Infective Endocarditis

 

• Background

  Pathophysiology

  • Infection of the endocardium, usually a valve, most commonly the mitral or aortic. Can affect prosthetic or native valves. Usually follows transient bacteraemia and turbulent flow past valve.
  • Leads to formation of vegetations on valves, containing bacteria, fibrin and platelets.
  • Individuals with prosthetic or abnormal native valves are at high risk, but half the cases occur in those with normal valves.
  • Disease is often systemic, due to septicaemia, and multi-system, due to septic or sterile emboli and immune-complex deposition.

  Causes

  • Bacterial: Strep Viridians is commonest in those with valve disease (Sick Valves). Staph Aureus is commonest in IV drug users (Substance Abusers) and those with Artificial valves. Enterococci are another common cause.
  • Fungal: candida, aspergillus.
  • Non-infective: SLE, cancer.

  Classification

  • Acute IE (50% of cases): develops over days-weeks, usually seen in normal valves and due to Staph. aureus.
  • Subacute IE (aka subacute bacterial endocarditis, SBE): develops over weeks-months, usually seen in abnormal valves and due to Strep viridians.
  • The distinction between these two can be blurry.

• Signs and symptoms

  Key features: murmur (85%) + fever.

  Septic signs and symptoms:

  • Fever, rigors, and night sweats.
  • Malaise
  • Weight loss.
  • Splenomegaly
  • Clubbing, suggesting subacute IE as it takes time to develop.

  Emboli can cause infarcts and abscesses, most commonly affecting brain (stroke), lung, and spleen.

  Immune-complex deposition and vasculitis usually suggests subacute disease. Signs include:

  • Petechiae and splinter haemorrhages: commonest signs.
  • Janeway lesions: painless ('Jentle') plantar/palmar lesions.
  • Osler's nodes: painful ('Ouch') infarcts in distal phalanges of fingers/toes.
  • Roth spots: retinal haemorrhages with pale centre.
  • Glomerulonephritis.

  Sometimes presents with acute HF.

• Risk factors

  Increased turbulent flow:

  • Valve disease.
  • Prosthetic valves.
  • Structural disease: unrepaired PDA, VSD, HCM.
  • Rheumatic heart disease.

  Increased pathogen entry and bacteraemia:

  • IV drug use.
  • Haemodialysis
  • Dermatitis

  Chronic disease:

  • Diabetes
  • Kidney disease.

• Investigations

  Blood cultures:

  • 3 sets from different sites before starting antibiotics.
  • Within 6 hours if subacute, within 1h30 if acute.
  • 90% sensitive.

  Bloods:

  • FBC: normocytic anaemia.
  • ↑Neutrophils.
  • ↑ESR/CRP.
  • Rheumatoid factor may be +ve (due to IE itself or RA).

  Heart investigations:

  • Echo: transthoracic echo, then transoesophageal echo if -ve.
  • CXR: cardiomegaly.
  • ECG: ↑PR interval. Monitor this to decide whether surgery required.

  Urinalysis: microhaematuria.

  Duke criteria

  Diagnosis requires any 1 of:

  • 2 major.
  • 1 major plus 3 minor.
  • 5 minor.

  Major criteria:

  • +ve blood culture x2 or persistent.
  • +ve echo: vegetation, abscess, new regurgitation, or prosthetic valve dehiscence.

  Minor criteria:

  • RF +ve.
  • Fever
  • Vascular immune-complex signs.
  • +ve blood culture (x1).
  • +ve echo for other abnormality.

• Treatment and prevention

  Acute management

  Antibiotics as soon as blood cultures taken:

  • 4-6 weeks, including at least 2 weeks IV initially.
  • Empiric therapy and for streptococci: benzylpenicillin (or amoxicillin) + gentamicin.
  • Staph. aureus: flucloxacillin if native valve, add rifampicin and gentamicin if prosthetic valve.

  Surgery:

  • Debridement, repair, or replacement required in 20%.
  • Indications: refractory HF, persistent sepsis or emboli, or fungal IE.

  Prevention

  Prophylactic antibiotics for high-risk dental procedures in patients at risk of IE (e.g. prosthetic valves) is controversial: European and American guidelines recommend it, but NICE do not.