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Cardiovascular System > Endocarditis > Flashcards

Endocarditis Flashcards

1
Q
A
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2
Q

Definition of endocarditis

A

Infection of endocardium or parts of in. Sometimes but not always infection.

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3
Q

Parts of endocardium more prone to infection

A

valve leaflets congenital defects the walls or chordae of the chambers paraprosthetic tissue the attachment of implanted shunts, conduits fistula,

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4
Q

Can IE be seen on an XRay

A

No

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5
Q

What conditions are more prone to endocarditis?

A

Valve or valve replacement, VSD, new regurgitant heart murmurs, mitral valve prolapse.

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6
Q

What is the male/female ratio of endocarditis?

A

2/1

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7
Q

What are the 2 components of the pathophysiology of IE?

A

Nonbacterial thrombotic endocarditis, transient bacteria.

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8
Q

What are the pathologic effects of IE from infection?

A

Local tissue destruction and embolic phenomena

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9
Q

What secondary autoimmune effects can result from IE?

A

Autoimmune: glomerulonephritis, vasculitis, arthritis.

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10
Q

How has the incidence of IE changed over time?

A

Increased from more invasive procedures but decreased from less rheumatic heart disease so evens out overall.

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11
Q

What are the obvious characteristic findings of IE?

A

Numerous positive blood cultures in the presence of a well recognized predisposing cardiac lesion , Evidence of endocardial involvement.

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12
Q

How many patients have no identifiable predisposing cardiac lesion at disease onset?

A

1/4-1/3

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13
Q

What needs to be checked in order to diagnose IE?

A

A careful history and physical examination, blood cultures and laboratory results, an electrocardiogram, a chest radiograph, an echocardiogram .

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14
Q

What is significant on a physical exam for IE?

A

New regurgitant murmurs heart failure, classic clinical stigmata of endocarditis, including evidence of small and large emboli with special attention to the fundi, conjunctivae, skin, and digits, a neurologic evaluation, associated peripheral cutaneous or mucocutaneous lesions of IE include petechiae, splinter hemorrhages, Janeway lesions, Osler’s nodes, and Roth spots.

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15
Q

What history is significant for IE?

A

Prior cardiac lesions , historical clues pointing towards a recent source of bacteremia such as indwelling intravascular catheters or intravenous drug use.

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16
Q

Types of skin lesions in IE

A

Petechiae, splinter hemorrhages, Janeway lesions, Ostler nodes, Roth spots, other emboli.

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17
Q

How do petechiae appear in IE?

A

not specific for IE
most common skin manifestation in IE
on the skin (usually on the extremities) or on mucous membranes (palate or conjunctivae)

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18
Q

How do splinter hemorrhages appear in IE?

A

nonspecific for endocarditis
nonblanching, linear reddish-brown lesions found under the nail bed caused by emboli reaching end of finger.

19
Q

Janeway lesions in IE

A 
more specific (but still not diagnostic) for IE, though less common (10% of patients).
 macular, blanching, nonpainful, erythematous, red lesions on the palms and soles.
20
Q

Osler’s nodes

A 
more specific (but still not diagnostic) for IE, though less common
 painful, violaceous nodules/papulopustules found in the pulp of fingers and toes and are seen more often in subacute than acute cases of IE due to immune complexes.
21
Q

Roth spots

A

More specific (but still not diagnostic) for IE, though maybe present in other disorders, such as diabetes, Leukemia, anemia, hypertension and HIV
rare (5%)
exudative, edematous hemorrhagic lesions of the retina (a cotton wool spot (infarct) with surrpunding hemorrhage)

22
Q

Other organs affected by embolic events

A

focal neurologic deficits,
renal and splenic infarcts,
septic pulmonary infarct in right-sided IE.

23
Q

How should blood cultures be performed in IE?

A

A minimum of 3, spread out, prior to antibiotic treatment.

24
Q

The Duke Criteria: Typical causes of IE

A

Staphylococcus aureus,
Viridans group streptococci and Streptococcus bovis,
Enterococci ,
HACEK group organisms

25
Q

Staph aureus in IE

A

huge problem can be anywhere in the body, loves to sit on valves, esp prosthetic, only good outcomes are with IV drug users

26
Q

Strep viridans and bovis in IE

A

sit on teeth and can enter. 2 blood cultures are very suspicious but doesn’t have to be.

