INFECTIVE ENDOCARDITIS.pptx1235678900000

INFECTIVE ENDOCARDITIS

1. INFECTIVE ENDOCARDITIS By Namuyangu Rebecca Mudondo

2. DEFINITION Infective endocarditis is infection of the endocardium, usually with bacteria (commonly, streptococci or staphylococci) or fungi.

3. EPIDEMIOLOGY Infective endocarditis can occur at any age. Men are affected about twice as often as women. Group at highest risk: IV drug abusers, immunocompromised patients, and patients with prosthetic heart valves and other intracardiac devices

4. ETIOLOGY The normal heart is relatively resistant to infection because Bacteria and fungi do not easily adhere to the endocardial surface, constant blood flow helps prevent them from settling on endocardial structures. Thus, 2 factors are typically required for endocarditis: A predisposing abnormality of the endocardium Microorganisms in the bloodstream (bacteremia) Rarely, massive bacteremia or particularly virulent microorganisms cause endocarditis on normal valves.

5. Endocardial factors: Major predisposing factors include congenital heart defects , rheumatic valvular disease , bicuspid or calcific  aortic valves , mitral valve prolapse , hypertrophic cardiomyopathy , and prior endocarditis Occasionally, mural thrombi,  ventricular septal defects , and  patent ductus arteriosus Microorganisms  streptococci and  Staphylococcus aureus  cause 80 to 90% of cases Enterococci, gram-negative bacilli,  HACEK organisms  ( H aemophilus  sp,  A ctinobacillus actinomycetemcomitans ,  C ardiobacterium hominis ,  E ikenella corrodens , and  K ingella kingae ), and fungi cause most of the rest.

6. The actual nidus for infection is usually a sterile fibrin-platelet vegetation formed when damaged endothelial cells release tissue factor. The disease develops in 3 stages: Bacteremia : Microorganisms are present in the blood Adhesion : The microorganism adheres to abnormal or damaged endothelium via surface adhesins Colonization : Proliferation of the organism together with inflammation, leading to a mature vegetation Many of the causative microorganisms produce polysaccharide biofilms that shield them from host immune defences and impede antibiotic penetration

7. SITES Infection most commonly involves heart valves (either native or prosthetic) may also occur on the low-pressure side of the ventricular septum at the site of a defect , the mural endocardium where it is damaged by aberrant jets of blood or foreign bodies, intracardiac devices themselves. occurs most often on the left side ( eg , mitral or aortic valve). About 10 to 20% of cases are right-sided (tricuspid or pulmonic valve). IV drug abusers have a much higher incidence of right-sided endocarditis (about 30 to 70%).

8. PATHOPHYSIOLOGY Endocarditis has local and systemic consequences. Local consequences include Myocardial abscesses with tissue destruction and sometimes conduction system abnormalities (usually with low septal abscesses). Sudden, severe valvular regurgitation, →  heart failure  → death (usually due to mitral or aortic valve lesions). Aortitis  ← contiguous spread of infection. Prosthetic valve infections are particularly likely to involve valve ring abscesses, obstructing vegetations, myocardial abscesses, and mycotic aneurysms manifested by valve obstruction, dehiscence, and conduction disturbances.

9. Systemic consequences primarily due to Embolization of infected material from the heart valve Immune-mediated phenomena (primarily in chronic infection) Right-sided lesions typically → septic pulmonary emboli, which may → pulmonary infarction , pneumonia , or empyema . Left-sided lesions may embolize to any tissue, particularly the kidneys , spleen , and CNS . Mycotic aneurysms can form in any major artery. Cutaneous and retinal emboli are common. Diffuse glomerulonephritis may result from immune complex deposition.

10. CLASSIFICATION Subacute bacterial endocarditis  (SBE) Acute bacterial endocarditis  (ABE) Prosthetic valvular endocarditis  (PVE) Aggressive, usually Develops insidiously and progresses slowly (i.e., over weeks to months) usually develops abruptly and progresses rapidly (ie, over days) develops in 2 to 3% of patients within 1 yr after valve replacement and in 0.5%/ yr thereafter Often,no source of infection or portal of entry is evident source of infection or portal of entry is often evident more common after aortic than after mitral valve replacement and affects mechanical and bioprosthetic valves equally caused most commonly by streptococci (especially viridans , microaerophilic, anaerobic, and nonenterococcal group D streptococci) Enterococci less commonly by  S. aureus and epidermidis ,  Gemella morbillorum ,  Abiotrophia defectiva  (formerly,  Streptococcus defectivus ),  Granulicatella  sp, fastidious  Haemophilus  sp usually caused by  S. aureus , group A hemolytic streptococci, pneumococci, or gonococci. Early-onset infections (< 2 mo after surgery) are caused mainly by contamination during surgery with antimicrobial-resistant bacteria (e.g.,  S. epidermidis , diphtheroids, coliform bacilli,  Candida  sp,  Aspergillus  sp).

