4. Introduction
• Infection of the endocardial surface of the heart (heart valves and
mural endocardium)
• Increasing in prevalence due to
• introduction of conduits (tubes),
• prosthetic materials and intracardiac devices
makes more susceptible
to infection in view of
the presence of these
foreign materials.
6. IE according to localisation of infection and presence of intracardiac material
• Left-sided native valve IE
• Left-sided PVE
>> Early PVE < 1 year after valve surgery
>> Late PVE > 1 year after valve surgery
• Right-sided native valve IE
• Device related IE
IE according to the mode of acquisition
• Healthcare associated IE
• Community acquired IE
• Intravenous drug abuseassociated IE
Acute endocarditis
• High grade and persistant fever
• Rapidldamages cardiac to structures,
• Seeds extracardiac sites
IF untreated progresses to death within weeks.
Subacute endocarditis
• Follows an slower course(slow cardiac damage)
• Rarely metastasizes; and
• Gradually progressive unless complicated by a major embolic event or a ruptured mycotic aneurysm.
7.
8. Common Organisms
• Native Valve and late prosthetic valve : Strep Viridans
• Early Prosthetic valve : Staph Epidermidis and Staph Aureus
• IVDU esp tricuspid valve is : S. aureus
• Non-infective:
• systemic lupus erythematosus (Libman-Sacks)
• malignancy: marantic endocarditis
• Culture negative causes
• Brucella
• Coxiella burnetii
• HACEK: Hemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
• Bartonella
• Prior antibiotic therapy
9.
10. Pre-existing risk factors
• Previous history of IE.
• Pre-existing cardiac disease.
• Presence of prosthetic valves or prosthetic cardiac material.
• Presence of intracardiac devices.
• History of IVDU.
• Presence of chronic intravenous access (e.g. haemodialysis catheters,chemoports
and neonate/paediatric patients with indwelling central venous catheters).
• Presence of CHD Elderly or immunocompromised patients.
• Co-existing conditions such as diabetes, human immunodeficiency virus (HIV)
• infection and malignancy.
11. General Clinical Presentation
• Fever (87%) with chills, poor appetite and weight loss.
• Heart failure may be present at admission (up to 58%)
• New or altered cardiac murmur (50-85%)
• Embolic events may also cause presenting symptoms (27-30%)
Fever + New/Altered murmur : IE until proven otherwise
• Pt do not often present with classic textbook manifestations of subacute or chronic endocarditis.
19. Investigation
• FBC : Raised white cell count and Low hb
• UFEME : Ery positive
• Inflammatory marker
• Elevated CRP and ESR.
• Renal profile
• LFT
• ECG
• Chest X-ray
• Blood cultures : three set from three different sites prior to
antibiotics
If blood cultures negative after 5 days of incubation and no history of prior antimicrobial use, consider
blood culture negative infective endocarditis (BCNIE), which can be caused by fungi or fastidious
microorganisms, and perform the appropriate microbiological tests.
