3. DEFINITION
Infective endocarditis is an infection of the endocardium and /or heart
valve that involves thrombus formation (vegetation),which damage the
endocardial tissues and /or valves.
4. EPIDEMIOLOGY
The precise incidence of IE is difficult to ascertain because case
definitions have varied over times between the authors and clinical
centres.
In addition ,the incidence of predisposing conditions such as
rheumatic heart diseases or injection drug users is variable over time
and between region, in low and high income countries.
5. RISK FACTORS ( PATIENTS FACTORS)
1) Age >60years
2) Injection drug users.IDUs induce bloodstream seedling with flora/oral flora or
organism contaminating the drugs or material used to for injection. Elicit drug
may induce valvular endothelial damage predisposing to subsequent infection.
3) Poor dentition or dental infection.
4) Male sex .Men predominant in most cases of IE
Male to female ratio range from 3:2 to 9:1
6. RISK FACTORS OF IE( COMORBID
CONDITIONS)
1) Structural heart diseases
2) Valvular disease. Rheumatic heart disease, mitral valve prolapse, aortic
valves disease and other valvular abnormalities.
3) Congenital heart disease. Heart lesions such as aortic stenosis,biscupid aortic
valve, pulmonary stenosis ventricular defect, patent ductus
artenosus,coartaion of the aorta and tetralogy of Fallot predispose to IE
7. 1) Chronic haemodialysis.
2) HIV infection. HIV is an independent risk factor for in injection users.
Unusual organism such as salmonella and listeria may cause IE in HIV
infected pts.
3) History if infective endocarditis
4) prosthetic heart valve
8. CAUSATIVE ORGANISM
90% of community acquired native valve infective endocarditis is caused by
staphylococci, streptococci or enterococci which are normal inhabitants of the
skin, oropharyngeal and urogenital tact respectively which have frequent
access to the blood stream.
They have specific receptors to attachment and adherence to damaged
endothelial surface
11. ENDOCARDITIS RELATED IE
INJECTION DRUGS USERS
A number of factors may uniquely predispose IDUS pts to IE.
a. Injection of particulate matter such talc along with illicit may damage the
endothelial to the tricuspid valve.
b. Repetitive use of injection drug (heroin) may produce cumulative subclinical
damage to the tricuspid valve.
c. Introduce bacterial (s. aureus)and fungi
d. Cocaine cause vasospasm which lead to tissue injuries.
12. 1. Most case of IE begins with a damaged endocardial surface which might
be due to inflammatory e.g. RHD to congenital e.g. mitral valve prolapse
to senile degeneration and calcification. Any excess turbulence or high
pressure gradient can cause injury to the nearby endocardium.
2. Fibrin –platelet aggregate at the site of the damaged endocardium to form
a sterile vegetation also called non bacterial thrombotic endocardium
13. when transient bacteraemia occur e.g. through health care procedure, injection
drugs users, gingival manipulation the previous sterile vegetation may be seeded
S.aures and streptococci adhere to the vegetation and evade innate endovascular
causing endocarditis.
The bacteria then proliferate within the vegetation causing invasion of the
endothelial surface
Lastly the surface of cardiac valves and vegetation are avascular thereby making
it antibiotic therapy and healing difficult.
15. CLINICAL PRESENTATION.
Patients complain of fever and non specific constitutional symptoms such as
fatigue, malaise and weight loss
50% complain of musculoskeletal symptoms varying from frank arthritis to
diffuse myalgia, and low back pain.
Injection drug users with tricuspid valve IE and pts with right heart
implantable devices endocarditis can present with pleauric chest pain and
multilobar pneumonia.
16. 90% present with fever.
peripheral stigmata: splinter haemorrhage ,Osler nodes Janeway lesion, petechiae
in conjunctival ,palate and extremities.
Finger clubbing
A widen pulse pressure in acute aortic insufficiency.
Fundoscopic examination: Roth spot in choriorenitis or endophthalmitis common
in fungal endocarditis.
Cardiac examination may reveal diastolic and systolic murmur.
17. PHYSICAL EXAMINATION CONT..
Abdominal examination, splenomegaly is come in subacute
endocarditis.
