endocarditis

1. INFECTIVEINFECTIVE
ENDOCARDITISENDOCARDITIS

2. Colonization or invasion of the heart valves orColonization or invasion of the heart valves or
mural endocardium by a microbemural endocardium by a microbe
 Leads to the development of bulky friableLeads to the development of bulky friable
vegetationsvegetations
 Vegetations : Composed ofVegetations : Composed of
thrombotic debris,thrombotic debris,
micro-organismsmicro-organisms
+/- ass. damage of underlying cardiac tissue+/- ass. damage of underlying cardiac tissue
 Usually bacterial ( a.k.a bacterial endocarditis).Usually bacterial ( a.k.a bacterial endocarditis).
 May be acute or subacuteMay be acute or subacute

3. ACUTE INFECTIVEACUTE INFECTIVE
ENDOCARDITISENDOCARDITIS
SUBACUTESUBACUTE
ENDOCARDITISENDOCARDITIS
(SABE)(SABE)
 BacteriaBacteria Very virulent.Very virulent.
Eg : Staph.aureusEg : Staph.aureus
Low virulenceLow virulence
Eg : Strep viridansEg : Strep viridans
 Valves beforeValves before
infectioninfection
NormalNormal DiseasedDiseased
 DurationDuration Days to weeksDays to weeks Insidious onset.Insidious onset.
Protracted courseProtracted course
 LesionLesion Severe infection -Severe infection -
Nerotising, ulcerativeNerotising, ulcerative
Less destructive,Less destructive,
Likely to healLikely to heal
 OutcomeOutcome FatalFatal Heals but withHeals but with
complicationscomplications
 TreatmentTreatment No response toNo response to
antibiotics.antibiotics.
Requires surgeryRequires surgery
Responds to antibioticsResponds to antibiotics

4. ETIOPATHOGENESISETIOPATHOGENESIS
Predisposing factors:Predisposing factors:
In the HeartIn the Heart::
 RHDRHD
 Myxomatous mitral valve,Myxomatous mitral valve,
 Degenerative calcific stenosisDegenerative calcific stenosis
 Bicuspid aortic valveBicuspid aortic valve
 Prosthetic valves, valve graftsProsthetic valves, valve grafts
Host factorsHost factors::
 Neutropenia,Neutropenia,
 MalignancyMalignancy
 Immunodeficiency,Immunodeficiency,
 Diabetes mellitus,Diabetes mellitus,
 Alcohol,Alcohol,
 IV drug abuse,IV drug abuse,
 Indwelling vascular catheters,Indwelling vascular catheters,
 Abnormal “jet streams” caused by pre-existing heart diseaseAbnormal “jet streams” caused by pre-existing heart disease

5. Causative organismsCausative organisms
 In previously damaged valves:In previously damaged valves:
streptococcus viridansstreptococcus viridans (50-60%)(50-60%)
 In normal or damaged valves, IV drugIn normal or damaged valves, IV drug
abusers:abusers: S aureusS aureus (10-20%)(10-20%)
 EnterococciEnterococci
 HACEKHACEK Group of oral commensalsGroup of oral commensals
((HHaemophilus,aemophilus, AActinobacillus,ctinobacillus,
CCardiobacterium,ardiobacterium, EEikenella,ikenella, KKingella)ingella)
 Coagulase neg staphCoagulase neg staph: prosthetic valve: prosthetic valve
infectioninfection

6.  Other agents: fungi, gram neg bacilliOther agents: fungi, gram neg bacilli
 In 10% Culture is negative. No organismIn 10% Culture is negative. No organism
can be isolatedcan be isolated
SOURCES OF ENTRY OF INFECTIONSOURCES OF ENTRY OF INFECTION
 Infection elsewhereInfection elsewhere
 Dental or surgical procedureDental or surgical procedure
 IV drug abuseIV drug abuse
 Occult sources in Gut, oral cavity etc.Occult sources in Gut, oral cavity etc.

7. PATHOGENESISPATHOGENESIS
Damaged valves are more prone to bacterial infectionDamaged valves are more prone to bacterial infection
 Hemodynamic stressHemodynamic stress
 Damaged endotheliumDamaged endothelium
 Platelet thrombiPlatelet thrombi
 Bacterial infectionBacterial infection
 BE / IEBE / IE

8. MORPHOLOGYMORPHOLOGY
Bulky friable, destructive vegetations, destroying valvesBulky friable, destructive vegetations, destroying valves

9. SITESITE
 Valves : Most common : mitral, aorticValves : Most common : mitral, aortic
 IV abusers : Tricuspid, pulmonaryIV abusers : Tricuspid, pulmonary
 EndocardiumEndocardium
GROSSGROSS
VEGETATIONSVEGETATIONS
 Single/ multipleSingle/ multiple
 1 or more valves involved1 or more valves involved
 Friable, bulky, destructiveFriable, bulky, destructive
Erode adjacent myocardiumErode adjacent myocardium
SABE : no erosion, perforationSABE : no erosion, perforation
 RING abscess.RING abscess.
APPEARANCE DEPENDS
UPON
1. Type of organism
BE : Bulky
SABE : Smaller
Fungal : Larger
2. Degree of host response
3. Previous antibiotic therapy

