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Supervisor :
Dr: Mohammed Al marwala
Presented by :
Dr :Areej Aljabali
Items of Presentation
General definitions
• Pathology
• Pathogenesis
• Pathophysiology
• Clinical features
• Diagnosis
• Treatment
• Prevention
•
Definition :
Infective endocarditis is characterized by
colonization or invasion of the heart
valves or the mural endocardium by a
microbe, leading to the formation of bulky
friable vegetations
composed of thromb and organisms, often
associated with destruction of the
underlying cardiac tissues.

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
55-75% of patients with native valve
endocarditis (NVE) have underlying valve
abnormalities
 MVP
 Rheumatic
 Congenital
 I.v. drug abuse
◦ 7-25% of cases involve prosthetic valves
◦ 25-45% of cases predisposing condition can
not be identified
Pathology :
◦ NVE infection is largely confined to leaflets
◦ PVE infection commonly extends beyond
valve ring into annulus/peri annular tissue
 Ring abscesses
 Septal abscesses
 Fistulae
 Prosthetic dehiscence
◦ Invasive infection more common in aortic
position and if onset is early
Pathogenesis :
Endothelial damage
Platelet-fibrin thrombi
Microorganism adherence
Nonbacterial Thrombotic Endocarditis
 Endothelial injury
 Hypercoagulable state
◦ Lesions seen at coaptation points of valves
 Atrial surface mitral/tricuspid
 Ventricular surface aortic/pulmonic
 Modes of endothelial injury
 High velocity jet
 Flow from high pressure to low pressure
chamber
 Flow across narrow orifice of high velocity
◦ Bacteria deposited on edges of low pressure
or site of jet impaction

Pathophysiology:

Clinical manifestations
◦ Direct
 Constitutional symptoms of infection (cytokine)
◦ Indirect
 Local destructive effects of infection
 Embolization – septic or bland
 Hematogenous seeding of infection may
present as local infection or persistent fever,
metastatic abscesses may be small
 Immune response
 Immune complex or complement-mediated
Local destructive effects
 Valvular distortion/destruction
 Chordal rupture
 Perforation/fistula formation
 Paravalvular abscess
 Conduction abnormalities
 Purulent pericarditis
 Functional valve obstruction
Embolization
 Clinically evident 11 – 43% of patients
 Pathologically present 45 – 65%
 High risk for embolization
 Large > 10 mm vegetation
 Hypermobile vegetation
 Mitral vegetations (esp. anterior leaflet)
 Pulmonary (septic) – 65 – 75% of i.v. drug
abusers with tricuspid IE
Clinical Features :
•
Fever, chills, weakness, lethargy, weight loss,
flu-like illness (not always present)
•
Longstanding IE (rarely seen now with
earlier diagnosis): splinter haemorrhages,
Janeway lesions, Osler nodes, Roth spots
•
Murmurs are present in 80 - 85% of patients
with left sided IE
Feature
Frequency, %
Fever
80–90
Chills and sweats
40–75
Anorexia, weight loss, malaise
25–50
Myalgias, arthralgias
15–30
Back pain
7–15
Heart murmur
80–85
New/worsened regurgitant murmur
10–40
Arterial emboli
20–50
Splenomegaly
15–50
Clubbing
10–20
Neurologic manifestations
20–40
Peripheral manifestations (Osler's nodes, subungual
hemorrhages, Janeway lesions, Roth's spots)
2–15
Petechiae
10–40
Laboratory manifestations
Anemia
70–90
Leukocytosis
20–30
Microscopic hematuria
30–50
Elevated erythrocyte sedimentation rate
>90
Elevated C-reactive protein level
>90
Rheumatoid factor
50
Circulating immune complexes
65–100
Decreased serum complement
5–40
Splinter Haemorrhages
Janeway Lesions
Osler Nodes
Roth Spots
•
In IVDU right sided IE usually affect the
tricuspid valve & occasionally the pulmonary
valve, instead of systemic issues pulmonary
embolism is the most important complication
which can evolve into:
• Pulmonary infarction
• Pulmonary abscess
• Bilateral pneumothoraces
• Pleural effusion
• Empyema
•
•
The severity of valvular destruction
depends on virulence of infecting
organism & infection duration
Heart failure can be the initial
presentation
Diagnosis :
Modified Duke criteria
It is based on clinical, microbiological & echo
findings providing high sensitivity & specificity
(~80%) for diagnosis of IE when applied to
patients with native valve IE with +ve BC
Modified Duke Criteria

