it is talk abou infection related to cardiac

1. INFECTIVE ENDOCARDITIS
Fitsum Getahun, MD; Ass. Prof of I.Medicine
Department of internal medicine
AMU, March 2018

2. Definition of Infective Endocarditis
• A serious infection of the endocardium of the
heart, particularly the heart valves, is
associated with a high degree of illness and
death.
• It generally occurs in patients with altered and
abnormal heart architecture, in combination
with
– exposure to bacteria through trauma and other
potentially high-risk activities involving transient
bacteraemia.

3. Definition
Infective Endocarditis (IE): an infection of the
heart’s endocardial surface
Main Classification:
– Native Valve IE
– Prosthetic Valve IE
Additional Consideration
– Intravenous drug abuse (IVDA) IE
– Nosocomial IE

4. Infective Endocarditis
• Febrile illness
• Persistent bacteremia
• Characteristic lesion of microbial infection of
the endothelial surface of the heart
– Variable in size
– Amorphous mass of fibrin & platelets
– Abundant organisms
– Few inflammatory cells
The vegetation

5. Bacterial Endocarditis
Predisposing Factors
1. Dental manipulation
2. Dental disease (caries, abscess)
3. Extra cardiac infection (lung, urinary tract,skin,
bone, abscess)
4. Instrumentation (urinary tract, GI tract, IV
infusions)
5. Cardiac surgery
6. Injection drug use
7. None apparent

6. Infective Endocarditis
• Acute
– Toxic presentation
– Progressive valve destruction & metastatic infection developing in
days to weeks
– Most commonly caused by S. aureus
• Sub acute
– Mild toxicity
– Presentation over weeks to months
– Rarely leads to metastatic infection
– Most commonly S. viridans or enterococcus

7. Infective Endocarditis
• Adult population
–Rheumatic Heart Disease
• 20 – 25% of cases of IE in 1970’s & 80’s
• 7 – 18% of cases in recent reported series
• Mitral site more common in women
• Aortic site more common in men
–Congenital Heart Disease
• 10 – 20% of cases in young adults
• 8% of cases in older adults
• PDA, VSD, bicuspid aortic valve (esp. in men>60)

8. Infective Endocarditis
• Intravenous Drug Abuse
– Risk is 2 – 5% per pt./year
– Tendency to involve right-sided valves
• Distribution in clinical series
– 46 – 78% tricuspid
– 24 – 32% mitral
– 8 – 19% aortic
– Underlying valve normal in 75 – 93%
– S. aureus predominant organism (>50%, 60-70%
of tricuspid cases)

9. Causes of Bacteraemia
Brushing teeth
Eating/chewing
Dental work
IV lines (colonised/infected)
IV drug use
Infected site/abscess
alpha-haemolytic
streptococci from
oral flora
Staphylococcus
aureus from
skin/nose
Strep. pneumoniae,
S.aureus

10. Infecting Organisms
Common bacteria
– Alpha haem streptococci (viridans – S. mitis, S. sanguis) SUBACUTE
– Enterococci (E. faecalis) SUBACUTE
– Coagulase Negative Staphylococci – PROSTHETIC VALVES, SUBACUTE
Less common bacteria
– S. aureus ACUTE
– B-Haemolytic streptococci ACUTE
– Streptococcus pneumonia
Not so common
– Fungi
– Pseudomonas / Coliforms
– HACEK group organisms

11. Bacterial Pathogens
HACEK Group
• Haemophilus spp.
• Actinobacillus
actinomycetemcomitans
• Cardiobacterium hominis
• Eikenella corrodens
• Kingella kingae

12. Infecting Organisms
Streptococci 60-80%
– Alpha-haemolytic Streptococci (viridans – S. mitis, S. oralis) 30-40%
(subacute)
– Enterococci (E. faecalis) 5-18% (subacute)
– Beta-haemolytic streptococci (e.g. Gp A Strep) – rare (acute)
Staphylococci 20-35%
– S. aureus 10-27% (acute)
– Coagulase negative staphylococci (Staph epidermidis) 1-3 %
(mainly prosthetic valve risk, subacute)
Fungi
– Candida – IVDU at risk (usually indolent)
– Aspergillus – rare
Gram-negative bacteria – rare
Culture-negative endocarditis HACEK, Q-fever – cases do occur, subacute

