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INFECTIVE ENDOCARDITIS
Infective endocarditis is an infection of the endocardial surface of the
heart. The disease may occur as an acute, fulminating infection, but more
commonly runs an insidious course and is known as subacute bacterial
endocarditis (SBE.) The term 'infective endocarditis' is preferred because
not all the infecting organisms are bacteria, and fungi can be responsible.
The annual incidence in the UK is 6-7 per 100 000, but it is more
common in developing countries. Without treatment the mortality
approaches 100% and even with treatment there is a significant morbidity
and mortality.
Aetiology
Endocarditis is usually the consequence of two factors: the presence of
organisms in the bloodstream and abnormal cardiac endothelium
facilitating their adherence and growth.
Factors causing a bacteraemia
Anything that results in a breach of the body's innate defences can
potentially cause a bacteraemia. In some cases the cause of the
bacteraemia is unknown; more often; there is an obvious factor that
facilitated the entry of organisms into the bloodstream. This may be
patient orientated: poor dental hygiene, intravenous drug use, soft tissue
infections; or iatrogenic: dental treatment, intravascular cannulae
(especially central), cardiac surgery, or permanent pacemakers.
Local cardiac factors
Damaged vascular endothelium will promote platelet and fibrin
deposition. It is these small thrombi that allow organisms to adhere and
grow. As they grow, more fibrin and platelets are deposited, forming the
characteristic infected vegetation. Abnormal vascular endothelium can
be the result of valvular lesions, which create areas of non-laminar blood
flow, or jet lesions resulting from ventricular septal defects or a patent
ductus arteriosus. Infective endocarditis is less likely to develop where
the haemodynamic disturbance is minimal (i.e. low-pressure systems).
Hence it is more common in ventricular septal defects than atrial septal
defects, and rare in mitral valve prolapse without significant
regurgitation.
Aortic and mitral valves are the commonest valves to be affected. Rightsided endocarditis is typically related to intravenous drug use, although
the exact pathological mechanisms that underlie this association are not
fully known. It may be that damage to right -sided valves results from the
injected particulate matter used to cut the drugs. Instrumentation of the
right heart (central venous catheter and temporary pacemaker insertion) is
also a common cause of right-sided endocarditis.
Virulent pathogens such as Staphylococcus aureus and Streptococcus
pneumoniae may adhere and multiply on previously normal valves.
Microbiology
Over three-quarters of cases are due to streptococci or staphylococci.
The viridans group of streptococci (Strep.mitis, Strep. sanguis) are
commensals in the upper respiratory .
Other organisms, including Enterococcus faecalis, E. faecium and Strep.
bovis, may enter the blood from the bowel or urinary tract.
Staph. aureus has now overtaken streptococci as the most common cause
of acute endocarditis. It originates from skin infections, abscesses or
vascular access sites (e.g. intravenous and central lines), or from
intravenous drug misuse. 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. There is frequently a history of post-operative
wound infection with the same organism. Staph. epidermidis occasionally
causes endocarditis in patients who have not had cardiac surgery, and its
presence in blood cultures may be contamination.
In Q fever endocarditis due to Coxiella burnetii, the patient often has a
history of contact with farm animals.
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.
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)
Clinical presentation
Patients can present with an acute illness and the classic features of a new
or changing heart murmur and a fever. However, they may present with a
subacute insidious illness. A high index of suspicion for the possibility of
endocarditis is therefore required;
Clinical signs tend to arise from the following pathological processes:
systemic features of infection; cardiac lesions; embolization, and immune
complex deposition
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
haemorrhages under the fingernails or toe nails. Osler’s nodes are painful
tender swellings at the fingertips that are probably the product of
vasculitis. 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. Abscesses may be detected on echocardiography.
Partially treated acute endocarditis behaves like subacute endocarditis.
Post-operative endocarditis
This may present as an unexplained fever in a patient who has had heart
valve surgery. The infectio may resemble subacute or acute endocarditis,
depending on the virulence of the organism.Morbidity and mortality are
high and redo surgery is required.
Investigations
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
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 key for detecting and following the progress of
vegetations, for assessing valve damage and for detecting abscess
formation. The sensitivity of transthoracic echo is approximately 65% but
that of transoesophageal echo is more than 90%. 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.
Principles of therapy
Therapy of endocarditis is difficult because organisms reside within a
protected site within the vegetation. High concentrations of intravenous
antibiotic are required for prolonged periods to achieve successful
treatment. Where possible, synergistic combinations of antibiotics are
used, in order to maximize the microbiocidal effect. This is best achieved
by a multidisciplinary approach consisting of clinicians, cardiologists,
cardiothoracic surgeons and microbiologists.
Drug therapy Empirical antibiotic treatment is started only after cultures
are taken. The regimen is then adjusted according to culture results. The
treatment should continue for 4-6 weeks, although studies of 2-week,
short-course therapy have shown that it is highly effective in
uncomplicated penicillin-sensitive Strep, viridans endocarditis. Typical
therapeutic regimens are shown in Table below.
Serum levels of gentamicin and vancomycin need to be monitored. In
patients with penicillin allergy one of the glycopeptide antibiotics,
vancomycin or teicoplanin, can be used. Penicillins, however, are
fundamental to the therapy of bacterial endocarditis; allergies therefore
seriously compromise the choice of antibiotics.
Persistent fever
Most patients with infective endocarditis should respond within 48 hours
of initiation of appropriate antibiotic therapy. This is evidenced by a
resolution of fever, reduction in serum markers of infection (CRP tends to
be the most sensitive) and relief of systemic symptoms of infection.
Failure of this to occur needs to be taken very seriously. The following
should be considered:
■perivalvular extension of infection and possible abscess formation
■drug reaction (the fever should promptly resolve after drug withdrawal)
■nosocomial infection (i.e. venous access site, UTI)
■pulmonary embolism(as a consequence of right-sided endocarditis or
prolonged hospitalization).
In such cases, samples for culture should be taken from all possible sites
and evidence sought for the above causes. Changing antibiotic dosage or
regimen should be avoided unless there are positive cultures or a drug
reaction is suspected.
Surgery
Surgical intervention should be considered in the following cases:
• 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
Prevention
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.