Mid Infective Endocarditis

Front 1

What are the pathological findings of infective endocarditis?

Back 1

The presence of often friable, valvular vegetations containing bacteria, fibrin, platelets and inflammatory cells. There is often valvular destruction with local intracardiac complications.

Front 2

What are some of the potential complications of infective endocarditis?

Back 2

-A chunk of friable vegation may break off and embolize
-Bacteria may seed other tissues causing metastatic infections

Front 3

Describe the underlying valvular disease in cases of infective endocarditis

Back 3

Rheumatic disease is not far less common and atherosclerotic cardiovascular disesasesas well as mitral valve prolapse with insufficiency have become more common. Patients with no antecedent history of valvular disease are also more common (25-30%)

Front 4

What bacteria typically cause bacterial endocarditis?

Back 4

-S. aureus (31.6%)
-Viridens group strep (18.0%)
-Enterococcus (10.6%)
-Coagulase negative staph (10.5%)
-S. bovis (6.5%)

Front 5

What is the major pathogen in subacute endocarditis?

Back 5

Viridens streptococcus

Front 6

What other disease is Streptococcus bovis associated with?

Back 6

Colonic carcinoma

Front 7

What is the predominant pathogen in IV drug use-related and nosocomial endocarditis?

Back 7

S. aureus

Front 8

What percentage of acute endocarditis cases are S. aureus?

Back 8

80%

Front 9

What is the major pathogen in prostetic valve endocarditis?

Back 9

Coagulase negative staph

Front 10

What are the predisposing factors for infective endocarditis?

Back 10

-Antecedal dental, GU or GI procedures that produce transient bacteremia
-IV drug abuse
-Invasive medical procedures such as IV lines, hemodialysis or surgical replacement of cardiac valves

Front 11

What is the sequence of events in infective endocarditis?

Back 11

-Transient bacteremia
-Seeding of a valvular surface
-Formation of a mature vegetation

Front 12

Explain nonbacterial thrombus

Back 12

In subacute infective endocarditis baceteria seed sites of previous micro or macroscopic damage. These sites are characterized by the deposition of platelet-fibrin thrombus. These are nonbacterial thrombus. These lesions form as a result of mechanical stress or antecedent valvular disease. In acture IE, the NBT may not be neccessary, the more virulent organisms appear capable of colonizing normal cardiac valvular surfaces

Front 13

Which valves are predominantly effects?

Back 13

The left sided ones. The proportion of cases involving the tricuspid valuve is greater with acute bacterial endocarditis and with drug addicts.

Front 14

What are the hemodynamic features that predict the anatomic site of vegetation formation?

Back 14

a) The presence of a high-pressure source
b) High velocity of flow through a narrow orifice
c) A low presure chamber or sink beyound hte orifice
-The infections occur on hte low-pressure side of things

Front 15

What bacterial factors are associated with infective endocarditis?

Back 15

-Gram positives are better than gram negatives because of surface adhesins that mediate binding to valvular surfaces
-Other factors include the serum resistance of gram positives and their capacity to interact with platelets

Front 16

Contrast the vegetations of acute and subacute IE

Back 16

There is often greater necrosis and friability of the lesions associated with acute IE

Front 17

What pathogenic processes explain the clinical manifestations of IE?

Back 17

1) Valvular destruction and local intracardiac complications
2) Bland or septic embolization of vegetations to other organs
3) Sustained bacteremia which contributes to metastatic seeding
4) Immunopathologic phenomena

Front 18

What are the clinical manifestations of IE?

Back 18

-Fever (85-90%)
-Fatigue
-Anorexia
-General malaise
-Weight loss (25%)
-Heart murmurs (85-99% in SBE, 1/3 of the time in acute IE involving the aorta or mitral valve)
-Development of a new regirgitant murmur tha tleads to congestive heart failure (>90%)
-Major arterial embolization with subsequent tissue infarction (coronary vessels, kidneys, CNS, spleen)
-ABE may lead to spsis
-Lungs are seeded with tricuspid valve ABE
-Sustained bacteremia
-Rheumatoid factor (~50%)
-Glomerulonephritis from circulating immune complexes
-Skin Petechiae (20-40%)
-CNS emboli (>1/3)
-Roth spots on retina, Osler's nodes, Janeway lesions or Spliner hemorrhages on skin

Front 19

What are laboratory results in IE?

Back 19

-Blood cultures Positive
-Anemia (50-80%)
-Hematuria (30-50%)
-RBC casts (12%)
-Hypocomplementemia (5-15%)
-Elevated ESR
-Immune complexes present

Front 20

Prosthetic Valuve Endocarditis

Back 20

-Follows insertion of a prosthetic cardiac valve
-Early (<60 days postsurg) and Late (>60 days)
-Early onset in <2% patients
-Mostly coagulase negative staphylococcus
-High mortality (40-80%)
-Therapy requires replacement of valve and antibiotics
-Late is 2-4% of patients
-Organisms from dental, GU or skin sources
-Low virulence streptococci most common
-Clinical manifestions similar to SBE
-Lower mortality and cure is achieved often w/o valve replacement

Front 21

What can cause culture-negative endocardititis?

Back 21

i) Infectious etiology: Fastidious G- (HACEK group), fungi, nutritionally variant strep, anaerobes, rickettsiae
ii) Noninfectious etiology- After prolonged illness as a result of immunologic clearing of bacteria from the bloodstream with bacterial persistence in valvular tissue. Mural endocarditis from infected pacer wires or thrombi.

Front 22

How do you diagnose IE?

Back 22

Duke criteria (modeled after Jones criteria)

Front 23

How do you treat IE?

Back 23

Bacteriocidal agents of relatively prolonged time period. Treatment should be started early to prevent rapid valve destruction. Urgency is required for acute but not subacute.

Front 24

What is the mortality of IE? From what? What factors adversely effect prognosis?

Back 24

5-30%. From congestive heart failure or emboli
Factors: Increased age, culture negative endocarditis, aortic valve involvement, congestive heart failure, relatively resistant or virulent pathogens or early prosthetic valve endocarditis.

Front 25

How do you prevent IE?

Back 25

Prophylaxis for those with known valvular disease going for dental, GU or GI procedures knowns to be associated with transient bacteremia.

Prophylax for viridans streptococci for upper respiratoryu tract or dental predures and against enterococci for GI and GU procedures. Generally GI and GU is for those at high risk. High risk means a prosthetic valve, complex congenital heart disease, previous endocarditis, cardiac transplant with valvulopathy.

Front 26

What diseases mimic IE

Back 26

-Atrial myxoma
-Marantic endocarditis
-Left atrial thrombus
-Acute rheumatic fever with carditis
-Collagen vascular disease (SLE)
-Neoplasms