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Infective endocarditis
- 2. GUIDELINES FOR INFECTIVE ENDOCARDITIS •Clinical Practice Guidelines for the Prevention, Diagnosis & Management of Infective Endocarditis 2017.
- 3. Contents • Introduction • Riskfactors • Classification • Common Organism • Clinical presentation • Investigations • Modified Duke’s criteria • Management • Summary
- 4. Introduction • Infection ofthe endocardial surface of the heart (heart valves and mural endocardium) • Increasing in prevalence due to • introduction of conduits (tubes), • prosthetic materials and intracardiac devices makes more susceptible to infection in view of the presence of these foreign materials.
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- 6. IE according tolocalisation of infection and presence of intracardiac material • Left-sided native valve IE • Left-sided PVE >> Early PVE < 1 year after valve surgery >> Late PVE > 1 year after valve surgery • Right-sided native valve IE • Device related IE IE according to the mode of acquisition • Healthcare associated IE • Community acquired IE • Intravenous drug abuseassociated IE Acute endocarditis • High grade and persistant fever • Rapidldamages cardiac to structures, • Seeds extracardiac sites IF untreated progresses to death within weeks. Subacute endocarditis • Follows an slower course(slow cardiac damage) • Rarely metastasizes; and • Gradually progressive unless complicated by a major embolic event or a ruptured mycotic aneurysm.
- 8. Common Organisms • NativeValve and late prosthetic valve : Strep Viridans • Early Prosthetic valve : Staph Epidermidis and Staph Aureus • IVDU esp tricuspid valve is : S. aureus • Non-infective: • systemic lupus erythematosus (Libman-Sacks) • malignancy: marantic endocarditis • Culture negative causes • Brucella • Coxiella burnetii • HACEK: Hemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella) • Bartonella • Prior antibiotic therapy
- 10. Pre-existing risk factors •Previous history of IE. • Pre-existing cardiac disease. • Presence of prosthetic valves or prosthetic cardiac material. • Presence of intracardiac devices. • History of IVDU. • Presence of chronic intravenous access (e.g. haemodialysis catheters,chemoports and neonate/paediatric patients with indwelling central venous catheters). • Presence of CHD Elderly or immunocompromised patients. • Co-existing conditions such as diabetes, human immunodeficiency virus (HIV) • infection and malignancy.
- 11. General Clinical Presentation •Fever (87%) with chills, poor appetite and weight loss. • Heart failure may be present at admission (up to 58%) • New or altered cardiac murmur (50-85%) • Embolic events may also cause presenting symptoms (27-30%) Fever + New/Altered murmur : IE until proven otherwise • Pt do not often present with classic textbook manifestations of subacute or chronic endocarditis.
- 12. Peripheral sign and symptom Dueto septic emboli or immune complex deposition
- 13. Peripheral sign and symptom SKIN Splinter hemorhage Janewaylesion >> Non-tender lesions >> 1-4 mm in diameter >>Often haemorrhagic Osler’s nodes Painful subcutane ous nodules Clubbing
- 14. Peripheral sign andsymptom EYES Conjuctival hemorhage Roth’s spot White centred retinal haemorrhages)
- 15. Clinical features Neurological Mycotic aneurysm vessel walls infected with bacteria, is digested and a false aneurysm forms, which is unstable and highly prone to rupture.
- 16. Clinical features Renal • Hematuria: due to glomerulonephritis
- 18. Differential diagnosis.. 1) AcuteRhematic heart fever 2) Endocarditis due SLE (Libman-Sacks) 3) Atrial myxoma
- 19. Investigation • FBC :Raised white cell count and Low hb • UFEME : Ery positive • Inflammatory marker • Elevated CRP and ESR. • Renal profile • LFT • ECG • Chest X-ray • Blood cultures : three set from three different sites prior to antibiotics If blood cultures negative after 5 days of incubation and no history of prior antimicrobial use, consider blood culture negative infective endocarditis (BCNIE), which can be caused by fungi or fastidious microorganisms, and perform the appropriate microbiological tests.
