INFECTIVE ENDOCARDITIS
M. VINOD KUMAR
DEFINITION
• INVASION AND MULTIPLICATION OF MICROORGANISMS ON
THE ENDOCARDIAL SURFACE,
- WITHIN THE ENDOCARDIUM ,
- WITHIN THE MYOCARDIUM,
- OR ON PROSTHETIC MATERIALS WITHIN AND AROUND
CARDIAC STRUCTURES.
DEFINITION
• CONDITIONS IN WHICH STRUCTURES OF THE HEART
( FREQUENTLY VALVES) HARBOR AN INFECTIVE PROCESS;
- THAT LEADS TO VALVAR DYSFUNCTION,
- LOCALISED OR GENERALISED SEPSIS,
- OR SITES FOR EMBOLISM
THE TERM COVERS ,,,,
a) A/C TO DURATION
- ACUTE,
- SUBACUTE,
- CHRONIC
b) A/C TO INFECTING AGENT
- BACTERIAL,
- VIRAL,
- RICKETTSIAL
- FUNGAL
c) A/C TO SITE OF INFECTION
- NATIVE VALVE,
- PROSTHETIC VALVE
HISTORICAL NOTE
• 1841 - BOUILLAUD - THE TERM ENDOCARDITIS
• 1885 - OSLER - CLASSICAL FEATURES
• 1950 - PRINCIPLES OF AB THERAPY ESTABLISHED
• 1961 - KAY & COLLEAGUES - FIRST SURGICAL Rx
• 1970s - STINSON , RICHARDSON & COLLEAGUES
MODERN CONCEPTS OF SURGICAL Rx
PATHOGENESIS
• MOST COMMON SITE IS :
- ATRIAL SIDE OF AV VALVES
- VENTRICULAR SIDE OF SEMILUNAR VALVES
• INJURY MAY RESULT FROM :
- PRE-EXISTING LESIONS ( RHEUMATIC VALVULITIS,VALVAR CALCIFICATION )
- CATHETER TRAUMA
- HEMODYNAMIC FACTORS ( JET EFFECT OF BLOOD FLOW THRU :
PDA,
RESTRICTIVE VSD,
MVP,
BAV)
VALVE
ENDOTHELIUM
ENDOTHELIAL
DAMAGE
(BIOFILM)
NBTE
ADHERENCE
MUCOUS
MEMBRANE
BACTEREMIA
MATURE
INFECTED
VEGETATION
VALVE RING
ABSCESS
VALVE
INCOMPETENCE
VALVE
PERFORATION
TRAUMA
TURBULENCE
TRAUMA
IV DRUG USE
PATHOGENESIS
RODBARD HYPOTHESIS
ORIFICE LOW PRESSURE SINK
HIGH
PRESSURE
SOURCE
VENA CONTRACTA
Rodbard S. Blood velocity and endocarditis. Circulation 1963,27:18.
LOCI OF INFECTIVE ENDOCARDITIS LESIONS
CONDITION HIGH – PRESSURE
SOURCE
ORIFICE LOW – PRESSURE
SINK
LOCATION OF
LESIONS
AR AORTA CLOSED AORTIC
CUSPS
LV VENTRICULAR
SURFACE OF AOV
MR LV CLOSED MITRAL
LEAFLETS
LA ATRIAL SURFACE
OF MV
TR RV CLOSED
TRICUSPID
LEAFLETS
RA ATRIAL SURFACE,
TRICUSPID
LEAFLETS
VSD LV DEFECT RV RV SURFACE OF
DEFECT
PDA AORTA DUCTUS PULMONARY
ARTERY
PULMONARY
ARTERY
REPRESENTATION OF IE AT A PDA
VEGETATIONS ARE DEPOSITED
ON PA WALL OPPOSITE A HIGH-
VELOCITY JET THRU AN OPEN
DUCTUS
MORPHOLOGY
• VEGETATIONS, EROSIVE CAVITIES – VENTRICULAR ASPECT OF AOV, ATRIAL
ASPECT OF MV
• OFTEN RESULT IN DISCONTINUITY AT
THE VA OR AV JUNCTION
• DISCRETE PERFORATIONS OF AOV
• DROP LESIONS ON AML
• PERIANNULAR PSEUODANEURYSMS
/ ABSCESS [ AOV > MV ]
CLINICAL FEATURES
• FEVER - 95 – 100%
• HEART MURMUR (CHANGING) - 85%-95%
• ANEMIA, HEMATURIA
• MYALGIAS
• ARTHRITIS/ARTHRALGIAS
• EMBOLIZATION ( CENTRAL / PERIPHERAL )
• CLASSIC PERIPHERAL SIGNS OF ENDOCARDITIS
• JANEWAY LESIONS – ALMOST ALWAYS BY STAPHYLOCOCCUS
• IN PRACTICE, DIAGNOSIS BASED ON TWO SETS :
1. POSITIVE BLOOD CULTURES
2. CARDIAC LESION CSTD BY NEW STENOSIS/REGURG OR VEGETATION
CLINICAL FEATURES
• EMBOLIC EVENTS = 24-67%
• BRAIN = MOST COMMON SITE OF EMBOLI
• NEUROLOGIC MANIFESTATIONS ARE PROTEAN ;
• INCLUDES - STROKE ( ISCHEMIC / HAEMORRHAGIC )
- TIA
- TOXIC ENCEPHALOPATHY
- MENINGITIS
- BRAIN ABSCESS
- SEIZURES
MODIFIED DUKE CRITERIA
MAJOR CRITERIA
BLOOD CULTURES POSITIVE FOR IE
1. TYPICAL MICROORGANISMS
2. PERSISTENT MICROORGANISMS
3. SINGLE POSITIVE BLOOD CULTURE FOR C . burnetti
EVIDENCE OF ENDOCARDIAL INVOLVEMENT
1. ECHO POSITIVE FOR IE
( VEGETATION, ABSCESS,
NEW PARTIAL DEHISCENCE OF PROSTHETIC VALVE )
2. NEW VALVULAR REGURGITATION
MINOR CRITERIA
1. PREDISPOSITION
2. FEVER
3. IMMUNOLOGIC PHENOMENA
4. VASCULAR PHENOMENA
5. MICROBIOLOGIC EVIDENCE
DEFINITE IE
2 MAJOR
1 MAJOR + 3 MINOR
5 MINOR
POSSIBLE IE
1 MAJOR + 1 MINOR
3 MINOR
VASCULAR PHENOMENA
JANEWAY LESIONS CONJUCTIVAL HEMORRHAGES
MYCOTIC ANEURYSMS
IMMUNOLOGIC PHENOMENA
OSLER NODES ROTH SPOTS
DIFFERENCES B/N BACTERIAL AND FUNGAL INFECTIVE
ENDOCARDITIS
PARAMETERS BACTERIAL FUNGAL
ONSET ACUTE INSIDOUS
CLINICAL COURSE FULMINANT PROTRACTED
TISSUE DESTRUCTION MASSIVE MINIMAL
VEGETATION SIZE USUALLY SMALL LARGE
PERIANNULAR ABSCESS PRESENT ABSENT
VASCULAR EMBOLI USUALLY INVOLVES
SMALLER VESSELS
USUALLY INVOLVES MAJOR
VESSELS
HEMATURIA COMMON NOT COMMON
SKIN LESIONS COMMON NOT COMMON
BLOOD CULTURES ARE USUALLY POSITIVE NEGATIVE
BLOOD SAMPLES VENOUS SAMPLE CAN BE
TAKEN
ARTERIAL SAMPLE FOR
LEFT SIDE LESION IS
NECESSARY FOR CULTURE
CULTURE NEGATIVE INFECTIVE ENDOCARDITIS
• ACCOUNTS FOR 5% OF ALL IE
• CAUSES :
1. PRIOR ANTIBIOTIC THERAPY
