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Infective
Endocarditis
PELİN ÖZKAN
FATİH KÖKDERE
EGEMEN SAV
Infective Endocarditis
Infective endocarditis (IE) is defined as an infection of the endocardial surface of the
heart, which may include one or more heart valves, the mural endocardium, or a septal
defect. Its intracardiac effects include severe valvular insufficiency, which may lead to
intractable congestive heart failure and myocardial abscesses. If left untreated, IE is
generally fatal.
• Infective endocarditis (IE) is a peculiar disease for
at least three reasons:
• First, neither the incidence nor the mortality of the
disease have decreased in the past 30 years.
• Secondly, IE is not a uniform disease, but presents
in a variety of different forms.
• Thirdly, guidelines are often based on expert
opinion because of the low incidence of the
disease
• The incidence of IE ranges from one country to
another within 3–10 episodes/100 000 personyears.
• the incidence of IE was very low in young patients
but increased dramatically with age—the peak
incidence was 14.5 episodes/100 000 person-years
in patients between 70 and 80 years of age.
• male:female ratio is 2:1, although this higher
proportion of men is poorly understood.
• female patients may have a worse prognosis
classification
• according to the site of infection
• the presence or absence of intracardiac foreign
material
• left-sided native valve IE,
• left-sided prosthetic valve IE,
• right-sided IE,
• device-related IE
Classification and definitions of infective endocarditis
• Mitral Valve: 85% (Left atrium/ventricle)
Common site for Strep viridans group
• Aortic valve: 55% (Left ventricle)
Emboli would effect systemic organs brain,
kidneys, spleen
• Tricuspid valve: 20% (Right atrium/ventricle)
Common site for IV drug users (Staph. spp)
Emboli to lung
• Pulmonary valve: 1% (Right ventricle)
1. Infective endocarditis with positive blood cultures:
a. Infective endocarditis due to streptococci and
enterococci:
Oral (formerly viridans) streptococci form a mixed
group of microorganisms, which includes species
such as S. sanguis, S. mitis, S. salivarius, S. mutans,
and Gemella morbillorum.
b. Staphylococcal infective endocarditis
s, S. aureus was the most frequent cause not only of
IE but also of prosthetic valve IE.
Pathophysiology
1. The valve endothelium
• The normal valve endothelium is resistant to
colonization and infection by circulating bacteria
• Endothelial damage may result from mechanical
lesions provoked by turbulent blood flow,
electrodes or catheters, inflammation, as in
rheumatic carditis, or degenerative changes in
elderly individuals, which are associated with
inflammation, microulcers, and microthrombi.
Pathophysiology
2. Transient bacteraemia
• The role of bacteraemia has been studied in animals
with catheterinduced NBTE.
• Both the magnitude of bacteraemia and the ability of
the pathogen to attach to damaged valves are
important.
• Bacteraemia does not occur only after invasive
procedures, but also as a consequence of chewing and
tooth brushing.
• Most cases of IE are unrelated to invasive procedures.
Pathophysiology
3. Microbial pathogens and host defences
• Classical IE pathogens (S. aureus,
Streptococcus spp., and Enterococcus spp.)
adhere to damaged valves
• Trigger platelet activation
Infective Endocarditis
Infective Endocarditis
Population at risk
• Patients with a prosthetic valve or with prosthetic material used for cardiac valve
repair
• Patients with previous IE
• Patients with untreated cyanotic congenital heart disease (CHD) and those
with CHD who have postoperative palliative shunts, conduits or other
prostheses
Risk faktörleri
• Intravenous drug abuse
• Artificial heart valves and pacemakers
• Acquired heart defects
Calcific aortic stenosis
Mitral valve prolapse with regurgitation
• Congenital heart defects
• Intravascular catheters
Risk faktörleri
• Rheumatic heart disease
• Prosthetic heart valves
• IV drug use
• Intravenous catherization/shunt procedures
• Congenital heart defects
• patent ductus arteriosus, intraventricular shunts
• Degenerative cardiac lesions
Infective Endocarditis
Prevention
• Antibiotic prophylaxis is recommended only for patients with the highest risk of IE
undergoing the highest risk dental procedures.
• Good oral hygiene and regular dental review are more important than antibiotic
prophylaxis to reduce the risk of IE.
• Aseptic measures are mandatory during venous catheter manipulation and during any
invasive procedures in order to reduce the rate of health care-associated IE.
• Although prophylaxis should be restricted to high-risk patients, preventive measures
should be maintained or extended to all patients and in particular to those with cardiac
disease.
