Infective Endocarditis
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1 Infective Endocarditis
2 Definition Historical perspective Classification Epidemiological Features Etiology Pathogenesis Clinical presentation Diagnosis Treatment options Prevention
3 Infective endocarditis (IE) is a disease that produces vegetations on the endocardium. It is virtually always fatal if untreated. A heart valve is usually involved, but the infection may develop on a septal defect or on the mural endocardium. It is typically a syndrome diagnosis that is determined on the basis of the presence of multiple findings rather than a single definitive test result. Although the presence of IE may be obvious when a patient with predisposing cardiac lesions has bacteremia without an obvious source, it is often a difficult diagnosis to establish in patients who are seen in routine clinical practice.
4 Historical perspective
5 Few diseases present greater difficulties in the way of diagnosis than malignant endocarditis, difficulties which in many cases are practically insurmountable. It is no disparagement to the many skilled physicians who have put their cases upon record to say that, in fully one-half the diagnosis was made post mortem. William Osler
6 In the pre-antibiotic era endocarditis was usually a fatal disease as a result of CHF. Osler s Gulstoian lectures provided the 1 st comprehensive overview of the disease. Lewis and Grant (1923) were the first to link a transient bacteremia with deformed valves as the two predominant risk factors for infection. The introduction of penicillin marked the first successful therapy for this otherwise lethal infection
7 Classification
8 Acute vs.subacute On basis of Causative agent Native valve vs. Prosthetic valve - Early PVE vs. Late PVE Right-sided vs. left-sided Culture-positive vs. culture-negative Nosocomial endocarditis
9 Epidemiology & Etiology
10 Predisposing Factors Aged Degenerative valvular disease. Increased exposure to nosocomial bacteremia Prosthetic valves Gender (M>F) Associated medical conditions : Long term Hemodialysis Diabetes Mellitus Poor dental hygiene HIV Congenital defects MVP (100/100,000 pt-yr, in advanced countries) MR Thickened leaflets ASD, VSD Injection-drug use (TV) Long-term indwelling intravenous catheters Rheumatic heart disease (primarily the young in developing countries)
11 Common Etiological Agents Streptococci -Represent approximately 50% of cases of IE down from 80% in the preantibiotic era -Viridans streptococci (30-40% of Streptococcal IE) S. sanguis and S. mitis each account for 30%-50% of the cases caused by the oral viridans streptococci Enterococci - Cause 5-15% of cases of IE Staphylococci - Responsible for about 20% of cases of IE Coagulase-negative staphylococci (e.g. S. epidermidis) cause 60% of prosthetic-valve IE Mortality rates associated with CONS in PVE have been decreasing, although the mortality rates of IE due to S. aureus remain ominously high.
12 Not so common Etiological Agents Other bacteria -The HACEK Group Haemophilus species, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella species Usual bacterial causes Bacillus cereus, Clostridium perfringens, Mycobacterium tuberculosis, Nocardia asteroides, Coxiella burnetii, etc. Fungi-Candida and Aspergillus species Emerging pathogens- Tropheryma whipplei and Bartonella spp. Abiotrophia defectiva, Granulicetella adiacens
13 Pathogenesis
14 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
15 Clinical Presentation Highly variable
16 Symptoms Acute High grade fever and chills SOB Arthralgias/ myalgias Abdominal pain Pleuritic chest pain Back pain Subacute Low grade fever Anorexia Weight loss Fatigue Arthralgias/ myalgias Abdominal pain N/V
17 Petechiae 1. Nonspecific 2. Often located on extremities or mucous membranes
18 Splinter Hemorrhages 1. Nonspecific 2. Non blanching 3. Linear reddish-brown lesions found under the nail bed 4. Usually do NOT extend the entire length of the nail
19 Osler s Nodes 1. Not specific 2. Painful and erythematous nodules 3. Located on pulp of fingers and toes 4. More common in subacute IE
20 Janeway Lesions 1. Thought to be embolic in origin 2. Erythematous, blanching macules 3. Nonpainful 4. Located on palms and soles
21 Roth Spots 1. Oval,pale retinal lesions surrounded by haemorrhage. 2. Near optic disk.
22 Diagnosis
23 The diagnosis of infective endocarditis requires the integration of clinical, laboratory, and echocardiographic data.
24 Making the Diagnosis Pelletier and Petersdorf criteria (1977) Von Reyn criteria (1981) Duke criteria (1994) von Reyn CF, Levy BS, Arbeit RD,et al. Infective endocarditis: An analysis based on strict case definitions. Ann Intern Med. 1982;94:505.Durack DT, Lukes AS, Bright DK: New criterion for dignosis of IE: utilization of specific echocardiographic findings,am j Med 1994;96:200
25 Modified Duke Criteria (2000) Definite IE Pathological criteria: Microorganism (via culture or histology) in a valvular vegetation, embolized vegetation, or intracardiac abscess. Histologic evidence of vegetation or intracardiac abscess. Clinical criteria: 2 Major criteria, or 1 Major and 3 minor criteria, or 5 minor criteria Ref: Li JS, Sexton DJ, Mick N, et al. Proposed modifications to the Duke criterion for the diagnosis of infective endocarditis. Clin infect Dis 2000; 30:633-8
26 Possible IE -Findings that fall short of definite IE,but are not rejected. - Clinical criteria 1 major and 1 minor, or 3 minor criteria Rejected IE Resolution of illness with four days or less of antibiotics. An alternative diagnosis is made. No pathological evidence at surgery/autopsy after antibiotic therapy of 4 days or less.
