Infective Endocarditis
Definitions & Background
Bacterial vegetations comprised of platelets, fibrin, microorganisms, and inflammatory cells generally involve the heart valves and intracardiac devices.
Endothelial injury allows for either direct infection or formation of a nonbacterial thrombotic endocarditis (NBTE) which can become infected during transient bacteremia. More virulent bugs tend to adhere directly to the endothelium. Other bugs tend to adhere to the NBTE. Risk factors for NBTE are valvular defects (MR, AS, AR), VSD, CHD, hypercoagulable states (marantic endocarditis), SLE, and antiphospholipid syndrome.
Organisms deep within the vegetation are metabolically inactive and difficult to eradicate. Embolization of vegetation fragments can lead to distant infection or infarction. Intracardiac structures can be damaged (perivalvular abscesses, conduction blocks), and tissue damage arises from immune complex deposition or responses to deposited bacterial antigens.
Risk factors are fairly obvious:
- congenital heart diseases
- chronic rheumatic heart disease
- IV drug use
- degenerative valves
- intracardiac devices (ICD, pacemaker, etc)
- old age
- prosthetic valves
- bioprosthetics and mechanicals have similar risk profiles
- risk is greatest in the first 6 to 12 mo
- risk declines to a low, stable level after
Causative organisms are typically bacteria, but can be fungal as well.
| Organism | Associations |
|---|---|
| viridans Streptococci | dental procedures |
| HACEK group | upper respiratory tract |
| CoNS |
|
| Streptococcus gallolyticus (bovis) | colon cancer |
| Enterococcus spp. | genitourinary tract |
| Staphylococcus aureus |
|
Breakdowns of common bugs varies by population and valve replacement status, but Streptococci and Staph aureus are by far the two most common.
Some conditions can mimic infectious endocarditis:
- atrial myxoma
- marantic endocarditis
- antiphospholipid syndrome/lupus (Libman-Sacks endocarditis)
Clinical Manifestations
Tempo of Disease
The time-course and aggression of disease is dictated by the causative organism.
- Acute endocarditis is a febrile and aggressive disease. It causes rapid damage to cardiac structures, seeds extracardiac sites, and causes death within weeks of untreated.
- beta-hemolytic strep, Staph aureus, pneumococci
- Subacute endocarditis has a more indolent course. It causes slow progressive damage and rarely metastasizes unless there is a major embolic event or rupture of a mycotic aneurysm.
- viridans Strep, CoNS, HACEK, Bartonella, Whipple's disease, Staph aureus
Clinical Manifestations
| System | Manifestations |
|---|---|
| Systemic | fevers, weight loss, constitutional symptoms |
| Cardiac | new regurgitant murmurs, heart failure, perivalvular abscess, heart block, coronary embolism |
| Extracardiac | Janeway lesions (immune), Osler nodes and splinter hemorrhages (vascular), MSK pain, distal embolization, stroke, glomerulonephritis |
Duke Criteria
The Duke Criteria are a highly sensitive and specific set of clinical, laboratory, and echocardiographic findings of infective endocarditis. It emphasizes bacteremia and echocardiography. To satisfy the criteria, you must have one of the following combinations:
Workup
- Blood cultures - at least 2 sets prior to antibiotics. Consider obtaining 3 two-bottle sets, separated by 2+ hours, if no antibiotics have been received within the past two weeks. 5 to 15% of cases have negative blood cultures, and much of this is due to either prior antibiotic exposure or fastidious organisms.
- Serology can be drawn for Brucella, Bartonella, Legionella, Chlamydia psittaci, and Coxiella burnetti, if you think these are likely.
- Start with an initial TTE for all patients.
- Consider TEE if TTE nondiagnostic, IE complications suspected, or there are intracardiac leads. (Class I indications). Extremely specific, but cannot image vegetations less than 2 mm diameter. False negative rate is 6 to 18% in initial imaging, and so likely endocarditis may require a second TEE in 7 to 10 days if the first TEE is negative.
- Staphylococcus aureus bacteremia is an indication for routine TEE, due to the high prevalence of infective endocarditis with this bug.
- Other imaging is less common, and may involve 3D TEE or FGD-PET/CT.
Management
Medical Treatment
See Enterococcal Bacteremia for more specific information on Enterococcal endocarditis. See Staph Aureus Bacteremia for more information for SA associated endocarditis.
De-Escalation to Oral Therapy
The POET (NEJM 2019) trial compared partial PO vs IV antibiotic therapy for IE. 400 adults with IE (SA, E faecalis, CoNS) randomized to full IV therapy vs transition to PO after >10 days of IV. No difference in the primary outcome of mortality/cardiac surgery/embolism/bacteremia relapse within 6 months between the two groups. However, patients were followed 3x weekly, all had TEE, mostly L sided IE, and very few IVDU.
POET (2019)
In select patients with left sided IE (Strep, E faecalis, S aureus, CNST) who are stable, consider transition to PO antibiotics after at least 10 days of IV therapy. Requires:
- TEE before the switch to PO to demonstrate no paravalvular infection
- Frequent and close followup
- Followup TEE 1-3 days before the completion of the antibiotic course.
Surgical Considerations (per 2021 AHA/ACC Guidelines)
Class I Indications
Class II Indications
Prophylaxis
References & Resources
- Harrison's Principles of Internal Medicine, 20e
- Lilly Pathophysiology of Heart Disease
- Hoen B and Duval X. Infective Endocarditis. New Eng J Med. 2013; 368:1425-33.
- 2021 IM Review Slides