20. Definite IE Pathological criteria:
Microorganisms demonstrated by culture or HPE of a vegetation, a vegetation
that has embolised, or an intracardiac abscess specimen;
or pathological lesions; vegetation or intracardiac abscess confirmed by HPE
showing active endocarditis
Clinical criteria:
2 major criteria
or
1 major criterion and 3 minor criteria
or
5 minor criteria
Possible IE 1 major criterion and 1 minor criterion
or
3 minor criteria
Rejected IE Firm alternative diagnosis explaining evidence of IE
or resolution of IE syndrome with antimicrobial therapy for ≤ 4 days
or no pathological evidence of IE at surgery or autopsy with antimicrobial
therapy for ≤ 4 days
or does not meet criteria for possible IE as above
21. Major Criteria
Blood culture positive for IE Evidence of endocardial involvement
Typical microorganisms consistent with IE from 2
separate blood cultures:
• VGS, Streptococcus bovis, HACEK group, S. aureus
Or community-acquired enterococci in the absence
of a primary focus
Or microorganisms consistent with IE from
persistently positive blood cultures defined as follows:
>> At least 2 positive cultures of blood samples drawn
> 12 hours apart
>>Or all of 3 or a majority of ≥ 4 separate cultures of
blood (with first and last sample drawn at least 1
hour apart)
• Single positive blood culture from Coxiella burnetii
or phase 1 IgG antibody titres > 1:800
Echocardiogram positive for IE defined as follows:
• Oscillating intracardiac mass on valve or supporting
structures, in the path of regurgitant jets, or on
implanted material in the absence of an alternative
anatomic explanation
• Abscess
Or new partial dehiscence of prosthetic valve
Or new valvular regurgitation (worsening or changing
or pre-existing murmur not sufficient)
22. Minor
criteria
Predisposition: predisposing heart condition or IVDU
Fever: temperature > 38°C
Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic
aneurysm, intracranial haemorrhage, conjunctival haemorrhages and Janeway
lesions
Immunological phenomena: glomerulonephritis, Osler nodes, Roth spots and
rheumatoid factor
Microbiological evidence: positive blood cultures but does not meet a major
criterion as noted above (excludes single positive cultures for coagulase
negative staphylococci and microorganisms that do not cause endocarditis) or
serological evidence of active infection with microorganism consistent with IE
24. Surgical or autopsy findings Echocardiography findings
Vegetation Infected mass attached to an
endocardial structure or on
implanted intracardiac material
Oscillating or non-oscillating
intracardiac mass on valve or
other endocardial structures, or on
implanted intracardiac material
Abscess Perivalvular cavity
with necrosis and purulent material
not communicating with the
cardiovascular lumen
Thickened, non-homogeneous
perivalvular area with echodense or
echolucent appearance
Pseudoaneurysms Perivalvular cavity communicating
with the cardiovascular lumen
Pulsatile perivalvular
echocardiographic-free space, with
colour-Doppler detected
Perforation Interruption of endocardial tissue
continuity
Interruption of endocardial tissue
continuity traversed by colour-
Doppler
Fistula Communication between two
neighbouring cavities through a
perforation
Colour-Doppler communication
between two neighbouring cavities
through a perforation
Valve aneurysm Saccular outpouching of valvular
tissue
Saccular bulging of valvular leaflet
tissue
Dehiscence of a
prosthetic valve
Dehiscence of the prosthesis Paravalvular regurgitation identified
by TTE/TEE, with or without rocking
motion of the prosthesis
29. The major goals of management of IE
are:
•To eradicate the infectious agent from
the endocardium.
•To address the complications of the
infection, both intra and extracardiac.
30. Things to monitor in Ward(1)
•General well being – septic looking, GCS
•Temperature : Fever usually resolves in a
few days after appropriate antibiotics
started
•Daily ECG – PR interval (conduction delay)
31. Things to monitor in Ward(2)
• Examined regularly for ssx of the following complications
• Heart failure: symptoms should be treated with standard medical therapy
and its severity regularly assessed. Heart failure may persist despite
microbiological resolution.
• Embolic events. - related to the migration of cardiac vegetations : liver,
spleen, kidneys and abdominal mesenteric vessels
• Common sites
• left-sided IE are the brain and spleen
• Right-sided IE – Pulmonary embolism
• Ongoing sepsis.
• Neurological sequelae. –ischemic and hemorhagic stroke, mycotic aneuryms,
cerebral abscess.
32. Things to monitor in Ward (3)
• Blood investigations
• Regular Inflammatory markers.
• Regular FBC to monitor WBCs, Hb and Plt
• Blood cultures
• BUSE for sign of AKI and it’s resolution.
• Echocardiography
• Monitor vegetation
• Resolution of IE: vegetations gradually reduce in size, mobility and increase in
echogenicity. In the long-term, these vegetations may not disappear or even change in
size, even with clinical treatment success.
• Risk of embolisation: vegetations increase in sizeand mobility.
35. Empirical
In our setting we use IV Ceftriaxone as empirical antibiotic
Add Cloxacillin if suspected Staph Aureus(IVDU or PVE)
Or
Vancomycin for suspected MRSA
1. Community-acquired native valves or
late prosthetic valves (≥ 12 months
post-surgery) endocarditis
Usually strep viridans
Ampicillin + Gentamicin (Low dose) +/-
Cloxacillin**
Or
Vancomycin + Gentamicin (Low dose)
2. Early PVE (< 12 months post-surgery) or
nosocomial and non-nosocomial
healthcare associated endocarditis.
