Infective Endocarditis: Causes, Diagnosis, and Management

Infective Endocarditis: Causes, Diagnosis, and Management

Infective Endocarditis (IE) is a life-threatening infection of the heart’s endocardium, most commonly affecting heart valves. It can lead to valvular destruction, heart failure, embolic events, and multi-organ complications. Early recognition and treatment are crucial to reduce morbidity and mortality.


2. Classification of Infective Endocarditis

Type Description
Acute IE Rapid onset, highly virulent organisms (e.g., Staphylococcus aureus), aggressive progression
Subacute IE Indolent course, less virulent organisms (e.g., Streptococcus viridans), occurs on pre-existing valve disease
Native Valve Endocarditis (NVE) Infection on natural heart valves
Prosthetic Valve Endocarditis (PVE) Infection on prosthetic heart valves (early: <1 year post-surgery, late: >1 year post-surgery)
Intravenous Drug Use (IVDU) Endocarditis Commonly affects the tricuspid valve, caused by Staphylococcus aureus

3. Risk Factors

Category Risk Factors
Structural Heart Disease Rheumatic heart disease, bicuspid aortic valve, mitral valve prolapse
Prosthetic Material Prosthetic valves, indwelling cardiac devices (pacemakers, ICDs)
IV Drug Use Staphylococcus aureus is the most common causative organism
Immunosuppression HIV, chemotherapy, long-term corticosteroids
Recent Procedures Dental procedures, hemodialysis, intravascular catheters

4. Pathophysiology

  1. Endothelial Injury → Turbulent blood flow (e.g., valvular disease) damages the endocardium.
  2. Platelet & Fibrin Deposition → Forms a non-bacterial thrombotic endocarditis (NBTE).
  3. Bacteremia → Organisms adhere to the thrombus, leading to vegetation formation.
  4. Embolization & Systemic Effects → Fragments of vegetation break off, causing stroke, infarcts, or septic emboli.

5. Clinical Features

(A) General Symptoms

Symptoms Findings
Fever & Malaise Most common symptom (present in ~90%)
Night Sweats & Weight Loss Seen in subacute IE
New or Changing Murmur Indicates valvular involvement

(B) Classic Signs of Infective Endocarditis

Sign Description
Osler’s Nodes Painful, red nodules on fingertips/toes (immune complex deposition)
Janeway Lesions Non-tender macules on palms/soles (microemboli)
Splinter Hemorrhages Linear hemorrhages under fingernails
Roth Spots Retinal hemorrhages with pale centers
Clubbing Chronic IE cases
Splenomegaly More common in subacute IE

(C) Embolic & Systemic Manifestations

Complication Affected Organ Presentation
Stroke Brain Focal neurological deficits
Renal Infarct Kidneys Hematuria, flank pain
Septic Pulmonary Emboli Lungs (IVDU-associated IE) Respiratory symptoms, cavitary lesions on CXR
Mycotic Aneurysm Blood vessels Risk of rupture and hemorrhage
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6. Diagnosis of Infective Endocarditis

(A) Duke Criteria for IE Diagnosis

IE is diagnosed using the Modified Duke Criteria, which include major and minor criteria.

Major Criteria

  1. Positive Blood Cultures
    • Staphylococcus aureus, Streptococcus viridans, Enterococcus (typical IE pathogens)
    • Persistent bacteremia (≥2 positive blood cultures >12 hours apart)
  2. Endocardial Involvement (Echocardiography)
    • Vegetation, abscess, or new dehiscence of prosthetic valve on transesophageal echocardiography (TEE)

Minor Criteria

  1. Predisposing Risk Factor (e.g., prosthetic valve, IVDU, heart disease)
  2. Fever >38°C
  3. Vascular Phenomena (e.g., Janeway lesions, embolic events)
  4. Immunologic Phenomena (e.g., Osler’s nodes, Roth spots)
  5. Microbiological Evidence (e.g., positive culture not meeting major criteria)

Definitive IE = 2 Major or 1 Major + 3 Minor or 5 Minor
Possible IE = 1 Major + 1 Minor or 3 Minor

(B) Laboratory & Imaging Workup

Investigation Findings
Blood Cultures (3 sets before antibiotics) Bacteremia
Full Blood Count (FBC) Leukocytosis, anemia
Inflammatory Markers ↑ ESR, CRP
Transesophageal Echocardiogram (TEE) Gold standard for detecting vegetations
ECG May show conduction abnormalities (suggests abscess)
CT/MRI To assess embolic complications

7. Management of Infective Endocarditis

(A) Empirical Antibiotic Therapy (Before Culture Results)

Suspected Organism First-Line Empirical Therapy
Native Valve (NVE) IV Vancomycin + IV Gentamicin
Prosthetic Valve (PVE) IV Vancomycin + IV Gentamicin + IV Rifampicin
IV Drug User (Tricuspid IE) IV Vancomycin

(B) Targeted Antibiotic Therapy (After Culture Results)

Causative Organism Antibiotic Regimen Duration
Staphylococcus aureus IV Flucloxacillin (MSSA) / IV Vancomycin (MRSA) 4–6 weeks
Streptococcus viridans IV Benzylpenicillin ± Gentamicin 4 weeks
Enterococcus spp. IV Ampicillin + Gentamicin 4–6 weeks
HACEK Group IV Ceftriaxone 4 weeks

🚨 Prosthetic Valve IE requires ≥6 weeks of therapy
🚨 IV to oral switch is NOT recommended

(C) Indications for Surgery

Indication Rationale
Severe Valve Dysfunction Refractory heart failure
Large Vegetations (>10 mm) High embolic risk
Persistent Infection Positive blood cultures despite antibiotics
Prosthetic Valve Endocarditis Higher risk of complications
Abscess Formation Conduction abnormalities (AV block on ECG)

8. Prevention of Infective Endocarditis

(A) Who Needs Prophylaxis?

High-Risk Group Examples
Prosthetic Valves Mechanical or bioprosthetic valves
Previous Infective Endocarditis History of IE
Congenital Heart Disease Unrepaired cyanotic defects, repaired defects with prosthetics
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(B) Antibiotic Prophylaxis for High-Risk Procedures

Procedure Prophylactic Antibiotic
Dental (gingival manipulation) Amoxicillin 2g PO (or Clindamycin 600mg if allergic)
Respiratory (bronchoscopy with biopsy) Amoxicillin 2g IV
GI/GU Procedures Not routinely recommended

9. Key Takeaways

Fever + new murmur = Suspect IE!
Duke Criteria guide diagnosis (TEE is the gold standard for vegetations).
Blood cultures BEFORE antibiotics!
Long-term IV antibiotics are required (4–6 weeks).
Surgery indicated for severe valve damage, large vegetations, or abscesses.

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