouped
into
1)Indicating the presence of an infection
2)Indicating involvement of the
cardiovascular system
3)Indicating the presence of an
immunological reaction to infection
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17. Clinical features
It may be acute or insidious in onset.
1.History of urinary tract manipulation, dental
work or any surgery
2.Unexplained low grade fever for 7-10days
3.Weight loss and cough
4.Anorexia
5.Malaise and fatigue
6.Body stiffness
7.Rigor
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18. 7.Muscle pain (myalgia), arthralgia (due to thrombi)
8.Head ache, seizures
9.Spleenomegaly
10.Murmur (incompetent valve)
11.Chest and abdominal pain
12.Night sweats
13.Tachycardia
14.Arrhythmias
15.Clubbing
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19. 16. Petecheae appears on skin,
17. Conjunctival bleeding,
18. Oral mucosal bleeding,
19. Roth’s spots on retina,
20. Hematuria from renal infarct
21. Left flank pain from spleenic infarct
22. G.I bleeding from mesenteric embolism
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20. Classic signs –
Roth spots (retinal hemorrhages with a pale
center),
Janeway lesions (nontender macules on
fingers and soles),
Osler nodes (painful lesions on hands and
feet),
splinter hemorrhage – are rare in children
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21. ROTH SPOT
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22. 23. Jane way lesions
( painless hemorrhagic lesions on palms and
soles)
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23. JERIN.T.S, 3RD YEAR BSC NURSING,
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24. 24. Splinter hemorrhage
darkened lines under the nails
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25. 25. Osler nodes
Tender small painful intradermal nodules in
the pads of fingers And toes
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26. JERIN.T.S, 3RD YEAR BSC NURSING,
KRSMCON MANGALORE. PH:
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27. JERIN.T.S, 3RD YEAR BSC NURSING,
KRSMCON MANGALORE. PH:
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28. Diagnostic measures
1.Positive blood culture
2.Elevated CRP
3.Hemolytic anemia Hb 10g%
4.Leukocytosis 15,000-20,000/cmm
5.Immune complexes
6.Hypergamaglobulenemia
7.Positive serum rheumatoid factor
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29. 8.Microscopic Hematuria & albuminuria
9.In Renal failure : azotemia, high creatinine
10.Chest X-Ray : bilateral infiltrates, nodules,
pleural effusion
11.Echocardiography evidence of valve
vegetation,

prosthetic valve dysfunction or leak,
myocardial abscess.
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30. Pathologic evidence of intracardiac or embolized
vegetation or intracardiac abscess OR
2 major, 1 major and 3 minor, or 5 minor of the Duke
Criteria:
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31. DUKE CRITERIA
Major:
1)Positive blood culture with typical
Infective Endocarditis microorganism
-S.viridans
-Streptococcus bovis
-Staphylococus aureus
2 positive blood culture samples drawn
>12 hours apart
2) Positive echocardiogram
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32. Minor
1)Predisposing factors
2)Fever >38
o
C
3)Embolism, infarct, Janeway Lesions ,
conjunctival hemorrage
4)Immunological problems- G. nephritis,
oslers nodes
5)Positive blood culture.
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33. Principles of management
Identification of the organism
Finding out the antibiotic sensitivity
Starting treatment as early as possible
Starting heavy doses of bactericidal
antimicrobial agents.
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34. Management
High dose of antibiotics for 2-8 week IV like
1)Crystalline penicillin 2-3lac units/kg/day for 4-6weeks
2)Cefazoline
3)Ampicillin, methicillin
4)Cloxacillin
5)Streptomycin
6)Gentamycin 2-4mg/kg/day
7)Amphotericin B for fungal
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35. Surgical management: valve replacement

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KRSMCON MANGALORE. PH:
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36. Nursing management
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NURSING, KRSMCON
MANGALORE. PH:
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37. Aims of nursing management
1)To reduce the cardiac demands & O
2

consumption
2)To reduce respiratory distress
3)To improve tissue oxygenation
4)Improve contractility of the heart
5)Assess the cardiac status
6)Maintain nutrition & hydration
7)Prevention of infection
8)Reduce anxiety & support parents
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38. JERIN.T.S, 3RD YEAR BSC NURSING,
KRSMCON MANGALORE. PH:
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39. a.Health education
b.Counseling of parents
c.Maintaining oral hygiene
d.Preparing the child for IV infusion
e.Observing for side effects of
antibiotics
f.Frequent blood culture
g.Observing the complications
h.Follow up
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KRSMCON MANGALORE. PH:
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40. Prevention
Antibiotic prophylaxis before
procedures such as dental resiratory,
G.I, genitourinary.
Amoxicillin
Ampicillin
Penicillin G
Erythromycin
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41. prognosis
Even with antibiotics mortality is
20-25%
Death due to C.C.F, cardiac
perforation, M.I from coronary
emboli.
Child may die with sudden epileptic
fits due to emboli blocking the
cerebral vessels
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42. Complications
Damage to valve cusps or perforation
Rupture of chordae tendinae
Embolic neaurological deficit
Renal infarcts with hematuria
Mesenteric infarcts & malena
Loss of fingers & toes due to loss of blood
supply
IgM, IgG complements deposited on
glomeruli causing nephritis
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