11. Subacute bacterial endocarditis  (SBE) Acute bacterial endocarditis  (ABE) Prosthetic valvular endocarditis  (PVE) Late-onset infections are caused mainly by contamination with low-virulence organisms during surgery or by transient asymptomatic bacteremias , most often with: streptococci;  S. epidermidis ; diphtheroids; and the fastidious gram-negative bacilli,  Haemophilus  sp ,  Actinobacillus actinomycetemcomitans , and  Cardiobacterium hominis . often develops on abnormal valves after asymptomatic bacteremia due to periodontal, GI, or GU infections. can affect normal valves when bacteria are virulent or bacterial exposure is massive

12. SYMPTOMS AND SIGNS Symptoms and signs vary based on the classification but are nonspecific. Subacute bacterial endocarditis  (SBE) ABE and PVE Right-sided endocarditis Initially, symptoms are vague: low-grade fever (< 39° C) and chills night sweats, fatigability, malaise, and weight loss. Arthralgia Symptoms and signs of valvular insufficiency may be a FIRST CLUE Physical examination may be normal or include : pallor , fever , change in a preexisting murmur or development of a new regurgitant murmur , and tachycardia . Initially, ≤ 15% of patients have fever or a murmur, but eventually almost all develop both Symptoms and signs similar to those of SBE, but course is MORE RAPID . Fever is almost always present initially, and patients appear toxic ; sometimes  septic shock  develops. Heart murmur is present initially in about 50 to 80% and eventually in > 90%. Rarely, purulent meningitis occurs. Septic pulmonary emboli may cause cough, pleuritic chest pain, and sometimes hemoptysis. A murmur of  tricuspid regurgitation  is typical.

13. Subacute bacterial endocarditis  (SBE) ABE and PVE Right-sided endocarditis Retinal emboli can → round or oval hemorrhagic retinal lesions with small white centers ( Roth spots ). Cutaneous manifestations include Petechiae (on the upper trunk, conjunctivae, mucous membranes, and distal extremities), painful erythematous subcutaneous nodules on the tips of digits ( Osler nodes ), Nontender Hemorrhagic Macules on the palms or soles ( Janeway lesions ), splinter hemorrhages under the nails. CNS effects (About 35% of patients), includes transient ischemic attacks ,  stroke , toxic encephalopathy , and, if a mycotic CNS aneurysm ruptures, → brain abscess and subarachnoid hemorrhage. Renal emboli may → flank pain and, rarely, gross hematuria . Splenic emboli may → LUQ pain. Prolonged infection may → splenomegaly or clubbing of fingers and toes.

14. DIAGNOSIS Suspected in patients with fever and no obvious source of infection, particularly if a heart murmur is present. Suspicion should be Very High if blood cultures are positive in patients : who have a history of a heart valve disorder, who have had certain recent invasive procedures , or who abuse IV drugs . Based on: Revised Duke Clinical Criteria for infective endocarditis and European Society of Cardiology (ESC) 2015 modified criteria Culture Echocardiography and sometimes other imaging modalities

15. REVISED DUKE CLINICAL CRITERIA FOR INFECTIVE ENDOCARDITIS Major criteria Minor criteria Two positive blood cultures for organisms typical of endocarditis drawn >12 h apart Predisposing heart disorder All of 3 or a majority of 4 or more positive blood cultures (with at least 1 h between first and last culture) for organisms consistent with endocarditis IV drug abuse Serologic evidence of  Coxiella burnetii  (IgG titer > 1:800) or one positive blood culture for  Coxiella burnetii Fever ≥ 38.0° C Echocardiographic evidence of endocardial involvement: Oscillating intracardiac mass on a heart valve, on supporting structures, in the path of regurgitant jets, or on implanted material without another anatomic explanation Cardiac abscess New dehiscence of prosthetic valve New valvular regurgitation † Vascular phenomena: Arterial embolism Septic pulmonary embolism Mycotic aneurysm Intracranial hemorrhage Conjunctival petechiae Janeway lesions Immunologic phenomena: Glomerulonephritis Osler nodes Roth spots Rheumatoid factor Microbiologic evidence of infection consistent with but not meeting major criteria Serologic evidence of infection with organisms consistent with endocarditis