2. FASTIDIOUS ORGANISMS
( GRAM NEGATIVE BACILLI, HACEK sps , BRUCELLA, FUNGI )
3. INTRACELLULAR BACTERIA
( C. burnetti, Bartonella, Chlamydia, T. whipplei )
• DIAGNOSIS :
– SEROLOGICAL TESTING
– CELL CULTURE
– GENE AMPLIFICATION
NATURAL HISTORY
• EPIDEMIOLOGY :
THEN NOW
YOUNGER POPULATION AFFECTS OLDER AGE GROUP
OFTEN IN PREXISTING VALVAR
DISEASE ( RHD )
EVEN IN NORMAL VALVES
STREPTOCOCCI WAS THE
LEADING CAUSE
STAPHYLOCOCCI IS THE
LEADING CAUSATIVE
ORGANISM
POOR DENTITION WAS ONE OF
THE MAJOR CAUSE
INVASIVE PROCEDURES (
HEMODIALYSIS , CATHETERS )
NATURAL HISTORY - EPIDEMIOLOGY
• PHV – STRONG RISK FACTOR
• RISK FACTORS FOR PVE
• CAUSATIVE FACTORS FOR PVE
• PEDIATRIC POPULATION
• ( PRE AND POST OP RISK FACTORS )
NATURAL HISTORY
50%
30%
10%
5%
5%
CAUSATIVE ORGANISMS
Staphylococcus aureus
Streptococcus
Enterococcus
Gram negative bacilli
others ( fungi, viral,
rickettsial )
NATURAL HISTORY
ACUTE BACTERIAL ENDOCARDITIS SUBACUTE BACTERIAL ENDOCARDITIS
OFTEN BY S. aureus OFTEN BY S. viridans
FULMINATING CLINICAL COURSE PROTRACTED CLINICAL COURSE
ANTIBIOTICS ALONE SELDOM CURES ANTIBIOTICS ALONE OFTEN CURES
JANEWAY LESION AND ROTH SPOTS ARE
SEEN ONLY IN ACUTE FORM
OSLER NODES, SPLINTER HEMORRHAGES,
NEW MURMUR IS COMMON TO BOTH
NO PREEXISTING VALVULAR DISEASE OFTEN ASSOC WITH PREEXISTING
VALVULAR DISEASE
NATURAL HISTORY - COMPLICATIONS
A) CARDIAC
1. HEART FAILURE
NVE – VALVAR REGURGITATION
PVE – PERIANNULAR LEAKAGE AND ABSCESS
2. MYOCARDIAL ABSCESS
3. CONDUCTION ABNORMALITIES
4. MYOCARDIAL PERFORATION
5. PERICARDITIS
B) RENAL COMPLICATIONS
1. PRERENAL FAILURE – LCOS
2. MICROABSCESS - SEPTIC EMBOLI
3. GLOMERULAR DYSFUNCTION – CIC’s
4. RENAL FAILURE - ANTIBIOTIC TOXICITY
C) EMBOLIC EVENTS
• INCIDENCE ( NVE > PVE )
• S. aureus, Candida, HACEK sps INCREASES THE RISK OF
EMBOLISM
• NEUROLOGIC MANIFESTATIONS ARE MOST COMMON
• MOST DEVASTATING NEUROLOGIC COMPLICATION IS ICH
SITE OF EMBOLISATION
Habib G. Management of infective endocarditis. Heart 2006;92:124-30.
RISK OF EMBOLIC EVENTS A/C TO VEGETATION SIZE
Vilacosta I, Graupner C, San Roman JA, Sarria C, Ronderos R, Fernandez C et al. Risk of
embolization after institution of antibiotic therapy for infective endocarditis. J Am Coll Cardiol
2002; 39:1489.
RECOMMENDED PLAN
NVE
PRIMARY
ANTIBIOTIC
THERAPY
SURGERY ONLY
FOR
COMPLICATIONS
EARLY PVE ANTIBIOTIC
THERAPY AND
SURGICAL
TREATMENT IS
ESSENTIAL
LATE PVE ANTIBIOTIC
THERAPY
SURGICAL
TREATMENT IF
REQUIRED
THERAPY - ANTIBIOTICS
• BLOOD CULTURES SHOULD BE OBTAINED BEFORE INITIATING
AB THERAPY
• PROLONGED PARENTERAL AB ADMN IS ADVISABLE
• AFTER INITIATING AB THERAPY – BLOOD CULTURES SHOULD
BE DRAWN EVERY 1-2 DAYS UNTIL THEY BECOME NEGATIVE
• AMINOGLYCOSIDES + CELL WALL ACTIVE AGENT = SYNERGY
ANTIBIOTIC Rx FOR STREPTOCOCCI ( MIC < 0.125 mg/L )
ANTIBIOTIC DOSAGE AND ROUTE DURATION
( WEEKS)
LEVEL OF
EVIDENCE
STANDARD TREATMENT
PENICILLIN G
Or
CEFTRIAXONE
12-18 MU/day i.v
2 g/day i.v or i.m 24 h
4
4
I B
I B
TWO – WEEK TREATMENT
PENICILLIN G
OR
CEFTRIAXONE
With
GENTAMICIN
12-18 MU/day i.v in 6 doses
2 g/day i.v or i.m in 1 dose
3 mg/kg/day i.v or i.m in 1 dose
2
2
2
I B
I B
I B
IN BETA-LACTAM ALLERGIC PATIENTS
VANCOMYCIN 15 mg/kg i.v q 12 h 4 I C
ANTIBIOTIC Rx FOR STREPTOCOCCI (MIC < 0.125 – 2 mg/L )
ANTIBIOTIC DOSAGE AND ROUTE DURATION
(WEEKS)
LEVEL OF
EVIDENCE
STANDARD TREATMENT
PENICILLIN G
WITH
GENTAMICIN
24 MU i.v per 24 h
3 mg/kg i.v / i.m q 24 h
4
2
I B
I B
IN BETA-LACTAM ALLERGIC PATIENTS
VANCOMYCIN
WITH
GENTAMICIN
15 mg/kg i.v 12 h
3 mg/kg/day i.v or i.m q 24 h
4
2
I C
ANTIBIOTIC Rx FOR STAPHYLOCOCCUS
ANTIBIOTIC DOSAGE AND ROUTE DURATION
( WEEKS )
LEVEL OF
EVIDENCE
A) NATIVE VALVES
METHICILLIN SUSCEPTIBLE
OXACILLIN
WITH
GENTAMICIN
2 g i.v in 4 h
1 mg/kg i.v or i.m 8 h
6
3-5 days
I B
METHICILLIN RESISTANT
VANCOMYCIN 15 mg/kg i.v in 12 h 6 I B
ANTIBIOTIC Rx FOR ENTEROCOCCUS
ANTIBIOTIC DOSAGE AND ROUTE DURATION
(WEEKS)
LEVEL OF
EVIDENCE
A ) IF SUSCEPTIBLE TO PENICILLIN
AMPICILLIN
PLUS
GENTAMICIN (OR)
2 g IV q 4 h
1 mg/kg IV/IM q 8 h
4-6
4-6
I B
PENICILLIN G
PLUS
GENTAMICIN
18-30 MU IV 24 h
PLUS
1 mg/kg IV/IM q 8 h
4-6
B) IF RESISTANT TO PENICILLIN
VANCOMYCIN
PLUS
GENTAMICIN
15 mg/kg IV Q 12 h
1 mg/kg IV / IM q 8 h
6 I B
ANTIBIOTIC Rx FOR STAPHYLOCOCCUS
ANTIBIOTIC DOSAGE AND ROUTE DURATION
( WEEKS )
LEVEL OF