27 Clinical criteria
28 Major criteria 1. Positive blood cultures Typical pathogen > 2 separate blood cultures in the absence of a primary focus (viridans strep, Strep bovis, HACEK group, Community acquired Staph aureus or Enterococci ) Persistently positive blood culture drawn more than 12 h apart or all of 3 or majority of 4 or more (with first and last culture drawn at least 1 hour apart) 2.Evidence of endocardial involvement - New evidence of valve regurgitation - Positive Echocardiogram -Oscillating intracardiac mass/vegetation on valve/implanted material/ supporting structures/in path of regurgitant jet. -Evidence of intra-cardiac abscess -New partial dehiscence of prosthetic valve
29 Minor Criteria Fever > 100.4F (38C) Immunologic : Roth Spots; Osler Nodes; glomerulonephritis; Rheumatoid Factor Vascular : Arterial embolus; Janeway Lesion; Intracranial hemorrhage; Septic pulmonary infarct Predisposing heart condition or IV drug abuse Microbiologic : Positive blood culture but, not meeting major criteria or serologic evidence supporting an organism which is known to cause IE Echo : Abnormal echo suggestive of IE but, not adequate for major criteria
30 The Essential Blood Test
31 Blood Cultures Minimum of three blood cultures Three separate venipuncture sites Adequate disinfection of the puncture site Very imp. Obtain 10-20mL in adults and 3-5mL in children Best time-fever spikes ( not very imp as continuous bacteremias) Before starting antibiotics. In acute cases, 2-3 cultures within 5 minutes of each other, while in subacute cases 3 or more cultures 30 min to 1 hour apart over several hours(24) Multiple cultures if pt has received antibiotics in the preceding 2 weeks. Anaerobic culture if suspiction of IE due to anaerobes.
32 Blood Cultures Automated blood culture system demonstrate recovery of organisms within 6-7 days. To maximize positive results, bottles can be kept for 3 wks. Manual blood culture bottles to be incubated for at least 2-3 weeks with repeated subcultures Negative blood culture in 2.5%-31% of cases
33 Echocardiography Attempt to visualize vegetation. Negative test does not rule out Endocarditis
34 Transthoracic echo(tte): Rapid & non-invasive Excellent specificity (98%) & Overall sensitivity (60-70%) Transesophageal echo(tee): Great sensitivity (75-95%) & Great specificity (85-98%) Particularly useful in patients with prosthetic valves
35 Laboratory Manifestations Anemia 70-90% Leukocytosis 20-30% Proteinuria 50-65% Microscopic 30-50% Hematuria Serum 10-20% creatinine ESR >90% Rheumatoid factor 50% Circulating immune % complexes Serum complement 5-40%
36 Some Clues for Diagnosis
37 Epidemiologic Clues: Travel to endemic region Coxiella burnetti, Brucella spp. Exposure to animals or their products Travel to endemic areas Intravenous drug use Homeless person, chronic alcoholism, HIV Poor dental hygiene C. Burnetti, Chlamydia psittaci, Brucella spp., Bartonella henselae Fungi, Corynebacterium spp. (Staph. aureus is the most common pathogen) Bartonella spp. HACEK group, nutritionally variant streptococci
38 Echocardiographic Clues Large vegetations Vegetations with fingerlike projections HACEK group, fungi Chlamydia spp.
39 Clinical Clues Underlying neoplasm (atrial myxoma, adenocarcinoma, lymphoma, rhabdomyosarcoma, carcinoid tumor Underlying autoimmune disease (rheumatic heart disease, SLE) Postvalvular operation Noninfective endocarditis Libman-Sacks endocarditis Noninfectious process (e.g. thrombus, sutures)
40 Treatment options
41 Principles of Therapy Use bactericidal antibiotics. IV better than oral. Prolonged therapy is necessary (weeks) Treatment is best started after multiple sets of blood cultures have been taken. Urgency in the initiation of therapy is required for acute but not subacute endocarditis. Synergistic combinations of antibiotics are used when available. Prevent or limit valvular damage and resulting CHF Maintain optimal nutritional status of patient Prevent embolic disease Advise patient &/or family regarding future need for antibiotic prophylaxis
42
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