Presentation of endocarditis
Key facts
• Highly variable presentation—depends on intracardiac pathology, virulence of organism, and extracardiac involvement.
• Presentation can be insidious, as in streptococcal infections, or with striking constitutional symptoms as in Staphylococcus aureus infection. Presenting features can include those discussed next.
General manifestations of sepsis
Includes malaise, anorexia, weight loss, fever, rigors, and night sweats. Longstanding infection produces anaemia, clubbing, and splenomegaly.
Cardiac manifestations of endocarditis
• Sepsis causing tachycardia, hypotension.
• Valve destruction results in a new or changing murmur. This may result in progressive heart failure and pulmonary oedema.
• A new harsh pansystolic murmur and acute deterioration may be due to perforation of the interventricular septum or rupture of a sinus of Valsalva aneurysm into the right ventricle.
• High-degree atrioventricular (AV) block (2–4% of infective endocarditis (IE)) occurs with intracardiac extension of infection into the interventricular septum (e.g. from aortic valve).
• Intracardiac abscess may be seen with any valve infection (25–50% of aortic endocarditis, 1–5% of mitral but rarely with tricuspid) and is most common in prosthetic valve endocarditis.
• Pericarditis.
Manifestations of immune complex deposition
Skin: Petechiae (most common), splinter haemorrhages; Osler’s nodes (small tender nodules (pulp infarcts) on hands and feet and persist hours to days); Janeway lesions (non-tender eryhthematous and/or haemorrhagic areas on the palms and soles).
Eye: Roth spots (oval retinal haemorrhages with a pale centre located near the optic disc), conjunctival splinter haemorrhages, retinal flame haemorrhages.
Renal: Microscopic haematuria, glomerulonephritis and renal impairment.
Cerebral: Toxic encephalopathy.
Musculoskeletal: Arthralgia or arthritis.
Systemic manifestations of endocarditis
General manifestations of sepsis
Includes malaise, anorexia, weight loss, fever, rigors, and night sweats. Longstanding infection produces anaemia, clubbing, and splenomegaly.
Septic emboli
• Septic emboli are seen in 20–45% of patients and may involve any circulation (brain, limbs, coronary, kidney, or spleen; pulmonary emboli with tricuspid endocarditis (see Right-sided endocarditis, p. 190).
• ∼40% of patients who have had an embolic event will have another.
• The risk depends on the organism (most common with Gram-negative infections, S. aureus or candida) and the presence and size of vegetations (emboli in 30% of patients with no vegetation on echocardiography, 40% with vegetations <5 mm and 65% with vegetations >5 mm).
• Ask specifically for a history of dental work, infections, surgery, intravenous (IV) drug use, or instrumentation, which may have led to a bacteraemia.
• Examine for any potential sources of infection, e.g. teeth/skin lesions.
• Risk factors for endocarditis are shown in the box below.
Risk factors for infective endocarditis
High risk
Prosthetic valves
Previous bacterial endocarditis
Aortic valve disease
Mitral regurgitation or mixed mitral disease
Cyanotic congenital heart disease
Patent ductus arteriosis
Uncorrected L→R shunt
Intracardiac and systemic-pulmonary shunts
Moderate risk
Mitral valve prolapse (MVP) with regurgitation or valve thickening
Isolated mitral stenosis
Tricuspid valve disease
Pulmonary stenosis
Hypertrophic cardiomyopathy
Bicuspid aortic valve disease
Degenerative valve disease in elderly
Mural thrombus (e.g. post infarction)
Low risk
MVP without regurgitation
Tricuspid incompetence without structural abnormality
Isolated atrial septal defect (ASD)
Surgically corrected L→R shunt with no residual shunt
Calcification of mitral valve (MV) annulus
Ischaemic heart disease and/or previous coronary artery bypass graft (CABG)
Permanent pacemaker
Atrial myxoma
Other predisposing factors
• Arterial prostheses or arteriovenous fistulae
• Recurrent bacteraemia, e.g. IV drug users, severe periodontal disease, colon carcinoma)
• Conditions predisposing to infections, e.g. diabetes, renal failure, alcoholism, immunosuppression)
• Recent central line.
In many cases no obvious risk factor is identified.
