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INFECTIVE ENDOCARDITIS

By
Dr Bashir Ahmed Dar
Chinkipora Sopore
Kashmir
Associate Professor
Medicine
Email
drbashir123@gmail.com
 From Right to Left
 Dr.Smitha associate
prof gynae
 Dr Bashir associate
professor Medicine
 Dr Udaman
neurologist
 Dr Patnaik HOD
ortho
 Dr Tin swe aye paeds
 From RT to Lt
 Professor Dr Datuk
rajagopal N
 Dr Bashir associate
professor medicine
 Dr Urala HOD
gynae
 Dr Nagi reddy
tamma HOD-
opthomology
 Dr Setharamarao
Prof ortho
INFECTIVE ENDOCARDITIS
A microbial infection of the endothelial
lining of the heart; most commonly
occurring as a vegetation on the valve
leaflets
INFECTIVE ENDOCARDITIS
 Annual incidence: Age Distribution
15,000 to 20,000 60%
 Forth leading cause of 50%
40%
life-threatening 30%

infectious disease 20%


10%
0%
<30 31-60 >60
 Male:female ratio is Age

1.7:1 (median age 50)


INFECTIVE ENDOCARDITIS
100% fatal if undiagnosed and untreated
• 20% fatal even if diagnosed and treated
appropriately.

•70% streptococcal
• 20% staphylococcal
Predisposing factors

 Any type of structural heart disease


– Rheumatic heart disease (37-76%) like MS,AS,AI,MI,etc
– Congenital heart disease (6-24%) Like ASD,VSD,PDA,etc
– Degenerative cardiac lesions (30-40%)
– Other (including prosthetic valves)
Predisposing factors
Already damaged valves by
RHD
Predisposing factors
Already damaged damaged
heart
– Congenital heart
by CHD
disease (6-24%)
Predisposing factors
Prosthetic valves &
 High risk
pacemakers
– prosthetic cardiac valve
– prior episodes of
endocarditis
– surgically constructed
systemic-pulmonary
shunts or conduits
– Pacemakers &
pacemaker leads
Predisposing factors
Prosthetic valves &
pacemakers
PREDISPOSING FACTORS
IV drug abusers
PREDISPOSING FACTORS
Alcohol abuse & sepsis
PREDISPOSING FACTORS

Neutropenia
&
Immunosupression
PREDISPOSING FACTORS
 Staph aureus accounts for the majority of
cases of endocarditis in case of IV drug
abusers and is recurrent polymicrobial
 tricuspid valve, either alone or in
combination, is most often infected
PREDISPOSING FACTORS
 Moderate risk
– patent ductus arteriosus
– VSD, primum ASD
– coarctation of the aorta
– bicuspid aortic valve
– hypertrophic cardiomyopathy
– acquired valvular dysfunction
– MVP with mitral regurgitation
PREDISPOSING FACTORS
 Low risk
– isolated secundum atrial septal defect
– ASD, VSD, or PDA >6 months past repair
– “innocent” heart murmur “
PREDISPOSING FACTORS
INVASIVE PROCEDURES
– G.I.
 Barium enema
 Colonoscopy

– Genitourinary
 Prostatectomy
PREDISPOSING FACTORS
INVASIVE PROCEDURES
 Tooth extraction
 Periodontal surgery
 Teeth cleaning
 Tooth brushing, flossing
 Using wooden
toothpicks
 Chewing food
PREDISPOSING FACTORS
INVASIVE PROCEDURES
 Biopsies,suture
removal, placing
orthodontic bands
 Tonsillectomy,Adenoid
ectomy,Bronchoscopy.
 Resp tract procedure to
drain abscess or
empyema
PREDISPOSING FACTORS
INVASIVE PROCEDURES
 Central venous
catheterization
 Bladder catheterization,
Endoscopies, shaving,
 Skin or
musculoskeletal
infections
PREDISPOSING FACTORS

