Transcript - Cardiothoracic Surgery

MEDICAL MANAGEMENT OF
INFECTIVE ENDOCARDITIS IN
CHILDREN
Ndubueze Ezemba
Chris Barnard Division of Cardiothoracic Surgery, University of
Cape Town
Hannes Meyer Symposium 13 April 2008
OUTLINE
Introduction
Epidemiology
Classification
Aetiopathogenesis
Management
Investigation
Treatment
Outcome
Conclusion
INTRODUCTION
DEFINITION
Infective endocarditis may be defined as conditions in which structures
of the heart, most frequently the valves, harbour an infective process
that leads to valvar dysfunction, localized or generalized sepsis, or sites
for embolism (1).
It includes acute, subacute, and chronic processes; infection of
bacterial, viral, rickettsial, or fungal aetiology.
It may be native valve endocarditis (NVE) or prosthetic endocarditis.
It is the most feared complications of structural heart lesions.
EPIDEMIOLOGY
The incidence of infective endocarditis(IE) is
difficult to estimate because true population
characteristics, including both cases and total
population at risk, are difficult to obtain.
There is an increasing incidence of IE in children.
One paediatric cardiology unit puts the incidence as
high as 32/1000 hospital admissions in children <
16 years of age (2).
CLASSIFICATION
MODE OF PRESENTATION
Acute
Subacute
Chronic
MICROBIOLOGICAL ORGANISM
Bacterial
Viral
Rickettsial
Fungal
Culture negative
CLASSIFICATION
STATUS OF THE HEART
Native Endocarditis
Replacement Device Endocarditis
i.
valve prostheses
ii.
Patch
iii. Shunts
iv. Homografts
v.
pacemaker
AETIOPATHOGENESIS:
Aetiology
Microbiology of Infective Endocarditis
A. Gram – Positive Cocci
a. Streptococci
Viridans streptococci remain the major
cause of endocarditis in children.
b. Staphylococci
Streptococci and staphylococci account
90% of culture positive IE (3,4).
for
80 –
AETIOPATHOGENESIS
Staphylococci cause at least 30 – 40% of cases of IE, and 80 – 90% of
these are due to coagulase-positive S. aureus.
This species is the causative agent in most cases of acute IE.
The organism may attack normal heart valves in approximately onethird of the patients.
The course is frequently fulminant when it involves the mitral or aortic
valve, with widespread metastatic infection, and result in death in
approximately 25 – 30 % of the patients.
AETIOPATHOGENESIS
Myocardial abscesses (with conduction disturbances),
purulent pericarditis, and peripheral foci of suppuration
are more common in staphylococcus IE than in other
forms of infective endocarditis.
The rare entity of neonatal endocarditis is also often
caused by S. aureus; survival is unusual.
THUS STAPHYLOCOCCUS AUREUS
ENDOCARDITIS FROM THE START MAY BE
CONSIDERED A SURGICAL DISEASE.
AETIOPATHOGENESIS
B.
Gram-Negative Bacilli
i. Enterobacteriaceae, Salmonella species are important cause of IE.
These organisms have an affinity for abnormal cardiac valves,
usually left sided heart valves.
ii. Pseudomonas endocarditis is rare in children being commoner in
replacement device endocarditis.
c.
HACEK and other unusual Gram-Negative Bacteria
The HACEK (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella,
Kingella) bacteria are fastidious and originally required 2 to 3 weks for
primary isolation.
They produce large large friable vegetations, frequent emboli, and the
development of CCF.
AETIOPATHOGENESIS
D. Gram-Positive Bacilli
i.
Corynebacteria(diphtheroids)
ii.
Listeria monocytogenes
E. Anaerobic Bacteria
i.
Bacteroides fragilis
These are all rare causes of infective endocarditis in children as in
adults.
AETIOPATHOGENESIS
F.
G.
Fungal
Most patients who have fungal endocarditis have undergone reconstructive
cardiovascular surgery, or may have received prolonged intravenous
antibiotic therapy.
The overall cure rate for fungal IE is poor(14.5%) in part due to;
a.
poor penetration of antifungal agents into the vegetation
b.
low toxic-therapeutic ratio of the available
antifungal agents
c.
the usual lack of fungicidal activity with these agents
A cure is usually impossible without surgical intervention.
