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تسلسل 56
تسلسل 56
Cardiology lectures

Infective endocarditis

This is caused by 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 preexisting endocardial damage, but infection with particularly virulent or aggressive organisms (e.g. Staphylococcus aureus) can cause endocarditis in a previously normal heart. Infection tends to occur at sites of endothelial damage because they attract deposits of platelets and fibrin that are vulnerable to colonization by blood-borne organisms.

The avascular valve tissue and presence of fibrin and platelet 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 or embolism. 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 autopsy, infarction of the spleen and kidneys and, sometimes, an immune glomerulonephritis are found.


Over three-quarters of cases are caused by streptococci or staphylococci. The viridans group of streptococci (Streptococcus 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 endocarditis. 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 is associated with large-bowel neoplasms.

Staph. aureus originates from skin infections, abscesses or vascular access sites (e.g. intravenous and central lines), or from intravenous drug use. It is highly virulent and invasive, 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), a

normal skin commensal. Another coagulase-negative staphylococcus, Staph. lugdenensis, causes a rapidly destructive acute endocarditis that is associated with previously normal valves and multiple emboli. Unless accurately identified, it may also be overlooked as a contaminant.

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 also be hepatitis, pneumonia and purpura. Life-long antibiotic therapy may be required.

Gram-negative bacteria of the so-called HACEK group (Haemophilus spp., Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella spp. And Kingella kingae) are slow-growing, fastidious organisms that are only 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 immunocompromised patients or those with indwelling intravenous lines. Abscesses and emboli are common, therapy is difficult (surgery is often required) and mortality is high. Concomitant bacterial infection may be present.


The incidence of infective endocarditis in community based studies ranges from 5 to 15 cases per 100 000 per annum. More than 50% of patients are over 60 years of age. In a large British study, the underlying

condition was rheumatic heart disease in 24% of patients, congenital heart disease in 19%, and other cardiac abnormalities (e.g. calcified aortic valve, floppy mitral valve) in 25%. The remaining 32% were not thought to have a pre-existing cardiac abnormality.

Clinical features:

Endocarditis can take either an acute or a more insidious ‘subacute’ form. However, there is considerable overlap because the clinical pattern is influenced not only by the organism, but also by the site of infection, prior antibiotic therapy and the presence of a valve or shunt prosthesis. The subacute form may abruptly develop acute life-threatening complications, such as valve disruption or emboli.

Subacute endocarditis:

This should be suspected when a patient with congenital or valvular heart disease develops a persistent fever, complains of unusual tiredness, night sweats or weight loss, or develops new signs of valve dysfunction or heart failure. Less often, it presents as an embolic stroke or peripheral arterial embolism. Other features include purpura and petechial haemorrhages in the skin and mucous membranes, and splinter haemorrhage under the fingernails or toe nails. Osler’s nodes are painful tender swellings at the fingertips that are probably the product of vasculitis; they are rare. Digital clubbing is a late sign. The spleen is frequently palpable; in Coxiella infections, the spleen and the liver may be considerably enlarged. Microscopic haematuria is common.

The finding of any of these features in a patient with persistent fever or malaise is an indication for re-examination to detect hitherto unrecognized heart disease.

Acute endocarditis:

This presents as a severe febrile illness with prominent and changing heart murmurs and petechiae. Clinical stigmata of chronic endocarditis are usually absent.

Embolic events are common, and cardiac or renal failure may develop rapidly. Abscesses may be detected on echocardiography. Partially treated acute endocarditis behaves like subacute endocarditis.

A clinical diagnosis of endocarditis can be made on the presence of two major, one major and three minor, or five minor criteria.


Blood culture is the crucial investigation because it may identify the infection and guide antibiotic therapy. Three to six sets of blood cultures should be taken prior to commencing therapy and should 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 minimized 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 key 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 echocardiography, and even smaller ones (1–1.5 mm) can be visualised by transoesophageal echocardiography (TOE), which is particularly valuable for identifying abscess formation and investigating patients with prosthetic heart valves. Failure to detect vegetations does not exclude the diagnosis.

Elevation of the ESR, a normocytic normochromic anaemia, and leucocytosis are common but not invariable.

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 AV block (due to aortic root abscess formation) and occasionally infarction due to emboli.

The chest X-ray may show evidence of cardiac failure and cardiomegaly.


The case fatality of bacterial endocarditis is approximately 20% and even higher in those with prosthetic valve endocarditis and those infected with antibiotic resistant organisms. A multidisciplinary approach, with cooperation between the physician, surgeon and microbiologist, increases the chance of a successful outcome.

Any source of infection should be removed as soon as possible; for example, a tooth with an apical abscess should be extracted.

Empirical treatment depends on the mode of presentation, the suspected organism, and whether the patient has a prosthetic valve or penicillin allergy, If the presentation is acute (suspecting staph aureus infection), flucloxacillin and gentamicin are recommended, while for a subacute or indolent presentation, benzyl penicillin and gentamicin are preferred.

In those with penicillin allergy, a prosthetic valve or suspected meticillin-resistant Staph. aureus (MRSA) infection, triple therapy with vancomycin, gentamicin and oral rifampicin should be considered.

A 2-week treatment regimen may be sufficient for fully sensitive strains of Strep. viridans and Strep. bovis, provided specific conditions are met.

Cardiac surgery (débridement of infected material and valve replacement) is advisable in a substantial proportion of patients, particularly those with Staph. Aureus and fungal infections. Antimicrobial therapy must be started before surgery.


Until recently, antibiotic prophylaxis was routinely given to people at risk of infective endocarditis undergoing interventional procedures. However, as this has not been proven to be effective and the link between episodes of infective endocarditis and interventional procedures has not been demonstrated, antibiotic prophylaxis is no longer offered routinely for defined interventional procedures.

Antibiotics only in high-risk group patients:

1. Prosthetic valve or foreign material used for heart repair.

2. History of IE

3. Congenital heart disease

Cyanotic without correction or with residual leakage

CHD without leakage but up to 6 months after surgery

Use amoxycilin 2gm orally or ampicylin 2gm i.m / i.v 30-60 min prior to intervention. In patients with penicillin allergy use Clindamycin 600mg orally or Azithromycin 500mg.

رفعت المحاضرة من قبل: Harir Radhwan
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