Download Infective Endocarditis

Infective Endocarditis
Faculty of Medicine
University of Brawijaya
Malang
INTRODUCTION
The term ‘bacterial endocarditis’ has been
replaced by ‘Infective endocarditis’ (IE) since fungi
are also involved as causative pathogens
IE is an uncommon but lifethreatening infection.
If the diagnosis is delayed or appropriate
therapeutic measures postpone, mortality is still
high
JADA, Vol. 138, 2007
European Heart Journal (2004) 00, 1-37
Guidelines AHA, Circulation. 2007;115:&NA;-.
INTRODUCTION
If untreated Infective Endocarditis (IE) is a fatal
disease. Major diagnostic (first of all
echocardiography) and therapeutic progress
(mainly surgery during active IE) have
contributed to some prognostic improvement.
In this respect, it is of utmost importance that:
– IE is considered early in every patients with fever or
septicaemia and cardiac murmurs.
– Echocardiography is applied without delay in
suspected IE.
– Cardiologist, microbiologists and cardiac surgeons
cooperate closely if IE is suspected or definite.
INTRODUCTION
Recent data suggest it may be increasing,
1. In industrialized nations, patients are living longer
2. There is an increase in nosocomial infections
3. Intravenous drug use has increased in industrialized
societies
4. Increasing application of cardiac surgery has provided
new substrates for endocardial infection
5. The increased use of indwelling intravascular lines and
implantable devices
6. the increased application of echocardiography
Cardiol Clin 21 (2003) 159–166
DEFINITION
IE is an endovascular, microbial
infection of intracardiac structures facing
the blood including infections of the large
intrathoracic vesseis and of intracardiac
foreign bodies.
The early characteristic lesion is a variably
sized vegetation, although destruction,
ulceration or abscess formation may be
seen earlier by echocardiography.
Definition
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
INFECTIVE ENDOCARDITIS
Characterized by inflammation or infection
two major predisposing factors:
– susceptible cardiac or vascular substrate
lesions associated with high-velocity flow, jet impact and
focal increases in the rate of shear
– source of bacteremia
Further Classification
Acute
– Affects normal heart
valves
– Rapidly destructive
– Metastatic foci
– Commonly Staph.
– If not treated, usually
fatal within 6 weeks
Subacute
– Often affects damaged
heart valves
– Indolent nature
– If not treated, usually
fatal by one year
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
Proposed scheme for the pathogenesis of infective
endocarditis
Mandell, Bennett, & Dolin:
Principles and Practice of Infectious Diseases, 6th ed
Epidemiology
Incidence difficult to ascertain and varies
according to location
Much more common in males than in
females
May occur in persons of any age and
increasingly common in elderly
Mortality ranges from 20-30%
Risk Factors
Intravenous drug abuse
Artificial heart valves and pacemakers
Acquired heart defects
– Calcific aortic stenosis
– Mitral valve prolapse with regurgitation
Congenital heart defects
Intravascular catheters
Infecting Organisms
Common bacteria
– S. aureus
– Streptococci
– Enterococci
Not so common bacteria
– Fungi
– Pseudomonas
– HACEK
HACEK organisms
• Hemophilus, Actinobacillus,
•
•
•
•
Cardiobacterium, Eikenella, Kingella
Gram negative inhabitants of the upper
airways.
Large vegetations, high likelihood of
embolization.
Slow growing: hold cultures for 3 weeks.
Traditionally sensitive to beta lactams, now
some produce beta lactamase.
Symptoms
Acute
– High grade fever and
chills
– SOB (shortness of
breath)
– Arthralgias/ myalgias
– Abdominal pain
– Pleuritic chest pain
– Back pain
Subacute
–
–
–
–
–
–
Low grade fever
Anorexia
Weight loss
Fatigue
Arthralgias/ myalgias
Abdominal pain
The onset of symptoms is usually ~2 weeks or less
from the initiating bacteremia
Signs
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
Petechiae
1. Nonspecific
2. Often located on extremities
or mucous membranes
dermatology.about.com/.../
blpetechiaephoto.htm
Photo credit, Josh Fierer, M.D.