EVIDENCE
A) PROSTHETIC VALVES
OXACILLIN - SUSCEPTIBLE
OXACILLIN
WITH
RIFAMPIN
AND
GENTAMICIN
2 g i.v I q 4 h
300 mg i.v or orally q 8 h
1 mg/kg i.v or i.m q 8 h
> 6
6
2
I B
OXACILLIN - RESISTANT
VANCOMYCIN
WITH
RIFAMPIN
AND
GENTAMICIN
15 mg/kg i.v q 12 h
300 mg i.v or orally q 8 h
1 mg/kg i.v or i.m q 8 h
> 6
> 6
2
I B
ANTIBIOTIC Rx FOR CULTURE NEGATIVE IE
PATHOGENS PROPOSED THERAPY TREATMENT OUTCOME
Brucella sps DOXYCYCLINE + COTRIMOXAZOLE +
RIFAMPIN > 3 MONTHS ORALLY
SUCCESS DEFINED AS
ANTIBODY TITRE < 1:60
Coxiella burnetti
(agent of Q fever)
DOXYCYCLINE + OFLOXACIN
( > 18 MONTHS TREATMENT )
SUCCESS DEFINED AS
ANTIBODY TITRE < 1:200
Bartonella spp DOXYCYCLINE ( 6 WEEKS ) SUCCESS EXPECTED IN > 90%
Legionella spp RIFAMPIN OR CIPROFLOXACIN
(6 WEEKS)
OPTIMAL Rx UNKNOWN
Mycoplasma spp NEWER FLUOROQUINOLONES OPTIMAL Rx UNKNOWN
Tropheryma Whipplei DOXYCYCLINE + HYDROXYCHLOROQUINE ( >
18 MONTHS )
LONG TERM TREATMENT
ECHOCARDIOGRAPHIC AND CLINICAL FEATURES S/O NEED FOR
SURGICAL INTERVENTION
VEGETATION
• PERSISTENT
• > 10 mm
• > 1 EMBOLIC EVENT
DURING FIRST 2 WKS
OF AB THERAPY
• INCREASE IN SIZE
AFTER 4 WKS OF AB
THERAPY
VALVAR
DYSFUNCTION
• ACUTE AR/MR WITH
SIGNS OF
VENTRICULAR
DILATATION
• HEART FAILURE
UNRESPONSIVE TO
MEDICAL THERAPY
• VALVE PERFORATION
/RUPTURE
PERIVALVAR
EXTENSION
• VALVAR DEHISCENCE,
RUPTURE, OR FISTULA
• NEW HEART BLOCK
• LARGE ABSCESS OR
EXTENSION OF
ABSCESS DESPITE AB
THERAPY
INDICATIONS FOR SURGERY
1. CHF
2. PERIANULAR EXTENSION
3. PERSISTENT SEPSIS
4. DIFFICULT ORGANISMS
5. PVE
1. SEVERE AR/MR
2. ELEVATED LVEDP / PAH
3. PROSTHETIC DEHISCENCE /
OBSTRUCTION
1. SYSTEMIC EMBOLISM
( RECURRENT EMBOLI ;
LARGE VEG > 10 mm;
LARGE VEG WITH COMPL.COURSE;
VERY LARGE VEG > 15 mm )
2. CEREBROVASCULAR
COMPLICATIONS
( TIA / ISCHEMIC STROKE )
1.FEVER OR POSITIVE BLOOD
CULTURE > 7 DAYS DESPITE
AB REGIMEN
2. RELAPSING IE ( NON
STREPTO ORGANISMS AND
IN PTS PHV )
S. aureus
MRSA, VRSA
PSEUDOMONAS
FUNGAL
Q FEVER
1. EARLY PVE
2. PVE CAUSED BY S. aureus
3. LATE PVE WITH CHF,
PERIANULAR EXTENSION,
PERSISTENT BACTEREMIA
SURGERY
• GOALS :
1. REMOVE INFECTED TISSUE AND DRAIN ABSCESSES
2. RESTORE OR RECONSTRUCT AV OR VA CONTINUITY
3. REVERSE THE HEMODYNAMIC ABNORMALITY
SURGICAL TREATMENT
ACTIVE INFECTIVE
ENDOCARDITIS
ONLY CUSPS
INVOLVED
VALVE REPAIR/
REPLACEMENT
CUSPS + ANNULUS
INVOLVED
RADICAL RESECTION
+ RECONSTRUCTION
SMALL DEFECT
(1-2 CM)
FRESH
AUTOLOGOUS
PERICARDIUM
LARGE DEFECTS
GLUTARALDHELYDE
FIXED BOVINE
PERICARDIUM
VALVE REPAIR/
REPLACEMENT
SURGICAL TREATMENT
MYOCARDIAL
PROTECTION
AVOIDANCE OF
CONTAMINATION
SURGICAL TREATMENT
VALVE REPAIR
VALVE
REPLACEMENT
AORTIC ROOT
ABSCESS
ONLY AORTIC
VALVE IS
INVOLVED
HOMOGRAFT
IS IDEAL
BIO /
MECHANICAL
PROSTHESIS
REPAIR OF AML PERFORATION ( DROP LESION)
SMOOTH SURFACE SHOULD FACE THE ATRIUM
REPAIR OF PML VEGETATION
P2 SEGMENT IS MOST COMMONLY INVOLVED
REPAIR OF TV INFECTIVE ENDOCARDITIS
NOTE : IN IV DRUG ABUSERS IF TRICUSPID
VALVE REPAIR IS NOT POSSIBLE, THEN
TRICUSPID VALVE RESECTION WITHOUT
REPLACEMENT IS ALSO AN OPTION.
SURGICAL TREATMENT
MECHANICAL
PROSTHESIS
BIO PROSTHESIS
POST OP CARE
• TISSUE GRAM STAIN AND CULTURE ANALYSIS IS MANDATORY
• USE OF PHENLYEPHRINE, VASOPRESSIN TO INC PERIPHERAL
RESISTANCE IN SEPTIC PATIENTS
• IV ANTIBIOTIC Rx FOR 4-6 WEEKS
• CANDIDA :ORAL KETOCONAZOLE / FLUCONAZOLE FOR 3-6 MONTHS
• ASPERGILLUS : ORAL VORICONAZOLE ( EVEN FOR LIFE LONG )
• MONITORING A) ANTIBIOTIC LEVELS
B) RENAL FUNCTION
C) CELL COUNTS
RESULTS
• EARLY DEATH
• TIME-RELATED SURVIVAL
• INCREMENTAL RISK FACTORS
• IN-HOSPITAL MORBIDITY
• RECURRENT INFECTION
1. NVE – EARLY DEATH
• FACTORS AFFECTING THE OUTCOME
- STAGE OF ENDOCARDITIS ( ACTIVE / HEALED)
- URGENCY OF THE SURGICAL INDICATION
- MODALITY OF THE TREATMENT ( OPERATIVE V/S NON-
OPERATIVE)
- COMPLEXITY OF THE PROCEDURE ( DURATION OF THE
ILLNESS AND INFECTING MICROORGANISM)
1. EARLY DEATH - PVE
• PVE – INCREMENTAL RISK FACTOR FOR OPERATIVE
MORTALITY IN THE DOMAIN OF ALL IE.
• FACTORS RESPONSIBLE FOR INCREASED MORTALITY
- REOPERATION
- PREVALENCE OF ABSCESS
- ANNULAR EROSION
- PERIANULAR ANEURYSM
- FASTIDIOUS/FUNGAL ORGANISM
2. TIME-RELATED SURVIVAL
Haydock D, Barratt-Boyes B, Macedo T, Kirklin JW Blackstone E. Aortic valve replacement for
active infectious endocarditis in 108 patients. Heart 2010;96:696-700.