Diagnosis of endocarditis
Key facts
• Clinical features can be non-specific and diagnosis difficult.
• Maintain a high index of suspicion in patients presenting with unexplained fever, a predisposing cardiac lesion, bacteraemia, and embolic phenomena.
Duke classification
• Developed in 1994 as a means of standardizing the diagnosis of IE
• Highly specific (99%) and sensitive (92%)
• Several modifications, the most current version is described next.
Major criteria
• Positive blood culture
• Evidence of endocardial involvement: positive echocardiogram
• oscillating intracardiac mass (vegetation)
• abscess
• new partial dehiscence of prosthetic valve
• new valve regurgitation.
Minor criteria
• Predisposing condition or drug use
• Fever >38oC
• Vascular phenomena: arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial and conjunctival haemorrhage, Janeway lesions
• Immunologic phenomena: glomerulonephritis, Osler’s nodes, Roth spots, rheumatoid factor
• Microbiological evidence: positive blood cultures but not meeting major criteria or serological evidence of organism consistent with IE
• Echocardiogram: positive for IE but not meeting major criteria
• Always consider this diagnosis in IV drug users (or patients with
• venous access).
• Endocarditis on endocardial permanent pacemaker leads is a rare but recognized cause.
Right-sided endocarditis
• Patients most commonly have staphylococcal infection and are unwell, requiring immediate treatment and often early surgery.
• Lesions may be sterilized with IV antibiotics.
• Surgery may be required for:
• resistant organisms (Staphylococcus aureus, Pseudomonas, Candida and infection with multiple organisms).
• increasing vegetation size in spite of therapy.
• infections on pacemaker leads (surgical removal of lead and repair or excision of tricuspid valve).
• recurrent mycotic emboli.
Criteria for definite diagnosis
• Definite endocarditis: 2 major criteria, or 1 major and 3 minor criteria, or 5 minor criteria
• Possible endocarditis: findings that fall short of definite endocarditis but are not rejected
• Rejected diagnosis: firm alternative diagnosis, or sustained resolution of clinical features with <4 days of antibiotic therapy
Common organisms in IE
50–60%
Streptococci (esp. Strep. viridans group)
10%
Enterococci
25%
Staphylococci
S. aureus = coagulase +ve
S. epidermidis = coagulase –ve
5–10%
Culture negative
<1%
Gram-negative bacilli
<1%
Multiple organisms
<1%
Diphtheroids
<1%
Fungi
Investigation of endocarditis
• Blood cultures
Take 3–4 sets of cultures from different sites at least an hour apart and inoculate a minimum of 10 mL/bottle for the optimal pick-up rate. Both aerobic and anaerobic bottles must be used. Lab should be advised that IE is a possibility, especially if unusual organisms are suspected. In stable patients on antibiotic therapy, doses must be delayed to allow culture on successive days. Ask for prolonged (fungal) cultures in IV drug users.
• Full blood count (FBC)
May show normochromic, normocytic anaemia (exclude haematinic deficiency), neutrophil leucocytosis, and perhaps thrombocytopenia.
• Urea and electrolytes (U&Es)
May be deranged (this should be monitored throughout treatment).
• Liver function tests (LFTs)
May be deranged, especially with an increase in alkaline phosphatase (ALP) and gamma glutamyl transferase (GGT).
• Erythrocyte sedinemtation rate (ESR)/C-reactive protein (CRP)
Acute phase reaction.
• Urinalysis
Microscopic haematuria ± proteinuria.
• Immunology
Polyclonal elevation in serum Igs, complement levels
• Electrocardiogram (ECG)
May have changes associated with any underlying cause. There may be atrioventricular (AV) block or conduction defects (especially aortic root abscess) and, rarely (embolic), acute myocardial infarction (MI).
• Chest X-ray (CXR)
May be normal. Look for pulmonary oedema or multiple infected or infarcted areas from septic emboli (tricuspid endocarditis).
• Echocardiography (ECHO)
Transthoracic ECHO may confirm the presence of valve lesions and/or demonstrate vegetations if >2 mm in size. Transoesophageal echocardiography (TOE) is more sensitive for aortic root abcess and mitral leaflet involvement. A normal ECHO does not exclude the diagnosis.