Neurological examination: evidence of major vessel emboli, cranial
nerve palsies ,visual deficient defect.
18.
19.
20. The gold standard for diagnosis of IE is culture of the pathologic organism
from the valve or other endothelial surface however unless the patients
undergoes valve replacement or postmortem examination, the diagnosis is
made clinically.
The most accepted criteria is the modified duke criteria. Which is estimated
76-100% sensitivity and 88-96% specificity with a negative predictive value
of at least 92%
21. major criteria
1. Blood culture positive
A. Typical organism (alpha hemolytic streptococcus, streptococcus bovis, HACEK
organism or community acquired S.Aureus or enterococci with primary cause) from 2
separate culture. OR
B. Persistent bacteremia with any organism( 2 positive culture > 12 hrs. apart or 3 positive
culture or a majority of > 4 cultures positive > 1 hr. apart. OR
C. Bacteremia with S. Aureus regardless of whether the bacteremia was nosocomial;
acquired or whether a removable focus of infection is found
22. 2. Evidence of endocardial involvement
A. Echocardiographic findings: mobile mass attached to valve or valve
apparatus, abscess, or new partial dehiscence of prosthetic valve.
B. New valvular regurgitation
3. Serology: single positive blood culture for Coxiella burnetii or antiphase 1
IgG antibody titer >1 : 800
23. minor criteria
1) Predisposing condition: IV drug use or predisposing cardiac condition
2) Fever ≥38° C
3) Vascular phenomena: arterial embolism, septic pulmonary emboli, mycotic aneurysm,
intracranial hemorrhage, conjunctival hemorrhages, Janeway lesions
4) Immunologic phenomena: glomerulonephritis, Osler nodes, Roth spots, rheumatoid factor
5) Echocardiogram findings consistent with endocarditis but not meeting major criteria
6) Microbiologic evidence: positive blood cultures not meeting major criteria or serologic
evidence of active infection consistent with endocarditis
24. DEFINITIVE INFECTIVE ENDOCARDITIS
1. Pathologically proven infective endocarditis Or Clinical criteria meeting
a. Two major criteria or
b. One major and three minor criteria or
c. five minor criteria
POSSIBLE INFECTIVE ENDOCARDITIS
Findings that fall short of definitive infective endocarditis but do not reject it
25. The role of ECHO in IE: to determine the underlying anatomy of valvular
structures
Determine the presence, location and number of vegetations
Define any function valvular abnormality/dysfunction resulting to vegetations
Determine the impact of valvular abnormality/ dysfunction if any on right or
left ventricular size and function
Recognizing intracardiac complication associated with endocarditis including,
regurgitant valve lesion, Valve perforation, Abscess, Fistula formation
26. Valvular vegetation is defined as a discrete mass of echogenic material adherent
at point of the leaflet surface and distinct in character from the remainder of the
leaflet. It has he following character:
a. Texture- gray scale and reflectance of myocardium
b. Location- upstream side of the valve in the path of the jet or prosthetic
material
c. Characteristics motion-chaotic and orbiting; independent of valve motion
d. Shape- lobulated and amorphous
e. Accompanying abnormality- abscess , fistula and pseudoaneurysm, prosthetic
dehiscence, paravalvular leak, preexisting or new vegetation.
27. The modified duke criteria for dx of IE include echocardiographic
structure finding as major criteria:
1. Presence of oscillating intracardiac mass
2. Presence of abscess
3. Partial dehiscence of a prosthetic valve.
New valvular regurgitation is a major criteria in the AHA Valvular Heart
Disease Guidelines.
28. Transthoracic echocardiography (TTE) should be done in all pts suspected to
having IE.
Transesophageal echocardiography (TEE) should be done if initial TTE images
are inadequate or negative in pts with an ongoing suspicion of IE, or with
initial positive TTE among patients with concern for intracardiac
complications.
If there is high suspicion for IE despite a negative TEE, a TEE should be
repeated after 3-5 days.
29. Complete blood count –anemia of chronic disease in subacute IE, elevated
white blood cell
Renal function test, serum electrolytes.
Urinalysis ( hematuria, proteinuria.)
