Overview of Infective Endocarditis: Etiology, Presentation, Diagnosis, and Management

 
ALI 
 
SOMILY
 
,
  
MD,
 
FRCP(C)
ali.somily@gmail.com
FAWZIA  ALOTAIBI,  MD
ofawzia@ksu.edu.sa
 
Infective
E
n
d
o
c
a
r
d
itis
 
Objectives
 
D
efine infective endocarditis
Recognize the bacteria such as staphylococcus aureus and streptococcus viridans as the most common etiologies
of IE
Know the different clinical presentation of acute and sub-acute IE
To recognize the different clinical presentation of IE; fever as the most common cause of pyerixia of unknown
origin (P.U.O).
TO the bacterial and host factors affecting the severity and outcome of the disease.
Recognize the sources of bacteria causing bacteremia preceding IE.
To know the pathogenesis of IE and the formation and importance of vegetations.
To know the predisposing factors such as RHD, CHD, prosthetic valves and IVDU.
To the common bacterial causes of IE associated with different sources and clinical conditions.
To realize the infection as a diagnostic challenge and to know the different diagnostic methods of IE including;
1.
Clinical presentation (signs & symptoms)
2.
Laboratory tests mainly multiple blood cultures.
3.
Echocardiogram for the presence of vegetations
To know the different regimens used to treat different types of organisms.
To know possible complications of IE.
 
 
 
 
.
 