• Magnetic resonance imaging (MRI, used rarely)
Useful in investigation of paravalvular extension, aortic root aneurysm, and fistulas.
• Dentition
All patients should have an OPG (orthopentamogram—a panoramic dental X-ray) and a dental opinion.
• Swabs
Any potential sites of infection (skin lesions).
• Ventilation/perfusion (V/Q) scan
In cases where right-sided endocarditis is suspected, this may show multiple mismatched defects.
• Save serum for:
Aspergillus precipitins; Candida antibodies (rise in titre); Q fever (Coxiella burnetti) complement fixation test; Chlamydia complement fixation test; Brucella agglutinins; Legionella antibodies; Bartonella species.
Further reading
Guidelines on the Prevention, Diagnosis, and Treatment of Infective Endocarditis (new version 2009), The Task Force on the Prevention, Diagnosis, and Treatment of Infective Endocarditis of the European Society of Cardiology (ESC). Eur Heart J 30: 2369–413. 
http://www.escardio.org/guidelines-surveys/esc-guidelines/Pages/infective-endocarditis.aspx
Antibiotics in endocarditis
Key facts
• Be guided by your local microbiologist and always follow local antibiotic prescription guidelines.
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• Septic emboli are seen in 20–45% of patients and may involve any circulation (brain, limbs, coronary, kidney, or spleen; pulmonary emboli with tricuspid endocarditis (see Right-sided endocarditis, p. 190).
• ∼40% of patients who have had an embolic event will have another.
• The risk depends on the organism (most common with Gram-negative infections, S. aureus or candida) and the presence and size of vegetations (emboli in 30% of patients with no vegetation on echocardiography, 40% with vegetations <5 mm and 65% with vegetations >5 mm).
• Ask specifically for a history of dental work, infections, surgery, intravenous (IV) drug use, or instrumentation, which may have led to a bacteraemia.
• Examine for any potential sources of infection, e.g. teeth/skin lesions.
• Risk factors for endocarditis are shown in the box below.
Risk factors for infective endocarditis
| High risk | Prosthetic valves Previous bacterial endocarditis Aortic valve disease Mitral regurgitation or mixed mitral disease Cyanotic congenital heart disease Patent ductus arteriosis Uncorrected L→R shunt Intracardiac and systemic-pulmonary shunts |
| Moderate risk | Mitral valve prolapse (MVP) with regurgitation or valve thickening Isolated mitral stenosis Tricuspid valve disease Pulmonary stenosis Hypertrophic cardiomyopathy Bicuspid aortic valve disease Degenerative valve disease in elderly Mural thrombus (e.g. post infarction) |
| Low risk | MVP without regurgitation Tricuspid incompetence without structural abnormality Isolated atrial septal defect (ASD) Surgically corrected L→R shunt with no residual shunt Calcification of mitral valve (MV) annulus Ischaemic heart disease and/or previous coronary artery bypass graft (CABG) Permanent pacemaker Atrial myxoma |
| Other predisposing factors • Arterial prostheses or arteriovenous fistulae • Recurrent bacteraemia, e.g. IV drug users, severe periodontal disease, colon carcinoma) • Conditions predisposing to infections, e.g. diabetes, renal failure, alcoholism, immunosuppression) • Recent central line. | |
| In many cases no obvious risk factor is identified. | |
• Clinical features can be non-specific and diagnosis difficult.
• Maintain a high index of suspicion in patients presenting with unexplained fever, a predisposing cardiac lesion, bacteraemia, and embolic phenomena.
• Developed in 1994 as a means of standardizing the diagnosis of IE
• Highly specific (99%) and sensitive (92%)
• Several modifications, the most current version is described next.
• Positive blood culture
• Evidence of endocardial involvement: positive echocardiogram
• oscillating intracardiac mass (vegetation)
• abscess
• new partial dehiscence of prosthetic valve
• new valve regurgitation.
• Predisposing condition or drug use
• Fever >38oC
• Vascular phenomena: arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial and conjunctival haemorrhage, Janeway lesions
• Immunologic phenomena: glomerulonephritis, Osler’s nodes, Roth spots, rheumatoid factor
• Microbiological evidence: positive blood cultures but not meeting major criteria or serological evidence of organism consistent with IE
• Echocardiogram: positive for IE but not meeting major criteria
• Always consider this diagnosis in IV drug users (or patients with
• venous access).
