endocarditis
TRANSCRIPT
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Endocarditis
By – Mr. Rahul P Kshirsagar M.Pharm (Ph.D)
Assistant Professor
Dept. of Pharmacology
School of Pharmacy, Anurag Group of Institutions
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Contents of Lecture
Endocarditis Definitions Epidemiology Pathogenesis Clinical Presentations Diagnosis Complications/Mortality
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Anatomy of Heart
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Endocarditis: Definition
Infective Endocarditis: is an inflammation of the
endocardium, the membrane lining the chambers of the
heart and covering the cusps of the heart valves
it refers to infection of the heart valves by various
microorganisms
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ENDOCARDITIS
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ENDOCARDITIS
Characteristic pathological lesion: vegetation, composed of platelets, fibrin, microorganisms and inflammatory cells.
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Classification:
• acute or subacute-chronic on temporal basis,
severity of presentation and progression
• By organism
• Native valve or prosthetic valve
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Acute • Toxic presentation• Progressive valve destruction & metastatic
infection developing in days to weeks• Most commonly caused by S. aureus
Subacute• Mild toxicity• Presentation over weeks to months• Rarely leads to metastatic infection• Most commonly S. viridans or enterococcus
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EPIDEMIOLOGY AND ETIOLOGY
• Infective endocarditis is an uncommon, but not rare,
infection affecting about 10,000 to 20,000 persons
annually in the United States.
• accounts for approximately 1 in every 1,000 hospital
admissions.
• The mean male-to-female ratio is 1.7:1.
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• Presence of a prosthetic valve (highest risk)• Previous endocarditis (highest risk)• Complex cyanotic congenital heart disease (e.g., single-
ventricle states)• Surgically constructed systemic pulmonary shunts or
conduits• Acquired valvular dysfunction (e.g., rheumatic heart
disease)• Hypertrophic cardiomyopathy• Mitral valve prolapse with regurgitation• IVDA (intravenous drug abuse).
IMPORTANT RISK FACTORS
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EPIDEMIOLOGY
Incidence in IVDA group is estimated at 2000 per
100,000 person-years, even higher if there is known
valvular heart disease
Increased longevity leads to more degenerative valvular
disease, placement of prosthetic valves and increased
exposure to nosocomial bacteremia
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PROSTHETIC VALVES
7-25% of cases of infective endocarditis The rates of infection are the same at 5 years for
both mechanical and bioprostheses, but higher for mechanical in first 3 months
Cumulative risk: 3.1% at 12 months and 5.7% at 60 months post surgery
Onset: within 2 months of surgery early and usually
hospital acquired 12 months post surgery late onset and usually
community acquired
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Nosocomial Infective Endocarditis
7-29% of alll cases seen in tertiary referral
hospitals
At least half linked to intravascular devices
Other sources GU and GIT procedures or
surgical-wound infection
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Aetiological Agents
1. Streptococci Viridans streptococci/α-haemolytic streptococci
S. mitis, S. sanguis, S. oralis S. bovis
Associated with colonic carcinoma
1. Enterococci E. faecalis, E. faecium Associated with GU/GI tract procedures Approx. 10% of patients with enterococcal
bacteraemia develop endocarditis
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Aetiological Agents
3. Staphylococci Staphylococcci have surpassed
viridans streptococci as the most common cause of infective endocarditis
S. aureus Native valves acute endocarditis
Coagulase-negative staphylococci Prosthetic valve endocarditis
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Aetiological Agents
4. Gram-negative rods HACEK group
Haemophilus aphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae.