medicine.ucsd.edu/clinicalimg/ Eye-Petechiae.html
Harden Library for the Health Sciences
www.lib.uiowa.edu/ hardin/
md/cdc/3184.html
Splinter Hemorrhages
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
American College of Rheumatology
webrheum.bham.ac.uk/.../ default/pages/3b5.htm
www.meddean.luc.edu/.../
Hand10/Hand10dx.html
1. More specific
2. Painful and erythematous nodules
3. Located on pulp of fingers and toes
4. More common in subacute IE
Janeway Lesions
1. More specific
2. Erythematous, blanching macules
3. Nonpainful
4. Located on palms and soles
The Essential Blood Test
Blood Cultures
– Minimum of three blood cultures1
– Three separate venipuncture sites
– Obtain 10-20mL in adults and 0.5-5mL in children2
Positive Result
– Typical organisms present in at least 2 separate samples
– Persistently positive blood culture (atypical organisms)
Two positive blood cultures obtained at least 12 hours apart
Three or a more positive blood cultures in which the first and
last samples were collected at least one hour apart
Additional Labs
CBC (complete blood count)
ESR (erythrocyte sedimentation rate) and
CRP (C reactive protein)
Complement levels (C3, C4, CH50)
RF (rheumatoid factors)
Urinalysis
Baseline chemistries and coagulations
Imaging
Chest x-ray
– Look for multiple focal infiltrates and
calcification of heart valves
EKG
– Rarely diagnostic
– Look for evidence of ischemia, conduction
delay, and arrhythmias
Echocardiography
Indications for Echocardiography
Transthoracic echocardiography (TTE)
– First line if suspected IE
– Native valves
Transesophageal echocardiography (TEE)
– Prosthetic valves
– Intracardiac complications
– Inadequate TTE
– Fungal or S. aureus or bacteremia
Making the Diagnosis
Pelletier and Petersdorf criteria (1977)
– Classification scheme of definite, probable, and possible IE
– Reasonably specific but lacked sensitivity
Von Reyn criteria (1981)
– Added “rejected” as a category
– Added more clinical criteria
– Improved specificity and clinical utility
Duke criteria (1994)
– Included the role of echocardiography in diagnosis
– Added IVDA as a “predisposing heart condition”
Modified Duke Criteria
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
CRITERIA THAT SHOULD RAISE
SUSPICION OF IE
High clinical suspicion (urgent indication for echocardiographic
screening and possibly hospital admission)
–
–
–
–
–
New valve lesion/(regurgitant) murmur
Embolic events of unknown origin (esp. cerebral and renal infarction)
Sepsis of unknown origin
Haematuria, glomerulonephritis, and suspected renal infarction
“Fever “ plus
Prosthetic material inside the heart
Other high predispositions of IE
Newly developed ventricular arrhythmias or conduction disturbances
First manifestation of chronic heart failure
Positive blood cultures (if the organism identified is typical for NVE/PVE)
Cutaneous (Osler, janeway) or ophthalmic (roth) manifestations
Multifocal/rapid changing pulmonary infiltrations (right heart IE)
Peripheral abscesses (renal, spienic, spine) of unknown origin
Predisposition and recent diagnostic/therapeutic interventions known to
result in significant bacteraemia
Low Clinical Suspicion
– Fever plus none of the above
ECHOCARDIOGRAPHY
Any patient suspected of having Native Valve Endocarditis (NVE) by
clinical criteria should be screened by Transthoracic
Echocardiography (TTE).
When images are of good quality and prove to be negative and
there is only a low clinical suspicion of IE, endocarditis is unlikely
and other diagnosis are to be considered.
If suspicion of IE is high, TransEsophageal Echocardiography (TEE)
should be performed in all TTE-negative cases, in suspected
Prosthetic Valve Endocarditis (PVE), and if TTE is positive but
complications are suspected or likely and before cardiac
surgery during active IE.
If TEE remains negative and there is still suspicion, it should be
repeated within one week. A repeatedly negative study should
virtually exclude the diagnosis.
Three echocardiographic findings are
considered to be major critetria in the
diagnosis of IE:
– A mobile, echodense mass attached to the
valvular or the mural endocardium or to
implanted prosthetic material
– Demonstration of abscesses or fistulas
– A new dehiscence of a valve prosthesis,
especially when occurring late after
implantation
Treatment
Parenteral antibiotics
– High serum concentrations to penetrate
vegetations
– Prolonged treatment to kill dormant bacteria
clustered in vegetations
Surgery
– Intracardiac complications
Surveillance blood cultures
ANTIMICROBIAL THERAPY
If initiation of antimicrobial therapy is urgent,
empiric antibiotic treatment can be started
thereafter (blood culture)
In all other cases it is recommended to postpone therapy until blood cultures become
positive.
Previous short term antibiotic  discontinue for
at least 3 day before taking blood cultures.
Previous long term antibiotic treatment 
discontinue for 6 - 7 days.
