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Serious potentially fatal infection of cardiac valves and endocardium usually by bacteria. Infective destructive vegetations form and erode and destroy the heart valves. Vegetations contain fibrin, platelets, microorganisms. These can embolise the cerebral circulation. A useful rule of thumb is that any patient with a prosthetic valve or valvular heart disease with a stroke (ischaemic or haemorrhagic) must be considered to have endocarditis until proven otherwise. The fact that haemorrhagic transformation from an embolised mycotic vegetation is common and bleeding is seen on CT can mislead the unwary. Co-existing anticoagulation can also distract and be blamed. Check the CRP, send cultures and get and arrange an urgent echocardiogram.

Potential Infective agentsDetails
Streptococcus viridans (alpha haemolytic) a low virulence organism seen where there is a history of rheumatic fever
Staphylococcus epidermidis Drug addicts and IV drug abusers have a tendency to RIGHT sided valve lesions particularly.
> Staphylococcus aureus causes a much more aggressive disease e.g. early following surgery especially to the heart or valve replacement.
Coxiella burnetii (Q fever)
Enterococci and other Gram negative bacteria
HACEK Haemophilus sp, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae


Approximately 60-80% of those with IE have a Predisposing heart lesions. High risk lesions include prosthetic valves, MR or AR, VSD, PDA. Medium risk are those with Aortic stenosis or Hypertrophic cardiomyopathy. Low risk are those with Mitral stenosis or ASD. Mitral valve prolapse only carries appreciable risk where there is associated MR. Other risk groups are those IV drug users who get a tricuspid valve endocarditis with Staph aureus. Those with Bicuspid aortic valve are also at risk of aortic valve endocarditis.

Markers of severity

These include Staph aureus infection, Prosthetic valve, Culture negative endocarditis and Low complement levels

Clinical Findings

Classically Fever, Malaise, Joint pains, arthropathy. Splinter haemorrhages - also seen in manual workers on dominant hand. Patients may have Stroke/TIA like episodes if emboli to brain/eye with infarction or infratction and secondary haemorrhage. Also have Peripheral emboli - gangrene / ischaemic bowel or to spinal cord. Finger clubbing - not common in less than 5% of SBE. Osler's nodes - painful, tender nodules on the pulps of fingers. Janeway lesions - small < 5 mm flat painless red spots seen on palms and soles. Roth's spots - haemorrhage and micro infarction of retinal vessels. New or changing murmurs, Splenomegaly


  • FBC - anaemia, Raised ESR and CRP, U&E
  • Urinalysis - microscopic haematuria
  • ECG -New AV block even a lengthened PR interval suggests Aortic valve involvement an dpossibly aortic root abscess.
  • CXR - evidence of cardiomegaly, mitral stenosis
  • Transthoracic echo - vegetations and valve disease may be seen. Root abscess.
  • Transoesphageal echo - shows much higher quality views of the heart valves. Look for valves structure and vegetations and abscess formation.
  • Blood cultures - multiple from multiple sites at different times with fastidious care to avoid contaminants

    Definite infective endocarditis

  • Pathological criteria positive OR Two major criteria OR One major and two minor criteria OR Five minor criteria

Pathological criteria

  • Positive histology or microbiology of pathological material obtained at autopsy or cardiac surgery (valve tissue, vegetations, embolic fragments, or intracardiac abscess content)

    Major criteria

  • Two positive blood cultures showing typical organisms consistent with infective endocarditis, such as Streptococcus viridans and the HACEK group OR
  • Persistent bacteraemia from two blood cultures taken more than 12 hours apart or three or more positive blood cultures where the pathogen is less specific, such as Staphylococcus aureus and Staph epidermidis OR
  • Positive serology for Coxiella burnetii, Bartonella species, or Chlamydia psittaci OR
  • Positive molecular assays for specific gene targets
  • Positive echocardiogram showing oscillating structures, abscess formation, new valvular regurgitation, or dehiscence of prosthetic valves

    Minor criteria

  • Predisposing heart disease
  • Fever > 38°C
  • Immunological phenomena such as glomerulonephritis, Osler's nodes, Roth spots, or positive rheumatoid factor
  • Microbiological evidence not fitting major criteria
  • Elevated C reactive protein or ESR
  • Vascular phenomena such as major emboli, splenomegaly, clubbing, splinter haemorrhages, petechiae, or purpura


The complications of Infective Endocarditis include Valve failure with heart failure, throwing off of further septic emboli e.g. stroke, Glomerulonephritis and progressive renal failure, Aortic root abscess formation, further valve destruction with regurgitation and severe cardiac failure. Valvular abscess and Pericarditis

Management of endocarditis

Medical: It is vitally important to try and obtain cultures of the organism to help guide therpay and so multiple aerobic and anaerobic blood cultures from multiple sites should be taken over 12-24 hrs prior to commencing antibiotics. If antibiotics have already been given this can make organism identification difficult. Ensure sufficient microbiological samples taken before starting blind therapy. Once the organism is known specific treatment is started usually a prolonged course of antibiotics is needed and determined by local advice and sensitivities. Usually requires 4-6 weeks of IV and then oral therapy. Streptococci - Penicillin G and Gentamicin. Methicillin Sensitive Staph Aureus - take expert guidance. Generally anticoagulation is avoided if possible as there is a high risk of bleeding into infarcted areas.

Cardiac Surgical: urgent assessment needed for cardiac failure due to valve damage, extensive MR/AR, large vegetations, septic emboli, abscess formation, fungal infection, antibiotic resistance, failure to respond to medical management. Surgery is evidently high risk with significant risk of complications. Cardiothoracic centres may be reluctant to take those with pre-existing large strokes with a poor prognosis. Patients may need moved to a local cardiothoracic centre perhaps under cardiology to have further assssment before any surgical intervention.

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