This book contains alot of information regarding infective endocarditis
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Language: en
Added: Jul 24, 2024
Slides: 26 pages
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This is an infection, usually bacterial, of the
endocardial surface of the heart
Prototypic lesion –the vegetations( mass of platelets,
fibrin, microcolonies of microorganisms, scant
inflammatory cells
Most commonly involves valves ( native and
prosthetic), may also affect mural endocardium,
intracardiac devices, A-V shunts, PDA, coarctation of
AO
Acute febrile illness, rapid damage of cardiac
structures, hematogenically seeds extracardiac sites
resulting in death within weeks if untreated
Subacute-cardiac damage is slow, gradual progression
Potentially any bacteria or fungi
1.COMMUNITY –ACQUIRED
mostly from oral cavity, skin, URT –Streptococci
viridans, Staphylococci, HACEK ( Haemophilis,
Actinobacilli, Cardiobacterius, Eikinella, Kingella)
GIT –Streptococcus bovis
GUT -enterococci
2. NOSOCOMIAL IE.
Prosthetic valve endocarditis 2 months after surgery –
intraoperative contamination-usually coagulase-
negative Staphylococci, Gram(-) bacilli, diphteroids,
fungi
Transvenouspacemaker leads or implanted
defibrillators –Staph.aureusand other Staph.
3. DRUG USERS
Staph.aureus, Pseudomonas aeruginosa, Candida
Fungi –difficult to diagnose and treat, mostly Candida
and Aspergilles
5-15% of ptswith IE have (-) blood culture. 1/3-1/2 of
them due to prior antibiotic exposure
Normal endocardium is resistant to infection ( by
most bacteria) and to thrombus formation
Endocardial injury (e.g. at the site of high velocity jets
or on the low pressure side of cardiac structure lesion)
–causes aberrant flow and allows direct infection by
virulent organism or the development of uninfected
platelet-fibrin thrombi –non-bacterial thrombotic
endocarditis (NBTE), subsequently site of bacterial
attachment
Organisms enter the bloodstream from mucosa, skin,
sites of focal infection
Some of them adhere directly to intact endocardium or
injured endothelium
Others –adhere to thrombi, where they proliferate and
form vegetations
Damage to cardiac structures causes hemodynamic
changes
Embolization –infarction of other organs
Infection of remote tissues due to dissemination of
infection, mycotic aneurysms
Tissue injury due to deposition of circulating immune
complexes or immune response to deposited bacterial
antigens
Cytokines release –constitutional symptoms
Very variable
Complete history including travel Hx and review of
systems, Hx of URTI, dental, surgical and other
procedures
Fever, constitutional symptoms ( fatigue, malaise,
weight loss)
Myalgias, arthritis, low back pain, pleuritic chest pain
Thorough examination , search for stigmata of IE
Fever
Splinter hemorrhages on nail beds
Osler’s nodes –painful nodes on palmar surfaces of toes
and fingers
Janeway lesions –hemorrhagic papules on the palm and
soles
Roth’s spots on fundoscopy
IV injection marks
Anemia
Heart –cardiac murmurs, feature of CHF ( due to
valvular lesions, myocarditis or intracardiac fistulas),
various heart blocks (infectious process affecting
conduction system)
Embolic events –extremities, spleen, kidneys, bowel,
brain
Neurological complications –meningitis, intracranial
hemorrhages due to hemorrhagic infarcts, or ruptured
mycotic aneurysms, seizure, encepalopathy,
microabscesses
Immune complex deposition on glomerular basement
membrane –diffuse glomerulonephritis and renal
dysfunction, emboli -hematuria
Drug users –infection of Tricuspid V, high fever, faint
murmur, cough, chest pain, pulmonary infiltrates,
pyopneumothorax
Prosthetic valves –CHF, arrhythmias, new murmurs
Blood culture (+) for above mentioned organisms, at
least initially 3 sets
FBC-Anemia of chronic illness
WBC –normal or increased
Urinalysis-Hematuria, proteinuria
Abnormal CXR
ECHO-Valvular Vegetations
ECG –conduction blocks, MI
Elevated ESR, (+) Rheumatoid factor
Direct valvular damage-valve erosion ( perforation), or
erosion of adjacent myocardial wall –fistula
Embolic events-large mobile vegetations on the MV
(high risk)-kidney, spleen, brain, large arteries, lungs
Metastatic infection-osteomyelitis, septic arthritis,
epidural abscess, purulent meningitis
Immunologic phenomena-Glomerulonephritis,
musculoskeletal conditions
Duke criteria remain the clinical gold standard for
diagnosis
2 major
1 major + 3 minor
5 minor
Major : 1-+veBlood culture in 2 separate
cultures;atleast24 hrs apart
2-Endocardialinvolvement, +veEcho.by
doing an echo e.gvulvularfunctions.
Minor : 1-predisposition.e.gpeople whozhad
extracted a tooth and
2-fever > 38°c
3-vascular/immunological signs.
(roth’sspots, splinter hemorrhages, osler’s
nodes & janewaylesions)
4-+veBlood Culture not meeting major
criteria.
5-+veEchocardiogram.e.gaffected heart
function .
CHF
Affected prosthetic valves
Persistent bacteremia
Lack of effective microbicide therapy ( Brucella, fungi)
Staph.aureus prosthetic valve IE
Relapse of prosthetic valve IE with optimal a/b
treatment
Large > 10 mm vegetations
Prognosis is poor :
Older age
Severe co morbidities.combination of different
conditions e.g cch and id and menngitis
Delayed diagnosis
Involvement of prosthetic valve or Aortic valve.e.g with
history of surgical RHD
S.aureus or Pseudomonas, yeasts
Intracardiac complications
Neurologic complications
Dental procedures: extraction, periodontal
procedures, implants, root canal, surgery beyond apex;
Respiratory procedures: operations involving mucosa,
bronchoscopy with rigid bronchoscope
GIT –esophageal stricture dilatation, sclerotherapy of
varices, endoscopic retrgrade cholangiography, biliary
tract surgery, surgery involving mucosa
Use of antibiotics before procedure:
Amoxyl 2 g PO 1 hour before or ampicillin 2 g IV 30
min before proceure, Cefazolin 1 g IV 30 min before.
If allergic to penicillin –clarythromycin 500 mg PO 1
hour before, Clindamycin 600 mg PO before
Ampicillin + Gentamycin
Vancomycin + Gentamycin
Maintain good dental hygiene
Aggressive treatment of local infections