 
O
utlines
 
Definition
Pathogenesis
Risk
 
factors
Clinical
 
presentation
Diagnosis
Culture 
negative
 
endocarditis
Management
Prophylaxis
 
D
e
f
initi
o
n
 
Infectious Endocarditis 
(IE): 
an 
infection
 
of
the 
heart’s 
endocardial
 
surface
Classified 
into 
four
 
groups:
Native 
Valve
 
IE
Prosthetic 
Valve
 
IE
Intravenous 
drug 
abuse
 
(IVDA) 
IE
Nosocomial
 
IE
 
Further
 
Classification
 
Acute:
Affects
 
normal
heart
 
valves
Rapidly
 
destructive
If 
not 
treated,
usually 
fatal
 
within
6
 
weeks
Commonly
 
Staph→
Metastatic
 
foci
 
Subacute:
Often 
affects
damaged
 
heart
valves
Indolent
 
nature
If 
not 
treated,
usually 
fatal 
by
 
one
year
Commonly
 
viridans
Streptococci
 
Pathophysiology
 
1.
Turbulent 
blood 
flow 
disrupts
 
the
endocardium 
making 
it
 
“sticky”
2.
Bacteremia 
delivers 
the
 
organisms 
to
the 
endocardial
 
surface
3.
Adherence
 
of
 
the
 
organisms
 
to
 
the
endocardial
 
surface
4.
Eventual 
invasion 
of 
the
 
valvular
leaflets
 
Epidemiology
 
Incidence: 
1.7— 
6.2 
/
 
100, 
000 
person 
years
M:F
 
1.7
Becoming 
a 
disease 
of 
the
 
elderly
Median
 
age
PreABx 
era
 
—35y
Now
 
—58y
Due 
to 
two
 
factors
The
 
decline
 
of
 
rheumatic
 
heart
 
disease
The 
increasing 
proportion 
of
 
elderly
 
Prosthetic
 
Valve
 
7 
-25 
% 
of 
cases 
of 
infective
 
endocarditis
Early
 
<12mons
Late 
>12
 
mons
0.94 
per 
100,000
 
bioprosthetic
Initially
 
mechanical
 
valves
 
at
 
greater
 
risk
for
 
first
 
3
 
mo,
 
then
 
risk
 
same
 
at
 
5y
1-3.1% 
risk 
at 
1
 
yr
2-5.7% 
at 
5
 
yr
 
Risk
 
Factors
 
Injection drug
 
use
100X
 
risk 
in
 
young
Staphylococcus
 
aureus
Other
 
risks:
1.
Poor 
dental
 
hygiene
2.
Hemodialysis
3.
DM
4.
HIV
 
IVDU
Rates 
150- 
2000/ 
100
 
000
person
 
years
Higher 
among 
patients
 
with
known 
valvular 
heart
disease
Structural
 
cardiac
abnormality
75% 
of 
pts 
will 
have 
a
preexisting
 
structural
cardiac
 
abnormality
10-20% 
have
 
congenital
heart
 
disease
 
Risk 
Factors 
; 
Cardiac
 
Abnormality
 
Previous 
IE 
4.5(2.5
to
 
9)%
Aortic 
valve
disease12 
to
 
30%
Rheumatic
 
valve
disease
Prosthetic
 
valve
Coarctation
Complex
 
cyanotic
congenital
 
High
 
risk
 
Moderate
 
risk
 
MVP 
w/
 
MR/thickened 
leaflets- 
5
to 
8 
times 
(100/100 
000 
person
years)
Mitral
 
Stenosis
tricuspid
 
valve
Pulmonary
 
Stenosis
Hypertrophic
 
Obstructive
Cardiomyopathy
 
(HOCM)
Low/no
 
risk
ASD
 
(secundum)
CABG
 
Risk
 
Factors
 
HIV
 
infection:
A
 
number
 
of
 
cases
 
of
 
IE
 
have
 
been
 
reported
 
in
 
patients
 
with
HIV
 
infection
It
 
has
 
been
 
suggested
 
that
 
HIV
 
infection
 
is
 
an
 
independent
risk 
factor 
for 
IE 
in
 
IDU
Rheumatic 
valve
 
disease:
Predisposition
 
for
 
young
 
in
 
some
 
countries
 
37%-76%
 
of
 
cases
Mitral 
85%, 
Aortic
 
50%
Degenerative 
valvular
 
lesions
MV
 
Prolapse
 
and
 
associated
 
mitral
 
regurgitation
 
-
 
5
 
to
 
8
 
times
higher 
IE
 
risk
Aortic
 
valve
 
disease
 
(stenosis
 
or/and
 
regurgitation)
 
is
 
present
in 
12 
to 
30 
% 
of
 
cases
 
Diagnostic
 
approach
 
History 
of 
prior 
cardiac
 
lesions
A 
recent 
source 
of
 
bacteremia
 
Symptoms
 
Acute
 
High 
grade 
fever
 
and
chills
SOB
Arthralgias/
 
myalgias
Abdominal
 
pain
Pleuritic 
chest
 
pain
Back
 
pain
 
Subacute
 
Low 
grade
 
fever
Anorexia
Weight
 
loss
Fatigue
Arthralgias/
 
myalgias
Abdominal
 
pain
N/V
 
The
 
onset
 
of
 
symptoms
 
is
 
usually
 
~2
 
weeks
 
or
 
less
from 
the 
initiating
 
bacteremia
 
Physical
 
examination
 
Look 
for 
small 
and
 
large
emboli 
with 
special
attention 
to 
the 
fundi,
conjunctivae, 
skin, 
and
digits
Cardiac 
examination
 
may
reveal 
signs 
of 
new
regurgitation 
murmurs
and 
signs 
of
 
CHF
Neurologic 
evaluation
may 
detect 
evidence
 
of
focal 
neurologic
impairment
 
Si
g
n
s
 
Fever
Heart
 
murmur
Nonspecific 
signs 
petechiae, 
subungal 
or
“splinter”
 
hemorrhages,
clubbing, 
splenomegaly,
neurologic
 
changes
More specific 
signs -
Osler’s 
Nodes, 
Janeway
lesions, 
and 
Roth
 
Spots
 
Other 
aspects 
clinical
 
diagnosis
 
WHICH 
VALVE? 
R 
or 
L 
heart 
where 
would
emboli
 
go?
HEART
 
FUNCTION?
Pump, 
acute 
valve 
dysfunction
 
conduction
Look 
for evidence
 
emboli
Bleed 
(intracranial, 
elsewhere
 
mycotic
aneurysm
 
)
 
Diagnostic
 
approach
 
1
Positive 
blood 
culture
 
results
A 
minimum 
of 
three 
blood 
cultures
 
should
be
 
obtained
 
over
 
a
 
time
 
period
 
based
 
upon
the 
severity 
of 
the
 
illness
2
Additional 
laboratory 
Nonspecific
 
test
An 
elevated 
ESR 
and/or 
an
 
elevated 
level 
of 
CRP 
is
usually
 
present
Most
 
patients
 
quickly
 
develop
 
a
 
normochromic
normocytic
 
anemia
The
 
WBC
 
count
 
may
 
be
 
normal
 
or
 
elevated
 
Additional 
laboratory
 
tests
 
a
b
n
o
r
m
a
l
 
u
r
i
n
a
l
y
s
i
s
The 
combination 
of 
RBC 
casts 
on 
urinalysis
and
 
a
 
low
 
serum
 
complement
 
level
 
may
 
be
 
an
indicator 
of 
immune-mediated 
glomerular
disease
E
C
G
:
New 
AV, 
fascicular, 
or 
bundle 
branch
 
block...
.?PERIVALVULAR 
INVAVSION­
 
monitoring,
??pacing
 
Native 
Valve
 
IE
Strep. 
(55%), 
mostly
 
S.
viridans
Staph. 
(30%), 
mostly
 
S.
aureus
Enterococci
 (5-10%),
GNB=HACEK
 
(5%),
Fungi
 
Prosthetic
 
Valve
IE
Early 
(0-2 
mo) 
1 
-
 
3.1%
50% 
Staphylococci 
S.
epi.> 
S. 
aureus
, 
gnb,
enterococci
Late 
(>12 
mo) 
2 
-
 
