Transcript Endocarditis

Infective Endocarditis in Adults
R4 Sung-Jin Kwon
Contents
Epidemiology
Etiology
Pathogenesis
Clinical Manifestation
Diagnosis
Complication
Treatment
Prevention
Introduction
Infective endocarditis : A microbial infection of the endocardial surface
- most commonly involves heart valves (either native or prosthetic)
- may also occur on the low-pressure side of the ventricular septum
- on the mural endocardium where it is damaged by aberrant jets
- on intracardiac devices themselves
Incidence : 2.6 to 7.0 cases per 100,000 population per year
notably increased among the elderly
Predisposing conditions shifting from chronic rheumatic heart disease
to illicit IV drug use, degenerative valve disease, intracardiac devices,
and health care–associated infection
Introduction
 Classified according to the temporal evolution of disease, the site of
infection, the cause of infection, or a predisposing risk factor
Acute
Affects normal heart valves
Rapidly destructive
Metastatic foci
Commonly by Staphylo
If not treated, usually fatal
within 6 weeks
Subacute
Often affects damaged
heart valves
Indolent nature
If not treated, usually fatal
by one year
5
Epidemiologic Change in Korea
Mean age : increase (48 yrs old)
Acute infective endocarditis : relatively increased
Classic clinical manifestations (Osler’s node, clubbing, Roth spot) : rare
Endocarditis d/t streptococcus infection : decreased trend
Gram negative bacilli, fungus or uncommon source infection : increase
Endocarditis in IV drug user : increase
Prosthetic valve endocarditis : abruptly increased (most common
underlying heart disease)
First manifestation as endocarditis in pts without underlying heart
disease : increase (54%)
Still consistent culture nagative incidence (30%) & high mortality (20%)
Epidemiology
Brouqui and Raoult, Clin Microbiol Rev, 2001
Fowler, V. JAMA, 2006
7
Etiology
Pathogens vary with the clinical types of endocarditis because of
different portals of entry
- The oral cavity, skin, and upper respiratory tract
: primary portals for viridans streptococci, staphylococci, and HACEK
organisms (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella,
and Kingella) → causing community-acquired native valve endocarditis
- Streptococcus bovis originates from the gastrointestinal tract
: associated with polyps and colonic tumors
- Enterococci enter the bloodstream from the genitourinary tract
- Health care–associated native valve endocarditis
: consequence of bacteremia arising from intravascular catheter
infections, nosocomial wound and urinary tract infections, chronic
invasive procedures such as hemodialysis
→ Staphylococcus aureus bacteremia is higher
Organisms Causing Major Clinical Forms of Endocarditis
Harrison 17th Table 118-1 9
Pathogenesis
Endothelium : resistant to infection by most bacteria and to thrombus
formation
Pressure drop → Turbulent Jet → Endothelial injury
(at the site of impact of high-velocity blood jets or on the low-pressure
side of a cardiac structural lesion)
→ Direct infection by virulent organisms or development of an
uninfected platelet-fibrin thrombus
(nonbacterial thrombotic endocarditis : NBTE)
→ Bacterial attachment on thrombus during transient bacteremia
→ Vegetation
Clinical Manifestation
1. Cardiac manifestation
Heart murmurs : predisposing cardiac pathology → valvular damage
and ruptured chordae result in new regurgitant murmurs
(In acute endocarditis only 30–45% → ultimately in 85%)
Congestive heart failure (30–40%)
Perivalvular abscess
Heart block : adjacent to either the right or the noncoronary cusp of
the aortic valve may interrupt the conduction system in the upper
interventricular septum
Myocardial infarction
Clinical Manifestation
2. Non-Cardiac manifestation
Septic embolization (subungual hemorrhage, Osler's nodes)
Arterial emboli (50%)
Embolic renal infarct
Musculoskeletal Sx : nonspecific inflammatory arthritis, back pain
Neurologic symptoms (40%) : mostly resulting from embolic stroke
aseptic or purulent meningitis, intracranial hemorrhage, ruptured my
cotic aneurysms, seizures, encephalopathy.
Hypocomplementemic glomerulonephritis & renal dysfunction
Endocarditis associated with injection drug use
: infection limited to the tricuspid valve (50%) and prominent
pulmonary findings (cough, pleuritic chest pain, nodular pulmonary
infiltrates, pyopneumothorax)
Clinical and Laboratory Features of Infective Endocarditis
The onset of symptoms is usually 2 weeks
or less from the initiating bacteremia
Harrison 17th Table 118-2
Petechiae
Nonspecific
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
Nonspecific
Nonblanching
Linear reddish-brown lesions found under the nail bed
Usually do NOT extend the entire length of the nail
Osler’s Nodes
More specific
Painful and erythematous nodules
Located on pulp of fingers and toes
More common in subacute IE
American College of Rheumatology
webrheum.bham.ac.uk/.../ default/pages/3b5.htm
www.meddean.luc.edu/.../
Hand10/Hand10dx.html
Janeway Lesions
More specific
Erythematous, blanching macules
Nonpainful
Located on palms and soles
Roth’s Spots
Diagnosis
 Endocarditis Milestones
1885
Osler-clinical syndrome
1944
Penicillin
1960
Operation
1973
Echocardiography Dx of vegetation
1977
Pelletier and Petersdorf criteria
1981
Von Reyn Criteria
1994
Duke Criteria
2000
Li → Modified Duke Criteria
Introduction to first of three seminal lectures
on endocarditis to the Royal College of
Physicians of London
Lancet 1885;1:415-418
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 IV drug abuser as a “predisposing heart condition”
Modified Duke Criteria for the Diagnosis of
Infective Endocarditis
21
Harrison 17th
Echocardiographic Roles in Endocarditis
Highly sensitive for detection of vegetations
Detection of underlying heart disease and complications
Response to therapy
Use in conjunction with clinical findings to define indications for
operation
Prognostic implications
Hallmark is vegetation !