• Usually MRSA
Vancomycin + Gentamicin (Low dose) +/-
Rifampicin** +/- Cefepime*
36. Definitive
Based on the culture
Ideally ,minimum inhibitory concentration(MIC) level is needed to
determine the number/dosage of the antimicrobial.
37. Native Valves
Methicillin-
Susceptible
Staphylococci (MSSA)
Complicated right sided
endocarditis: renal failure, extra
pulmonary metastatic infections
such as osteomyelitis, aortic or
mitral valve involvement,
meningitis, or infection by MRSA
Left sided endocarditis and
complicated right sided :
Cloxacillin 2gm IV in q4h for 6
weeks +/- Gentamicin 1mg/kg
IV/IM q8h for 3-5 days
Right sided endocarditis (tricuspid
valve) in uncomplicated
endocarditis :
Cloxacillin 2gm IV q4h for 2 weeks
+
Gentamicin 1mg/kg IM/IV q8h for
2 weeks
39. Native Valves
MRSA
left-sided and right-sided
Vancomycin
15-20 mg/kg/ dose (actual body weight)
IV every 8-12 hourly; not to
Exceed 2 g/dose
For 4-6 weeks
Prosthetic Valves
MRSA
Vancomycin 25-30mg/kg loading dose then
15mg/kg IV q12h for > 6 weeks, not to exceed
2gm/24h
PLUS
Rifampicin 300mg PO q8h for > 6 weeks
PLUS
Gentamicin 1mg/kg IM/IV q8h for 2 weeks
40. Surgical Intervention
Indications
• Severe valvular incompetence, haemodynamic instability or heart
failure.
• Uncontrolled sepsis and paravalvular extension of infection.
• Fungal or multiresistant endocarditis.
• Large vegetations (> 10 mm for left-sided IE) and recurrent systemic
embolisation.
NBTE also arises as a result of a hypercoagulable state; this gives
rise to mara n tic endocarditis (uninfected vegetations seen in patients
with malignancy and chronic diseases) and to bland vegetations complicating systemic lupus erythematosus and the antiphosphoIipid
antibody syndrome.
ECG:
&gt;&gt; Should be done daily to monitor heart rhythm and to look for conduction
defects. This is especially important in cases of prosthetic valve IE or
native valve IE as they are at higher risk for extension of infection to the
conduction pathways which can occur very abruptly.
&gt;&gt; Conduction defects may be a sign of perivalvular extension of infection
especially in cases involving the aortic valve.
lowest concentration of an antimicrobial (like an antifungal, antibiotic or bacteriostatic) drug that will inhibit the visible growth of a microorganism.
**For patients with suspected S. aureus infections (such as IVDU or patients with prosthesis) and acute presentation
**Rifampicin is only recommended for PVE and it should be started 3-5 days later than vancomycin and gentamicin
^Cefepime is indicated if local Epidemiology suggests for non-HACEK Gram- negative rod infections (such as Pseudomonas)
lowest concentration of an antimicrobial (like an antifungal, antibiotic or bacteriostatic) drug that will inhibit the visible growth of a microorganism.
The undamaged endothelium is resistant to infection by most bacteria and to thrombus formation.
Endothelial injury (e.g.at the site of impact of high relocity blood jets or on the low-pressure side of a cardiac structural lesion) allows either direct infection by virulent organisms or the development of a platelet-fibrin thrombus-acondition called nonbacterial thrombotic endocarditis (NBTE). This thrombus serves as a site of bacterial attachment during transient bacteremia. The cardiac conditions most commonly resulting in NBTE are mitral regurgitation， aortic stenosis， aortic regurgitation， ventricular septal defects， and complex congenital heart disease. NBTE also arises as a result of a hypercoagulable state; this gives rise to marantic endocarditis (uninfected vegetations seen in patients with malignancy and chronic diseases) and to bland vegetations.