5.7%
IE 
in 
IV 
drug
abusers
Staph.
 
aureus(50-60%)
 
Case 
Definition:
 
IE
 
Duke
 
criteria
In 
1994 
investigators 
from 
Duke
 
University
modified
 
the
 
previous
 
criteria
 
to
 
include
The
 
role
 
of
 
echocardiography
 
in
 
diagnosis
They 
also 
expanded 
the 
category 
of
predisposing
 
heart
 
conditions
 
to
 
include
intravenous drug
 
use
 
Modified 
Duke
 
criteria
 
Proposed: 
2000,
 
Addresses
TEE, 
Broad 
“possible
categories.
S. 
aureus 
risks 
(13-25% 
S.
aureus 
bacteremia 
have
 
IE 
)
Definite
 
IE
Microorganism 
(via 
culture
 
or
histology) 
in 
a
 
valvular
vegetation, 
embolized
vegetation, 
or
 
intracardiac
abscess
Histologic 
evidence 
of
 
vegetation
or 
intracardiac
 
abscess
 
Possible
 
IE
2
 
major
1 
major 
and 
3
 
minor
5
 
minor
Rejected
 
IE
Resolution 
of 
illness 
with
 
four
days 
or 
less 
of
 
antibiotics
 
Major
 
criteria
 
1.
MICROBIOLOGY
 
 
 
Typical 
organism from
 
2
separate 
cultures
 
OR
Microorganism 
from
persistently 
positive 
BC 
OR
Single 
BC 
+ 
for 
Coxiella 
burnetii,
or 
titer
 
>1:800
 
2.
ENDOCARDIAL
 
INVOLVEMEMT
 
 
New 
(not 
changed) 
murmur
 
of
regurgitation
3.
POSITIVE
 
ECHO
 
(TEE 
if 
prosthetic 
valve,
complicated, 
or 
pretest
probability 
possible
 
IE
 
Minor 
criteria
Predisposition 
(heart 
condition
 
or
IV 
drug
 
use)
1.
Fever 
>/=
 
38
o
C
2.
Vascular 
phenomenon
 
(excludes
petechiae, 
splinter hemorrhage)
3.
major 
arterial
 
emboli,
 
 
Mycotic 
aneurysm,
intracranial 
or
 
conjunctival
hemorrhages. 
Janeway
lesions
4.
Immunologic
 
phenomena
RF,.Roth’s 
spots
glomerulonephritis, 
Osler’s
nodes
6.
Microbiologic
 
evidence
Not 
meeting 
major 
criteria
single 
BC 
not 
CNS,
 
serology
 
P
e
te
c
hia
e
 
Photo 
credit, 
Josh 
Fierer,
 
M.D.
 
Harden
 
Library
 
for
 
the
 
Health
 
Sciences
 
1.
Nonspecific
2.
Often 
located 
on
 
extremities
or 
mucous
 
membranes
 
S
plinte
r
 
He
m
o
rr
ha
ge
s
 
1.
Nonspecific
2.
Nonblanching
3.
Linear
 
reddish-brown
 
lesions
 
found
 
under
 
the
 
nail
 
bed
4.
Usually
 
do
 
NOT
 
extend
 
the
 
entire
 
length
 
of
 
the
 
nail
 
Osler’s
 
Nodes
 
1.
More
 
specific
2.
Painful 
and 
erythematous
 
nodules
3.
Located
 
on
 
pulp
 
of
 
fingers
 
and
 
toes
4.
More 
common 
in 
subacute
 
IE
 
American 
College 
of
 
Rheumatology
 
Janeway
 
Lesions
 
1.
More
 
specific
2.
Erythematous, blanching
 
macules
3.
Nonpainful
4.
Located 
on 
palms 
and
 
soles
 
Complications
 
Four
 
etiologies
Embolic
Local 
spread 
of
 
infection
Metastatic 
spread 
of
 
infection
Formation 
of 
immune 
complexes
 
glomerulonephritis 
and
 
arthritis
 
Embolic
 
Complications
 
Occur 
in 
up 
to
 
40% 
of
patients 
with
 
IE
Predictors 
of
 
embolization
Size 
of
 
vegetation
Left-sided
 
vegetations
Fungal 
pathogens, 
S.
 
aureus,
and 
Strep.
 
