endocarditis

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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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Page 1: Endocarditis

Endocarditis

By – Mr. Rahul P Kshirsagar M.Pharm (Ph.D)

Assistant Professor

Dept. of Pharmacology

School of Pharmacy, Anurag Group of Institutions

Page 2: Endocarditis

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