Infective Endocarditis

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What is Infective Endocarditis?

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Infective endocarditis: infection involving the endocardial surface of the heart, most commonly the heart valves.

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Describe Acute endocarditis:

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Acute endocarditis has a rapid fulminant course, and is often fatal within several weeks after onset; affects normal valves.

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Describe subacute endocarditis:

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Subacute endocarditis usually affects previously damaged valves, and may cause symptoms for weeks or months prior to admission.

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Epidemiology of endocarditis:

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*Infective endocarditis is a relatively uncommon infection: accounts for about 1 case/1000 hospital admissions.
*More likely with artificial valves
*Overall, over 50% of cases occur in persons over age 50.

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Predisposing conditions for endocarditis:

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-Prosthetic heart valves
-Previous infective endocarditis
-Intravenous drug use
-Degenerative conditions involving heart valves
-Hypertrophic cardiomyopathy
-Congenital heart disease (& repair)
-Rheumatic heart disease
-Mitral valve prolapse

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left: strep visible
right: gram neg diplococci (gonorrhea)

*both on heart valves

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Pathogenesis of endocarditis:

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*Damage due to trauma, turbulence and underlying disease provides a suitable site for bacterial attachment.
*Platelets and fibrin form a thrombus on damaged endothelium.

*Transient bacteremia results in colonization of the platelet-fibrin thrombus; Forms a "vegetation."
*The vegetation enlarges and growth or organisms proceeds within the thrombus.

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Describe the deposition of ICs in the development of endocarditis:

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*Persistent bacteremia leads to septic emboli, formation of immune complexes and formation of rheumatoid factor antibodies.
*Septic emboli can affect any organ; may cause Osler’s nodes or Janeway lesions.
*Immune complex deposition may produce focal or diffuse glomerulonephritis, arthralgias, fever, pleuritic pain.

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What kind of pathology in the heart do you see in endocarditis?

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*Valves affected: mitral 85% of cases, aortic 55%, tricuspid 15%, pulmonic <1%.
*Infection may cause perforation of valve leaflets, valve ring abscesses, rupture of chordae tendinae, or disruption of the conduction system.
*Occasionally, myocarditis or pericarditis accompany IE.
*Myocardial infarction may result if emboli lodge in the coronary arteries.
*Vegetations may occlude valve orifice.

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*mitral valve showing large vegetation damaging flow of blood thru the valve.
*Valve itself appears fibrotic

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*Right sided endocarditis
*pulmonic valve affected

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*tricuspid
*a ruptured chordae tendinae

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*Aortic valve destroyed by staph aureus

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*fibrotic valve affected by rheumatic heart disease

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-Vegetation is calcified

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What kinds of systemic effects do you see related to endocarditis?

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*Splenic infarctions are common, but are often not diagnosed clinically.
*Renal infarcts; seldom cause renal failure.
*Diffuse glomerulonephritis (GN) or immune complex GN may result in renal failure.
*Cerebral emboli usually involve the MCA; mycotic (arterial wall) aneurysms may develop.
*Pulmonary emboli, infarction, effusions and empyema common with right-sided endocarditis.

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*Brain abscess 2˚ to endocarditis
*Many endocarditis pts (80%) will have SOME kind of brain effects, but this is extreme and uncommon.

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*mycotic aneurysm
*vegetation visible

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*glomerulonephritis 2˚ to endocarditis

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*lighter colored scabs are infarcts to the spleen, 2˚ to endocarditis.

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What bugs cause Endocarditis?

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*Streptococci and enterococci: 40-50% of cases
*Staphylococci: 40-50% of cases
*Gram-negative bacilli: 2-10% of cases
*Fastidious Gram-negative organisms: (“HACEK”) group and other “Culture-negative” endocarditis (Q fever, Coxiella burnetii)
*Gram-positive bacilli: uncommon
*Anaerobic bacteria and fungi: uncommon

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What is the HACEK group?

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Haemophilus
Aggregatibacter aphrophilus
Cardiobacterium hominis
Eikenella corrodens
Kingella (Kingella kingae)

*less common causes of endocarditis

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Clinical manifestations of endocarditis:

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*Infective endocarditis often causes fever, anemia, murmur & emboli (FAME).
*Murmur is present in 85-95% of cases. “Changing” murmurs and new murmurs are relatively uncommon.
*Fever occurs in 80% of patients.
*Chills, night sweats, weight loss and malaise are common.
*Arthralgias (including nonspecific back pain) and myalgias are common, and may be chief complaint.
*Splenomegaly occurs mainly in subacute form.