Bovis
Incidence 
decreases
significantly 
after
initiation 
of
 
effective
antibiotics
 
Stroke
Myocardial
 
Infarction
Fragments 
of
 
valvular
vegetation
 
or
vegetation-induced
 
stenosis
of 
coronary
 
ostia
Ischemic
 
limbs
Hypoxia 
from
 
pulmonary
emboli
Abdominal 
pain
 
(splenic
or 
renal
 
infarction)
 
Septic
 
Pulmonary
 
Emboli
 
Septic 
Retinal
 
embolus
 
http://www.emedicine.com/emerg/topic164.htm
 
Local 
Spread 
of
 
Infection
 
Heart
 
failure
Extensive 
valvular
 
damage
Paravalvular 
abscess
 
(30-40%)
Most 
common 
in aortic 
valve, 
IVDU, 
and
 
S. 
aureus
May
 
extend
 
into
 
adjacent
 
conduction
 
tissue
 
causing
arrythmias
Higher
 
rates
 
of
 
embolization
 
and
 
mortality
Pericarditis
Fistulous 
intracardiac
 
connections
 
Local
 
Spread
 
of
 
Infection
 
Acute 
S. 
aureus 
IE 
with perforation 
of 
the
aortic
 
valve
 
and
 
aortic
 
valve
 
vegetations.
 
Acute 
S. 
aureus 
IE 
with 
mitral 
valve 
ring
abscess 
extending 
into
 
myocardium.
 
Metastatic 
Spread
 
of
Infection
 
Metastatic
 
abscess
Kidneys, 
spleen, 
brain, 
soft
 
tissues
Meningitis 
and/or
 
encephalitis
Vertebral
 
osteomyelitis
Septic
 
arthritis
 
Poor 
Prognostic
 
Factors
 
Female
S.
 
aureus
Vegetation
 
size
Aortic
 
valve
Prosthetic
 
valve
Older
 
age
 
Diabetes
 
mellitus
Low 
serum
albumen
Apache 
II
 
score
Heart
 
failure
P
a
r
a
va
l
vu
l
a
r
abscess
Embolic
 
events
 
Echocardiographic
 
findings
 
1.
 
Oscillating 
intracardiac
 
mass
o 
On 
valve 
or 
supporting
 
structure,
In
 
the
 
path
 
of
 
regurgitation
 
jets,
On
 
implanted
 
material,
 
in
 
the
 
absence
 
of
 
an
altenate 
anatomic
 
explanation
3.
abscess
1.
New 
partial 
dehiscence 
of 
prosthetic
 
valve
2.
New 
valvular 
regurgitation 
(increase
 
or
change 
in 
pre-existing 
murmur 
not
sufficient)
 
Improved 
diagnostic 
value of 
echocardiography 
in patients
with 
infective 
endocarditis 
by 
transoesophageal 
approach
 
A
prospective
 
study
 
Eur 
Heart 
J, 
1988 
Jan;9(i):43.5396 
patients 
were
 
studied
consecutively 
with 
TEE 
and
 
TTE
TEE 
sensitivity 
100 
percent 
for 
vegetations
 
as
compared
 
to
 
63
 
percent
 
with
 
TTE
Both 
TTE 
and 
TEE 
had 
specificity 
of
 
98%
25% 
of 
vegetations 
less 
than 
5
 
mm,
69% 
of 
vegetations 
6-10 
mm,
 
and
100%
 
of
 
vegetations
 
greater
 
than
 
11 
mm
 
detected
 
by
TEE 
were 
also 
observed 
with
 
TTE
 
Culture 
Negative”
 
IE
 
How 
hard 
did
 
you
look?
(50% 
culture 
neg
 
are
d/t 
previous
antibiotics)
HACEK: 
- 
2-3 
wk
incubation,
subculturing,
Tend 
to 
see
 
subacute
w/ 
valve
destruction/CHF
 
H
e
m
o
p
h
i
l
u
s
p
a
r
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i
n
g
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l
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s
p
p
.
 
Lab 
Diagnosis! 
Etiologies“Culture 
Negative” 
IE
Based 
on 
clinical
 
setting
 
PCR 
of
 
vegetation/emboli:
T
r
o
p
h
e
r
y
m
a
 
w
h
i
p
p
e
l
e
i
,
 
b
a
r
t
o
n
e
l
l
a
Histology/stain 
/culture 
of
 
vegetation/emboli:
Fungus
Prolonged, 
enriched
 
cultures:
HACEK
Lysis 
centrifugation 
system
 
(Isolator):
Bartonella, legionella
 
(BCYE),fungal
Serology:
Endemic 
fungi, 
bartonella, 
Q 
fever, 
brucella, 
legionella,
 
chiamydia
Thioglycolate 
or 
cysteine 
supplemented
 
media.
S.aureus 
satellitism: Abiotrophia
 
(NVS)
 
endocarditis
 
GENERAL
 
CONSIDERATIONS
Antimicrobial
 
therapy
 
should
 
be
 
administered
 
in
a 
dose 
designed 
to 
give 
sustained 
bactericidal
serum concentrations 
throughout 
much 
or 
all 
of
the 
dosing
 
interval.
In 
vitro 
determination 
of 
the 
minimum
inhibitory 
concentration 
of 
the 
etiologic
 
cause
of 
the 
endocarditis 
should 
be 
performed 
in 
all
patients.
 
