INFECTIVE

ENDOCARDITIS
DR ANGELA ODIKE
DEFINITION
 Infective endocarditis (IE) is an infection
of the endocardial surfaces of the heart
that involves the valves and adjacent
structures.
 It includes:
1. Acute and sub acute bacterial
endocarditis
2. Non bacterial endocarditis caused by
viruses, fungi and other agents
INFECTIVE ENDOCARDITIS
IMAGE
DEFINITION
 Acute IE — develops suddenly and may
become life threatening within days
 Sub acute or chronic IE (or sub acute
bacterial endocarditis) — develops
slowly over a period of weeks to several
months.
 It is a significant cause of morbidity and
mortality in children and adolescents
 It can be fatal without treatment
REASONS FOR
MORBIDITY
 Changing nature of infecting organisms
despite prophylaxis
 Insufficient awareness in physicians,
dentists and public of the risks of IE and
prophylaxis
 Delayed diagnosis
 Emergence of a new risk group: iv drug
users, survivors of cardiac surgery, HIV
patients
AETIOLOGY
 Leading causative agents in paediatrics
are- viridans type streptococci ( ἀ-
hemolytic streptococci) and staph
aureus
 Group d enterococcus- strep bovis, s.
Faecalis
 H. Influenza
 Strep pneumonia
 Neisseria gonorrhoea
 Pseudomonas aeruginosa
CONTD
 Staph endocarditis is common in
patients with no underlying heart
disease
 Viridens IE is more common after dental
procedure
 Group d enterococci after lower bowel or
genitourinary manipulations
 Pseudomonas aerogenosa in iv drug
users
 Fungal in open heart surgery
EPIDEMIOLOGY
 The incidence has risen from 2-4 cases/
100,000 persons per year in the USA to
12.7 cases /100,000 persons per year
 The incidence is similar in other
countries
 > 50% of cases are older than 50 years
 Male: female is 3:1
 No racial predilection
EPIDEMIOLOGY
 IE usually occur in :Acquired valve diseases
(rheumatic heart disease) including mitral
valve prolapse with valve regurgitation
(leaking) and/or thickened valve leaflets.
 Congenital heart defects- VSD, ASD, PDA etc
 An artificial (prosthetic) heart valve, including
bio prosthetic and homograft valves.
 Previous bacterial endocarditis.
 A device, such as a pacemaker
 A suppressed immune system.
 An intravenous drug abuse habit.
 Hypertrophic cardiomyopathy (HCM).
CONTD
 Can also occur in children with normal
hearts
 Autopsy of cases in UCH over 30 years
in children aged 4week-13 years
-37% had underlying congenital
heart disease
-21% of them had underlying rheumatic
heart disease
-53% had no pre-existing heart lesion
 Mortality is as high as 20%
PATHOPHYSIOLOGY
 The pathophysiology of infective
endocarditis comprises at least three critical
elements:
1.Preparation of the cardiac valve for bacterial
adherence
2. Adhesion of circulating bacteria to the
prepared valvular surface
3. Survival of the adherent bacteria on the
surface, with propagation of the infected
vegetation.
 It appears that circulating bacteria do not
readily adhere to normal endothelial
surfaces.
PATHOPHYSIOLOGY
 There is usually a predisposing condition
that leads to generation of a turbulent
blood flow leading to endocardial
damage
 Platelets and fibrin are deposited at the
site of damage as an attempt to repair
the area of injury
 There is formation of a non- bacterial
thrombotic vegetation (NBTV)
CONTD
 Transient bacteremia may lead to
colonization of the NBTV
 Multiplication of the bacteria causes the
vegetation to grow
 More platelets and fibrins are deposited
 The colonized NBTV causes a constant
bacteremia and re-seeding of the
circulating organism unto the enlarging
vegetation
PATHOPHYSIOLOGY
INFECTIVE ENDOCARDITIS
INFECTIVE ENDOCARDITIS
CONTD
 Bacterial zone is largely protected from
the normal host defensive mechanism
and antibiotics
 This allows bacterial proliferation to go
unchecked
 Vegetations can be single or multiple
 Can range from few mm to several
centimeters and obstructing blood flow
CONTD
 Involvement of heart valves will lead to
ulceration, perforation, and chordal
rupture
 This will result in sudden congestive
heart failure
 Some vegetations are friable and can
lead to embolisation to distant organs
like those caused by candida albicans,
haemophilus spp and staph aureus
CONTD
 The sites involved are:
- Lungs
- Kidney
- Brain
- Spleen
CLINICAL
MANIFESTATIONS
 A high index of suspicion is required for
early diagnosis, because of non specific
signs and symptoms
 There maybe a pre-existing congenital
or rheumatic heart disease
 History of preceding dental, urinary
tract or intestinal procedure
 Or patient is an iv drug user
 Presence of central venous line or
prosthetic heart valve
CONTD
 Fever, may have a mild onset. Usually prolonged
and persists for weeks and even month ( viridens) or
acute, severe with high intermittent fever and
prostration as seen in staph aureus
 Chills
 Chest and abdominal pain
 Arthralgia, myalgia
 Dyspnea
 Malaise
 Night sweat
 Weight loss
 Seizures
 Strokes
 Headaches
CONTD