10.  vegetations are composed of fibrin,vegetations are composed of fibrin,
inflammatory cells, bacteria and otherinflammatory cells, bacteria and other
organismsorganisms

11. MICROSCOPYMICROSCOPY
BEBE
 NecrosisNecrosis
 Fibrin + Bacteria + Dense NeutrophilsFibrin + Bacteria + Dense Neutrophils
SABESABE
 Granulation tissue at baseGranulation tissue at base
 Chronic inflammationChronic inflammation
 Fibrosis, calcifiedFibrosis, calcified

12. CLINICAL FEATURESCLINICAL FEATURES
Fever, especially in BEFever, especially in BE
 ABE :ABE :
Stormy onsetStormy onset
Fever with chillsFever with chills
Weakness, lassitudeWeakness, lassitude
 SABE : nonsp :SABE : nonsp :
Fatigue, flu like symp, wt lossFatigue, flu like symp, wt loss
 Uncommon :Uncommon :
Petechiae, subungual hge, Roth spots.Petechiae, subungual hge, Roth spots.

13. COMPLICATIONSCOMPLICATIONS
1. CARDIAC1. CARDIAC
 Valvular insufficiencyValvular insufficiency
 Myocardial ring abscessMyocardial ring abscess
 Cardiac failureCardiac failure
 Suppurative pericarditisSuppurative pericarditis
 Partial dehiscence with paravalvular leakPartial dehiscence with paravalvular leak
2. EMBOLIC2. EMBOLIC
 Left sided : Brain, heart, spleen, kidneyLeft sided : Brain, heart, spleen, kidney
 Right sided : Lungs : Infarct, abscess, pneumoniaRight sided : Lungs : Infarct, abscess, pneumonia
3. RENAL3. RENAL
 Embolic infarctionEmbolic infarction
 Focal / diffuse glomerulonephritisFocal / diffuse glomerulonephritis
 Multiple abscessesMultiple abscesses

14. Vegetation in Acute RheumaticVegetation in Acute Rheumatic
FeverFever
Small warty vegetations along line of closure of valve

15. Vegetations in infectiveVegetations in infective
endocarditisendocarditis
Large irregular masses on the chordae that can extend
onto chordae

16. Nonbacterial ThromboticNonbacterial Thrombotic
EndocarditisEndocarditis
(marantic endocarditis)(marantic endocarditis)
Small bland vegetations along the line of closure

17. NBTENBTE
Characterised by deposition of small masses of fibrin, platelets, andCharacterised by deposition of small masses of fibrin, platelets, and
other blood components on the leaflets of cardiac valves.other blood components on the leaflets of cardiac valves.
 VegetationsVegetations
Sterile, nondestructiveSterile, nondestructive
Small (1-5mm)Small (1-5mm)
Along line of closure of the leaflets or cuspsAlong line of closure of the leaflets or cusps
On either side of leafletsOn either side of leaflets
 Occurs in debilitated patients (marantic)Occurs in debilitated patients (marantic)
 May be due to hypercoagulable states that occur inMay be due to hypercoagulable states that occur in
association with cancerassociation with cancer
 Eg : Mucinous AdenoCa pancreasEg : Mucinous AdenoCa pancreas
AML – M3AML – M3
Indwelling catheter – endocardial traumaIndwelling catheter – endocardial trauma

18. Libman Sacks EndocarditisLibman Sacks Endocarditis
endocarditis of SLEendocarditis of SLE
Small medium sized vegetations on either or both
sides of the valve

19. Endocarditis of SLE (LSE)Endocarditis of SLE (LSE)
 Small sterile (bland) vegetations on mitralSmall sterile (bland) vegetations on mitral
and tricuspid valvesand tricuspid valves
On undersurface of AV valvesOn undersurface of AV valves
Valvular endocardiumValvular endocardium
ChordsChords
Mural endocardium of ventricles or atriaMural endocardium of ventricles or atria
 Micro :Micro :
Granular fibrinous materialGranular fibrinous material
Hematoxyphilic bodiesHematoxyphilic bodies
Fibrinoid necrosisFibrinoid necrosis

20. Diagnostic criteriaDiagnostic criteria
( Dukes criteria)( Dukes criteria)

21. Pathological criteriaPathological criteria
 Microorganisms demonstrated by cultureMicroorganisms demonstrated by culture
or histological examination. Found in aor histological examination. Found in a
vegetation, embolus from a vegetation, orvegetation, embolus from a vegetation, or
intracardiac abscessintracardiac abscess
 Histological confirmation of activeHistological confirmation of active
endocarditis in a vegetation or intracardiacendocarditis in a vegetation or intracardiac
abscessabscess