16. Diagnostic Requirements for Infective Endocarditis According to the Revised Duke Criteria Clinical Diagnosis Status Criteria Definite endocarditis One of the following: 2 major criteria 1 major and 3 minor 5 minor Possible endocarditis One of the following: 1 major and 1 minor 3 minor Endocarditis rejected One of the following: Firm alternative diagnosis explaining the findings of infective endocarditis Resolution of symptoms and signs after ≤ 4 d of antimicrobial therapy No pathologic evidence of infective endocarditis found during surgery or autopsy Failure to meet the clinical criteria for possible endocarditis Adapted from Durack DT, Lukes AS, Bright DK: New criteria for diagnosis of infective endocarditis: Utilization of specific echocardiographic findings; Duke Endocarditis Service. American Journal of Medicine 96 (3):200–209, 1994.

17. European Society of Cardiology (ESC) 2015 modified criteria The ESC criteria are similar to the modified Duke criteria but include expanded imaging results as major criteria as follows: Vegetation, abscess, pseudoaneurysm, intracardiac fistula, valvular perforation or aneurysm, or new partial dehiscence of prosthetic valve identified by echocardiography Abnormal activity around a prosthetic valve (implanted > 3 mo earlier) detected by PET/CT or SPECT/CT with radiolabelled leukocytes Paravalvular lesions identified by cardiac CT The ESC also differs from the modified Duke minor criteria by specifying that detecting silent vascular phenomena by imaging only is sufficient .

18. Culture 3 blood cultures (20 mL each) should be obtained within 24 h (if presentation suggests ABE, 2 cultures within the first 1 to 2 h) Each set of cultures should be obtained from a separate, fresh venipuncture site (ie, not from preexisting vascular catheters) When endocarditis is present and no prior antibiotic therapy was given, all 3 blood cultures usually are positive because the bacteremia is continuous; at least one culture is positive in 99%.

19. NB: Premature use of empiric antibiotic therapy should be avoided in patients with acquired or congenital valvular or shunt lesions to avoid culture-negative endocarditis. If prior antimicrobial therapy was given, blood cultures should still be obtained, but results may be negative.

20. Reasons for negative blood culture: Other organism, e.g. Aspergillus sp suppression due to prior antimicrobial therapy, infection with organisms that do not grow in standard culture media: Some organisms require serodiagnosis , e.g.  Coxiella burnetii ,  Bartonella  sp,  Chlamydia psittaci ,  Brucella  sp others require special culture media e.g.,  Legionella pneumophila ; or others require PCR e.g.,  Tropheryma whippelii ). another diagnosis ( differential diagnosis ), e.g.: noninfective endocarditis, atrial myxoma with embolic phenomena, vasculitis

21. Imaging studies Echography Initially transthoracic (TTE) rather than transesophageal (TEE), should be done. NB:TEE is more sensitive (ie, capable of revealing vegetations too small to be seen on TTE). Transesophageal echocardiography  should be done when: Patients have a prosthetic valve Transthoracic echocardiogram is nondiagnostic Diagnosis of infective endocarditis has been established clinically (done to detect perforations, abscesses, and fistulas) CT  is used occasionally when TEE fails to : fully define paravalvular abscesses detect mycotic aneurysms PET scanning = emerging tool for the diagnosis of endocarditis originating in prosthetic and intracardiac devices. NB: CT and PET abnormalities are now included as major criteria in the European guidelines.

22. Other investigations: CBC , infection can cause: normocytic-normochromic anemia, elevated WBC count, ESR : increased Ig levels : increased presence of circulating immune complexes and rheumatoid factor , Urinalysis often shows : microscopic hematuria occasionally, RBC casts, pyuria, or bacteriuria.

