Download TF_Infectious Endocarditis_2015_cleaned

Infectious
Endocarditis
-prevention, diagnosis, treatment.
ESC Guidelines 2015.
Tomasz Fabiszak
1
2
Why IE is a problem?
1.
The mortality due to IE have decreased, but this disease still carries a
poor prognosis and a high mortality.
3
Why IE is a problem?
2.
IE is not a uniform disease, but presents in a variety of different forms,
varying according to:
•
•
•
•
•
the initial clinical manifestation,
the underlying cardiac disease (if any),
the microorganism involved,
the presence or absence of complications,
underlying patient characteristics.
4
Why IE is a problem?
3.
IE requires a collaborative approach involving:
•
•
•
•
•
•
•
•
•
primary care physicians,
cardiologists,
surgeons,
microbiologists,
infectious disease specialists,
neurologists,
neurosurgeons,
radiologists,
pathologists.
5
Definition
Endovascular infection, which may include:
• the structure of the heart (valves, endocardial wall)
• large vessels of the chest (patent ductus arteriosus,
coarctation of the aorta, arteriovenous fistula)
• foreign material placed in the cavities of the heart (valvular
prostheses, intracardiac electrodes, surgically created
vascular connections)
6
Definition
The most characteristic part of the disease is vegetationvarious size formation, composed of platelets, fibrin and red
blood cells, mixed with bacteria and inflammatory cells.
Abnormal
blood flow
Endothelial
damage
Non-infected
vegetation
(nonbacterial
thrombotic
endocarditis)
IE
Bacteria
7
Epidemiology
•
•
•
•
3-10/100 000/year
The peak incidence (14,5/100 000/y)-70-80 years of age
Male > Female - 2:1
Older > younger
• Female have a worse prognosis and undergo valve surgery
less frequently than their male counterparts.
8
Changing Epidemiology of Native Valve
Infective Endocarditis
Distribution of the number of cases of native valve infective endocarditis in
non-intravenous drug users during the study period.
Rev Esp Cardiol. 2011;64:594-8. - Vol.964
Classification
ACTIVE
RECURRENCE
RELAPSE
•IE with persistent fever and positive
blood cultures, or
•Active inflammatory morphology found
at surgery, or
•Patient still under antibiotic therapy, or
•Histopathological evidence of active IE
•Repeat episode of IE
caused by the same
microorganism < 6
months after the
initial episode
REINFECTION
•Infection with the
different
microorganism
•Repeat episode of IE
caused by the same
microorganism > 6
months after the
initial episode
11
Predispositions
• mitral valve prolapse- the most common cause of IE
on native valve in adults (risk 3,5-8,2%)
• rheumatic valvular disease- 7-18% of IE (F-mitral
valve, M-aortic valve)
• congenital heart disease- 10-20% young adults, 9%
adults (patent ductus arteriosus, VSD, bicuspid aortic
valve, coarctation of the aorta)
• no risk factors- 25-47%
12
Etiology
•
•
•
•
Streptococci - 50-70% of NVE
Staphylococci -25% of NVE
Enterococci- 10% of NVE
Gram-negative bacilli [HACEK]
–
–
–
–
–
–
–
–
–
Haemophilus parainfluenzae,
H. aphrophilus,
H. paraphrophilus,
H. influenzae,
Actinobacillus
actinomycetemcomitans,
Cardiobacterium hominis,
Eikenella corrodens,
Kingella kingae,
K. denitrificans
• Other: bacterias, fungi, rickettsiae,
mycobacteria, mycoplasma,
chlamydia.
13
Etiology
Streptococci
Staphylococci
Enterococci
Other
5%
10%
25%
60%
14
Pathophysiology
Inflammatory process
Proliferation and destruction of the valves
Leaflet perforation, papilary muscle
rapture
Abscesses, fistulas
Penetration into the myocardium- AVconductions disorders
15
IE - prevention
1. Antibiotic prophylaxis limited to pts:
1.
2.
with the highest risk of IE
undergoing the highest risk dental procedure
2. Good oral hygiene and regular dental review more important
than antibiotic prophylaxis
3. Aseptic measures – mandatory for venous catherization and
invasive procedures
16
22
Diagnosis
• Clinical features
• Echocardiography
• Microbiological diagnosis
• Diagnostic criteria and their limitations
23
IE - Symptoms
Symptoms
•
•
•
•
•
•
•
•
•
Fever - 80 - 90%
Shivers - 40 - 75%
Sweating - 25%
Lack of apetite - 25-55%
Weight Loss - 25 - 35%
Malaise - 25 - 40%
Headaches
Muscles, joints, back- aches
Confusion
25
Signs
• Heart murmur (new) - 80 - 90%
• Peripheral embolism -10 -40% (arteries of the brain, Valsalva’s
sinus, mesenteric artery, splenic artery, coronary arteries,
pulmonary artery, vasa vasorum)
• Strokes - 15 - 20%
• Splenomegaly - 15 - 50%
• Osler’s nodes - 7 - 10%
• Janeway lesions - 6 - 10%
• Petechiae - 5 - 15%
• Roth's spots - 4 - 10%
• Clubbed fingers - 7 - 10%
26
Janeway lesions
• Non-tender, small erythematous or haemorrhagic macular
or nodular lesions on the palms.
• Pathologically, the lesion is described to be a microabscess of
the dermis with marked necrosis and inflammatory infiltrate
not involving the epidermis.
