Download ENDOCARDITIS

Dr. M. A. SOFI
MD; FRCP (London); FRCPEdin; FRCSEdin
Definition:
Infective endocarditis (IE) is defined as an infection of the endocardial
surface of the heart, which may include one or more heart valves, the mural
endocardium, or a septal defect
Signs and symptoms
 Osler nodes: Tender
subcutaneous nodules usually
 Fever possibly low-grade and
found on the distal pads of the
intermittent
90%.
digits
 Heart murmurs 85%
 Janeway lesions: Non-tender
 Petechiae: Common, but
maculae on the palms and
nonspecific, finding
soles
 Subungual (splinter)
 Roth spots: Retinal
hemorrhages: Dark-red, linear
hemorrhages with small, clear
lesions in the nail beds
centers; rare
Other signs of IE include the following
 Splenomegaly
 Gallops
 Stiff neck
 Rales
 Delirium
 Cardiac arrhythmia
 Paralysis, hemiparesis,
 Pericardial rub
aphasia
 Conjunctival
hemorrhage
 Pallor
 Pleural friction rub
Petechiae
Janeway lesions
Osler node
Splinter hemorrhage
Subacute native valve endocarditis
The symptoms of early subacute native valve endocarditis (NVE) are usually
subtle and nonspecific; they include the following:
 Low-grade fever:
Absent in 3-15% of
patients
 Anorexia
 Weight loss
 Influenza-like
syndromes
 Polymyalgia-like
syndromes
Pleuritic pain
 Syndromes similar to
rheumatic fever, such as
fever, dulled sensorium (as
in typhoid), headaches
 Abdominal symptoms,
such as right upper
quadrant pain, vomiting,
postprandial distress,
appendicitis-like
symptoms

Diagnosis
The Duke diagnostic criteria, developed by Durack and colleagues, are generally used to
make a definitive diagnosis of IE. The criteria combine the clinical, microbiologic,
pathologic, and echocardiographic characteristics of a specific case
Blood culture criteria for IE:
 Two blood cultures positive for
organisms typically found in
patients with IE
 Blood cultures persistently
positive for one of these
organisms, from cultures drawn
more than 12 hours apart
 Three or more separate blood
cultures drawn at least 1 hour apart
Echocardiographic criteria for IE
 Oscillating intracardiac mass on a
valve or on supporting structures,
in the path of regurgitant jets, or
on implanted material.
 Myocardial abscess
 Development of partial
dehiscence of a prosthetic valve
 New-onset valvular regurgitation
Minor criteria for IE include the following:
 Predisposing heart condition
or intravenous drug use
 Fever of 38°C or higher
 Vascular phenomenon:
 Major arterial emboli
 Septic pulmonary infarcts
 Mycotic aneurysm
 Intracranial hemorrhage
 Conjunctival hemorrhage
 Janeway lesions
 Immunologic phenomenon:
 Glomerulonephritis
 Osler nodes
 Roth spots
 Rheumatoid factor
 Positive blood culture results not
meeting major criteria or serologic
evidence of active infection with an
organism consistent with IE
 Echocardiogram results consistent
with IE but not meeting major
echocardiographic criteria
A definitive clinical diagnosis can be
made based on the following:
 2 major criteria
 1 major criterion and 3 minor
criteria
 5 minor criteria
Native valve endocarditis: Main underlying causes of NVE
RHD (30% of NVE) - Primarily
involves the mitral valve
followed by the aortic valve
 Congenital heart disease (15%
of NVE) - Underlying etiologies
include:
 Patent ductus arteriosus
 Ventricular septal defect
 Tetralogy of Fallot
 Native or surgical high-flow
lesion.

 Mitral valve prolapse with an
associated murmur (20% of
NVE)
Degenerative heart disease:
 Calcific aortic stenosis due to
a bicuspid valve
 Marfan syndrome
 Syphilitic disease
Approximately 70% of infections in NVE are caused by Streptococcus
species, including S viridans, Streptococcus bovis, and enterococci.