Infective Endocarditis
1- Prophylaxis for dental procedures
2- Prophylaxis for non-dental procedures
• Respiratory tract procedures
• Gastrointestinal or genitourinary procedures
• Dermatological or musculoskeletal procedures
• Body piercing and tattooing
• Cardiac or vascular interventions
• Healthcare-associated infective endocarditis
Clinical Features
Symptoms
• Acute
• High grade fever and
chills
• SOB
• Arthralgias/ myalgias
• Abdominal pain
• Pleuritic chest pain
• Back pain
• Subacute
•
•
•
•
•
•
•
Low grade fever
Anorexia
Weight loss
Fatigue
Arthralgias/ myalgias
Abdominal pain
N/V
The onset of symptoms is usually ~2 weeks or less
from the initiating bacteremia
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
Janeway Lesions
1.
2.
3.
4.
5.
More specific
Erythematous, blanching macules
Nonpainful
Located on palms and soles
Microabscess of the dermis with marked necrosis and inflammatory
infiltrate not involving the epidermis.
Osler’s Nodes
1. More specific
2. Painful and erythematous nodules
3. Located on pulp of fingers and toes
Splinter Hemorrhages
1.
2.
3.
4.
5.
Nonspecific
Nonblanching
Linear reddish-brown lesions found under the nail bed
Usually do NOT extend the entire length of the nail
vessel damage from swelling of the blood vessels (vasculitis) or tiny
clots that damage the small capillaries (microemboli).
Petechiae
1. Nonspecific
2. Often located on extremities
or mucous membranes
DIAGNOSIS
Microbiological diagnosis
• Blood culture:
• At least three sets are taken at 30-min intervals.
•
each containing 10 mL of blood,.
•
incubated both aerobic and anaerobic atmospheres.
•
Sampling peripheral vein rather than from a central venous catheter .
•
using a meticulous sterile technique.
• no rationale for delaying blood sampling with peaks of
fever.
• When a microorganism has been identified, blood
cultures should be repeated after 48–72 h to check the
effectiveness oftreatment.
I.
Blood culture–positive infective endocarditis
II.
Blood culture–negative infective endocarditis 31%.
-consequence of previous antibiotic administration
-fungi or fastidious bacteria, obligatory intracellular bacteria
• systematic serological testing
Coxiella burnetii,Bartonella spp., Aspergillus spp., Mycoplasma pneumonia,
Brucella spp. and Legionella pneumophila
• specific polymerase chain reaction (PCR) assays
Tropheryma whipplei, Bartonella spp. and fungi (Candida spp., Aspergillus spp.)
Most studies using blood PCR for the diagnosis of BCNIE have highlighted the
importance of Streptococcus gallolyticus and Streptococcus mitis, enterococci, S.
aureus, Escherichia coli and fastidious bacteria, the respective prevalence of which
varies according to the status and condition.
Imaging
•
•
•
•
Echocardiography
Multislice Computed Tomography
Magnetic Resonance Imaging
Nuclear Imaging
Echocardiography
MODIFIED DUKE
CRITERIA
DIAGNOSIS
2015 ESC ALGORITHM
2015 ESC CRITERIA
INFECTIVE ENDOCARDITIS
TREATMENT
Treatment
• Treatment involves antimicrobial therapy
targeted to the identified organism.
• Surgical indications include heart failure,
uncontrolled infection, and prevention of
embolic events.
Antimicrobial Therapy
•Five important recommendations:
• The indications and pattern of use of
aminoglycosides have changed. no longer
recommended in staphylococcal NVE because their
clinical benefits have not been demonstrated, but
they can increase renal toxicity.
• Rifampin should be used only in foreign body
infections such as PVE after 3–5 days of effective
antibiotic therapy, once the bacteraemia has been
cleared.
• Daptomycin and fosfomycin have been recommended
for treating staphylococcal endocarditis and netilmicin
for treating penicillin-susceptible oral and digestive
streptococci. not available in all European countries.
• Drug treatment of PVE should last longer (at least 6
weeks) than that of native valve endocarditis (NVE) (2–
6 weeks), but is otherwise similar, except for
staphylococcal PVE, where the regimen should include
rifampin whenever the strain is susceptible.
• In NVE needing valve replacement by a prosthesis
during antibiotic therapy, the postoperative antibiotic
regimen should be that recommended for NVE, not for
PVE.
Fungal IE
• Fungi are most frequently observed in PVE and in IE
affecting IVDAs and immunocompromised patients.
• Candida and Aspergillus spp. predominate, the latter
resulting in BCNIE.
• Mortality is very high (50%), and treatment necessitates
dual antifungal administration and valve replacement.
