1. INFECTIVE ENDOCARDITIS
HA MWKYOMA, MD

2. DEFINITION OF IE
Is a microbial infection of the endocardial surface of the heart and has been classified as "acute" or "subacute –chronic" on the basis of severity of the clinical presentation and the progression of the untreated disease.
The characteristic lesion, a vegetation, is composed of a collection of
platelets,
fibrin,
microorganisms, and
inflammatory cells

3. IE
It most commonly involves heart valves but may also occur at the site of a septal defect, on the chordae tendineae, or on the mural endocardium. 
Men are more often affected than women.

4. Infective Endocarditis
Essential characteristics,
General definitions and epidemiology
NVE
I.V. drug abuse
PVE
Pathogenesis
Pathophysiology
Clinical features
Treatment

5. Epidemiology
Underlying valvular abnormality predisposing to infective endocarditis
rheumatic fever a common cause in the past
mitral valve prolapse currently represents the most common underlying cardiac abnormality

6. Risk for Endocarditis High risk prosthetic cardiac valve
prior episodes of endocarditis
complex congenital cardiac defect
surgically constructed systemic-pulmonary shunts or conduits

7. Risk for Endocarditis Moderate risk patent ductus arteriosus
VSD, primum ASD
coarctation of the aorta
bicuspid aortic valve
hypertrophic cardiomyopathy
acquired valvular dysfunction
MVP with mitral regurgitation

8. Risk for Endocarditis Low risk isolated secundum atrial septal defect
ASD, VSD, or PDA >6 months past repair
“innocent” heart murmur by auscultation in the pediatric population
“innocent” heart murmur by echocardiography in adult patients

9. Infective Endocarditis
General characteristics
Febrile illness
Persistent bacteremia
Characteristic lesion of microbial infection of the endothelial surface of the heart ( the vegetation)
Variable in size
Amorphous mass of fibrin & platelets
Abundant organisms
Few inflammatory cells

11. Infective Endocarditis
Typically involves the valves
May involve all structures of the heart
Chordae tendinae
Sites of shunting
Mural lesions
Infection of vascular shunts, by strict definition, is endarteritis, but lesion is the same
Majority of cases caused by
Gram-positive bacteria namely;
streptococcus,
staphylococcus,
enterococcus, or fastidious gram negative cocco-bacillary forms

12. Infective Endocarditis
Gram negative organisms
P. aeruginosa most common
HACEK - slow growing, fastidious organisms that may need 3 weeks to grow out of culture
Haemophilus sp.
Actinobacillus
Cardiobacterium
Eikenella
Kingella

13. Infective Endocarditis
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

14. Infective Endocarditis
Case rate may vary between 2-3 cases /100,000 to as high as 15-30/100,000 depending on incidence of i.v. drug abuse and age of the population
55-75% of patients with native valve endocarditis (NVE) have underlying valve abnormalities
MVP
Rheumatic
Congenital
i.v. drug abuse

15. Infective Endocarditis
Pediatric population
The vast majority (75-90%) of cases after the neonatal period are associated with an underlying congenital abnormality
Aortic valve
VSD
Tetralogy of Fallot
Risk of post-op infection in children with IE is 50%
Microbiology
Neonates: S. aureus, coag – staph, group B strep
Older children: 40% strep, S. aureus

16. Infective Endocarditis
Adult population
MVP – prominent predisposing factor
High prevalence in population
2-4%
20% in young women
Relative risk in MVP ~3.5 – 8.2, largely confined to patients with murmur, but also increased in men and patients >45 years old

17. Infective Endocarditis
Adult population
Rheumatic Heart Disease
20 – 25% of cases of IE in 1970’s & 80’s
7 – 18% of cases in recent reported series
Mitral site more common in women
Aortic site more common in men
Congenital Heart Disease
10 – 20% of cases in young adults
8% of cases in older adults
PDA, VSD, bicuspid aortic valve (esp. in men>60)

18. Infective Endocarditis
Intravenous Drug Abuse
Increased frequency of gram negative infection such as P. aeruginosa & fungal infections
High concordance of HIV positivity & IE (27-73%)
HIV status does not in itself modify clinical picture
Survival is decreased if CD4 count < 200/mm3

19. Infective Endocarditis
Intravenous Drug Abuse
Risk is 2 – 5% per pt./year
Tendency to involve right-sided valves
Distribution in clinical series
46 – 78% tricuspid
24 – 32% mitral
8 – 19% aortic
Underlying valve normal in 75 – 93%
S. aureus predominant organism (>50%, 60-70% of tricuspid cases)

20. Infective Endocarditis
Prosthetic Valve Endocarditis (PVE)
10 – 30% of all cases in developed nations
Early PVE – within 60 days
Nosocomial (S. epid. predominates)
Late PVE – after 60 days
Community (same organisms as NVE)

21. Infective Endocarditis
Pathology
NVE infection is largely confined to leaflets
PVE infection commonly extends beyond valve ring into annulus/periannular tissue
Ring abscesses
Septal abscesses
Fistulae
Prosthetic dehiscence
Invasive infection more common in aortic position and if onset is early

