creation date: 2025-10-28 14:59
tags: Pathologies
Infective Endocarditis
Background
Definitions
Infective endocarditis, formerly known as infectious endocarditis, refers to the inflammation of the endocardium and the heart valves.
Microbiology
Owing to its infective nature, the cause of IE involve bacterial infection. The exact bacteria depends on the nature and origin of the disease.
Native valve endocarditis
Oral, skin, or upper respiratory portals:
- Streptococcus viridans
- Staphylcocci
- HACEK (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
Gut origin:
- Streptococcus bovis
Genitourinary tract:
- Enterococci
Nosocomial:
- Staphylcoccus aureus
- Coagulase-negative staphylococci (intracardiac devices)
Prosthetic valve endocarditis
<2 months post-surgery:
- Coagulase-negative staphylococcus
- Pseudomonas
- Candida
2-12 months post-surgery:
- Staphylococcus aureus
- Candida
- Enterococci
>12 months post-surgery:
- Streptococci
- Staphylococcus aureus
- Enterococci
IV drug use
Right-sided endocarditis (tricuspid/pulmonic):
- Staphylococcus aureus
Left-sided endocarditis:
- Staphylococcus aureus
- Enterococci
- Streptococci
- Gram-negative rods
- Candida
Pathogenesis
The pathogenesis of endocarditis begins with some initial damage to the endocardium. This may be from direct mechanical trauma from catheter, secondary to turbulent flow from disease valves, or from particulate matter co-injected with drug use.
As the left side of the heart experiences higher pressures and thus turbulence, the left-sided heart valves (mitral, aortic) have a high prevalence of endocarditis. The exception is with IV drug use, where direct inoculation can happen from the systemic blood flow.
The damage predisposes the endocardium to formation of thrombotic vegetation on the valve through platelet aggregation and activation of the coagulation cascade.
Subsequent bacteremia allows for colonization of the vegetation. This can stem from an established source of infection or transiently through hematogenous inoculation (eg. from dental procedure). In some cases, bacteremia can mediate platelet aggregation.
Clinical Presentation
Signs & Symptoms
IE may present as an acute, rapidly progressive infection (more virulent pathogens, sg. S. aureus) or as a subacute/chronic disease (less virulent pathogens, eg. Streptococcus viridans).
Symptoms occur with no temporal pattern:
- Fever
- Malaise (and myalgias, arthralgias)
- Anorexia
- Weight loss, night sweats
- Abdominal pain
- Dyspnea
Signs observed are:
- New or changing cardiac murmur
- Splenomegaly
- Cutaneous manifestations (petechiae or splinter hemorrhages)
Some findings, although uncommon, are highly specific of IE:
- Janeway lesions (nontender erythematous macules no palms and soles)
- Osler nodes (tender subcutaneous violaceos nodules on pads of fingers and toes)
- Roth spots (exudative, edematous hemorrhagic lesions of retina with pale centers)
In subacute cases, findings may only be nonspecific symptoms and low-grade fever.
Patients may also present with complications.
History & Physical Exam
Physical exam should include cardiac auscultation and evaluation of complications.
Risk factors
Infective endocarditis is generally rare but pre-disposing factors elevate risk:
- Congenital heart disease
- Illicit IV drug use
- Degenerative valvular disease
- Intra-cardiac devices
- Prosthetic heart valves (especially within 6 months of implantation)
Diagnosis
Criteria
Diagnosis is made based on clinical manifestations, blood cultures/microbiologic data, and cardiac imaging. This is summarized by the updated Modified Duke Criteria.
Work-up
Blood cultures
Blood cultures are collected on suspicion of IE and 48 hours after antimicrobial therapy has begun, repeated every 48 hours until bacteremia is cleared.
At least two sets should be obtained, 30-60 minutes spaced, but ≥3 is preferred to distinguish bacteremia from skin contamination.
Cardiac imaging
Transthoracic echocardiography (sn 75%, sp ~100%) is the first line diagnostic test. However, TEE has higher sensitivity. Additionally, cardiac CT may be considered.
Note, while specificity is very high, a negative echo does not exclude IE. In such cases where there is a high clinical suspicion for IE (eg. persistent bacteremia or fever with risk factors for IE), repeat TEEs should be undergone (after a week).
Dental care
For patients with IE due to common oral organisms, a dental evaluation is indicated to find the source of bacteremia.
Differential
Patients with bacteremia without evidence of valvular vegetation should be evaluated for alternative causes:
- Intravascular catheter infection
- Cardiac device infection
- Prosthetic joint infection
- Hematogenous osteomyelitis
- Septic thrombophlebitis
- Infected arterial aneurysm
Red Flags / Complications
IE is associated with severe complications due to septic embolization:
- Cardiac (valve regurgitation, heart failure, conduction abnormalities)
- Neurologic (embolic stroke, intracerebral hemorrhage, brain abscess)
- Septic emboli (infarction of organs, pulmonary emboli for right-sided)
- Metastatic infection (vertebral osteomyelitis, septic arthritis, splenic or psoas abscess)
- Systemic immune reaction (eg. glomerulonephritis)
Management
Management follows the following process:
- Prompt administration of antimicrobial therapy with diagnosis
- Assessment of need to remove infected implanted device, AV shunt, or graft
- Consideration for valve surgery
- Monitoring for resolution of bacteremia
Antimicrobial Therapy
Empiric therapy should be administered after ≥2 sets of blood cultures have been drawn. Treatment typically consist of 2-4 weeks of IV antibiotics.
A reasonable empiric regimen for suspected native valve endocarditis is:
- Vancomycin plus ceftriaxone
- Vancomycin plus ampicillin-sulbactam
- Replace ceftriaxone with cefepime or pip-tazo for Pseudomonas coverage
Monitoring for clearance of bacteremia is done every 48 hours with blood cultures. Antibiotic therapy should be guided with culture and sensitivity.
Further Treatment
In the context of catheter- or cardiac device-associated endocarditis, surgical removal/replacement may be necessary.
In patients with complicated IE (eg. IE-associated valve dysfunction), early valve surgery may be necessary. Right-sided valve surgery may be needed for large vegetations, recurrent septic pulmonary emboli, or persistent bacteremia.
Note, antithrombotic therapy is not indicated as evidence does not suggest they reduce risk of septic embolism.
Prophylaxis
For patients at risk of IE, prophylactic antibiotics may be indicated prior to dental work. Management is deferred to dentist.
References
Tools / Guidelines
2023 Duke-International Society for Infective Endocarditis