Infective Endocarditis (34) Flashcards
What is endocarditis?
Inflammation of the endocardial surfaces of the heart including heart valves which is caused by certain microorganisms.
Why are rheumatic heart and valve replacement patients more susceptible to IE?
Blood usually flows smoothly over valves, when these valves are damaged (as in rheumatic heart) or in valve replacement, there will be an increased chance for bacterial colonization on damaged tissues.
What are the types of endocarditis?
- Infective endocarditis
- Microbes colonize heart valves and form friable vegetations
- Two types of IE: acute and subacute
- Diagnosis via Duke’s criteria
- Non-bacterial thrombotic endocarditis (marantic endocarditis)
- Characteristically occurs in the settings of cancers (e.g. adenocarcinomas)
- Libman-Sacks endocarditis
- Occurs in the settings of cancers (e.g. adenocarcinoma)
What is the pathophysiology of Rheumatic heart disease?
- Acute rheumatic fever is a result of host immune responses to group A streptococcal antigens that cross-react with host proteins.
- Antibodies and CD4+ T cells directed against streptococcal M proteins can also, in some cases, recognize cardiac self-antigens.
- Antibody binding can activate complement, as well as recruit Fc-receptor bearing cells (neutrophils and macrophages); cytokine production by the stimulated T cells leads to macrophage activation (e.g., within Aschoff bodies).
- Damage to heart tissue may be caused by a combination of antibody and T cell-mediated reactions.
- Recurrent inflammation, progressive fibrosis, narrowing and stiffening of the valve leaflets with commissural fusion, retraction of the leaflet edges, valve thickening, calcification leading to stenosis.
What are the gross findings in endocarditis on echo?
- Acute phase: Valvular vegetations (verrucae) along the lines of closure, having little effect on cardiac function
- Chronic phase: Commissural fibrosis, valve thickening, and calcification + shortened and fused chordae tendinea (fish mouth shape)
What are the microscopic findings in endocarditis?
- Aschoff bodies, a form of granulomatous inflammation consisting of a central zone of degenerating ECM infiltrated by lymphocytes, plasma cells, and Anitschkow cells.
- Found in all three layers of the heart (pericardium, myocardium, or endocardium)
What investigation is used to identify vegetations?
2D echo
What should be looked for in 2D echo?
- Valvular regurgitation
- A regurgitant jet >1 cm in length and peak velocity >2.5 m/s
- Leaflet
- Prolapse, coaptation failure, thickening (>4 mm), reduced mobility, nodules
- Annular dilatation
- Chordal elongation/rupture
- Increased echogenicity of subvalvular apparatus
- Pericardial effusion
- Ventricular dilatation and dysfunction (almost always with significant regurgitation)
What are the common organisms that cause endocarditis?
- Viridans Strep. or Staph.
- Coagulase-negative staph.
- Enterococci
- HACEK group of microorganisms (oropharyngeal commensals)
- Haemophilus species, Aggregatibacter species, Cardiobacterium hominis, Eikenella corrodens, and Kingella species
What are the causes and risk factors of endocarditis?
Cardiac
- Acquired valvular heart disease with stenosis or regurgitation
- Valve replacement
- Structural congenital heart disease, including surgically corrected, but excluding isolated ASD, fully repaired VSD/PDA
- HOCM (hypertrophic obstructive cardiomyopathy)
- Devices (Implantable cardioverter-defibrillators)
- Cyanotic congenital heart defects
- RHD
- Previous IE
Non-cardiac
- HIV
- Malignancy
- Diabetes mellitus
- Alcohol
- Tooth extractions
- Colorectal cancer (Streptococcus bovis)
- UTI (enterococci)
- IVDU
What are the complications of endocarditis?
Cardiac
- AMI
- Pericarditis
- Arrhythmia
- Valvular insufficiency
- CCF (congestive cardiac failure)
- Sinus of Valsalva (aneurysm of the aortic sinus)
- Aneurysm
- Intra-cardiac abscess
- Arterial emboli
Non-cardiac
- GN (endocarditis-associated glomerulonephritis)
- AKI
- Stroke
- Mesenteric/splenic abscess or infarct
What are the signs in hand?
- Osler nodes
- Painful, raised, red lesions due to immune complex deposition
- Janeway lesions
- Non-painful, nodular or macular red lesions due to septic emboli which deposit bacteria forming microabscesses
- Splinter hemorrhages: tiny blood clots under nails
What is the treatment for endocarditis?
IV antibiotics depending on culture and sensitivity for 6 weeks (IV ceftriaxone and vancomycin)
Why are restrictions in place for endocarditis treatment?
- Valves do not have specific blood supply so antibiotics cannot reach.
- Organisms lie inside the vegetations.
- Bacteria form a biofilm (glycocalyx covering) that shields them from antibiotics.
What is matched before heart transplantation?
HLA antigen
What are the major criteria for diagnosing endocarditis?
Blood cultures positive for endocarditis
- Typical microorganisms consistent with IE from 2 separate blood cultures, microorganisms consistent with IE
from persistently positive blood cultures, single positive blood culture for Coxiella burnetii or antiphase I IgG
antibody titer >1:800.
Evidence of endocardial involvement
- Echocardiogram positive for IE, abscess, new partial dehiscence of prosthetic valve, new valvular regurgitation.
- Note: Worsening or changing of pre-existing murmur NOT sufficient.
What are the minor criteria for diagnosing endocarditis?
- Predisposition
- Heart condition or IV drug use
- Fever
- Greater than or equal 38ᵒc
- Vascular phenomena
- Major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, and Janeway’s lesions.
- Immunologic phenomena
- Glomerulonephritis, Osler’s nodes, Roth’s spots, and rheumatoid factor.
- Microbiological evidence
- Positive blood culture but does not meet a major criterion as noted above or serological evidence of active infection with organism consistent with IE.
- Echocardiographic findings consistent with endocarditis but do not meet a major criterion as noted above
What is the mechanism of action of immunosuppressant drugs?
