This slide carefully elucidates the etiology, causes, signs, symptoms and management of endocarditis.

1. INFECTIVE
ENDOCARDITIS
BY DR C.E AMADI

2. Infective endocarditis: The
Backstory

3. A 28- year old man with a medical history of mitral
regurgitation presented at the ER after an episode of
transient weakness in his right arm and slurred speech. He
under went dental scaling a month earlier. He in addition
has recurrent history of fevers, general malaise and weight
loss. On cardiac exam he has anaemia, finger clubbing and
unchanged intensity of the MR.
Echocardiography shows a mobile 1.2cm mitral valve
vegetation and moderately severe MR

4. Cont’d
A 45 year old Nurse with background history
of CHF had prosthetic mitral valve
replacement 11 months ago. She presented at
the Cardiology OPD with 3 weeks history of
fever, worsening symptoms of heart failure
and chest infection.
Cardiac exam showed increased intensity of
the MR while echo showed partial dehiscence
of the prosthetic valve, para-valvar turbulent
flow and mobile vegetation along the valve
commissures

5. Cont’d
A 45 year old man with advanced NHL
was admitted for chemotherapy. 48
hours later he developed high grade
fever and mitral regurgitation.
Echocardiography showed hyperechoic
masses on the anterior mitral valve
leaflets and moderate MR
Blood culture showed pure isolates of
Staph aureus

6. DEFINITION
• A infection of the endocardial surfaces of
the heart which may include
• One or more valves ( native or prosthetic)
• mural endocardium
• Septal defects
• Endothelial surfaces of the great arteries.

7. Also includes infection of intravascular
lines/implants such as central lines,
dialysis catheters, pacemaker leads ,
intra-cardiac devices
Infections of patent ductus arterious
and coarctation also constitute IE
The infection is usually bacteria but
occasionally fungi, mycoplasma,
chlamydia may be involved

8. Usually causes severe valvar
damage and incompetence, heart
failure and extra-cardiac
complications.
Usually fatal if not properly treated

9. History of IE
1674
In 1674, Lazaire Rivere first described
the gross autopsy findings of IE in this
work Opera medica
1885
In1885 William Osler presented the
first comprehensive description on IE
in English
1966
The first scientific publication of IE
was in the New England Journal of
Medicine in 1966 by Lerner and
Weinstein

10. Classification
Native valve IE (Acute
or Sub acute)
Prosthetic Valve IE
(Early or Late)
Intravenous Drug
Abuse ( IVDA) IE
Nosocomial Hospital
Associated IE

11. Native
Valve IE
Usually constitutes
about 50-60% of cases
of IE
Affects natural valves
Two types viz Acute
and Sub-acute

12. Acute NVIE usually affects normal valves in
debilitated people
Usually no associated structural heart disease
Has an aggressive course leading to valve
destruction and embolic complications especially
stroke
Fatal under 6 wks if not treated
Typical causative organism:
Staph aureus
Group B Strep

13. Sub-acute NVIE usually
affects abnormal or damaged
valves
There may be associated
congenital heart diseases
(repaired or unrepaired) e.g.
PDA, VSD, TOF , MVP
Degenerative heart diseases
such as Marfan’s syndrome,
Aortic stenosis

14. Usually runs an indolent cause
Metastatic infection is rare
Fatal if not treated under 1 yr
Typical organisms are
Strept viridans viz bovis, sanguis, mitis;
Enterococci
Coagulase negative Staph aureus
Gram -ve bacilli

15. Prosthetic
Valve
Endocarditis

16. Prosthetic
Valve IE
PVIE accounts for 10-20% of
IE
Mechanical valves more at
risk within 3 months of
surgery; Mitral valves more at
risk than aortic valves
Two types viz Early and PVIE

17. Early PVIE occurs within 12
months of valve replacement
Usually caused by
Coagulase –ve Staph(Staph
epidermidis),
Gram –ve bacilli and
Staph aureus
Usually due to contamination at
the time of surgery