The 
duration 
of 
therapy 
has 
to 
be
sufficient 
to 
eradicate
 
microorganisms
growing 
within 
the 
valvular
vegetations.
The 
need 
for 
prolonged 
therapy 
in
treating 
endocarditis 
has
 
stimulated
interest 
in 
using 
combination
therapy 
to 
treat
 
endocarditis.
 
Indications
 
for
 
surgery 
in
 
IE
 
Combined 
therapy 
generally 
advised
 
with
Refractory 
CHF 
(mortality 
56-86% 
w/o
surgery 
vs 
11-35%
 
w/surgery)
Perivalvualr 
invasive
 
disease
Uncontrolled infection 
on 
maximal
 
medical
therapy
Recurrent
 
systemic
 
emboli,
 
particularly
 
in
 
the
presence 
of 
large
 
vegetations
SOME 
pathogens: 
Pseudomonas, 
brucella,
coxiella, 
fungi,
 
enterococci
 
Prosthetic 
same 
as 
native
 
valve
endocarditis
 
Perivalvular 
infection
 
valve
Dehiscence
Excessively 
mobile 
prosthesis 
on
 
echo
results in 
hemodynamic
 
instability
 
Prosthetic 
valve 
endocarditis 
that
one 
may 
attempt
 
medical 
treatment
alone:
1.
>l2mo 
post
 
surgical
2.
VGS 
or 
HACEK 
or
 
enterococci
3.
No 
perivalvular
 
extension
Recurrence 
after 
surgery 
about
 
7% 
/
6
 
years
Relapse,
S. 
aureus 
usually 
means
 
surgery
S. 
aureus- 
RR 
death 
0.18 
in 
surgery 
plus 
AB 
vs
ABx
 
alone
 
P
r
o
phy
la
xis
 
For 
High 
or 
Mod.
 
cardiac
risk 
conditions
 
(previous
list)
For 
Dental, 
rigid
bronchoscopy,
esophageal 
procedures,
 
G
I 
mucosal 
procedures,
cystoscopy, 
prostate
surgery
Antibiotic 
Prophraxis
(American 
Heart
 
Assoc.
JAMA
 
Timing
One 
hour 
prior
 
to
procedure:
2gm Amoxicillin 
oraly
 
or
600 
mg
 
Clindamycin
orally
 
or
2gm 
Cephalexin 
orally
or
500mg 
Clarithromycin
orally
 
or
2 
gm 
Ampicillin
i
n
tr
a
mu
scu
l
a
r
i
y
 
Dental 
procedures
where 
endocarditic
prophylaxis
 
indicated:
 
1.
Extraction
2.
Periodontal
 
procedures
3.
Implants
4.
Root 
canal
5.
Subgingival
 
antibiotics
fiber/strips
6.
Initial 
orthodontic 
bands
 
(not
brackets)
7.
Intraligamentary
 
local
anesthetic
8.
Cleaning 
of 
teeth/implants
 
if
bleeding
 
anticipated
 
Dental 
procedures
where
 
endocarditic
prophylaxis 
NOT
indicated:
1.
Filling 
cavity 
or
 
local
anesthetic
2.
Placement 
of 
rubber
 
dam
3.
Suture removal
4.
Orthodontic 
removal
5.
Orthodontic 
adjustments
6.
Dental
 
X-rays
7.
Shedding 
of
 
primary
teeth
 
ALI 
 
SOMILY
 
,
  
MD,
 
FRCP(C)
ali.somily@gmail.com
 
FAWZIA  ALOTAIBI,  MD
ofawzia@ksu.edu.sa
 
Male tutor                                                           Female tutor
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Infective endocarditis is an infection of the heart's endocardial surface that can be classified into four groups. It is crucial to recognize common bacteria causing IE, understand clinical presentations, diagnostic methods, and management strategies. The pathophysiology involves turbulent blood flow leading to bacterial adherence to the endocardium. The disease predominantly affects the elderly population, with a changing incidence due to factors like rheumatic heart disease decline and aging demographics.


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  1. Infective Endocarditis ALI SOMILY,MD,FRCP(C) ali.somily@gmail.com FAWZIA ALOTAIBI, MD ofawzia@ksu.edu.sa

  2. Objectives Define infective endocarditis Recognize the bacteria such as staphylococcus aureus and streptococcus viridans as the most common etiologies of IE Know the different clinical presentation of acute and sub-acute IE To recognize the different clinical presentation of IE; fever as the most common cause of pyerixia of unknown origin (P.U.O). TO the bacterial and host factors affecting the severity and outcome of the disease. Recognize the sources of bacteria causing bacteremia preceding IE. To know the pathogenesis of IE and the formation and importance of vegetations. To know the predisposing factors such as RHD, CHD, prosthetic valves and IVDU. To the common bacterial causes of IE associated with different sources and clinical conditions. To realize the infection as a diagnostic challenge and to know the different diagnostic methods of IE including; Clinical presentation (signs & symptoms) 1. Laboratory tests mainly multiple blood cultures. 2. Echocardiogram for the presence of vegetations 3. To know the different regimens used to treat different types of organisms. To know possible complications of IE.

