Lisa Salberg
03-11-2003, 04:04 PM
March 3, 2003
SECTION: Pg. 162
LENGTH: 3137 words
HEADLINE: When should you suspect endocarditis?
BODY:
* When should the GP suspect infective endocarditis in practice?
* Why is prompt diagnosis and referral essential?
* What prophylaxis should be given to which patients?
SHRILLA BANERJEE MD, MRCP, Specialist Registrar in Cardiology, The Heart
Hospital, UCLH NHS Trust, London
R HOWARD SWANTON MA, MD, FRCP, FESC, Consultant Cardiologist, The Heart
Hospital, UCLH NHS Trust, London
Infective endocarditis is an infection of the heart valves or other
endothelial surfaces of the heart. The lesion or vegetation represents a mass of
fibrin, platelets, inflammatory cells and microorganisms. Vegetations usually
occur on heart valves, normal or diseased, and can occur in septal defects,
chordae tendinae and mural surfaces.
The clinical presentation is often non-specific, and infective endocarditis
should be high up on the list of differential diagnoses, especially in patients
with congenital heart defects, previous endocarditis and prosthetic heart
valves.
Prompt diagnosis and referral are essential, as the morbidity and mortality
associated with this condition is high - in some categories of patients,
mortality may be as high as 50 per cent.
In this review we discuss the epidemiology, diagnosis, management and
recommended prophylaxis for this important group of patients.
* Epidemiology The incidence worldwide varies between 1.7-6.2 per 100,000
patient years. Current estimates of the incidence1 in England and Wales are 2.0
per 100,000 population, equating to 1500-2000 cases annually.
The condition is multifaceted: it can occur on undiseased or diseased heart
valves, prosthetic or native valves. Men are more commonly affected than women
(ratio 1.7:1). In our ageing population degenerative valve disease is becoming
more commonly observed and hence the median age of those affected has risen to
47-69 years.2 However, endocarditis in intravenous drug abusers (IVDA) tends to
occur in younger age groups.
Many conditions predispose to infection with endocarditis (see table 1).
Predisposing conditions may be identified in 25-45 per cent of patients.
* Causative organisms and associated mortality rates The commonest cause of
native valve endocarditis is the viridans group of streptococci, which cause 50
per cent of endocarditis episodes, and are commonly found in the oral and
respiratory tracts.
Infection with Staphylococcus aureus infection is found in 20 per cent of
all episodes overall; however, in IVDA 50-60 per cent of episodes are related to
infection with S aureus.3
Mortality rates vary depending on the causative organism. Mortality with
viridans group streptococci and Streptococcus bovis varies between 4-16 per
cent. Cases of endocarditis associated with enterococcal infection have
mortality rates of between 15-25 per cent. S aureus cases have associated
mortality rates of 25-47 per cent.4 Endocarditis caused by fungal infections
will result in death in 50 per cent of patients.3
Prosthetic valve endocarditis (PVE) can occur early (usually within the
first two months, but up to one year) or late (more than one year after surgery)
and is usually associated with characteristic pathogens.5
The pathogen in early PVE is often coagulase-negative staphylococcus, and is
thought to be due to intra-operative contamination. Late infections are
associated with viridans group streptococci, S aureus or coagulase-negative
staphylococci6 (see table 2 for possible routes of entry).
* Clinical presentation Fever is the most common manifestation of infection
with endocarditis, but may be absent or minimal in the elderly or those with
comorbidities including congestive heart failure, chronic renal impairment or
severe debility, or in patients already partially treated with antibiotics.
Constitutional symptoms including weight loss, anorexia and malaise are
common.
Pallor due to anaemia may be present.
Heart murmurs are found in 80-85 per cent of patients with native valve
endocarditis and may be new or changing.7
Petechiae may be found in the conjunctiva, buccal and palatal mucosa.
Splinter haemorrhages (see figure 1) are dark red or brown lines found in
the nail beds of both the fingers and toes. They are often related to trauma and
hence innocent, but in the setting of a patient with a persistent fever and a
murmur they should be addressed.
