INFECTIVE ENDOCARDITIS

INFECTIVE ENDOCARDITIS

Infective endocarditis is due to microbial infection of a heart valve (native or prosthetic), the lining of a cardiac chamber or blood vessel, or a congenital anomaly (e.g. septal defect).

The causative organism is usually a bacterium, but may be a rickettsia, chlamydia or fungus.

Infective endocarditis typically occurs at sites of pre-existing endocardial damage. However, infection with particularly virulent or aggressive organisms (e.g. Staphylococcus aureus) can cause endocarditis in a previously normal heart; for example, staphylococcal endocarditis of the tricuspid valve is a common complication of intravenous drug misuse

 high-pressure jet of blood, such as ventricular septal defect, mitral regurgitation and aortic regurgitation, many of which are haemodynamically insignificant. In contrast, the risk of endocarditis at the site of many haemodynamically important low-pressure lesions (e.g. a large atrial septal defect) is negligible

Infection tends to occur at sites of endothelial damage because these areas attract deposits of platelets and fibrin, which are vulnerable to colonisation by blood-borne organisms. The avascular valve tissue and presence of fibrin aggregates help to protect proliferating organisms from host defence mechanisms

When the infection is established, vegetations composed of organisms, fibrin and platelets grow and may become large enough to cause obstruction;

 they may also break away as emboli. Adjacent tissues are destroyed and abscesses may form;

valve regurgitation may develop or increase if the affected valve is damaged by tissue distortion, cusp perforation or disruption of chordae.

Extracardiac manifestations such as vasculitis and skin lesions are due to emboli or immune complex deposition. Mycotic aneurysms may develop in arteries at the site of infected emboli.

 At postmortem it is common to find infarction of the spleen and kidneys, and sometimes an immune glomerulonephritis.

Microbiology

Bacteria

• Streptococci  Viridans group30-40

%  Enterococci10

-15%  Other streptococci20-25%• Staphylococci  Staph. aureus9-27%  

Coagulase-negative1-3%• Gram-negative bacilliTotal 3-8%•

Haemophilus• AnaerobesOther organisms• Rickettsiae, fungi< 2%

The viridans group of streptococci (Strep. mitis, Strep. sanguis) are commensals in the upper respiratory tract that may enter the blood stream on chewing or teeth-brushing, or at the time of dental treatment, and are common causes of subacute endocardit

). Other organisms, including Enterococcus faecalis, E. faecium and Strep. bovis, may enter the blood from the bowel or urinary tract

. Strep. milleri and Strep. bovis endocarditis are sometimes associated with large-bowel neoplasms.

Staph. aureus is a common cause of acute endocarditis, originating from skin infections, abscesses or vascular access sites (e.g. intravenous and central lines), or from intravenous drug misuse.

 It is a highly virulent and invasive organism, usually producing florid vegetations, rapid valve destruction and abscess formation.

 Other causes of acute endocarditis include Strep. pneumoniae and Strep. pyogenes.

Post-operative endocarditis after cardiac surgery may affect native or prosthetic heart valves or other prosthetic materials. The most common organism is a coagulase-negative staphylococcus (Staph. epidermidis), which is a normal skin commensal. There is frequently a history of post-operative wound infection with the same organism.

In Q fever endocarditis due to Coxiella burnetii, the patient often has a history of contact with farm animals. The aortic valve is usually affected and there may be hepatic complications and purpura. Life-long antibiotic therapy may be required.

Gram-negative bacteria of the so-called HACEK group (Haemophilus spp; Actinobacillus actinomycetem-comitans; Cardiobacterium hominis; Eikenella spp. and Kingella kingae) are slow-growing fastidious organisms that may only be revealed after prolonged culture and may be resistant to penicillin

Brucella is associated with a history of contact with goats or cattle and often affects the aortic valve.

Yeasts and fungi (Candida, Aspergillus) may attack previously normal or prosthetic valves, particularly in immuno-compromised patients or those with indwelling intravenous lines. Abscesses and emboli are common, therapy is difficult (surgery is often required) and the mortality is high

the underlying condition was rheumatic heart disease in 24% of patients, congenital heart disease in 19%, and some other cardiac abnormality (e.g. calcified atrial valve, floppy mitral valve) in 25%. The remainder (32%) were not thought to have a pre-existing cardiac abnormality. More than 50% of patients with infective endocarditis are over 60 years of age.

Clinical features

DIAGNOSIS OF INFECTIVE ENDOCARDITIS (MODIFIED DUKE CRITERIA

Major criteria

Positive blood culture

Typical organism from two cultures

Persistent positive blood cultures taken > 12 hours apart

Three or more positive cultures taken over more than 1 hour

Endocardial involvement

Positive echocardiographic findings of vegetations

New valvular regurgitation

Minor criteria

Predisposing valvular or cardiac abnormality

Intravenous drug misuse

Pyrexia ≥38°C

Embolic phenomenon

Vasculitic phenomenon

Blood cultures suggestive-organism grown but not achievingmajor criteria

Suggestive echocardiographic findings

Definite endocarditis: two major, or one major and three minor, or five minor

Possible endocarditis: one major and one minor, or three minor

Blood culture is the crucial investigation because it may identify the infection and guide antibiotic therapy.

Three sets of blood cultures should be taken prior to commencing therapy, and these need not wait for episodes of pyrexia.

 The first two specimens will detect bacteraemia in 90% of culture-positive cases.

Aseptic technique is essential and the risk of contaminants should be minimised by sampling from different venepuncture sites.

 An in-dwelling line should not be used to take cultures. Aerobic and anaerobic cultures are required.

Echocardiography is the key investigation for detecting and following the progress of vegetations, for assessing valve damage and for detecting abscess formation.

 Vegetations as small as 2-4 mm can be detected by transthoracic echo, and even smaller ones (1-1.5 mm) can be visualised by transoesophageal echo, which is particularly valuable for identifying abscess formation and investigating patients with prosthetic heart valves.

Vegetations may be difficult to distinguish in the presence of an abnormal valve; the sensitivity of transthoracic echo is approximately 65% but that of transoesophageal echo is more than 90%.

Elevation of the ESR, a normocytic, normochromic anaemia and leucocytosis are common but not invariable, and thrombocytopenia may be present. Measurement of serum CRP is more reliable than the ESR in monitoring progress.

 Proteinuria may occur and microscopic haematuria is usually present

The ECG may show the development of atrioventricular block (due to abscess formation) and occasionally infarction due to emboli. The chest X-ray may show evidence of cardiac failure and cardiomegaly

Management

• Empirical treatment depends on the mode of presentation, the suspected organism, and whether the patient has a prosthetic valve and/or penicillin allergy. For example, if the presentation is acute, flucloxacillin and gentamicin are recommended,
•  and for a subacute or indolent presentation, benzyl penicillin and gentamicin.
•  In those with either penicillin allergy, a prosthetic valve or suspected meticillin-resistant Staph. aureus (MRSA) infection, triple therapy with vancomycin, gentamicin and oral rifampicin should be considered.
• Following identification of the causal organism, determination of the minimum inhibitory concentration (MIC) is essential to guide antibiotic therapy

INDICATIONS FOR CARDIAC SURGERY IN INFECTIVE ENDOCARDITIS

Heart failure due to valve damage

Failure of antibiotic therapy (persistent or uncontrolled infection)

Large vegetations on left-sided heart valves with evidence or'high risk' of systemic emboli

Abscess formation