Staphylococcus species cause 25% of cases and generally demonstrate a more
aggressive acute course.
Prosthetic valve endocarditis
Early PVE, which presents shortly after surgery, has a different bacteriology and
prognosis than late PVE, which presents in a subacute fashion similar to NVE.
Infection associated with aortic
valve prostheses is particularly
associated with
 local abscess and fistula formation
 Valvular dehiscence.
This may lead to:
Shock
 Heart failure
 Heart block
 Shunting of blood to the right
atrium
 Pericardial tamponade
 Peripheral emboli to the central
nervous system and elsewhere.

Early PVE may be caused by a
variety of pathogens, including:
 S aureus and S epidermidis.
These nosocomially acquired
organisms are often methicillinresistant (eg, MRSA).
 Late disease is most commonly
caused by streptococci.
 Overall, CoNS are the most
frequent cause of PVE (30%).
IVDA infective endocarditis
Diagnosis of endocarditis in IV drug
users can be difficult and requires
a high index of suspicion.
 2/3 of patients have no previous
history of heart disease or murmur
on admission.
 A murmur may be absent in those
with tricuspid disease.
 Pulmonary manifestations may be
prominent in patients with
tricuspid infection:
 1/3 have pleuritic chest pain, and
three quarters demonstrate chest
radiographic abnormalities.
S aureus is the most common (<
50% of cases) etiologic organism in
patients with IVDA IE.
 MRSA accounts for an increasing
portion of S aureus infections and
has been associated with previous
hospitalizations, long-term
addiction, and non-prescribed
antibiotic use.
 Groups A, C, and G streptococci and
enterococci are also recovered from
patients with IVDA IE.

Nosocomial/healthcare-associated infective endocarditis
Endocarditis may be associated with:
 Central or peripheral IV catheters
 Pacemakers and defibrillators
 Hemodialysis shunts
 Hyperalimentation lines
 These patients tend to have
significant comorbidities, more
advanced age, and predominant
infection with S aureus.
 The mortality rate is high in this
group.
The organisms that cause
NIE/HCIE obviously are related
to the type of underlying
bacteremia. The gram-positive
cocci (ie, S aureus, CoNS,
enterococci, nonenterococcal
streptococci) are the most
common pathogens.
Fungal endocarditis is found in
IV drug users and ICU patients
who receive broad-spectrum
antibiotics. Blood cultures are
often negative, and diagnosis
frequently is made after
microscopic examination of
large emboli.
Clinical features associated with different pathogens
Clinical Features of Infective Endocarditis According to Causative Organism
Causative Organism(s)
Staphylococcus aureus
Clinical Features of IE
Overall, S aureus infection is the most common cause of
IE, including PVE, acute IE, and IVDA IE.
Approximately 35-60.5% of staphylococcal bacteremias are
complicated by IE.
More than half the cases are not associated with underlying
valvular disease.
The mortality rate of S aureus IE is 40-50%.
S aureus infection is the second most common cause of
nosocomial BSIs, second only to CoNS infection.
The incidence of MRSA infections, both the hospital- and
community-acquired varieties, has dramatically increased
(50% of isolates)
The primary risk factor for S aureus BSI is the presence of
intravascular lines. Other risk factors include cancer,
Clinical features associated with different pathogens
Clinical Features of Infective Endocarditis According to Causative Organism
Causative Organism(s)
Streptococcus viridans
Streptococcus intermedius
group
Abiotrophia
Clinical Features of IE
•This organism accounts for approximately 50-60% of
cases of subacute disease.
•Most clinical signs and symptoms are mediated
immunologically.
•These infections may be acute or subacute.
•S intermedius infection accounts for 15% of streptococcal
IE cases.
•Members of the S intermedius group, especially S
anginosus, are unique among the streptococci in that they
can actively invade tissue and form abscesses, often in the
CNS.