  3. Outlines Definition Pathogenesis Riskfactors Clinical presentation Diagnosis Culture negativeendocarditis Management Prophylaxis

  4. Definition Infectious Endocarditis (IE): an infectionof the heart s endocardialsurface Classified into fourgroups: Native ValveIE Prosthetic ValveIE Intravenous drug abuse(IVDA) IE Nosocomial IE

  5. Further Classification Acute: Affectsnormal heart valves Subacute: Often affects damaged heart valves Rapidlydestructive If not treated, usually fatalwithin 6weeks Commonly Staph Metastatic foci Indolent nature If not treated, usually fatal byone year Commonly viridans Streptococci

  6. Pathophysiology 1. Turbulent blood flow disruptsthe endocardium making it sticky 2. Bacteremia delivers theorganisms to the endocardialsurface 3. Adherence of the organisms to the endocardial surface 4. Eventual invasion of thevalvular leaflets

  7. Epidemiology Incidence: 1.7 6.2 / 100, 000 person years M:F1.7 Becoming a disease of theelderly Median age PreABx era 35y Now 58y Due to twofactors The decline of rheumatic heart disease The increasing proportion ofelderly

  8. Prosthetic Valve 7 -25 % of cases of infectiveendocarditis Early <12mons Late >12mons 0.94 per 100,000bioprosthetic Initially mechanical valves at greater risk for first 3mo, then risk same at 5y 1-3.1% risk at 1yr 2-5.7% at 5yr

  9. Risk Factors Injection drug use 100X risk inyoung Staphylococcusaureus Other risks: Poor dentalhygiene Hemodialysis DM HIV IVDU Rates 150-2000/ 100000 person years Higher among patientswith known valvular heart disease Structural cardiac abnormality 75% of pts will have a preexisting structural cardiac abnormality 10-20% have congenital heart disease 1. 2. 3. 4.

  10. Risk Factors ; Cardiac Abnormality High risk Moderate risk MVP w/ MR/thickened leaflets- 5 to 8 times (100/100 000 person years) Previous IE 4.5(2.5 to 9)% Aortic valve disease12 to30% Rheumaticvalve disease Prosthetic valve Coarctation Complexcyanotic congenital MitralStenosis tricuspidvalve Pulmonary Stenosis Hypertrophic Obstructive Cardiomyopathy (HOCM) Low/no risk ASD(secundum) CABG

  11. Risk Factors HIVinfection: Anumber of cases of IEhave been reported in patients with HIVinfection It has been suggested that HIVinfection is an independent risk factor for IE inIDU Rheumatic valve disease: Predisposition for young in some countries 37%-76%ofcases Mitral 85%, Aortic50% Degenerative valvularlesions MVProlapse and associated mitral regurgitation - 5to 8times higher IErisk Aortic valve disease (stenosis or/and regurgitation) is present in 12 to 30 % ofcases

  12. Diagnostic approach History of prior cardiaclesions A recent source ofbacteremia

  13. Symptoms Acute High grade feverand chills SOB Arthralgias/ myalgias Abdominal pain Pleuritic chest pain Backpain Subacute Low grade fever Anorexia Weight loss Fatigue Arthralgias/ myalgias Abdominal pain N/V The onset of symptoms is usually ~2weeks or less from the initiatingbacteremia

  14. Physical examination Signs Fever Heart murmur Nonspecific signs petechiae, subungal or splinter hemorrhages, clubbing, splenomegaly, neurologic changes More specific signs - Osler s Nodes, Janeway lesions, and RothSpots Look for small andlarge emboli with special attention to the fundi, conjunctivae, skin, and digits Cardiac examinationmay reveal signs of new regurgitation murmurs and signs ofCHF Neurologic evaluation may detect evidenceof focal neurologic impairment

  15. Other aspects clinical diagnosis WHICH V ALVE? R or L heart where would emboli go? HEARTFUNCTION? Pump, acute valve dysfunctionconduction Look for evidence emboli Bleed (intracranial, elsewheremycotic aneurysm )

  16. Diagnostic approach 1 Positive blood cultureresults Aminimum of three blood cultures should be obtained over a time period based upon the severity of theillness 2 Additional laboratory Nonspecifictest An elevated ESR and/or anelevated level of CRP is usually present Most patients quickly develop a normochromic normocytic anemia The WBCcount may be normal or elevated

  17. Additional laboratory tests abnormalurinalysis The combination of RBC casts on urinalysis and a low serum complement level may be an indicator of immune-mediated glomerular disease ECG: New A V , fascicular, or bundle branchblock... .?PERIV ALVULAR INVAVSION monitoring, ??pacing