18. Late PVIE occurs more one yr following
valve implantation
Usually community acquired
Typical microbes include
Streptococci,
Enterococci
Staph aureus
Recent data suggest that Staph aureus is
often implicated in both early and late PVIE

19. Early PVE is commoner than late
PVE
Mechanical valves are at higher
risk than bio-prosthetic (tissue)
valves within the first yr;
Risk higher for bio-prosthetic
valves after 1 year
Risk comparable after 5 yrs of
valve replacement

20. Intravenous
Drug Abuse
IE
Common in i.v drug abusers and
HIV patients
About 75% of patients do not
have any structural heart
disease
The tricuspid valve is affected in
about 60% of cases, aorta
(25%), mitral(5%); mixed (5%)
Aortic or mitral valve may be
affected

21. IVDA IE
Staph aureus is the most common
causative agent(50%);
Pseudomonas,
Candida,
Streptococci
Enterococci
HACEK group of bacteria

22. HACEK are Gram negative fastidious
slow growing bacteria.
Haemophilus parainfluenza
Actinobacillus actinomycetecomitans
Cardiobacterium hominis
Eikenella corrodens
Kingella kingae
Commensals of upper airway and
oropharnyx

23. Nosocomial
IE
Also called Healthcare Associated
endocarditis
Usually manifests 48 hrs following
admission or associated with a
hospital based procedure e.g. central
lines, dialysis shunts/catheters
Commonly caused by Staph aureus,
and enterococci

24. Two types of NIE viz
Right sided NIE caused by
injury due a normal valve
during vascular procedures
Left sided NIE from a
previously damaged valve

25. Epidemiology
Incidence varies globally; 2-4
cases/100,000 to 15-30/100,000
depending on the age and
prevalence of i.v drug abuse
Males are 3X more affected than
females
No racial predilection

26. Depends on age and region
Younger age group:
Congenital heart diseases & repair in
developed countries;
Rheumatic heart dx primarily and
congential heart disease/repair in
developing countries

27. Older age group:
Degenerative heart Dx, IVDA,
increased use of invasive
procedures in developed
countries;
Increasing use of intra-cardiac
devices , prosthetic valves and
degenerative heart Dx in the
developing countries

28. Valvular
Distribution
of IE
Mitral 28-45%
Aortic 5-36%
Both 0-35%
Tricuspid 0-6%
Pulmonary < 1%

29. Predisposing Factors
• Age
• DM
• Immunosuppression
• HIV
• Long term dialysis
• Poor dental hygiene
• Previous IE
• Use of intravascular
lines/catheters
• Rheumatic disease
• Valve repairs/replacement

30. Aetiopathogenesis of
IE
Prerequisite for IE;
Damaged endothelium
Bacteraemia
Host Factors
Virulence and Inoculum of the
organism

31. Aetiopathogenesis
Cont’d
Damaged endothelium viz:
Disease e.g RHDx,
Intravascular procedures
Flow from high pressure to low
pressure chamber
Flow across a narrow orifice at high
velocity
Repeated injection of solid particles
in IVDA

32. Aetiopathogenesis
Cont’d
Bacteraemia :
Poor dental hygiene
IVDA
Soft tissue injuries
Genito-urinary procedures
Colonic procedures
Procedures on septic loci

33. Etiopathogenesis
Cont’d
Host Factors(Immunity)
viz:
Local
Systemic
Virulence and inoculum
of the Organism

34. Pathophysiology
Normal endocardium
Laminar blood flow
Resistant to bacteria colonization
Damaged endocardium
Turbulent blood flow with eddy current
(Venturi effect)
Easily colonised by bacteria
Hypercoaguable state usually results

35. Pathophysiology
Cont’d
Promotes platelet & fibrin
deposition leading to formation of
sterile vegetation( Non-Bacterial
Thrombotic Endocarditis)
In the event of sufficient virulent
bacteraemia and poor host factors
bacteria adhere to the platelet and
fibrin rich NBTE
This complex is called vegetation,
the pathologic hallmark of IE