3. INCREMENTAL RISK FACTORS
Moon MR, Miller DC, Moore KA,Oyer PE, Mitchell RS, Robbins RC, et al. Treatment of endocarditis
with valve replacement : the question of tissue versus mechanical prosthesis. Ann Thorac Surg
2001;71:1164.
4. IN-HOSPITAL MORBIDITY
• CONTINUING EPISODES OF SEPSIS AFTER SURGERY
• NEW CONDUCTION ABNORMALITIES
• POST OP BLEEDING
• NEW / DEEPENING NEUROLOGIC DEFICIT
5. RECURRENT INFECTION
• INCIDENCE INCREASES WITH :
- NONSTREPTOCOCCAL ORGANISMS
- ANNULAR DESTRUCTION
- AORTIC VALVE IS INVOLVED
- IV DRUG ABUSERS
• AORTIC NVE / PVE / MITRAL NVE/ MITRAL PVE :
( ALLOGRAFTS > MECHANICAL = BIOPROSTHESIS )
5. RECURRENT INFECTION
Haydock D, Baratt-Boyes B, Macedo T, Kirklin JW, Blackstone E. Aortic valve replacement for
active infectious endocarditis in 108 patients. J Thorac Cardiovasc Surg 1992;103:130.
RECURRENT ENDOCARDITIS
McGiffin DC, et al. Aortic Valve infection. Risk factors for death and recurrent endocarditis
after aortic valve replacement. J Thorac Cardiovasc Surg 1992;104:511
TIMING OF SURGERY
EMERGENCY SURGERY ( WITHIN 24 HRS )
1. NVE / PVE WITH SEVERE CHF / CARDIOGENIC SHOCK
CAUSED BY
- ACUTE VALVAR REGURGITATION
- SEVERE PROSTHETIC DYSFUNCTION
- FISTULA INTO A CARDIAC CHAMBER / PERICARDIAL SPACE
TIMING OF SURGERY
URGENT SURGERY ( WITHIN DAYS )
1. NVE / PVE WITH PERSISTING CHF, SIGNS OF POOR HEMODYNAMIC
TOLERANCE OR ABSCESS
2. PVE BY STAPHYLOCOCCI OR GRAM – NEGATIVE ORGANISMS
3. LARGE VEGETATION ( 10 mm ) WITH AN EMBOLIC EVENT
4. LARGE VEGETATION WITH OTHER COMPLICATED COURSE
5. VERY LARGE VEGETATION (> 15 mm)
6. LARGE ABSCESS / PERIANNULAR INVOLVEMENT
TIMING OF SURGERY
ELECTIVE SURGERY ( DURING IN-HOSPITAL STAY )
1. SEVERE AR / MR WITH CHF – RESPONSIVE TO MEDICAL THERAPY
2. PVE WITH VALVAR DEHISCENCE / CHF – RESPONSIVE TO MEDICAL THERAPY
3. PRESENCE OF ABSCESS /PERIANULAR EXTENSION
4. FUNGAL / OTHER INFECTIONS RESISTANT TO MEDICAL CARE
ANTIBIOTIC PROPHYLAXIS RECOMMENDATIONS
S.NO : RECOMMENDATION : PROPHYLAXIS CLASS LEVEL
1. ONLY BE CONSIDERED FOR PATIENTS AT HIGH
RISK :
A) PATIENTS WITH A PROSTHETIC VALVE
B) PATIENTS WITH PREVIOUS IE
C) PATIENTS WITH CYANOTIC CONGENITAL
HEART DISEASE ( ONLY IN SOME CASES )
IIa C
2 NO LONGER RECOMMENDED IN OTHER FORMS
OF VALVULAR OR CONGENITAL HEART DISEASE
III C
PROCEDURAL ANTIBIOTIC PROPHYLAXIS
S.NO : RECOMMENDATIONS PROPHYLAXIS LEVEL CLASS
1. DENTAL PROCEDURES :
A) SHOULD ONLY BE CONSIDERED FOR
MANIPULATION OF THE GINGIVA
B) SHOULD NOT BE CONSIDERED FOR
LOCAL ANAESTHETIC INJ, REMOVAL OF SUTURES
IIa
III
C
C
2. RESPIRATORY TRACT PROCEDURES :
NOT RECOMMENDED
III C
3. GI OR UROGENITAL PROCEDURES :
NOT RECOMMENDED
III C
4. SKIN AND SOFT TISSUE :
NOT RECOMMENDED FOR ANY PROCEDURE
III C
RECOMMENDED PROPHYLAXIS FOR DENTAL PROCEDURES AT RISK
Single dose 30-60 min before procedure
SITUATION ANTIBIOTIC ADULTS CHILDREN
NO ALLERGY TO
PENICILLIN/
AMPICILLIN
AMOXYCILLIN/
AMPICILLIN
2 gm p.o/i.v 50 mg/kg p.o / i.v
ALLERGY TO
PENICILLIN /
AMPICILLIN
CLINDAMYCIN/
CEPHALEXIN
600 mg p.o / i.v
2 gm
20 mg /kg p.o / i.v
50 mg /kg
Infective endocardiitis

Infective endocardiitis

  • 1.
  • 2.
    DEFINITION • INVASION ANDMULTIPLICATION OF MICROORGANISMS ON THE ENDOCARDIAL SURFACE, - WITHIN THE ENDOCARDIUM , - WITHIN THE MYOCARDIUM, - OR ON PROSTHETIC MATERIALS WITHIN AND AROUND CARDIAC STRUCTURES.
  • 3.
    DEFINITION • CONDITIONS INWHICH STRUCTURES OF THE HEART ( FREQUENTLY VALVES) HARBOR AN INFECTIVE PROCESS; - THAT LEADS TO VALVAR DYSFUNCTION, - LOCALISED OR GENERALISED SEPSIS, - OR SITES FOR EMBOLISM
  • 4.
    THE TERM COVERS,,,, a) A/C TO DURATION - ACUTE, - SUBACUTE, - CHRONIC b) A/C TO INFECTING AGENT - BACTERIAL, - VIRAL, - RICKETTSIAL - FUNGAL c) A/C TO SITE OF INFECTION - NATIVE VALVE, - PROSTHETIC VALVE
  • 5.
    HISTORICAL NOTE • 1841- BOUILLAUD - THE TERM ENDOCARDITIS • 1885 - OSLER - CLASSICAL FEATURES • 1950 - PRINCIPLES OF AB THERAPY ESTABLISHED • 1961 - KAY & COLLEAGUES - FIRST SURGICAL Rx • 1970s - STINSON , RICHARDSON & COLLEAGUES MODERN CONCEPTS OF SURGICAL Rx
  • 6.
    PATHOGENESIS • MOST COMMONSITE IS : - ATRIAL SIDE OF AV VALVES - VENTRICULAR SIDE OF SEMILUNAR VALVES • INJURY MAY RESULT FROM : - PRE-EXISTING LESIONS ( RHEUMATIC VALVULITIS,VALVAR CALCIFICATION ) - CATHETER TRAUMA - HEMODYNAMIC FACTORS ( JET EFFECT OF BLOOD FLOW THRU : PDA, RESTRICTIVE VSD, MVP, BAV)
  • 7.
  • 8.
    RODBARD HYPOTHESIS ORIFICE LOWPRESSURE SINK HIGH PRESSURE SOURCE VENA CONTRACTA Rodbard S. Blood velocity and endocarditis. Circulation 1963,27:18.
  • 9.
    LOCI OF INFECTIVEENDOCARDITIS LESIONS CONDITION HIGH – PRESSURE SOURCE ORIFICE LOW – PRESSURE SINK LOCATION OF LESIONS AR AORTA CLOSED AORTIC CUSPS LV VENTRICULAR SURFACE OF AOV MR LV CLOSED MITRAL LEAFLETS LA ATRIAL SURFACE OF MV TR RV CLOSED TRICUSPID LEAFLETS RA ATRIAL SURFACE, TRICUSPID LEAFLETS VSD LV DEFECT RV RV SURFACE OF DEFECT PDA AORTA DUCTUS PULMONARY ARTERY PULMONARY ARTERY
  • 10.
