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.
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.
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 | ||||||||||
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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
Persistently positive blood culture2
Single positive blood culture for Coxiella Burnettii or phase I
antibody
Titre to C. Burnettii >1:800
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 >38°C
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
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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.
Once diagnosis is confirmed (or even suspected), explain to the patient the need for a prolonged parenteral (usually IV) course of antibiotics.
Microbiology will determine sensitivities to, and minimum inhibitory concentration (MIC) of, appropriate antibiotics—if fully sensitive organism with ‘low’ MIC then shorter courses of antibiotics may suffice (and the latter part of the course may be completed on an outpatient basis). Evidence shows that combination therapy is more effective than single chemotherapeutic agents.
Identification of an organism is invaluable for further management, and blood cultures should be taken before antibiotics, with meticulous attention to detail.
Fully sensitive (MIC of penicillin <0.1 mg/L)—native valve endocarditis (NVE): benzylpenicillin 1.2 g/4 h IV for 4 weeks, occasionally can successfully treat with 2-week course of benzylpenicillin and gentamicin. For prosthetic valve endocarditis (PVE): benzylpenicillin for 6 weeks (in combination with gentamicin for first 2 weeks).
Mild penicillin resistance (MIC of penicillin >0.1-0.5 mg/L)—NVE: benzylpenicillin for 4 weeks with gentamicin for first 2 weeks. PVE: benzylpenicillin for 6 weeks with gentamicin for first 4 weeks.
Moderate penicillin resistance (MIC>0.5 mg/L)—NVE: benzylpenicillin (or amoxicillin) and gentamicin for 4-6 weeks. PVE: benzylpenicillin (or amoxicillin) and gentamicin for at least 6 weeks.
NB: can use vancomycin if allergic to penicillin.
Meticillin-sensitive staphylococci—NVE: flucloxacillin 2 g/6 hours IV for 4-6 weeks with gentamicin for at least 1st week. PVE: flucloxacillin for 6 weeks + gentamicin for first 2 weeks + rifampicin 600 mg bd PO for 6 weeks.
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