Infective endocarditis is a microbial infection of the heart valves or intracardiac devices. It is classified as either acute or subacute based on clinical presentation. Acute IE is caused by pyogenic bacteria and results in sepsis, while subacute IE is usually caused by Streptococcus viridans. Diagnosis relies on the modified Duke criteria and blood cultures, while echocardiography can identify valvular vegetations. Common manifestations include fever, heart murmurs, embolic phenomena, and immunological findings such as Roth spots.

1. INFECTIVE ENDOCARDITIS
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1

2. Definition
 Infective endocarditis (IE) is a microbial
infection of the endothelial surface of the heart or
iatrogenic foreign bodies like prosthetic valves or
other intracardiac devices
 Infective Endarteritis – AV shunts,
Arterioarterial shunts, Coarctation of aorta
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3. Traditionally, IE has been classified on
clinical grounds into acute and subacute forms.
1. Acute IE
2. Subacute IE
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4. 1.Acute IE :The strong pathogenic pyogenic bacteria
（carbuncle, puerperal fever, osteomyelitis ）
> Immune resistance down > bacteria get into the
blood>sepsis > invasion of normal endocardium
>invasion of mitral valve, aortic valve>acute septic
endocarditis>bacterial vegetations
2.Subacute IE: Streptococcus viridans (localized
infection focus in vivo or iatrogenic infection)>
bacteria into the blood >the mitral valve or/and aortic
valve with original lesions (80%, congenital heart
disease, RHD or valve repair) >Subacute IE
>bacterial vegetations 6/25/2023
4

5. The prototypic lesion
The vegetation
 Variable in size
 Amorphous mass of fibrin & platelets
 Abundant organisms
 Few inflammatory cells
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6. In the aortic opening a larger, irregular red vegetations, this mostly by Staphylococcus
aureus infection. 6/25/2023
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7. Pathogenesis
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8. Infective Endocarditis
 Nonbacterial Thrombotic Endocarditis
• Endothelial injury
• Hypercoagulable state
 Lesions seen at coaptation points of valves
 Atrial surface mitral/tricuspid
 Ventricular surface aortic/pulmonic
 Modes of endothelial injury
 High velocity jet
 Flow from high pressure to low pressure chamber
 Flow across narrow orifice of high velocity
Platelet-fibrin thrombi
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9. Conversion of NBTE to BE
 Transient bacteremia
 Traumatization of mucosal surface colonized with bacteria
(oral, GI)
 Low grade, cleared in 15-30 minutes
 Susceptibility to complement-mediated bacterial killing
 Leads to concept of prophylaxis
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10. Infective Endocarditis
• Pathology
– Native Valve Endocarditis infection is largely confined to
leaflets
– Prosthetic Valve Endocarditis infection commonly extends
beyond valve ring into annulus/periannular tissue
• Ring abscesses
• Septal abscesses
• Fistulae
• Prosthetic dehiscence
– Invasive infection more common in aortic position
and if onset is early
– Bracht Wachter bodies – myocardial microabcesses
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11. Epidemiology
• 1.7 to 6.2 cases per 100,000 population per year in
US
• The cumulative rate of prosthetic valve
endocarditis is 1.5 to 3.0% at 1 year after valve
replacement.
• 3 to 6% at 5 years; the risk is greatest during the
first 6 months after valve replacement.
• Men predominate in most case series, with male-
to-female ratios ranging from 2:1 to 9:1
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12. Risk Factors
• Structural heart disease
– Rheumatic, congenital, aging
– Prosthetic heart valves
• Injected drug use
• Invasive procedures (Intracardiac pacemaker,
Implatable Cardio Defibrillator , AV Fistula)
• Indwelling vascular devices
• Other infection with bacteremia (e.g.
pneumonia, meningitis)
• Immunocompromised states
• History of infective endocarditis
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13. The causative organisms in IE
Viridans Streptococci
 30-65% of native valve endocarditis
 Normal oral commensals
 A group, composed of several species:
 S. mitior, S. sanguis, S. mutans,etc.
 Alpha-hemolytic, non-typable
 Typical agents of classic “SBE”
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14. Other Streptococci
• S. bovis
– Lancefield group D
– Gut flora: associated with GI pathology
• S. pneumonia
– 1-3% of cases of IE with predilection for AV
– Usually, in those with immune suppression
• DM and Alcoholism
• Group B Streptococci
– Elderly with chronic disease
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15. Enterococcus
 Normal inhabitant of GI tract.