•Approximately 5% of subacute cases of IE are due to
infection with Abiotrophia species.
•They require metabolically active forms of vitamin B-6 for
Clinical features associated with different pathogens
Clinical Features of Infective Endocarditis According to Causative Organism
Causative Organism(s)
Group D streptococci
Nonenterococcal group D
Group B streptococci
Clinical Features of IE
•Most cases are subacute.
•The source is the gastrointestinal or genitourinary tract.
•It is the third most common cause of IE.
•They pose major resistance problems for antibiotics.
•The clinical course is subacute.
•Infection often reflects underlying abnormalities of the
large bowel (eg, ulcerative colitis, polyps, cancer).
•The organisms are sensitive to penicillin.
•Acute disease develops in pregnant patients and older
patients with underlying diseases (eg, cancer, diabetes,
alcoholism).
•The mortality rate is 40%.
•Complications include metastatic infection, arterial
thrombi, and congestive heart failure.
Clinical features associated with different pathogens
Clinical Features of Infective Endocarditis According to Causative Organism
Causative Organism(s)
Group A, C, and G
streptococci
Coagulase-negative S
aureus
Pseudomonas
aeruginosa
Clinical Features of IE
•Acute disease resembles that of S aureus IE (3070% mortality rate), with suppurative
complications.
•Group A organisms respond to penicillin alone.
•Group C and G organisms require a combination
of synergistic antibiotics (as with enterococci).
•This causes subacute disease.
•It behaves similarly to S viridans infection.
•It accounts for approximately 30% of PVE cases
and less than 5% of NVE cases.[21]
•This is usually acute, except when it involves the
right side of the heart in IVDA IE.
Clinical features associated with different pathogens
Clinical Features of Infective Endocarditis According to Causative Organism
Causative Organism(s)
HACEK (ie, Haemophilus
aphrophilus, Actinobacillus
actinomycetemcomitans,
Cardiobacterium hominis,
Eikenella corrodens,
Kingella kingae)
Fungal
Bartonella
Clinical Features of IE
•These organisms usually cause subacute disease.
•They account for approximately 5% of IE cases.
•They are the most common gram-negative organisms
isolated from patients with IE.
•Complications may include massive arterial emboli and
congestive heart failure.
•Cure requires ampicillin, gentamicin, and surgery.
•These usually cause subacute disease.
•The most common organism of both fungal NVE and
fungal PVE is Candida albicans.
•Fungal IVDA IE is usually caused by Candida
parapsilosis or Candida tropicalis.
•Aspergillus species are observed in fungal PVE and NIE.
•The most commonly involved species is Bartonella quintana.
Differential Diagnoses
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Thrombotic nonbacterial
endocarditis
Vasculitis
Temporal arteritis
Marantic endocarditis
Connective tissue disease
Fever of unknown origin (FUO)
Intra-abdominal infections
Septic pulmonary infarction
Tricuspid regurgitation
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Antiphospholipid Syndrome
Atrial Myxoma
Cardiac Neoplasms, Primary
Endocarditis
Lyme Disease
Polymyalgia Rheumatica
Reactive Arthritis
Systemic Lupus Erythematosus
Diagnostic work up:
The criterion standard test for diagnosing infective endocarditis (IE) is the documentation of a continuous
bacteremia (>30 min in duration) based on blood culture results
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25% of S aureus bloodstream
infections (BSIs) represent IE or
metastatic infections
S aureus to produce an endotheliosis,
the presence of a continuous
bacteremia does not necessarily
imply an infected valvular vegetation
Clue to continuous bacteremia/IE is
the presence of S aureus bacteriuria
associated with hematuria
25% of patients with staphylococcal
bacteremia and 23% of those with
catheters as the primary focus have
evidence of IE based on
transesophageal echocardiography
(TEE) findings, in the absence of
clinical and transthoracic
echocardiography (TTE) findings.
