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Bacteial Endocarditis in Pediatrics

Bacteial Endocarditis in Pediatrics
by

Hania Salama

on 9 January 2014

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Transcript of Bacteial Endocarditis in Pediatrics

Content Specs for Infective Endocarditis
Know the epidemiology of infective endocarditis, including risk factors
Know that a blood culture is the most important test for the diagnosis of infective endocarditis
Know the microbiology of infective endocarditis
Know the clinical manifestations of infective endocarditis
Know the management of infective endocarditis
Know the indications for antibiotic prophylaxis in children with congenital heart lesions
Know the drugs of choice for the prophylaxis of infective endocarditis

Infective Endocarditis
Hania Salama, M.D.
12/12/13

Epidemiology
Children at
highest risk of adverse outcome
after infective endocarditis include:
An artificial heart valve or who have had a heart valve repaired with artificial material.
history of endocarditis.
heart transplant with abnormal heart valve function
Certain congenital heart defects including:
Cyanotic congenital heart disease (birth defects with oxygen levels lower than normal), that has not been fully repaired, including children who have had a surgical shunts and conduits.
A congenital heart defect that's been completely repaired with artificial material or a device for the first six months after the repair procedure.
Repaired congenital heart disease with residual defects, such as persisting leaks or abnormal flow at or adjacent to a prosthetic patch or prosthetic device
Common Microorganisms
Most common pathogens in children
Streptococcus viridians and S bovis as well as Staphylococcus aureus

Other potential organisms
include Enterococcus, coagulase-negative Staphylococcus, fungi, and a group of bacteria referred to as the HACEK organisms
Clinical Manifestations of Infective Endocarditis
Etiology
an infection that involves the endocardial surface of the heart.
composed of microorganisms trapped in a fibrin mesh that extends into the bloodstream
most commonly on the cardiac valves
also may be seen on the margins of VSD, along chordae supporting AV valves, along vascular grafts, along foreign material such as prosthetic valve
Require high doses of bactericidal antibiotics for an extended period of treatment, because antibiotics must reach the organisms by passive diffusion through the fibrin mesh
Haemophilus
Actinobacillus actinomycetemcomitans
Cardiobacterium hominis
Eikenella corrodens
Kingella kingae

These gram-negative oral and pharyngeal flora are fastidious, slow-growing, and often require growth factors and carbon dioxide to provide positive test results in isolation.

HACEK organisms
Early Symptoms
Nonspecific
Low-grade fever with afternoon elevations, fatigue, myalgia, arthralgia, headache, and, at times, chills, nausea, and vomiting.
New or changing heart murmurs
are common, particularly with associated heart failure.
Splenomegaly and petechiae

Serious Neurologic Complications
Cardiac Complications
Pulmonary Complications
Classic Skin Findings

Especially high suspicion in children with congenital heart disease and child with unexplained illness after dental or surgical procedure
Serious neurologic complications:
embolic strokes, cerebral abscesses, mycotic aneurysms, and hemorrhage are most often associated with staphylococcal disease and may be late manifestations
Meningismus, increased intracranial pressure, altered sensorium, and focal neurologic
Cardiac complications:
Myocardial abscesses may occur with staphylococcal disease
damage the cardiac conducting system
cause heart block
rupture into the pericardium and produce purulent pericarditis.
Pulmonary and other systemic emboli
associated with fungal disease
Classic skin findings
develop late in the course of the disease
rarely seen in appropriately treated patients, may represent vasculitis produced by circulating antigen-antibody complexes
Osler nodes
Janeway lesions
splinter hemorrhages
Splinter Hemorrhages

Osler Nodes:
Painful, palpable red lesions usually on fingers/toes. They are caused by immune complexes.

Janeway Lesions:
Non-painful, macular lesions, usually on palms/soles, caused by septic emboli, more common in S. aureus endocarditis

Splinter Hemorrhages
Nonspecific finding associated with trauma most commonly, also seen with subacute bacterial endocarditis and scleroderma

Embolic phenomena Review
Three-dimensional echocardiogram of a retro-aortic abscess seen as an echolucent space behind the aortic valve in a teenaged boy with staphylococcal endocarditis.

