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Infective Endocarditis

Infective Endocarditis
• Outline
– Definition
– Classification
– Epidemiology
– Pathogenesis
– Etiologic agent
– Clinical manifestations
– Diagnosis
– Treatment
– Complications
– Prevention

11/20/23
Definition
• Infective Endocarditis (IE): an infection of the
heart’s endocardial surface
• Classified into four groups:
– Native Valve IE
– Prosthetic Valve IE
– Intravenous drug abuse (IVDA) IE
– Nosocomial IE

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Further Classification
• Acute • Subacute
– Affects normal heart – Often affects damaged
valves heart valves
– Rapidly destructive – Indolent nature
– Metastatic foci – If not treated, usually
– Commonly Staph. fatal by one year
– If not treated, usually
fatal within 6 weeks

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Pathophysiology
1. Turbulent blood flow disrupts the endocardium making it
“sticky”
2. Bacteremia delivers the organisms to the endocardial
surface
3. Adherence of the organisms to the endocardial surface
4. Eventual invasion of the valvular leaflets

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Location of vegetations
– Vegetations tend to occur when blood travels from an area of
high pressure through a narrow orifice into an area of lower
pressure
• Vegetations in patients with preexisting valvular lesions are
usually located on the atrial surface of incompetent
atrioventricular valves, or the ventricular surfaces of
incompetent semilunar valves.
• Patients with ventricular septal defects tend to develop
vegetations on the orifice of the defect, on the right
ventricular side of the opening, and secondarily on the
tricuspid and pulmonic valves

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Epidemiology
• Incidence difficult to ascertain and varies according to
location
• Much more common in males than in females
• May occur in persons of any age and increasingly common in
elderly
• In ≈30% of patients with infective endocarditis, a predisposing
factor is presumably recognized.
• Although a preceding dental procedure may be identified in
10-20% of patients, the time of the procedure may range
from 1 to 6 mo prior to the onset of symptoms
• Mortality ranges from 20-30%
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Risk Factors

• Artificial heart valves and pacemakers


• Acquired heart defects
– Rheumatic heart disease
– Calcific aortic stenosis
• Congenital heart defects
– VSD
– PDA
– Coarctation
– TOF
– Mitral valve prolapse with regurgitation
• Intravascular catheters
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Infecting Organisms
• Common bacteria
– Viridans group streptococci (S. mutans, S. sanguis, S. mitis)
– Staphylococcus aureus
– Group D streptococcus (enterococcus) (S. bovis, S. faecalis)
• Not so common bacteria
– Pseudomonas
– HACEK (Haemophilus species , Actinobacillus actinomycetemcomitans,
Cardiobacterium hominis, Eikenella corrodens, and Kingella species)
• Fungi

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Symptoms
• Acute • Subacute
– High grade fever and – Low grade fever
chills – Anorexia
– SOB – Weight loss
– Arthralgias/ myalgias – Fatigue
– Abdominal pain – Arthralgias/ myalgias
– Pleuritic chest pain – Abdominal pain
– Back pain – N/V
The onset of symptoms is usually ~2 weeks or less
from the initiating bacteremia

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Signs
• Fever
• Heart murmur( new or changing murmur)
• Nonspecific signs – petechiae, subungal or
“splinter” hemorrhages, clubbing,
splenomegaly, neurologic changes
• More specific signs - Osler’s Nodes, Janeway
lesions, and Roth Spots

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Petechiae
1. Nonspecific
2. Often located on extremities
or mucous membranes

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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
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Janeway lesions

1.Erythematous, blanching macules


2.Nonpainful
3.More specific
4.Located on palms and soles
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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
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The Essential Blood Test
• Blood Cultures
– Minimum of three blood cultures over a period of hrs to
two days depending on the severity of the disease
– Three separate venipuncture sites
– Obtain 10-20mL in adults and 1 to 3 mL in infants and
young children, and 5 to 7 mL in older children
• Positive Result
– Typical organisms present in at least 2 separate samples
collected 12 hr apart
– Persistently positive blood culture (atypical organisms)
• Three or more positive blood cultures in which the first
and last samples were collected at least one hour apart

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Additional Labs
• CBC
• ESR and CRP
• Complement levels (C3, C4, CH50)
• RF
• Urinalysis
• Baseline chemistries and coagulation tests

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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
• Cerebral imaging — routine magnetic resonance imaging (MRI) may be
useful in patients with definite or suspected IE

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Indications for Echocardiography
• Transthoracic echocardiography (TTE)
– First line if suspected IE
– Native valves
• Transesophageal echocardiography (TEE)
– Prosthetic valves
– Intracardiac complications
– Inadequate TTE
– Fungal or S. aureus or bacteremia

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Making the Diagnosis
• 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”

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Modified Duke Criteria
• Definite IE
– Pathologic criteria
• Microorganism: (via culture or histology) in a valvular
vegetation, embolized vegetation, or intracardiac
abscess
• Pathological lesions: vegetation or intracardiac abscess
present, confirmed by histology showing active
endocarditis
– Clinical criteria
• Two major criteria, or
• One major and three minor criteria, or
• Five minor criteria
(2,4,5)
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Con’d
• Possible IE
 One major criterion and one minor criterion or three
minor criteria
• Rejected IE
 Firm alternative diagnosis for manifestations of
endocarditis, or
 Sustained resolution of manifestations of endocarditis,
with antibiotic therapy for 4 days or less, or
 No pathological evidence of infective endocarditis at
surgery or autopsy, after antibiotic therapy for 4 days or
less