 Frequently encountered in UTIs.
 Up to 40% of cases without identified underlying
predisposition to IE.
 Difficult to treat due to drug resistance.
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16. Staphylococci
 Coagulase Positive (Staph. aureus)
 a major causative agent in all populations of IE
 typically produces “acute” IE
 fulminant, rapidly progressive with few immunologic signs.
 CNS complications in 30-50%
 Coagulase Negative (Staph. Epi)
 Major cause of PVE and 3-8% of NVE.
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17. HACEK organisms
• Hemophilus, Actinobacillus, Cardiobacterium,
Eikenella, Kingella
• Gram negative inhabitants of the upper airways.
• Large vegetations, high likelihood of
embolization.
• Slow growing: hold cultures for 3 weeks.
• Traditionally sensitive to beta lactams, now
some produce beta lactamase.
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18. Fungi
• Commonly encountered agents:
– Candida, Torulopsis, Aspergillus
• Predispositions
– Prosthetic valves
– IV Drug Addicts
– Immunosupression
– Parentral nutrition
– Prolonged antibiotic treatment
• Large vegetations and frequent embolic events.
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19. Other Organisms
 Pseudomonas
 Diphtheroids
 Listeria
 Bartonella
 Coxiella,Legionella,Salmonella,Brucella
 Chlamydia,Abiotropia
 Bartonella ,tropheryma, streptobacillus
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20. BCNE
• Blood culture (negative) sterile in 31 % (western
data)
• Sterile culture in India – 48 to 54 %
• Blood culture is positive only on 67.7% of the cases
in recently published data from India
• Causes
– Antibiotic therapy before blood culture
– Fastidius or atypical organisms do not grow in routine
culture media
– Fungal or viral Endocarditis
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20

21. IV Drug Users
 Accounts for 25% of
cases of IE in US.
 5:1 male:female
 Pre-existing valvular
diseases uncommon.
 Variable
microbiology.
 Mortality<10%.
AV
6%
MV
24%
TV
70%
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22. Prosthetic Valve IE
 Affects 3% of prosthesis patients.
 Highest risk in first 6 months post op.
 Accounts for 10-20% of all IE cases.
 Increased risk in;
 Males
 Blacks
 Multiple valve replacement
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23. Prosthetic Valve IE
 “Early” (<2 months)-Staphylococcus
 “Late” (after 2 months)- mimics NVE
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24. Clinical features
• High index of clinical suspicion is the
cornerstone of early diagnosis
• Symptoms
– Fever, sweats, chills
– Anorexia, malaise, weight loss
• Signs
– Anemia (normochromic, normocytic)
– Splenomegaly
– Microscopic hematuria, proteinuria
– New or changing heart murmur, CHF
– Embolic or immunologic dermatologic signs
– Hypergammaglobulinemia, elevated ESR, CRP,
RF 6/25/2023
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25. CLINICAL MANIFESTATIONS
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26.  Fever is the most common symptom and sign in
patients with IE.
Fever may be absent or minimal in
 elderly
 in those with CHF,
 severe debility,
 chronic renal failure
 NVE caused by coagulase-negative staphylococci
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27. Cardiac murmur
 New changing regurgitant murmur is the hallmark
of IE
 Murmurs are commonly not audible in
 Tricuspid valve IE
 Acute NVE due to S. aureus
 Murmurs are heard in only 30 to 45 percent of
patients on initial evaluation but are ultimately
noted in 75 to 85 percent.
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28.  Embolic phenomena include systemic,cerebral and
pumonary emboli are common in >50 % cases.