– AIDS patients
– Cancer patients
– Leukemia
– Lymphomas
MICROBIAL AGENTS
RESPONSIBLE FOR IE
 The commonest cause is  Then is enterococci
streptococci (alpha
hemolytic) and constitutes 10%
about 70%.among which  And other streptococci
 Streptococci viridans is 35%
that reside in oral cavity 10%
along with HACK associated
with dental procedures.
 Then is streptococcus bovis
that resides in oral &
colon.colonic cancers 15%
MICROBIAL AGENTS
RESPONSIBLE FOR IE
 Staphylococcus aureus:  Prosthetic valve
healthy or deformed valves, endocarditis also occurs
esp. in intravenous drug
abusers and prosthetic
by Candida and
valves. aspergillosis but form
 Prosthetic valve large vegetations.
endocarditis during the
perioperative period or
60 after operation also
by s.epidermitides.
MICROBIAL AGENTS
RESPONSIBLE FOR IE

 HACEK group consists of Haemophilus,


Actinobacillus, Cardiobacterium, Eikenella, &
Kingella (as I said are commensals of oral cavity)
MICROBIAL AGENTS
RESPONSIBLE FOR IE
 Enterococcus
 Normal inhabitants of the GI tract, occasionally anterior
urethra
 Mostly subacute and affect men (mean age 59) after
genitourinary manipulations or women (mean age 37) after
obstetrics procedures.
 E. faecalis 85% of enterococcal IE
MICROBIAL AGENTS
RESPONSIBLE FOR IE
 Others are
 Fungi (Candida,aspergillosis).
 Rickettsiae
 Chlamydia
 These infections occur in a particular
situation.
MICROBIAL AGENTS
RESPONSIBLE FOR IE
 Stillother organisms are
 Pseudomonas
 Brucella
 Diphtheroids
 Listeria
 Bartonella
 Coxsiella
 Chlamydia
PATHOGENESIS OF
INFECTIVE ENDOCARDITIS
 Previously damaged endocardial surface of valve for
example by rheumatic heart disease forms rough surface
over the damaged valve.
 Due to this rough surface palatelets stick and adhere to
this area forming small small thrombi over the cusp of
valves.fibrin also deposits on this area, the lesions now
called as Nonbacterial Thrombotic Endocarditis (NBTE).
PATHOGENESIS OF
INFECTIVE ENDOCARDITIS
 This deposition of sterile vegetations in the form
of thrombi on the leaflets of cardiac valves, is also
called MARANTIC ENDOCARDITIS
NONBACTERIAL
THROMBOTIC
ENDOCARDITIS (NBTE)
 These vegetations are sterile, nondestructive,
noninflammatory & small (1-5mm),made of
platelets,fibrin & other blood elements and
may occur singly or multiply along the lines
of closure of heart valves
NONBACTERIAL
THROMBOTIC
ENDOCARDITIS (NBTE)
 Probably occurs as a consequence of a
hypercoagulable state
 Seem with concomitant venous thrombosis
&/or pulmonary embolism
 May be seen with hyperestrogenic state,
extensive burns, or endocardial trauma from
indwelling catheters
NONBACTERIAL
THROMBOTIC
ENDOCARDITIS (NBTE)
 Importance
 Localeffect on valve unimportant
 May produce emboli with resultant infarcts
 May eventually heal with fibrosis.
PATHOGENESIS OF
INFECTIVE ENDOCARDITIS
 Bacteria reach this thrombotic vegetation site
and produce colonization and deposit deep
within this thrombi and remain hidden and
protected and then multiply easily there.
 The surface may further covered by platelets
and fibrin.
Infectious Endocarditis
Vegetation

Stick in Perforation

Mitral Valve

Infective endocarditis with perforation of mitral valve leaflet


PATHOGENESIS OF
INFECTIVE ENDOCARDITIS
 The reason why bacteria lodge there is because of
Venturi effect as the blood carrying bacteria flows
with high jet and force from high pressure to low
pressure chamber below.
 Since the valve is deformed and stenosed so
bubbles of blood are sprinkled that fall over the
atrial surface of valve along free margins and
deposit within thrombi.
Venturi Effect
PATHOGENESIS OF
INFECTIVE ENDOCARDITIS
 In systemic lupus erythematosus the
vegetations may form on the undersurface
of valve towards ventricular side called as
libman sacks syndrome.
PATHOGENESIS OF
INFECTIVE ENDOCARDITIS
 Theadherence of the organism to NBTE is a
crucial step.
1. FimA is a surface adhesin of S.viridans that serves as
an important colonization factor. Homologues of fimA
genes were found in many S.viridans strains and
enterococci.
2. Fibronectin is implicated as the host receptor within
NBTE.
PATHOGENESIS OF
INFECTIVE ENDOCARDITIS
Adherence of some streptococci to blood clot
is facilitated by dextran (a cell wall
component) (especially of Streptococcus
mutans, a viridans group.