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Describe Embolic phenomena in Endocarditis patients:

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*Embolic phenomena occur in 25-35% of patients.
-Splinter hemorrhages in 15% of cases.
-Petechiae are relatively uncommon.
-Osler’s nodes (nodular lesions usually in the finger pads)
-Janeway lesions (hemorrhagic skin lesions on palms or soles)
-Roth spots (red lesions with a white center, involve the retina)
-Cerebral emboli occur in 10-30% of patients.
-Major artery emboli due to bulky vegetations more common with fungi and Haemophilus species.

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*conjunctival hemorrhage due to endocarditis

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*scleral hemorrhage due to endocarditis

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*roth spot in endocarditis

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*flame hemorrhages in endocarditis.

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*Janeway lesion in endocarditis; subtle

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*splinter hemorrhages on left
*osler's nodes on right

*both due to endocarditis

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*left: petechiae, splinter hemorrhages
*right: janeway lesions

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*embolic spots related to endocarditis

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*embolic spots related to endocarditis

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*clubbing and a splinter hemorrhage
*seen in subacute endocarditis as well as COPD

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Describe staph aureus left-sided endocarditis:

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*40% mortality in younger patients; 80% mortality in older persons.
*1/3 of patients will have “normal valves”.
*High incidence of complications.
-CHF, embolic phenomena, myocardial abscess
-Neurological complications

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*aortic valve completely destroyed by s. aureus

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Describe right-sided endocarditis:

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*Associated with IV drug use; 75% of infective endocarditis in IV drug users is right-sided, 10% of infective endocarditis in non-IV drug users is right-sided.
*Fever with multiple pulmonary infarcts.
*Staph auerus bacteremia.

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-Staph aureus in right sided endocarditis.

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ORGANISMS CAUSING INFECTIVE ENDOCARDITIS IN INTRAVENOUS DRUG USERS:

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*S. aureus is most common.

*Pseudomonas much more common than in other patients.

*Candida and Aspergillus fungi more common than in other risk groups.

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LABORATORY FINDINGS in endocarditis:

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*Erythrocyte sedimentation rates are elevated in almost all cases.
*Anemic of chronic disease is present in 70-90% of cases.
*Microscopic hematuria is relatively common.
*Rheumatoid factor antibodies often present in patients with subacute endocarditis.

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*example of a positive blood culture in endocarditis
*gram + diplococci --> strep

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How do you diagnose endocarditis?

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*Blood cultures are the most important diagnostic test for diagnosing infective endocarditis.
*Draw blood cultures before starting empiric antibiotics.
*In patients who have not been on antibiotics, 2 sets of timed blood cultures will yield the causative organism in >90% of cases.
*Ideally, 3 sets of cultures before antibiotics.

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Describe the role of echo in diagnosing endocarditis:

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*Echocardiogram (ECHO) may be useful.
*Sensitivity and specificity for detecting vegetations vary with ultrasound technique used
Transthoracic (TTE) Transesophageal (TEE)
Sensitivity 60-70% 90-95%
Specificity 90-95% 95-98%

*Negative predictive value of a single TEE is about 90%.

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*echo showing a large embolus in endocarditis

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LOCAL COMPLICATIONS OF INFECTIVE ENDOCARDITIS:

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*ECHO can identify perivalvular extension of infection, valvular dysfunction or instability, degree of aortic insufficiency.
*ECHOs are seldom useful if blood cultures are negative (don't screen for no reason; must be suspicious of endocarditis or valve dysfunction first)

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Therapy for Endocarditis:

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*Long-term intravenous antibiotics with bactericidal agents required.
*Monitoring the efficacy of antibiotic therapy by determining the MIC of the organism is often necessary.
*Surgery is needed in a significant number of patients.

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When should you perform surgical therapy for endocarditis?

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*Refractory CHF
*Perivalvular or myocardial abscess, conduction abnormalities on EKG
*Fungal endocarditis
*More than one serious embolic episode
*Persistent bacteremia despite appropriate antibiotics

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Who should receive prophylactic treatment for endocarditis?

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*Prosthetic cardiac valve
*Previous IE
*Congenital heart disease
-unrepaired cyanotic CHD
-repaired with prosthetic materials during first 6 months after procedure
-repaired with residual defects at site
*Cardiac transplantation recipients who develop valvulopathy