23. Treatment ANTIMICROBIAL THERAPY It is difficult to eradicate bacteria from the avascular vegetation in infective endocarditis because this is relatively inaccessible to host defency Since all bacteria in the vegetation must be killed, therapy for endocarditis must be bactericidal and must be given for prolonged periods. high serum concentrations that will, through passive diffusion, lead to effective concentrations in the depths of the vegetation

24. Other considerations endocarditis involving prosthetic valves (except for staphylococcal infections) are similar to those used to treat native valve infection. The initiation of treatment before a cause is defined must balance the need to establish a microbiologic diagnosis against the potential progression of disease Blood cultures should be repeated until sterile and should be rechecked if there is recrudescent fever and at 4–6 weeks after therapy to document cure

25. if acute endocarditis start antibiotic treatment as soon as three sets of blood culture samples are obtained, but stable pts with subacute disease should have antibiotics withheld until a diagnosis is made. Pts treated with vancomycin or an aminoglycoside should have serum drug levels monitored.

26. STREPTOCOCCI Penicillin- susceptible b streptococci, S. bovis Relatively penicillin-resistant streptococci Penicillin G 2–3 million units IV q4h for 4 weeks — Penicillin G 2–3 million units IV q4h plus gentamicin c 1 mg/kg IM or IV q8h, both for 2 weeks Ceftriaxone 2 g/d IV as single dose for 4 weeks Vancomycin 15 mg/kg IV q12h for 4 weeks Penicillin G 3 million units IV q4h for 4–6 weeks plus gentamicinc 1 mg/kg IV q8h for 2 weeks

27. Moderately penicillin-resistant streptococci, pyridoxal -requiring streptococci ( Abiotrophia spp.) ENTEROCOCCI Penicillin G 3–4 million units IV q4h plus gentamicin 1 mg/kg IV q8h, both for 4–6 weeks Penicillin G 3–4 million units IV q4h plus gentamicin 1 mg/kg IV q8h, both for 4–6 weeks Ampicillin 2 g IV q4h plus gentamicinc 1 mg/kg IV q8h, both for 4–6 weeks Vancomycind 15 mg/kg IV q12h plus gentamicin 1 mg/kg IV q8h, both for 4–6 weeks

28. STAPHLOCOCCI Methicillin -susceptible, infecting native valves (no foreign devices) Methicillin -resistant, infecting native valves (no foreign devices) Methicillin -susceptible, infecting prosthetic valves Nafcillin or oxacillin 2 g IV q4h for 4–6 weeks plus (optional) gentamicinc 1 mg/kg IM or IV q8h for 3–5 days Cefazolin 2 g IV q8h for 4–6 weeks plus (optional) gentamicin 1 mg/kg IM or IV q8h for 3–5 days Vancomycin 15 mg/kg IV q12h for 4–6 weeks Nafcillin or oxacillin 2 g IV q4h for 6–8 weeks plus gentamicin1 mg/kg IM or IV q8h for 2 weeks plus rifampinh 300 mg PO q8h for 6–8 weeks

29. Methicillin -resistant, infecting prosthetic Valves HACEK organisms Vancomycin 15 mg/kg IV q12h for 6–8 weeks plus gentamicin 1 mg/kg IM or IV q8h for 2 weeks plus rifampin 300 mg PO q8h for 6–8weeks Ceftriaxone 2 g/d IV as single dose for 4 weeks Ampicillin 2 g IV q4h plus gentamicin 1 mg/kg IM or IV q8h, both for 4 weeks May use another third-generation cephalosporin at comparable dosage Determine ampicillin susceptibility; do not use ampicillin if beta - lactamase is produced

30. Staphylococcal PVE is treated for 6–8 weeks with a multidrug regimen. Rifampin is important because it kills organisms adherent to foreign material. Susceptibility testing for gentamicin should be performed before rifampin is given; if the strain is resistant, another aminoglycoside or a fluoroquinolone should be substituted. Pts with negative blood cultures and without confounding prior antibiotic treatment should receive ceftriaxone plus gentamicin . If the pt has a prosthetic valve, those two drugs plus vancomycin should be given

31. Indications for Cardiac Surgical Intervention Surgery required for optimal outcome; Moderate to severe CHF due to valve dysfunction Partially dehisced unstable prosthetic valve Persistent bacteremia despite optimal antimicrobial therapy Lack of effective microbicidal therapy (e.g., fungal or Brucella endocarditis ) S. aureus PVE with an intracardiac complication and Relapse of PVE after optimal antimicrobial therapy

32. Surgery should be considered early in the course of illness in pts with the indications listed above Although most of these indications are not absolute. However, pts who develop acute aortic regurgitation with preclosure of the mitral valve or a sinus of Valsalva abscess rupture into the right heart require emergent surgery.

