11/14/24, 10\:59 AM Infective Endocarditis

Infective Endocarditis

Table of contents
Key points ⚡
Succinct notes to superpower your revision
Infective endocarditis\: in
Mortality rate\: approximately 40%; incidence of 1.7 - 6.2 cases per 100,000 patient years.
Risk factors\: more common in men (ratio >2\:1), elderly, multimorbid patients, those with internal cardiac devices, and
intravenous drug users.
Classi
Left-sided (mitral/aortic valve) or right-sided (tricuspid/pulmonary valve).
Native valve endocarditis vs. prosthetic valve endocarditis (PVE).
Pathophysiology\:
Transient bacteraemia, damage to valvular tissue, formation of vegetations.
Pathogens enter bloodstream, aggregate with platelets and
Vegetations can embolise, causing further complications.
Microbiology\:
Most commonly by and caused S t a p h y l o c o c c u s a u r e u s , S t r e p t o c o c c u s v i r i d a n s , enterococci, Blood culture-negative cases may involve HACEK organisms, C o x i e l l a b u r n e t t i , and B a r t o n e l l a .
Risk factors\:
HACEK organisms.
Intrinsic\: valvular stenosis/regurgitation, hypertrophic cardiomyopathy, structural heart disease, prosthetic heart valves,
previous endocarditis.
Extrinsic\: intravenous drug use, invasive vascular procedures, poor oral hygiene.
Clinical features\:
Systemic\: fever, malaise, night sweats, weight loss, anorexia, fatigue, breathlessness.
Examination\: fever, tachycardia, new/changing heart murmur, splinter haemorrhages, Osler's nodes, Janeway lesions, Roth
spots, clubbing, splenomegaly, lung crepitations.
Di
Autoimmune\: systemic lupus erythematosus, antiphospholipid syndrome, vasculitis.
Infective\: Lyme disease, meningitis, tuberculosis.
Neoplastic\: atrial myxoma.
Investigations\:
Bedside\: vital signs, 12-lead ECG (prolongation of PR interval may indicate
abscess), urine dipstick.
Laboratory\: blood cultures (3 sets at least 30 mins apart from three separate peripheral sites), FBC, CRP/ESR, U&E.
Imaging\: transthoracic echocardiogram (
Diagnosis\: based on Duke criteria; classi
Management\:
Medical\: prolonged IV antibiotics (2-6 weeks), close liaison with multidisciplinary team.
Surgical\: indicated for heart failure, uncontrolled infection, prevention of embolism.
Complications\:
Localised\: valve destruction, heart failure, arrhythmias, myocardial infarction, pericarditis, aortic root abscess.
Systemic\: emboli, immune complex deposition, septicaemia, death.
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Prognosis\: high annual mortality (30-40%), recurrence in 2-6% of survivors, worse outcomes in elderly, multimorbid patients,
those with prosthetic valves, and severe complications.
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A comprehensive topic overview

Introduction

Infective endocarditis is when the heart's inner lining (the endocardium) becomes in
Infective endocarditis occurs worldwide and has, on average, around a 40% mortality rate. However, it remains a rare
disease, especially in the West, with an incidence of approximately 1.7 - 6.2 cases per 100,000 patient years.
1
Men are more commonly a
those with internal cardiac devices and intravenous drug users.
1,2

Aetiology

Anatomy

The wall of the heart is divided into three main layers\:
An outer epicardium (connective tissue and fat)
A middle muscular myocardium
An inner endocardium
The endocardium is the heart's thin, smooth interior lining covering the heart valves. It comprises a specialised
endothelium (similar to that in blood vessels) and connective tissue.
3
Figure 1. Layers of the heart wall.
4

Classi

Depending on the valve a
(tricuspid/pulmonary valve). Most cases involve the left side; only 5-10% are right-sided.
5
This may be further subdivided into native valve endocarditis (where the patient’s own heart valves are a
prosthetic valve endocarditis (a
Prosthetic valve endocarditis (PVE) makes up 20% of all endocarditis cases. 6
and the prognosis is often poor.
This is the most severe form of endocarditis,
Early PVE is seen within 12 months of surgery due to intraoperative contamination or spread to the valve via the blood
within days or weeks of the operation. S t a p h y l o c o c c u s a u r e u s is most commonly associated with early PVE.
Late PVE, on the other hand, is a community-acquired infection that occurs more than 12 months post-op and is caused by
similar microorganisms to those found in native valve endocarditis (streptococci, S t a p h y l o c o c c u s a u r e u s ).