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29. 6/25/2023
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30. Cardiac Pathologic Changes
 Vegetations on valve closure lines
 Destruction and perforation of valve leaflet
 Rupture of chordae tendinae, intraventricular
septum, papillary muscles
 Valve ring abscess
 Myocardial abscess
 Conduction abnormalities
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31. S. Aureus mitral valve vegetation, anterior leaflet
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32. 6/25/2023
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33. Pathologic Changes
 Kidney
 Immune complex glomerulonephritis
 Emboli with infarction, abscess
 Aortic mycotic aneurysms
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34. Pathologic Changes
 Splenic enlargement, infarction
 Septic pulmonary embolism
 Skin
 Petechiae
 Osler nodes: diffuse infiltrate of neutrophils, and
monocytes in the dermal vessels with immune
complex deposition. Tender and erythematous
 Janeway lesions: septic emboli with bacteria,
neutrophils and S/C hemorrhage and necrosis.
Blanching and non-tender. Palms and soles
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35. MUSCULOSKELETAL
 Vertebral osteomyelitis - rare.
 Osteomyelitis - S. aureus endocarditis .
 Acute septic arthritis
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36. Metastatic
Abscess
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37. Splinter Hemorrhages
1. Nonspecific
2. Nonblanching
3. Linear reddish-brown lesions found under the nail bed
4. Usually do NOT extend the entire length of the nail
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38. Osler’s Nodes
1. More specific
2. Painful and erythematous nodules
3. Located on pulp of fingers and toes
4. More common in subacute IE
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39. Janeway Lesions
1. More specific
2. Erythematous, blanching macules
3. Nonpainful
4. Located on palms and soles
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40. Septic emboli with hemorrhage and infarction due to
acute
S. aureus endocarditis
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41. Roth spots
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42.  Enlargement of the spleen is noted in 15 to 50
percent of patients and is more common in subacute
IE of long duration.
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43. Diagnosis of IE:Duke’s v/s modified Dukes
 Duke’s sensitivity -76 % in western
 Major deficiency is inability to diagnose benign
disease
 Major additions in modified dukes includes Q fever
serology, staphylococcal bacteremia in the absence
of other primary focus as major criteria, serological
evidence of other organism consistent with
endocarditis as minor criteria.
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44. Modified Duke Criteria
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45. Two major criteria,
OR
One major and three minor
criteria,
OR
Five minor criteria allows a clinical
diagnosis of definite endocarditis.
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46. Rejected IE
 If an alternative diagnosis is established,
 If symptoms resolve and do not recur with 4 days of
antibiotic therapy, or
 If surgery or autopsy after 4 days of antimicrobial
therapy yields no histologic evidence of endocarditis.
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47. Possible IE
 Illnesses not classified as definite endocarditis or rejected
 When either one major and one minor criteria or three minor
criteria are identified.
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48. St Thomas modifications
From the Division of Infection, United Medical and Dental School,
St. Thomas’ Hospital, London, United Kingdom
LAMAS & EYKYN et al
 Inclusion of ESR , CRP, Presence of newly diagnosed
clubbing, splenomegaly and microhematuria, as
minor criteria
 Increases sensitivity by 10 %
 More appropriate in Indian /African patients
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49. St Thomas modifications
From the Division of Infection, United Medical and Dental School,
St. Thomas’ Hospital, London, United Kingdom
 Pathologically proven yet culture negative
Endocarditis
 21 % were classified definite by Original Duke’s
 32 % were definite by modified Duke’s
 62 % were definite by St Thomas modification
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50. Blood Cultures in IE
 3 separate venepunctures during one hour period
at least 10 ml blood before giving antibiotics.
 Adherence to above practice yields positive
culture in 90 %
 But at least 30 % are prescribed antibiotics before
taking culture.