    REPRESENTATION OF IEAT A PDA VEGETATIONS ARE DEPOSITED ON PA WALL OPPOSITE A HIGH- VELOCITY JET THRU AN OPEN DUCTUS
  • 11.
    MORPHOLOGY • VEGETATIONS, EROSIVECAVITIES – VENTRICULAR ASPECT OF AOV, ATRIAL ASPECT OF MV • OFTEN RESULT IN DISCONTINUITY AT THE VA OR AV JUNCTION • DISCRETE PERFORATIONS OF AOV • DROP LESIONS ON AML • PERIANNULAR PSEUODANEURYSMS / ABSCESS [ AOV > MV ]
  • 12.
    CLINICAL FEATURES • FEVER- 95 – 100% • HEART MURMUR (CHANGING) - 85%-95% • ANEMIA, HEMATURIA • MYALGIAS • ARTHRITIS/ARTHRALGIAS • EMBOLIZATION ( CENTRAL / PERIPHERAL ) • CLASSIC PERIPHERAL SIGNS OF ENDOCARDITIS • JANEWAY LESIONS – ALMOST ALWAYS BY STAPHYLOCOCCUS • IN PRACTICE, DIAGNOSIS BASED ON TWO SETS : 1. POSITIVE BLOOD CULTURES 2. CARDIAC LESION CSTD BY NEW STENOSIS/REGURG OR VEGETATION
  • 13.
    CLINICAL FEATURES • EMBOLICEVENTS = 24-67% • BRAIN = MOST COMMON SITE OF EMBOLI • NEUROLOGIC MANIFESTATIONS ARE PROTEAN ; • INCLUDES - STROKE ( ISCHEMIC / HAEMORRHAGIC ) - TIA - TOXIC ENCEPHALOPATHY - MENINGITIS - BRAIN ABSCESS - SEIZURES
  • 14.
    MODIFIED DUKE CRITERIA MAJORCRITERIA BLOOD CULTURES POSITIVE FOR IE 1. TYPICAL MICROORGANISMS 2. PERSISTENT MICROORGANISMS 3. SINGLE POSITIVE BLOOD CULTURE FOR C . burnetti EVIDENCE OF ENDOCARDIAL INVOLVEMENT 1. ECHO POSITIVE FOR IE ( VEGETATION, ABSCESS, NEW PARTIAL DEHISCENCE OF PROSTHETIC VALVE ) 2. NEW VALVULAR REGURGITATION MINOR CRITERIA 1. PREDISPOSITION 2. FEVER 3. IMMUNOLOGIC PHENOMENA 4. VASCULAR PHENOMENA 5. MICROBIOLOGIC EVIDENCE DEFINITE IE 2 MAJOR 1 MAJOR + 3 MINOR 5 MINOR POSSIBLE IE 1 MAJOR + 1 MINOR 3 MINOR
  • 15.
    VASCULAR PHENOMENA JANEWAY LESIONSCONJUCTIVAL HEMORRHAGES MYCOTIC ANEURYSMS
  • 16.
  • 17.
    DIFFERENCES B/N BACTERIALAND FUNGAL INFECTIVE ENDOCARDITIS PARAMETERS BACTERIAL FUNGAL ONSET ACUTE INSIDOUS CLINICAL COURSE FULMINANT PROTRACTED TISSUE DESTRUCTION MASSIVE MINIMAL VEGETATION SIZE USUALLY SMALL LARGE PERIANNULAR ABSCESS PRESENT ABSENT VASCULAR EMBOLI USUALLY INVOLVES SMALLER VESSELS USUALLY INVOLVES MAJOR VESSELS HEMATURIA COMMON NOT COMMON SKIN LESIONS COMMON NOT COMMON BLOOD CULTURES ARE USUALLY POSITIVE NEGATIVE BLOOD SAMPLES VENOUS SAMPLE CAN BE TAKEN ARTERIAL SAMPLE FOR LEFT SIDE LESION IS NECESSARY FOR CULTURE
  • 18.
    CULTURE NEGATIVE INFECTIVEENDOCARDITIS • ACCOUNTS FOR 5% OF ALL IE • CAUSES : 1. PRIOR ANTIBIOTIC THERAPY 2. FASTIDIOUS ORGANISMS ( GRAM NEGATIVE BACILLI, HACEK sps , BRUCELLA, FUNGI ) 3. INTRACELLULAR BACTERIA ( C. burnetti, Bartonella, Chlamydia, T. whipplei ) • DIAGNOSIS : – SEROLOGICAL TESTING – CELL CULTURE – GENE AMPLIFICATION
  • 19.
    NATURAL HISTORY • EPIDEMIOLOGY: THEN NOW YOUNGER POPULATION AFFECTS OLDER AGE GROUP OFTEN IN PREXISTING VALVAR DISEASE ( RHD ) EVEN IN NORMAL VALVES STREPTOCOCCI WAS THE LEADING CAUSE STAPHYLOCOCCI IS THE LEADING CAUSATIVE ORGANISM POOR DENTITION WAS ONE OF THE MAJOR CAUSE INVASIVE PROCEDURES ( HEMODIALYSIS , CATHETERS )
  • 20.
    NATURAL HISTORY -EPIDEMIOLOGY • PHV – STRONG RISK FACTOR • RISK FACTORS FOR PVE • CAUSATIVE FACTORS FOR PVE • PEDIATRIC POPULATION • ( PRE AND POST OP RISK FACTORS )
  • 21.
    NATURAL HISTORY 50% 30% 10% 5% 5% CAUSATIVE ORGANISMS Staphylococcusaureus Streptococcus Enterococcus Gram negative bacilli others ( fungi, viral, rickettsial )
  • 22.
    NATURAL HISTORY ACUTE BACTERIALENDOCARDITIS SUBACUTE BACTERIAL ENDOCARDITIS OFTEN BY S. aureus OFTEN BY S. viridans FULMINATING CLINICAL COURSE PROTRACTED CLINICAL COURSE ANTIBIOTICS ALONE SELDOM CURES ANTIBIOTICS ALONE OFTEN CURES JANEWAY LESION AND ROTH SPOTS ARE SEEN ONLY IN ACUTE FORM OSLER NODES, SPLINTER HEMORRHAGES, NEW MURMUR IS COMMON TO BOTH NO PREEXISTING VALVULAR DISEASE OFTEN ASSOC WITH PREEXISTING VALVULAR DISEASE
  • 23.
    NATURAL HISTORY -COMPLICATIONS A) CARDIAC 1. HEART FAILURE NVE – VALVAR REGURGITATION PVE – PERIANNULAR LEAKAGE AND ABSCESS 2. MYOCARDIAL ABSCESS 3. CONDUCTION ABNORMALITIES 4. MYOCARDIAL PERFORATION 5. PERICARDITIS
  • 24.
    B) RENAL COMPLICATIONS 1.PRERENAL FAILURE – LCOS 2. MICROABSCESS - SEPTIC EMBOLI 3. GLOMERULAR DYSFUNCTION – CIC’s 4. RENAL FAILURE - ANTIBIOTIC TOXICITY
  • 25.
    C) EMBOLIC EVENTS •INCIDENCE ( NVE > PVE ) • S. aureus, Candida, HACEK sps INCREASES THE RISK OF EMBOLISM • NEUROLOGIC MANIFESTATIONS ARE MOST COMMON • MOST DEVASTATING NEUROLOGIC COMPLICATION IS ICH
  • 26.
    SITE OF EMBOLISATION HabibG. Management of infective endocarditis. Heart 2006;92:124-30.