22. Infective Endocarditis
Nonbacterial Thrombotic Endocarditis (NBTE)
Endothelial injury
Hypercoagulable state
Lesions seen at coaptation points of valves
Atrial surface mitral/tricuspid
Ventricular surface aortic/pulmonic
Modes of endothelial injury
High velocity jet
Flow from high pressure to low pressure chamber
Flow across narrow orifice of high velocity
Bacteria deposited on edges of low pressure sink or site of jet impaction
Platelet-fibrin thrombi

23. Infective Endocarditis
Pathogenesis
Endothelial damage
Platelet-fibrin thrombi
Microorganism adherence

24. Pathogenesis
Disruption of the endocardial layer as a complication of abnormal blood flow associated with underlying cardiac defect
Bacterium-endothelium interaction with bacterial attachment and invasion of endothelial cells

25. Pathophysiology Clinical manifestations Direct Indirect
Constitutional symptoms of infection (cytokine)
Indirect
Local destructive effects of infection
Embolization – septic or bland
Hematogenous seeding of infection
N.B. may present as local infection or persistent fever, metastatic abscesses may be small, miliary
Immune response
Immune complex or complement-mediated

26. Pathophysiology Local destructive effects
Valvular distortion/destruction
Chordal rupture
Perforation/fistula formation
Paravalvular abscess
Conduction abnormalities
Purulent pericarditis
Functional valve obstruction

27. Pathophysiology Embolization Clinically evident 11 – 43% of patients
Pathologically present 45 – 65%
High risk for embolization
Large > 10 mm vegetation
Hypermobile vegetation
Mitral vegetations (esp. anterior leaflet)
Pulmonary (septic) – 65 – 75% of i.v. drug abusers with tricuspid IE

28. Coagulase-negative Staphylococci
can produce native-valve endocarditis in mitral valve prolapse
usually subacute, difficult to diagnose, and disregarded as a contaminant
delay in diagnosis and treatment may account for the severe complications
myocardial abscess formation
valvular insufficiency requiring valve surgery
death

29. Prosthetic Heart Valve
positive blood culture in hospitalized patients with underlying prosthetic valves can be a harbinger of endocarditis
43% patients with nosocomial bacteremia or fungemia had prosthetic valve infection
a serious complication

30. Clinical Features
Interval between index bacteremia & onset of sx’s usually < 2 weeks
May be substantially longer in early PVE
Fever most common sign
May be absent in elderly/debilitated pt.
Murmur present in 80 – 85%
Generally indication of underlying lesion
Frequently absent in tricuspid IE
Changing murmur

31. Classical Peripheral Manifestations
Less common today
Not seen in tricuspid endocarditis
Petechiae most common

32. Janeway Lesions

33. Splinter Hemorrhage

34. Osler’s Nodes

35. Subconjunctival Hemorrhages

36. Roth’s Spots

37. Clinical Features Systemic emboli Neurological sequelae CHF
Incidence decreases with effective anti-microbial Rx
Neurological sequelae
Embolic stroke 15 – 20% of patients
Mycotic aneurysm
Cerebritis
CHF
Due to mechanical disruption
High mortality without surgical intervention
Renal insufficiency
Immune complex mediated
Impaired hemodynamics/drug toxicity

38. Diagnosis Published criteria for diagnostic purposes in obscure cases
High index of suspicion in patients with predisposing anatomy or behavior
Blood cultures
Echocardiography

39. Goals of Therapy Eradicate infection
Definitively treat sequelae of destructive intra-cardiac and extra-cardiac lesions

40. Antibiotic Therapy Treatment tailored to etiologic agent
Important to note relationship for each causative organism and the antibiotic used
High serum concentration necessary to penetrate avascular vegetation

41. Antibiotic Therapy Treatment before blood cultures turn positive
Suspected ABE
Hemodynamic instability
Neither appropriate nor necessary in patient with suspected SBE who is hemodynamically stable

42. Antibiotic Therapy
Effective antimicrobial treatment should lead to defervescence within 7 – 10 days
Persistent fever in:
IE due to staph, pseudomonas, culture negative
IE with microvascular complications/major emboli
Intracardiac/extracardiac septic complications
Drug reaction

43. Prevention Prophylactic regimen targeted against likely organism
Strep. viridans – oral, respiratory, eosphogeal
Enterococcus – genitourinary, gastrointestinal
S. aureus – infected skin, mucosal surfaces

44. Prevention – the procedure
Dental procedures known to produce bleeding
Tonsillectomy
Surgery involving GI, respiratory mucosa
Esophageal dilation
Gallbladder surgery
Cystoscopy, urethral dilation
Urethral catheter if infection present
Urinary tract surgery, including prostate
I&D of infected tissue

45. Prevention – the underlying lesion
High risk lesions
Prosthetic valves
Prior IE
Cyanotic congenital heart disease
PDA
AR, AS, MR,MS with MR
VSD
Coarctation
Surgical systemic-pulmonary shunts
Intermediate risk
MVP with murmur
Pure MS
Tricuspid disease
Pulmonary stenosis
ASH
Bicuspid Ao valve with no hemodynamic significance
Lesions at highest risk

46. Summary
You need to go to medical school (and graduate) in order to take care of patients with endocarditis.