Osler's nodes are small tender subcutaneous nodules found in the nail pulps,
and may persist for hours or days.
Janeway lesions are non-tender erythematous, sometimes haemorrhagic or
pustular, lesions found on the palms and soles. They are the result of septic
emboli.
Roth spots occur in more fulminant forms of the condition; these are
described as boat-shaped haemorrhages with a pale centre.
Septic emboli occur in up to 40 per cent of patients. The emboli may deposit
anywhere including the coronary arteries, spleen, brain, kidney, retina (see
figure 2) or lungs (right-heart endocarditis).
Embolic stroke classically involves the middle cerebral artery territory.
Neurological symptoms including confusion and stupor, meningism, seizures and
focal neurological deficits are often a result of septic emboli.
Emboli are more common in patients with S aureus endocarditis.
Heart failure is associated with endocarditis resulting in severe valvular
destruction or destruction of the valvar apparatus (chordae tendinae). This
presentation is associated with a very severe outcome if not treated rapidly
with surgical intervention.
Renal impairment may be due to immune-complex deposition and presents with
haematuria.7
Splenomegaly is found in 15-50 per cent of patients, more commonly in those
with a prolonged disease course and sub-acute presentation. It is often found in
association with clubbing.
Patients may present with any combination of these signs and symptoms and
hence the diagnosis is usually difficult. The most important thing to watch out
for is unexplained constitutional symptoms in a patient with either high or
medium risk cardiac abnormalities (see table 1).
Remember to ask about recent procedures, especially dental, and any new skin
lesions, which the patient will often fail to mention as they are felt to be
unrelated.
The prescription of antibiotics should be avoided. Instead thought should be
given regarding further urgent referral and investigation.
* Investigations A number of investigations are indicated in suspected
endocarditis:
* Microbiology Three separate blood culture samples from different sites and
at peak fever should be taken. Clinicians must state the suspicion of
endocarditis on the request form to allow the appropriate cultures to be
performed. Previous therapy with antibiotics reduces the rate of detection to
35-40 per cent.
Approximately ten per cent of all endocarditis is culture-negative.8 In
these cases, prolonged cultures and serological testing may be helpful.9
* Blood tests The erythrocyte sedimentation rate (ESR) and C-reactive protein
(CRP) are both helpful in differentiating transient infection from persistent
infection such as endocarditis. Anaemia with an elevated neutrophil count and
ESR are common.
* Urinanalysis Proteinuria and microscopic haematuria are found in 50 per
cent of patients with endocarditis, even while the renal function may be normal.
* Echocardiography Trans-thoracic echocardiography provides adequate imaging
of vegetations in 98 per cent of cases of endocarditis. However, in certain
patients with prosthetic valve endocarditis or aortic valve involvement
trans-oesophageal echocardiography (TOE) is superior to transthoracic
imaging.10,11
* Electrocardiogram The ECG may demonstrate prolonging PR intervals and new
bundle branch block indicative of infection infiltrating the conduction
pathways.
* Who should be referred, and when? Patients in the high and moderate risk
categories12,13 (see table 1) who have fever with weight loss and other
constitutional symptoms, should be referred as soon as possible to a
cardiologist for assessment.
If they are following a less acute course with a more diffuse diagnosis,
then blood cultures, blood tests for inflammatory markers and an urgent
outpatient echocardiogram should be organised.
Patients will be rapidly referred on to a cardiothoracic centre with the
facilities for TOE and surgical intervention.
* Treatment This will depend on the presentation, the organism and the
sensitivity to antibiotics. In a few patients it is possible to treat with a
course of oral antibiotics with outpatient hospital monitoring. However, the
majority will need an in-patient stay with therapy tailored to the particular
causative organism.
* Outcomes The overall mortality for endocarditis, both native valve and
prosthetic valve, is 20-25 per cent.14,15 Death is usually a result of emboli to
the central nervous system, or severe haemodynamic compromise. Right-sided
endocarditis mortality rates are around ten per cent.
