Ebright: Infective Endocarditis Flashcards
Infective Endocarditis
DEFINITION
Infection of the endocardial surface of the
heart
Implies the physical presence of
microorganisms in the lesion
Organism location (6)
• Heart valves (most common) • Septal defects • Mural endocardium • Arterio-venous shunts • Arterio-arterial shunts (patent ductus arteriosus – persistent communication between left pulmonary artery and the descending aorta) • Coarctation of aorta
Epidemiology
- Approximately 1 case per 1000 hospital admissions
- More than 50% of cases are older than 50 years
- Males more commonly affected (ratio 1.7:1)
Epidemiology - Valve Involved
Left
• mitral 28-45%
• aortic 5-36%
- mitral/aortic combined 0-35%
- tricuspid 0-6%
- pulmonic <1%
Epidemiology - Association with Underlying
Valvular Disease
Rheumatic heart disease:
Congential heart disease:
IE essentially does not occur with:
Rheumatic heart disease (25%)
•mitral most common
Congential heart disease
•patent ductus arteriosus, ventricular septal defect,
coarctation of the aorta, tetralogy of Fallot
•congenitally bicuspid aortic valve (20% of cases >age 60 poor prognosis)
*IE essentially does not occur with secundum atrial
defects (low-pressure shunt; little turbulence)
Epidemiology - Association with Underlying Valvular
Disease
“Degenerative” cardiac lesions
Other conditions
“Degenerative” cardiac lesions (30-40% cases without underlying valve disease)
• Ex: calcified mitral annulus, post myocardial infarction, thrombus
- syphilitic heart disease
- arterioatrial fistulas
- hemodialysis shunts/fistulas
- intracardiac pacemaker wires
- intracardiac prostheses
- intravenous drug abuse
- mitral valve prolapse with mitral regurgitation
Pathogenesis
What results in deposition of platelets
and fibrin?
Turbulent flow results in deposition of platelets and fibrin (nonbacterial thrombotic endocarditis).
Pathogenesis
Non-bacterial thrombotic endocarditis (NBTE)
What is a prerequisite for bacterial colonization?
Found in:
What are pathogenic mechanisms?
Found most frequently on which side of cardiac valve?
Along what line?
• Alteration of valve surface is prerequisite for bacterial colonization
• Found in many conditions causing acute/chronic illness
• Hypercoagulability and/or endothelial damage are
pathogenic mechanisms
• Found most frequently on low-pressure side of cardiac valve
• Along the line of closure
Pathogenesis
Hemodynamic factors
Lesions with high degrees of turbulence readily create conditions that lead to bacterial colonization
*low flow states (secundum atrial defects) rarely associated with IE
Pathogenesis
Transient bacteremia:
Where does it occur?
How long does it usually take to clear the bloodstream?
What can the bacteria in the bloodstream then do?
- Occurs when mucosal surface heavily colonized with bacteria is traumatized
- Bloodstream is usually clear 15-30 minutes after the procedure
- Bacteria in bloodstream can then colonize NBTE lesions
Pathogenesis
Microorganism - NBTE Interaction
How do organisms differ?
What do bacteria do once they bind?
What does vegetation create?
- Organisms differ in their propensity to cause (Infective Endocarditis) IE
- Once bacteria bind they proliferate, causing further platelet –fibrin deposition.
- Vegetation creates an environment of impaired host resistance (bacteria covered by platelets/fibrin)
Pathogenesis
Immunopathologic Factors
- Stimulation of humoral and cellular immunity
- Rhematoid factor can be positive
- Antinuclear antibodies can be present
- Circulating immune complexes
Pathologic Changes
Vegetation located:
Complications:
Vegetation located along line of closure of valve leaflet
Complications – valve ring abscess – perforation of valve leaflet – myocardial abscesses (20%) – rupture of chordae tendinae, interventricular septum, papillary muscle – valvular stenosis (large lesions) – myocarditis – pericarditis – myocardial infarction (40-60% of autopsied cases)
Vegetations
Pathologic Changes
Kidney
• abscess
• infarction
• glomerulonephritis (focal or diffuse)
secondary to immune complex deposition
Pathologic Changes
Mycotic aneurysm:
Usually develop during: Tend to occur where? Mechanism leads to: direct bacterial invasion: embolic occlusion of: immune complex deposition: Clinically silent until:
• Usually develop during active disease, but can occur
months to years later
• tend to occur at bifurcation points
• mechanism leading to aneurysm
• direct bacterial invasion of arterial wall with
abscess formation
• embolic occlusion of vasovasorum
• immune complex deposition with injury to
vessel wall
• Clinically silent until rupture occurs
Pathologic Changes
CNS
Spleen
Lung (Rt. Sided)
Central nervous system
• cerebral emboli (1/3 of cases)
•also mycotic aneurysms, cerebritis, abscesses
Spleen
•infarctions common (but usually clinically silent)
•abscesses
Lung (Rt. Sided)
•embolic
•pleural effusion/empyema
Pathologic Changes
Skin
Eyes
Skin
•petechiae 20-40%
•Osler’s nodes (immune complex)
•Janeway lesions (septic emboli)
Eyes
•Roth spots
Clinical Manifestations
“Incubation period”
Average: Symptom onset to diagnosis
Process contributing to the clinical picture (4)
Clinical Manifestations
“Incubation period” 2 weeks but time from symptom onset to diagnosis averages 5 weeks (and depends on causative organism)
Process contributing to the clinical picture
– infectious process on the valve
– bland/septic emboli to any organ system
– constant bacteremia (with metastatic foci)
– circulating immune complexes
Clinical Manifestations
Fever:
Nonspecific Symptoms:
Heart Murmur:
Fever (95%)
• Usually remittent
• absent in: CHF, renal failure, older age,
terminal illness, prior antibiotic therapy
Nonspecific Symptoms
• anorexia, weight loss, fatigue, chills,
weakness, nausea, vomiting, night sweats
• often result in incorrect initial diagnosis
Heart murmur (85%) (classically a new or changing murmur)