Very Unusual Microorganisms
i.
Coxiella burnetii (Q fever)
ii.
Chlamydia
AETIOPATHOGENESIS
H.
“CULTURE –NEGATIVE” ENDOCARDITIS
The prevalence of “culture negative” endocarditis in a recent study in Western
Cape is put at >50% 5.
Factors responsible for this include;
i.
prior administration of antibiotics
ii.
cultures taken towards the end of a
chronic course
iii.
mural endocarditis as in VSDs
iv.
Slow growth of fastidious organisms
such as anaerobes
v.
fungal endocarditis
vi.
endocarditis due to obligate intracellular
parasites, eg rickettsia
When strict diagnostic criteria are applied blood cultures are negative in only about
5% of patients with IE (6).
PATHOGENESIS
Predisposing Factors to IE
Rheumatic heart disease
Congenital heart diseases
Previous cardiac interventional procedures
With a few exceptions, the endothelial lining of the heart and valves is generally resistant
to infection.
Development of endocarditis involves a complex interaction between;
i.
The host immune system
ii.
The haemostatic mechanism
iii.
Cardiac anatomic chambers
iv.
Surface properties of the microorganism
v.
Enzymes and toxins produced by microorganism
vi.
Peripheral events that have caused the bacteraemia
PATHOGENESIS
Endothelial damage is the inciting event
Platelet – fibrin deposition provides a milieu for bacterial colonization
Bacteria must be present to colonize the vegetation
Adherence of the microoganism to the vegetation or the intact valve endothelium mediated by
adhesion molecules(MSCRAMMS)
Multiplication and internalization within the host cells
Invasion of the endothelium causing cell death and disruption of the endothelial surface further
promotes platelet – fibrin deposits.
Fig:1 steps in the development of
endocarditis lesion
Fig. 2 Sites of high-velocity jets where endocarditis vegetations
occur.
The areas of vegetation
formation
are similar to those where blood
flow injury is likely to occur.
These are;
a. atrial side of AV valves
b. ventricular side of semilunar
valves
c. jet lesions(McCallum patches)
PATHOPHYSIOLOGY
Endocarditis vegetation on native valve interferes with
valve motion resulting in regurgitation
Vegetation growth results in leaflet perforation and
may cause chordal rupture
Infection extension into surrounding structures such
as sinotubular juction, annulus, myocardium,
conduction tissue
PATHOPHYSIOLOGY
Cavitation in the aortic wall leads to periaortic abscess
Abscess may occasionally erode into pericardium or another
cardiac chamber.
Large vegetations on prosthetic valves can lead to both
regurgitation and obstruction.
Vegetations on patches leads to dehiscence
Vegetation may embolize
Complications of IE
• Congestive heart failure
50–60%
• Embolization
• CVA
15%
20–25%
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•
•
•
Other emboli
Limb 2–3%
Mesenteric 2%
Splenic 2–3%
Complications of IE
•
•
•
•
•
•
•
•
•
•
•
Glomerulonephritis
Anular abscess
Myocotic aneurysm
Conduction system involvement
CNS abscess
Other less common complications
Pericarditis
Myocarditis
Myocardial infarction
Intracardiac fistula
Metastatic abscess
15–25%
10–15%
10–15%
5–10%
3–4%
1–2%
MANAGEMENT
DIAGNOSTIC MEASURES
Clinical features
Blood culture, FBC, CUE, LFT
- blood culture results provide much useful information that has
immediate importance for management decisions.
i. Provides the identity of the presumed organism
ii. May point to the source of bacteraemia which is useful in preventive
measures
iii. Provides initial guidance with regard to antibiotic therapy
iv. It gives important prognostic information about the likelihood of
surgical intervention.
DIAGNOSTIC MEASURES
Optimal procedures must be used in obtaining samples for
blood culture (6):
a. Optimal antiseptic skin preparation
b. Optimal timing of blood culture
c. Optimal number of blood cultures
d. The volume must be optimal;
i.
ii.
iii.
iv.
1-2ml/culture for neonates
2-3ml/culture for infants aged 1 month to 2 years
3-5ml for older children
10-20ml for adolescents
e.
