INFECTIVE ENDOCARDITIS

2. INFECTIVE ENDOCARDITIS

3. INTRODUCTION • Endocarditis is defined as an infection, usually bacterial, of the endocardial surface of the heart. • Infective endocarditis primarily affects the cardiac valves, although the septa between the chambers or the mural endocardium may be involved in some cases.

4. infective endocarditis has been categorized as acute or subacute, depending on the length of symptoms before presentation; . A classification that considers the causative organism and the valve involved is more clinically relevant

5. ACUTE IE • Acute IE is most commonly caused by Staphylococcus aureus. It presents with marked toxicity and progresses over days to several weeks to valvular destruction and metastatic infection

6. SUB ACUTE IE • Subacute IE, usually caused by viridans streptococci, enterococci, coagulase-negative staphylococci, or gram-negative coccobacilli, evolves over weeks to months with only modest toxicity and rarely causes metastatic infection.

7. Incidence Of Infective Endocarditis • The incidence of infective endocarditis is approximately 1.7-6.2 cases per 100 000 patient /year,although rates are higher in at risk cohorts such as intravenous drug users. • Men are more often affected than women (in a ratio of 2:1), and the incidence progressively increases with age. Underlying degenerative aortic and mitral valve disease now predominate over rheumatic disease, although in one recent French study 47% of patients with infective endocarditis presented without previous knowledge of an underlying cardiac disorder

8.  PREDISPOSING CONDITIONS ASSOCIATED WITH INCREASED RISK OF ENDOCARDITIS • More Common • Mitral valve prolapse with murmur • Degenerative valvular disease • Intravenous drug use • Prosthetic valve. • Congenital abnormalities (valvular or septal defect)

9. Less Common • Rheumatic heart disease • Hypertrophic obstructive cardiomyopathy • Pulmonary-systemic shunts. • Coarctation of the aorta • Complex cyanotic congenital heart disease

10. Infective endocarditis: patient groups • Children with IE: congenital heart disease Staphylococcus (neonate), Streptococcus group B (children), S. pneumonia (rare) • Adults with IE: Rheumatic heart disease: MV (F>M), AV (M>F) Congenital heart disease: PDA, VSD, bicuspid AV

11. Infective endocarditis:patient groups • IV drug abusers with IE: TV (46—78%)  MV (24—32%)  AV (8—19%) S. aureus, GNB (Pseudomonas), polymicrobial HIV: 73%; increased mortality (CD4 < 200) • Prosthetic valves with IE: early (< 60 days): surgical complication, late (> 60 days): community or nosocomial ring abscess, annular invasion, paravalvular regurgitation

12. Infective endocarditis: nosocomial • Infected intracardiac device and catheter • GI or GU tract surgery or instrumentation • High mortality (40—56%) • GPC ( S. aureus, CONS, Enterococcus) • S. aureus catheter related bacteremia .

13. Infective endocarditis: microorganism • Streptococcus viridans: 35 — 65% NVE normal flora of the oropharynx • Streptococcus pneumoniae: alcoholism aortic valve concurrent pneumonia or meningitis • Enterococcus: normal GI tract flora and cause GU infection 5—15% NVE and PVE

14. Infective endocarditis: microorganism • Staphylococcus: Coagulase-positive: S. aureus highly toxic febrile 30—50% CNS involvement Coagulase-negative: S epidermidis Major cause of PVE

15. Infective endocarditis: microorganism • Gram negative bacteria: upper respiratory tract and oropharyngeal flora P. aeruginosa: most common in GNB IE HACEK: haemophilus spp., Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae • Fungus: drug abuser and prosthetic valve common: C. albicans (PVE); C. parapsilosis (NVE)

16. Pathogenesis of Endocarditis • Inoculation of bacteria colonizing a mucosal (e.g., oral mucosa) or peripheral tissue site into the bloodstream • Transient bacteremia of a serum-resistant pathogen capable of adhering to a cardiac valvular surface. • Turbulent blood flow across the valve • • Bacterial adherence to cardiac valvular surface • Pathogen - host tissue interaction resulting in vegetation formation and local tissue damage • – Bacterial persistence • Dissemination of infection to other tissue sites and elicitation of systemic findings

17. Factors Contributing to the Pathogenesisof Endocarditis • Hemodynamics - blood flow patterns • Bacterial properties • Host factors

18. Local destruction of intracardiac infection: valve, chordae tendineae, fistula, paravalvular abscess, conduction • Distant embolization with infarct or infection: • Hematogenous seeding with bacteremia: metasttic infection, • Immune-complex or antibody reaction: IgM, IgA, IgG, Osler’s node, Rheumatoid factor, Roth’s spot

19. Sepsis Pneumonia Meningitis Brain abscess Stroke Malaria Acute pericarditis Vasculitis DIC Differential Diagnosis: ABE

20. As FUO Rheumatic fever Osteomyelitis Tuberculosis Meningitis Abdominal infection Glomerulonephritis Myocardial infarction Stroke Connective tissue diseases Occult malignancy Chronic heart failure Pericarditis Differential Diagnosis: SBE

21. Clinical P R E S E N T A T I O N

22. INFECTIVE ENDOCARDITIS:Symptoms • High grade fever and chills • SOB • Arthralgias/ myalgias • Abdominal pain • Pleuritic chest pain • Back pain

