Cardiology > Infective endocarditis (IE)  

Background 

Infective endocarditis (IE) is a microbial infection of the endocardial surface of the heart, typically involving the heart valves. It results in vegetation formation—comprising fibrin, platelets, microorganisms, and inflammatory cells—which can cause valvular destruction, systemic embolization, and immunologic phenomena. IE can be acute or subacute, with varied presentations depending on the causative organism and host factors. 

II) Classification/Types 

By Clinical Course: 

• • Acute IE: Rapid onset with high fever and rapid valvular destruction; commonly due to Staphylococcus aureus 

• • Subacute IE: Insidious onset with milder symptoms; often caused by viridans streptococci 

By Valve Type: 

• • Native Valve Endocarditis (NVE): Affects normal or previously diseased native valves 

• • Prosthetic Valve Endocarditis (PVE): Early (<60 days) or late (>60 days) post-valve replacement 

• • Device-related IE: Involving pacemakers, defibrillators, or central venous catheters 

By Etiologic Agent: 

• • Bacterial (most common): Staph aureus, Strep viridans, Enterococci 

• • Fungal: Candida, Aspergillus (more common in immunocompromised or IV drug users) 

Pathophysiology 

IE begins with endothelial damage due to turbulence or trauma. This promotes thrombus formation, creating a nidus for bacterial adhesion during transient bacteremia. Microbial colonization leads to vegetation formation, valvular destruction, and systemic embolization. Septic emboli may affect the brain, spleen, kidneys, and lungs. Immune complex deposition can cause glomerulonephritis or Osler nodes. 

Epidemiology 

• • Incidence: 3–10 per 100,000 person-years 

• • More common in older adults, IV drug users, and patients with prosthetic valves or cardiac devices 

• • Increasingly healthcare-associated 

• • Staph aureus is now the leading cause, especially in developed countries 

Etiology 

I) Causes 

• • Staphylococcus aureus (acute, common in healthcare and IV drug users) 

• • Viridans streptococci (dental origin, subacute) 

• • Enterococci (genitourinary or gastrointestinal procedures) 

• • Coagulase-negative staphylococci (prosthetic valve IE) 

• • Fungi (immunosuppressed hosts) 

II) Risk Factors 

• • Pre-existing valvular heart disease 

• • Prosthetic heart valves or devices 

• • Intravenous drug use (IVDU) 

• • Recent dental or surgical procedures 

• • Immunosuppression 

• • Poor dental hygiene 

Clinical Presentation 

I) History (Symptoms) 

• • Fever, chills, night sweats 

• • Fatigue, malaise 

• • Weight loss 

• • Dyspnea or chest pain 

• • Symptoms of embolic events (stroke, hematuria, flank pain) 

• • Back pain (vertebral osteomyelitis) 

II) Physical Exam (Signs) 

• • New or changing heart murmur 

• • Petechiae (palate, conjunctivae, extremities) 

• • Splinter hemorrhages (nails) 

• • Janeway lesions (painless, on palms/soles) 

• • Osler nodes (tender, on fingers/toes) 

• • Roth spots (retinal hemorrhages) 

• • Signs of heart failure in advanced cases 

Differential Diagnosis (DDx) 

• • Rheumatic heart disease 

• • Nonbacterial thrombotic endocarditis (NBTE) 

• • Systemic lupus erythematosus (Libman-Sacks endocarditis) 

• • Acute rheumatic fever 

• • Vasculitis 

• • Malignancy-associated fever 

Diagnostic Tests 

Initial Work-Up 

• • Blood cultures (3 sets from different sites before antibiotics) 

• • CBC: Anemia of chronic disease, leukocytosis 

• • ESR/CRP: Elevated 

• • Echocardiography: 

• • Transthoracic (TTE): First-line 

• • Transesophageal (TEE): Higher sensitivity, especially in prosthetic valves 

• • Urinalysis: Hematuria, RBC casts 

• • ECG: May show conduction abnormalities (if abscess extends to septum) 

Modified Duke Criteria (2023 AHA/ESC Update) 

Major Criteria: 

• • Positive blood cultures (typical organisms, persistent) 

• • Evidence of endocardial involvement on echo (vegetation, abscess, new dehiscence of prosthetic valve) 

Minor Criteria: 

• • Predisposing condition (e.g., valve disease, IVDU) 

• • Fever ≥38°C 

• • Vascular phenomena (Janeway lesions, emboli) 

• • Immunologic phenomena (Osler nodes, glomerulonephritis) 

• • Positive blood cultures not meeting major criteria 

Diagnosis: 

• • Definite IE: 2 major OR 1 major + 3 minor OR 5 minor criteria 

• • Possible IE: 1 major + 1 minor OR 3 minor criteria 

Treatment 

I) Initial Approach 

• • Empirical IV antibiotics after blood cultures 

• • Adjust antibiotics based on culture/sensitivity 

• • Monitor for embolic complications 

• • Valve surgery if complications arise 

II) Medications 

Patient Education, Screening, Vaccines 

Education 

• • Importance of completing antibiotic therapy (often 4–6 weeks IV) 

• • Notify providers of history of IE before invasive procedures 

• • Monitor for signs of embolic events or heart failure 

Screening/Prevention 

• • Dental hygiene maintenance 

• • Antibiotic prophylaxis in high-risk patients before dental procedures 

• • Prosthetic heart valves 

• • Prior history of IE 

• • Certain congenital heart diseases 

Vaccinations 

• • Influenza and pneumococcal to reduce secondary infections 

• • COVID-19 vaccine as per guidelines 

Consults/Referrals 

• • Infectious Disease: For antibiotic management and duration 

• • Cardiology/Cardiothoracic Surgery: If valve damage, abscess, or CHF 

• • Neurology: If embolic stroke 

• • Nephrology: For glomerulonephritis or renal impairment 

Follow-Up 

Short-Term 

• • Monitor response to antibiotics (fever curve, labs, blood cultures) 

• • Repeat echocardiography if no improvement or new symptoms 

• • Monitor for antibiotic toxicity (renal, auditory, cytopenias) 

Long-Term 

• • Serial echocardiography for valve function 

• • Evaluate for surgical valve replacement if indicated 

• • Educate on recurrence prevention 

• • Long-term suppressive therapy in select high-risk patients 

Prognosis 

• • Prognosis depends on causative organism, host factors, and timing of intervention 

• • Early treatment improves outcomes 

• • Complications if untreated or delayed: 

• • • Heart failure 

• • • Embolic stroke 

• • • Valve destruction 

• • • Death