1. INFECTIVE ENDOCARDITIS

2. INFECTIVE ENDOCARDITIS: DEFINITION
Microbial infection of the endothelial surface of the heart
Characteristic lesion: VEGETATION

3. IE: DEFINITION: VEGETATIONS
Mass of platelets and fibrin, rich in bacteria, scanty inflammatory cells
Sites: heart valves, septal defect, chordae tendineae or mural endocardium

4. INFECTIVE ENDOCARDITIS: DEFINITION
Infection of arteriovenous shunts or PDA or coarctation of the aorta is called infective endarteritis, but clinically resembles IE

5. INFECTIVE ENDOCARDITIS: DEFINITION
Causative organism: bacteria, fungi, and rickettsiae
Most frequent organisms: streptococci, staphylococci, enterococci, and fastidious gram-negative coccobacilli

6. INFECTIVE ENDOCARDITIS: PATHOGENESIS
vegetations
Bacterial proliferation
Colonization with bacteria during bacteremia
Deposition of platelets & fibrin
Endocardial damage
High pressure jet

7. Vegatations on the mitral valve

8. Vegetations on top of mitral stenosis

9. Vegetations on a biologic valve

10. IE: UNDERLYING HEART DISEASE
High pressure gradient or narrowed tracts:
Mitral regurgitation
Aortic regurgitation
VSD
Aortic stenosis
Mitral stenosis
Tetralogy of Fallot
Coarctation of the aorta, PDA

11. IE: UNDERLYING HEART DISEASE
Cardiac lesions with low or no pressure gradients are unlikely to be complicated by IE e.g. ASD

12. IE: MICRO-ORGANISMS S. viridans Enterococcus fecalis
Staphylococcus aureus
Coagulase negative Staphylococci
Gram-negative bacilli
Brucella
Rickettsia
Fungi

13. CLINICAL MANIFESTATIONS
The local destructive effects of intracardiac infection
Embolization of bland or septic fragments of vegetations to distant sites: infarction or infection
Hemato seeding of remote sites during continuous bacteremia
Antibody response to MO: immune complex deposition or Ab-complement interaction

14. IE: CLINICAL MANIFESTATIONS
Fever
Heart murmur
Splenomegaly
Peripheral manifestations

16. IE: PERIPHERAL MANIFESTATIONS
Splinter hemorrhage
Osler’s nodes: subcutaneous nodules, tender

17. Osler’s nodes

18. Dermal infarcts

19. IE: EYE MANIFESTATIONS
Janeway’s lesions: macular non-tender lesions
Roth’s spots: on fundoscopy

20. IE: EYE MANIFESTATIONS
Subconjunctival hemorrhage

21. IE: PERIPHERAL MANIFESTATIONS: THE EYE
Petechiae: conjunctiva, buccal mucosa, limbs

22. CLINICAL MANIFESTATIONS
The local destructive effects of intracardiac infection
Embolization of bland or septic fragments of vegetations to distant sites: infarction or infection
Hemato seeding of remote sites during continuous bacteremia
Antibody response to MO: immune complex deposition or Ab-complement interaction

23. LOCAL DESTRUCTIVE EFFECTS
Destruction of valve leaflets, ruptured chordae
Abscess formation
Perforations or fistulas
Disruption of conductive system
Large vegetations lead to valve obstruction

24. IE: SYSTEMIC EMBOLI CNS embolization: focal neurologic deficits
Spleen: pain, splenomegaly
Limbs: ischemia and gangrene
Mesenteric: abdominal pain, hematochezia

25. IE: NEUROLOGICAL MANIFESTATIONS
Headache
Confusion
Convulsions
Long tract signs & focal neurological deficit
Meningeal irritation

26. IE: RENAL MANIFESTATIONS
Renal failure:
immune-complex deposition
Congestive heart failure
drug-induced
Glomerulonephritis
Focal renal infarcts: hematuria

27. IE: CLINICAL SETUP depending on the clinical presentation: Acute IE:
Subacute IE (SBE)
Postoperative IE: following cardiac surgery

28. ACUTE IE Caused by virulent organisms on top of normal heart:
Usually staphylococcus aureus
E.g. cannula infection, staphylococcal septicemia, drug abusers

29. ACUTE IE 5:Vegetations on top of normal endocardial tissue
1:Bacteremia or septicemia
2:Direct damage of endocardium
3:Colonization: virulent organisms
4:Deposition of platelets & fibrin
5:Vegetations on top of normal endocardial tissue

30. ACUTE IE: CLINICAL MANIFESTATIONS
Severe febrile illness
Petechiae
Embolic events common
Rapid progression of cardiac and renal failure

31. SUBACUTE IE
Caused by infection with low-virulence organisms on top of pre-existing cardiac disease
Persistent fever, tiredness, weight loss, night sweats

32. PROSTHETIC VALVE ENDOCARDITIS
IE following cardiac surgery
Early postoperative IE:
infection is acquired at the time of surgery
High mortality: repeat surgery often required
Late postoperative IE:
Community-acquired infection
Complication rates lower than early form

33. IE: INVESTIGATIONS Blood cultures
Echocardiography: transthoracic (TTE) and transesophageal (TEE)
Vegetations
Serial follow up
Valve damage
Abscess fromation

34. Vegatations on the aortic valve

35. VEGETATIONS

40. IE: INVESTIGATIONS High ESR Anemia of chronic disease
Neutrophil leucocytosis
CRP
Hematuria
Proteinuria
Low serum complement
Rheumatoid factor

41. IE: INVESTIGATIONS
ECG:
Heart block
Bundle branch block
arrhythmia

42. IE: TREATMENT
Combination antibiotic therapy according to culture & sensitivity
Empirical regimes pending the results of blood culture

43. IE: TREATMENT Large doses Given intravenously
Protracted duration of therapy:
usually 4 weeks
6 weeks in PVE

44. Combination AB therapy
Benzyl penicillin or ampicillin i.v
Plus gentamycin
For penicillin resistant or allergic: vancomycin infusion plus gentamycin
Oral rifampicin when staphylococcal infection suspected or confirmed

45. CARIAC SURGERY: INDICATIONS
Failure to respond to medical treatment
Heart failure due to valve insufficiency
Large vegetations
Abscess formation

46. PREVENTION OF IE
Susceptible patients: those with valvular or congenital heart disease
Good dental hygiene

47. PREVENTION OF IE
Avoidance of bacteremia
Antibiotic prophylaxis:
Dental manipulation
Genito-urinary tract catheterization or surgery

48. PROPHYLAXIS
For dental procedures:
Oral amoxicillin given 30 min before and 6 hours after the procedure