• Most cases are treated with various forms of
Amphotericin B with or without azoles, recent case
reports describe successful therapy with the new
echinocandin caspofungin
Cure rates for NVE
• For S viridans and S bovis infection, the rate is 98%.
• For enterococci and S aureus infection in individuals
who abuse intravenous drugs, the rate is 90%.
• For community-acquired S aureus infection in
individuals who do not abuse intravenous drugs, the
rate is 60-70%.
• For infection with aerobic gram-negative organisms,
the rate is 40-60%.
• For infection with fungal organisms, the rate is lower
than 50%.
Cure rates for PVE
• Rates are 10-15% lower for each of the above
categories, for both early and late PVE.
• Surgery is required far more frequently.
• Approximately 60% of early CoNS PVE cases
and 70% of late CoNS PVE cases are curable.
*Coagulase-negative staphylococci (CoNS)
Main complications
infective endocarditis
•
Heart failure
•
Uncontrolled infection
•
systemic embolism
•
Neurological complications
•
Infectious aneurysms
•
Splenic complications
•
Myocarditis and pericarditis
•
Heart rhythm and conduction disturbances
•
Musculoskeletal manifestations
•
Acute renal failure
Heart
failure
• the most frequent complication of IE
• the most common indication for surgery in IE.
• observed in 42–60% of cases of NVE.
• Caused by worsening severe AR or MR, intracardiac fistulae and
valve obstruction
• MR or AR: Mitral chordal rupture, leaflet rupture (flail leaflet),
leaflet perforation or interference of the vegetation mass with
leaflet closure.
• dyspnoea, pulmonary oedema and cardiogenic shock (66% NYHA
Class III-IV)
• Echocardiography ,Troponin and BNP- poor prognosis.
Uncontrolled infection
•
fever + positive cultures after 7–10 days of antb treatment.
•
Persisting fever:
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•
•
•
•
•
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inadequate antb therapy,
resistant microrganisms,
infected lines,
locally uncontrolled infection,
embolic complications
extracardiac site of infection
adverse reaction to antibiotics
•
Perivalvular extension:abscess formation, pseudoaneurysms and fistulae
•
Perivalvular abscess :aortic IE (10–40% in NVE), in PVE (56–100%).In mitral IE:usually located
posteriorly or laterally. In aortic IE: in the mitral-aortic intervalvular fibrosa .
•
Risk factors for perivalvular complications : prosthetic valve, aortic location and mo:CoNS
•
Perivalvular extension should be suspected in cases with persistent unexplained fever or new
atrio-ventricular block.(serial ECG,TTE,TEO,BT,SPECT)
Systemic embolism
frequent and life-threatening complication of IE 20–50%
brain ,spleen and pulmonary branches
silent in 20–50% of patients with IE,
systematic abdominal and cerebral CT scanning (kontrast
media !)
• the risk of new events (occurring after initiation of
antibiotic therapy) is only 6–21%.
• risk of embolism:
• size, location and mobility of vegetation,(>10 mm
in length are at higher risk)
• mo (S. aureus,S. bovis, Candida spp.),
• previous embolism,
• multivalvular IE
• biological markers.
•
•
•
•
Neurological complications
• Symptomatic(TIA, intracerebral or subarachnoidal
haemorrhage, brain abscess, meningitis and toxic
encephalopathy neurological) complications occur in 15–
30%.
• silent cerebral embolisms occur in 35–60% .
• associated with an excess mortality, sequelae,
particularly in the case of stroke.
• Rapid diagnosis and antb therapy prevent a first or
recurrent NC.
• Early surgery in high-risk patients mainstay of
embolism prevention
Infectious aneurysms
• Septic arterial embolism(vaso vasaorum) %2
• Thin Wall and friable-High tendency to rupture
• Size is not predictor of rupture
• variable clinical presentation .(focal neurological deficit, headache,
confusion, Seizures)
• Cerebral CT and MRI
• İf ruptured or the size increase under antb therapy: surgical or
endovascular procedures
• İf unruptured or the size decrease under antb theraphy:follow up under
antb.
• if the infectious aneurysm is voluminous and symptomatic,
neurosurgery or endovascular therapy.
Other complications
• Splenic infarcts
• Myocarditis and pericarditis
• Heart rhythm and conduction disturbances
• Acute renal failure
Complications requiring
surgery
• Infected prosthetic material: less than 1 year
out from original heart surgery
• Refractory congestive heart failure (Leading
cause of death)
• Unresponsive infection/ continued infection
despite appropriate antibiotics
• Pt. experiences more than 1 major emboli
•Reference
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