33. Prophylaxis for Prevention – the procedure Dental procedures known to produce bleeding Tonsillectomy Surgery involving GI, respiratory mucosa Esophageal dilation ERCP for obstruction Gallbladder surgery Cystoscopy, urethral dilation Urethral catheter if infection present Urinary tract surgery, including prostate I&D of infected tissue

34. Cardiac Lesions for which Endocarditis Prophylaxis Is Advised High Risk Prosthetic heart valves Prior bacterial endocarditis Complex cyanotic congenital heart disease; other complex congenital lesions after correction -Patent ductus arteriosus - Coarctation of the aorta iv. Surgically constructed systemicpulmonary shunts Moderate Risk Congenital cardiac malformations (other than high-/low-risk lesions), ventricularseptal defect, bicuspid aortic valve Acquired aortic and mitral valve dysfunction Hypertrophic cardiomyopathy (asymmetric septal hypertrophy) Mitral valve prolapse with valvular regurgitation and/or thickened leaflets

35. Chemoprophylaxis Adult Prophylaxis: Dental, Oral, Respiratory, Esophageal Standard Regimen Amoxicillin 2g PO 1h before procedure or Ampicillin 2g IM/IV 30m before procedure Penicillin Allergic Clindamycin 600 mg PO 1h before procedure or 600 mg IV 30m before Cephalexin OR Cefadroxil 2g PO 1 hour before Cefazolin 1.0g IM/IV 30 min before procedure Azithromycin or Clarithromycin 500mg PO 1h before

36. Adult Genitourinary or Gastrointestinal Procedures High Risk Patients Standard Regimen Before procedure (30 minutes): Ampicillin 2g IV/IM AND Gentamicin 1.5 mg/kg (MAX 120 mg) IM/IV After procedure (6 hours later) Ampicillin 1g IM/IV OR Amoxicillin 1g PO Penicillin Allergic Complete infusion 30 minutes before procedure Vancomycin 1g IV over 1-2h AND Gentamicin 1.5 mg/kg IV/IM (MAX 120 mg) Moderate Risk Patients Standard Regimen Amoxicillin 2g PO 1h before OR Ampicillin 2g IM/IV 30m before Penicillin Allergic Vancomycin 1g IV over 1-2h, complete 30m before

37. COMPLICATIONS Four etiologies Embolic Local spread of infection Metastatic spread of infection Formation of immune complexes ( glomerulonephritis and arthritis )

38. Embolic , occur up to 40% predictated by size of vegetation, left sided vegetation, fungal pathology, s. aureas . Strep bovis Incidence decrease with effect. Antibiotics MI, STROKE, ISCHEMIC LIMB, ABD. PAIN LOCAL SPREAD Extensive valvular damage Paravalvular abscess ( 30- 40) Pericarditis Fistulous intra cardia connection

39. Metarstatic spread Metastatic abscess ( kidney , spleen , brain meningitis , vertebral osteomyelits , septic arthritis Poor prognostic factors Female prosthetic valves S. aureus dm Low serum albumin heart failure Vegetation size Aortic valve involv Paravalvular abscess

40. REFERENCES Habib G, Lancellotti P, Antunes MJ, et al : 2015 ESC Guidelines for the management of infective endocarditis: The Task Force for the Management of Infective Endocarditis of the European Society of Cardiology (ESC). Endorsed by: European Association for Cardio-Thoracic Surgery (EACTS), the European Association of Nuclear Medicine (EANM).  Eur Heart J 36:3075–3123, 2015. Baddour LM, Wilson WR, Bayer AS, et al : Infective endocarditis in adults: Diagnosis, antimicrobial therapy, and management of complications: A scientific statement for healthcare professionals from the American Heart Association. Circulation 132:1435–1486, 2015. Cahill TJ, Baddour LM, Habib G, et al : Challenges in infective endocarditis. J Am Coll Cardiol  69(3):325–344, 2017.