  • 27.
    RISK OF EMBOLICEVENTS A/C TO VEGETATION SIZE Vilacosta I, Graupner C, San Roman JA, Sarria C, Ronderos R, Fernandez C et al. Risk of embolization after institution of antibiotic therapy for infective endocarditis. J Am Coll Cardiol 2002; 39:1489.
  • 28.
    RECOMMENDED PLAN NVE PRIMARY ANTIBIOTIC THERAPY SURGERY ONLY FOR COMPLICATIONS EARLYPVE ANTIBIOTIC THERAPY AND SURGICAL TREATMENT IS ESSENTIAL LATE PVE ANTIBIOTIC THERAPY SURGICAL TREATMENT IF REQUIRED
  • 29.
    THERAPY - ANTIBIOTICS •BLOOD CULTURES SHOULD BE OBTAINED BEFORE INITIATING AB THERAPY • PROLONGED PARENTERAL AB ADMN IS ADVISABLE • AFTER INITIATING AB THERAPY – BLOOD CULTURES SHOULD BE DRAWN EVERY 1-2 DAYS UNTIL THEY BECOME NEGATIVE • AMINOGLYCOSIDES + CELL WALL ACTIVE AGENT = SYNERGY
  • 30.
    ANTIBIOTIC Rx FORSTREPTOCOCCI ( MIC < 0.125 mg/L ) ANTIBIOTIC DOSAGE AND ROUTE DURATION ( WEEKS) LEVEL OF EVIDENCE STANDARD TREATMENT PENICILLIN G Or CEFTRIAXONE 12-18 MU/day i.v 2 g/day i.v or i.m 24 h 4 4 I B I B TWO – WEEK TREATMENT PENICILLIN G OR CEFTRIAXONE With GENTAMICIN 12-18 MU/day i.v in 6 doses 2 g/day i.v or i.m in 1 dose 3 mg/kg/day i.v or i.m in 1 dose 2 2 2 I B I B I B IN BETA-LACTAM ALLERGIC PATIENTS VANCOMYCIN 15 mg/kg i.v q 12 h 4 I C
  • 31.
    ANTIBIOTIC Rx FORSTREPTOCOCCI (MIC < 0.125 – 2 mg/L ) ANTIBIOTIC DOSAGE AND ROUTE DURATION (WEEKS) LEVEL OF EVIDENCE STANDARD TREATMENT PENICILLIN G WITH GENTAMICIN 24 MU i.v per 24 h 3 mg/kg i.v / i.m q 24 h 4 2 I B I B IN BETA-LACTAM ALLERGIC PATIENTS VANCOMYCIN WITH GENTAMICIN 15 mg/kg i.v 12 h 3 mg/kg/day i.v or i.m q 24 h 4 2 I C
  • 32.
    ANTIBIOTIC Rx FORSTAPHYLOCOCCUS ANTIBIOTIC DOSAGE AND ROUTE DURATION ( WEEKS ) LEVEL OF EVIDENCE A) NATIVE VALVES METHICILLIN SUSCEPTIBLE OXACILLIN WITH GENTAMICIN 2 g i.v in 4 h 1 mg/kg i.v or i.m 8 h 6 3-5 days I B METHICILLIN RESISTANT VANCOMYCIN 15 mg/kg i.v in 12 h 6 I B
  • 33.
    ANTIBIOTIC Rx FORENTEROCOCCUS ANTIBIOTIC DOSAGE AND ROUTE DURATION (WEEKS) LEVEL OF EVIDENCE A ) IF SUSCEPTIBLE TO PENICILLIN AMPICILLIN PLUS GENTAMICIN (OR) 2 g IV q 4 h 1 mg/kg IV/IM q 8 h 4-6 4-6 I B PENICILLIN G PLUS GENTAMICIN 18-30 MU IV 24 h PLUS 1 mg/kg IV/IM q 8 h 4-6 B) IF RESISTANT TO PENICILLIN VANCOMYCIN PLUS GENTAMICIN 15 mg/kg IV Q 12 h 1 mg/kg IV / IM q 8 h 6 I B
  • 34.
    ANTIBIOTIC Rx FORSTAPHYLOCOCCUS ANTIBIOTIC DOSAGE AND ROUTE DURATION ( WEEKS ) LEVEL OF EVIDENCE A) PROSTHETIC VALVES OXACILLIN - SUSCEPTIBLE OXACILLIN WITH RIFAMPIN AND GENTAMICIN 2 g i.v I q 4 h 300 mg i.v or orally q 8 h 1 mg/kg i.v or i.m q 8 h > 6 6 2 I B OXACILLIN - RESISTANT VANCOMYCIN WITH RIFAMPIN AND GENTAMICIN 15 mg/kg i.v q 12 h 300 mg i.v or orally q 8 h 1 mg/kg i.v or i.m q 8 h > 6 > 6 2 I B
  • 35.
    ANTIBIOTIC Rx FORCULTURE NEGATIVE IE PATHOGENS PROPOSED THERAPY TREATMENT OUTCOME Brucella sps DOXYCYCLINE + COTRIMOXAZOLE + RIFAMPIN > 3 MONTHS ORALLY SUCCESS DEFINED AS ANTIBODY TITRE < 1:60 Coxiella burnetti (agent of Q fever) DOXYCYCLINE + OFLOXACIN ( > 18 MONTHS TREATMENT ) SUCCESS DEFINED AS ANTIBODY TITRE < 1:200 Bartonella spp DOXYCYCLINE ( 6 WEEKS ) SUCCESS EXPECTED IN > 90% Legionella spp RIFAMPIN OR CIPROFLOXACIN (6 WEEKS) OPTIMAL Rx UNKNOWN Mycoplasma spp NEWER FLUOROQUINOLONES OPTIMAL Rx UNKNOWN Tropheryma Whipplei DOXYCYCLINE + HYDROXYCHLOROQUINE ( > 18 MONTHS ) LONG TERM TREATMENT
  • 36.
    ECHOCARDIOGRAPHIC AND CLINICALFEATURES S/O NEED FOR SURGICAL INTERVENTION VEGETATION • PERSISTENT • > 10 mm • > 1 EMBOLIC EVENT DURING FIRST 2 WKS OF AB THERAPY • INCREASE IN SIZE AFTER 4 WKS OF AB THERAPY VALVAR DYSFUNCTION • ACUTE AR/MR WITH SIGNS OF VENTRICULAR DILATATION • HEART FAILURE UNRESPONSIVE TO MEDICAL THERAPY • VALVE PERFORATION /RUPTURE PERIVALVAR EXTENSION • VALVAR DEHISCENCE, RUPTURE, OR FISTULA • NEW HEART BLOCK • LARGE ABSCESS OR EXTENSION OF ABSCESS DESPITE AB THERAPY
  • 37.
    INDICATIONS FOR SURGERY 1.CHF 2. PERIANULAR EXTENSION 3. PERSISTENT SEPSIS 4. DIFFICULT ORGANISMS 5. PVE 1. SEVERE AR/MR 2. ELEVATED LVEDP / PAH 3. PROSTHETIC DEHISCENCE / OBSTRUCTION 1. SYSTEMIC EMBOLISM ( RECURRENT EMBOLI ; LARGE VEG > 10 mm; LARGE VEG WITH COMPL.COURSE; VERY LARGE VEG > 15 mm ) 2. CEREBROVASCULAR COMPLICATIONS ( TIA / ISCHEMIC STROKE ) 1.FEVER OR POSITIVE BLOOD CULTURE > 7 DAYS DESPITE AB REGIMEN 2. RELAPSING IE ( NON STREPTO ORGANISMS AND IN PTS PHV ) S. aureus MRSA, VRSA PSEUDOMONAS FUNGAL Q FEVER 1. EARLY PVE 2. PVE CAUSED BY S. aureus 3. LATE PVE WITH CHF, PERIANULAR EXTENSION, PERSISTENT BACTEREMIA
  • 38.