23. Signs • Fever • Changing Heart murmur • Nonspecific signs – • petechiae, “splinter” hemorrhages, • clubbing, • splenomegaly, • neurologic changes • More specific signs – • Osler’s Nodes, • Janeway lesions, • Roth Spots

24. Petechiae • Nonspecific • Often located on extremities • or mucous membranes

25. Splinter Hemorrhages • Nonspecific • Nonblanching • Linear reddish-brown lesions found under the nail bed • Usually do NOT extend the entire length of the nail

27. Osler’s Nodes • More specific • Painful and erythematous nodules • Located on pulp of fingers and toes • More common in subacute IE

28. Janeway Lesions • More specific • Erythematous, blanching macules • Nonpainful • Located on palms and soles

30. Duke Criteria For The Diagnosis Of Infective Endocarditis • Major Criteria • Positive blood culture . • A). Typical micro-organism consistent with infective endocarditis from two separate blood cultures : • i) Streptococciviridans ,Streptococcus bovis HACEK group OR   (ii) community-acquired Staphylococcus aureusenterococci, in the absence of a primary focus or

31. B. Micro-organisms consistent with infective endocarditis from persistently positive blood cultures defined as: i) at least two positive cultures of blood samples drawn > 12h apart or ii) all three of these or a majority of four or more separate cultures of blood (with first and last sample drawn at least 1h apart).

32. 2. Evidence of endocardial involvement • A. Positive echocardiogram for infective endocarditis as defined as: • (i) oscillating intracardiac mass on valve or supporting structures, in the path of regurgitant jets, or on implanted material in the absence of an alternative anatomical explanation or   (ii) abscess or, (iii) new partial dehiscence of prosthetic valve. B. New valvular regurgitation (worsening or changing of pre-existing murmur not sufficient)

33. Minor Criteria • 1. Predisposition: predisposing heart condition or intravenous drug use2. Fever: temperature > 38 °C3. Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial haemorrhages, and Janeway's lesions

34. 4. Immunological phenomena: glomerulonephritis, Osler's nodes, Roth spots, and rheumatoid factor • 5. Microbiological evidence: positive blood culture but does not meet a major criteria or serological evidence of active infection with organism consistent with infective endocarditis • 6. Echocardiographic findings: consistent with infective endocarditis but do not meet a major criteria.

35. investigations

36. Lab: CBC • Anemia • Mild to moderate • Normocytic normochromic • Leukocytosis: not reliable

37. Routine Tests • Elevated ESR: 90% • Elevated CRP: 96% • Urinalysis • Microscopic hematuria or proteinuria: >50% • RBC casts & heavy proteinuria: glomerulonephritis • Gross hematuria: renal infarction

38. Blood Culture • B/C should be done in all patients with undiagnosed fever and a heart murmur • B/C send on the first day • Aerobic + anaerobic • Additional B/C on day 3 if necessary (when diagnosis is likely but B/C yielded negative results)

39. ECG • Repeated or even continuous ECG monitoring • Frequent APC or PVC • Prolonged PR interval • Myocardial infarction

41. Echocardiography • The diagnosis of infective endocarditis is frequently suggested on the basis of echocardiography, which is the diagnostic procedure of choice for detecting valvular vegetations.

42. The echocardiographic features typical for infective endocarditis are • (a) an oscillating intracardiac mass on a valve or supporting structure or in the path of a regurgitation jet or on a device, • (b) abscesses, • (c) new partial dehiscence of a prosthetic valve, or • (d) new valvular regurgitation. The initial attachment site of a vegetation is usually on the ventricular surface of the semilunar valves and on the atrial surface of the atrioventricular valves

45. Image Study: CXR • Provide evidence of early CHF • Valvular calcification • Multiple small, patchy infiltrates in the lungs of an Iv drug user with fever: septic emboli from right-sided IE

46. Image Study: CT/MRI • For defining the cause of focal neurologic lesions • Cerebral emboli

47. Image Study: Cardiac Cath • Indication: • In patients >40 y/o (for possible concurrent CAD) • When surgical intervention is considered

49. Diagnostic Criteria • DEFINITE INFECTIVE ENDOCARDITIS • Pathologically proven infective endocarditis or Clinical criteria meeting either   Two major criteria or   one major and three minor criteria or   five minor criteria • POSSIBLE INFECTIVE ENDOCARDITIS • One major or one minor or three minor criteria • REJECTED INFECTIVE ENDOCARDITIS • Firm alternative diagnosis or Resolution of infective endocarditis syndrome with antibiotic therapy of ≤4 days or No pathologic evidence of infective endocarditis at surgery or autopsy with antibiotic therapy of ≤4 days

50. Culture-Negative Infective Endocarditis • Blood cultures fail to isolate an etiologic agent in 3% to 23% of cases . Culture-negative IE is most often associated with antibiotic use within the previous 2 weeks. Less frequently, intracellular pathogens not detected using standard culture approaches may be the cause . If blood cultures are negative , consideration should be made to analyze serum for Bartonella, Coxiella, and Chlamydia species antibodies . If the patient requires valve surgery, RNA polymerase chain reaction amplification of valve tissue often yields an etiologic agent • the search for a causative organism remains fruitless, consider noninfectious etiologies such as marantic or Libman-Sacks endocarditis and atrial myxoma.