Relapse of infection usually occurs within two months of stopping therapy.
Rates of relapse vary with the pathogen, with the highest rates in patients with
enteroccocal infections. The prosthetic valve endocarditis relapse rate is 10-15
per cent.
* Prophylaxis should be provided to all patients with cardiac lesions in the
high and moderate risk groups (see table 1) who are undergoing the following:
* Any dental work;
* Any surgical procedure;
* Cystoscopy and urinary tract instrumentation;
* Trans-rectal prostatic biopsy; and
* Insertion of permanent pacemakers.
It is safer to advise patients to have prophylactic antibiotics prior to
every dental procedure. The same antibiotic regime should not be used within a
month. Chlorhexidine gel and mouthwashes significantly reduce the bacteraemia
associated with dental work.
The antibiotic regime shown in table 5 is recommended by the British Society
for Antimicrobial Chemotherapy.
* The future The International Collaboration on Endocarditis is developing a
large global database of patients with endocarditis to guide future management
of patients with this condition.
Most available data is of limited quality arising from case reports and
retrospective reviews of cases. This important collaboration will eventually
provide randomised controlled trial evidence on varying therapeutic strategies
to guide our management.
CLINICAL FOCUS
* Infective endocarditis can occur on undiseased or diseased heart valves,
prosthetic or native valves. Men are more often affected than women. In our
ageing population degenerative valve disease is becoming more common and the
median age of those affected has risen to 47-69 years
* The clinical presentation is frequently non-specific, and infective
endocarditis should be high up on the list of differential diagnoses, especially
in those patients with congenital heart defects, previous endocarditis and
prosthetic heart valves
* Fever is the most common manifestation of infection with endocarditis, but
may be absent or minimal in the elderly or those with comorbidities.
Constitutional symptoms including weight loss, anorexia and malaise are common.
Pallor due to anaemia may be present. Heart murmurs are found in 80-85 per cent
of patients with native valve endocarditis and may be new or changing. Petechiae
may be found in the conjunctiva, buccal and palatal mucosa
* Prompt diagnosis and referral are essential, as the morbidity and mortality
associated with this condition is high - in some categories of patients,
mortality may be as high as 50 per cent
* Prophylaxis should be provided to all patients with cardiac lesions in high
and moderate risk groups who are undergoing the following: any dental work; any
surgical procedure; cystoscopy and urinary tract instrumentation; trans-rectal
prostatic biopsy; and insertion of permanent pacemakers. It is safer to advise
patients to have prophylactic antibiotics prior to every dental procedure. The
same antibiotic regime should not be used within a month
Table 1 Conditions predisposing to infective endocarditis
CARDIAC CONDITIONS
High risk
* Previous infective endocarditis
* Aortic valve disease
* Rheumatic heart disease
* Prosthetic heart valve
* Coarctation of the aorta
* Complex cyanotic congenital heart disease
Medium risk
* Mitral valve prolapse with regurgitation or thickened leaflets
* Isolated mitral stenosis
* Tricuspid valve disease
* Pulmonary stenosis
* Hypertrophic cardiomyopathy
Low or no risk
* Secundum atrial septal defect
* Ischaemic heart disease
* Previous coronary artery bypass grafts
* Mitral valve prolapse without regurgitation and with thin
leaflets
Non-cardiac conditions
* Poor dental hygiene
* Intravenous drug users
* Systemic sepsis
* Diabetes mellitus
* Haemodialysis
* Immunosuppression
Table 2 Routes of entry of causative organisms
* Dental work - even a routine scale and polish may be sufficient
* Poor dental hygiene or badly fitting dentures
* Urinary tract infection or instrumentation
* Respiratory tract infection
* Bowel lesions, including carcinoma of the colon (classically
treptococcus bovis)
* Skin lesions - purulent lesions, wound infections, leg ulcers,
burns
* Intravenous drug abuse
* Chronic haemodialysis
* Gall bladder disease
* Surgery
Table 3 The Modified Duke Criteria for diagnosing endocarditis
Definite cases require two of the major criteria, or either one major and
three minor criteria, or five minor criteria
Possible cases require one major and one minor criterion, or three minor
criteria
Major criteria:
* Two or more positive blood cultures with typical disease-causing bacteria,
eg viridans group
* Echocardiographic demonstration of vegetations, or new para- prosthetic
leak/dehiscence
Minor criteria:
* Cardiac conditions predisposing to endocarditis or intravenous drug abuse
(see table 1)
* Fever >38degC
* Vascular phenomena, excluding petechiae and splinter haemorrhages
* Immunological phenomena, including rheumatoid factor, Osler's nodes,
glomerulonephritis, Roth's spots
* Microbiological findings, including positive blood cultures not meeting
major criteria, and serological evidence of infection
Table 4 Differential diagnosis of endocarditis
* Polymyalgia rheumatica
* Collagen vascular disease
* Atrial myxoma
* Malignancy
* Sarcoid
* Drug reactions
Table 5 Antibiotic cover for patients with congenital heart disease or
acquired valve disease receiving dental treatment or any operative procedure
Without anaesthetic or under local anaesthesia
* Amocicillin 3g orally one hour before procedure.
