Infective endocarditis (IE) is an infectious inflammation of the endocardium that affects the heart valves. The condition is usually a result of bacteremia, which is most commonly caused by dental procedures, surgery, distant primary infections, and nonsterile injections. IE may be acute (developing over hours or days) or subacute (progressive over weeks to months). Acute bacterial endocarditis is usually caused by Staphylococcus aureus and causes rapid endocardium destruction, while subacute bacterial endocarditis is most commonly caused by viridans streptococci and generally affects individuals with preexisting damage to the heart valves, structural heart defects, or prosthetic valves. Clinical features include constitutional symptoms (fatigue, fever/chills, malaise), signs of pathological cardiac changes (e.g., new or changed heart murmur, heart failure signs), and, in some cases, manifestations of subsequent damage to other organs (e.g., glomerulonephritis, septic embolic stroke). Management is complex and infectious disease (ID) specialists should be involved early. Diagnosis is made based on the Duke criteria, the main features of which are positive blood cultures and evidence of endocardial involvement on echocardiography. Initial treatment of IE consists of empiric IV antibiotics, which are then adapted to blood culture results and continued for several weeks. Categorization into native valve endocarditis or prosthetic valve endocarditis helps to further tailor regimens. Surgery may be necessary for complex cases (e.g., valve perforation). Prophylaxis is only administered in specific circumstances, e.g., in patients with preexisting heart conditions undergoing dental or surgical procedures. If left untreated, infective endocarditis can be fatal within a few weeks.
Staphylococcus aureus (45–65%)
HEAving your KING-size bed from IKEa into your CAR AGGREGATes joy: Native valve endocarditis is caused by haemophilus, kingella, eikenella, cardiobacterium, and aggregatibacter.
Risk factors for infective endocarditis
- Male sex
- Age > 60 years
- Preexisting conditions
Pathogenesis: localized infection or contamination → bacteremia → bacterial colonization of damaged valve areas → formation of fibrin clots encasing the vegetation → valve destruction with loss of function
- Preexisting valvular endothelial damage or prosthetic valves predispose to bacterial colonization, especially organisms that cause subacute IE
- Frequency of valve involvement: mitral valve > aortic valve > tricuspid valve > pulmonary valve
- The tricuspid valve is the most commonly affected valve in IV drug users (associated with Pseudomonas, S. aureus, and Candida).
- Clinical consequences
Don't tri drugs for the sake of your tricuspid valves.
- Fever and chills (∼ 90% of cases), tachycardia
- General malaise, weakness, night sweats, weight loss
- Dyspnea; , cough, pleuritic chest pain
- Arthralgias, myalgias
New heart murmur development or change to a preexisting one
- → holosystolic murmur, loudest at the heart's apex, and radiates to the left axilla
- Tricuspid valve regurgitation → holosystolic murmur; loudest at the left sternal border; ; seen in IV drug users; and concomitant HIV infection; , immunosuppressed patients,; and patients with central venous catheters
- → early diastolic murmur; loudest at the left sternal border
- Signs of progressive heart failure (e.g., dyspnea, edema) due to valve insufficiency
- Signs of acute cardiac decompensation (pulmonary edema)
With the exception of pulmonary embolic manifestations, extracardiac symptoms are more common in left-sided endocarditis.
- These manifestations are mainly caused by bacterial microemboli and/or the precipitation of immune complexes.
- Petechiae; especially splinter hemorrhages (hemorrhages underneath fingernails)
- Janeway lesions
- Painful nodules on pads of the fingers and toes
- Caused by immune complex deposition
- Roth spots: round retinal hemorrhages with pale centers
- Signs of acute renal injury, including hematuria and anuria; (due to renal artery occlusion or glomerulonephritis)
- Splenomegaly and possible LUQ pain (caused by splenic artery occlusion or a splenic abscess, which can lead to rupture)
- Neurological manifestations; (e.g., seizures, paresis): due to septic embolic stroke, hemorrhages, meningitis, encephalitis, and/or abscess.
- Signs of pulmonary embolism (e.g., dyspnea); : typically caused by septic emboli resulting from tricuspid valve involvement
- Possible arthritis
FROM JANE - Fever, Roth spots, Osler nodes (Ouch = painful), Murmur, Janeway lesions, Anemia, Nail bed hemorrhage, Emboli
Infective endocarditis can be classified based on the type of valve (native vs. prosthetic), acuity of the infection, and location of the infection (left- vs. right-sided). Although this is not a definitive classification system, it can help in the approach to management and selection of empiric antibiotic regimens.
|Classified by type of valve involved and clinical course|
|Native valve endocarditis||Prosthetic valve endocarditis|
|Acute bacterial endocarditis||Subacute bacterial endocarditis|
|Distinguishing clinical features|| |
|Affected valves|| || || |
|Classified by location of valves involved|
|Right-sided endocarditis ||Left-sided endocarditis|
|Distinguishing clinical features|| |
|Affected valves|| || |
- Suspect IE based on clinical findings (e.g., fever without focus combined with a new murmur) and predisposing conditions.