Further Some strains of bacteria are


stimulators of platelet aggregation
PATHOGENESIS OF
INFECTIVE ENDOCARDITIS
 Once these thrombotic vegetations are laden with
microbial organisms they become large even upto
3cms,friable and easily detachable in contrast to
vegetations of RHD that are not easily detachable.
 The colour of vegetations is tan grey red or brown
and situated along the line of closure of valve.
PATHOGENESIS OF
INFECTIVE ENDOCARDITIS
Microscopic Pathology

Fibrin, platelets, masses of organisms,


+/- necrosis, +/- neutrophils

Later: +/-lymphocytes, +/- macrophages,


+/- fibroblasts, +/- fibrosis
LOCAL EFFECTS OF
INFECTIVE ENDOCARDITIS
 Firstthe leukocytes are unable to penetrate
the vegetations as additional layers of fibrin
are added. Treatment with antibiotics can
also be problematic because the bacteria
within the vegetation often become less
metabolically active, and many antibiotics
require active bacterial growth to be
effective.
LOCAL EFFECTS OF
INFECTIVE ENDOCARDITIS
 Infection may extends beyond valve cusp
may erode & perforate valve, & may erode
into underlying myocardium to produce an
abscess (ring abscess) or Paravalvular
abscess
 Septal abscesses & adjacent abscess
 Fistulae
 Prosthetic dehiscence
LOCAL EFFECTS OF
INFECTIVE ENDOCARDITIS
 Valvular distortion/destruction chordal rupture.
 Conduction abnormalities
 Purulent pericarditis
 Functional valve obstruction
 With treatment, healing occurs by fibrosis and
occasionally calcification.
DISTANT EFFECTS OF
INFECTIVE ENDOCARDITIS
 Vegetations may become detached and
produce embolic effects.
 Embolic phenomena are common (15-
35%). septic infarcts involving: renal,
splenic, coronary, or cerebral circulation.
 Risk for emboli is increased when
vegetation >1cm.
IMMUNOLOGICAL EFFECTS OF IE