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Con’d
 Major Criteria
 Positive blood culture
 Typical microorganism for infective endocarditis from two
separate blood cultures
 Persistently positive blood culture, defined as recovery of a
microorganism consistent with infective endocarditis from:

 Blood cultures (≥2) drawn more than 12 hr apart, or


 All of three or a majority of four or more separate blood
cultures, with first and last drawn at least 1 hr apart
 Single positive blood culture for Coxiella burnetii or
antiphase I IgG antibody titer >1:800
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Con’d
 Evidence of endocardial involvement
– Positive echocardiogram
• Oscillating intracardiac mass, on valve or supporting
structures, or in the path of regurgitant jets, or on
implanted material, in the absence of an alternative
anatomical explanation, or
• Abscess, or
• New partial dehiscence of prosthetic valve, or
– New valvular regurgitation (increase or change in
preexisting murmur not sufficient)

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Con’d
 Minor Criteria
– Predisposition: predisposing heart condition or intravenous
drug use
– Fever ≥38.0°C (100.4°F)
– Vascular phenomena: major arterial emboli, septic pulmonary
infarcts, mycotic aneurysm, intracranial hemorrhage,
conjunctival hemorrhages, Janeway lesions
– Immunological phenomena: glomerulonephritis, Osler nodes,
Roth spots, rheumatoid factor
– Microbiological evidence: positive blood culture but not
meeting major criterion as noted previously[*] or serologic
evidence of active infection with organism consistent with
infective endocarditis

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Con’d
• The following minor criteria are added to those already listed:
– the presence of newly diagnosed clubbing
– splenomegaly
– splinter hemorrhages, and petechiae
– a high erythrocyte sedimentation rate
– a high C-reactive protein level
– the presence of central nonfeeding lines
– peripheral lines
– microscopic hematuria

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Treatment
• Parenteral antibiotics
– High serum concentrations to penetrate vegetations
– Prolonged treatment to kill dormant bacteria clustered in
vegetations
• Surgery
– Intracardiac complications
– intractable heart failure
– failure to sterilize the blood despite adequate antibiotic
levels
– increasing size of vegetations while receiving therapy
• Surveillance blood cultures

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Prevention
• Antimicrobial prophylaxis before various high risk procedures
for high risk patients
• The following are patients with the highest risk:
1. Prosthetic heart valves, including bioprosthetic and
homograft valves.
2. A prior history of IE.
3. Unrepaired cyanotic congenital heart disease, including
palliative shunts and conduits.
4. Completely repaired congenital heart defects with prosthetic
material or device, whether placed by surgery or by catheter
intervention, during the first six months after the procedure.
5. Repaired congenital heart disease with residual defects at the
site or adjacent to the site of the prosthetic device.

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Cont…
• High risk procedure which needs prophylaxis
1. All dental procedures that involve manipulation of either
gingival tissue or the periapical region of teeth or perforation
of the oral mucosa.
2. Procedures of the respiratory tract that involve incision or
biopsy of the respiratory mucosa.
3. Procedures in patients with ongoing GI or GU tract infection.
4. Procedures on infected skin, skin structure, or
musculoskeletal tissue.
5. Surgery to place prosthetic heart valves or prosthetic
intravascular or intracardiac materials

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

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Risk factors for complication
• Prosthetic cardiac valves
• Left-sided involvement
• Staphylococcus aureus or fungal IE
• Previous IE
• Prolonged symptoms ≥3 months
• Cyanotic congenital heart disease
• Systemic-to-pulmonary shunts
• Poor clinical response to antimicrobial therapy
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Embolic Complications
 Occur in up to 40% of patients with IE
 Predictors of embolization
 Size of vegetation
 Left-sided vegetations
 Fungal pathogens, S. aureus, and Strep. Bovis
 Incidence decreases significantly after initiation of effective
antibiotics
 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)

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Local Spread of Infection
• Heart failure
– Extensive valvular damage
• Paravalvular abscess (30-40%)
– Most common in aortic valve, IVDA, and S. aureus
– May extend into adjacent conduction tissue causing
arrythmias
– Higher rates of embolization and mortality
• Pericarditis
• Fistulous intracardiac connections

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

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Poor Prognostic Factors
• Female • Diabetes mellitus
• S. aureus • Low serum albumen
• Candida infection • Heart failure
• Vegetation size • Paravalvular abscess
• Aortic valve • Embolic events
• Prosthetic valve

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IE Mortality Rates

• 100% fatal if not treated


• With antibiotic treatment, fatality rate:
– NVE (native valve)
• Streptococcus <10%
• Staphylococcus 25-40%
• Gram negatives 75-83%
• Fungi 50-60%
– Late PVE (prosthetic valve) 30-53%

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Thank You!!!
11/20/23

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