22. Clinical criteriaClinical criteria
Major and minorMajor and minor

23. Major clinical criteriaMajor clinical criteria
Positive blood culturePositive blood culture
ECG findings of mass or abscessECG findings of mass or abscess
New valvular regurgitationNew valvular regurgitation

24. MINOR CRITERIAMINOR CRITERIA
 FeverFever
 Predisposing heart lesion, IV drug abusePredisposing heart lesion, IV drug abuse
 Vascular lesionsVascular lesions
 Immunological phenomenaImmunological phenomena
 Microbiological evidenceMicrobiological evidence
 ECG findings consistent but not diagnosticECG findings consistent but not diagnostic
of IEof IE

25. Vascular lesionsVascular lesions
 Arterial petechiaeArterial petechiae
 Subungual /splinter hemorrhagesSubungual /splinter hemorrhages
 Emboli, septic infarctsEmboli, septic infarcts
 Mycotic aneurysmMycotic aneurysm
 Janeway lesions( Small erythematousJaneway lesions( Small erythematous
lesions on palms and soles due to septiclesions on palms and soles due to septic
emboli)emboli)

26. Janeway lesions Splinter hemorrhages

27. Immunological phenomenaImmunological phenomena
 GlomerulonephritisGlomerulonephritis
 Oslers nodesOslers nodes: small tender subcutaneous: small tender subcutaneous
nodules in the pulp of the digitsnodules in the pulp of the digits
 Roths spotsRoths spots: Oval retinal hemorrhages: Oval retinal hemorrhages
with pale centreswith pale centres

28. For diagnosisFor diagnosis
 Either pathological criteriaEither pathological criteria
 If clinical criteria are usedIf clinical criteria are used
• 2 major2 major
• 1 major and 3 minor1 major and 3 minor
• 5 minor criteria for diagnosis5 minor criteria for diagnosis

29. CONGENITAL HEARTCONGENITAL HEART
DISEASEDISEASE

30. CATEGORIESCATEGORIES
 Malformations associated with left to rightMalformations associated with left to right
shuntsshunts
 Malformations associated right to leftMalformations associated right to left
shunts (cyanotic heart disease)shunts (cyanotic heart disease)
 Malformations associated with obstructionMalformations associated with obstruction

34. Tetralogy of Fallot (TOF)Tetralogy of Fallot (TOF)
 The most common congenital cyanoticThe most common congenital cyanotic
heart diseaseheart disease
FeaturesFeatures
 Ventricular septal defectVentricular septal defect
 Obstruction to rt ventricular outflow tractObstruction to rt ventricular outflow tract
(subpulmonary stenosis)(subpulmonary stenosis)
 Aorta that overrides the VSDAorta that overrides the VSD
 Rt ventricular hypertrophyRt ventricular hypertrophy

35. Tetralogy of Fallot (TOF)Tetralogy of Fallot (TOF)
 The most common congenital cyanoticThe most common congenital cyanotic
heart diseaseheart disease

36. FEATURESFEATURES
 Ventricular septal defectVentricular septal defect
 Obstruction to rt ventricularObstruction to rt ventricular
outflow tract (subpulmonaryoutflow tract (subpulmonary
stenosis)stenosis)
 Aorta that overrides the VSDAorta that overrides the VSD
 Rt ventricular hypertrophyRt ventricular hypertrophy

38.  Embryologically due to an anterosuperiorEmbryologically due to an anterosuperior
displacement of the infundibular septum indisplacement of the infundibular septum in
the truncus arteriosusthe truncus arteriosus

39. MorphologyMorphology
 Boot shaped heart due to rt ventricularBoot shaped heart due to rt ventricular
hypertrophy pronounced at apexhypertrophy pronounced at apex

40.  Direction of blood flow is determined byDirection of blood flow is determined by
the severity of pulmonic stenosisthe severity of pulmonic stenosis
 If mild , shunt functions like a VSDIf mild , shunt functions like a VSD (pink(pink
tetralogy)tetralogy)
 When pulmonic obstruction increases,When pulmonic obstruction increases,
resistance to rt outflow increasesresistance to rt outflow increases
 When it reaches the level of systemicWhen it reaches the level of systemic
resistance a rt to left shunt occursresistance a rt to left shunt occurs
(cyanosis occurs) “CLASSIC TOF”(cyanosis occurs) “CLASSIC TOF”

41.  TheThe tighter the subpulmonic stenosis, thetighter the subpulmonic stenosis, the
larger the aorta and the more hypoplasticlarger the aorta and the more hypoplastic
the pulmonary arteriesthe pulmonary arteries
 However, the stenosis protects theHowever, the stenosis protects the
pulmonary arteries from pressure overloadpulmonary arteries from pressure overload
 Rt ventricle decompresses through VSDRt ventricle decompresses through VSD
into left ventricle and aorta.into left ventricle and aorta.
 Hence Rt ventricular failure rareHence Rt ventricular failure rare
 Treatment : surgicalTreatment : surgical