5.7 Infective endocarditis
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).
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