 IE cause both humural and cellular response


 Rheumatoid factor:
– titers correlate with the level of hypergammaglobulinemia and decrease with
therapy
 Antinuclear antibodies:
– may contribute to the musculoskeletal manifestations, low-grade fever, or
pleuritic pain
 Circulating immune complexes:
– Connected with long duration of illness, extravascular manifestations,
hypocomplemenemia
– May cause diffuse glomerulonephritis, and some of the peripheral
manifestations such as Osler nodes
EFFECTS OF IE ON KIDENY
 Pathologicalprocesses: abscess, infarction,
glomerulonephritis (focal, segmental),
membranoproliferative GN
 May be normal is size or slightly swollen
 10 to 15% of IE exhibit immune complex GN (as in
SLE). Supporting IC rather than emboli:
1. Bacteria rarely seen in lesion
2. GN can occur with right-sided IE
3. GN is rare in acute IE even though large vegetation result in
metastatic abscess formation
4. IF staining reveals IC-typical distribution
5. Antibacterial antibodies eluted from lesions
OTHER EFFECTS OF IE
1.Mycotic aneurysm is a
localized, irreversible
arterial dilatation due
to destruction of the
vessel wall by
infection
 More common with
S.viridans
OTHER EFFECTS OF IE
 May arise by the following
mechanisms:
– direct bacterial invasion of the
arterial wall with subsequent
abscess formation or rupture
– septic or bland emoblic
occlusion of the vasa vasorum
– immune complex deposition
with resultant injury to arterial
wall
OTHER EFFECTS OF IE
 Tend to occur at
bifurcation areas;
middle cerebral artery is
most common,Clinically
silent until rupture
EFFECTS ON
CNS,SPLEEN,LUNG
 CNS
– cerebral emboli (>30% of IE)
– Mycotic aneurysms
 Spleen
– infarctions (44% of autopsy cases)
– enlargement associated with hyperplasia of lymphoid follicles,
increase in secondary follicles, focal necrosis,abscess
 Lung
– associated with right-sided IE
– pulmonary embolism, acute pneumonia, pleural effusion, or
empyema
EFFECTS ON
CNS,SPLEEN,LUNG
 CNS
– cerebral emboli (>30% of
IE)
– Mycotic aneurysms
EFFECTS ON
CNS,SPLEEN,LUNG
 Spleen
– infarctions (44% of autopsy
cases)
– enlargement associated with
hyperplasia of lymphoid
follicles, increase in
secondary follicles, focal
necrosis,abscess
EFFECTS ON
CNS,SPLEEN,LUNG
 Lung
– associated with right-sided
IE
– pulmonary embolism, acute
pneumonia, pleural
effusion, or empyema
EFFECTS ON SKIN&EYE
– Petechiae, may result
from local vasculitis or
emboli
– Petechiae are red
because they contain
red blood that has
leaked from the
capillaries
EFFECTS ON SKIN&EYE
 Osler nodes, painful
nodes on finger or toe
pads
 Due to immune
complexes in dermal
vessels
EFFECTS ON SKIN&EYE
 Osler’s Nodes:
1. red, raised lesions
 Tender, subcutaneous
nodules.4 P’s:
 Pink
 Painful
 Pea-sized
 Pulp of the fingers/toes.
– Immunological origin?
EFFECTS ON SKIN&EYE
 Janeway lesions (due
to septic emboli),
painless plaques on
palms or soles.
 non-tender, small
erythematous or
hemorrhagic macular
or nodular lesions on
the palms or soles only
a few millimeters.
EFFECTS ON SKIN&EYE
 Pathologically, the
Janeway lesion is
described to be a
microabscess of the
dermis with marked
necrosis and inflammatory
infiltrate not involving the
epidermis, which is due to
the deposition of
circulating immune
complexes in small blood
vessels.
Janeway Lesions
EFFECTS ON SKIN&EYE
 Splinter hemorrhage
(linear lines beneath
fingernails)
EFFECTS ON SKIN&EYE
 Eye
– Roth spots
– Roth's spots are retinal
hemorrhages with white or
pale centers composed of
coagulated fibrin. They are
typically observed via
fundoscopy (using an
ophthalmoscope to view
inside the eye) or slit lamp
exam
EFFECTS ON SKIN&EYE
 Eye
– Roth spots
– They are usually caused by
immune complex mediated
vasculitis often resulting
from bacterial endocarditis.
Roth's spots may be
observed in leukemia,
diabetes, subacute bacterial
endocarditis, pernicious
anemia, ischemic events,
and rarely in HIV
retinopathy.
EFFECTS ON SKIN&EYE
 Infective endocarditis
also can give rise to
conjunctival
haemorrhages
EFFECTS ON SKIN&EYE
 Clubbing is also
known to occur in
infective endocarditis.
Summary of Infective
Endocarditis

Endothelial damage

Platelet-fibrin thrombi

Microorganism adherence
Summary of
Pathogenesis BE
 Turbulent blood flow (from congenital or
acquired heart dz)Endothelial trauma
 Platelets and fibrin deposit on damaged
endothelium  Nonbacterial Thrombotic
Endocarditis (NBTE)
 Bacteremia Colonization of NBTE 
Bacterial Vegetation
THINGS TO REMEMBER IN
INFECTIVE ENDOCARDITIS
 Infective endocarditis affects

