1.
INFECTIVE ENDOCARDITIS (IE)
BHADRA TRIVEDI, MD Pediatrics
Pediatric cardiologist
Room – 5 , B & M Patel cardiology centre
Bhadrayt@charutarhealth.org

2.
Compare and Contrast
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Similarities – Blue Sky and
Contrast – Vegetation
Dessert

3.
“VEGETATION”
what it has to do with
IE?
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4.
CARDIAC LAYERS & VALVES
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5.
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Carditis
Rubor, Calor, Tumor, Dolor, Functio Laesa
Endo
Involves endocardium Only Spares other layers
Infective
Infective Non Infective
Acute
Fulminating Life Threatening
Sub
Milder Variant
Sub(Acute) Infective Endo Carditis

6.
Carditis – Inflammation – R,C,T,D,F
1. Rubor - Redness
2. Calor - Heat
3. Tumor – Swelling – tissue edema
4. Dolor - Pain
5. Functio Laesa – Fn of MV in
Systole?
MV Regurgitation
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7.
Old Hard Disease
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• Knowledge about the
origins of endocarditis
stems from the work of
Fernel in the early
1500s, and yet this
infection still presents
physicians with major
diagnostic and
management
dilemmas.

8.
Infective Endocarditis
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• Febrile illness
• Persistent bacteremia
• Characteristic lesion of microbial infection of the endothelial surface of the
heart
The vegetation
– Variable in size
– Amorphous mass of fibrin & platelets
– Abundant organisms
– Few inflammatory cells

9.
Predisposing Factors
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1. Dental manipulation
2. Extra cardiac infection (lung, urinary tract,
skin, bone, abscess)
3. Instrumentation (urinary tract, GI tract, IV
infusions)
4. Cardiac surgery
5. Injection drug use
6. Intravenous catheters

10.
Infective Endocarditis
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• Acute
– Toxic presentation
– Progressive valve destruction & metastatic infection developing in
days to weeks
– Most commonly caused by S. aureus
• Sub acute
– Mild toxicity
– Presentation over weeks to months
– Rarely leads to metastatic infection
– Most commonly S. viridans or enterococcus

11.
Infecting Organisms
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Common bacteria
– Alpha haem streptococci (viridans – S. mitis, S. sanguis) SUBACUTE
– Enterococci (E. faecalis) SUBACUTE
– Coagulase Negative Staphylococci – PROSTHETIC VALVES, SUBACUTE
Less common bacteria
– S. aureus ACUTE
– B-Haemolytic streptococci ACUTE
– Streptococcus pneumonia
Not so common
– Fungi
– Pseudomonas / Coliforms
– HACEK group organisms

12.
Bacterial Pathogens
HACEK Group
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• Haemophilus spp.
• Actinobacillus
actinomycetemcomitans
• Cardiobacterium hominis
• Eikenella corrodens
• Kingella kingae

13.
Infecting Organisms
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Streptococci 60-80%
– Alpha-haemolytic Streptococci (viridans – S. mitis, S. oralis) 30-40%
(subacute)
– Enterococci (E. faecalis) 5-18% (subacute)
– Beta-haemolytic streptococci (e.g. Gp A Strep) – rare (acute)
Staphylococci 20-35%
– S. aureus 10-27% (acute)
– Coagulase negative staphylococci (Staph epidermidis) 1-3 %
(mainly prosthetic valve risk, subacute)
Fungi
– Candida – IVDU at risk (usually indolent)
– Aspergillus – rare
Gram-negative bacteria – rare
Culture-negative endocarditis HACEK, Q-fever – cases do occur, subacute

14.
Infective Endocarditis
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• Pathology
– NVE infection is largely confined to leaflets
– PVE infection commonly extends beyond valve ring
into annulus/periannular tissue
• Ring abscesses
• Septal abscesses
• Fistulae
• Prosthetic dehiscence
– Invasive infection more common
in aortic position and if onset is early

