Transcript ENDOCARDITISx

INFECTIVE 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)
hemorrhages: Dark-red, linear  Roth spots: Retinal
hemorrhages
with
small,
clear
lesions in the nail beds
centers; rare
Other signs of IE include the following
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Splenomegaly
Stiff neck
Delirium
Paralysis, hemiparesis,
aphasia
• Conjunctival hemorrhage
• Pallor
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Gallops
Rales
Cardiac arrhythmia
Pericardial rub
Pleural friction rub
Patients with IE may have
involvement of other organs:
• Metastatic infection (eg,
vertebral osteomyelitis),
• Embolic events (eg, focal
neurologic deficits, renal infarct,
splenic infarct).
• Systemic immune reaction (eg,
glomerulonephritis).
• In right-sided endocarditis,
septic pulmonary emboli may be
seen
Chest radiograph of a patient with
tricuspid valve endocarditis due to
S. aureus
Multiple cavitating lung nodules
due to septic pulmonary emboli.
Petechiae
Janeway lesions
Osler node
Splinter hemorrhage
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, dull sensorium,
headaches
• Abdominal symptoms,
such as right upper
quadrant pain, vomiting,
postprandial distress,
appendicitis-like
symptoms
Diagnosis
The Duke diagnostic criteria, 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:
Echocardiographic criteria for IE
• Typical microorganism for
• Oscillating intracardiac mass on a
infective endocarditis from two
valve or on supporting structures,
separate blood cultures
in the path of regurgitant jets, or
on implanted material.
• Blood cultures persistently positive
for one of these organisms, from
• Myocardial abscess
cultures drawn more than 12
• Development of partial
hours apart
dehiscence of a prosthetic valve
• Three or more separate blood
• New-onset valvular regurgitation
cultures drawn at least 1 hour
apart
Minor criteria for IE include the following:
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Predisposing heart condition or
intravenous drug use
Fever of 38°C or higher
Vascular phenomenon:
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Major arterial emboli
Septic pulmonary infarcts
Mycotic aneurysm
Intracranial hemorrhage
Conjunctival hemorrhage
Janeway lesions
Immunologic phenomenon:
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Glomerulonephritis
Osler nodes
Roth spots
Rheumatoid factor
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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 rt. 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.
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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.
Differential Diagnoses
• 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
• 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.
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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CBC (Leukocytosis in acute stage)
ESR (Elevated in 90%)
BUN
Coagulation Profile
RF (+50%)
Proteinuria
Hematuria
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.
• 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.
• 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
Class I - There is evidence and/or general agreement that TTE or TEE should be performed in patients with
native or prosthetic valve IE.
Class IIa - The weight of evidence or opinion is in favor of the usefulness of TTE or TEE in patients with
native or prosthetic valve IE.
Class IIb - The weight of evidence or opinion is less well-established for the usefulness of TTE or TEE in
patients with native or prosthetic valve IE.
CT: computed tomography; IE: infective endocarditis; NVE: native valve endocarditis; PVE: prosthetic valve
endocarditis; TEE: transesophageal echocardiography; TTE: transthoracic echocardiography.
* Repeat TEE and/or TTE recommended for re-evaluation of patients with IE and a change in clinical signs
or symptoms and in patients at high risk of complications.
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
• 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)
• 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
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.