Pathophysiology

Infective endocarditis arises from three key factors occurring simultaneously\:
1. Transient bacteraemia
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2. Damage to valvular tissue
3. Formation of vegetations
Pathogens must
contamination or intravenous drug use.
Endocarditis is typically seen in patients with damaged or prosthetic heart valves, although it may occasionally occur in
healthy valves.
When the valve is damaged (e.g. by trauma or the infecting organism itself), the endothelium is exposed, leading to an
aggregation of platelets and
The circulating pathogen binds to this platelet-
continued deposition of platelets,
7
This explains why removing the organism is di
vascularised and di
clear the infection.
7,8
These vegetations have the potential to embolise and cause further complications. Emboli resulting from left-sided
endocarditis may cause cerebral infarcts (strokes) or cerebral abscesses, whereas those from right-sided endocarditis may
lead to mycotic aneurysms, pulmonary infarcts or pulmonary abscesses.
Deposition of circulating immune complexes in organs such as the skin, kidneys and eyes (an example of a type 3
hypersensitivity reaction) is also seen.

Microbiology

Bacteria cause most cases of endocarditis, with Staphylococci now overtaking Streptococci as the leading pathogen.
2
S t a p h y l o c o c c u s a u r e u s is particularly linked to endocarditis in patients with prosthetic valves, acute endocarditis and
intravenous drug use.
9
Table 1. Causative pathogens of infective endocarditis.
Class of pathogen Causative organisms
Gram-positive bacteria
Staphylococci (e.g. Streptococci (e.g. Groups A, B, C, D, G)
Enterococci
S t a p h a u r e u s )
S t r e p v i r i d a n s , S t r e p i n t e r m e d i u s ,
Gram-negative bacteria
HACEK organisms*
Non-HACEK organisms (e.g. P s e u d o m o n a s a e r u g i n o s a ,
N e i s s e r i a e l o n g a t a )
*H a e m o p h i l u s s p p ., A g g r e g a t i b a c t e r
a c t i n o m y c e t e m c o m i t a n s , C a r d i o b a c t e r i u m s p p ., E i k e n e l l a
c o r r o d e n s , K i n g e l l a k i n g a e
C a n d i d a
Fungi
A s p e r g i l l u s
Blood culture-negative infective endocarditis
In a signi
methods - so-called blood culture-negative infective endocarditis (BCNIE).
9
This is often due to the patient receiving antibiotic therapy before blood cultures are taken. Still, there are several
important bacteria to remember, as further investigations may be required to identify them (e.g. serology).
Culture-negative bacteria may include\:
HACEK organisms
C o x i e l l a b u r n e t t i (Q fever)
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Chlamydia spp
Bartonella spp (trench fever and cat-scratch disease)
Legionella

Risk factors

Endocarditis risk factors may be divided into those related to the heart (intrinsic) and those external to the heart
(extrinsic).
9,10,11
Intrinsic risk factors include\:
Valvular stenosis or regurgitation\: congenital or acquired
Hypertrophic cardiomyopathy
Structural heart disease with turbulent
Prosthetic heart valves\: these will require replacement if infected
Previous infection (infective endocarditis/rheumatic fever) causing structural damage
Extrinsic risk factors include\:
Intravenous drug use (right-sided endocarditis)
Invasive vascular procedures (e.g. central lines)
Poor oral hygiene/dental infections

Clinical features

Patients with infective endocarditis may present acutely (otherwise known as fulminant endocarditis) or subacutely over
weeks to months.
9,10

History

Presentation is variable, but patients may complain of systemic features of infection (such as fever, malaise, night sweats,
weight loss, anorexia) and symptoms of anaemia (such as fatigue and breathlessness).

Clinical examination

All patients with suspected infective endocarditis require a thorough cardiovascular examination.
Typical clinical
Fever
Tachycardia
New or changing heart murmur
Splinter haemorrhages\: nailbed petechial haemorrhages
Osler's nodes (tender subcutaneous nodules in the
the palms)\: see Table 2
Roth spots (boat-shaped retinal haemorrhages, pale in the centre)
Clubbing\: typically a late sign
Mild splenomegaly
Bi-basal lung crepitations\: heart failure in severe cases
Patients may also present with clinical features from emboli (e.g. weakness from a stroke).
Table 2. Comparison between Osler’s nodes and Janeway lesions.
12
Osler’s nodes Janeway lesions
Painful (Osler’s Ow!) Painless
Typically a
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Nodules Macules/papules
Purple-pink with a pale centre Erythematous/haemorrhagic
Localised immune-mediated response Septic emboli
Subacute endocarditis Acute endocarditis
Last hours to days Last days to weeks
The "classical” stigmata should not be used to make the diagnosis alone as these are unreliable. Instead, diagnosis is based
on the Duke criteria (see diagnosis section).
Figure 2. Finger clubbing (a late feature of endocarditis).
13
Figure 3. Osler’s Nodes.
14
Figure 4. Janeway lesions.
15
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Di