Rheumatic factor, ESR,C-reactive protein
ECG( EKG)-Prolonged PR interval, new AVB, fascicular or BBB.
30. OBTAIN CULTURE DATA FIRST!! (but don’t delay treatment in acute ill pts with complication of
endocarditis and pts with high risk of endocarditis such as prosthetic valve recipeints.)
1. Native Valve, Empiric therapy
Ugandan Guidelines:
Benzylpenicillin 4MU IV every 4 hours + Gentamicin 1mg/kg every 8 hours (NO Gent in pregnancy)
Alternate Guidelines:
[PCN G or AMP] + [Nafcillin or Oxacillin]+ Gentamicin
Adjust Antibiotic Regimen based on organism and sensitivities!!!
-This is because the organisms (S. Bovis, Viridians Strep, Enterococci, Staph aureus, HACEK group, and
culture negative endocarditis have different regimens)
31.
32.
33.
34.
35. Duration is 4-6 weeks.
First, the counting of days of recommended duration of therapy should
begin on the first day on which blood cultures were negative in cases in
which blood cultures were initially positive.
At least 2 sets of blood cultures should be obtained every 24 to 48 hours
until bloodstream infection is cleared.”
Blood cultures to ensure eradication
36. Bartonella spp treated with doxycycline for 6 weeks +gentamicin for 2 weeks
Brucella is treated with at least 3 drugs: Aminoglycoside+tetracycycline
+rifampicin.
Fungal infection traditionally primary indication of valvular surgery and
amphotericin b
Candida endocarditis can be treated with azole containing antimicrobial agent
with or without amphotericin.
37. EASE TRIALS
Kang DH,et al. Early surgery vs conventional treatment for IE
Clinical question: among pt. with left sided native valve endocarditis at high risk embolic events, does early surgery
reduce mortality and embolic event as compared to conventional treatment?
Outcomes: Comparison are early surgery vs. Conventional treatment
Primary outcome
In hospital mortality or embolic event- 3%vs 23% (p=0.03)
Secondary outcomes
In-hospital mortality 3% vs.3% (p=01.00)
All cause mortality at 6 months 3% vs.5%(p=0.59)
Mortality, Embolic events ,recurrence of IE at 6months3% vs.28% p=0.02
38. NATIVE VALVE
ENDOCARDITIS)
i. Acute aortic insufficiency or mitral regurgitation with heart failure
ii. Acute aortic insufficiency with tachycardia and early closure of the mitral valve on
echocardiogram
iii. Evidence of valve dysfunction and persistent infection after a prolonged period (7-10 days)
of appropriate therapy, provided there are no noncardiac causes of infection
iv. Evidence of annular or aortic abscess, sinus or aortic true or false aneurysm, valvular
dehiscence, rupture, perforation, or fistula
v. Recurrent emboli after appropriate antibiotic therapy
vi. Fungal endocarditis
39. Early prosthetic valve endocarditis (<2 month after surgery)
Heart failure with prosthetic valve dysfunction
Nonstreptococcal endocarditis
Evidence of perivalvular leak, annular or aortic abscess, sinus or aortic true or
false aneurysm, fistula formation, or new-onset conduction disturbances
Persistent bacteremia after 7-10 days of appropriate antibiotic therapy, with
noncardiac causes for bacteremia excluded
40. Indication of antithrombotic therapy.
1. Pts with mechanical prosthetic valves after ECHO/HEAD CT
SCAN to exclude ischemic stroke, intracerebral hemorrhage.
2. Atrial fibrillation with IE with CHADS2 score > 2
3. Atrial fibrillation with mitral stenosis with IE regardless of the
CHADS2 score
42. IE prophylaxis for dental procedures is reasonable only for patients with
certain underlying cardiac conditions
Dental procedures that involve manipulation of gingival tissue or the
periapical region of teeth or perforation of the oral mucosa.
Administration of antibiotics solely to prevent endocarditis is not
recommended for patients who undergo a genitourinary or gastrointestinal
tract procedure
43.
