Infective endocarditis

• Infective endocarditis refers to infection of the endothelium (the inner surface) of the heart. Most commonly, it affects the heart valves. It can be acute, subacute or chronic, depending on how rapidly and acutely the symptoms present and the causative organism.
• Risk Factors

  • Intravenous drug use
  • Poor dentition
  • Structural heart pathology - including artificial valves
  • Chronic kidney disease (particularly on dialysis)
  • Immunocompromised
  • History of infective endocarditis
• The most common cause of infective endocarditis is Staphylococcus aureus.
• Presentation

  The presenting symptoms are non-specific for an infection:

  • Fever
  • Fatigue
  • Night sweats
  • Muscle aches
  • Anorexia
• The key examination findings are:

  • New or “changing” heart murmur
  • Splinter haemorrhages
  • Petechiae
  • Janeway lesions
  • Osler’s nodes
  • Splenomegaly (in longstanding disease)
  • Finger clubbing (in longstanding disease)
  • Bi-basal lung crepitations - heart failure in severe cases
• A fever with a new heart murmur is infective endocarditis until proven otherwise
• The modified Duke criteria is used for diagnosis of infective endocarditis:

  • 1 major + 3 minor criteria or
  • 5 minor criteria
• Blood cultures need to be taken before the start of antibiotics

  3 samples are needed, 6 hours apart from different sites
• Echocardiography is the usual imaging investigation. Vegetations (an abnormal mass or collection) may be seen on the valves.
• Management of infective endocarditis:

  • IV broad spectrum antibiotics - amoxicillin
  • 4 weeks or 6 if prosthetic valve
  • Surgery may be needed
• Infective endocarditis has a high mortality rate. Key complications include:

  • Heart valve damage, causing regurgitation
  • Heart failure
  • Infective and non-infective emboli
  • renal impairment
• Depending on the valve affected, endocarditis may be classified as left-sided (mitral/aortic valve) or right-sided (tricuspid/pulmonary valve). Most cases involve the left side; only 5-10% are right-sided.
• Infective endocarditis arises from three key factors occurring simultaneously:

  1. Transient bacteraemia
  2. Damage to valvular tissue
  3. Formation of vegetations
• Causative organisms:

  • Most common - Staphylococci e.g. staphylococcus aureus is particularly linked with prosthetic valves, acute endocarditis and IV drug use
  • Streptococci
  • HACEK organisms
  • Non- HACEK organisms
  • Candida
  • Aspergillus
• HACEK organisms:

  • Haemophilus
  • Aggregatibacter actinomycetemcomitans
  • Cardibacterium
  • Eikenella corrodens
  • Kingella kingae
• Non-HACEK organisms:

  • Pseudomonas aeruginosa
  • Neisseria elongata
• Blood culture negative IE:

  • In a significant proportion of cases no organism is identified from standard blood culture methods
  • Can be due to patient receiving antibiotics before blood cultures are taken
  • Serology is needed
  • HACEK organisms
  • Coxiella burnetti
  • Chlamydia
  • Legionella
• Intrinsic risk factors include:

  • Valvular stenosis or regurgitation: congenital or acquired
  • Hypertrophic cardiomyopathy
  • Structural heart disease with turbulent flow (e.g. VSD, PDA): but NOT isolated ASD or fully repaired VSD or PDA
  • Prosthetic heart valves: these will require replacement if infected
  • Previous infection (infective endocarditis/rheumatic fever) causing structural damage
• Extrinsic risk factors include: 

  • Intravenous drug use (right-sided endocarditis)
  • Invasive vascular procedures (e.g. central lines)
  • Poor oral hygiene/dental infections
• Relevant bedside investigations include:

  • Basic observations (vital signs): signs of infection (fever, tachycardia).
  • 12-lead ECG: to exclude first degree AV block. This may be seen in aortic root abscesses, which are a rare complication of infective endocarditis.
  • Urine dipstick: microscopic haematuria.
• The European Society of Cardiology (ESC) recommends that three sets of blood cultures (i.e. six bottles in total) be taken, at least 30 mins apart, from three separate peripheral sites. A minimum of 10 ml of blood per bottle should be collected.
• Other relevant laboratory investigations include:

  • Full blood count: to exclude anaemia (↓Hb) and check white cell count (WCC) to track the progress of the infection and response to treatment.
  • CRP/ESR: inflammatory markers, used together with WCC (CRP more so). CRP may lag slightly behind WCC.
  • Urea & electrolytes: baseline renal function and creatinine clearance is required if starting on nephrotoxic antibiotics such as gentamicin.
• Transthoracic echocardiogram is the first-line imaging investigation in endocarditis and should be performed as soon the diagnosis of endocarditis is suspected. Note that not all vegetations are picked up on echocardiogram.
• The start of the antibiotic course is taken from the first day a negative set of blood cultures is obtained
• Every patient with prosthetic valve endocarditis should have an urgent surgical review.
• Indications for surgery include:

  • Heart failure (i.e severe valve disease, pulmonary oedema or cardiogenic shock)
  • Uncontrolled infection
  • Prevention of embolism (large vegetations)
• Localised complications include:

  • Valve destruction
  • Heart failure (secondary to valve regurgitation)
  • Arrhythmias and conduction disorders (e.g. AV block)
  • Myocardial infarction
  • Pericarditis
  • Aortic root abscess
• Systemic complications include:

  • Emboli (e.g. stroke, splenic infarction)
  • Immune complex deposition (e.g. glomerulonephritis)
  • Septicaemia
  • Death
• Native valve endocarditis initial treatment:

  • Amoxicillin
  • Consider adding low dose gentamicin
  • If penicillin-allergic, or if meticillin-resistant Staphylococcus aureus suspected, or if severe sepsis, use vancomycin + low-dose gentamicin
  • If severe sepsis with risk factors for Gram-negative infection, use vancomycin + meropenem
• If prosthetic valve endocarditis, vancomycin + rifampicin + low-dose gentamicin