15.
Turbulent Blood Flow
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Rheumatic fever history
Old age – calcified valves
Mitral valve prolapse with regurgitation
Prosthetic heart valves
Congenital defects / any structural defect
Cardiac surgery
Central lines
Pacemakers
Intravenous drug abuse

16.
Sub-Acute Vs Acute
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Feature Acute Subacute
Underlying Heart Heart may be normal RHD,CHD, etc.
Disease
Organism S. aureus, Pneumococcus
S. pyogenes,
Enterococcus
viridans
Streptococci,
Entercoccus
Therapy Prompt, vigorous and initiated
on empirical ground
Can often be delayed
until culture reports and
susceptibilities
available

17.
Bacterial Endocarditis
Clinical Features
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1. Fever. Antibiotics, salicylates, steroids, severe CHF, uremia may
mask temperature elevations.
2. Murmurs
3. Petechial and cutaneous manifestations. Roth spots Conjunctival
and mucosal petechiae, splinter hemorrhages, Osler nodes and
Janway lesions.
4. Splenomegaly
5. Embolism. Septic or sterile. CNS, spleen, lung, retinal
vessels, coronary artery, large vessels.
6. Renal disease, infarction. Multiple abscesses.
Glomerulonephritis and uremia
7. CHF
8. General. Weight loss, anorexia, debilitation, loss of libido.

18.
Symptoms
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Acute
– High grade fever and
chills
– SOB
– Arthralgias/ myalgias
– Abdominal pain
– Pleuritic chest pain
– Back pain
Sub acute
– Low grade fever
– Anorexia
– Weight loss
– Fatigue
– Arthralgia's/ myalgia's
– Abdominal pain
– N/V
The onset of symptoms is usually ~2 weeks or less
from the initiating bacteremia

19.
Signs
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• Fever
• Heart murmur
• Nonspecific signs – petechiae, subungal or “splinter”
hemorrhages, clubbing, splenomegaly, neurologic
changes
• More specific signs - Osler’s Nodes,
• Janeway lesions
• Roth Spots
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20.
Janeway Lesions
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21.
Janeway Lesions
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1. More specific
2. Erythematous, blanching macules
3. Nonpainful
4. Located on palms and soles

22.
Splinter Hemorrhages
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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

23.
Subconjuctival Hemorrhages
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24.
Roth’s Spots
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25.
Osler’s Nodes
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1. More specific
2. Painful and erythematous nodules
3. Located on pulp of fingers and toes
4. More common on in Sub-Acute 32

26.
Bacterial Endocarditis Laboratory
Features
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1. Anemia
2. Most commonly elevated WBC
3. ESR elevated
4. Microscopic hematuria
5. Bacteremia.

27.
Blood cultures
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• Recommendation: Blood cultures remain a
cornerstone of the diagnosis of IE cases and
should be taken prior to starting treatment in
all case
• Meticulous aseptic technique is required
when taking blood cultures, to reduce the risk
of contamination with skin
commensals, which can lead to misdiagnosis.
Guidelines for best practice should be
consulted

28.
When to Collect the blood
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• In patients with a chronic or sub acute
presentation, three sets of optimally filled blood
cultures should be taken from peripheral sites with
≥6 h between them prior to commencing
antimicrobial therapy.
• Taking blood cultures at different times is critical to
identifying a constant bacteraemia, a hallmark of
endocarditis.

29.
Timing of blood collection
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• In patients with suspected IE and severe
sepsis or septic shock at the time of
presentation, two sets of optimally filled
blood cultures should be taken at different
times within 1 h prior to commencement of
empirical therapy, to avoid undue delay in
commencing empirical antimicrobial therapy.

30.
Start with Empherical Treatment
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• It is not always appropriate to withhold antimicrobial
therapy while three sets of blood cultures are taken
over a 12 h period. This recommendation is
intended to be pragmatic, allowing time to take at
least two sets of blood cultures (the minimum for a
secure microbiological diagnosis) prior to
commencing antimicrobial therapy.