Left-sided valves 75%


Right-sided valves 15%
Both 5%
Other 5%
THINGS TO REMEMBER IN
INFECTIVE ENDOCARDITIS
Mitral valve alone 35%
Aortic valve alone 20%
Mitral plus aortic 20%
Tricuspid 14%
Pulmonic 1%
With changing murmurs in character
pitch duration etc.fungal vegetations
are large vegetations.
THINGS TO REMEMBER IN
INFECTIVE ENDOCARDITIS
 Infectiveendocarditis may be culture
negative either due to prior antibiotic
treatment or due to atypical microbial
organisms or due to fungus etc.then called
as non bacterial endocarditis.
CLASSIFICATION OF
BACTERIAL ENDOCARDITIS
1. Acute Bacterial Endocarditis (“ABE”)
usually fulminant, due to highly virulent
organisms (e.g. Staphylococcus aureus)

versus

Subacute Bacterial Endocarditis (“SBE”)


with insidious onset over weeks, due to less
virulent organisms (e.g. viridans streptococci)
CLASSIFICATION OF
BACTERIAL ENDOCARDITIS
 Acute: Rapid progression of symptoms
– Less than 6 weeks duration
– Significant systemic signs/symptoms
 Fever
 Elevated systemic WBC/ left shift
 Subacute: Slower, more chronic progression of
symptoms
– Low grade fevers
– Vague clinical signs/symptoms
 weakness, anorexia, malaise,etc.
CLASSIFICATION OF
BACTERIAL ENDOCARDITIS
 Acute
– Toxic presentation
– Progressive valve destruction & metastatic infection
developing in days to weeks
– Most commonly caused by S. aureus
 Subacute
– Mild toxicity
– Presentation over weeks to months
– Rarely leads to metastatic infection
– Most commonly S. viridans or enterococcus
CLINICAL FEATURES OF
ENDOCARDITIS
Common Symptoms
Fever 80%
Chills 40%
Weakness 40%
Dyspnea 40%
CLINICAL FEATURES OF
ENDOCARDITIS
Uncommon Symptoms

Cough 25%
Sweats 25%
Anorexia 25%
Weight loss 25%
Malaise 25%
Skin lesions 20%
Nausea/vomiting 20%
Stroke 20%
CLINICAL FEATURES OF
ENDOCARDITIS
More Uncommon Symptoms

Headache 15%
Myalgia/arthralgia 15%
Edema 15%
Chest pain 15%
Abdominal pain15%
Delirium/coma 15%
Back pain 10%
Hemoptysis 10%
CLINICAL FEATURES OF
ENDOCARDITIS
Common Physical Signs

Fever 90%
Heart murmur 85%
Splenomegaly 30%
Petechiae 30%
CLINICAL FEATURES OF
ENDOCARDITIS
Uncommon Physical Signs

Osler nodes 15%


(pea-sized tender finger/toe nodules)
Subungual splinter hemorrhages 15%
Changing heart murmur 10%
CLINICAL FEATURES OF
ENDOCARDITIS
More Uncommon Physical Signs

Janeway lesions 5%
(small palm/sole hemorrhages)

New heart murmur 5%

Roth spots (on retina) 2%


(white dots with surrounding hemorrhage)
LABORATORY FINDINGS
Laboratory Findings

Elevated ESR (mean 57 mm/hr) 95%


(erythrocyte sedimentation rate)

Circulating immune complexes 90%

Anemia 80%

Proteinuria 60%
LABORATORY FINDINGS
Laboratory Findings

Rheumatoid factor 50%


(anti-IgG antibodies)
Hematuria 40%
Leukocytosis 25%
Hypergammaglobulinemia 25%
Elevated creatinine 10%
Leukopenia 10%
Thrombocytopenia 10%
LABORATORY FINDINGS
 ECG should be done in all pts with suspected IE
– Nonspecific usually
– Conduction abnormalities ( new LBBB, Prolonged PR
interval, new RBBB, complete heart block)
– Junctional tachycardia
 Chest Xray
– Pulmonic emboli or CHF
LABORATORY FINDINGS
 Blood cultures critical for specific diagnosis
3 sites 30-60 minutes apart
before starting antibiotics.
86 – 96% of 1st cultures positive
98 – 100% of 1st 2 cultures positive
Blood cultures may be negative if the patient
has already received antibiotics; a few cases
of infective endocarditis are “culture-negative”
LABORATORY FINDINGS
 All patients with suspected bacteremia
should have blood cultures drawn in the ED
prior to abx
 Blood cultures should be drawn in 3
different sites
 Minimum of 10 ml blood in each bottle
 Minimum of one hour between first and last
bottle
LABORATORY FINDINGS
 Negative culture can occur in 5% of
patients.
 1/3 to ½ are negative due to prior antibiotic
use
 In patients with culture negative IE, advise
lab to allow specialized testing to recover
the causative organism which is needed to
adequately treat
LABORATORY FINDINGS
Transthoracic (TTE)echocardiography
60% sensitivity for vegetations