44. Ugandan Guideline:
“Prophylactic Amoxicillin 2g plus Gentamicin 1 hour before plus 500mgs 8 hourly
for 48 hours after dental extraction and tonsillectomy in individuals with cardiac
valve defects “
Alternate Guideline examples: (all 30 to 60 mins prior to surgery)
Amoxicillin 2grams x once; Ceftriaxone 1 gram IM or IV x once; Clindamycin 600
mg IM or IV x once
45. Valvular regurgitation- bacterial infection infiltrate and proliferate in the
valve tissues and destroy the leaflet integrity leading to regurgitation.
Perivalvular abscess or fistula
Leaflet perforation( valve perforation)
True aneurysm formation
Emboli formation( myocardium infarction)
Metastatic infection from bacteremia.
46. Overall mortality rate from both native and prosthetic valve endocarditis remain fairly
high ranging from 17-36%
Viridian group streptococci endocarditis have lower risk of death while, pts with
S.Aureus ,fungal and zoonotic endocarditis have high mortality rate.
Heart failure and CNS events are the most frequent cause of dead.
Endocarditis recur in about 12-16% and more common in IDUs, elderly people,
prosthetic valve
Rate of relapse varies depending on causative organism. Viridians group streptococci
have lower rates 5% but more diffuse to eradicate organism may have higher rates.
47. 1. Goldman-Cecil,Medecine,25th edition, Elsevier
2. Upto date
3. David S.Bach,MD,FACC,Infective endocarditis in adults;2015 AHA update.
4. Wilson, W., Taubert, K. A., Gewitz, M., Lockhart, P. B., Larry, M., Levison, M., Bolger, A.,
Cabell, C. H., Takahashi, M., Baltimore, R. S., Newburger, J. W., Strom, B. L., Tani, L. Y.,
Bonow, R. O., Pallasch, T., Shulman, S. T., Rowley, A. H., Burns, J. C., Ferrieri, P., …
Durack, D. T. (2007). Downloaded from http://circ.ahajournals.org/ by guest on January 6,
2012. https://doi.org/10.1161/CIRCULATIONAHA.106.183095
5. Cultures, B., Therapy, A., & Evaluation, A. (n.d.). Infective Endocarditis - Adult – Inpatient
Clinical Practice Guideline.
6. Yun, S., Ph, D., Song, J., & Ph, D. (2012). Early Surgery versus Conventional Treatment for
Infective Endocarditis.
In 2000-2011,the incidence of IE in the US increased from 11 per 100,000 population to 15 per 100.000 population.
Older patients are likely to develop degenerative valve diseases and require valve replacemet both which are associated with increased risk of IE.
--dental procedures that involves manipulation if gingival tissues or periapical region of the teeth or perforation, increase risk of IE.
Preexisting with heart dx are more likely to ne immunosuppressed and more likely to acquire IE
--Mitral valve prolapse is associated with viridians group streptococci. Aortic valve dx( sclerosis,stenosis,and regurgitation occur in 12-30% of IE cases.
Pts on chronic dialysis are at risk of IE DUE to intravenous acces,calcific valvular disease and immune impairment.
--Bacteraemia is associated with the presence of central line Cather, or invasive intravenous procedures.peritoneovenous shunt for control of intractable ascites and ventriculoarterial shunt for mnx of hydrocephalus .
Staphylococcal spp are the most common cause of IE in health associated IE.
streptococcal IE is the most commonest of community acquired IE.
Zoonotic endocarditis is usually culture negative commonly caused by bartonella spp, c.burneti and brucella spp
Pts with ulcerative of the colon due to CA, or inflammatory bowel disease have predilection develop IE due to streptococcus bovis.
Fungal endocarditis is often difficult to diagnose and treat. Common in pts with hx of injection drug users, recent cardiac valve surgery, prolonged us of indwelling vascular catheter especially those for total parental nutrition.aspergillus and cadida spp are common.
Native valve acute endocarditis usually has an aggressive course. Virulent organisms, such as Staphylococcus aureus and group B streptococci, are typically the causative agents of this type of endocarditis. Underlying structural valve disease may not be present.
Subacute endocarditis usually has a more indolent course than the acute form. Alpha-hemolytic streptococci or enterococci, usually in the setting of underlying structural valve disease, typically are the causative agents of this type of endocarditis.