36. Complications
of vegetation
Cardiac
Valve destruction & haemodynamic changes
Infection may extend to paravalvular tissue
leading to mural abscess
Large vegetations may cause functional stenosis
Cardiac failure
Arrhythmias
Pericarditis

37. Embolic/Metastatic
(Large, mobile,
mitral, Staph)
Lung abscess
Septic arthritis Splenic infarction
Renal abscess/renal
failure from AGN
Cerebral abscess,
spinal abscess,
Stroke Osteomyelitis
Mycotic aneurysm

38. Microbiology of
IE
Staph aureus (40%)
Strept viridans (34%
Enterococci (6%)
Coagulase –ve Staph aureus (5%)
Gram –ve bacilli (6%)
Fungi (2%)
HACEK group/Polymicrobe (3%)
Culture negative IE (4%)

39. Clinical features
Fever & chills are
the most common
symptoms (80%)
Constitutional
symptoms:
Malaise
Weight loss Anorexia Arthralgia
Headaches Night sweats Cough
Shortness of
breathe
Chest pain Abd pains

40. Features of CHF
Embolic complications
Stroke
Acute Kidney Injury
Haematuria
Septic arthritis
Osteomyelitis
Immune mediated vasculitis

41. Roth’s
Spots

42. Janeway Lesions

43. Splinter Hemorrhage

44. Osler’s Nodes

45. Clinical signs
Fever most common sign(80%)
New or changing murmur(48%
and 20%)
Non specifics viz splenomegaly,
splinter haemorrages, petechie,
neurol signs, digital clubbing
Osler nodes, Roth spots,
Janeway lesions
Signs of CHF

46. Lab Investigations
• Blood cultures are key to diagnosis;
• Minimum of 3 samples from different sites over
30 min-24 hr; must include anaerobic culture.
Positive result is growth of typical microbes in at
least 2 samples.
• Culture negative samples are caused by prior
antibiotic use, fastidious organisms, poor
techniques, inadequate blood volume

47. Fastidious
Organisms

48. Lab
Cont’d
Echocardiography:
Visualising vegetations,
Abscesses
Structural lesions
Ventricular functions
CHF diagnosis
Predicting embolic complications of IE

49. Echocardiography
Echocardiography can be:
i) TTE
ii) TEE
TEE more sensitive than TTE in
visualising smaller vegetations <
10mm, right sided lesions, PVIE

50. Echocardiographic Predictors of systemic
embolization:
Large valvular vegetations > 10mm in diameter
Multiple vegetations
Mobile but pedunculated vegetations
Noncalcified vegetations
Vegetations that are increasing in size
Prolapsing vegetations

51. Others…..
FBC: anaemia,
leucocytosis, are
common
ESR, CRP: usually
elevated
Decreased C3, C4
and CH50
Pro-calcitonin may
be elevated
Urinalysis;
microscopic
haematuria &
protienuria
E/U/Cr

52. Others……
Plasma Glucose to
r/o DM
Lipid Profile
CXR: Septic
emboli; features of
CHF
CT/MRI of the
Brain for cerebral
complications
ECG: 1st degree A-
V Block and new
IVCD: Bad
prognosis

53. CXR:
Features of CHF
Pulmonary infiltrates esp
in right sided endocarditis
ECG:
Conduction defects
Myocardial infarction
Arrhythmias

54. Diagnostic
criteria
Modified Duke's criteria ( Major &
Minor)
Major criteria include:
Positive blood culture of typical
organisms in the absence of a primary
focus in 2 or more blood cultures
A positive serologic titre for Q fever or
PCR for fastidious organisms

56. Echo evidence of IE viz
Vegetations
Abscess
Prosthetic valve dehiscence
New valve regurgitation

57. Diagnostic Criteria
• Duke's Minor Criteria:
• Predisposing cardiac condition or iv drug use
• Fever; Temp > 38 degrees centigrade
• Vascular phenomena viz major arterial emboli, septic pulmonary
infarcts, mycotic aneurysm, intracranial/conjunctival hhages, Janeway
lesions
• Immunologic phenomena; AGN, Oslers nodes, Roth spots, positive
Rheumatoid Factor

58. Microbial evidence: A positive
blood culture but not meeting
major criteria or a positive
serologic evidence of an active
infection that can cause IE
Echo consistent with IE but not
meeting major criteria.

