149 Endocarditis Flashcards
Endocarditis
Noninfective endocarditis
- •Nonbacterial thrombotic endocarditis (NBTE, marantic endocarditis)
- •Rheumatic endocarditis
- •Libman-Sacks endocarditis (manifestation of systemic lupus erythematosis (SLE)
Infective endocarditis
Nonbacterial Thrombotic Endocarditis
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Definition: The deposition of small masses of fibrin, platelets, and other blood components on leaflets of cardiac valves.
- Lesions do not contain microorganisms
- Valvular damage not a prerequisite; valves usually previously normal
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Pathogenesis
- Subtle endothelial abnormalities
- Hypercoagulable states
- malignancies (especially adenocarcinomas) found in 50% of cases
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Morphologic Features
- small nodules on lines of valve closure
- nodules may be bulky and friable
- valve leaflets otherwise normal
- aortic valve most common, mitral valve next most frequently involved
Infective Endocarditis
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Definition: Infection of the cardiac valves or mural surface of the endocardium, with formation of adherent mass of thrombotic debris and organisms, termed a “vegetation”.
- Any microorganism may be present, but most cases are bacterial
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Acute Endocarditis
- –High virulence organisms: may affect normal valves
- •Staphylococcus aureus
- rapid destruction, no inflammatory response, embolize infarct
- –High virulence organisms: may affect normal valves
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•Subacute Endocarditis
- –Lower virulence organisms: affects previously abnormal valves
- •alpha-hemolytic streptococci
- Less firm than acute, cause less valve damage, systemic emboli
- –Lower virulence organisms: affects previously abnormal valves
-
•Pathogenesis
- –Organisms implanted during bacteremia
- –Conditions which increase risk: preexisting cardiac abnormalities, Endothelial injury, Turbulent flow (due to scarred valve of congenital heart defect, e.g. V.S.D.), prosthetic heart valves, intravenous drug abuse
Fungal endocarditis
- Prosthetic valves are especially susceptible to colonization since it is a foreign material
- Common location around sewing ring
- Also frequently involved with sterile thrombotic vegetations
Acute Rheumatic Carditis
•Endocardium
–Most pronounced in mitral & aortic valves
–Inflammation, edema, fibrinoid necrosis
–Aschoff nodules not common
–Verrucous endocarditis
- Small excrescences along lines of valve closure
- Lesions may resolve or undergo fibrosis
Anitschkow cells are found in Aschoff nodules
They are histiocytes with vesicular nuclei and abundant cytoplasm
Nuclei resemble owl eyes!
Causes of mitral stenosis
Postinflammatory scarring (rheumatic heart disease)
Causes of mitral valve regurgitation
Mitral Valve Prolapse
–Most common cause of isolated mitral regurgitation
–Affects women > men
–Mitral valve “floppy” or incompetent
–May occur with Marfan’s syndrome
–Mitral valve cusps (especially posterior cusp) soft, enlarged, and ballooned into left atrium during systole
–Cordae may rupture
–Loose, edematous, basophilic ground substance in valve leaflets and chordae
•Identified by midsystolic click
Aortic Stenosis + causes
•Most frequent valvular abnormality
•Acquired >> congenital
•Senile calcification, degenerative, “wear and tear” > 10% due to rheumatic fever
1-2% congenitally bicuspid
•Heaped-up calcified masses in sinuses of Valsalva
- •Postinflammatory scarring (rheumatic heart disease 30-60 yrs old)
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•Senile calcific aortic stenosis (>60yrs)
- Heaped up calcifications in the sinus of Valsalva
- Moderately thickened free edge
- Absence of fusion of the commisures
- •Calcification of congenitally deformed valve (30-50yrs)
- Thickening of the free edges of the valve cusps
- Fusion of the cusps
- Normal sinus of Valsalva
Causes of aortic regurgitation
Ankylosing spondylitis
- •Systemic disease affecting joints, lungs, heart and eyes.
- •Inflammation can involve the aorta and heart
- •Can cause aortic regurgitation due to dilatation of the aorta and scarring of valve cusps
Pericardial Physiology
- •not needed to sustain life
- •physiologic functions
- –limit cardiac dilatation
- –maintain normal ventricular compliance
- –reduce friction to cardiac movement
- –barrier to inflammation
- –limit cardiac displacement
Pericardial Inflammation
pathogenesis
- •Contiguous spread
- –lungs, pleura, mediastinal lymph nodes, myocardium, aorta, esophagus, liver
- •Hematogenous spread
- –septicemia, toxins, neoplasm, metabolic
- •Lymphangetic spread
- •Traumatic or irradiation
- •Inflammation provokes a fibrinous exudate with or without serous effusion
- •The normal transparent and glistening pericardium is turned into a dull, opaque, and “sandy” sac
- •Can cause pericardial scarring with adhesions and fibrosis
Causes of Pericarditis
- Rheumatic Fever
- Scleroderma
- Postcardiotomy
- Drug-hypersensistivity reaction
- Systemic lupus erythematosus
- Postmyocardial infarction (Dressler) syndrome
Dressler’s Syndrome
•Described by Dressler in 1956
•fever, pericarditis, pleuritis
(typically with a low grade fever and a pericardial friction rub)
- occurs in the first few days to several weeks following MI or heart surgery
- incidence of 6-25%
- treat with high-dose aspirin
Constrictive Pericarditis
- An uncommon post inflammatory disorder
- the encasement of the heart by a rigid, nonpliable pericardium
- characterized by a thickened, fibrotic, and frequently calcified pericardium
- rarely develop after an episode of acute idiopathic pericarditis
- more likely to develop after subacute pericarditis with effusion that evolve over several weeks
Etiologies of Cardiac Tamponade
- Fluid accumulation within the pericardial space resulting in increased intracardiac pressure
- Progressive limitation of ventricular diastolic filling
- Reduction of stroke volume and cardiac output
Effect of volume and timing of fluid accumulation on intrapericardial pressure/tampanode