Transesophageal(TEE) echocardiography
>90% sensitivity for vegetations

The absence of vegetations on echocardiogram


does not exclude the diagnosis of endocarditis
Duke’s Criteria For Diagnosis
of Infective Endocarditis
Duke Criteria – Simplified

 Requires 2 major,
 or 1 major + 3 minor
 or 5 minor criteria
Duke’s Major Criteria
Major Criteria
 1. Positive blood culture
– typical microorganism (strep viridans, strep bovis,
HACEK group, staph aureus or enterococci in the
absence of a primary locus) for endocarditis from two
separate blood cultures
– persistently positive blood culture from:
 blood cultures drawn more than 12 hr apart, or
 all of 3 or a majority of 4 or more separate blood cultures, with
first and last drqwn at least 1 hr apart
Duke’s Major Criteria

 2.Positive Echocardiogram showing


 Vegetation
 Abscess,
 Detached prosthesis
 Regurgitation
Duke’s Minor Criteria
Minor Criteria
 Predisposition (predisposing heart condition or iv
drug use)
 Fever of 100.40F or higher
 Vascular phenomena (major arterial emboli, septic
pulmonary infarcts, mycotic aneurysm,
intracranial hemorrhage, conjunctive
hemorrhages, Janeway lesions).
Duke’s Minor Criteria
 Immunologic phenomena (glomerulonephritis,
Osler’s nodes, Roth spots, rheumatoid factor)
 Microbiologic evidence (positive blood culture not
meeting major criteria or serologic evidence of
active infection with organism consistent with IE)
 Echocardiogram (consistent with IE but not
meeting major criteria)
COMPLICATIONS OF
INFECTIVE ENDOCARDITIS
Heart failure 67%

Septic emboli 55%


to kidneys 55%
to heart 50%
to spleen 44%
to brain 33%
COMPLICATIONS OF
INFECTIVE ENDOCARDITIS
Uncommon Complications