    SURGERY • GOALS : 1.REMOVE INFECTED TISSUE AND DRAIN ABSCESSES 2. RESTORE OR RECONSTRUCT AV OR VA CONTINUITY 3. REVERSE THE HEMODYNAMIC ABNORMALITY
  • 39.
    SURGICAL TREATMENT ACTIVE INFECTIVE ENDOCARDITIS ONLYCUSPS INVOLVED VALVE REPAIR/ REPLACEMENT CUSPS + ANNULUS INVOLVED RADICAL RESECTION + RECONSTRUCTION SMALL DEFECT (1-2 CM) FRESH AUTOLOGOUS PERICARDIUM LARGE DEFECTS GLUTARALDHELYDE FIXED BOVINE PERICARDIUM VALVE REPAIR/ REPLACEMENT
  • 40.
  • 41.
    SURGICAL TREATMENT VALVE REPAIR VALVE REPLACEMENT AORTICROOT ABSCESS ONLY AORTIC VALVE IS INVOLVED HOMOGRAFT IS IDEAL BIO / MECHANICAL PROSTHESIS
  • 42.
    REPAIR OF AMLPERFORATION ( DROP LESION) SMOOTH SURFACE SHOULD FACE THE ATRIUM
  • 43.
    REPAIR OF PMLVEGETATION P2 SEGMENT IS MOST COMMONLY INVOLVED
  • 44.
    REPAIR OF TVINFECTIVE ENDOCARDITIS NOTE : IN IV DRUG ABUSERS IF TRICUSPID VALVE REPAIR IS NOT POSSIBLE, THEN TRICUSPID VALVE RESECTION WITHOUT REPLACEMENT IS ALSO AN OPTION.
  • 45.
  • 46.
    POST OP CARE •TISSUE GRAM STAIN AND CULTURE ANALYSIS IS MANDATORY • USE OF PHENLYEPHRINE, VASOPRESSIN TO INC PERIPHERAL RESISTANCE IN SEPTIC PATIENTS • IV ANTIBIOTIC Rx FOR 4-6 WEEKS • CANDIDA :ORAL KETOCONAZOLE / FLUCONAZOLE FOR 3-6 MONTHS • ASPERGILLUS : ORAL VORICONAZOLE ( EVEN FOR LIFE LONG ) • MONITORING A) ANTIBIOTIC LEVELS B) RENAL FUNCTION C) CELL COUNTS
  • 47.
    RESULTS • EARLY DEATH •TIME-RELATED SURVIVAL • INCREMENTAL RISK FACTORS • IN-HOSPITAL MORBIDITY • RECURRENT INFECTION
  • 48.
    1. NVE –EARLY DEATH • FACTORS AFFECTING THE OUTCOME - STAGE OF ENDOCARDITIS ( ACTIVE / HEALED) - URGENCY OF THE SURGICAL INDICATION - MODALITY OF THE TREATMENT ( OPERATIVE V/S NON- OPERATIVE) - COMPLEXITY OF THE PROCEDURE ( DURATION OF THE ILLNESS AND INFECTING MICROORGANISM)
  • 49.
    1. EARLY DEATH- PVE • PVE – INCREMENTAL RISK FACTOR FOR OPERATIVE MORTALITY IN THE DOMAIN OF ALL IE. • FACTORS RESPONSIBLE FOR INCREASED MORTALITY - REOPERATION - PREVALENCE OF ABSCESS - ANNULAR EROSION - PERIANULAR ANEURYSM - FASTIDIOUS/FUNGAL ORGANISM
  • 50.
    2. TIME-RELATED SURVIVAL HaydockD, Barratt-Boyes B, Macedo T, Kirklin JW Blackstone E. Aortic valve replacement for active infectious endocarditis in 108 patients. Heart 2010;96:696-700.
  • 51.
    3. INCREMENTAL RISKFACTORS Moon MR, Miller DC, Moore KA,Oyer PE, Mitchell RS, Robbins RC, et al. Treatment of endocarditis with valve replacement : the question of tissue versus mechanical prosthesis. Ann Thorac Surg 2001;71:1164.
  • 52.
    4. IN-HOSPITAL MORBIDITY •CONTINUING EPISODES OF SEPSIS AFTER SURGERY • NEW CONDUCTION ABNORMALITIES • POST OP BLEEDING • NEW / DEEPENING NEUROLOGIC DEFICIT
  • 53.
    5. RECURRENT INFECTION •INCIDENCE INCREASES WITH : - NONSTREPTOCOCCAL ORGANISMS - ANNULAR DESTRUCTION - AORTIC VALVE IS INVOLVED - IV DRUG ABUSERS • AORTIC NVE / PVE / MITRAL NVE/ MITRAL PVE : ( ALLOGRAFTS > MECHANICAL = BIOPROSTHESIS )
  • 54.
    5. RECURRENT INFECTION HaydockD, Baratt-Boyes B, Macedo T, Kirklin JW, Blackstone E. Aortic valve replacement for active infectious endocarditis in 108 patients. J Thorac Cardiovasc Surg 1992;103:130.
  • 55.
    RECURRENT ENDOCARDITIS McGiffin DC,et al. Aortic Valve infection. Risk factors for death and recurrent endocarditis after aortic valve replacement. J Thorac Cardiovasc Surg 1992;104:511
  • 56.
    TIMING OF SURGERY EMERGENCYSURGERY ( WITHIN 24 HRS ) 1. NVE / PVE WITH SEVERE CHF / CARDIOGENIC SHOCK CAUSED BY - ACUTE VALVAR REGURGITATION - SEVERE PROSTHETIC DYSFUNCTION - FISTULA INTO A CARDIAC CHAMBER / PERICARDIAL SPACE
  • 57.
    TIMING OF SURGERY URGENTSURGERY ( WITHIN DAYS ) 1. NVE / PVE WITH PERSISTING CHF, SIGNS OF POOR HEMODYNAMIC TOLERANCE OR ABSCESS 2. PVE BY STAPHYLOCOCCI OR GRAM – NEGATIVE ORGANISMS 3. LARGE VEGETATION ( 10 mm ) WITH AN EMBOLIC EVENT 4. LARGE VEGETATION WITH OTHER COMPLICATED COURSE 5. VERY LARGE VEGETATION (> 15 mm) 6. LARGE ABSCESS / PERIANNULAR INVOLVEMENT
  • 58.
    TIMING OF SURGERY ELECTIVESURGERY ( DURING IN-HOSPITAL STAY ) 1. SEVERE AR / MR WITH CHF – RESPONSIVE TO MEDICAL THERAPY 2. PVE WITH VALVAR DEHISCENCE / CHF – RESPONSIVE TO MEDICAL THERAPY 3. PRESENCE OF ABSCESS /PERIANULAR EXTENSION 4. FUNGAL / OTHER INFECTIONS RESISTANT TO MEDICAL CARE
  • 59.
    ANTIBIOTIC PROPHYLAXIS RECOMMENDATIONS S.NO: RECOMMENDATION : PROPHYLAXIS CLASS LEVEL 1. ONLY BE CONSIDERED FOR PATIENTS AT HIGH RISK : A) PATIENTS WITH A PROSTHETIC VALVE B) PATIENTS WITH PREVIOUS IE C) PATIENTS WITH CYANOTIC CONGENITAL HEART DISEASE ( ONLY IN SOME CASES ) IIa C 2 NO LONGER RECOMMENDED IN OTHER FORMS OF VALVULAR OR CONGENITAL HEART DISEASE III C
  • 60.