* For patients allergic to penicillin or who have had amoxicillin in the last
month: either clindamycin 600mg as a single dose one hour before procedure; or
erythromycin stearate 1.5g orally before procedure plus 0.5g six hours later.
The 1.5g dose may cause nausea and the single dose of clindamycin is better
tolerated.
* For children: age 5-10 years, halve adult doses for all three drugs above
age <5 years, one-quarter of the adult dose
Under general anaesthetic
* Ampicillin 1g iv with premedication (or amoxicillin 1g in 2.5mL 1%
lignocaine im) plus 0.5g orally six hours later
* For patients allergic to penicillin or who have had amoxicillin or
ampicillin in the last month: either vancomycin 1g slowly iv over
* 100 mins plus gentamicin 120mg iv just before induction; or teicoplanin
400mg iv plus gentamicin 120mg iv just before induction (this is the easiest
regime); or clindamycin 300mg in 50mL normal saline over 10 mins iv just before
induction followed by clindamycin 150mg orally or by iv injection over 10 mins
six hours later (this is not suitable for patients undergoing pelvic
instrumentation, genitourinary or gastrointestinal procedures)
* For children: either vancomycin 20mg/kg plus gentamicin 2mg/kg iv; or
clindamycin 150mg iv (age 5-10 years) or 75mg iv (age <5 years) diluted as above
Special risk patients
* Patients with prosthetic heart valves or history of previous infective
endocarditis: ampicillin 1g plus gentamicin 120mg iv with premedication plus
amoxicillin 0.5g orally at six hours
* For penicillin allergy use regime described for Under general anaesthetic'
above
References
1 Mylonakis E, Calderwood SB. Infective endocarditis in adults. N Engl J Med
2001;345:1318-1330
2 Cabell CH, Jollis JG, Peterson GE et al. Changing patient characteristics
and the effect on mortality in endocarditis. Arch Intern Med 2002;162:90-94
3 Cabell CH, Abrutyn E. Progress toward a global understanding of infective
endocarditis. Early lessons from the International Collaboration on Endocarditis
investigation. Infect Dis Clin North Am 2002;16:255-272
4 Management of infective endocarditis. Drug Ther Bull 2002;40(4):26-30
5 Calderwood SB, Swinski LA, Karchmer AW et al. Prosthetic valve
endocarditis: analysis of factors affecting outcome of therapy. J Thorac
Cardiovasc Surg 1986;92:776-783
6 Eykyn SJ. Valve disease - endocarditis: basics. Heart 2001;86:476-480
7 Bayer AS, Bolger AF, Taubert KA et al. Diagnosis and management of
infective endocarditis and its complications. Circulation 1998;98:2936-2948
8 Hoen B, Selton-Suty C, Lacassin F et al. Infective endocarditis in
patients with negative blood cultures: analysis of 88 cases from a one- year
nationwide survey in France. Clin Infect Dis 1995;20:501-506
9 Prendergast BD. Diagnosis of infective endocarditis. BMJ 2002;325:845-846
10 Sachdev M, Peterson GE, Jollis JG. Imaging techniques for diagnosis of
infective endocarditis. Infect Dis Clin North Am 2002;16:319-337
11 Shively BK, Gurule FT, Roldan CA et al. Diagnostic value of
transesophageal compared with transthoracic echocardiography in infective