31.
Blood Cultures
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Blood Cultures
– Minimum of three blood cultures (ideally spread over 24
hrs)
– Three separate venipuncture sites ideally
–Obtain correct volume of blood for culture bottles
Positive Result
– 1 set gives 90% sensitivity, remaining 2 sets add 8%
– Multiple same cultures are important in confirming
significance, especially for less typical organisms
Negative Result
– Prior antibiotic therapy
– ‘Culture negative endocarditis’ – fastidous orgs / non-
culturable
– May support a non-endocarditis patient diagnosis

32.
Culture Negative Results may yield
..less known microbes
• Microorganisms that
should be considered
first include Coxiella
burnetii (Q fever) and
Bartonella spp.
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33.
Additional Tests
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CBC
ESR and CRP
Complement levels (C3, C4, CH50)
RF
Urinalysis
Baseline chemistries

34.
Imaging
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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

35.
Echocardiography
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Transthoracic echocardiography (TTE)
– First line if suspected IE
– Native valves
Trans esophageal echocardiography (TEE)
– Prosthetic valves
– Intracardiac complications
– Inadequate TTE
– Fungal or S. aureus or bacteremia

36.
Making the Diagnosis
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Pelletier and Petersdorf criteria (1977)
– Classification scheme of definite, probable, and possible IE
– Reasonably specific but lacked sensitivity
Von Reyn criteria (1981)
– Added “rejected” as a category
– Added more clinical criteria
– Improved specificity and clinical utility
Duke criteria (1994)
– Included the role of echocardiography in diagnosis
– Added IVDA as a “predisposing heart condition”

37.
Modified Duke Criteria
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Definite IE
– Microorganism (via culture or histology) in a valvular
vegetation, embolized vegetation, or intracardiac abscess
– Histologic evidence of vegetation or intracardiac abscess
Possible IE
– 2 major
– 1 major and 3 minor
– 5 minor
Rejected IE
– Resolution of illness with four days or less of antibiotics

38.
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39.
Treatment
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Parenteral (IV) antibiotics
– High serum concentrations to penetrate vegetation's
– Prolonged treatment to kill dormant bacteria
clustered in vegetation’s
– Empirical in Acute Condition
Surgery
– Intracardiac complications/paravalve abscess
51

40.
Treatment - Specific
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• Modify empiric therapy once
cultures/sensitivities known
• Long duration 4-6 weeks Rx is required
• Liaise with Microbiologist
• Liaise with Cardiac Surgeon if needed Monitor response
to treatment
• (clinical, CRP, ECHO) & look for complications

41.
Complications
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Four etiologies
–Embolic
–Local spread of infection
–Metastatic spread of infection
–Formation of immune complexes –
glomerulonephritis and arthritis

42.
Embolic Complications
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Occur in up to 40% of patients with IE
Predictors of embolization
–Size of vegetation
–Left-sided vegetation's
–Fungal pathogens, S. aureus, and Strep.
Bovis
Incidence decreases significantly after
initiation of effective antibiotics

43.
Embolic Complications
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Stroke
Myocardial Infarction
– Fragments of valvular vegetation or vegetation-
induced stenosis of coronary ostia
Ischemic limbs
Hypoxia from pulmonary emboli
Abdominal pain (splenic or renal infarction)

44.
Metastatic Spread of Infection
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Meningitis and/or encephalitis
Vertebral osteomyelitis
Metastatic abscess
–Kidneys, spleen, brain, soft tissues
Septic arthritis

45.
Prevention
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• Prophylactic regimen targeted against likely
organism
– Strep. viridans – oral, respiratory,
esophageal
– Enterococcus – genitourinary,
gastrointestinal
– S. aureus – infected skin, mucosal surfaces

46.
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