 Sterile culture ---western =2.5 to 31%
--- Indian = 48 to 54 %
? Kenyan
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51. Blood Cultures
 MULTIPLE BLOOD CULTURES BEFORE
EMPIRIC THERAPY
 If not critically ill
 3 blood cultures over 12-24 hour period
 ? Delay therapy until diagnosis confirmed
 If critically ill
 3 blood cultures one hour apart
 No more than 2 from same venepuncture
 Relatively constant bacteremia
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52. “Culture Negative” IE
 Less common with improved blood culture
methods
 Special media required
 Brucella, Mycoplasma, Chlamydia, Histoplasma,
Legionella, Bartonella
 Longer incubation may be required
 HACEK
 Coxiella burnetii (Q Fever), Trophyrema
whipplei will not grow in cell-free media
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53. Use of Echo in Diagnosis of IE
 Native Valves-ACC Guidelines:
 Detection/characterization of valvular lesions
 Detection of vegetations and characterization of lesions in
patients with CHD
 Detection of associated abnormalities
 Reevaluation studies in complex IE
 Evaluation of patients with high suspicion of culture-negative
IE
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54. Use of Echo in Diagnosis of IE
 Prosthetic Valves-ACC Guidelines:
 Detection/characterisation of valvular lesions
 Detection of associated abnormalities
 Reevaluation in complex IE
 Evaluation of suspected IE and negative cultures
 Evaluation of persistent fever without known source
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55. Typical Echo features
 Oscillating intracardiac mass on a valve or
supporting structure or device or in the path of a
regurgitant stream
 Abscess
 New partial dehiscence of prosthetic valve
 New valvular regurgitation
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56.  Echo is useful in predicting complications based on
the size of the vegetation, mobility , extent,&
consistency, either embolisation or destruction.
 Vegetations greater than 10 mm often embolise
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57. TTE v/s TEE
 Transthoracic echocardiographyTTE ;Initial echo.
Sensitive in VSD and aortic valve repair. vegetation
above AV or suture site
 Transesophageal echorcardiography TEE;
- Can detect structure upto 1 mm
 Pulmonic and prosthetic valve lesion aare better visualised
 Sensitivity 81- 100%
 Specificity – 91 to 100%
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58. Use of Echo in Diagnosis of IE
 TEE:
 Prosthetic valves
 Poor visualization on TTE and high suspicion
 Detection of associated complications
 Preoperative
 Reevaluation in complex IE
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59. Other tests
 Electrocardiogram
 Conduction delays
 Ischemia or infarction
 Chest X-ray
 Septic emboli in right-sided IE
 Valve calcification
 CHF
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60. Microbiological advances to increase
culture yield
 In patients with previous antibiotic therapy the yield
of blood culture can be enhanced by diluting the
culture broth and adding sodium
polyanetholsulfonate or a dedicated adsorbant
resin.
 Atypical fastidious growing organisms are
subcultured on Chocolate agar
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61. Serology in IE
 Serology
 Coxiella burnetii – endocarditis presents only during
chronic infection with coxiella
 Bartonella
 Brucella
 Legionella
 Chlamydophila
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62. Molecular diagnostic techniques in
IE
 PCR
 RT PCR
 Proteomics ( protein signatures of the organism used
to identify the pathogens)
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63. Molecular diagnostic techniques in IE
 PCR useful in
 Coxiella burnetii
 Tropheryma whipplei
 Bartonella henselae
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64. Procalcitonin
 116 amino acid peptide
 No known hormonal activity
 Under normal metabolic conditions, PCT is only
present in the C cell of the thyroid gland
 In sepsis it is released to circulation
 Values exceeding 2.3 ng/ml in a suspected case of
IE has a sensitivity of 81 %& specificity of 85 %.
