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Roth's spots are retinal hemorrhages with white or pale centers.

The original retinal spots


identified in 1872 were attributed to nerve-fibres that had burst or exploded. Present-day
analysis shows that they can be composed of coagulated fibrin including platelets, focal
ischemia, inflammatory infiltrate, infectious organisms, or neoplastic cells. [1] They are
typically observed via fundoscopy (using an ophthalmoscope to view inside the eye) or slit
lamp exam.
They are usually caused by immune complex mediated vasculitis often resulting from
bacterial endocarditis. Roth's spots may be observed in leukemia, diabetes, subacute bacterial
endocarditis, pernicious anemia, ischemic events, hypertensive retinopathy and rarely in HIV
retinopathy.
Roth's spots are named after Moritz Roth.[

Janeway lesions are non-tender, small erythematous or haemorrhagic macular or nodular


lesions on the palms or soles only a few millimeters in diameter that are indicative of
infective endocarditis.[1] Pathologically, the lesion is described to be a microabscess of the
dermis with marked necrosis and inflammatory infiltrate not involving the epidermis.[1] They
are caused by septic emboli which deposit bacteria, forming microabscesses. [2] Janeway
lesions are distal, flat, ecchymotic, and painless.
Osler's nodes and Janeway lesions are similar, but Osler's nodes present with tenderness and
are of immunologic origin

Infective Endocarditis
Epidemiology:

Incidence of endocarditis estimated as 2-6 cases/100,000 person years

90% of endocarditis occurs in patients with pre-existing heart disease

Worldwide, condition that most predisposes individuals to endocarditis is rheumatic


heart disease; nationwide, it is mitral valve prolapse

Endocarditis continues to have a high mortality, estimated at 10-20% among


hospitalized patients

Greatest morbidity occurs among those with recent cardiac prostheses, status-post
heart transplant, or prior endocarditis

Pathogenesis

Step 1: Formation of non-bacterial thrombotic embolus (vegetation)


o Turbulent flow from acquired or congenital heart disease traumatizes
endothelium
o Traumitized endothelium serves as a nidus for fibrin and platelet deposition

Step 2: Pathogen seeds blood; generally occurs via trauma to a mucosal surface from
such daily activities as teeth brushing or chewing, or invasive activities like dental,
GI, or GU procedures

Step 3: Pathogen adheres to fibrin-laden endothelium or device


o Gram-positive cocci (Staph, Strep) most common pathogens
o Gram-negative bacteria (HACEK organisms) and fungi (Candida, Aspergillus)
can also adhere

Step 4: Pathogen promotes fibrin deposition


o Micro-organism stimulates more fibrin deposition on pre-exisiting aseptic
vegetation
o Creates secluded area within which pathogen can proliferate

Sequelae

Valvular damage: Pathogen destroys valves - cause regurgitation and possibly even
heart failure

Emboli: Septic emboli travel to lung, brain, kidney, or extremities and cause local
infection and ischemia/infarction

Immune-mediated: Circulating
glomerulonephritis or vasculitis

immune

complexes

can

possibly

mediate

Clinical Presentation:

Overview:
o Non-specific signs fever, myalgia, arthralgia, headache, malaise, anorexia,
weight loss are common
o Classic signs Roth spots (retinal hemorrhages with a pale center), Janeway
lesions (nontender macules on fingers and soles), Osler nodes (painful
lesions on hands and feet), and splinter hemorrhage are rare in children

Making the diagnosis:

o Pathologic evidence of intracardiac or embolized vegetation or intracardiac


abscess OR
o 2 major, 1 major and 3 minor, or 5 minor of the Duke Criteria:

Duke Criteria

Major Criteria
Positive blood culture*
Positive echocardiogram (vegetation, paravalvular abscess, or valve dehiscence after
surgery). While transesophageal echo recommended in adults, transthoracic echo is fine in
children.
New valvular regurgitation (by auscultation, not echocardiogram)
Minor Criteria
Predisposing heart condition (including prior IE)
Injection drug use
Fever (temperature >100.4 F [38 C])
Major arterial emboli
Septic pulmonary infarcts
Mycotic aneurysm
Intracranial hemorrhage
Conjunctival hemorrhage
Janeway lesions (painless hemorrhagic lesions on palms and soles)
Glomerulonephritis
Osler nodes (painful lesions at fingertips)
Roth spots (retinal hemorrhages)
Positive rheumatoid factor

Single positive blood culture


Serologic evidence of active infection with an organism consistent with IE

Note: Splinter hemorrhagees and erythrocyte sedimention rate are not criteria. Also, there are
no minor echo criteria, ie, valvular regurgitation alone is not a criterion.
*A positive blood culture is a major criterion when 1) there is growth on two occasions of a
microorganism typical for IE (eg, viridans group Streptococcus, Staphylococcus aureus, or
enterococcus), OR 2) there are persistently postiive blood cultures (two positive cultures
from samples 12 h apart or three positive cultures drawn 1 h apart) of a microorganism
consistent with IE, such as S epidermidis, OR 3) Coxiella burnetii (Q fever) grows from a
single blood culture, or there is serologic evidence of C burnetii (IgG titer _1:800).
From Li JS, Sexton DJ, Mick N, et al. Proposed modifications to the Duke Criteria for the
diagnosis of infective endocarditis. Clin Infect Dis.
2000;30:633638. Used with permission from the University of Chicago Press.

Treatment

If blood cultures have not come back and need to begin treatment, generally begin
empiric coverage against staph and strep with penicillin or ampicillin plus gent for 4-6
weeks; IV treatment most effective

Surgery indicated in those with persistent blood cultures after two weeks of
appropriate treatment, fungal vegetations, abscess formation, worsening heart failure,
or systemic emboli

Prophylaxis
In 2007, the American Heart Association (AHA) revised its criteria for bacterial prophylaxis
against endocarditis. Current guidelines state that only those individuals with the following
conditions require one dose antibiotic prophylaxis prior to undergoing dental procedures:
1. Prosthetic cardiac valve or prosthetic material used for cardiac valve repair
2. Previous infectious endocarditis
3. Of those with congenital heart disease (CHD), those with
1. Unrepaired cyanotic CHD, including palliative shunts and conduits
2. Completely repaired congenital heart defect with prosthetic material or device
for the first 6 months after the procedure

3. Repaired CHD with residual defects at the site or adjacent to the site of a
prosthetic patch or prosthetic device
4. Cardiac transplantation recipients who develop cardiac valvulopathy
The rationale for the revised criteria is that the majority of endocarditis in non-IV drug users
is caused by transient bacteremia resulting from daily activities, such as chewing food,
flossing, and brushing teeth, rather than semi-annual, invasive dental procedures. However,
by the reasoning of the AHA, in the aforementioned groups, the risk of serious adverse
outcome from endocarditis is so great as to warrant prophylaxis.

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