 Tachycardia
 New and changing murmur
 Splenomegaly
 Arthritis
 Heart failure
 Hepatomegaly
 Digital clubbing
 Arrhythmias
CONTD
 Roth spots- small pale retinal lesions
with areas of hemorrhage and usually
located near the optic disc
 Osler node – tender pea sized
intradermal nodules on the pads of the
fingers and toes.
 Jane way lesions- painless small
erythematous/hemorrhagic lesions on
the palms and soles
ROTH SPOT
OSLER NODE/ JANEWAY
LESION
JANEWAY LESION
CONTD
 Splinter hemorrhages- linear lesions
beneath the nails ( vasculitis from
antigen antibody reaction.
 Petechiae
PETECHIAE
PETECHIAE
SPLINTER HEMORRHAGE
METASTATIC INFECTIONS
 Arthritis
 Meningitis
 Mycotic arterial aneurysm
 Cerebral abscess/ abscesses
 Pericarditis
 Septic pulmonary embolism
INVESTIGATIONS
 Blood culture – by strict aseptic procedure
at least 3 blood samples must be taken
for aerobic and anaerobic cultures for
isolation of organism over 24-48 hours
 If patient is on antibiotics, discontinue
antibiotics for 48 hours before culture
 Culture is about 90% positive
 And 50% - 60% in the presence of
antibiotics
 Abscesses, synovial fluid and skin
scrapings can be cultured
CONTD
 ESR- usually elevated but low in CCF and
renal failure
 Positive rheumatoid factor
 Urine – microscopic hematuria
 FBC – leucocytosis
 S/E/U/Cr – azothemia, increased creatinine
 CXR – bilateral infiltrates and pleural
effusion
 Serology- immune complexes,
hypocomplementemia and
hypogammaglobulinaemia
CONTD
 Echo – valve vegetations, prosthetic
valve dysfunction and leak, valve
insufficiency, myocardial abscesses and
masses
 Absence of vegetation does not exclude
infective endocarditis as it may not be
seen at the early stages and in complex
cardiac lesions
DUKES CRITERIA FOR
DIAGNOSIS
MAJOR CRITERIA
1.Positive blood culture- usually 2 for
common pathogens and 2 or more for less
common pathogens
2.Evidence of endocarditis on ECHO-
a. Intra- cardiac mass on valve or other sites
b. Abscess
c. Regurgitant flow near a prosthetic valve
d. Partial dehiscence of prosthetic valve
e. New valve regurgitant flow( not just
changing murmurs by auscultation)
MINOR CRITERIA
1.Fever > 38 degrees
2.Embolic vascular signs- pulmonary
embolism
3.Existing cardiac lesion or iv drug use
4.Immune complex phenomena
A. Glomerulonephritis
B. Arthritis
C. Rheumatoid factor
D. Osler nodes
E. Roth spot
CONTD
5.A single positive blood culture or
serological evidence of infection
6.Echo signs not meeting the major criteria
7.Clubbing
8.Splenomegaly
9.Increased ESR
10.Increased C-reactive protein
11.Splinter hemorrhages/ petechiae
12.Microscopic hematuria
13. Presence of a central line or peripheral
lines
DIAGNOSIS
 Two major criteria or
 One major and 3 minors or
 5 minor criteria
TREATMENT
 Immediate administration of antibiotics
- For bacterial infection:
1. Iv penicillin G- 300,000 iu/kg/day in 4-6
divided doses + gentamycin 5-7mg/kg/
day in one dose or 3 divided doses
2. Ceftriaxone – 100mg/kg/ day in one
dose + gentamycin for 4-6 weeks
3. Vancomycin at 30mg/kg/day in 2 divided
doses in case of penicillin allergy
4.Nafcillin or cloxacillin- 100mg/kg in 4 divide
doses in staph infection and used 6 weeks or
more
FUNGAL
 Very difficult to diagnose and treat
 20% survival
 Amphotericin B- the drug of choice, 0.5-
1mg/kg/day with or without 5-
florocytosine.
SURGICAL
INTERVENTIONS
 Replacement of perforated valve leaflets
and infected prosthetic valves
 Resection of mycotic aneurysm
 Embolectomy- removal of vegetations
 Repair of underlying cardiac defects

 Treatment of CCF
PROFILAXIS
 Use of antibiotics before or during any
procedure that induces transient
bacteremia
 Recommended in:

1. Prosthetic cardiac valves

Recommended profilaxis
 Amoxycillin- 3g orally 1 hour before
procedure then 1.5g 6 hrs after
(50mg/kg initial dose then 25mg/kg 6
hrs later)
 Erythromycin (penicillin allergy)-
20mg/kg initial dose then 10mg/kg 6hrs
later
 Clindamycin- 10mg/kg initial dose then
5mg/kg 6 hours later
COMPLICATIONS /
PROGNOSIS
 Fatal without antibiotics
 20% - 25% mortality with antibiotics
 50%- 60% of children will have morbidity

- Heart failure
- Myocardial abscesses
- Toxic myocarditis
- Arrhythmias
- Systemic embolism especially in the
CNS
CONTD
-Pulmonary embolism
-Acquired VSD
-Obstruction to flow due to large
vegetation
-Heart block
-Metastatic infections
ANY QUESTIONS

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