Endocarditis is inflammation of your heart's inner lining, called the endocardium. It's usually caused by bacteria. When the inflammation is caused by infection, the condition is called infective endocarditis. Endocarditis is uncommon in people with healthy hearts.
Endocarditis is inflammation of your heart's inner lining, called the endocardium. It's usually caused by bacteria. When the inflammation is caused by infection, the condition is called infective endocarditis. Endocarditis is uncommon in people with healthy hearts.
Seminar of Endocarditis by Sudeep,(Pharm.D.)SUDEEP
Presentation of Endocarditis.
Pharmaco therapeutics of disease endocarditis(Inflammation of endocardium).
Definition,causes,etiology,symptoms and treatment of disease.
A powerpoint presentation about infective Endocarditis, with the most recent updates from the most reliable sources. I highlighted an introduction, pathology, approach to disease & different management plans in this presentation. 2018. Please don't forget to give me credit to my work.
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4. Endocarditis: Definition
Infective Endocarditis: is an inflammation of the
endocardium, the membrane lining the chambers of the
heart and covering the cusps of the heart valves
it refers to infection of the heart valves by various
microorganisms
7. Classification:
• acute or subacute-chronic on temporal basis,
severity of presentation and progression
• By organism
• Native valve or prosthetic valve
8. 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
9. EPIDEMIOLOGY AND ETIOLOGY
• Infective endocarditis is an uncommon, but not rare,
infection affecting about 10,000 to 20,000 persons
annually in the United States.
• accounts for approximately 1 in every 1,000 hospital
admissions.
• The mean male-to-female ratio is 1.7:1.
10. IMPORTANT RISK FACTORS
• Presence of a prosthetic valve (highest risk)
• Previous endocarditis (highest risk)
• Complex cyanotic congenital heart disease (e.g., single-ventricle
states)
• Surgically constructed systemic pulmonary shunts or
conduits
• Acquired valvular dysfunction (e.g., rheumatic heart
disease)
• Hypertrophic cardiomyopathy
• Mitral valve prolapse with regurgitation
• IVDA (intravenous drug abuse).
11. EPIDEMIOLOGY
Incidence in IVDA group is estimated at 2000 per
100,000 person-years, even higher if there is known
valvular heart disease
Increased longevity leads to more degenerative valvular
disease, placement of prosthetic valves and increased
exposure to nosocomial bacteremia
12. PROSTHETIC VALVES
7-25% of cases of infective endocarditis
The rates of infection are the same at 5 years for
both mechanical and bioprostheses, but higher for
mechanical in first 3 months
Cumulative risk: 3.1% at 12 months and 5.7% at 60
months post surgery
Onset:
within 2 months of surgery early and usually
hospital acquired
12 months post surgery late onset and usually
community acquired
13. Nosocomial Infective Endocarditis
7-29% of alll cases seen in tertiary referral
hospitals
At least half linked to intravascular devices
Other sources GU and GIT procedures or
surgical-wound infection
14. Aetiological Agents
1. Streptococci
Viridans streptococci/α-haemolytic streptococci
S. mitis, S. sanguis, S. oralis
S. bovis
Associated with colonic carcinoma
1. Enterococci
E. faecalis, E. faecium
Associated with GU/GI tract procedures
Approx. 10% of patients with enterococcal
bacteraemia develop endocarditis
15. Aetiological Agents
3. Staphylococci
Staphylococcci have surpassed
viridans streptococci as the most common
cause of infective endocarditis
S. aureus
Native valves
acute endocarditis
Coagulase-negative staphylococci
Prosthetic valve endocarditis
19. Pathogenesis
Altered valve surface
Animal experiments suggest that IE is almost
impossible to establish unless the valve surface is
damaged
Deposition of platelets and fibrin – nonbacterial
thrombotic vegetation (NBTE)
Bacteraemia – attaches to platelet-fibrin deposits
Covered by more fibrin
Protected from neutrophils
Division of bacteria
Mature vegetation
20.
21. Pathogenesis
Bacteraemia
Transient bacteraemia occurs when a heavily
colonised mucosal surface is traumatised
Dental extraction
Periodontal surgery
Tooth brushing
Tonsillectomy
Operations involving the respiratory, GI or GU tract mucosa
Oesophageal dilatation
Biliary tract surgery
22. Site of Infection
Aortic valve more common than mitral
Aortic:
Vegetation usually on ventricular aspect, all 3
cusps usually affected
Perforation or dysfunction of valve
Root abscess
Mitral:
Dysfunction by rupture of chordae tendineae
23. Clinical Manifestations
Fever, most common symptom, sign (but may be
absent)
Anorexia, weight-loss, malaise, night sweats
Heart murmur
Petechiae on the skin, conjunctivae, oral mucosa
Right-sided endocarditis is not associated with
peripheral emboli/phenomena but pulmonary findings
predominate
24. Janeway Lesions
Janeway lesions—Hemorrhagic, painless plaques on the palms
of the hands or soles of the feet. These lesions are believed to
be embolic in origin.