• caused by septic emboli which deposit bacteria, forming
microabscesses.
• Janeway lesions are distal, flat, ecchymotic, and painless.
27
28
Osler's nodes
• Painful, red, raised lesions found on the hands and feet.
• Result from the deposition of immune complexes.
• Osler's nodes and Janeway lesions are similar, but Osler's
nodes present with tenderness and are of immunologic origin
29
30
Splinter haemorrhage
31
Roth's spots
• Retinal hemorrhages with white or pale centers composed
of coagulated fibrin.
• They are typically observed via fundoscopy (using
an ophthalmoscope to view inside the eye) or slit lamp exam.
• Usually caused by immune complex mediated vasculitis often
resulting from bacterial endocarditis.
32
Roth’s spots
33
WARNING
•
•
•
•
•
Roth's spots may also be observed with:
Leukemia
DM
Pernicious anaemia
Ischemic events
HIV retinopathy
34
Conjunctival haemorrhages
35
Clubbed
fingers
36
Right-sided endocarditis
•
•
•
•
•
•
Cough
Chest pain
Dyspnoea
Hemoptysis
Lung infarction, lung abscess, pneumothorax
Occasionally, extensive damage to the lungs, leading to RDS
(respiratory distress syndrome)
• 60 - 75% of IE in drug abused persons
37
Lab findings
• Inflammation parameters:
–
–
–
–
CRP
OB
LEU
Gamma-Globulins
• Anaemia
• Erythrocyturia
38
Blood cultures
ECHO
IE
DIAGNOSIS
40
Venous blood culture:
•
•
•
•
At least 3x
Separated by at least 1 hour
Each time with a different injection site
5 - 10 ml blood into tubes with liquid medium (aerobic bacteria), and
semi-solid (anaerobic bacteria)
• If possible, before the start of antibiotic therapy
• If antibiotic therapy was started, 3 days after its discontinuation
• The probability of (+) culture depends on the quality of blood and prior
antibiotic therapy (in Poland 40 - 50% of blood cultures are negative)
49
ECHO
Transthoracic
(TTE)
Transesophageal
(TEE)
• reveals vegetations
in about 50% of the
patients (45 - 75%)
• reveals vegetations on
native valve in about
90-94% of the patients
• reveals vegetations on
prostetic valve in about
90-100% of the patients
52
(e.g. frailty,
immunosuppression,
renal or pulmonary
diseaase)
Antimicrobial therapy
General principles:
• Blood culture guided
• I.v.
• Therapy duration:
– 2-6 weeks for native valve IE
– 6-8 weeks for prosthetic valve IE
• Empirical therapy
– Negative blood cultures
– the patient’s condition is poor
55
56
57
58
59
60
Indications for surgery
1. Heart failure
2. Uncontrolled infection
3. Prevention of embolism
Emergency = within 24 hrs
Urgent = a few days
Elective = after 1-2 weeks
61
Indications for surgery
62
Indications for surgery
63
Indications for surgery
64
Right-sided infective endocarditis
• Right-sided IE accounts for 5–10% of cases of IE
• May occur in patients with a PPM, ICD, central venous catheter, or CHD,
this situation is most frequently observed in IVDAs
• Tricuspid valve is the usual site of infection in IVDAs, pulmonary and
eustachian valve infection may also be observed
• Diagnostic features include respiratory symptoms and fever
• TTE is of major value in these patients
• Despite relatively low in-hospital mortality, right-sided IE has a high risk of
recurrence in IVDAs and a conservative approach to surgery is
recommended in this group
66
Outcomes after discharge and long-term prognosis
• The risk of recurrence amongst survivors of IE varies between 2.7 and
22.5%.
• Progressive HF can occur as a consequence of valve destruction, even
when infection is healed
• Long-term survival is 60–90% at 10 years
• Relapse- Repeat episode of IE caused by the same microorganism < 6
months after the initial episode
• Reinfection- Infection with the different microorganism, repeat episode
of IE caused by the same microorganism > 6 months after the initial
episode
68
69
Infective endocarditis on pacemakers and implantable
defibrillators
•
•
•
•
•
•
•
One of the most difficult forms of IE to diagnose
Must be suspected in the presence of frequently misleading symptoms,
particularly in elderly patients
Blood cultures are positive in 77% of cases
Staphylococci are the most frequent pathogens
The Duke criteria are difficult to apply in these patients because of low sensitivity
In the majority of patients must be treated by prolonged antibiotic therapy and
device removal (4-6 weeks)
Infective endocarditis on pacemakers and implantable defibrillators is
associated with high mortality
70
Infective endocarditis on pacemakers and implantable
defibrillators
•
•
•
•
Blood cultures – 3 or more
Lead-tip culture at CIED explantation
TTE not sensitive enough -> go for TOE / ICE
Suspected CDRIE with +ve cultures, but –ve
ECHO -> radiolabelled leukocyte scintigraphy
and 18F-FDG PET/CT scanning
71
Infective endocarditis on pacemakers and implantable
defibrillators
Indications for hardware removal*:
•Definite CDRIE (+prolonged antibiotic therapy)
•Presumably isolated pocket infection
•Occult infection w/o another apparent source of infection
•NVE/PVE + no evidence of associated device infection ??
*Percutaneous extraction preferred even with vegetations >10 mm
72
Thank you
for
your attention
73