Detailed description of infective endocarditis

1. Infective Endocarditis

2. Definition
Infection of the endocardial surface ofheart
characterized by
- Colonization or invasion of theheart
valves (native or prosthetic) or the mural
endocardium by amicrobe,
- leading to formation ofbulky, friable
vegetation composed of thrombotic debris andorganisms
- often associated with destruction of
underlyingcardiac tissue.

3. Sites involved
•Heart valves
•Ventricular septum defects
•Mural endocardium
•Intracardiac devices

4. ACUTEENDOCARDITIS
• Destructive infection
frequently of a previously
normal heart valve, with a
highly virulent organism
• Hematogenoulsy seeds
• If untreated, leads todeath
within weeks
SUBACUTE ENDOCARDITIS
• Organismsof low virulence
causing infection in a
previously abnormal heart,
particularly on deformed
valves.
• Diseaseappear insidiously and
pursue aprotracted course of
weeks to month
• Recoverafter appropriate
antibiotic treatment
Classification

5. Prosthetic cardiac valves
Unrepaired cyanotic CHD
Completely repaired defect with prosthetic device or device within 6 months of
procedure
Repaired CHD with residual defects
Valve stenosis or insufficiency occurring after heart transplantation
Previous infective endocarditis
Permanent valve diseases resulting from RHD
Patient with high flow leisons (VSD, AS)
Predisposing factors

6. Microbiology
•Staphylococcus aureus : Either healthy or deformed valves, IVdrug
abusers (polymicrobial), devices
•Streptococcus viridans : previouslydamaged/abnormal valves
•Enterococci : bowl and genitourinary manipulations
•CoNS - S.epidermidis : Prosthetic valve endocarditis, devices
•G–ve bacilli of HACEKgroup
•Yeastand Fungi :openheartsurgery
•Culture negative endocarditis

7. Pathogenesis
Portal of entry:
◦ Dental / SurgicalProcedures
◦ Contamination by IVdrug use
◦ Obvious infections (RS/Skin)
◦ Occult source from gut, oralcavity
◦ Trivial injuries.
◦ Intravascular catheter infection
◦ Nosocomial wounds
◦ Chronic invasive procedures

8. PATHOGENESIS
Patient with CHD where there is a turbulent blood flow because of hole
or stenotic orifice especially if there is a high gradient across defect.
Turbulent blood flow traumatises vascular endothelium creating a
substrate deposition of fibrin and platelets: NBTE.
Biofilm formed on implanted mechanical devices also serve as an
adhesive substrate for infection.
Development of transient bacteraemia then colonises the NBTE or
biofilm leading to proliferation of bacteria within the lesion

9. Endothelial Injury
Uninfected Platelet-Fibrin thrombus(NBTE)
Transient bacteremia and attachmentat
NBTE
Proliferation and pro-coagulantstate
Infected, friable, bulkyvegetation

10. Morphology
• Friable, bulky vegetation containing fibrin, inflammatory cells, andmicrobes
• Aortic and mitral valves involved mostcommonly.
• Right side valve involvement in iv drugusers.

11. Clinical features
IE is uncommon in less than 2 years of age
Clinical features may be grouped as
1) indicating presence of infection
fever, rigors, chills, sweats, generalised malaise, weakness, loss of
appetite and amenorrhoea in females. Arthralgia and myalgia may occur but
arthritis doesn’t occur
2) features indicating involvement of cvs
- left or right heart failure
-development of new or change in pre existing murmur
-presence of embolic events in various parts of body
-regurgitant leisons appear when valves are damaged leading to
hemodynamic changes resulting in CHF.

12. 3) features of immunological response
presents as vasculitis – arthralgia myalgia, clubbing,
splenomegaly and haematuria
petechial lesion's over skin mucosal membrane and
conjunctiva
splinter haemorrhages
Osler nodes
Jane way lesions

13. .