Nadas’ Pediatric Cardiology, 467-476, 2006

Positive blood culture
Elevated erythrocyte sedimentation rate; may be low with heart or renal failure
Elevated C-reactive protein
Anemia
Leukocytosis
Immune complexes
Hypergammaglobulinemia
Hypocomplementemia
Cryoglobulinemia
Rheumatoid factor
Hematuria
Renal failure: azotemia, high creatinine (glomerulonephritis)

Lab/Imaging Findings
Chest radiograph:
bilateral infiltrates, nodules, pleural effusions

Echocardiographic
evidence of valve vegetations, prosthetic valve dysfunction or leak, myocardial abscess, new-onset valve insufficiency
The Duke Criteria:
Two major criteria, one major and three minor, or five minor criteria suggest definite endocarditis.

Major criteria include:
Blood culture positive for IE
Typical microorganisms consistent with IE from 2 separate blood cultures: Viridans streptococci, Streptococcus bovis, HACEK group, Staphylococcus 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 h apart; or all of 3 or a majority of ≥4 separate cultures of blood (with first and last sample drawn at least 1 h apart)
 Single positive blood culture for Coxiella burnetii or anti–phase 1 IgG antibody titer >1:800
Evidence of endocardial involveEchocardiogram positive for IE (TEE recommended for patients with prosthetic valves, rated at least “possible IE” by clinical criteria, or complicated IE [paravalvular abscess]; TTE as first test in other patients) 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; or abscess; or new partial dehiscence of prosthetic valve; new valvular regurgitation (worsening or changing or preexisting murmur not sufficient)
Endocarditis treatment depends on the organism isolated from the blood or tissue of the infected patient
.
Empirical therapy
: vancomycin plus gentamicin in patients without a prosthetic valve and when there is a high risk of S. aureus enterococcus or viridians streptococci

S. Auerus:
6 week of B-lactamase-resistant penicillin, Oxacillin or nafcillin or vancomycin IV for patients with penicillin allergy
Enterococcus:
6 wk Ampicillin and Gentamicin IV
Viridans streptococci:
4 to 6 wk with penicillin G or Ampicillin IV

Culture negative Endocarditis: should be treated for 4 to 6 weeks with antibiotics covering for staphylococcal, streptococcal (including S. pneumonia and HACEK organisms

Fungal Endocarditis: medical therapy (amphotericin B with 5-fluorocystosine)often unsuccessful and require surgical intervention

Surgery is reserved for patients who develop severe congestive heart failure from severe valve regurgitation, fungal infection, and annular abscess that is not responding to antibiotic therapy.

Management of Infective Endocarditis
20-25% mortality, despite antibiotics treatment
50-60% of children will end up with serious morbidity
Most common complication is heart failure caused by vegetations involving the aortic or mitral valve
Myocardial abscesses and toxic myocarditis
Systemic emboli, often with central nervous system manifestations,
Pulmonary emboli may occur in children with ventricular septal defect or the tetralogy of Fallot

Other complications include
mycotic aneurysms, rupture of a sinus of Valsalva, obstruction of a valve secondary to large vegetations, acquired ventricular septal defect, and heart block as a result of involvement (abscess) of the conduction system.

Additional non-cardiac complications include meningitis, osteomyelitis, arthritis, renal abscess, purulent pericarditis, and immune complex-mediated glomerulonephritis.
Prognosis and Complications
The dentist in your community health center’s clinic calls you with a question about a patient that he is seeing later that day. The child is 14 years old and underwent surgical repair of his congenital heart disease 5 years ago. The dentist wants to know if this patient’s cardiac condition warrants antibiotic prophylaxis for a routine dental cleaning. Of the following, the condition for which antibiotic prophylaxis is MOST appropriate when the patient is at risk for bacteremia is:

A. atrial septal defect transcatheter device closure with no residual shunt
B. complete atrioventricular septal defect repair with moderate mitral regurgitation
C. prosthetic aortic valve with no residual stenosis or regurgitation
D. tetralogy of Fallot repair with mild pulmonary stenosis and regurgitation
E. ventricular septal defect repair with aortic insufficiency

The dentist in your community health center’s clinic calls you with a question about a patient that he is seeing later that day. The child is 14 years old and underwent surgical repair of his congenital heart disease 5 years ago. The dentist wants to know if this patient’s cardiac condition warrants antibiotic prophylaxis for a routine dental cleaning. Of the following, the condition for which antibiotic prophylaxis is MOST appropriate when the patient is at risk for bacteremia is:

A. atrial septal defect transcatheter device closure with no residual shunt
B. complete atrioventricular septal defect repair with moderate mitral regurgitation
C. prosthetic aortic valve with no residual stenosis or regurgitation
D. tetralogy of Fallot repair with mild pulmonary stenosis and regurgitation
E. ventricular septal defect repair with aortic insufficiency

PREP 2010 – Q 165
C. prosthetic aortic valve with no residual stenosis or regurgitation

Antibiotic prophylaxis should be reserved for those children and adults who have the greatest risk for a poor outcome from endocarditis.