Important di
9
Autoimmune/rheumatological di
Systemic lupus erythematosus\: may present with non-infective (Libman-Sacks) endocarditis
Antiphospholipid syndrome\: thromboemboli, cardiac valve disease
Vasculitis
Polymyalgia rheumatica\: myalgia, raised in
Reactive arthritis
Infective di
Lyme disease\: fever, myocarditis (rarely)
Meningitis\: fever, rash
Tuberculosis\: fever, night sweats, weight loss
Neoplastic di
Atrial myxoma\: fever, new murmur (“tumour plop”
, mid-diastolic rumble)

Investigations

Bedside investigations

Relevant bedside investigations include\:
Basic observations (vital signs)\: signs of infection (fever, tachycardia).
12-lead ECG\: to exclude
complication of infective endocarditis.
11
Urine dipstick\: microscopic haematuria.
10
Figure 5. Prolongation of the PR interval,
indicating
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be a sign of aortic root abscess, a rare

Laboratory investigations

complication of endocarditis.
16
Blood cultures
Blood cultures are a key part of the workup for endocarditis and should ideally be obtained before starting antibiotic
therapy. This will reduce the number of negative cultures and help to guide appropriate treatment.
The European Society of Cardiology (ESC) recommends that three sets of blood cultures (i.e. six bottles in total) be taken,
at least 30 mins apart, from three separate peripheral sites. A minimum of 10 ml of blood per bottle should be collected.
5
Other laboratory investigations
Other relevant laboratory investigations include\:
Full blood count\: to exclude anaemia (↓Hb) and check white cell count (WCC) to track the progress of the infection and
response to treatment.
CRP/ESR\: in
Urea & electrolytes\: baseline renal function and creatinine clearance is required if starting on nephrotoxic antibiotics
such as gentamicin.

Imaging investigations

Transthoracic echocardiogram is the
the diagnosis of endocarditis is suspected. Note that not all vegetations are picked up on echocardiogram.
10
Figure 6. Vegetation on tricuspid valve
visualised on echocardiography. Arrow
denotes the vegetation.
17
Other relevant imaging investigations include\:
Transoesophageal echocardiogram\: more invasive but provides more detail than TTE. It can aid in diagnosis where
endocarditis is clinically suspected but initial TTE is negative. It may also be used to rule out local complications in
patients with a positive initial TTE.
5
Chest X-ray\: may be requested as part of the initial infection screen where the diagnosis is unclear. It may also be
requested when heart failure (a serious complication of endocarditis) is suspected.
CT chest\: this can be helpful if a root abscess is present and if the patient is considered for surgery. When planning a re-
do-sternotomy for prosthetic endocarditis, a pre-operative CT will be required as the heart structures may be stuck to
the sternum.

Diagnosis

Diagnosis of endocarditis is based on the Duke criteria, rather than clinical features alone.
Suspected cases may be classi
5,10,18

Major criteria

Positive blood cultures
These must meet ONE of the following criteria\:
1. Positive for typical microorganisms on two or more separate occasions including S t r e p v i r i d a n s , S t r e p b o v i s , HACEK
group, S t a p h a u r e u s , Community-acquired enterococci (in the absence of a primary focus)
2. Persistently positive cultures for microorganisms consistent with IE\: ≥2 positive blood cultures of blood samples drawn >12
h apart or all of 3 or a majority of ≥4 separate cultures of blood (with ≥1 h apart)
3. A single positive culture for C o x i e l l a b u r n e t t i or high antibody titre (>1\:800)
Evidence of endocardial involvement
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Evidence on echocardiogram of\:
Intra-cardiac vegetation (oscillating intracardiac mass)
Abscess
New valvular regurgitation (change in pre-existing murmurs is not included)
New partial dehiscence of prosthetic valve

Minor criteria

Minor Duke criteria include\:
1. Risk factors for infective endocarditis (see risk factors section)
o
2. Fever > 38 C
3. Vascular phenomena\: septic emboli, Janeway lesions, conjunctival haemorrhage, intracranial haemorrhage
4. Immunological phenomena\: glomerulonephritis, Osler’s nodes, Roth spots, positive rheumatoid factor
5. Microbiological evidence\: positive blood cultures which do not meet the major criteria