ESC guideline; European Heart J 2004
2 weeks regimen (combination) has similar
cure rates to 4 week regimen
4 week regimen (monotherapy) preferred in
– patients >65 yo
– with 8th cranial nerve impairment
– renal dysfunction
– Cardiac/extracardiac abscess
Vancomycin only for patients not tolerate to
penicillin / ceftriaxone
For combination antibiotics  given at
same time or close together to increase
synergistic effect
IE IN INTRAVENOUS DRUG USER
(IVDU)
Most common: S aureus *, **
MRSA had been emerging (60-70% in
Europe)**
Other organisms: P aeruginosa, Candida,
enterococci, streptococci *, **
Polymicrobial infection 5-10% **
* AHA guidelines IE. Circulation 2005;111;e394-e433
** ESC guidelines Infective Endocarditis 2004
ANTIBIOTIC PROPHYLAXIS
Background for prophylaxis:
– Bacteremia causes endocarditis
– Viridans group streptococci are part of normal oral flora,
and enterococci are part of normal GI and GU tract
flora
– These microorganisms were usually susceptible to
antibiotics recommended for prophylaxis
– Antibiotic prophylaxis prevents viridans group
streptococcal or enterococcal experimental endocarditis
in animals
AHA guideline: Prevention of Infective Endocarditis. Circulation 2007;115
– Large number of poorly documented case
reports implicated a dental procedure as a
cause of IE
– In some cases, there was a temporal
relationship between a dental procedure and
the onset of symptoms of IE
– The risk of significant adverse reactions to an
antibiotic is low in an individual patient
– Morbidity and mortality from IE are high.
Cardiac condition in Which
Antimicrobial Prophylaxis is Indicated
High Risk
–
–
–
–
Prosthetic heart valves
Complex congenital cyanotic heart diseases
Previous infective endocarditis
Surgically constructed systemic or pulmonary
conduits
Moderate Risk
– Acquired valvular heart disease
– Mitral valve prolapse with valvular regurgitation or
severe valve thickening
– Non-cyanotic congenital heart diseases (except for
secundum type Atrial Septal Defect) including
bicuspid aortic valves
– Hypertrophic cardiomyopathy
Predisposing diagnostic and therapeutic
interventions
Procedure which may cause bacteraemia and for which
antimicrobial prophylaxis is recommended
Diagnostic and therapeutic interventions likely to produce
bacteraemia
–
–
–
–
–
–
–
–
–
–
–
Bronchoscopy (rigid instrument)
Cystoscopy during urinary tract infection
Biopsy of urinary tract/prostate
Dental procedures with the risk of gingival/mucosal trauma
Tonsillectomy and adenoidectomy
Oesophageal dilatation/ sclerotherapy
Instrumentation of obstructed biliary tracts
Transurethral resection of prostate
Urethral instrumentation/ dilation
Lithotripsy
Gynaecologic procedures in the presence of infection
New from AHA for IE prophylaxis
Bacteremia from daily activities (chewing food,
tooth brushing and flossing, use of wooden
toothpicks, use of water irrigation devices) is
much more likely to cause IE than a dental
procedure
Extremely small number of IE might be
prevented by antibiotic prophylaxis, even if
prophylaxis is 100% effective
AHA guideline: Prevention of Infective Endocarditis. Circulation 2007;115
Limit prophylaxis only to conditions with
high adverse outcome from endocarditis
Maintenance of optimal oral health and
hygiene may reduce the incidence of
bacteremia from daily activities and is
more important than prophylactic
antibiotics
AHA guideline: Prevention of Infective Endocarditis. Circulation 2007;115
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
Embolic Complications
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
http://www.emedicine.com/emerg/topic164.htm
Septic Retinal Embolus
Local Spread of Infection
Heart failure
– Extensive valvular damage
Paravalvular abscess (30-40%)
– Most common in aortic valve, IVDA, 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
Paravalvular abscess
Embolic events
Summary
IVDA and the elderly are at greatest risk of
developing IE.
The signs and symptoms of IE are
nonspecific and varied.
A thorough but timely evaluation (including
serial blood cultures, adjunct labs, and an
echo) is crucial to accurately diagnose and
treat IE.
Beware of life-threatening complications.
THANK YOU
ACUTE
PERICARDITIS
Faculty of Medicine
Universitas Brawijaya
Malang
Incidence
Exact incidence and prevalence are
unknown
Diagnosed in 0.1% of hospitalized
patients and 5% of patients admitted for
non-acute MI chest pain
Observational study: 27.7 cases/100,000
population/year
Etiology: Can be Tricky. . .
