Infective endocarditis

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5.7 Infective endocarditis

Sarah Dalton

Essentials

1 Infective endocarditis is the microbial infection of cardiac endothelium.
2 Risk factors include congenital heart disease, central venous access, intravenous drug use and immunodeficiency.
3 Diagnosis is based on the presence of positive blood cultures with evidence of carditis, peripheral embolisation and immunological phenomena.
4 Acute management includes elimination of causative organisms and treatment of associated complications such as congestive heart failure.
5 Long-term chemoprophylaxis is recommended for procedures likely to result in bacteraemia in at-risk patients.

Introduction

Infective endocarditis (IE) is the microbial infection of the endothelial lining of the heart. Infection may be bacterial or fungal, and may arise in both structurally normal and abnormal hearts. Presentation can be acute or subacute and the long-term morbidity and mortality is high.

Epidemiology

Over the last decade the incidence of IE has increased owing to the improved survival of children with congenital heart disease and an increase in patients with central venous catheters. Up to 75% of children with bacterial endocarditis are known to have pre-existing cardiac abnormalities, most commonly ventricular septal defect and tetralogy of Fallot. Other risk factors include acquired valve disease, intravenous drug use, immunodeficiency and previous bacterial endocarditis.

Pathophysiology

Turbulent cardiac blood flow through a structurally abnormal heart can damage endothelium and lead to overlying thrombus formation. Transient bacteraemia may infect the thrombus and a vegetation is formed. The local effects of vegetations include valvular insufficiency, valvular obstruction, and perivalvular extension leading to intracardiac fistulae and conduction system abnormalities. Extracardiac manifestations result from peripheral embolisation of thrombus material with subsequent infarction or infection of involved tissue. Mycotic aneurysms are secondary to bacterial embolisation causing infection and distension of the arterial wall and are most common in intracranial arteries.

Microbiology

Streptococcus viridans and Staphylococcus aureus are the most frequently encountered organisms in children with IE. Less common aetiological agents include enterococci, Staphylococcus epidermidis and Gram-negative HACEK bacilli – Haemophilus, Actinobacillus, Cardiobacterium, Eikenella and Kingella species. Fungal species such as Candida and Aspergillus may cause IE in neonates, immunocompromised patients and those with long-term central venous lines. Other agents such as Coxiella, Pneumococcus and Listeria are rare causes of endocarditis.

History

Patients with acute IE are often readily identified by systemic toxicity and high fever of short duration. The presentation of subacute endocarditis is more non-specific and usually includes fever, anorexia, malaise, cough, headache and arthralgia. A high degree of suspicion is required to identify these patients. Any presentation of unexplained prolonged fever, new neurological deficit or other embolic phenomena should be evaluated for endocarditis. Systemic embolisation occurs in up to 50% of patients with IE, and is most frequently seen in the first month post-diagnosis. Embolic events may cause infarction or abscess formation in the brain, lungs, kidneys, spleen, bone and extremities. Peripheral embolisation is often absent in acute endocarditis and right-sided heart disease, making their diagnosis more difficult. Endocarditis may also present with cardiac failure secondary to acute valvular dysfunction, fistulous tract formation or prosthetic dehiscence.

Examination

The physical signs of endocarditis may be subtle. A new or changing murmur may signify valvulitis, but can be difficult to distinguish from an innocent murmur or that of a pre-existing cardiac abnormality. Other findings include congestive heart failure or evidence of peripheral embolisation such as Osler nodes (tender, red nodules of finger pulps), Janeway lesions (non-painful, haemorrhagic areas of palms or soles) and splinter and subungual haemorrhages. These stigmata, which develop late in the course of disease, are unusual in children. Roth spots (retinal haemorrhages with a pale centre) are occasionally seen on funduscopy. Neurological deficit arises in 30–40% of patients from embolic infarcts, abscesses or intracerebral haemorrhage. Associated findings include splenomegaly in up to 30% of patients, and new onset clubbing may occur. Immune-mediated glomerulonephritis may result in haematuria, proteinuria and renal impairment.

Diagnosis is based on the modified Duke Criteria for Diagnosis of Infective Endocarditis (see below).

Modified Duke criteria

Major criteria

• Typical microorganisms from at least two separate blood cultures or a single positive blood culture for Coxiella burnetii.
• Mobile echodense intracardiac mass depicted on echocardiogram.
• Periannular abscess depicted on echocardiogram.
• New partial dehiscence of prosthetic valve depicted on echocardiogram.
• New valvular regurgitation depicted on echocardiogram.

Minor criteria

• Predisposing factor – history of intravenous (IV) drug use or congenital heart disease.
• Fever >38°C.
• Vascular phenomena – arterial emboli, pulmonary infarcts, mycotic aneurysm, intracranial haemorrhage, conjunctival haemorrhage, Janeway lesions.
• Immunological phenomena – glomerulonephritis, Osler nodes, Roth spots, positive rheumatoid factor.
• Positive blood cultures or serological evidence of infection not meeting above criteria.

These criteria determine three diagnostic categories: definite endocarditis, possible endocarditis and rejected cases. Definite diagnosis requires the presence of two major, one major with three minor, or five minor criteria. Possible endocarditis is defined by one major with one minor, or three minor criteria. Rejected cases are those where manifestations are explained by a clear alternate diagnosis or resolve after antibiotic therapy for 4 days or less.