  18. Prosthetic Valve IE Early (0-2 mo) 1 -3.1% 50% Staphylococci S. epi.> S. aureus, gnb, enterococci Late (>12 mo) 2 -5.7% IE in IV drug abusers Native Valve IE Strep. (55%), mostly S. viridans Staph. (30%), mostly S. aureus Enterococci (5-10%), GNB=HACEK(5%), Fungi Staph.aureus(50-60%)

  19. Case Definition: IE Dukecriteria In 1994 investigators from DukeUniversity modified the previous criteria to include The role of echocardiography in diagnosis They also expanded the category of predisposing heart conditions to include intravenous drug use

  20. Modified Duke criteria Possible IE 2major 1 major and 3minor 5minor Rejected IE Resolution of illness withfour days or less ofantibiotics Proposed: 2000,Addresses TEE, Broad possible categories. S. aureus risks (13-25% S. aureus bacteremia haveIE ) Definite IE Microorganism (via cultureor histology) in avalvular vegetation, embolized vegetation, orintracardiac abscess Histologic evidence ofvegetation or intracardiac abscess

  21. Major criteria 1.MICROBIOLOGY Minor criteria Predisposition (heart conditionor IV drug use) Typical organism from2 separate culturesOR Microorganism from persistently positive BC OR Single BC + for Coxiella burnetii, or titer>1:800 2.ENDOCARDIALINVOLVEMEMT New (not changed) murmurof regurgitation 3.POSITIVEECHO (TEEif prosthetic valve, complicated, or pretest probability possibleIE 1.Fever >/=38oC 2.Vascular phenomenon(excludes petechiae, splinter hemorrhage) 3.major arterial emboli, Mycotic aneurysm, intracranial orconjunctival hemorrhages. Janeway lesions 4.Immunologic phenomena RF,.Roth s spots glomerulonephritis, Osler s nodes 6.Microbiologicevidence Not meeting major criteria single BC not CNS,serology

  22. Petechiae 1. Nonspecific 2. Often located onextremities or mucousmembranes Harden Libraryfor the Health Sciences Photo credit, Josh Fierer,M.D.

  23. Splinter Hemorrhages 1. Nonspecific 2. Nonblanching 3. Linear reddish-brown lesions found under the nail bed 4. Usuallydo NOTextend the entire length of the nail

  24. Oslers Nodes American College ofRheumatology 1. More specific 2. Painful and erythematousnodules 3. Locatedon pulp of fingers and toes 4. More common in subacuteIE

  25. Janeway Lesions 1. More specific 2. Erythematous, blanchingmacules 3. Nonpainful 4. Located on palms andsoles

  26. Complications Four etiologies Embolic Local spread ofinfection Metastatic spread ofinfection Formation of immune complexes glomerulonephritis and arthritis

  27. Embolic Complications Stroke MyocardialInfarction Fragments ofvalvular vegetation or vegetation-induced stenosis of coronary ostia Ischemic limbs Hypoxia frompulmonary emboli Abdominal pain(splenic or renalinfarction) Occur in up to40% of patients withIE Predictors ofembolization Size ofvegetation Left-sided vegetations Fungal pathogens, S.aureus, and Strep.Bovis Incidence decreases significantly after initiation ofeffective antibiotics

  28. Septic Pulmonary Emboli Septic Retinalembolus http://www.emedicine.com/emerg/topic164.htm

  29. Local Spread of Infection Heart failure Extensive valvular damage Paravalvular abscess(30-40%) Most common in aortic valve, IVDU, andS. aureus May extend into adjacent conduction tissue causing arrythmias Higher rates of embolization and mortality Pericarditis Fistulous intracardiac connections

  30. Local Spread of Infection Acute S. aureus IE with perforation of the aortic valve and aortic valve vegetations. Acute S. aureus IE with mitral valve ring abscess extending intomyocardium.

  31. Metastatic Spread of Infection Metastatic abscess Kidneys, spleen, brain, softtissues Meningitis and/or encephalitis Vertebral osteomyelitis Septic arthritis

  32. Poor Prognostic Factors Female S.aureus Vegetation size Aortic valve Prosthetic valve Older age Diabetes mellitus Low serum albumen Apache IIscore Heart failure Paravalvular abscess Embolic events

  33. Echocardiographic findings 1. Oscillating intracardiac mass o On valve or supportingstructure, In the path of regurgitation jets, Onimplanted material, in the absence of an altenate anatomicexplanation 3. abscess 1. New partial dehiscence of prostheticvalve 2. New valvular regurgitation (increaseor change in pre-existing murmur not sufficient)