    PROCEDURAL ANTIBIOTIC PROPHYLAXIS S.NO: RECOMMENDATIONS PROPHYLAXIS LEVEL CLASS 1. DENTAL PROCEDURES : A) SHOULD ONLY BE CONSIDERED FOR MANIPULATION OF THE GINGIVA B) SHOULD NOT BE CONSIDERED FOR LOCAL ANAESTHETIC INJ, REMOVAL OF SUTURES IIa III C C 2. RESPIRATORY TRACT PROCEDURES : NOT RECOMMENDED III C 3. GI OR UROGENITAL PROCEDURES : NOT RECOMMENDED III C 4. SKIN AND SOFT TISSUE : NOT RECOMMENDED FOR ANY PROCEDURE III C
  • 61.
    RECOMMENDED PROPHYLAXIS FORDENTAL PROCEDURES AT RISK Single dose 30-60 min before procedure SITUATION ANTIBIOTIC ADULTS CHILDREN NO ALLERGY TO PENICILLIN/ AMPICILLIN AMOXYCILLIN/ AMPICILLIN 2 gm p.o/i.v 50 mg/kg p.o / i.v ALLERGY TO PENICILLIN / AMPICILLIN CLINDAMYCIN/ CEPHALEXIN 600 mg p.o / i.v 2 gm 20 mg /kg p.o / i.v 50 mg /kg

Editor's Notes

  • #7 THE PREPONDERANCE OF THE BACTERIA BELOW THE SURFACE OF THE VEGETATION PROVIDES PROTECTION FROM PHAGOCYTES AND HIGH AB CONCENTRATION AND HENCE THE NEED FOR PROLONGED AB THERAPY.
  • #9 IT IS AT THE VENA CONTRACTA THAT BACTERIA AND OTHER FORMED ELEMENTS IN BLOOD ACCUMULATE. VENA CONTRACTA IS THE POINT AT WHICH THERE IS DIAMETER IS LEAST AND VELOCITY OF BLOOD IS HIGH.
  • #13 FEVER MAY BE LOW GRADE OR SPIKING, FOLLOWS PEAKS OF BACTEREMIA BY ABOUT 2 HRS, PTS AT RISK FOR IE WHO DEVELOP UNEXPLAINED FEVER FOR > 48 HRS SHOULD HAVE TWO OR MORE SETS OF BLOOD CULTURES DRAWN FROM DIFFERENT SITES. ADMN OF AB SHOULD BE DELAYED UNTIL BLOOD CULTURES HAVE BEEN OBTAINED. CHANGING MURMURS OCCUR LESS FREQUENTLY. SHORT DM IN INF INVOLVING AORTIC ROOT, MR MURMUR RADIATING POSTERIORLY DUE TO AML PERFORATION, DIASTOLIC MURMUR IN LARGE VEGETATIONS OBSTRUCTING MV CAUSING MS. ( OSLER NODES, JANEWAY LESIONS, ROTH SPOTS, PETECHIAE, CLUBBING ARE LATE MFSTS AND INFREQUENTLY SEEN TODAY ).
  • #15 TYPICAL MICROORGANISMS INCLUDES S. viridans, S. aureus, HACEK GROUP, COMMUNITY ACQUIRED ENTEROCOCCI IN THE ABSENCE OF A PRIMARY FOCUS FROM TWO SEPARATE BLOOD CULTURES, ATLEAST TWO PERSISTENT POSITIVE BLOOD CULTURES DRAWN 12 HRS APART, ALL THREE OR MAJORITY OF MORE THAN 4 POSTIVE FIRST AND LAST DRAWN MORE THAN 1 HR APART,
  • #20 THE PROFILE HAS CHANGED FROM RHD, POOR DENTITION TO OLD AGE AND INVASIVE MEDICAL PROCEDURES
  • #21 . RISK FACTORS FOR PVE ARE PTS OPERATED FOR NVE, MECHANICAL PROSTHESIS, BLACK RACE, MALE GENDER, LONGER CPB, REOPERATION. INTRAOPERATIVE SURFACE CONTAMINATION, INTRODUCTION OF CONTAMINATED BLOOD, BACTERIAL COLONISATION OF MEMBER OF SURGICAL TEAM, BACTERIAL AEROSOLISATION IN VENTILATORS, NASAL COLONIZATION OF THE PATIENT, PREEXISTING UROSEPSIS. VSD AND VALVAR AS AS PREOP RISK FACTOR IN PEDIATRIC POPULATION AND AORTIC VALVOTOMY, VALVE REPLACEMENT, RV-PA CONDUIT AS POST OP RISK FACTORS. MVP IN BOTH PEDIATRIC AND ADULT POPULATION
  • #22 Early PVE ( within 2 months) caused by Staph epidermidis. Late PVE has the same general spectrum of causative organism as NVE. CANDIDA IN NVE AND ASPERGILLUS IN PVE.
  • #24 CICs – Circulating Immune Complexes. ICH - Intra Cerebral Hemorrhage.MEDICAL Rx ALONE INCREASES THE RISK OF EMBOLISM. HOWEVER DELAYING SURGICAL REPAIR IN THE PRESENCE OF CNS COMPLICATIONS ARE ADVISABLE. MORBIDITY IS LESS WHEN REPAIR IS DONE IN THE PRESENCE OF CEREBRAL INFARCTION V/S CEREBRAL HEMORRHAGE.
  • #30 Total duration of antibiotic therapy is counted from the time of the first negative culture.
  • #32 IN PVE, THE DURATION IS FOR 6 WEEKS WITH SAME AB DOSE
  • #35 Rifampin is believed to play a special role in prosthetic device infection because it helps eradicate bacteria attached to foreign material. Rifampin should always be used in combination with another effective antistaphylococcal drug, to minimize the risk of resistant mutant selection.
  • #41 The two important aspects of surgical treatment are myocardial protection since pts are already in chf and avoidance of contamination of surgical field, instruments, drapes and gloves with vegetation, pus. Suction equipment, gloves and local drapes should be changed.
  • #46 NO EVIDENCE THAT BIO IS BETTER THAN MECHANICAL IN CASES OF ACTIVE IE
  • #49 THE MORE URGENT THE SURGICAL INDICATION AND THE MORE SEVERE THE HEART FAILURE, THE BETTER THE SURGICAL RESULTS COMPARED WITH MEDICAL THERAPY.
  • #51 LOWER SURVIVAL IN PTS WITH PVE THAN IN THOSE WITH NVE
  • #53 SPLENIC ABSCESSES, RENAL EMBOLI, CEREBRAL MYCOTIC ANEURYSMS; DUE TO RADICAL DEBRIDEMENT AROUND AORTIC ROOT, MV APPARATUS AND IVS; COMPLEX RECONSTRUCTIONS, RENAL DYSFN, PLATELET DYSFN; – CEREBRAL SEPTIC EMBOLI
  • #54 NO SUPERIORITY OF XENOGRAFTS OVER MECHANICAL IN AOV PVE, MV NVE, MV PVE
  • #60 Pts with cyanotic CHD without surgical repair, or with residual defects, shunts or conduits or chd with prosthetic material placed during complete repair upto 6 months of the procedure, or chd with residual defect persists at the site of implantation of the device or during procedure
  • #61 ALSO NOT RECOMMENDED FOR SHEDDING OF DECIDOUS TEETH, DENTAL X RAYS, PLACEMENT OF ADJUSTABLE ORTHODONTIC BRACES, TRAUMA TO LIPS/ORAL MUCOSA. NOT RECOMMENDED FOR ANY RESPIRATORY TRACT PROCEDURE LIKE LARYNGOSCOPY/BRONCHOSCOPY/TRANSNASAL OR ENDOTRACHEAL INTUBATION. GI OR UROLOGICAL PROCEDURES LIKE GASTROSCOPY/COLONOSCOPY/TEE, CYSTOSCOPY.