A slide on infective endocarditis

1. INFECTIVE ENDOCARDITIS
AGNES MTAJA – BSCHB; MBCHB, MMED PED; DIP UKMP

2. Outline
 Definition
 Aetiology
 Epidemiology
 Clinical manifestations
 Diagnosis
 Prognosis and complications
 Treatment
 Prevention

3. Definition
 An infection of the endocardium and/or heart valves that involves
thrombus formation (vegetation) which then damage the endocardial
tissue and/or valves.
 Includes acute, subacute bacterial endocarditis + non bacterial
endocarditis to include:
 Viruses
 Fungi
 Autoimmunity
 May occur on a previously healthy native heart

4. Two important factors
 A damaged area of endothelium (1)
 Bacteraemia (even transient) (2)
 Structural abnormalities in the heart with significant pressure gradient or
turbulence produce endothelial damage
 Endothelial damage induces thrombus formation with deposition of sterile
clumps of platelets and fibrin (non bacterial thrombus)
 Non bacterial thrombus provides a nidus for bacteria to adhere and
eventually form infected vegetation

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

6. High risk lesions for IE
 TOF
 VSD
 Aortic valve disease
 PDA
 Prosthetic valves

7. Infective Endocarditis
 Nonbacterial Thrombotic Endocarditis
 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
Venturi Effect
Platelet-fibrin
thrombi

8. Venturi Effect

9. Aetiology
 Streptococci viridans (post dental procedure) and staphylococcus aureus
(normal native valve) are the leading causes
 Group D enterococci – post lower bowel or genitourinary manipulation
 CONS – indwelling central venous catheter
 Pseudomonous/serratia – IV drug users
 HACEK (Haemophilus, Actinobacillus, cardiobacterium, Eikenella and
Kingella) – neonates and immunocompromised children
 Fungal endocarditis is a severe disease with poor prognosis

10. Epidemiology
 Patients with CHD in which blood is ejected at high velocities through a
hole or stenotic orifice are most susceptible
 Often complicates RHD
 May occur in children with normal valves and children with no cardiac
malformations
 It is rare in infancy, but may occur post open heart surgery

11. Risk factors
 Cyanotic congenital heart disease
 Valvular lesions
 Previous episode of bacterial endocarditis
 Prosthetic valve
 Central venous catheters
 Residual cardiac defect post surgical or catheter intervention for that
defect

12. Features of endocarditis are due to:
 Bacteraemia
 Local cardiac invasion by organisms leading to valve detruction and or
rupture of chordae tendinae and hence acute HF
 Peripheral embolizaton which may produce septic embolic phenomena
(osteomyelitis, meningitis and pneumonia)
 Formation of immune complexes, in circulation will cause vasculitis

13. Janeway Lesions

14. Splinter Hemorrhage

16. Osler’s Nodes

17. Subconjunctival Hemorrhages

18. Roth’s Spots

19. Manifestations
 May be acute, sub acute or even chronic
 May be very non specific with fevers going on for months
 “B symptoms”
 New or changing murmers with associated CCF
 Skin manifestation..more common in the chronic type
 Splenomegaly and petechiae
 Stroke
 Cerebral abscesses
 Mycotic aneurysms

20. Symptoms/signs in order of
prevalence
 Fever – 85-99%
 Splenomegaly - 70%
 Petechiae – 20-40%
 Changing murmur – 21%
 Hepatosplenomegaly – 14%
 CCF – 9%
 Splenomegaly 7%
 Osler nodes – 4% (rare in children)
 Arthritis 3%

21. The Modified Duke Criteria
 Majors
 Positive blood culture
 Echo positive
 Minors
 Predisposing conditions
 Fever
 Embolic vascular signs
 Immune complex phenomena
 Newly diagnosed clubbing, splenomegaly, ↑ESR/CRP

22. Diagnosis from Duke…
 Two majors
 One major and 3 minors
 Five minors

23. Diagnosis
 BLOOD CULTURE, BLOOD CULTURE, BLOOD CULTURE!!
 3 – 5 samples needed
 Transthoracic + transoesophageal echo may help localize vegetations
 Normal echo does not exclude endocarditis

24. Laboratory Parameters
 FBC – Anaemia in 70-90% (normocytic normochromic)
 Leukocytosis – 50%
 ESR –Elevated in 100% patients mean about 55mm/h
 C-reactive protein – elevated in almost all patients. Decreases with
successful treatment and therefore can be used to monitor response to
antibiotic therapy
 Urinalysis – proteinuria (50-60%); microscopic haematuria (30-50%)

25. Prognosis and complications
 Is fatal without antibiotics
 Mortality still as high as 40% even with use of antibiotics
 Severe CCF, life threatening arrhythmias
 CNS emboli

26. Treatment
 Recognize that vegetations house organisms that now become
inaccessible as these are avascular
 Broad spectrum antibiotics 1st
line Xpen/Gentamicin
 4 – 6 weeks duration
 Treat the CCF (digoxin, salt restriction, diuretics)
 Surgery may be indicated for severe aortic or mitral involvement

27. Prevention
 Good oral/dental hygiene
 Antibiotic prophylaxis for various procedures:
 Dental cleaning or any form of dental manipulation
 Scopic examinations: endo,broncho,cystoscopy