 More valuable than CRP in Sepsis
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65. Treatment of IE
 Native vs. Prosthetic Valve
 Bactericidal therapy is necessary
 Eradication of bacteria in the vegetation
 May be metabolically inactive (stationary phase)
 May need higher concentrations of antimicrobial agents
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66. Antimicrobial Therapy
 Blood culture become sterile within 2 days
 Fever resolves in 4 to 7 days
 If fever persists despite 7 days of antibiotics evaluate
for paravalvular or extracardiac abscess
 Combination therapy most important for
 Shorter course regimens
 Enterococcal endocarditis
 Prosthetic valve infections
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67. Streptococci susceptible to pencillin
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68. 6/25/2023
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69. 6/25/2023
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70. 6/25/2023
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71. 6/25/2023
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72. 6/25/2023
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73. NVE
 Fungal
 Amphotericin
 Fluconazole
 Caspofungin (little data)
 Surgery usually necessary 1-2 weeks into treatment
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74. Prosthetic Valve IE
 Staphylococci most common
 Coagulase negative staphylococci
 Enterococcus
 Nutritonally variant streptococci
 Fungi
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75. OTHER ORGANISMS
Streptococcus pneumoniae
• Penicillin if sensitive- can be treated with
intravenous penicillin
• Cftriaxone (2 g/d as a single dose), or cefotaxime (at
a comparable dosage).
• Infection caused by penicillin resistant strains
should be treated with vancomycin.
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76.  P. aeruginosa endocarditis is treated with an
antipseudomonal penicillin (ticarcillin or
piperacillin) and high doses of tobramycin (8 mg/kg
per day in three divided doses).
 Endocarditis caused by Enterobacteriaceae is treated
with a potent beta-lactam antibiotic plus an
aminoglycoside.
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77. • Corynebacterial endocarditis is treated with
penicillin plus an aminoglycoside (if the organism is
susceptible to the aminoglycoside) or with
vancomycin.
• Therapy for Candida endocarditis consists of
amphotericin B plus flucytosine and early surgery;
long-term suppression with fluconazole is also used.
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78. Empirical Therapy
• Therapy without culture data (i.e., before
culture results are known or when cultures
are negative).
• For acute endocarditis in an injection drug
user should cover methicillin-resistant S.
aureus and gram-negative bacilli.
• The initiation of treatment with vancomycin
plus gentamicin immediately after blood is
obtained for cultures covers these as well as
many other potential causes.
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79. • In culture-negative -marantic endocarditis
must be excluded and fastidious organisms
sought serologically.
• In the absence of prior antibiotic therapy, it
is unlikely to be due to S. aureus, coagulase-
negative staphylococcal, or enterococcal.
• Blood culture–negative subacute native
valve endocarditis is treated with ceftriaxone
plus gentamicin.
• These two antimicrobials plus vancomycin
should be used if prosthetic valves are
involved.
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80.  Serologic abnormalities (e.g.ESR , RF)
resolve slowly and do not reflect response to
treatment.
 Vegetations become smaller with effective
therapy, but at 3 months after cure half are
unchanged and 25% are slightly larger.
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81. Prophylactic Therapy for IE
Recommendations
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82. 1997 American Heart Assoc. Guidelines:
Endocarditis Prophylaxis Recommended:
High-risk category
Prosthetic cardiac valves, including bioprosthetic and homograft valves
Previous bacterial endocarditis
Complex cyanotic congenital heart disease (eg, single ventricle states, transposition of the
great arteries, tetralogy of Fallot)
Surgically constructed systemic pulmonary shunts or conduits
Moderate-risk category
Most other congenital cardiac malformations (other than above and below)
Acquired valvar dysfunction (eg, rheumatic heart disease)
Hypertrophic cardiomyopathy
Mitral valve prolapse with valvar regurgitation and/or thickened leaflets
Endocarditis Prophylaxis Not Recommended:
Negligible-risk category (no greater risk than the general population)
Isolated secundum atrial septal defect
Surgical repair of atrial septal defect, ventricular septal defect, or patent ductus arteriosus
(without residua beyond 6 mo)
Previous coronary artery bypass graft surgery
Mitral valve prolapse without valvar regurgitation1
Physiologic, functional, or innocent heart murmurs1
Previous Kawasaki disease without valvar dysfunction
Previous rheumatic fever without valvar dysfunction
Cardiac pacemakers (intravascular and epicardial) and implanted defibrillators
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83. 1997 AHA Guidelines
 Assumptions:
 Bacteremia with organisms known to cause IE occurs
in assoc. with invasive dental/GI/GU procedures
 Antibiotic prophylaxis was proven effective in animals
 Antibiotic prophylaxis thought to be effective in
human
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84. Reasons for 2007 Revision
 IE more likely due to frequent exposure to random
bacteremias from daily activities than from
bacteremia during dental/GI/GU procedure
 Prophylaxis may prevent only small number of
cases of IE, even if 100% effective
 Risk of antibiotic-assoc. adverse events exceeds the
benefit, if any, from prophylaxis
 To reduce the risk of bacteremia from
dental procedure: maintaining good oral
health and hygiene is more important than
Antibiotic prophylaxis
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85. Frequency of Transient Bacteremia
 Tooth extraction 10-100%
 Periodontal surgery 36-88%
 Teeth cleaning 40%
 Tooth brushing, 20-68%
 Using wooden toothpicks 20-40%
 Chewing food 7-51%
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86. 2007 guideline: Who gets
prophylaxis for IE?