13. Infective Endocarditis
• Prosthetic Valve Endocarditis (PVE)
– 10 – 30% of all cases in developed nations
– Cumulative incidence
• 1.4 – 3.1% at 12 months
• 3.2 – 5.7% at 5 years
– Early PVE – within 60 days
• Nosocomial (s. epi predominates)
– Late PVE – after 60 days
• Community (same organisms as NVE)

14. Infective Endocarditis
• Pathology
– NVE infection is largely confined to leaflets
– PVE 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

15. Pathophysiology
Turbulent blood flow within the heart - most often
(but not always) – patient has risk factors for this
Turbulent blood flow disrupts valve surface
(endocardium) to produce suitable (sticky) site for
bacterial attachment
Platelet deposition + fibrin may lead to non-bacterial
thrombus or vegetation
Bacteraemia – delivers organisms to the damaged
(sticky) endocardial surface resulting in adherence &
colonisation
Eventual invasion of valve leaflets results in infected
vegetation (sheath of fibrin & platelets, ideal
conditions for further bacterial multiplications,
protection from polymorphs)

16. Infected vs Normal Valve

17. Local Spread of Infection
Acute S. aureus IE with perforation of the
aortic valve and aortic valve vegetation.
Acute S. aureus IE with mitral valve ring
abscess extending into myocardium.

18. Turbulent Blood Flow
Rheumatic fever history
Old age – calcified valves
Mitral valve prolapse with regurgitation
Prosthetic heart valves
Congenital defects / any structural defect
Cardiac surgery
Central lines
Pacemakers
Intravenous drug abuse
Varying predisposing conditions exist, but in over 50% of cases, no identified valvular
lesion can be found.

19. Distinction between Acute and
Subacute Bacterial Endocarditis
Feature Acute Subacute
Underlying Heart
Disease
Heart may be normal RHD,CHD, etc.
Organism S. aureus, Pneumococcus
S. pyogenes,
Enterococcus
viridans
Streptococci,
Entercoccus
Therapy Prompt, vigorous and initiated
on empirical ground
Can often be delayed
until culture reports and
susceptibilities
available

20. Symptoms
Acute
– High grade fever and
chills
– SOB
– Arthralgias/ myalgias
– Abdominal pain
– Pleuritic chest pain
– Back pain
Sub acute
– Low grade fever
– Anorexia
– Weight loss
– Fatigue
– Arthralgia's/ myalgia's
– Abdominal pain
– N/V
The onset of symptoms is usually ~2 weeks or less
from the initiating bacteremia

21. Signs
Fever
Heart murmur
Nonspecific signs – petechiae,
subungal or “splinter” hemorrhages,
clubbing, splenomegaly, neurologic
changes
More specific signs - Osler’s Nodes,
Janeway lesions, and Roth Spots

22. Janeway Lesions

23. Janeway Lesions
1. More specific
2. Erythematous, blanching macules
3. Nonpainful
4. Located on palms and soles

24. Splinter Hemorrhage

25. 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

26. Subconjuctival Hemorrhages

27. Septic Retinal Embolus

28. Roth’s Spots

30. 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

31. Bacterial Endocarditis
Laboratory Features
1. Anemia
2. Most commonly elevated WBC
3. ESR elevated, ↓ C′ in patients with
glomerulonephritis
4. Microscopic hematuria
5. Bacteremia. Persistent.≥ 3, ≤ 5 blood cultures.
Aerobic and anaerobic. Different sites.

32. Blood cultures
• Recommendation: Blood cultures remain a
cornerstone of the diagnosis of IE cases and
should be taken prior to starting treatment in all
case
• Meticulous aseptic technique is required when
taking blood cultures, to reduce the risk of
contamination with skin commensals, which can
lead to misdiagnosis.
• Guidelines for best practice should be consulted

33. When to Collect the blood
• In patients with a chronic or sub acute
presentation, three sets of optimally
filled blood cultures should be taken
from peripheral sites with ≥6 h between
them prior to commencing antimicrobial
therapy.
• Taking blood cultures at different times is
critical to identifying a constant
bacteraemia, a hallmark of endocarditis.

