Harvey's Garden

Infective endocarditis

4 min read

Etiology

  • Infection of the endocardium, most commonly affecting heart valves.
  • Pathogenesis: Endothelial damage → sterile platelet-fibrin thrombus (nonbacterial thrombotic endocarditis) → transient bacteremia seeds the thrombus → vegetation formation.

Pathogens

  • ** S. aureus **: Most common cause overall, especially in IV drug users (IVDU), healthcare-associated infections, and acute, aggressive presentations.
  • ** Viridans group streptococci ** (S. sanguinis): Associated with poor dentition and recent dental procedures; typically causes subacute IE on previously damaged valves.
  • ** S. bovis (S. gallolyticus) **: Strongly associated with colon cancer; a workup for colonic malignancy is required if isolated.
  • Enterococci (E. faecalis): Common after GU/GI procedures and in nosocomial settings.
  • Coagulase-negative staphylococci (S. epidermidis): Associated with prosthetic valves, especially within the first year of placement.
  • HACEK organisms: Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella. Part of normal oral flora, associated with culture-negative endocarditis.
  • Fungi (Candida, Aspergillus): Seen in immunocompromised patients, IVDU, and after prolonged antibiotic therapy.

Risk factors for infective endocarditis

  • Cardiac conditions
  • Noncardiac risk factors
    • Poor dental status
    • Dental procedures
    • Nonsterile venous injections (e.g., in IV drug use)
    • Intravascular devices
    • Surgery

Pathophysiology

  • Pathogenesis
    1. Damaged valvular endothelium → exposure of the subendothelial layer → adherence of platelets and fibrin → sterile vegetation (microthrombus)
    2. Localized infection or contamination → bacteremia → bacterial colonization of vegetation → formation of fibrin clots encasing the vegetation → valve destruction with loss of function (valve regurgitation)
  • Clinical consequences
    • Bacterial vegetation → bacterial thromboemboli → vessel occlusion → infarctions
    • Emboli can lead to metastatic infections of other organs.

Classifications

Coagulase-negative staphylococci (CoNS): Staphylococcus epidermidis, Staphylococcus saprophyticus

Clinical features

Cardiac manifestations

  • Development of a new heart murmur or change in a preexisting murmur
    • Tricuspid valve regurgitation
      • Holosystolic murmur that is loudest at the left sternal border
      • Seen in persons who inject drugs, immunocompromised individuals, patients with congenital heart disease, and patients with instrumentation in the right heart (e.g., central venous catheters)
    • Aortic valve regurgitation: early diastolic murmur that is loudest at the left 3rd and 4thintercostal spaces and along the left sternal border
    • Mitral valve regurgitation: holosystolic murmur that is loudest at the heart’s apex and radiates to the left axilla

Extracardiac manifestations of IE

  • Pulmonary manifestations: caused by septic emboli resulting from tricuspid valve involvement
    • Signs of pulmonary embolism (e.g., dyspnea)
    • Signs of pulmonary infection, e.g., multifocal pneumonia, lung abscess, and/or empyema.

Diagnostics

vs rheumatic fever

Treatment

  1. Hemodynamic Stabilization: ABCs, manage acute HF if present.
  2. Empiric Abx (After 3 sets of blood cx):
    • Native valve: IV Vancomycin (covers MRSA) + Ceftriaxone (covers HACEK/Strep).
    • Prosthetic valve: IV Vancomycin + Gentamicin + Cefepime/Carbapenem (add Rifampin later once organism known/staph confirmed).
  3. Targeted Abx (Based on Cx/Sensitivities, usually 4-6 weeks IV):
    • MSSA: Nafcillin or Oxacillin.
    • MRSA: Vancomycin.
    • Viridans Strep: Penicillin G or Ceftriaxone.
  4. Surgical Valve Replacement (Indications for early surgery):
    • Severe heart failure (refractory). c
    • Cardiogenic shock / Hemodynamic instability.
    • Perivalvular abscess / New heart block.
    • Persistent bacteremia > 7 days despite appropriate IV Abx.
    • Fungal or highly resistant organisms.
    • Recurrent emboli.
  5. Prophylaxis (for future procedures):
    • Who: ONLY highest risk (prosthetic valve, prior IE, unrepaired cyanotic CHD, repaired CHD w/ residual defect, cardiac transplant w/ abnormal valve).
    • When: ONLY high-risk procedures (dental work w/ gingival manipulation, resp tract incisions, infected skin/MSK procedures). Not for routine GI/GU procedures.
    • What: Amoxicillin PO (or Ampicillin/Ceftriaxone IV). Clindamycin/Azithromycin if PCN allergic.

Complications

Perivalvular abscess

  • Epidemiology & Risk Factors
    • High-risk complication of Infective Endocarditis (IE); occurs in ~30-40% of cases.
    • Prosthetic valves (PVE) > Native valves (NVE).
    • Location: Aortic valve (most common) > Mitral valve.
  • Clinical Features
    • Persistent fever/bacteremia despite appropriate IV Abx therapy.
    • New-onset conduction abnormality: Pathognomonic for extension of infection into the septum/conduction system. c
    • Symptoms of worsening Heart Failure (HF): Dyspnea, orthopnea, pulmonary edema.
    • New or changing heart murmur (e.g., new AR murmur in aortic root abscess).
  • Diagnosis
    • Initial Step: EKG. Look for new 1st-degree AV block, bundle branch block, or complete heart block.
    • Confirmatory/Best Imaging: Transesophageal Echocardiogram (TEE).
      • Sensitivity for abscess: TEE (>90%) vs. TTE (<40%).
      • Necessary to visualize perivalvular extension, vegetations, or fistula.
    • Blood Cultures: Persistently (+) despite therapy.
  • Differential Diagnostics
    • Uncomplicated IE: Fever/murmur but no conduction delay; responds to Abx.
    • Acute Rheumatic Fever: Post-strep, Jones criteria, usually younger pts, migratory polyarthritis.
    • Myocarditis: Viral prodrome, diffuse ST changes, elevated troponin, global LV dysfunction.
    • Aortic Dissection: Sudden tearing chest pain, asymmetric BPs, widened mediastinum on CXR.
  • Management
    1. Surgical Intervention (Essential): Indicated for almost all perivalvular abscesses (debridement + valve replacement).
    2. Medical Therapy: High-dose IV Abx (tailored to culture/sensitivities) for 6+ weeks.
    3. Supportive: Stabilization of hemodynamics, management of HF symptoms (diuretics).

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