• Clinical science

Infective endocarditis

Summary

Infective endocarditis (IE) is an infectious inflammation of the endocardium that affects the heart valves. The condition is a result of bacteremia, which is most commonly caused by dental procedures, surgery, distant primary infections, and nonsterile injections. IE clinically presents with either an acute or subacute course. Acute disease is usually caused by Staphylococcus aureus and causes rapid endocardium destruction. Subacute progression is most commonly caused by viridans streptococci species and generally affects individuals with pre-existing damage to the heart valves, structural heart defects, or the presence of prosthetic valves. Unlike acute disease, in which patients develop symptoms over a period of hours to days, subacute disease is associated with a progression of symptoms over weeks to months. Clinical features include constitutional symptoms (fatigue, fever/chills, malaise) in combination with signs of pathological cardiac changes (e.g., new or changed heart murmur, heart failure signs) and possibly manifestations of subsequent damage to other organs (e.g., glomerulonephritis, septic embolic stroke). Diagnosis is made based on the Duke criteria, whose main features include positive blood cultures and evidence of endocardial involvement in echocardiography. Initial treatment of IE consists of empiric IV antibiotic therapy, which is then adapted to blood culture results and continued for four to six weeks. Prophylaxis is only administered in specific circumstances, e.g., in patients with preexisting heart conditions undergoing dental or surgical procedures. If left untreated, infective endocarditis can be fatal within a few weeks.

Etiology

Pathogens

Main pathogens Characteristics

Staphylococcus aureus (45–65%)

  • Most common cause of acute IE for all groups (including IV drug users and patients with prosthetic valves or pacemakers/ICDs)
  • Affects previously healthy valves
  • Usually fatal within 6 weeks (if left untreated)

Viridans streptococci (30%): S. sanguinis, S. mutans, S. mitis

Staphylococcus epidermidis

Enterococci, especially Enterococcus faecalis (< 10%)

Streptococcus gallolyticus (S. bovis)

Gram-negative HACEK group (Haemophilus species, Aggregatibacter actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae)

  • Physiological oral pharyngeal flora (∼ 3% of cases of IE)
  • In patients with poor dental hygiene and/or periodontal infection

Candida species

Aspergillus fumigatus

  • Causes IE in immunosuppressed patients
  • Causes IE in IV drug abusers
  • Cause of IE after cardiosurgical interventions

Coxiella burnetii

Bartonella species

  • Gram-negative pathogens responsible for culture-negative endocarditis

HEAving your KING-size bed from IKEa into your CAR AGGREGATes joy: native valve endocarditis is caused by haemophilus, kingella, eikenella, cardiobacterium, and aggregatibacter.

Risk factors

References:[3][4][5][6][1][7][8][9][10][11][12][13][14][2]

Pathophysiology

Don't tri drugs for the sake of your tricuspid valves.

References:[15][16][7][17]

Clinical features

Course of disease

Acute bacterial endocarditis Subacute bacterial endocarditis Prosthetic valve endocarditis
Course
  • Acute onset
  • Rapid, fulminant progression (days to weeks)
  • More severe constitutional symptoms (e.g., high fever)
  • Insidious onset
  • Slow progression (weeks to months)
  • Less severe constitutional symptoms (e.g., low fever possible, often absent)
  • Early-onset: < 60 days after surgery
  • Late-onset: ≥ 60 days after surgery
Main pathogens
  • Most common: S. aureus (associated with large vegetations that can destroy the valves)
  • Others: group A hemolytic streptococci, S.pneumoniae, N.gonorrhoeae
Affected valves
  • Native healthy valves
  • Native previously injured or congenitally defect valves

Constitutional symptoms

Cardiac manifestations

Extracardiac manifestations

Infective endocarditis should always be considered as a cause of fever of unknown origin (FUO), especially if a new heart murmur develops!

FROM JANE - Fever, Roth spots, Osler nodes (Ouch = painful), Murmur, Janeway lesions, Anemia, Nail bed hemorrhage, Emboli

References:[16][1][7][18][19][20][21][22][23][24][2]

Diagnostics

Laboratory studies

Echocardiography

  • Detects valve vegetations; , new valvular regurgitation, abscess, dehiscence of prosthetic valve
  • Transthoracic echocardiography (TTE) usually performed first (sensitivity: ∼ 75%)
  • Transesophageal echocardiography (TEE) to confirm findings; higher sensitivity (> 90%) than TTE

(Modified) Duke criteria

  • The Duke criteria help to diagnose infective endocarditis. To confirm the diagnosis, one of the following requirements must be met:
    • Two major criteria
    • One major and three minor criteria
    • Five minor criteria
  • Major diagnostic criteria
    • Two separate blood cultures positive for typical pathogens (see “Etiology” above)
    • Evidence of endocardial involvement in echocardiography
      • Valve vegetation or abscess or new dehiscence of artificial valves
      • A new valvular regurgitation (worsening of a pre-existing murmur is not sufficient)
  • Minor diagnostic criteria
    1. Predisposition: underlying heart disease or IV drug abuse
    2. Fever ≥ 38°C (100.4F)
    3. Vascular abnormalities
    4. Immunologic disorder
    5. Microbiology

Only negative findings on transesophageal echocardiography (TEE) can reliably rule out endocarditis, as transthoracic echocardiography (TTE) is not sensitive enough! References:[15][16][7][20][25]

Pathology

Pathogenesis

  • Acute disease (leading to valve insufficiency, septic embolic infarcts, tendinous cord rupture)
    1. Erosionfibrin deposits on valves
    2. Ulceration
    3. Perforation → adaptation of valve edges not possible
  • Chronic disease (leading to valve insufficiency and valve stenosis)
    1. Erosion → reorganization of fibrin layer
    2. Granulation tissue → valve scarring/fibrosis
    3. Calcification → thickened and/or shortened tendinous cords


References:[7]

Differential diagnoses

Noninfective endocarditis (nonbacterial thrombotic endocarditis)

Prosthetic valve thrombosis

References:[26][27]

The differential diagnoses listed here are not exhaustive.

Treatment

Empirical therapy

Condition/patient group Antibiotic therapy

Native valves

Prosthetic valves

IV drug users

Indications for surgery: congestive heart failure, uncontrolled infection, systemic embolization, prosthetic valve, fungal endocarditis

If infective endocarditis is suspected: 1. Obtain blood cultures → 2. Start empiric antibiotic therapy → 3. adapt the therapy according to culture results.

Targeted therapy

HACEK organisms

References:[16][7][17][28][29][30][31]

Prevention

Endocarditis prophylaxis:

References:[15][32][33]