De

To make a de
Direct evidence of infective endocarditis by histology or culture of organisms (e.g. from a vegetation)
TWO major criteria
ONE major + THREE minor criteria
FIVE minor criteria

Possible endocarditis

Endocarditis is possible when there are\:
ONE major and ONE minor criterion
THREE minor criteria
In other words, there is some evidence of endocarditis but not enough to make a de

Rejected endocarditis

A diagnosis of endocarditis is rejected when there is\:
A
Sustained symptom resolution after \<4 days of antibiotics

Management

Medical management

The mainstay of treatment of infective endocarditis is prolonged courses of antibiotics (or antifungals if the infection is of
fungal aetiology).
Antibiotics are initially given intravenously for at least two weeks before switching to oral preparations.
10
The European Society of Cardiology (ESC) advises that treatment should last for at least six weeks in patients with
prosthetic valves and two to six weeks for native valve endocarditis.
The start of the antibiotic course is taken from the
antibiotics will have been given before this).
5
The choice of antibiotic regimen depends on multiple factors including previous antibiotic use, the type of valve a
(native vs prosthetic), the microorganism involved and the antibiotic sensitivity of the particular organism.
5
Local antimicrobial guidelines should always be followed. Close liaison with microbiology/infectious diseases, cardiology
and cardiothoracics (if surgery is a possibility) is required with a discussion at the infective endocarditis multidisciplinary
team meeting.
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The ESC emphasises the high importance of having an established endocarditis team at each heart centre to speci
manage endocarditis.
5

Surgical management

Occasionally, antibiotics alone may not be enough to treat the infection and surgery to repair or replace the valve may be
required.
Every patient with prosthetic valve endocarditis should have an urgent surgical review.
Indications for surgery include\:
5
Heart failure (i.e severe valve disease, pulmonary oedema or cardiogenic shock)
Uncontrolled infection
Prevention of embolism (large vegetations)

Prophylaxis

Patients at risk of endocarditis may have other unrelated medical conditions requiring intervention.
Currently, in the United Kingdom, the National Institute for Health and Care Excellence (NICE) does not recommend using
prophylactic antibiotics against endocarditis for patients underging dental procedures, or procedures a
gastrointestinal, genitourinary or respiratory tracts. This is also true of chlorhexidine mouthwash for dental procedures.
19
However, if these patients undergo a gastrointestinal or genitourinary procedure and subsequently require antibiotics for a
suspected infection, the antibiotics selected should also provide e
Clinicians should provide patients at risk of endocarditis with clear and consistent information about prevention, including\:
The bene
recommended
The importance of maintaining good oral health
Symptoms that may indicate infective endocarditis and when to seek expert advice
The risks of undergoing invasive procedures including non-medical procedures such as body piercing or tattooing

Complications

Infective endocarditis can cause localised and systemic complications.
9,18
Localised complications include\:
Valve destruction
Heart failure (secondary to valve regurgitation)
Arrhythmias and conduction disorders (e.g. AV block)
Myocardial infarction
Pericarditis
Aortic root abscess
Systemic complications include\:
Emboli (e.g. stroke, splenic infarction)
Immune complex deposition (e.g. glomerulonephritis)
Septicaemia
Death

Prognosis

While progress has been made in managing patients with endocarditis, annual mortality still remains high at around 30-
40%. 1,2 5
Recurrence may be seen between two and six percent of survivors.
Patients who are elderly, who have multiple comorbidities and those who have prosthetic valves generally have worse
outcomes, as do those with severe complications from endocarditis such as heart failure or stroke.
9
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Certain micro-organisms are associated with more aggressive forms of the disease and can lead to higher mortality rates
(e.g. S t a p h y l o c o c c u s a u r e u s , non-HACEK Gram-negative bacilli, fungi).
Similarly, echocardiograms may demonstrate pathology associated with a poor prognosis, such as large vegetations,
severe left-sided valve regurgitation and low left ventricular ejection fraction.

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in

Reviewer

Miss Charlotte Holmes
Cardiothoracic Surgery Registrar

Related notes

Acute Coronary Syndrome (ACS)
Acute Heart Failure
Atrial Fibrillation (AF)
Atrioventricular Block
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Brugada Syndrome

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Contents

Introduction
Aetiology
Risk factors
Clinical features
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