Infective Endocarditis
A serious bacterial infection of the heart valves that can destroy the valve and spread infected clots throughout the body.
- Sudden onset focal neurologic deficit (stroke from septic embolus).
- New heart block on ECG (suspect paravalvular abscess).
Emergency Management: Acute cardiogenic shock from acute severe aortic/mitral regurgitation. Requires emergent cardiac surgery.
Infective Endocarditis (IE) is a life-threatening infection of the endocardial surface of the heart, most commonly affecting the cardiac valves, characterized by the formation of infected vegetations composed of platelets, fibrin, microorganisms, and inflammatory cells.
Detailed Overview
IE requires a confluence of endothelial damage (which forms a sterile platelet-fibrin thrombus) and transient bacteremia (which seeds the thrombus). Left-sided valves (mitral and aortic) are most commonly affected, except in IV drug users where the tricuspid valve is highly involved. The disease presents systemically with fever and bacteremia, and locally with valve destruction, heart failure, and embolic phenomena. Prompt diagnosis via blood cultures and echocardiography, followed by prolonged bactericidal IV antibiotics, is critical.
Epidemiology & Demographics
Incidence of 3-10 per 100,000. Male to female ratio is 2:1. Increasing incidence in healthcare-associated cases and IV drug users.
Etiological Mechanism
Primarily bacterial. Staphylococcus aureus is the most common overall (30-40%), followed by Viridans group streptococci, Enterococci, and the HACEK group.
Primary Causes
Bacterial seeding of damaged endocardium
- Intravenous drug use: High risk for right-sided (tricuspid) S. aureus IE.
- Prosthetic heart valves: Highest risk group, particularly in the first year post-surgery.
- Prior history of IE: Altered valve anatomy predisposes to recurrence.
- Structural heart disease: Unrepaired cyanotic congenital heart disease or rheumatic heart disease.
Endothelial injury (from turbulent blood flow, catheters, or electrodes) exposes subendothelial collagen, causing deposition of a sterile platelet-fibrin thrombus (Non-Bacterial Thrombotic Endocarditis). Transient bacteremia (from dental procedures, IV drug use, or GI/GU mucosal trauma) allows bacteria to adhere to this thrombus. The bacteria proliferate inside the vegetation, protected from host immune cells. The infection destroys the valve leaflet leading to acute regurgitation and heart failure. Fragments of the vegetation can embolize systemically to the brain, spleen, kidneys, or lungs (if right-sided).
Characteristic Clinical Presentation
- Fever and Chills: Present in >90% of cases, often low-grade in subacute, high and spiking in acute.
- Malaise and Fatigue: Non-specific systemic symptoms.
- Dyspnea: Secondary to acute congestive heart failure from valve destruction.
Physical Examination Signs
- New or changing heart murmur (usually regurgitant).
- Osler nodes (painful, raised nodules on finger/toe pads - immune complex mediated).
- Janeway lesions (painless, erythematous macules on palms/soles - septic microemboli).
- Roth spots (retinal hemorrhages with pale centers).
- Splinter hemorrhages under the nail beds.
- Congestive Heart Failure: Most common cause of death, due to acute severe valvular regurgitation.
- Embolic Stroke: Septic emboli to the middle cerebral artery territory.
- Paravalvular Abscess: Infection extends into the myocardium, causing AV block (suggested by new prolonged PR interval).
Diagnostic Criteria & Guidelines
Modified Duke Criteria. Requires 2 Major OR 1 Major + 3 Minor OR 5 Minor criteria. Major: 2 positive blood cultures with typical organisms, evidence of endocardial involvement on Echo (vegetation, abscess, new regurgitation).
Differential Diagnosis
- Rheumatic Fever
- Systemic Lupus Erythematosus (Libman-Sacks endocarditis)
- Meningitis
- Occult malignancy
Laboratory Tests & Biomarkers
- Blood Cultures: 3 sets drawn from different venipuncture sites before antibiotics; consistently positive.
- ESR and CRP: Markedly elevated.
- Urinalysis: Microscopic hematuria or RBC casts (glomerulonephritis).
Imaging Modalities & Findings
- Transesophageal Echocardiogram (TEE):
- Transthoracic Echocardiogram (TTE):
-
Acute IE
Rapidly progressive, highly destructive, toxic presentation. Often S. aureus on normal valves.
-
Subacute IE
Indolent course over weeks/months. Often Viridans streptococci on previously damaged valves.
Empiric IV antibiotics covering MRSA, Streptococci, and Enterococci: Vancomycin 15-20 mg/kg IV q8-12h PLUS Ceftriaxone 2g IV daily. Tailor to culture results. Treat for 4-6 weeks.
Second-Line & Adjunctive Therapy
Targeted therapy: For MSSA, Nafcillin 2g IV q4h for 6 weeks. For Viridans Strep, Penicillin G 12-18 million units/day IV for 4 weeks.
Surgical & Procedural Management
Early valve replacement surgery indicated for: Heart failure, left-sided S. aureus, paravalvular abscess, fungal IE, or large vegetations (>10mm) with prior embolization.
Recommended Lifestyle Changes
- Strict dental hygiene (frequent brushing, flossing, and professional cleanings).
Patient Counseling & Advice
Explain the need for prolonged IV antibiotics, often via a PICC line at home. Emphasize importance of declaring their history of IE to all future dentists/doctors for prophylaxis.
Follow-Up & Monitoring Schedule
Repeat blood cultures every 48-72h until negative. Weekly inflammatory markers and renal function while on antibiotics. Repeat Echo before discharge to establish a new baseline.
Preventive Strategies
Antibiotic prophylaxis (Amoxicillin 2g PO 1 hour before procedure) for dental procedures ONLY in high-risk patients (prosthetic valves, prior IE, unrepaired cyanotic congenital heart disease).
In-hospital mortality is 15-20%. S. aureus and prosthetic valve endocarditis have the highest mortality rates.
Frequently Asked Questions
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