Length of incubation must be adequate
DIAGNOSTIC MEASURES
Echo: Characteristics of IE
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•
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•
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Vegetation
Abscess
Aneurysm
Fistulae
Leaflet perforation
Valvular dehiscence
ECHO
Fistula formation during IE: infected sinus of Valsalva
aneurysm that has ruptured into RVOT and RA
DIAGNOSTIC MEASURES
ECG
CXR
OTHERS
CT
SEROLOGY
MAKING A DIAGNOSIS: THE
MODIFIED DUKE’S CRITERIA
The modified Duke criteria*
1. Major criteria
a. Microbiologic
Typical microorganisms isolated from two separate blood cultures, or
microorganism isolated from persistently positive blood cultures, or
single positive blood culture for
Coxiella burnetii (or phase I IgG antibody titer to C. burnetii 1:800)
b. Evidence of endocardial involvement
New valvular regurgitation or positive echocardiogram (intracardiac
mass, or periannular abscess, or new dehiscence of prosthetic valve)
MODIFIED DUKE’S
CRITERIA
2. Minor criteria
a. Predisposition to infective endocarditis
i. Previous infective endocarditis
ii. Injection drug use
iii. Prosthetic heart valve
iv. Mitral valve prolapse
v. Cyanotic congential heart disease
vi. Other cardiac lesions creating turbulent flow within the intracardiac chambers
b. Fever
c. Vascular phenomena (eg, embolic event)
d. Immunologic phenomena (eg, presence of serologic markers, glomerulonephritis,
Osler’s nodes, or Roth spots)
e. Microbiologic findings not meeting major criteria
*Definite endocarditis requires 2 major criteria or 1 major and 3 minor criteria or 5 minor.
Possible endocarditis requires 1 major and 1 minor or 3 minor criteria
TREATMENT
Principles for medical treatment of IE (7)
A. Bactericidal therapy must be used
ideally culture-directed
Adequate dosing of the appropriate antibiotic
(monitor the MIC).
B. Prolonged course of therapy.
C. Other adjuctive measures
diurectics
ACE inhibitors
inotropes
ventilatory support.
E. Evaluation of clinical response and early surgical consultation
TREATMENT
OUTCOME/PREDICTORS OF MORTALITY
(8)
1. Vegetation size ≥20mm
2. Age<1 year
3. Presence of heart failure
4. S. aureus as causative organism
CONCLUSION
Infective endocarditis remains a common disease in
children.
Streptococci and Staphylococci account for over 80% of
cases.
Staphylococci infective endocarditis is usually a fulminant
disease.
Best medical treatment hinges on culture directed
antimicrobial with early surgical consultation.
References
1.
Kouchoukos NT, Blackstone EH, Doty DB, Hanley FL, Karp RB (eds). Cardiac Surgery 3ed 2003;
Churchill Livingstone, Philadelphia. Chapter 15:689-711
2.
Sadiq M, Nazir M, Sheikh SA. Infective Endocarditis in Children- incidence, pattern, diagnosis and
treatment in a developing country. Int J Cardiol 2001; 78:175-182
3.
Bashore TM, Cabell C, Fowler V. Update on infective endocarditis. Curr Probl Cardiol 2006;
31:274-352
4.
Koegelenberg CFN, Doubell AF, Orth H, Reuter H. Infective endocarditis in the Western Cape
Province of South Africa; a three-year prospective study. Q J Med 2003; 96:217-225
5.
Koegelenberg CFN, Doubell AF, Orth H, Reuter H. Infective Endocarditis: improving the
diagnostic yield. Cardiovasc J South Afr 2004; 15:14-20
6.
Towns ML, Reller LB. Diagnostic methods. Current best practices and guidelines for isolation of
bacteria and fungi in infective endocarditis. Cardiol Clin 2003; 21:197-205
References
7.
Sexton DJ, Spelman D. Current best practices and guidelines. Assessment and management of
complications in infective endocarditis. Cardiol Clin 2003; 21:273-282
8.
Yoshinaga M, Niwa K, Niwa A, Ishiwada N, Takahashi H, Echigo S. Risk Factors for InHospital Mortality During Infective Endocarditis in Patients With Congenital Heart Disease.
Am J Cardiol 2008; 101:114-118