59. Guidelines on the prevention, diagnosis, and treatment of infective endocarditis (new version 2009)

60. Categories
of IE
diagnosis
Definite IE:
Demonstration of microbes in
vegetations, on cardiac tissues or on
valves
Histologic evidence of vegetations on
cardiac tissues
2 major Duke’s criteria; 1 major 3 minor
or 5 minor criteria

61. Possible IE:
1 major and 1 minor; or 3 minor criteria
No IE:
Resolution of fever under 4 days of
antibiotic regimen, absence of microbial
and echo evidence of IE

62. Goal of Treatment
Eradication of causative
microbe
Treatment of complications

63. Treatment
Parenteral antibiotics is
mainstay of treatment
Antibiotics with high MIC/MBC
should used
Bactericidal antibiotics in
combination is a must
Antibiotics should be used for 4-
6weeks
Antibiotics should be used
based on blood culture results

64. NVIE with penicillin
susceptible organisms( no
staph) use iv Pen G 4-6 MU 4
hrly x 4-6 wks or iv
ceftriaxone 2g daily x 4 wks
plus
Iv Getamycin 1mg/kg 8hrly x
2 wks

65. For suspected cases of
staph endocarditis iv
vancomycin 30mg/kg in
2 divided doses x 4-
6wks plus
iv gentamycin 1mg/kg 8
hrly x 2 wks

66. For Early PVIE and IVDA use
vancomycin & gentamycin as
above
For penicillin allergic patients
use vancomycin and gentamycin
as above
HACEK organisms use
ceftriaxone and gentamycin
Fungal endocarditis use
fluconazole or Amphotericin B

67. Indications for
surgery viz
Failed antibiotic
therapy
Persistent
vegetation after
systemic
embolization
Fungal endocarditis
Increase in size of
vegetation after
antibiotic Rx
Valvular
damage/destruction

68. Complications
Cardiac 33-50%
Neurologic 25-35%
Embolic 15-35%
Metastatic < 15%

69. Neurologic complications include:
Acute encephalopathy
Meningitis
Embolic stroke
Cerebral haemorrhage
Brain abscess

70. Cardiac Complications
CHF
Paravalvular abscess
Pericarditis
Fistulous intracardiac
connections

71. Embolic complications
Stroke
Ischaemic extremities
Paralysis from embolic infarction of
brain or spinal cord
Pulmonary emboli
Abdominal pain from splenic/renal
infarction

72. Metastatic Complications
Brain abscess
Septic arthritis
Vertebral osteomyelitis
Meningitis
Splenic/Renal abscess

73. Poor
Prognostic
Factors
• Female Gender
• Staph aureus infection
• Large vegetation
• Aortic valve vegetation
• Prosthetic valve
• Advanced Age
• DM
• Immunosuppression
• Heart Failure
• Acute lung injury
• Paravalvalar abscess
• Embolic
complications

74. Prophylaxis
• High risk cardiac lesions include
Prosthetic valves
CHDx viz unrepaired cyanotic heart dx,
completely repaired CHDx with prosthetic
material/device, repaired CHDx with
residual defects
Cardiac Transplant recipients with diseased
valves

75. Procedures
requiring
antibiotic
prophylaxis
• Dental procedures
• Invasive respiratory procedures
• Tonsillectomy
• Adenoidectomy
• Bronchoscopy with biopsy
• Gentiourinary procedures

76. Antibiotic
prophylaxis
Oral amoxicillin 2g 30- 60 mins
before procedure
i.v ampicillin 2g for those who
cannot take orally
Oral clindamycin 600mg for
penicillin allergic individuals or i.v
for those who cannot take orally