• Endocarditis on endocardial permanent pacemaker leads is a rare but recognized cause.
• Patients most commonly have staphylococcal infection and are unwell, requiring immediate treatment and often early surgery.
• Lesions may be sterilized with IV antibiotics.
• Surgery may be required for:
• resistant organisms (Staphylococcus aureus, Pseudomonas, Candida and infection with multiple organisms).
• increasing vegetation size in spite of therapy.
• infections on pacemaker leads (surgical removal of lead and repair or excision of tricuspid valve).
• recurrent mycotic emboli.
• Definite endocarditis: 2 major criteria, or 1 major and 3 minor criteria, or 5 minor criteria
• Possible endocarditis: findings that fall short of definite endocarditis but are not rejected
• Rejected diagnosis: firm alternative diagnosis, or sustained resolution of clinical features with <4 days of antibiotic therapy
Common organisms in IE
| 50–60% | Streptococci (esp. Strep. viridans group) |
| 10% | Enterococci |
| 25% | Staphylococci |
| S. aureus = coagulase +ve | |
| S. epidermidis = coagulase –ve | |
| 5–10% | Culture negative |
| <1% | Gram-negative bacilli |
| <1% | Multiple organisms |
| <1% | Diphtheroids |
| <1% | Fungi |
• Blood cultures | Take 3–4 sets of cultures from different sites at least an hour apart and inoculate a minimum of 10 mL/bottle for the optimal pick-up rate. Both aerobic and anaerobic bottles must be used. Lab should be advised that IE is a possibility, especially if unusual organisms are suspected. In stable patients on antibiotic therapy, doses must be delayed to allow culture on successive days. Ask for prolonged (fungal) cultures in IV drug users. |
• Full blood count (FBC) | May show normochromic, normocytic anaemia (exclude haematinic deficiency), neutrophil leucocytosis, and perhaps thrombocytopenia. |
• Urea and electrolytes (U&Es) | May be deranged (this should be monitored throughout treatment). |
• Liver function tests (LFTs) | May be deranged, especially with an increase in alkaline phosphatase (ALP) and gamma glutamyl transferase (GGT). |
• Erythrocyte sedinemtation rate (ESR)/C-reactive protein (CRP) | Acute phase reaction. |
• Urinalysis | Microscopic haematuria ± proteinuria. |
• Immunology | Polyclonal elevation in serum Igs, complement levels |
• Electrocardiogram (ECG) | May have changes associated with any underlying cause. There may be atrioventricular (AV) block or conduction defects (especially aortic root abscess) and, rarely (embolic), acute myocardial infarction (MI). |
• Chest X-ray (CXR) | May be normal. Look for pulmonary oedema or multiple infected or infarcted areas from septic emboli (tricuspid endocarditis). |
• Echocardiography (ECHO) | Transthoracic ECHO may confirm the presence of valve lesions and/or demonstrate vegetations if >2 mm in size. Transoesophageal echocardiography (TOE) is more sensitive for aortic root abcess and mitral leaflet involvement. A normal ECHO does not exclude the diagnosis. |
• Magnetic resonance imaging (MRI, used rarely) | Useful in investigation of paravalvular extension, aortic root aneurysm, and fistulas. |
• Dentition | All patients should have an OPG (orthopentamogram—a panoramic dental X-ray) and a dental opinion. |
• Swabs | Any potential sites of infection (skin lesions). |
• Ventilation/perfusion (V/Q) scan | In cases where right-sided endocarditis is suspected, this may show multiple mismatched defects. |
• Save serum for: | Aspergillus precipitins; Candida antibodies (rise in titre); Q fever (Coxiella burnetti) complement fixation test; Chlamydia complement fixation test; Brucella agglutinins; Legionella antibodies; Bartonella species. |
http://www.escardio.org/guidelines-surveys/esc-guidelines/Pages/infective-endocarditis.aspx• Be guided by your local microbiologist and always follow local antibiotic prescription guidelines.
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Full access? Get Clinical Tree