  34. Improved diagnostic value of echocardiography in patients with infective endocarditis by transoesophageal approachA prospective study Eur Heart J, 1988 Jan;9(i):43.5396 patients werestudied consecutively with TEE andTTE TEE sensitivity 100 percent for vegetationsas compared to 63percent with TTE Both TTE and TEE had specificity of98% 25% of vegetations less than 5mm, 69% of vegetations 6-10 mm, and 100%of vegetations greater than 11 mm detected by TEE were also observed withTTE

  35. Culture Negative IE Hemophilus paraphrophilus, aphrophilus. Parainfluenzae Aggregatibacter(Actino b acillus) actinomycetemcomitans Cardiobacterium hominis Eikenella corrodens Kingellaspp. How hard didyou look? (50% culture negare d/t previous antibiotics) HACEK: - 2-3 wk incubation, subculturing, Tend to seesubacute w/ valve destruction/CHF

  36. Lab Diagnosis! EtiologiesCulture Negative IE Based on clinical setting PCR ofvegetation/emboli: Tropheryma whippelei, bartonella Histology/stain /culture ofvegetation/emboli: Fungus Prolonged, enriched cultures: HACEK Lysis centrifugation system (Isolator): Bartonella, legionella (BCYE),fungal Serology: Endemic fungi, bartonella, Q fever, brucella, legionella,chiamydia Thioglycolate or cysteine supplementedmedia. S.aureus satellitism: Abiotrophia(NVS)

  37. endocarditis GENERALCONSIDERA TIONS Antimicrobial therapy should be administered in a dose designed to give sustained bactericidal serum concentrations throughout much or all of the dosinginterval. In vitro determination of the minimum inhibitory concentration of the etiologiccause of the endocarditis should be performed in all patients.

  38. The duration of therapy has to be sufficient to eradicatemicroorganisms growing within the valvular vegetations. The need for prolonged therapy in treating endocarditis hasstimulated interest in using combination therapy to treatendocarditis.

  39. Indications for surgery in IE Combined therapy generally advisedwith Refractory CHF (mortality 56-86% w/o surgery vs 11-35%w/surgery) Perivalvualr invasivedisease Uncontrolled infection on maximalmedical therapy Recurrent systemic emboli, particularly in the presence of largevegetations SOME pathogens: Pseudomonas, brucella, coxiella, fungi,enterococci

  40. Prosthetic same as native valve endocarditis Perivalvular infectionvalve Dehiscence Excessively mobile prosthesis onecho results in hemodynamicinstability

  41. Prosthetic valve endocarditis that one may attemptmedical treatment alone: 1. >l2mo post surgical 2. VGS or HACEK or enterococci 3. No perivalvular extension Recurrence after surgery about7% / 6years Relapse, S. aureus usually meanssurgery S. aureus-RR death 0.18 in surgery plus AB vs ABxalone

  42. VGS, NVS, sreptococcus MIC(ug/mI) Native valve prosthetic valve PenG or Ceph3 4wk PenG 6wkplus Gent 2wk <0.1 PenG 6wkPlus Gent 4wk >0.1 0.5 PenG 4wk plus Gent 2wk >0.5 PenG or Amp plus Gent for 4-6 wk total 6 wk Cloxacillin / Vancomycin 4-6 wk +/- gent X3-5d cloxacillin / vancomycin 6wk, gentamicin 2wk, rifampin 6 wk MSSA/ MRSA: Most common org IDU w/ R sided IE Clox plus gent 2wk, (not if complicated or febrile >lwk, large vegetations) HACEK Ceph3 for 4wk 6wk Aminoglycoside and flouroquinolones(or B-Lactam) Bartonella Doxycycline +or-hydroxychloroquine 26 months untill the titer below1:400 Q-fever 35% surgical

  43. Prophylaxis Timing One hour priorto procedure: For High or Mod. cardiac risk conditions (previous list) For Dental, rigid bronchoscopy, esophageal procedures,G I mucosal procedures, cystoscopy, prostate surgery Antibiotic Prophraxis (American HeartAssoc. JAMA 2gm Amoxicillin oralyor 600 mg Clindamycin orally or 2gm Cephalexin orally or 500mg Clarithromycin orally or 2 gm Ampicillin intramusculariy

  44. Dental procedures where endocarditic prophylaxis indicated: 1.Extraction 2.Periodontal procedures 3.Implants 4.Root canal 5.Subgingivalantibiotics fiber/strips 6.Initial orthodontic bands(not brackets) 7.Intraligamentary local anesthetic 8.Cleaning of teeth/implants if bleeding anticipated Dental procedures where endocarditic prophylaxis NOT indicated: 1.Filling cavity orlocal anesthetic 2.Placement of rubberdam 3.Suture removal 4.Orthodontic removal 5.Orthodontic adjustments 6.Dental X-rays 7.Shedding ofprimary teeth

  45. Male tutor Female tutor ALI SOMILY,MD,FRCP(C) ali.somily@gmail.com FAWZIA ALOTAIBI, MD ofawzia@ksu.edu.sa

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