Major Criteria:
Positive blood cultures
Typical microorganism for IE from 2 separate
blood culures
Viridans sreptococci
Sreptococcus bovis
HACEK group
Saph . Auresus
Community acquired enerococci , in the
absence of primary focus
Persistently positive blood culture , defined as
recovery of a microorganism consistent with IE
from:
Blood culture drawn more than 12 h apart OR
All of 3or majority of 4 or more separate blood
cultures , with first last drawn at least one h
apart
Single positive blood culture for Coxiella burnetii
or antiphase I IgG AB titer more than 1: 800
Evidence of endocardial involvement
Positive echocardiogram for IE
 TEE recommended in patients with PV
,rated at least possible IE by clinical
crieria ,or complicated IE ( paravalvular
abscess ) TTE as first test in other patients
Definition of positive ECHO
- Oscillating intracardiac mass, on valve or
supporting structures , or in the path or
regurgitant jets , or on implanted material , in he
absence of an alternative anatomic explanation
- Intracardiac abscess
- New partial dehiscence of prosthetic valve
New valvular regurgitation
Increase in or change in preexisting murmur not
sufficent

Minor Criteria
Predisposition such as a heart condition or IV
drug use
 Fever
 Vascular phenomena - major arterial emboli,
septic pulmonary infarcts, mycotic aneurysm,
intracranial haemorrhage, conjunctival
haemorrhage, & Janeway lesions

immunological phenomena –
glomerulonephritis , Osler s nodes , Roth
spots , rheumatoid factor
 Other microbial evidence - serological
tests, or a positive blood culture but does
not meet a major criteria ( excluding
single positive cultures for coagulase
negative staph and organisms that do not
cause endocarditis )

Definite IE
2 major criteria
OR
1 major + 3 minor
OR
5 minor criteria
Possible IE
1 major + 1 minor
OR
3 minor
Rejected :
Firm alternate diagnosis for manifestation of
endocarditis OR
Resolution of manifestation of endocarditis , with
antibiotic therapy for 4 days or less OR
No pathologic evidence of IE at surgery or
autopsy after antibiotic therapy for 4 days or
less
Does not meet criteria for possible IE , as above
TREATMENT :
Goals of Therapy
Eradicate infection
Definitively treat sequelae of destructive
intra-cardiac and extra-cardiac lesions
Antibiotics :
•
Benzylpenicillin is the first choice for
Streptococcus or Enterococcus penicillinsusceptible strains
• Empirical treatment; flucloxacillin &
gentamicin are the usual first line
• Vancomycin is used in pts with intracardiac
prosthetic material or suspected MRSA
• For vanc-resistant MRSA: teicoplanin,
lipopeptide daptomycin or oxazilidones
(linezolid) is recommended
•
IV Abx is normally continued for 4-6
weeks, with the aim of sterilising the
vegetations
Indications for Cardiac Surgical Intervention
in Patients with Endocarditis
Surgery required for optimal outcome
 Moderate to severe congestive heart failure due
to valve dysfunction
 Partially dehisced unstable prosthetic valve
 Persistent bacteremia despite optimal
antimicrobial therapy
 Lack of effective microbicidal therapy (e.g.,
fungal or Brucella endocarditis)
 S. aureus prosthetic valve endocarditis with an
intracardiac complication
 Relapse of prosthetic valve endocarditis after
optimal antimicrobial therapy
Surgery to be strongly considered for
improved outcomea
 Perivalvular extension of infection
 Poorly responsive S. aureus endocarditis
involving the aortic or mitral valve
 Large (>10-mm diameter) hypermobile
vegetations with increased risk of embolism
 Persistent unexplained fever (10 days) in
culture-negative native valve endocarditis
 Poorly responsive or relapsed endocarditis due
to highly antibiotic-resistant enterococci or
gram-negative bacilli
Complications
1.
Congestive heart failure
•
•
•
2.
Uncontrolled infection
•
•
3.
Most common complication
Main indication to surgical treatment
~60% of IE patients
Persisting infection
Perivalvular extension in infective endocarditis
Systemic embolism
•
•
•
Brain, spleen and lungs
30% of IE patients
May be the first symptom
5.
6.
7.
8.
Neurologic events
Acute renal failure
Rheumatic problems
Myocarditis
High-Risk Cardiac Lesions for Which
Endocarditis Prophylaxis Is Advised before
Dental Procedures






Prosthetic heart valves
Prior endocarditis
Unrepaired cyanotic congenital heart disease,
including palliative shunts
Completely repaired congenital heart defects
during the 6 months after repair
Incompletely repaired congenital heart disease
with residual defects adjacent to prosthetic material
Valvulopathy developing after cardiac
transplantation
Antibiotic Regimens for Prophylaxis of
Endocarditis in Adults with High-Risk Cardiac
Lesionsa,b
A. Standard oral regimen
 1. Amoxicillin 2.0 g PO 1 h before procedure
B. Inability to take oral medication
 1. Ampicillin 2.0 g IV or IM within 1 h before
procedure
C. Penicillin allergy
 1. Clarithromycin or azithromycin 500 mg PO 1
h before procedure
 2. Cephalexinc 2.0 g PO 1 h before procedure
 3. Clindamycin 600 mg PO 1 h before
procedure
D. Penicillin allergy, inability to take oral
medication
 1. Cefazolinc or ceftriaxonec 1.0 g IV or IM 30
min before procedure
 2. Clindamycin 600 mg IV or IM 1 h before
procedure
THANK YOU

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