25. Splinter Hemorrhage
Splinter hemorrhages—
Thin, linear hemorrhages
found under the nail beds
of the fingers or toes.
26. Osler’s Nodes
Osler nodes — Purplish or
erythematous subcutaneous
papules or nodules on the pads
of the fingers and toes. These
lesions are 2 to 15 mm in size
and are painful and tender.
27. Petechiae
Petechiae—Small (usually 1 to 2
mm in diameter), erythematous,
painless, hemorrhagic lesions.
These lesions appear anywhere
on the skin but more frequently on
the anterior trunk, buccal mucosa
and palate, and conjunctivae..
28. Roth’s Spots
Roth spots—Retinal
infarct with central
pallor and surrounding
hemorrhage.
30. Diagnosis: Duke Criteria
In 1994 a group at Duke University
standardised criteria for assessing patients
with suspected endocarditis
Include
-Predisposing Factors
-Blood culture isolates or persistence of
bacteremia
-Echocardiogram findings with other clinical,
laboratory findings
31. Duke Criteria
Definite
: 2 major criteria
: 1 major and 3 minor criteria
: 5 minor criteria
: pathology/histology findings
Possible : 1 major and 1 minor criteria
: 3 minor criteria
Rejected : firm alternate diagnosis
: resolution of manifestations of IE with
4 days antimicrobial therapy or less
32.
33.
34.
35. Echocardiography
Trans Thoracic Echocardiograpy (TTE)
rapid, non-invasive – excellent specificity (98%)
but poor sensitivity
obesity, chronic obstructive pulmonary disease
and chest wall deformities
Transesophageal Echo (TOE)
more invasive, sensitivity up to 95%, useful for
prosthetic valves and to evaluate myocardial
invasion
Negative predictive valve of 92%
TOE more cost effective in those with S. aureus
catheter-associated bacteraemia and
bacteraemia/fever and recent IVDA
36.
37. COMPLICATIONS OF ENDOCARDITIS
Cardiac :
congestive cardiac failure-valvular damage, more
common with aortic valve endocarditis, infection
beyond valve→ CCF, higher mortality, need for
surgery, A-V, fascicular or bundle branch block,
pericarditis, tamponade or fistulae
Systemic emboli
Risk depends on valve (mitral>aortic), size of
vegetation, (high risk if >10 mm)
20-40% of patients with endocarditis,
risk decreases once appropriate antimicrobial
therapy started.
38. Goals of Therapy
1. Eradicate infection
2. Definitively treat sequel of destructive
intra-cardiac and extra-cardiac lesions
39. Therapy
Antimicrobial therapy
Use a bactericidal regimen
Use a recommended regimen for the organism
isolated
E.g. American Heart Association JAMA 1995; 274: 1706-13.,
British Society for Antimicrobial Chemotherapy
Repeat blood cultures until blood is demonstrated to
be sterile
Surgery
40.
41.
42.
43.
44.
45.
46.
47.
48.
49. Surgical Therapy
Indications:
Congestive cardiac failure
perivalvular invasive disease
uncontrolled infection despite maximal
antimicrobial therapy
Pseudomonas aeruginosa, Brucella species, Coxiella
burnetti, Candida and fungi
Presence of prosthetic valve endocarditis
unless late infection
Large vegetation
Major embolus
Heart block
50. Prevention
Antimicrobial prophylaxis is given to at risk
patients when bacteraemia-inducing procedures
are performed
Look up and follow guidelines
American Heart Association. Circulation 1997; 96:
358-366
British Society for Antimicrobial Chemotherapy.
Journal of Antimicrobial Chemotherapy 1993; 31:
347-438
BNF
Editor's Notes
Early steps in bacterial valve colonisation. (A) Colonisation of damaged epithelium: exposed stromal cells and extracellular matrix proteins trigger deposition of fibrin-platelet clots to which streptococci bind (upper panel); fibrin adherent streptococci attract monocytes and induce them to produce tissue factor activity (TFA) and cytokines (middle panel); these mediators activate coagulation cascades, attract and activate blood platelets, and induce cytokine, integrin, and TFA production from neighbouring endothelial cells (lower panel), encouraging vegetation growth. (B) Colonisation of inflamed valve tissues: in response to local inflammation, endothelial cells express integrins that bind plasma fibronectin, to which microorganisms adhere by wall attached fibronectin binding proteins, resulting in endothelial internalisation of bacteria (upper panel); in response to invasion, endothelial cells produce TFA and cytokines, triggering blood clotting and extension of inflammation, and promoting formation of the vegetation (middle panel); internalised bacteria eventually lyse endothelial cells by secreting membrane active proteins such as haemolysins (lower panel).
These lesions are not specific for infective endocarditis and more commonly are the result of traumatic injuries. Distal lesions are more likely the result of trauma, whereas proximal lesions tend to be associated with infective endocarditis.
These nodes are
not specific for infective endocarditis and may be the result of
embolism, immunologic phenomena, or both.
Petechiae are nonblanching and resolve after a few days