• Infective endocarditis
is due to microbial infection of the heart valve (native or
prosthetic), the lining of the heart chamber or blood vessel
or a congenital anomaly e.g.
septal defect.
• The causative
organisms are
Streptococcus viridans 30-40%
Enterococci 10-15%
Other Streptococci 20-25%
Staphylococcus aureus 9-27%
Gram negative bacilli
Haemophilus spp
Anaerobes
• There are two
types of infective endocarditis namely acute and sub-acute endocarditis.
Acute endocarditis caused by virulent organisms and infection
occurs in normal
valves and endocardium.
Sub-acute endocarditis caused by less virulent organisims
and infection more
commonly in the damaged valves and endocardium.
Pathophysiology
• Infective
endocarditis typically occurs at sites of pre-existing endocardial damage.
• Virulent or
aggressive organisms e.g. Staphylococcus aureus can
cause endocarditis in a
previously normal heart such as in intravenous drug misuse.
• 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.
• The affected
valves develop vegetations composed of organisms, fibrin and platelets and
the vegetation may become large enough to cause obstruction
or may break away as
emboli. Regurgitations may develop or increase.
Clinical
Features, Differential Diagnosis and Investigations of Sub-acute
Bacterial
Endocarditis
Clinical Features
• Persistent fever
• Complain of
unusual tiredness
• Night sweats
• Weight loss
• Development of
new signs of valve dysfunction
• Infective
endocarditis should be considered when a patient with congenital or valvular
heart disease develops some of features mentioned above.
• In patients with
sub acute presentations
Fever is typically low-grade and rarely exceeds 39.4°C
(103°F).
In contrast, temperatures between 39.4 and 40°C (103 and
104°F) are often noted in
acute endocarditis.
• In acute
endocarditis involving a normal valve, murmurs are heard on presentation in only
30 to 45% of patients but ultimately are detected in 85%.
• Congestive heart
failure develops in 30 to 40% of patients; it is usually a consequence of
valvular dysfunction.
• Occasionally
endocarditis-associated myocarditis or an intracardiac fistula may cause
congestive heart failure.
• 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
(rare).
Painful and tender swellings at the fingertips.
Probably the product of vasculitis.
• Digital clubbing
is a late sign.
• The spleen is
frequently palpable, in coxiella infections the spleen and the liver may be
considerably enlarged.
• Microscopic
hematuria is common.
Differential Diagnosis
• Rheumatic Heart
Disease
• Congenital Heart
Disease
• Myocardial
Infarction
• Congestive
Cardiac failure
• Septicaemia
Investigations
• It is better
that patient suspected of having endocarditis be referred for specific
investigations at hospital level. This is because facilities
for such diagnosis are lacking in
the primary health care facilities (dispensary and health
centre).
• Investigations
done at hospital levels include
Blood culture
FBP and ESR
Chest X-ray
Echocardiography
ECG
Duke Criteria for Diagnosis of
Infective Endocarditis
Major Criteria
Positive Blood culture for Infective Endocarditis
• Typical
microorganism consistent with IE from 2 separate blood cultures, as noted
below:
viridans streptococci, Streptococcus bovis,
or HACEK group (H. parainfluenzae,
Actinobacillus
actinomycetemcomitans, Cardiobacterium hominis, Eikenella
corrodens, Kingellae kingae)
or
community-acquired Staphylococcus aureus or
enterococci, in the absence of a
primary focus
Or
• Microorganisms
consistent with IE from persistently positive blood cultures defined as:
2 positive cultures of blood samples drawn >12 hours
apart, or
all of 3 or a majority of 4 separate cultures of blood (with
first and last sample drawn
1 hour apart)
Evidence of endocardial
involvement
• Positive
echocardiogram for IE defined as :
oscillating intracardiac mass on valve or supporting
structures, in the path of
regurgitant jets, or on implanted material in the absence of
an alternative anatomic
explanation, or
abscess, or
new partial dehiscence of prosthetic valve
Or
• New valvular
regurgitation (worsening or changing of preexisting murmur not sufficient)
Minor Criteria
Predisposition:
predisposing heart condition or intravenous drug use
Fever: temperature >
38.0° C (100.4° F)
Vascular phenomena:
major arterial emboli, septic pulmonary infarcts, mycotic aneurysm,
intracranial hemorrhage, conjunctival hemorrhages, and
Janeway lesions.