Myocardial abscess20%
Glomerulonephritis15%
(immune complexes)
“Mycotic aneurysm” 10%
Pericarditis (S.aureus) rare
INDICATIONS FOR
PROPHYLAXIS
Prophylaxis is indicated for
 Prosthetic heart valves
 Congenital heart disease with manifestations
 Acquired heart disease with manifestations
 Hypertrophic cardiomyopathy
 Mitral valve prolapse with regurgitation
 Previous history of endocarditis
 Dental procedures known to produce bleeding
 Surgery involving GI, respiratory mucosa
INDICATIONS FOR
PROPHYLAXIS
 Tonsillectomy
 Esophageal dilation
 ERCP for obstruction
 Gallbladder surgery
 Cystoscopy, urethral dilation
 Urethral catheter if infection present
 Urinary tract surgery
 Tonsillectomy
 Rigid bronchoscopy.
INDICATIONS FOR
PROPHYLAXIS
 Esophageal sclerotherapy or stricture dilation
 Respiratory: Consider if pt will be cut or biopsied
 Periodontal procedures (surgery, scaling, and root
planing, probing, and recall maintenance)
 Implant placement and reimplantation of avulsed
teeth
 Endodontic instrumentation beyond the apex
 Subgingival placement of antibiotic fibers or strips
 Placement of orthodontic bands but not brackets.
INDICATIONS FOR
PROPHYLAXIS
 ERCP
 Billiary surgery
 Prostate surgery
 Cystoscopy
 Cardiac transplants
 Extractions of teeth
 Intraligamentary injections
 Prophylactic cleaning of teeth or implants where
bleeding is anticipated
No Prophylaxis
 Vaginal delivery  Radiographs
 Hysterectomy  Orthodontic adjustments
 Shedding of primary teeth
 Local anesthetic injections
 IUDs
 Placement of oral rubber  Circumcision
dams  MVP without regurgitation
 Post-op suture removal  Pacemakers but see if not
 Placement of removable already infected
appliances  Physiologic murmurs
 Fluoride treatment
Indications for Surgery
 (When removal of an infected valve is necessary).
 Refractory CHF
 Severe valvular dysfunction
 Uncontrolled infection
 Valve perforation
 Dehiscence
 Fistula
 Abscess
Indications for Surgery
 Embolic event with persistent large vegetation
 or >1 episode of embolization
 Prosthetic valve infection
 Fungal IE
 New heart block
 Refractory CHF
 Uncontrolled infection
 Ineffective antimicrobial therapy
Indications for Surgery
 Resection of mycotic  Large (>1cm diameter)
aneurysms
anterior mitral valve
 antibiotic-resistant pathogens)
vegetation
 Local suppurative
complications including  Acute mitral insufficiency
perivalvular or myocardial
abscesses
 Valve perforation or
 Persistent vegetations after a rupture
major systemic embolic  Increase in vegetation size
episode 4 weeks after antibiotic
therapy
Indications for Surgery
 Periannular extension of  Unresponsive
infection infection/ continued
 Infected prosthetic infection despite
material: less than 1 year appropriate antibiotics
out from original heart
surgery
 Refractory congestive
heart failure (Leading
cause of death)
Indications for Surgery
 Pt. experiences more than  Persistent bacteremia
1 major emboli  Acute AR or MR with
 Severe valvular heart failure.
dysfunction: Acute CHF
or impaired hemodynamic
 Acute AR with
status tachycardia and early
 Relapsing prosthetic valve closure of the MV.
endocarditis  Annular or aortic abscess.
 Fungal endocarditis  Sinus or aortic aneurysm.
 New conduction defects or  Persistent bacteremia and
arrhythmias valve dysfunction
Indications for Surgery
 Recurrent emboli after  Increase in vegetation
appropriate Abx. size after antimicrobial
 Mobile vegetations therapy
>10 mm.  Valvular dysfunction
 Persistent pyrexia and  Fungal endocarditis
leucocytosis with
negative blood
cultures.
TREATMENT OF INFECTIVE
ENDOCARDITIS
 Purpose of Prophylaxis
 To give antibiotics and kill blood-borne bacteria
or interfere with their metabolism, hindering their
ability to adhere to a damaged heart valve.
 However antibiotic resistance is increasing. Only
administered prior to “high risk” surgeries Include
dental procedures, surgery on the gastrointestinal
or urinary tract, surgery on infected tissues
TREATMENT OF INFECTIVE
ENDOCARDITIS
 50% of some valvular infections do not respond
to antimicrobial therapy or surgery
 Today’s highly virulent causative agents have
led to an increase in dangerous complications

