Download Infective Endocarditis

Infective Endocarditis
Associated professor
Kantemirova M.G.
Infective Endocarditis
Infective endocarditis:
• 1. acute and subacute bacterial endocarditis
• 2. nonbacterial endocarditis caused byviruses, -fungi - other microbiologic agents.
IE can occur in children without any abnormal
valves or cardiac malformations
Edematous cusp of mitral valve: the onset
of vegitation formation (fibrin)
Special risk groups
• 1. survivors of cardiac surgery
• 2. patients taking immunosuppressant
medications
• 3. patients who require chronic intravascular
catheters
• 4. patients with CHD and acquired heart
defects (rheumatic heart disease)
• 5. intravenous drug users
ETIOLOGY.
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Viridans-type streptococci (α-hemolytic streptococci) and Staphylococcus aureus
are the leading causative agents for endocarditis in pediatric patients.
Other organisms cause endocarditis less frequently
in ≈6% of cases, blood cultures are negative for any organisms. Many patients with
culture-negative endocarditis have Q fever (Coxiella burnetii) or Bartonella species.
No relationship exists between the infecting organism and the type of congenital
defect, the duration of illness, or the age of the child.
Staphylococcal endocarditis is more common in patients with no underlying heart
disease;
viridans group streptococcal infection is more common after dental procedures;
group D enterococci are seen more often after lower bowel or genitourinary
manipulation;
Pseudomonas aeruginosa or Serratia marcescens is seen more frequently in
intravenous drug users;
and fungal organisms are encountered after open heart surgery.
Coagulase-negative staphylococci are common in the presence of an indwelling
central venous catheter.
Bacterial Agents in Pediatric
Infective Endocarditis
• COMMON: NATIVE VALVE OR OTHER CARDIAC LESIONS
Viridans group streptococci (S. mutans, S. sanguis, S. mitis), Staphylococcus
aureus, Group D streptococcus (enterococcus) (S. bovis, S. faecalis)
• UNCOMMON: NATIVE VALVE OR OTHER CARDIAC LESIONS
Streptococcus pneumoniae, Haemophilus influenzae, Coagulage-negative
staphylococci, Coxiella burnetii (Q fever), Neisseria gonorrhoeae, Brucella,
Chlamydiae, Bartonella, HACEK group: Haemophilus species (H.
paraphrophilus, H. parainfluenzae, H. aphrophilus), Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and
Kingella species.
• PROSTHETIC VALVE
Staphylococcus epidermidis, Staphylococcus aureus, Viridans group
streptococcus, Pseudomonas aeruginosa, Serratia marcescens, HACEK group
Pathogenic factors
• Prolonged bacteremia
• The presence in the heart the site of endocardial or intimal
erosion that results from the turbulent flow (congenital
heart lesions in which blood is ejected at high velocity
through a hole or stenotic orifice: VSD, left-sided valvular
disease such as aortic stenosis, tetralogy of Fallot, and
systemic-pulmonary arterial communications (patent
ductus arteriosus or Blalock-Taussig shunts; congenital
bicuspid aortic valves and mitral valve prolapse with
regurgitation)
• Changes in coagulation with tendency to hypercoagulation
(vegetation is a complex of bacteria , fibrin, platelets)
Predisposing factors
• A surgical procedure (Tonsillectomy or adenoidectomy,
Bronchoscopy with a rigid broncoscope,
Gastrointestinal Tract, Genitourinary Tract, Cystoscopy)
• Dental procedure
• Poor dental hygiene in children with cyanotic heart
disease
• Heart surgery
• Primary bacteremia with Staphylococcus aureus
(purulent dermatitis, otitis, lympfodenitis)
CLINICAL MANIFESTATIONS
• I. HISTORY
• Prior congenital or rheumatic heart disease
• Preceding dental, urinary tract, or intestinal
procedure
• Intravenous drug use
• Central venous catheter
• Prosthetic heart valve
CLINICAL MANIFESTATIONS
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II. SYMPTOMS of infectious toxic syndrome
Fever
Chills
Chest and abdominal pain
Arthralgia, myalgia
Dyspnea
Malaise
Night sweats
Weight loss
CLINICAL MANIFESTATIONS
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III. SIGNS of cardio-vascular syndrome
Tachycardia
New or changing murmur
Heart failure
Arrhythmias
Muffled heart souds
Hemorrhagic rash
CLINICAL MANIFESTATIONS
• IV. SYMPTOMS of immune pathological syndrome
and embolic syndrome
• Embolic phenomena (Roth spots, petechiae, splinter
nail bed hemorrhages, Osler nodes, CNS or ocular
lesions)
• Glomerulonepfritis
• Splenomegaly
• Petechiae, hemorrhagic rash
• Embolic strokes
• Pulmonary and other systemic emboli
• Clubbing
Vasculitis produced by circulating antigen-antibody
complexes:
• Osler nodes (tender, pea-sized intradermal
nodules in the pads of the fingers and toes)
• Janeway lesions (painless small erythematous
or hemorrhagic lesions on the palms and
soles)
• splinter hemorrhages (linear lesions beneath
the nails)
LABORATORY data
• 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
• Rheumatoid factor
• Hematuria
• Renal failure: azotemia, high creatinine (glomerulonephritis)
• Chest radiograph: bilateral infiltrates, nodules, pleural effusions
• Echocardiographic evidence of valve vegetations, prosthetic valve
dysfunction or leak, myocardial abscess, new-onset valve insufficiency
The most important for diagnosis of infective endocarditis is
a positive blood cultures and evidence of vegetations
• The absence of vegetations does not exclude
endocarditis, and vegetations are often not visualized
in the early phases of the disease or in patients with
complex congenital heart lesions.