Immunologic phenomena:
glomerulonephritis, Osler's nodes, Roth spots (white-centered
retinal haemorrhages), and rheumatoid factor.
Microbiological evidence:
positive blood culture but does not meet a major criterion as
noted above (Excludes single positive cultures for
coagulase-negative staphylococci,
diphtheroids, and organisms that do not commonly cause
endocarditis) or serological
evidence of active infection with organism consistent with
IE.
Echocardiographic findings:
consistent with IE but do not meet a major criterion as noted
above
Clinical criteria for infective
endocarditis requires
• Two major
criteria, or
• One major and
three minor criteria, or
• Five minor
criteria
Treatment,
Prevention and Complications of Sub-acute Bacterial
Endocarditis
Treatment
• Refer the
patient immediately after initial antibiotic doses for expert care.
• 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.
• 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.
• In sub-acute or
indolent presentation, benzyl penicillin and gentamicin can be used.
• Those with
penicillin allergy, a prosthetic valve or suspected Methicillin Resistant
Staphylococcus aureus (MRSA)
infection, should be treated with vancomycin and
gentamicin.
• The duration of
treatment is usually 4-6 weeks with intravenous antibiotics.
Doses
• Benzylpenicillin
(Penicillin G) - 7.2g daily IV in 6 divided doses. In children, 75-
100mg/kg daily in divided doses.
• Ampicillin 500mg
IV every 4-6 hours
• Gentamycin
3-5mg/kg daily in divided doses every 8 hours.
• Vancomycin 500mg
IV infusion over at least 60 minutes every 6 hours or 1g over at least
100m minutes every 12 hours. In children 10-15mg/kg every
6-12 hours.
• Flucloxacillin
12g daily in 6 divided doses
Prevention
• Make sure that
antibiotics have been administered in conjunction with selected
procedures considered to entail a risk for bacteremia and
endocarditis.
• Maintaining good
oral hygiene is probably more effective in the overall prevention of
valvular infection because gingivitis is the most common
source of spontaneous
bacteremia.
• Prevention of
vascular catheter infections is an important prophylactic approach in
preventing nosocomial infective endocarditis (NIE).
Complications
• Monitor patients
for the development of the following complications.
Valvular dysfunction, usually insufficiency of the mitral or
aortic valves
Myocardial or septal abscesses
Congestive heart failure
Metastatic infection
Embolic phenomenon
Organ dysfunction resulting from immunological processes.
Congestive heart failure resulting from valvular
insufficiency and embolization may
occur after bacteriologic cure has been achieved.
REFFERNCES;
Braunwald &
Fauci (2001). Harrison’s principles of internal medicine 15th Ed. Oxford: McGraw Hill
Davidson, S
(2006). Principles and practice of medicine 20th Ed. Churchill: Livingstone.
Kumar &
Clark (2003) Textbook of clinical medicine. Churchill: Livingstone.
Douglas Model (2006): Making sense of Clinical
Examination of the Adult patient. 1st Ed. Hodder Arnold
Longmore, M., Wilkinson, I., Baldwin, A., &
Wallin, E. (2014). Oxford handbook of clinical medicine. Oxford
Macleod, J. (2009). Macleod's clinical
examination. G. Douglas, E. F. Nicol, & C. E. Robertson (Eds.).
Elsevier Health Sciences.
Nicholson N., (1999), Medicine of Non-communicable
diseases in adults. AMREF
Stuart and Saunders (2004): Mental health Nursing
principles and practice. 1st Ed. Mosby
Swash, M., &
Glynn, M. (2011). Hutchison's clinical methods: An integrated approach to
clinical practice.

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