27
Q

Enterococci in IE

A

Very hard to treat, lots of complications

28
Q

HACEK organisms in IE

A

Fastidious gram-negative bacilli, need to grow for 2-3 weeks to see:

Haemophilus aphrophilus
Actinobacillus actinomycetemcomitans
Cardiobacterium hominis
Eikenella corrodens
Kingella kingae.

29
Q

Other pathogens in IE

A

culture negative endocarditis (8%-unknown antibiotic)

polymicrobial (1%)

a variety of other organisms (3%-including Brucellosis in the Negev, other gram negatives)

Fungus (usually candida)

30
Q

Definite criteria for IE

A
31
Q

Diagnostic criteria for IE

A
32
Q

Why is echo used for IE?

A

because of its high sensitivity for valvular vegetations and complications of IE, is considered mandatory in the clinical diagnosis and treatment of this disorder

33
Q

What are the major criteria involving echo structural findings?

A

presence of an oscillating intracardiac mass/valvular vegetation
presence of an abscess
partial dehiscence of a prosthetic valve
(New valvular regurgitation is also a major criterion)

34
Q

What are the disadvantage of the Transthoracic Echo (TTE)

A

sensitivity (62-79%), less sensitive than TEE (92%)
measurements of structures in echo studies are limited by lower image resolution
underestimates the size and complexity of large vegetations
fails to detect small vegetations (<3 mm in diameter)

35
Q

What are the disadvantage of TEE (transesophageal echo)

A

Invasive, expensive.

36
Q

When is a TEE indicated over a TTE?

A

When TTE is nondiagnostic or to diagnose prosthetic valve endocarditis and assess complications.

37
Q

Noninfectious causes of endocarditis

A

Libman-Sacks endocarditis (also known as verrucous, marantic, or nonbacterial thrombotic endocarditis)
Loeffler’s endocarditis
Granulomatous diseases
Scleroderma

Lupus

38
Q

What are the criteria for culture-negative IE?

A

Endocarditis without etiology following inoculation of at least three independent blood samples in a standard blood culture system with negative cultures after seven days of incubation and subculturing

39
Q

What are the main causes for culture-negative IE?

A

Previous administration of antimicrobial agents
Inadequate microbiological techniques
Infection with highly fastidious bacteria or nonbacterial pathogens (eg, fungi).

The HACEK organisms (Haemophilus aphrophilus; Actinobacillus actinomycetemcomitans; Cardiobacterium hominis; Eikenella corrodens; and Kingella kingae)
Fastidious organisms [e.g., zoonotic agents (Bartonella spp., Coxiella burnetii, Brucella spp.) and fungi]
Streptococcal spp. in patients who have received previous antibiotic treatment

40
Q

How can culture-negative IE be diagnosed?

A

Special culturing techniques (eg, shell vial and lysis centrifugation)
Molecular techniques (eg, polymerase chain reaction and serologic assays)
Histopathology evaluation of valvular tissue when surgical excision is performed.

41
Q

What is the survival rate of IE?

A

Approximately 80% of patients with endocarditis now survive their infections (1/6 patients with IE does not survive the initial hospitalization), and up to 1/3 of patients infected with highly virulent organisms (such as Staphylococcus aureus) may die as a direct or indirect result of their valvular infection.

42
Q

What is the treatment for IE?

A

Only bactericidal, not bacteriostatic therapy is effective in treating endocarditis
Antimicrobial therapy should be administered in a dose designed to give sustained bactericidal (not bacteriostatic) serum concentrations throughout much or the entire dosing interval.

Most is IV.

Often empirical therapy: only after 2-3 cultures obtained.

Monitor other complications and response to antibiotics after treatment begins.

43
Q

Complications of IE

A

Myocardial infarction, pericarditis, cardiac arrhythmia
Cardiac valvular insufficiency
Congestive heart failure
Sinus of Valsalva aneurysm
Aortic root or myocardial abscesses
Arterial emboli, infarcts, mycotic aneurysms
Arthritis, myositis
Glomerulonephritis, acute renal failure
Stroke syndromes
Mesenteric or splenic abscess or infarct

Cardiovascular System (28 decks)

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