- 20. Definite IE Pathologicalcriteria: Microorganisms demonstrated by culture or HPE of a vegetation, a vegetation that has embolised, or an intracardiac abscess specimen; or pathological lesions; vegetation or intracardiac abscess confirmed by HPE showing active endocarditis Clinical criteria: 2 major criteria or 1 major criterion and 3 minor criteria or 5 minor criteria Possible IE 1 major criterion and 1 minor criterion or 3 minor criteria Rejected IE Firm alternative diagnosis explaining evidence of IE or resolution of IE syndrome with antimicrobial therapy for ≤ 4 days or no pathological evidence of IE at surgery or autopsy with antimicrobial therapy for ≤ 4 days or does not meet criteria for possible IE as above
- 21. Major Criteria Blood culturepositive for IE Evidence of endocardial involvement Typical microorganisms consistent with IE from 2 separate blood cultures: • VGS, Streptococcus bovis, HACEK group, S. 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 hours apart >>Or all of 3 or a majority of ≥ 4 separate cultures of blood (with first and last sample drawn at least 1 hour apart) • Single positive blood culture from Coxiella burnetii or phase 1 IgG antibody titres > 1:800 Echocardiogram positive for IE 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 • Abscess Or new partial dehiscence of prosthetic valve Or new valvular regurgitation (worsening or changing or pre-existing murmur not sufficient)
- 22. Minor criteria Predisposition: predisposing heartcondition or IVDU Fever: temperature > 38°C Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial haemorrhage, conjunctival haemorrhages and Janeway lesions Immunological phenomena: glomerulonephritis, Osler nodes, Roth spots and rheumatoid factor Microbiological evidence: positive blood cultures but does not meet a major criterion as noted above (excludes single positive cultures for coagulase negative staphylococci and microorganisms that do not cause endocarditis) or serological evidence of active infection with microorganism consistent with IE
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- 24. Surgical or autopsyfindings Echocardiography findings Vegetation Infected mass attached to an endocardial structure or on implanted intracardiac material Oscillating or non-oscillating intracardiac mass on valve or other endocardial structures, or on implanted intracardiac material Abscess Perivalvular cavity with necrosis and purulent material not communicating with the cardiovascular lumen Thickened, non-homogeneous perivalvular area with echodense or echolucent appearance Pseudoaneurysms Perivalvular cavity communicating with the cardiovascular lumen Pulsatile perivalvular echocardiographic-free space, with colour-Doppler detected Perforation Interruption of endocardial tissue continuity Interruption of endocardial tissue continuity traversed by colour- Doppler Fistula Communication between two neighbouring cavities through a perforation Colour-Doppler communication between two neighbouring cavities through a perforation Valve aneurysm Saccular outpouching of valvular tissue Saccular bulging of valvular leaflet tissue Dehiscence of a prosthetic valve Dehiscence of the prosthesis Paravalvular regurgitation identified by TTE/TEE, with or without rocking motion of the prosthesis
- 25. Video Vegetation • 2chamber view
- 26. Video – Aorticabscess Mercedes benz sign – aortic valve
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- 29. The major goalsof management of IE are: •To eradicate the infectious agent from the endocardium. •To address the complications of the infection, both intra and extracardiac.
- 30. Things to monitorin Ward(1) •General well being – septic looking, GCS •Temperature : Fever usually resolves in a few days after appropriate antibiotics started •Daily ECG – PR interval (conduction delay)
- 31. Things to monitorin Ward(2) • Examined regularly for ssx of the following complications • Heart failure: symptoms should be treated with standard medical therapy and its severity regularly assessed. Heart failure may persist despite microbiological resolution. • Embolic events. - related to the migration of cardiac vegetations : liver, spleen, kidneys and abdominal mesenteric vessels • Common sites • left-sided IE are the brain and spleen • Right-sided IE – Pulmonary embolism • Ongoing sepsis. • Neurological sequelae. –ischemic and hemorhagic stroke, mycotic aneuryms, cerebral abscess.
- 32. Things to monitorin Ward (3) • Blood investigations • Regular Inflammatory markers. • Regular FBC to monitor WBCs, Hb and Plt • Blood cultures • BUSE for sign of AKI and it’s resolution. • Echocardiography • Monitor vegetation • Resolution of IE: vegetations gradually reduce in size, mobility and increase in echogenicity. In the long-term, these vegetations may not disappear or even change in size, even with clinical treatment success. • Risk of embolisation: vegetations increase in sizeand mobility.
- 33. Antimicrobial management 1) Empirical antibiotic– based on clinical suspicion. 2) Definitive treatment – based on C+S.
