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When should you suspect endocarditis

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  • When should you suspect endocarditis

    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
    Knowledge is power ... Stay informed!
    YOU can make a difference - all you have to do is try!

    Dx age 12 current age 46 and counting!
    lost: 5 family members to HCM (SCD, Stroke, CHF)
    Others diagnosed living with HCM (or gene +) include - daughter, niece, nephew, cousin, sister and many many friends!
    Therapy - ICD (implanted 97, 01, 04 and 11, medication
    Currently not obstructed
    Complications - unnecessary pacemaker and stroke (unrelated to each other)

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