34. Timing of blood collection
• In patients with suspected IE and severe
sepsis or septic shock at the time of
presentation, two sets of optimally filled
blood cultures should be taken at
different times within 1 h prior to
commencement of empirical therapy, to
avoid undue delay in commencing
empirical antimicrobial therapy.

35. Start with Empherical Treatment
• It is not always appropriate to withhold
antimicrobial therapy while three sets of
blood cultures are taken over a 12 h period.
• This recommendation is intended to be
pragmatic, allowing time to take at least two
sets of blood cultures (the minimum for a
secure microbiological diagnosis) prior to
commencing antimicrobial therapy.

36. How to collect the Blood
• Sampling of
intravascular lines
should be avoided,
unless part of paired
through-line and
peripheral sampling to
diagnose concurrent
intravascular catheter-
related bloodstream
infection.

37. Blood Cultures
Blood Cultures
– Minimum of three blood cultures (ideally spread over 24
hrs)
– Three separate venipuncture sites ideally
– Obtain correct volume of blood for culture bottles
Positive Result
– 1 set gives 90% sensitivity, remaining 2 sets add 8%
– Multiple same cultures are important in confirming
significance, especially for less typical organisms
Negative Result
– Prior antibiotic therapy
– ‘Culture negative endocarditis’ – fastidous orgs / non-
culturable
– May support a non-endocarditis patient diagnosis

38. Blood Cultures
Always need to get full identification
of bacteria from positive blood
cultures in suspected endocarditis
Full sensitivity testing
Need full MIC (minimum inhibitory
concentration) for Penicillin
Liaison with Lab/microbiologist in
cases where endocarditis
suspected/diagnosed

39. Be cautious when you send
multiple samples
• Bacteraemia is
continuous in IE
rather than
intermittent, so
positive results from
only one set out of
several blood
cultures should be
regarded with
caution.

40. Prior administration of Antibiotics give
Negative Culture Results
• Failure to culture a causative microorganism in IE
is often due to
– the administration of antimicrobials prior to blood
culture
– infection caused by fastidious or slow-growing
microorganisms.
• Diagnostic methods should include serological
investigations where they are available and a
systematic approach is advised, based on the
clinical history of the patient and their exposure
to possible risk factors.

41. Culture Negative Results may yield
..less known microbes
• Microorganisms
that should be
considered first
include Coxiella
burnetii (Q
fever) and
Bartonella spp.

42. Additional Tests
CBC
ESR and CRP
Complement levels (C3, C4, CH50)
RF
Urinalysis
Baseline chemistries

43. Imaging
Chest x-ray
– Look for multiple focal infiltrates and calcification
of heart valves
ECG
– Rarely diagnostic
– Look for evidence of ischemia, conduction delay,
and arrhythmias
Echocardiography

44. Indications for Echocardiography
Transthoracic echocardiography (TTE)
–First line if suspected IE
–Native valves
Trans esophageal echocardiography (TEE)
–Prosthetic valves
–Intracardiac complications
–Inadequate TTE
–Fungal or S. aureus or bacteremia

45. The Duke Criteria for the Clinical Diagnosis of Infective
Endocarditis

46. Making the Diagnosis
Pelletier and Petersdorf criteria (1977)
– Classification scheme of definite, probable, and possible IE
– Reasonably specific but lacked sensitivity
Von Reyn criteria (1981)
– Added “rejected” as a category
– Added more clinical criteria
– Improved specificity and clinical utility
Duke criteria (1994)
– Included the role of echocardiography in diagnosis
– Added IVDA as a “predisposing heart condition”

47. Modified Duke Criteria
Definite IE
– Microorganism (via culture or histology) in a valvular
vegetation, embolized vegetation, or intracardiac abscess
– Histologic evidence of vegetation or intracardiac abscess
Possible IE
– 2 major
– 1 major and 3 minor
– 5 minor
Rejected IE
– Resolution of illness with four days or less of antibiotics

48. Bacterial Endocarditis
Therapy and Prophylaxis
1. Prolonged; high dosages; use of bactericidal
drugs
2. Serum antibiotic levels and MBC of the
organism
3. Viridans streptococci, Enterococcus, S. aureus,
S. pneumoniae, S. pyogenes
4. Institution of therapy on empirical grounds
5. Proven negative blood cultures on Abx
6. Prophylaxis: dental extraction, GU.