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CBC (Leukocytosis in acute stage)
ESR (Elevated in 90%)
BUN
Coagulation Profile
RF (+50%)
Proteinuria
Hematuria
50%
3-5 sets of blood cultures over 24
hours
3 sets may be drawn over 30 minutes
(with separate venipunctures)
Culture-negative infective
endocarditis
 Vasculitis
 Prior antibiotic therapy
 Fungal infections
 Atypical organisms
Echocardiography:
Echocardiography has become the indirect diagnostic method of choice. The diagnosis of IE can never be
excluded based on negative echocardiogram findings, either from TTE or from TEE.
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TTE sensitivity of approximately
60% for identification of valvular
lesions in patients with NVE.
TTE has a sensitivity of 20% in
patients with PVE.
The sensitivity of TEE in detecting
the vegetations of NVE is 90-100%.
In patients with PVE, the sensitivity
of TEE is greater than 90%.
TEE successfully visualizes
vegetations of the tricuspid valve in
more than 90% of cases of
pacemaker IE, compared with less
than the 50% achieved by TTE.
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Echocardiography is useful for
predicting the potential complications
of IE, especially those that are embolic
in nature
Echocardiographic predictors of
systemic embolization in patients with
IE are the following
◦ Large valvular vegetations (>10 mm
in diameter)
◦ Multiple vegetations
◦ Mobile but pedunculated vegetations
◦ Prolapsing vegetations
Echocardiography is also highly useful
for detecting abscesses
Treatment
The major goals of therapy for
infective endocarditis (IE)
are:
1. Eradicate the infectious agent
from the thrombus
2. Intra cardiac and extra
cardiac consequences of IE.
3. Surgical intervention.
4. Emergency care: Correct
diagnosis & stabilization
General Measures:
 Treatment of congestive heart
failure
 Oxygen
 Hemodialysis (may be
required in patients with RF)
 Empiric antibiotic therapy is
chosen based on the most
likely infecting organisms.
Treatment
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Native valve endocarditis
(NVE): Penicillin G wih
gentamicin for synergistic
coverage of streptococci
Patients with IVdrug use have
been treated with nafcillin and
gentamicin to cover for
methicillin-sensitive
staphylococci.
Prosthetic valve endocarditis
(PVE) may be caused by MRSA
or coagulase-negative
staphylococci (CoNS)
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Culture-negative NVE is
usually treated with vancomycin
and gentamicin
Patients with culture-negative
PVE are usually given
vancomycin and gentamicin,
targeting enterococcal or CoNS
infections
Approximately 15-25% of patients with IE eventually require surgery.
Indications for surgical intervention in patients with NVE are as follows:
CHF refractory to standard
medical therapy
 Fungal IE (except that caused
by Histoplasma capsulatum)
 Persistent sepsis after 72
hours of appropriate
antibiotic Rx
 Recurrent septic emboli,
especially after 2 weeks of
antibiotic treatment

Rupture of an aneurysm of
the sinus of Valsalva
 Conduction disturbances
caused by a septal abscess
 Kissing infection of the
anterior mitral leaflet in
patients with IE of the aortic
valve
 Paravalvular abscess and
intracardiac fistula almost
always require surgical
intervention
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Prevention of Infective Endocarditis:
15-25% cases of IE are due to procedures that produce bacteremia
Patients at higher risk include:
 Presence of prosthetic heart
valve
 History of endocarditis
 Cardiac transplant recipients
who develop cardiac
valvulopathy
 Congenital heart disease with
a high-pressure gradient
lesion
Also consider prophylaxis in
procedures involving:
 Manipulation of gingival tissue or
the periapical region of teeth, or
perforation of the oral mucosa
 Incision in the respiratory mucosa
 Infected skin or musculoskeletal
tissue including incision and
drainage of an abscess
 Prophylaxis is no longer routinely
recommended for GI procedures.