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
-