Only patients with the highest risk of adverse
outcomes (heart failure, surgery, death) from
endocarditis:
1. Prosthetic cardiac valve
2. Previous IE
3. Cardiac transplant recipients who develop cardiac
valvulopathy
4. Congenital Heart Disease
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87. Which categories of Congenital Heart
Disease require prophylaxis?
 Unrepaired cyanotic CHD
 Tetralogy of Fallot, Transposition of Great Arteries,
including palliative shunts and conduits
 Completely repaired congenital heart defect with
prosthetic material or device during 1st 6 months
after surgery
 Repaired CHD with residual defects at or near a
prosthetic patch/device (which inhibit
endothelialization)
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88. What about “Moderate-Risk” Pts?
1997’s “Moderate Risk” Category NO LONGER gets
prophylaxis:
 MVP with regurg and/or thickened leaflets
 Hypertrophic cardiomyopathy
 Acquired Valvular Dysfunction (eg rheumatic heart
disease)
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89. Dental Procedures
 “If it bleeds, give prophylaxis”
 High-risk pts undergoing all dental procedures
that involve manipulation of gingival tissues
OR periapical region of teeth OR perforation
of oral mucosa
 i.e. biopsies, suture removal, placing orthodontic bands
 NO PROPHYLAXIS:
 Xray, anesthetic injections, fluoride treatments
 Shedding of deciduous teeth
 Placement/adjustment of removable prosthodontic or
orthodontic appliances
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90. Prophylaxis for Dental Procedures
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91. Concern over resistant Strep Viridans
 Quinolones or IV Vancomycin not recommended
for prophylaxis due to concern of creating new
drug resistance
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92. Respiratory Tract Procedures
 No published data linking resp tract procedures
and IE..
 Consider prophylaxis for High-risk pts
undergoing Invasive Procedure in resp tract
with incision or biopsy of resp mucosa:
 Tonsillectomy
 Adenoidectomy
 Bronchoscopy WITH biopsy (not for BAL alone)
 Resp tract procedure to drain abscess or empyema
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92

93. Procedures on Infected Skin/Skin
Structure, or msk Tissue
In patients who are HIGH-risk for IE:
 The antibiotic regimen given to treat the skin or
musculoskeletal infection should contain an Anti-
staphylococcal Pencillin or cephalosporin
 If unable to take PO or Pencillin-allergic:
Clindamycin or Vancomycin
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94. Summary: IE prophylaxis
 Need high-risk patient PLUS high-risk procedure
 High-risk pts:
1. Prosthetic cardiac valve
2. Previous IE
3. Cardiac transplants with valvulopathy
4. Congenital Heart Disease
 High-risk procedures:
1. Dental: “If it bleeds, give prophylaxis”
2. Respiratory: Consider if pt will be cut or biopsied
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95. No Prophylaxis
 Endotracheal intubation
 Cardiac cath/stent
 Pacer/ICD implantation
 GI/GU procedures
 OGD, Colonoscopy
 Barium Enema
 TEE
 Incision/Bx of surgically scrubbed skin
 Circumcision
 Vaginal delivery
 Hysterectomy
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95