49. Treatment
Parenteral (IV) antibiotics
–High serum concentrations to penetrate
vegetation's
–Prolonged treatment to kill dormant
bacteria clustered in vegetation's
Surgery
–Intracardiac complications/paravalve
abscess

50. Treatment - Specific
Modify empiric therapy once
cultures/sensitivities known
Long duration 4-6 weeks Rx is required
Monitor response to treatment (clinical, CRP,
ECHO) & look for complications

51. Complications
Four etiologies
–Embolic
–Local spread of infection
–Metastatic spread of infection
–Formation of immune complexes –
glomerulonephritis and arthritis

52. Embolic Complications
Occur in up to 40% of patients with IE
Predictors of embolization
–Size of vegetation
–Left-sided vegetation's
–Fungal pathogens, S. aureus, and Strep.
Bovis
Incidence decreases significantly after
initiation of effective antibiotics

53. Embolic Complications
Stroke
Myocardial Infarction
– Fragments of valvular vegetation or vegetation-
induced stenosis of coronary ostia
Ischemic limbs
Hypoxia from pulmonary emboli
Abdominal pain (splenic or renal infarction)

54. Metastatic Spread of Infection
Meningitis and/or encephalitis
Vertebral osteomyelitis
Metastatic abscess
–Kidneys, spleen, brain, soft tissues
Septic arthritis

55. Prevention – the procedure
• Dental procedures
known to produce
bleeding
• Tonsillectomy
• Surgery involving GI,
respiratory mucosa
• Esophageal dilation
• ERCP for obstruction
• Gallbladder surgery
• Cystoscopy, urethral
dilation
• Urethral catheter if
infection present
• Urinary tract surgery,
including prostate
• I&D of infected tissue

56. Antibiotic Therapy
• Treatment tailored to etiologic agent
–Important to note MIC/MBC
relationship for each causative
organism and the antibiotic used
–High serum concentration necessary to
penetrate avascular vegetation

57. Antibiotic Therapy
• Effective antimicrobial treatment should
lead to defervescence within 7 – 10 days
–Persistent fever in:
• IE due to staph, pseudomonas, culture negative
• IE with micro vascular complications/major
emboli
• Intracardiac/extra cardiac septic complications
• Drug reaction

58. ANTIBIOTIC TREATEMENT OF IE

59. ANTIBIOTIC TREATEMENT OF IE

60. ANTIBIOTIC TREATEMENT OF IE

61. INDICATIONS FOR CARDIAC SURGICAL
INTERVENTION IN IE

62. GENERAL MEASURES FOR THE PREVENTION
OF IE
• The incidence of IE can be significantly
reduced by total surgical correction of
some congenital lesions, such as patent
ductus arteriosus, ventricular septal
defect, and pulmonary stenosis
• Maintaining good oral hygiene, which
decreases the frequency of bacteremia
that accompanies daily activities, is an
important preventive measure
• Infections associated with bacteremia
must be treated promptly and, if possible,

63. CHEMOPROPHYLAXIS
• Prophylactic antibiotics are advised only for those
patients at highest risk for severe morbidity or
death from endocarditis
• Prophylaxis is recommended only for dental
procedures wherein there is manipulation of
gingival tissue or the periapical region of the teeth
or perforation of the oral mucosa (including
surgery on the respiratory tract)
• Although prophylaxis is not advised for patients
undergoing gastrointestinal or genitourinary tract
procedures, it is recommended that effective
treatment be given to these high-risk patients
before or when they undergo procedures on an
infected genitourinary tract or on infected skin and
related soft tissue

64. High-Risk Cardiac Lesions for Which Endocarditis
Prophylaxis Is Advised before Dental Procedures