INFECTIVE ENDOCARDITIS

FEVER
t NEW MURMUR = ENDOCARDITIS UNTILL PROVEN OTHERWISE

Infection of the endocardium → Loss of function

Clotting through Ca cascade → coagulation

* ACUTE; NORMALVALVES Acute HE ± Emboli # I Staph Aweus

;
- =

Risk Factors
;
Skin breaches ,
Renal failure , Immunosuppression ,
DM

* SUBACUTE ; ABNORMAL VALVES # I strep Vi ri dans within

Early 60 days
→

, =
after
surgery→ Staph
Risk Factors ; Aortic I Mitral Valve disease , Tricuspid Valves in N Coaction , PDA , VSD, Prosthetic Valves Epidemic is
drug users ,
poor prognosis
=

↳ Late
=

strep viridis
=
-

Bacteria : • # I strep Vi ri dans

A wens C Acute IN
# 2 Staph drug users tricuspid valve 1mV Normal Valve )
•
-

Needs
colonoscopy ; Malignancy ?
Bovis →
•
strep a

•
Entercocci (9
'd
'
efiniomwain
EEE
botnets) ,
coxiella Bwnetii , Dypheioids , chlamydia
CAUSES bacteria ; Haemophilus , Actinobacil us , Cardiobacterium,
•

Rarely HACEK gram

-
ve EiKerala , Kinsella
C Most cannon in colonic resectionis bacteroids)

•
Strep memory ; found in Colon, Metastatic lesions I septic foci in brain → IBD a CA Cohn

Fungi :
Candida, His
toplasma , Aspergillus } usually in Drug users I Immunocompromised I prosthetic valves
C High Mortality ,
Need
surgery)
Others : SLE ( Libman Sacks Endocarditis ) , Malignancy
-

PATHOPHYSIOLOGY
II Abnormal Cardiac endothelium , facilitating bacterial adherence 's Growth
II Presence of organisms in theblood stream C Increased Attack } Decreased defence)

turbulentBlood flow → Endothelial

Damage →
platelet he Fibrin Activation → colonisation by blood bow ne organisms
→
Infection → Vegitatiars ( Fibrin t Platelets t organisms) grow → obstruction IEmboli Iperforation /fibrosis → stenosis/

Abscess formation →
Regurgitation
If vezithtiins in arteries → MI
coronary
•

•
Dilation of aortic root CudSava sign ) →
Affects Carney arteries

Mycolic Aneurysms
*
 RISK FACTORS →

•
No I =
Rheumatic Meet Disease or previous episode of IE

Heat problems ; VSD , PDA , Mitral Valve prolapse primary sclerotic Valves prosthetic valves
•

, ,

Host factors ; Immunocompromised , HIV

•

°
ASD isn't a risk factor because no press we difference or turbulence

CLINICAL PICTURE →
( Nwmocytic
Normo chromic)
SEPTIC SIGNS : fever , Rigors , Night sweats weight loss
, ,
malaise , Anemia , splenomegaly , clubbing

CARDIAC LESIONS :
New mwmw , worsening of preexisting murmur , Aortic root abscess → prolonged PR Interval or complete AV block LUH
,
ImInFt)
↳
IMMUNE COMPLEX DEPOSITION :
vasculitis , Microscopic Hematuria; GN 7 AKI
. ,
Roth spots , Splinter hemorrhage, osiers Nodes

EMBOLIC PHENOMENA : Abscesses in organs ( G Lungif Rs , Multiple inbrain) , or

Skin =
Janeway Lesions , Myocardial Abscess → Hypokinesics ofventricles → HF

SUBACUTE → pt with Congenital /

valvular heart disease t Resistantfever

putmore
Infection
→ Right Sudden
sided IE Right Hypo -
Stroke I Rend fail weI Ischemiclesions
→ Chandra
Rhin splenic
=

intact Acute Meet failure -

- Cause of Deem

ccoxielk? Emerged spleen} Live)

pericarditis → severe infection 1141
-

ACUTE → severe fever t prominent

(Microscopic)

(vasculitis) W
chasing murmurs t petichiae

( Leucocytosis) 1=4
.wks
-

* chronic Stigmata
=
Absent

* Embolic events = common

*
Rapid Rend , Heart Failure

* Abscess → seen on Echo

*
partially treated Acute behaves

Like subacute
INVESTIGATIONS
→

I .
CBC } ESR ICRP Cmore reliable) * Leucocytosis * Namo lytic NW mo chromic Anemia * High ESR E CRP

Rheumatoid factor tue, USE , MgLETS

"
(others :
, )

2. URINE → microscopic Hematuria 3 proteinuria

3. BLOOD CULTURE =
3 Sets ,
From different sites ,
At different times (36W intervals)

85 90%
-

diagnosed fran 1st 2 sets

,
10% =
culture negative → I .
prior Antibiotic treatment 4 .

Fungal Infections

z .
Organism requires special aetwe 5-
Wrong Diagnosis

3 . Slow growing organisms ey . HACEK

4 . ECHO: Detecting
-

Vegetation ,
value
damage , Abscesses

* Trans thoracic
; 2-4mm vegitaticns

* Trans eosoph
aged ; I -
i. 5mm Vegitaticns , prosthetic values , Aortic Root abscess

5 ECG : AV block , Prolonged PR segment , ST elevation Infarctiondue to Emboli

,
.

G . Cx R : Cardiac failure 4 cardiomegaly

7 .
CT : To look for Emboli

8. Complement level : for prognosis ; Ct t C4)

DIAGNOSIS →

( possible = I
major t I minor or 3 minor )
MANAGEMENT →
=
N Antibiotics (4 -

6 weeks
According to
sensitivity)

SUBACUTE → Amoxicillin ( IBenzyl penicillin) ± Getanyair

ACUTE →
Vancomycin (lfhrdoxacillin) t
Gertamyai ( Also pencil
in Allergy )

PROSTHETIC VALVE →
Vancomycin t
Gertamycin t Oral Rifampicin

SURGERY → PREVENTION →

* Heart failure due to value

damage Prophylactic Antibiotics
-

Obstruction C Large vegetation esp Left value w/ high risk of embolization) Good oral
valvular
Hygeine
-

* .

C Except Histoplasmosis) Risks of invasive

* Engel IE
procedures
-

* Persistent Bacteremia I Failure of Antibiotic therapy)

* Repeated emboli POOR PROGNOSIS →

*
Myocardial Abscess
-

Staph . A =
( Acute IE )
* Unstable infected prosthetic Valve
Fungal IE
-

Prosthetic Value IE

how Complement
Heavy Bacteremia
-