endocarditis. J Am Coll Cardiol 1991;18:391-397
12 Li JS, Sexton DJ, Mick N et al. Proposed modifications to the Duke
criteria for the diagnosis of infective endocarditis. Clin Infect Dis
2000;30:633-638
13 Durack DT, Lukes AS, Bright DK. New criteria for diagnosis of infective
endocarditis: utilization of specific echocardiographic findings. Am J Med
1994;96:200-209
14 Wallace SM, Walton BI, Kharbanda RK et al. Mortality from infective
endocarditis: clinical predictors of outcome. Heart 2002;88:53-60
15 Alexiou C, Langley SM, Stafford H et al. Surgery for active culture-
positive endocarditis: determinants of early and late outcome. Ann Thorac Surg
2000;69:1448-1454
SECTION: Pg. 162
LENGTH: 3137 words
HEADLINE: When should you suspect endocarditis?
BODY:
* When should the GP suspect infective endocarditis in practice?
* Why is prompt diagnosis and referral essential?
* What prophylaxis should be given to which patients?
SHRILLA BANERJEE MD, MRCP, Specialist Registrar in Cardiology, The Heart
Hospital, UCLH NHS Trust, London
R HOWARD SWANTON MA, MD, FRCP, FESC, Consultant Cardiologist, The Heart
Hospital, UCLH NHS Trust, London
Infective endocarditis is an infection of the heart valves or other
endothelial surfaces of the heart. The lesion or vegetation represents a mass of
fibrin, platelets, inflammatory cells and microorganisms. Vegetations usually
occur on heart valves, normal or diseased, and can occur in septal defects,
chordae tendinae and mural surfaces.
The clinical presentation is often non-specific, and infective endocarditis
should be high up on the list of differential diagnoses, especially in patients
with congenital heart defects, previous endocarditis and prosthetic heart
valves.
Prompt diagnosis and referral are essential, as the morbidity and mortality
associated with this condition is high - in some categories of patients,
mortality may be as high as 50 per cent.
In this review we discuss the epidemiology, diagnosis, management and
recommended prophylaxis for this important group of patients.
* Epidemiology The incidence worldwide varies between 1.7-6.2 per 100,000
patient years. Current estimates of the incidence1 in England and Wales are 2.0
per 100,000 population, equating to 1500-2000 cases annually.
The condition is multifaceted: it can occur on undiseased or diseased heart
valves, prosthetic or native valves. Men are more commonly affected than women
(ratio 1.7:1). In our ageing population degenerative valve disease is becoming
more commonly observed and hence the median age of those affected has risen to
47-69 years.2 However, endocarditis in intravenous drug abusers (IVDA) tends to
occur in younger age groups.
Many conditions predispose to infection with endocarditis (see table 1).
Predisposing conditions may be identified in 25-45 per cent of patients.
* Causative organisms and associated mortality rates The commonest cause of
native valve endocarditis is the viridans group of streptococci, which cause 50
per cent of endocarditis episodes, and are commonly found in the oral and
respiratory tracts.