The modified Duke criteria help categorize the diagnostic likelihood of IE: definite vs. possible vs. rejected. 
- Used as a diagnostic guide; not a substitute for clinical judgment
- Incorporate clinical, microbiological, pathological, and imaging criteria.
- All patients require multiple blood cultures and echocardiography.
- Additional diagnostics (e.g., serology, additional imaging) help assess blood culture-negative endocarditis and complications.
- Consult infectious disease (ID) if the diagnosis is uncertain.
|Modified Duke criteria |
Laboratory studies 
- CBC: leukocytosis with left shift
- Inflammatory markers: ↑ CRP, ↑ ESR 
- BMP: assessment of renal function for antibiotic dosing
Blood cultures 
- Prior to treatment: 3 sets from different venipuncture sites 
- Monitoring: 2 sets every 24–48 hours until clearance
- Positive bacterial cultures: Assess according to the modified Duke criteria.
- Negative bacterial cultures do not completely rule out endocarditis. False negatives can be due to: 
Transthoracic echocardiography (TTE) is the initial test of choice for all patients with suspected IE. It should ideally be performed within 12 hours of presentation and repeated after completing treatment. Transesophageal echocardiography (TEE) is more invasive and is added in select cases. 
- Indications for TEE include:
- Echocardiographic findings fulfilling Duke criteria for IE: similar in TTE and TEE 
- Other high-risk findings include:
Additional investigations 
- Serology: to assess blood-culture negative endocarditis (in consultation with the infectious disease service)
- Tissue sampling (after surgery)
- ECG: indicated in every patient to assess for complications (e.g., AV block/branch blocks in paravalvular extension) 
- Additional imaging: in individual cases to investigate for complications (e.g., emboli)
- Dental assessment: in all patients with confirmed IE regardless of the initial source of bacteremia
- Colonoscopy: in patients with bacteremia involving S. gallolyticus to rule out colon cancer and mucosal lesions
- Acute disease (leading to valve insufficiency, septic embolic infarcts, tendinous cord rupture)
- Chronic disease (leading to valve insufficiency and valve stenosis)
Noninfective endocarditis (nonbacterial thrombotic endocarditis)
- Description: rare, noninfectious form of endocarditis due to sterile platelet thrombus formation on the heart valves (usually mitral and aortic valves)
- Most commonly associated with underlying trauma (e.g., catheters), malignancy, hypercoagulable states, previous rheumatic fever, chronic infections (e.g., TB, pneumonia, osteomyelitis), or autoimmune conditions (systemic lupus erythematosus, rheumatoid arthritis, antiphospholipid syndrome, etc.)
- A nonbacterial thrombotic endocarditis with verrucous vegetations in a patient with systemic lupus erythematosus or antiphospholipid syndrome is also referred to as Libman-Sacks endocarditis. Vegetations are usually found on the undersurface of the mitral or aortic valve.
- Clinical features
- Treatment: anticoagulation with heparin and treatment of the underlying condition
Prosthetic valve thrombosis
- Insufficient anticoagulatory therapy after valve replacement
- Usually affects mechanic valves
- Rare if anticoagulation is adequate
- Presence of a cardiac defect raises the risk of recurrent endocarditis
- Clinical course
- Diagnostics: transesophageal echocardiography
- Treatment: anticoagulation and fibrinolysis, surgical valve replacement
The differential diagnoses listed here are not exhaustive.
General principles 
|Therapeutic approach to infective endocarditis |
|Empiric antibiotics|| |
|Targeted antibiotics|| |
|Empiric antibiotic therapy for infective endocarditis |
|Valve type||Clinical presentation||Common regimen|
|Native valve endocarditis||(days)|
|Prosthetic valve endocarditis||≤ 1 year after valve placement|
|> 1 year after valve placement|
|Targeted antimicrobial therapy for infective endocarditis |
|Organism||Native valve endocarditis (common regimens)||Prosthetic valve endocarditis (common regimens)|
|Methicillin-susceptible staphylococci (e.g., MSSA)|
|Methicillin-resistant staphylococci (e.g., MRSA)|
|Viridans group streptococci, S. gallolyticus|
|Enterococcus spp. (penicillin-sensitive)|
|Enterococcus spp. (penicillin-resistant)|
These procedures typically follow a multidisciplinary decision made by cardiology, cardiothoracic surgery, and infectious disease services.
- Indications for surgical consultation include:
- Options: valve replacement or valve repair (See “Treatment” in “Valvular heart diseases”.)
Endocarditis prophylaxis 
Common indications 
- Prior to the implantation of cardiac implantable electronic devices (e.g., AICD) 
- Some dental procedures in patients with high-risk cardiac features, such as:
- Common regimens (usually administered 30–60 minutes prior to the procedure)