Armando Hasudungan
Biology and Medicine videos

Infective Endocarditis

by Armando HF and Emily Qian

Overview

Overview Infective endocarditis is a condition which occurs in the setting of bacteraemia whereby endothelial surfaces of the heart, such as valvular structures, become infected. It can present acutely or subacutely, and is often associated with fevers, new heart murmurs, constitutional symptoms and embolic phenomena. The classical organism associated is Staphylcoccus aureus, however there are many other organisms which can cause infective endocarditis. This is particularly dependent on the presence of native or prosthetic valves, history of intravenous drug use and recent cardiac surgery.

Definition
Infective endocarditis: A microbial process of the endocardium, usually involving the heart valves
Janeway lesions: Painless hemorrhagic macules on the palms and soles that are consistent with infectious endocarditis, thought to be caused by septic emboli, resulting in microabscesses
Osler Node: Painful, palpable, erythematous lesions most often involving the pads of the fingers and toes, they represent vasculitic lesions caused by immune complexes.
Roth spots: Hemorrhagic retinal lesions with white centers, due to infectious endocarditis, also thought to be an immune-complex–mediated vasculitis

Risk factors

  • Prosthetic heart valves
  • Previous infective endocarditis
  • Intravenous drug use
  • Congenital heart disease
  • Rheumatic heart disease
  • Cardiac transplant
  • Hypertrophic cardiomyopathy
  • Poor dentition
  • Haemodialysis
  • Diabetes mellitus

Signs and symptoms

Infective Endocarditis presents with non-specific signs and symptoms. Highly variable presentation—depends on intracardiac pathology, virulence of organism, and extracardiac involvement. Only a small proportion of people actually present with the risk factors mentioned above.

  • Fever (95% of cases)
  • Chills
  • Weakness
  • Weight loss
  • Murmurs (90% of patients with left-sided infective endocarditis)

Clinical Examination

  • Clubbing (subacute)
  • Regurgitant murmur (new onset or increased intensity)
  • Congestive cardiac failure signs
    • Raised JVP, bibasal crepitations, stony dull percussion, sacral oedema, peripheral oedema
  • Embolic phenomena
    • Petechiae, splinter haemorrhages (reddish brown lesions in nailbed)
    • Janeway lesions (painless 5mm diameter, erythematous pustular lesions over palms)
    • Focal neurology (in setting of CNS emboli)
    • Splenomegaly
    • Microscopic haematuria, flank pain (renal emboli)
  • Immune complex phenomena
    • Osler’s nodes (painful, raised reddish brown lesions on pulps of fingers)
    • Arthritis
    • Roth spots

Investigations

General

  • FBC
  • EUC
  • LFT
  • ABG
  • CRP/ESR
  • Blood culture x3 (different sites before antibiotics start!)
  • Chest X-ray
  • Urinalysis/ Urine MCS
  • ECG – Prolonged PR interval may indicate perivalvular abscess

Additional

  • Transthoracic echocardiogram (first line)
  • Transoesophageal echocardiogram (more sensitive)
  • CT brain
  • CT abdomen

Diagnostic criteria – Duke criteria for IE – Must meet 2 major criteria or 1 major and 3 minor criteria or 5 minor criteria.

Major criteria:

  • Positive blood culture for infective endocarditis (IE):
    • Typical micro-organism for IE from 2 separate blood cultures
    • Persistently positive blood cultures.
  • Evidence of endocardial involvement:
    • Oscillating intracardiac mass on valve/supporting structures, or in the path of regurgitant jet in the absence of an alternative anatomical explanation
    • Abscess
    • New partial dehiscence of prosthetic valve or new valvular regurgitation.

Minor criteria:

  • Predisposing heart condition or intravenous drug use
  • Fever over 38°C (>100.4°F)
  • Vascular phenomenon such as major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial haemorrhage, conjunctival haemorrhage, Janeway lesions
  • Immunological phenomenon:
    • Glomerulonephritis
    • Osler nodes
    • Roth spots
    • Rheumatoid factor
  • Microbiological evidence:
    • Positive blood cultures not meeting major criteria
  • Echocardiogram:

Consistent with IE but not meeting major criterion

Aetiology

Gram positive bacteria

  • Viridans group streptococci (most common dental/oral cause)
  • staphylococcus aureus – coag positive (most common cause of IE)
  • staphylococcus epidermidis – coag negative

Zoonosis (Coxiella burnetii – Q fever)

Enterococcus faecalis

Fungal

HACEK group (fastidious gram negative bacteria)

  • Culture negative Haemophilus species
  • Actinobacillus actinomycetemcomitans
  • Cardiobacterium hominis
  • Eikenella corrodens
  • Kingella species

Pathophysiology

Turbulent blood flow across valvular surfaces can lead to endothelial damage which acts as substrate for platelets and fibrin to adhere. In the setting of bacteraemia, these areas become colonised which perpetuate further deposition of fibrin and platelets. This ultimately leads to vegetation formation which can produce new heart murmurs from regurgitant valves. In addition, it can cause distal embolic phenomena.

  • Cardiac valves involved: Mitral valve > aortic valve > tricuspid valve > pulmonary valve (except for IVDU, in which case 50% of cases affect tricuspid valve)

Depending on patient risk factors, there are a number of organisms which can cause infective endocarditis (above). There are several clinical patterns which can help predict the organism associated:

  • Native valve involvement
    • Absent IVDU – Staphylcocci, Enterococci, Streptococci viridans group
    • With IVDU (often right sided involvement) – Staphylcocci, Streptococci, gram negative bacilli, polymicrobial infections
  • Prosthetic valve (greatest risk 3 months post-operatively)
    • Streptococcus, coagulase negative staphylcocci, Staphylcoccus aureus, Staphylcoccus epidermidis, Enterococci, gram negative bacilli

Pathology

Pathology Vegetation on heart valves are the classic hallmarks of infective endocarditis. The vegetations are friable, bulky, potentially destructive lesions containing fibrin, inflammatory cells, and bacteria or other organisms.

Management

Overview IV Antibiotics over 4-6 weeks with monitoring.

Empirical antibiotic treatment

  • Native valve endocarditis
    • Gentamicin
    • Benzylpenillcin
    • Flucloxacillin (IF MRSA suspected replace with Vancomycin)
  • Prosthetic valve/cardiac implantable electronic device
    • Gentamicin
    • Benzylpenillcin
    • Vancomycin

Targeted antibiotic therapy

  • Based on organism, sensitivities, valve involvement and complications
  • For Step Viridans
    • Benzylpenicllin
    • Gentamicin
Remember The three most common causes of IE worldwide are staphylococci, streptococci, and enterococci. s.aureus is now the most common cause of IE

Surgical management

  • Most commonly required for refractory congestive cardiac failure
  • Also indicated in valvular ring abscess, fungal causes, valvular perforation, ≥2 major emboli, antimicrobial failure, mycotic aneurysms, or staphylococcus infection of prosthetic valve

Prognosis

Greatest mortality in prosthetic valve infective endocarditis (25-50%)

Adverse prognostic factors include…

  • Congestive cardiac failure
  • Cardiac abscesses
  • Prosthetic vale infection
  • Embolic phenomena
  • Persistent bacteraemia
  • Altered mental status

References

UpToDate
BMJ
eTG