→ No single characteristics on echocardiography
Positive feature
Negative feature
Low reflectance
Attached to valve, upstream side
Irregular shape, amorphous
Mobile, oscillating
Asso. tissue change, valvular regurgitation
High echogenicity
Nonvalvular location
Smooth surface or fibrillar
Non-mobile
Absence of regurgitation
Feigenbaum’s Echocardiography 6th Ed
Indication for TEE
High clinical suspicion of IE
Fever of unknown etiology
Bacteremia of unknown etiology
Clinical aggravation during treatment of IE
Presence of prosthesis & inadequate TTE
TTE detection rate 60-70 %, size 2-4 mm
TEE detection rate 98 %,
size 1-2 mm
Sensitivity & Specificity of Echo in Dx of Native-Valve Endocarditis
Sensitivity & Specificity of Echo in Dx of Prosthetic-Valve Endocarditis
Diagnostic Use of TTE and TEE
Harrison 17th Figure 118-4
Mimics of Infective Endocarditis
Atrial myxoma
Marantic endocarditis
Left atrial thrombus
Acute rheumatic fever with carditis
Collagen vascular disease (SLE)
Neoplasms (carcinoid)
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
Subclinical emboli are often found on autopsy
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 to a coronary artery
- vegetation-induced stenosis of coronary ostia
Embolic events often with infarction involving the extremities,
spleen, kidneys, bowel
- ischemic limbs
- embolic renal infarct : cause flank pain and hematuria but
rarely cause renal dysfunction
Hypoxia from pulmonary emboli
Abdominal pain (splenic or renal infarction)
Local Spread of Infection
Heart failure (30–40%)
usually consequence of valvular dysfunction
occasionally d/t endocarditis-associated myocarditis or an
intracardiac fistula
Paravalvular abscess (30-40%)
extension of infection beyond valve leaflets into adjacent annular
or myocardial tissue
most common in aortic valve, IV drug abuser, S. aureus
may extend into adjacent conduction tissue causing arrythmias
higher rates of embolization and mortality
Pericarditis
Fistulous intracardiac connections
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
- Splenic abscess (3–5%)
: effective therapy requires either image-guided percutaneous
drainage or splenectomy
Meningitis and/or encephalitis
Vertebral osteomyelitis
Septic arthritis
Extracardiac Complications
Mycotic aneurysms : 2–15%
- half of cases involve the cerebral arteries
- present as headaches, focal neurologic symptoms, or hemorrhage
-.some cerebral aneurysms resolve with effective antimicrobial therapy
- if persist, enlarge, or leak should be treated surgically
Extracerebral aneurysms
- present as local pain, mass, local ischemia, or bleeding
- treated by resection
Endocarditis - Cause of Death
CHF
Embolic phenomena
Mycotic aneurysm rupture
Complications from cardiovascular surgery
PVE
Inadequate response to antibiotics
Treatment
1. Parenteral antibiotics
 Difficult to eradicate bacteria from the avascular vegetation
 High serum concentrations to penetrate vegetations
 Must be bactericidal
 Prolonged treatment to kill dormant bacteria clustered in vegetations
2. Surgery
Treatment – Antibiotic Therapy
Organism-Specific Therapies
Streptococci
- Minimum inhibitory concentration (MIC) of penicillin must be
determined
- 2-week penicillin/gentamicin or ceftriaxone/gentamicin regimens
should not be used to treat complicated native valve infection or
prosthetic valve endocarditis
- Endocarditis caused by organisms of group B, C, or G : regimen
recommended for relatively penicillin-resistant streptococci is
advocated
Antibiotic Treatment for Infective Endocarditis
Caused by Common Organisms
Surgical Treatment
 Most of the clinical indications for surgery are not absolute
Harrison 17th Table 118-5
Timing of Cardiac Surgical Intervention
in Patients with Endocarditis
Harrison 17th Table 118-6
Prevention
Antibiotic prophylaxis in selected procedures considered to entail a
risk for bacteremia and endocarditis
The benefits of prophylaxis are not established and in fact may be
modest
Dental treatments, most widely accepted as predisposing to
endocarditis, are no more frequent during the 3 months preceding
endocarditis
AHA restricted the recommendations for antibiotic prophylaxis
Harrison 17th Table 118-7,8