Infection with Staphylococcus aureus infection is found in 20 per cent of
all episodes overall; however, in IVDA 50-60 per cent of episodes are related to
infection with S aureus.3
Mortality rates vary depending on the causative organism. Mortality with
viridans group streptococci and Streptococcus bovis varies between 4-16 per
cent. Cases of endocarditis associated with enterococcal infection have
mortality rates of between 15-25 per cent. S aureus cases have associated
mortality rates of 25-47 per cent.4 Endocarditis caused by fungal infections
will result in death in 50 per cent of patients.3
Prosthetic valve endocarditis (PVE) can occur early (usually within the
first two months, but up to one year) or late (more than one year after surgery)
and is usually associated with characteristic pathogens.5
The pathogen in early PVE is often coagulase-negative staphylococcus, and is
thought to be due to intra-operative contamination. Late infections are
associated with viridans group streptococci, S aureus or coagulase-negative
staphylococci6 (see table 2 for possible routes of entry).
* Clinical presentation Fever is the most common manifestation of infection
with endocarditis, but may be absent or minimal in the elderly or those with
comorbidities including congestive heart failure, chronic renal impairment or
severe debility, or in patients already partially treated with antibiotics.
Constitutional symptoms including weight loss, anorexia and malaise are
common.
Pallor due to anaemia may be present.
Heart murmurs are found in 80-85 per cent of patients with native valve
endocarditis and may be new or changing.7
Petechiae may be found in the conjunctiva, buccal and palatal mucosa.
Splinter haemorrhages (see figure 1) are dark red or brown lines found in
the nail beds of both the fingers and toes. They are often related to trauma and
hence innocent, but in the setting of a patient with a persistent fever and a
murmur they should be addressed.
Osler's nodes are small tender subcutaneous nodules found in the nail pulps,
and may persist for hours or days.
Janeway lesions are non-tender erythematous, sometimes haemorrhagic or
pustular, lesions found on the palms and soles. They are the result of septic
emboli.
Roth spots occur in more fulminant forms of the condition; these are
described as boat-shaped haemorrhages with a pale centre.
Septic emboli occur in up to 40 per cent of patients. The emboli may deposit
anywhere including the coronary arteries, spleen, brain, kidney, retina (see
figure 2) or lungs (right-heart endocarditis).
Embolic stroke classically involves the middle cerebral artery territory.
Neurological symptoms including confusion and stupor, meningism, seizures and
focal neurological deficits are often a result of septic emboli.
Emboli are more common in patients with S aureus endocarditis.
Heart failure is associated with endocarditis resulting in severe valvular
destruction or destruction of the valvar apparatus (chordae tendinae). This
presentation is associated with a very severe outcome if not treated rapidly
with surgical intervention.
Renal impairment may be due to immune-complex deposition and presents with
haematuria.7
Splenomegaly is found in 15-50 per cent of patients, more commonly in those
with a prolonged disease course and sub-acute presentation. It is often found in
association with clubbing.
Patients may present with any combination of these signs and symptoms and
hence the diagnosis is usually difficult. The most important thing to watch out
for is unexplained constitutional symptoms in a patient with either high or
medium risk cardiac abnormalities (see table 1).
Remember to ask about recent procedures, especially dental, and any new skin
lesions, which the patient will often fail to mention as they are felt to be
unrelated.
The prescription of antibiotics should be avoided. Instead thought should be
given regarding further urgent referral and investigation.
* Investigations A number of investigations are indicated in suspected
endocarditis:
* Microbiology Three separate blood culture samples from different sites and
at peak fever should be taken. Clinicians must state the suspicion of
endocarditis on the request form to allow the appropriate cultures to be
performed. Previous therapy with antibiotics reduces the rate of detection to
35-40 per cent.
Approximately ten per cent of all endocarditis is culture-negative.8 In
these cases, prolonged cultures and serological testing may be helpful.9
* Blood tests The erythrocyte sedimentation rate (ESR) and C-reactive protein
(CRP) are both helpful in differentiating transient infection from persistent
infection such as endocarditis. Anaemia with an elevated neutrophil count and
ESR are common.
* Urinanalysis Proteinuria and microscopic haematuria are found in 50 per
cent of patients with endocarditis, even while the renal function may be normal.
* Echocardiography Trans-thoracic echocardiography provides adequate imaging
of vegetations in 98 per cent of cases of endocarditis. However, in certain
patients with prosthetic valve endocarditis or aortic valve involvement
trans-oesophageal echocardiography (TOE) is superior to transthoracic
imaging.10,11
* Electrocardiogram The ECG may demonstrate prolonging PR intervals and new
bundle branch block indicative of infection infiltrating the conduction
pathways.