Investigations

Laboratory

The most definitive test for IE is the identification of a known causative organism from more than one blood culture. In all cases of suspected endocarditis three sets of blood cultures should be collected from different peripheral sites prior to antibiotic administration. Up to 10% of all cases of IE remain culture negative, usually where organisms are highly fastidious, non-bacterial, or microbiological techniques are insufficient. Non-specific inflammatory markers such as white cell count, C-reactive protein, erythrocyte sedimentation rate and rheumatoid factor may also be abnormal.

Imaging

The investigation of possible endocarditis should include an electrocardiogram (ECG) and chest X-ray (CXR) but findings are non-specific. A CXR may reveal evidence of cardiac or pulmonary complications but is not diagnostic of IE. Transthoracic echocardiography is the most definitive investigation and yields excellent images in most paediatric patients.

Accuracy can be increased using transoesophageal echocardiography (TOE), which should be considered in high-risk groups. Echocardiographic findings are also used to guide management such as surgical intervention.

Differential diagnosis

The presentation of IE is similar to many systemic inflammatory conditions. Positive blood cultures often distinguish the diagnosis, but in suggestive presentations where blood cultures remain negative, other diagnoses must be considered. Rheumatic fever, Kawasaki disease, systemic lupus erythematosus and leukaemia all have similar presentations, hence the need for rigorous diagnostic criteria.

Treatment

Medical

The medical management of IE includes eliminating causative microorganisms and treating complications such as congestive heart failure. The bacterial infection of vegetations is relatively protected and must be completely eradicated with prolonged parenteral therapy. As the aetiological agent is usually unknown at presentation, empiric antibiotic therapy should be commenced. Australian antibiotic guidelines recommend benzylpenicillin (45 mg kg–1, max. 1.8 g) and flucloxacillin (50 mg kg–1, max. 2 g) intravenously every 4 hours with daily IV gentamicin (4–6 mg kg–1, max. 160 mg). Vancomycin should be added if there is a prosthetic valve, penicillin allergy, nosocomial infection or risk of methicillin-resistant Staphylococcus aureus. The duration of parenteral therapy is usually 4–6 weeks, modified by the aetiological agent and therapeutic response. Monitoring of drug levels and consultation with microbiologists should be undertaken to optimise therapy.

Surgical

The need for surgical management of IE depends on the severity of complications and response to medical management. Perivalvular abscesses, obstructive vegetations, cardiac fistulae and prosthetic dehiscence often require surgery. Other indications include persistent bacteraemia, recurrent embolisation, and some cases of fungal endocarditis.

Prognosis

The overall mortality of IE remains approximately 25% and morbidity is also considerable, with up to 60% of confirmed cases developing significant complications. Poor prognosis is associated with Staphylococcus aureus infection and fungal disease. Severe cardiac failure, prolonged clinical symptoms and poor response to antibiotics are also associated with worse outcomes.

Prevention

Antibiotic prophylaxis for IE is recommended internationally but guidelines are based on expert consensus and vary across the world. Australian guidelines adopt recommendations from the American Heart Association and consider the underlying cardiac condition and risk of the proposed procedure.

Recommended conditions requiring prophylaxis:

• prosthetic cardiac valves;
• cardiac transplant with subsequent valvulopathy;
• rheumatic heart disease with valvular pathology;
• previous infective endocarditis;
• congenital heart disease if:

image unrepaired cyanotic defect;
image completely repaired defect with prosthetic material up to 6 months post procedure;
image repaired defects with residual defect at prosthetic part.

Chemoprophylaxis depends on the procedure being performed. Australian guidelines suggest dental and upper respiratory tract procedures (e.g. reimplantation of avulsed tooth) receive amoxicillin (50 mg kg–1 orally) as a single dose 1 hour before the procedure. Cephalexin or clindamycin are alternatives for penicillin sensitivity. Genitourinary and gastrointestinal procedures require ampicillin (50 mg kg–1 IV) just before the procedure, or vancomycin (25 mg kg-1 IV) if pencillin allergic. Endotracheal intubation and urinary catheterisation do not require antibiotic prophylaxis. Current therapeutic guidelines should be consulted to optimise management in each case.

Controversies

There is no published evidence to show that antibiotic prophylaxis prevents IE. Endocarditis is thought more likely to result from random bacteraemia than from that associated with dental, GI or GU procedures. The American Heart Association has recently revised guidelines to reduce the categories of patients for whom prophylaxis is recommended and Australian guidelines are in keeping with these recommendations.

Further reading

Baddour L.M., Wilson W.R., Bayer A.R., et al. Infective Endocarditis; Diagnosis, Antimicrobial Therapy, and Management of Complications: A Statement for Healthcare Professionals. Circulation. 2005;111:3167-3184.

Fuster V. The AHA Guidelines and Scientific Statements Handbook. Wiley-Blackwell, 2009.

Milazzo A.S., Li J.S. Bacterial endocarditis in infants and children. Paediatr Infect Dis J. 2001;20(8):799-801.

Prendergast B.D. The changing face of infective endocarditis. Heart. 2006;92:879-885.

Therapeutic Guidelines: Antibiotics, Version 13. Therapeutic Guidelines Limited, 2006.

Therapeutic Guidelines: Prevention of Endocarditis. Therapeutic Guidelines Limited, 2008.

Wilson W., Taubert K.A., Gewitz M., et al. Prevention of Infective Endocarditis. Circulation. 2007;116:1736-1754.

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