Patients who have congenital heart disease and are at the greatest danger of poor outcomes from endocarditis and for whom preventive antibiotics prior to a dental, oral or respiratory procedures are worth the risks include those who have:
Prosthetic cardiac valves
Previous infective endocarditis
Unrepaired cyanotic congenital heart disease, including palliative shunts and conduits
Completely repaired congenital heart defect with prosthetic material or device, during the first six months after the procedure
Repaired congenital heart disease with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device (which inhibit endothelialization)
Cardiac transplant recipients with cardiac valvulopathy
Rheumatic heart disease if prosthetic valves or prosthetic material used in valve repair

PREP 2010 - 165 Answer
Infective Endocarditis Antibiotic Prophylaxis
1. Keane, John F.; Lock, James E., and Fyler Donald C. Nadas’ Pediatric Cardiology, Pg 467-476.

2. Kliegman, Robert M.; Stanton, Bonita M.D.; St. Geme, Joseph; Behrman, Richard E.; Schor, Nina F (2011-06-01). Nelson Textbook of Pediatrics: Expert Consult (Kindle Locations 153689-153695). Elsevier Health.

3. Werdan, K. et al. (2013) Mechanisms of infective endocarditis: pathogen–host interaction and risk states Nat. Rev. Cardiol. doi:10.1038/nrcardio.2013.174
References
a | Valve colonization as a consequence of mechanical injury. (1) Nonbacterial thrombotic endocarditis. (2) Bacteria bind to coagulum and colonize it during transient bacteraemia. Adhered monocytes release tissue factor and cytokines. (3) More platelets are attracted and become activated, and the vegetation grows. (4) Endothelial cells are infected, and can be lysed by bacterial products, or bacteria can persist inside the cells by changing phenotype into small colony variants.

b | Valve colonization as a consequence of an inflammatory endothelial lesion. (1) Activated endothelial cells express integrins that promote the local deposition of fibronectin; bacteria such as Staphylococcus aureus adhere to this protein. (2) Bacteria are internalized, and endothelial cells release tissue factor and cytokines, causing blood clotting and promoting the extension of inflammation and vegetation formation. (3) Infected endothelial cells can be lysed by bacterial products, or bacteria can persist inside the cells by changing phenotype into small colony variants.
Werdan, K. et al. (2013) Mechanisms of infective endocarditis: pathogen–host interaction and risk states Nat. Rev. Cardiol. doi:10.1038/nrcardio.2013.174
This is infective endocarditis. The aortic valve demonstrates a large, irregular, reddish tan vegetation.Virulent organisms, such as Staphylococcus aureus, produce an "acute" bacterial endocarditis, while some organisms such as Streptococcus viridans produce a "subacute" bacterial endocarditis
[http://library.med.utah.edu].
Extensive, large vegetations on mitral valve leaflets extending onto chordae tendinae
[http://infectionnet.org/supporting-content/bacterial-endocarditis-pathology/]
Acute: IE:
-Commonly S. aureus but also Group A/B/C/G steps, Pseudomonas

Subacute: IE:
-More commonly S. viridans but also Group D streps, HACEK, fungi

Prosthetic valve:
-<6 months since insertion (associated with organisms from procedure e.g. coagulase –ve Staph (S. epidermidis) and S. aureus)
->6 months since insertion (associated with any causative organism)

Native valve:
◦Viridans streptococci (54%)- alpha-haemolytic organisms, from URT, pencillin-resistant
-S mutans dental plaques
-S sanguis from oropharynx
-S mitis from oropharynx
-S. bovis from gut,
-S milleri from gut

◦Staph aureus (19%)
◦Enterococci (9%) from colon, more resistant
◦Other strep (5%)
◦Candida spp (4%) from skin, lemon juice used to dissolve heroin, in IVDU

Minor criteria include:
Predisposition, predisposing heart condition, or IDU
Fever, temperature >38°C
Vascular phenomena, major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, and Janeway’s lesions
Immunologic phenomena: glomerulonephritis, Osler’s nodes, Roth’s spots, and rheumatoid factor
Microbiological evidence: positive blood culture but does not meet a major criterion as noted above* or serological evidence of active infection with organism consistent with IE

10 to 15% of cases not confirmed by positive BCx
Referred to as Culture Negative Endocarditis
Diagnosis
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