* Who should be referred, and when? Patients in the high and moderate risk
categories12,13 (see table 1) who have fever with weight loss and other
constitutional symptoms, should be referred as soon as possible to a
cardiologist for assessment.
If they are following a less acute course with a more diffuse diagnosis,
then blood cultures, blood tests for inflammatory markers and an urgent
outpatient echocardiogram should be organised.
Patients will be rapidly referred on to a cardiothoracic centre with the
facilities for TOE and surgical intervention.
* Treatment This will depend on the presentation, the organism and the
sensitivity to antibiotics. In a few patients it is possible to treat with a
course of oral antibiotics with outpatient hospital monitoring. However, the
majority will need an in-patient stay with therapy tailored to the particular
causative organism.
* Outcomes The overall mortality for endocarditis, both native valve and
prosthetic valve, is 20-25 per cent.14,15 Death is usually a result of emboli to
the central nervous system, or severe haemodynamic compromise. Right-sided
endocarditis mortality rates are around ten per cent.
Relapse of infection usually occurs within two months of stopping therapy.
Rates of relapse vary with the pathogen, with the highest rates in patients with
enteroccocal infections. The prosthetic valve endocarditis relapse rate is 10-15
per cent.
* Prophylaxis should be provided to all patients with cardiac lesions in the
high and moderate risk groups (see table 1) who are undergoing the following:
* Any dental work;
* Any surgical procedure;
* Cystoscopy and urinary tract instrumentation;
* Trans-rectal prostatic biopsy; and
* Insertion of permanent pacemakers.
It is safer to advise patients to have prophylactic antibiotics prior to
every dental procedure. The same antibiotic regime should not be used within a
month. Chlorhexidine gel and mouthwashes significantly reduce the bacteraemia
associated with dental work.
The antibiotic regime shown in table 5 is recommended by the British Society
for Antimicrobial Chemotherapy.
* The future The International Collaboration on Endocarditis is developing a
large global database of patients with endocarditis to guide future management
of patients with this condition.
Most available data is of limited quality arising from case reports and
retrospective reviews of cases. This important collaboration will eventually
provide randomised controlled trial evidence on varying therapeutic strategies
to guide our management.
CLINICAL FOCUS
* Infective endocarditis can occur on undiseased or diseased heart valves,
prosthetic or native valves. Men are more often affected than women. In our
ageing population degenerative valve disease is becoming more common and the
median age of those affected has risen to 47-69 years
* The clinical presentation is frequently non-specific, and infective
endocarditis should be high up on the list of differential diagnoses, especially
in those patients with congenital heart defects, previous endocarditis and
prosthetic heart valves
* Fever is the most common manifestation of infection with endocarditis, but
may be absent or minimal in the elderly or those with comorbidities.
Constitutional symptoms including weight loss, anorexia and malaise are common.