 Don’t need to memorize individual procedures


PROPHYLACTIC
TREATMENT
 Standard Prophylactic Regimen
 Single dose, 30-60 min prior to any
procedure
 Amoxycillin 2.0 grams orally or iv
Ampicillin 2gm IV/IM or Ceftriaxone 1g
IV/IM
 IV, PCN-allergic Ceftriaxone 1g IV/IM
PROPHYLACTIC
TREATMENT
 Prophylaxis for Patients Already Taking
Amoxycillin or have allergy to pencillin or
microbial may have developed resistance to
Amoxycillin options then are
 Ceftriaxone 1g IV/IM before and after procedure
 Clindamycin 600mg PO or Clarithromycin 500 mg
or Azithromycin 500mg PO
 Quinolones or IV Vancomycin not recommended
for prophylaxis due to concern of creating new
drug resistance
SUMMARY PROPHYLACTIC
TREATMENT
 Summary of Standard Regimen
 Ampicillin 1g IM/IV
 Gentamicin 1 to 1.5 mg/kg IV/IM (MAX
120 mg)
 Ceftriaxone 1gm IV
 Vancomycin 1g IV over 1-2h
TREATMENT OF IE
GENERAL COMMENTS
 IE treatment should be considered in
 All febrile IDUs
 Pts with a cardiac prosthesis and fever
 Pts with new murmur or change in murmur with
evidence of vasculitis or embolization
 Any cardiac risk factor with unexplained fever
 Any patient with a prolonged fever (>2 weeks)
TREATMENT OF IE
GENERAL COMMENTS
 Most patients will require 4 to 6 weeks of
antibiotic therapy.
 Antifungals alone are not enough to cure fungal
IE, although Amphotericin B is often administered
in conjunction with surgery.
 Culture-negative native-valve endocarditis should
be individualized and generally includes
ampicillin, Ceftriaxone, or Vancomycin, +/-
Aminoglycoside
TREATMENT OF IE
GENERAL COMMENTS
 Complete eradication takes weeks, relapses may
occur. This is due to:
 1. The infection exists in an area of impaired host
defense and is tightly encased in a fibrin
meshwork
 2. The bacteria reach very high population
densities, such that the organism may exist in a
state of reduced metabolic activity and cell
division
TREATMENT OF IE
GENERAL COMMENTS
 Etiologic agent must be isolated in pure culture.
MIC and MBC should be determined.
 All patients with suspected bacteremia should
have blood cultures drawn in the ED prior to abx
 Blood cultures should be drawn in 3 different sites
 Minimum of 10 ml blood in each bottle
 Minimum of one hour between first and last bottle
 Aspirin may decrease the growth of vegetative
lesions and prevent cerebral emboli
TREATMENT OF IE
GENERAL COMMENTS
 Parenteral antibiotics are  Blood cultures should be
recommended over oral obtained during the early
drugs phase of therapy to ensure
 Antibiotic combinations eradication
should produce a rapid  Use of anticoagulants
effect during therapy for native
 Selection of antibiotics valve IE is not
should be based on recommended. With
susceptibility tests, and mechanical valves,
treatment should be anticoagulation should be
monitored with clinical maintained (if indicated)
improvement. within therapeutic range
TREATMENT OF IE
GENERAL COMMENTS
 Effective antimicrobial  OOPS! You didn’t
treatment should lead to premedicate patient and
defervescence within 7 – you encounter unexpected
10 days bleeding!Don’t Panic
 Persistent fever in IE may  Stop procedure,
be due to staph, administer antibiotics, and
pseudomonas, culture resume working
negative IE or with  Antibiotics administered
microvascular up to 2 hours following a
complications/major procedure may still
emboli or due to drug protective
reaction.
TREATMENT OF IE
GENERAL COMMENTS
 Anticoagulation for  Pts with prosthetic
native valve valves who are treated
endocarditis has not with anticoagulation
been shown to be can be maintained on
beneficial because of their regimen with
Increase of risk of proper caution for
intracranial CNS complications
hemorrhage
TREATMENT OF IE
GENERAL COMMENTS
 “Ifanticoagulation is indicated for
 Another reason it should be continued.
 Anticoagulation does not prevent
TREATMENT OF IE
 Highly penicillin-susceptible Streptococcus
viridans or bovis
 Once-daily ceftriaxone for 4 wks
 cure rate > 98%
 Or Once-daily ceftriaxone 2 g for 2wks
followed by oral Amoxycillin qid for 2 wks
TREATMENT OF IE
 Iforganisms are resistant to this then give
 Vancomycin, 15mg/kg IV 12 hourly daily,
plus Gentamicin 1 to 1.5 mg/kg 8 hourly,
both 4 to 6 weeks.
TREATMENT OF IE
 Ampicillin 2gm 4 hourly plus Gentamicin
60-80mg 8 hourly
 HACEK organisms (IE) Ceftriaxone
monotherapy (1 to 2gm IV/BD daily) or
Ampicillin Plus Gentamicin x 4 to 6 weeks.
TREATMENT OF IE
 Staph IE with Prosthetic Material
 Triple drug regimens
 Methicillin-sensitive staph spp.
 Nafcillin/Oxacillin Plus Rifampin (6 weeks)
 Methicillin-resistant staph spp Vancomycin
Plus Rifampin 300mg PO 8hrly (6 to 8
weeks) Plus Ampicillin &Gentamicin (2
weeks).
TREATMENT OF IE
 Or Ceftriaxone (2 g/d IV as a single dose
for 4 weeks) plus Rifampicin (300 mg PO
q8h for 6-8 weeks).
THANK YOU
HELP THOSE IN
SUFFERING