Fastidious oropharyngeal GNBs E. coli, Klebsiella etc
Uncommon Pseudomonas aeruginosa
IVDA Neisseria gonorrhoae
Rare since introduction of penicillin
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Aetiological Agents
5. Others Fungi
Candida species, Aspergillus species
Chlamydia Bartonella Legionella
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MICROBIOLOGY OF NATIVE VALVE ENDOCARDITIS
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Pathogenesis
Altered valve surface Animal experiments suggest that IE is almost
impossible to establish unless the valve surface is damaged
Deposition of platelets and fibrin – nonbacterial thrombotic vegetation (NBTE)
Bacteraemia – attaches to platelet-fibrin deposits Covered by more fibrin Protected from neutrophils Division of bacteria Mature vegetation
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Pathogenesis
Bacteraemia Transient bacteraemia occurs when a heavily
colonised mucosal surface is traumatised Dental extraction Periodontal surgery Tooth brushing Tonsillectomy Operations involving the respiratory, GI or GU tract mucosa Oesophageal dilatation Biliary tract surgery
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Site of Infection
Aortic valve more common than mitral Aortic:
Vegetation usually on ventricular aspect, all 3 cusps usually affected
Perforation or dysfunction of valve Root abscess
Mitral: Dysfunction by rupture of chordae tendineae
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Clinical Manifestations
Fever, most common symptom, sign (but may be
absent)
Anorexia, weight-loss, malaise, night sweats
Heart murmur
Petechiae on the skin, conjunctivae, oral mucosa
Right-sided endocarditis is not associated with
peripheral emboli/phenomena but pulmonary findings
predominate
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Janeway Lesions
Janeway lesions—Hemorrhagic, painless plaques on the palmsof the hands or soles of the feet. These lesions are believed tobe embolic in origin.
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Splinter Hemorrhage
Splinter hemorrhages—
Thin, linear hemorrhages
found under the nail beds
of the fingers or toes.
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Osler’s Nodes
Osler nodes — Purplish or erythematous subcutaneous papules or nodules on the pads of the fingers and toes. These lesions are 2 to 15 mm in size and are painful and tender.
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Petechiae
Petechiae—Small (usually 1 to 2
mm in diameter), erythematous,
painless, hemorrhagic lesions.
These lesions appear anywhere
on the skin but more frequently on
the anterior trunk, buccal mucosa
and palate, and conjunctivae..
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Roth’s Spots
Roth spots—Retinal
infarct with central
pallor and surrounding
hemorrhage.
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Investigations
1. Blood culture
2. Echo TTE TOE
1. FBC/ESR/CRP
2. Rheumatoid Factor
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Diagnosis: Duke Criteria In 1994 a group at Duke University
standardised criteria for assessing patients with suspected endocarditis
Include
-Predisposing Factors
-Blood culture isolates or persistence of bacteremia
-Echocardiogram findings with other clinical, laboratory findings
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Duke Criteria
Definite : 2 major criteria : 1 major and 3 minor criteria : 5 minor criteria : pathology/histology findingsPossible : 1 major and 1 minor criteria : 3 minor criteria Rejected : firm alternate diagnosis
: resolution of manifestations of IE with 4 days antimicrobial therapy or less
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Echocardiography Trans Thoracic Echocardiograpy (TTE)
rapid, non-invasive – excellent specificity (98%) but poor sensitivity
obesity, chronic obstructive pulmonary disease and chest wall deformities
Transesophageal Echo (TOE) more invasive, sensitivity up to 95%, useful for
prosthetic valves and to evaluate myocardial invasion
Negative predictive valve of 92% TOE more cost effective in those with S. aureus
catheter-associated bacteraemia and bacteraemia/fever and recent IVDA
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COMPLICATIONS OF ENDOCARDITIS
Cardiac : congestive cardiac failure-valvular damage, more
common with aortic valve endocarditis, infection beyond valve→ CCF, higher mortality, need for surgery, A-V, fascicular or bundle branch block, pericarditis, tamponade or fistulae
Systemic emboli Risk depends on valve (mitral>aortic), size of
vegetation, (high risk if >10 mm) 20-40% of patients with endocarditis, risk decreases once appropriate antimicrobial
therapy started.
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Goals of Therapy
1. Eradicate infection
2. Definitively treat sequel of destructive intra-cardiac and extra-cardiac lesions
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Therapy
Antimicrobial therapy Use a bactericidal regimen Use a recommended regimen for the organism
isolated E.g. American Heart Association JAMA 1995; 274: 1706-13.,
British Society for Antimicrobial Chemotherapy Repeat blood cultures until blood is demonstrated to
be sterile Surgery
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Surgical Therapy
Indications: Congestive cardiac failure perivalvular invasive disease uncontrolled infection despite maximal
antimicrobial therapy Pseudomonas aeruginosa, Brucella species, Coxiella
burnetti, Candida and fungi Presence of prosthetic valve endocarditis
unless late infection Large vegetation Major embolus Heart block
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Prevention
Antimicrobial prophylaxis is given to at risk patients when bacteraemia-inducing procedures are performed
Look up and follow guidelines American Heart Association. Circulation 1997; 96:
358-366 British Society for Antimicrobial Chemotherapy.
Journal of Antimicrobial Chemotherapy 1993; 31: 347-438
BNF