• Three to five separate blood collections should be
obtained. The blood can be cultured on enriched
media for longer than usual (>7 days) – it increases the
chance to reveal pathological agent. Antimicrobial
pretreatment of the patient reduces the yield of
blood cultures to 50–60%.
Vegetation in the tricuspid valve
Big vegetation, later – abscess
Haemophilus parainfluenzae Endocarditis
Value of Echocardiography with Doppler:
• identify the size, shape, location, and mobility of the
lesion
• presence of valve dysfunction (regurgitation,
obstruction) can be determined
• asses left ventricular function
• predicts embolic complications (Echocardiography may
also be helpful in predicting embolic complications,
given that lesions >1 cm and fungating masses are at
greatest risk for embolization.
• reveals valve vegetations, prosthetic valve dysfunction
or leak, myocardial abscess
The modified Duke criteria of infective endocarditis:
I. Major criteria : 1. positive blood cultures (two separate cultures for a
usual pathogen, two or more for less typical pathogens)
2. evidence of endocarditis on echocardiography
(intracardiac mass on a valve or other site, regurgitant flow near a
prosthesis, abscess, partial dehiscence of prosthetic valves, or new valve
regurgitant flow).
II. Minor criteria: 1. predisposing conditions,
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2. fever
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3. embolic-vascular signs,
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4. immune complex phenomena (glomerulonephritis,
arthritis, rheumatoid factor, Osler nodes, Roth spots)
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5. a single positive blood culture or serologic evidence of
infection
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6. echocardiographic signs not meeting the major criteria
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7. the presence of newly diagnosed clubbing, splenomegaly,
splinter hemorrhages, and petechiae;
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8. a high erythrocyte sedimentation rate; a high C-reactive
protein level; microscopic hematuria
Two major criteria, one major and three minor, or five minor criteria
suggest definite endocarditis.
PROGNOSIS AND COMPLICATIONS.
• Despite the use of antibiotic agents, mortality remains at 20–25%.
• The most common 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 VSD or the tetralogy
of Fallot,
• Heart block as a result of involvement (abscess) of the conduction
system
• Additional complications include meningitis, osteomyelitis, arthritis,
renal abscess, and immune complex–mediated
glomerulonephritis.β
TREATMENT.
• Antibiotic therapy should be instituted immediately once a definitive
diagnosis is made. Main principles: 1. IV 2. According to sensitivity of
agent 3. High doses 4. Not less 4-6 weeks (start therapy β-lactam
antibiotics or Ceftriaxone sodium + amynoglycosides or Vancomycin
hydrochloride )
• Immune therapy : replacement first – IVIG –( IgM ) - Pentaglobin
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than immune stimulation - thymus preparations
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• Treatment of cardiac failure
• Correctiom of coagulation changes (to lyse intracardiac vegetations,
thrombs: anticoagulants – heparin, fraxiparin, fragmine; recombinant
tissue plasminogen activation )
• NSAID – in myocarditis, pericarditis
• Fungal endocarditis - the drugs of choice are amphotericin B (liposomal or
standard preparation) and 5-fluorocytosine.
• Surgical intervention for infective endocarditis is indicated for severe
aortic or mitral valve involvement with intractable heart failure.
PREVENTION.
• Antimicrobial prophylaxis before various procedures and other forms of
dental manipulation may reduce the incidence of infective endocarditis in
susceptible patients
Special risk groups(Susceptible patients):
• 1. survivors of cardiac surgery
• 2. patients taking immunosuppressant medications
• 3. patients who require chronic intravascular catheters
• 4. patients with CHD and acquired heart defects (rheumatic heart disease)
• 5. intravenous drug users
• Antimicrobial prophylaxis: oral or IV/IM amoxicillin, amoxiclav,
clindamycin, cepfalosporins II,III
Prophylaxis before 1. A surgical procedure (Tonsillectomy or
adenoidectomy, Bronchoscopy with a rigid broncoscope, Gastrointestinal
Tract, Genitourinary Tract, Cystoscopy)
2. Dental procedure