Infective Endocarditis Associated professor Kantemirova M.G.

Infective Endocarditis

Infective endocarditis: 1. acute and subacute bacterial endocarditis 2. nonbacterial endocarditis caused by- viruses, -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. 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 actino- mycetemcomitans, 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 II. SYMPTOMS of infectious toxic syndrome Fever Chills Chest and abdominal pain Arthralgia, myalgia Dyspnea Malaise Night sweats Weight loss

CLINICAL MANIFESTATIONS 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, 2. fever 3. embolic-vascular signs, 4. immune complex phenomena (glomerulonephritis, arthritis, rheumatoid factor, Osler nodes, Roth spots) 5. a single positive blood culture or serologic evidence of infection 6. echocardiographic signs not meeting the major criteria 7. the presence of newly diagnosed clubbing, splenomegaly, splinter hemorrhages, and petechiae; 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 than immune stimulation - thymus preparations 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