Early prosthetic valve endocarditis occurs within 60 days of valve implantation. Staphylococci, gram-negative bacilli, and Candida species are the common infecting organisms.
Late prosthetic valve endocarditis occurs 60 days or more after valve implantation. Alpha-hemolytic streptococci, enterococci, and staphylococci are the common causative organisms.
Particulate matter (talc) may damage the endothelial tricuspid valve,( 8-10mcm pass pulmonary capillary and damage endothelial of mitral and aortic valve.
Heroin damage tricuspid valve
Non bacterial thrombotic endocardium can occur in pts with systemic illness such as marantic endocarditis in malignancy or wasting diseases or libman sack endocarditis in systemic lupus erythematous .
Implantable devices disrupts the endothelial surface and predispose the infection and formation of the biofilm
In IDUs right sided infective endocarditis (tricuspid valve IE is often more frequent than pulmonic valve. Triscupid valve IIE do not have murmur. Metastatic infection is common due to S.aureus.metastatic infection can involve the kidney,eyes,brain and spine.
Pneumonia and septic pulmonary embolism is common.
IDUs with IE have coinfection with HIV,HEP C and B
Osler node are small painful nodules on palmar surface of the finger or toes. Its an immunological phenomena initiated by micro emboli.
Janeway lesion are hemorrhagic non painful macules on palm or sole. Origin of emboli
Splinter hemorrhage are nonblinding, linear brownish red lesion in the nail bed parallel to the direction of the nail bed.
JANEWAY (vascular lesions) – actual septic emboli, “microabscesses” – FOOT picture
OSLER NODES (immunologic) – deposition of immune complexes, leading to massive inflammatory response, can be associated with necrosis, PAINFUL
Janeway lesion is a VASCULAR phenomena!!
Echo finding suggestive of surgery: severe valvular regurgitation with signs of heart failure, abcess, large vegetation >10mm,prosthetic dehiscence or increased in vegetation size despite appropriate antibiotic therapy
With either TTE/TEE methods, a valvular vegetation is defined as a discrete mass of echogenic material adherent at point of the leaflet surface and distinct in character from the remainder of the leaflet
Less common ECHO finding in IE: pseudoaneurysm, fistula, valve perforation.
Both TTE/TEE have high specificity (98%)when used as part of the diagnostic evaluation of suspected endocarditis. contrast TEE has much higher sensitivity (90-95%)than TTE (48-68%)
TEE should also be repeated in a pt. with an initially positive TEE if clinical features suggest a new intracardiac complication and after the completion of antibiotics.
ECG. Suggestive of an aortic ring abscess or frank MI.
Definitive antibiotic treatment of infective endocarditis is guided by antimicrobial susceptibility testing of the responsible pathogen isolated from clinical cultures
Parenteral antibiotics
Short term therapy = high risk of relapse
Inpatient (or daily outpt follow-up) for first 2 weeks of tx
zoonotic endocarditis is usually culture negative and mostly commonly caused by bartonella spp,C.burneti,brucella spp.
Other culture negative: Chlamydia spp, Legionella spp, Tropheryma whipplei.
Study randomized pt. with newly dx left sided NVE to either surgery with 48hrs of randomization or conventional therapy alone, consisting of antibiotics and supportive care with surgery performed on urgent indication or persistent symptoms despite completion of antibiotics. Primary outcome endpoint was in-hospital death or occurrence of embolic events within weeks of randomization.
Persistent fever and leukocytosis with negative blood cultures.
Increase in vegetation size despite appropriate antimicrobial therapy
Recurrent peripheral embolus despite therapy
Vegetation of any size seen on or near the prosthesis
Anticoagulant/antiplatelet therapy is not indicated to reduce the risk of thrombolytic complication since they don’t reduce the risk of embolism in infective endocarditis.
CNS IMAGING should be performed to detect intracranial mycotic aneurysm or CNS bleeding in pt with severe localized headache, neurological deficient or meningeal signs.
Abscess formation is mostly due to s. aureus.
Myocardium abscess formation is the increasing cause morbidity and mortality in IE