Pallor due to anaemia may be present. Heart murmurs are found in 80-85 per cent
of patients with native valve endocarditis and may be new or changing. Petechiae
may be found in the conjunctiva, buccal and palatal mucosa
* Prompt diagnosis and referral are essential, as the morbidity and mortality
associated with this condition is high - in some categories of patients,
mortality may be as high as 50 per cent
* Prophylaxis should be provided to all patients with cardiac lesions in high
and moderate risk groups who are undergoing the following: any dental work; any
surgical procedure; cystoscopy and urinary tract instrumentation; trans-rectal
prostatic biopsy; and insertion of permanent pacemakers. It is safer to advise
patients to have prophylactic antibiotics prior to every dental procedure. The
same antibiotic regime should not be used within a month
Table 1 Conditions predisposing to infective endocarditis
CARDIAC CONDITIONS
High risk
* Previous infective endocarditis
* Aortic valve disease
* Rheumatic heart disease
* Prosthetic heart valve
* Coarctation of the aorta
* Complex cyanotic congenital heart disease
Medium risk
* Mitral valve prolapse with regurgitation or thickened leaflets
* Isolated mitral stenosis
* Tricuspid valve disease
* Pulmonary stenosis
* Hypertrophic cardiomyopathy
Low or no risk
* Secundum atrial septal defect
* Ischaemic heart disease
* Previous coronary artery bypass grafts
* Mitral valve prolapse without regurgitation and with thin
leaflets
Non-cardiac conditions
* Poor dental hygiene
* Intravenous drug users
* Systemic sepsis
* Diabetes mellitus
* Haemodialysis
* Immunosuppression
Table 2 Routes of entry of causative organisms
* Dental work - even a routine scale and polish may be sufficient
* Poor dental hygiene or badly fitting dentures
* Urinary tract infection or instrumentation
* Respiratory tract infection
* Bowel lesions, including carcinoma of the colon (classically
treptococcus bovis)
* Skin lesions - purulent lesions, wound infections, leg ulcers,
burns
* Intravenous drug abuse
* Chronic haemodialysis
* Gall bladder disease
* Surgery
Table 3 The Modified Duke Criteria for diagnosing endocarditis
Definite cases require two of the major criteria, or either one major and
three minor criteria, or five minor criteria
Possible cases require one major and one minor criterion, or three minor
criteria
Major criteria:
* Two or more positive blood cultures with typical disease-causing bacteria,
eg viridans group
* Echocardiographic demonstration of vegetations, or new para- prosthetic
leak/dehiscence
Minor criteria:
* Cardiac conditions predisposing to endocarditis or intravenous drug abuse
(see table 1)
* Fever >38degC
* Vascular phenomena, excluding petechiae and splinter haemorrhages
* Immunological phenomena, including rheumatoid factor, Osler's nodes,
glomerulonephritis, Roth's spots
* Microbiological findings, including positive blood cultures not meeting
major criteria, and serological evidence of infection
Table 4 Differential diagnosis of endocarditis
* Polymyalgia rheumatica
* Collagen vascular disease
* Atrial myxoma
* Malignancy
* Sarcoid
* Drug reactions
Table 5 Antibiotic cover for patients with congenital heart disease or
acquired valve disease receiving dental treatment or any operative procedure
Without anaesthetic or under local anaesthesia
* Amocicillin 3g orally one hour before procedure.
* For patients allergic to penicillin or who have had amoxicillin in the last
month: either clindamycin 600mg as a single dose one hour before procedure; or
erythromycin stearate 1.5g orally before procedure plus 0.5g six hours later.
The 1.5g dose may cause nausea and the single dose of clindamycin is better
tolerated.
* For children: age 5-10 years, halve adult doses for all three drugs above
age <5 years, one-quarter of the adult dose
Under general anaesthetic
* Ampicillin 1g iv with premedication (or amoxicillin 1g in 2.5mL 1%
lignocaine im) plus 0.5g orally six hours later
* For patients allergic to penicillin or who have had amoxicillin or
ampicillin in the last month: either vancomycin 1g slowly iv over
* 100 mins plus gentamicin 120mg iv just before induction; or teicoplanin
400mg iv plus gentamicin 120mg iv just before induction (this is the easiest
regime); or clindamycin 300mg in 50mL normal saline over 10 mins iv just before
induction followed by clindamycin 150mg orally or by iv injection over 10 mins
six hours later (this is not suitable for patients undergoing pelvic
instrumentation, genitourinary or gastrointestinal procedures)
* For children: either vancomycin 20mg/kg plus gentamicin 2mg/kg iv; or
clindamycin 150mg iv (age 5-10 years) or 75mg iv (age <5 years) diluted as above
Special risk patients
* Patients with prosthetic heart valves or history of previous infective
endocarditis: ampicillin 1g plus gentamicin 120mg iv with premedication plus
amoxicillin 0.5g orally at six hours
* For penicillin allergy use regime described for Under general anaesthetic'
above
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