15. Definitive Endocarditisif,
- Twomajor or,
- Onemajor and three minor or,
- five minor
Possible Endocarditisif,
- Onemajor and one minor or,
- Three minor
Modified Dukes Criteria for diagnosis
of Infective Endocarditis

16. Major Criteria
Positive bloodculture
◦Typical organism from two cultures
◦Persistent positive blood cultures taken >12 hoursapart
◦Three or more positive cultures taken over more than 1
hour apart.
Endocardial involvement
◦Positive echocardiographic findings of vegetations
◦New valvular regurgitation

17. Minor Criteria
Fever
Immune complex phenomenon (glomerulonephritis,
rheumatic fever, oslers nodes roths spot)
Embolic vascular signs
Positive single blood culture
ECHO signs not matching the major criteria

18. Following minor criteria are added in modified dukes criteria
Presence of newly diagnosed clubbing
Splenomegaly
Splinter haemorrhage
Petechial haemorrhages
High ESR
High CRP
Peripheral lines
Central feeding lines
Microscopic haemorrhages

19. INVESTIGATIONS

20. Microbiology
 Blood cultures:
Keydiagnostic investigation in infective endocarditis.
Isolation of microorganism from culture is importantfor
diagnosis and also for treatment.
At least 3 sets of samples should be taken from different
venepuncture sites over 24 hours.

21. Serology
Canbe sent when the diagnosis is suspected and the
cultures are negative.
Theyaid in caseswhere the organisms will notgrow in
blood cultures(Coxiella,Legionella,Bartonella)
ECG
Todetect complications like MI,conduction
abnormalities.
CHESTXRAY

22. Echocardiography
It canidentify the presence and sizeof
vegetations,detect intracardiac complications and
assesscardiac function.
Transthoracic echocardiography is noninvasive and has
high specificity for visualisingvegetations.
Transoesophageal echocardiography is more sensitive
than TTE.Itcandetect small vegetations,prosthetic
endocarditis and intra cardiaccomplications.

23. .
Complete blood counts
may show anamia and increased WBCcounts.
Urea and Creatinine:
may be elevated due to glomerulonephritis
Liver biochemistry:
Serumalkaline phosphatase may be increased
Inflammatory markers
CRPare increased in infection .CRPalso helps in
monotoring response to therapy.
Urine
proteinuria and hematuria occur frequently.

24. TREATMENT
AntimicrobialTherapy
Therapy requires identification of specificpathogen
and its susceptibility to antimicrobials.
Empirical therapy should be started assoon as
possible targeting most likely pathogens.
Bactericidal drugs should be used.

25. Resolution of fever occurs in 5 to 7 days.iffever
persists patient should be evaluated for complications
like paravalvular abscessand extracardiac abscess.
Serologic abnormalities resolve slowly and donot
reflect response to treatment.

26. Antibotic regimenfor infectiveendocarditis
 Streptococciviridians Penicillin/AMG 4wk
 Ceftriaxone/AMG
 Grp A streptococci Penicillin/AMG 4WK
Ceftriaxone/AMG
Strep. Faecalis Penicillin/AMG 4…6wk
Vancomycin/AMG
Staph aureus Cloxacillin /AMG 6wk
Vancomycin/AMG
E Coli Ceftriaxone/AMG 6WK
Ampicillin/AMG
Pseudomonas Ticarcillin/AMG 6WK
Meropenem/AMG

27. Culture negative Ampicillin / AMG
Ampicillin /AMG
Fungal endocarditis AMB + FLUCYTOSINE for 2-3 wk
operate to remove fungal mass
f/b
AMB + Flucytosine for 6 wks

28. Surgery
Indications
patients with direct extension ofinfection to
myocardial structuires.
Prosthetic valve dysfunction.
Congestive heart failure.
Badly damaged valves.
IEcausedby fungi or gram-ve or resistantorganisms.
Largevegetations on echocardiography
Recurrent embolic attacks.

29. Prophylaxis
High risk category
prosthetic cardiac valves
Previous bacterial endocarditis,even in absenseof
heart disease.
Complex cyanotic congenital heart disease(TGA,TOF)
Surgically constructed systemic pulmonary shunts.
During ist 6months fallowing complete repair of CHD
by surgery or catheter intervention using prothetic
valves
Repair of CHD with residual defects
Cardiac implant recipients

30. Moderate risk category
Rheumatic and other valvulardysfunction
Congenital cardiac malformations
Hypertrophic cardiomyopathy
Mitral valve prolapse with valvularregurgitation

31. Prophylactic antibiotic regimen
Oral Amoxicillin 50mg/kg
Unable to take oral Ampicillin 50mg/kg or
Ceftriaxone 50mg/kg
Allergic to penicillin…oral Cephalexin 50mg/kg or
Clindamycin 25 mg/kg or
Azithromycin 15mg/kg
Allergic to pn and unable to take oral Cefazolin or ceftriaxone 50mg/kg
Clindamycin 20mg/kg.

32. Thank you.