description of IE etiology, epidemiology, clinical signs and symptoms, pathophysiology, and treatment

1. Infective
Endocarditis
Presented by:
Daren Nicole N. Perez
BSPH-5A

2. Anatomy and Physiology of Endocardium

3. Endocarditis

4. Infective
Endocarditis
• A microbial infection of a
cardiac valve or the
endocardium caused by
bacteria, fungi, or chlamydia
• Pathological findings include
the presence of friable valvular
vegetations containing bacteria,
fibrin and inflammatory cells.
There is often valvular
destruction with extension to
adjacent structures.
– Embolic lesions may
demonstrate
similar findings

5. Etiology
The normal heart is relatively resistant to infection. Bacteria
and fungi do not easily adhere to the endocardial surface, and
constant blood flow helps prevent them from settling on
endocardial structures.
2 factors are typically required for endocarditis:
•A predisposing abnormality of the endocardium
•Microorganisms in the bloodstream (bacteremia)
Rarely, massive bacteremia or particularly virulent
microorganisms cause endocarditis on normal valves

6. Etiology

7. Etiology
• Usually Bacterial
•Staphylococcus aureus Endocarditis
•Streptococcus viridans Endocarditis
•Actinobacillus actinomycetemcomitans
Endocarditis
• Sometimes Fungal
•Candida albicans Endocarditis

8. Etiology

9. Etiology
HACEK organisms
The HACEK group of organisms –
Haemophilus parainfluenza,
Haemophilus aphrophilus,
Actinobacillus (Haemophilus)
actinomycetemcomitans
Cardiobacterium hominis,
Eikenella
Kingella species – also commonly cause IE
and can be difficult to diagnose.

10. Epidemiology
Population Groups At Greater Risk:
•Rheumatic Fever History
•Hemodialysis
•Previous History Of Endocarditis
•Patients With Prosthetic Valves
•IV Drug Users (30% Risk Within 2
Years)

11. •More Common In Men
•Median Age 50 Years
•Acute Cases Increasing
•Streptococcal Cases ↓
Slightly; Fungal And Gram
Negative Cases Increasing
Epidemiology

12. •Incidence Increases With Age, Probably
Due To Increased Cardiac Disease And
Decreased Immunity
•Prosthetic Heart Valve Infections Are
Increasing
Epidemiology

13. Mortality
•Overall Rate About 40%
•Death Usually Due To Heart
Failure Resulting From Valve
Dysfunction
•Highest Death Rate Is In Early
Prosthetic Valve Endocarditis

14. Pathophysiology

15. Clinical Features

18. Janeway Lesions

19. Splinter Hemorrhage – tiny blood
clots that tend to run vertically under
the nails.

20. Osler’s Nodes

21. Subconjunctival Hemorrhages

22. Roth’s Spots

23. Investigations

25. Investigations
• Blood cultures
•Echocardiography
• key investigation as it can assess underlying cardiac function as well as:
• identify the presence and size of vegetations.
• Detect intracardiac complications
• pre-existing rheumatic disease
• valve apparatus can be examined and the degree of valve
incompetence assessed.
Transthoracic echocardiography is noninvasive and
has high specificity for visualising vegetations.
Transoesophageal echocardiography is more sensitive
than TTE.It can detect small vegetations,prosthetic
endocarditis and intra cardiac complications.

26. Investigations
Other investigations include the following:
•Blood count – normochromic normocytic anemia
is usual, while neutrophil leucocytosis is common
•ESR – this may be raised
•renal and liver function test – levels of creatinine
may be raised; levels of liver enzymes may be
raised in a hepatocellular (nonobstructive) pattern
•CRP – increases acutely in bacterial infection
•Urine Microscopy – microscopic hematuria is
common in early disease
•Culture – culture any skin lesion, drip site, or other
focus of infectio

27. Investigations
Major criteria
•Two positive blood cultures for organisms typical of
endocarditis
•Three positive blood cultures for organisms consistent with
endocarditis
•Serologic evidence of Coxiella burnetii (or one positive blood
culture)
Echocardiographic evidence of endocardial involvement:
•Oscillating intracardiac mass on a heart valve, on supporting
structures, in the path of regurgitant jets, or on implanted
material without another anatomic explanation
•Cardiac abscess
•New dehiscence of prosthetic valve
•New valvular regurgitation
Revised Duke Clinical Diagnostic
Criteria for Infective Endocarditis

29. Natural History
Further Classification
•Acute
• Affects normal heart
valves
• Rapidly destructive
• Metastatic foci
• Commonly Staph.
• If not treated, usually
fatal within 6 weeks
•Subacute
• Often affects damaged
heart valves
• Indolent nature
• If not treated, usually
fatal by one year

30. Treatment

32. Prognosis
• With effective treatment, patients with IE have a 70%
survival rate.
• The prognosis is worse if there is no identifiable
organism or if there is a resistant organism.
• Fungal infections are associated with increased
mortality, as is prosthetic valve endocarditis.
• Overall death rates are:
• 20% for native valve endocarditis
• 30% for staphylococcal infections
• 20%–30% for late prosthetic valve infection
. The most common cause of death is intractable
heart failure.

33. Reference
• http://www.clevelandclinicmeded.com/medicalpubs/disea
semanagement/infectious-disease/infective-endocarditis/
• https://www.merckmanuals.com/professional/cardiovascu
lar-disorders/endocarditis/infective-endocarditis
• http://www.ncbi.nlm.nih.gov/books/NBK2208/
• http://www.columbia.edu/itc/hs/medical/pathophys/id/2
005/MID-LowyEndoColor.pdf
• http://www.ncbi.nlm.nih.gov/pubmed/9658947
• Pharmacotherapy Handbook, 7th
edition. Barbara G. Wells
et.al.