Standard diagnostic evaluations are
oftentimes relatively low yield
One series elucidated a cause in only
16% of patients
Leading possibilities:
– Neoplasia
– Tuberculosis
– Non-tuberculous infection
– Rheumatic disease
Initial clinical and echocardiographic
evaluation of patients with suspected acute
pericarditis
Diagnostic Criteria
 Chest pain: anterior chest, sudden onset, pleuritic;
may decrease in intensity when leans forward, may
radiate to one or both trapezius ridges
 Pericardial friction rub: most specific, heard best at
LSB (Left sternal border)
 EKG changes: new widespread ST elevation or PR
depression
 Pericardial effusion: absence of does not exclude
diagnosis of pericarditis
 Supporting signs/symptoms:
Elevated ESR (erythrocyte sedimentation rate), CRP (C
reactive protein)
Fever
Leukocytosis
EKG
Electrocardiogram in acute pericarditis showing diffuse upsloping ST segment elevations seen best here in
leads II, III, aVF, and V2 to V6. There is also subtle PR segment deviation (positive in aVR, negative
in most other leads). ST segment elevation is due to a ventricular current of injury associated with epicardial
inflammation; similarly, the PR segment changes are due to an atrial current of injury which, in pericarditis,
typically displaces the PR segment upward in lead aVR and downward in most other leads.
Pericardial Effusion
Cardiomegaly due to a massive pericardial effusion. At least 200 mL of
pericardial fluid must accumulate before the cardiac silhouette enlarges.
Tests
 EKG
 CXR
 PPD
 ANA
 HIV
 Blood cultures
 Urgent echocardiogram if evidence of pericardial
effusion
 Not necessary:
Viral studies b/c yield is low and management is not
altered
Treatment
 NSAIDs + PPI
 Aspirin (2-5 g/day)
 Ibuprofen (300-800 mg q6-8H)*
 Ketorolac
 Theoretical concern that anti-platelet agents promote development of
hemorrhagic pericardial effusion has not been substantiated
 Colchicine (0.5-1 mg/day) : may prevent recurrence
 Glucocorticoids (prednisone 1 mg/kg/day): ? increased rate of
complications. Should be restricted to:
 Acute pericarditis due to connective tissue disease
 Autoreactive (immune-mediated) pericarditis
 Uremic pericarditis
*NSAID of choice unless associated with acute MI, where all non-ASA NSAIDs should be avoided
Prognosis for acute idiopathic
pericarditis
Good long-term prognosis
Cardiac tamponade is rare, but up to 70%
in cases with specific etiologies (eg.
Neoplastic, tuberculous, purulent)
Constrictive pericarditis occurs in about
1% of patients
15-30% of patients not treated with
colchicine develop either recurrent or
incessant disease
Recurrent Pericarditis
Exact recurrence rate unknown
Most cases considered to be autoimmune
Risk Factors:
– Lack of response to aspirin or other NSAID
– Glucocorticoid therapy
– Inappropriate pericardiotomy
– Creation of a pericardial window
For some patients, symptoms can only be
controlled with steroidal therapy
Autoreactive Pericarditis:
diagnostic criteria
 Pericardial fluid revealing >5000/mm3 mononuclear
cells or antisarcolemmal antibodies
 Inflammation in epicardial/endomyocardial biopsies
by >14 cells/mm2
 Exclusion of active viral infection both in pericardial
effusion and endocardial/epicardial biopsies
 Exclusion of tuberculosis, borrelia burgdorferi,
chlamydia pneumoniae and other bacterial infection
 Absence of neoplastic infiltration in effusion and
biopsy samples
 Exclusion of systemic, metabolic disorders and
uremia
Treatment




Aspirin
NSAIDs
Colchicine: can reduce or eliminate need for glucocorticoids
Glucocorticoids: should be avoided unless required to treat patients
who fail NSAID and colchicine therapy
 Many believe that prednisone may perpetuate recurrences
 Intrapericardial glucocorticoid therapy: sx improvement and prevention
of recurrence in 90% of patients at 3 months and 84% at one year
 Other immunosuppression
 Azothoprine (75-100 mg/day)
 Cyclophosphamide
 Mycophenolate: anecdotal evidence only
 Methotrexate: limited data
 IVIG: limited data
 Pericardiectomy: To avoid poor wound healing, recommended to be
off prednisone for one year. Reserved for the following cases:
 If >1 recurrence is accompanied by tamponade
 If recurrence is principally manifested by persistent pain despite an
intensive medical trial and evidence of serious glucocorticoid toxicity