- 35. Empirical In our settingwe use IV Ceftriaxone as empirical antibiotic Add Cloxacillin if suspected Staph Aureus(IVDU or PVE) Or Vancomycin for suspected MRSA 1. Community-acquired native valves or late prosthetic valves (≥ 12 months post-surgery) endocarditis Usually strep viridans Ampicillin + Gentamicin (Low dose) +/- Cloxacillin** Or Vancomycin + Gentamicin (Low dose) 2. Early PVE (< 12 months post-surgery) or nosocomial and non-nosocomial healthcare associated endocarditis. • Usually MRSA Vancomycin + Gentamicin (Low dose) +/- Rifampicin** +/- Cefepime*
- 36. Definitive Based on theculture Ideally ,minimum inhibitory concentration(MIC) level is needed to determine the number/dosage of the antimicrobial.
- 37. Native Valves Methicillin- Susceptible Staphylococci (MSSA) Complicatedright sided endocarditis: renal failure, extra pulmonary metastatic infections such as osteomyelitis, aortic or mitral valve involvement, meningitis, or infection by MRSA Left sided endocarditis and complicated right sided : Cloxacillin 2gm IV in q4h for 6 weeks +/- Gentamicin 1mg/kg IV/IM q8h for 3-5 days Right sided endocarditis (tricuspid valve) in uncomplicated endocarditis : Cloxacillin 2gm IV q4h for 2 weeks + Gentamicin 1mg/kg IM/IV q8h for 2 weeks
- 38. Prosthetic Valves Methicillin-Susceptible Staphylococci Cloxacillin 2gm IVin q4h for > 6 weeks PLUS Rifampicin 300mg PO q8h for > 6 weeks PLUS Gentamicin 1mg/kg IM/IV q8h for 2 weeks
- 39. Native Valves MRSA left-sided andright-sided Vancomycin 15-20 mg/kg/ dose (actual body weight) IV every 8-12 hourly; not to Exceed 2 g/dose For 4-6 weeks Prosthetic Valves MRSA Vancomycin 25-30mg/kg loading dose then 15mg/kg IV q12h for > 6 weeks, not to exceed 2gm/24h PLUS Rifampicin 300mg PO q8h for > 6 weeks PLUS Gentamicin 1mg/kg IM/IV q8h for 2 weeks
- 40. Surgical Intervention Indications • Severevalvular incompetence, haemodynamic instability or heart failure. • Uncontrolled sepsis and paravalvular extension of infection. • Fungal or multiresistant endocarditis. • Large vegetations (> 10 mm for left-sided IE) and recurrent systemic embolisation.
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- 46. The modified Dukecriteria
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Editor's Notes
- #9 NBTE also arises as a result of a hypercoagulable state; this gives rise to mara n tic endocarditis (uninfected vegetations seen in patients with malignancy and chronic diseases) and to bland vegetations complicating systemic lupus erythematosus and the antiphosphoIipid antibody syndrome.
- #31 ECG: &gt;&gt; Should be done daily to monitor heart rhythm and to look for conduction defects. This is especially important in cases of prosthetic valve IE or native valve IE as they are at higher risk for extension of infection to the conduction pathways which can occur very abruptly. &gt;&gt; Conduction defects may be a sign of perivalvular extension of infection especially in cases involving the aortic valve.
- #34 lowest concentration of an antimicrobial (like an antifungal, antibiotic or bacteriostatic) drug that will inhibit the visible growth of a microorganism.
- #36 **For patients with suspected S. aureus infections (such as IVDU or patients with prosthesis) and acute presentation **Rifampicin is only recommended for PVE and it should be started 3-5 days later than vancomycin and gentamicin ^Cefepime is indicated if local Epidemiology suggests for non-HACEK Gram- negative rod infections (such as Pseudomonas)
- #37 lowest concentration of an antimicrobial (like an antifungal, antibiotic or bacteriostatic) drug that will inhibit the visible growth of a microorganism.
- #59 The undamaged endothelium is resistant to infection by most bacteria and to thrombus formation. Endothelial injury (e.g.at the site of impact of high relocity blood jets or on the low-pressure side of a cardiac structural lesion) allows either direct infection by virulent organisms or the development of a platelet-fibrin thrombus-acondition called nonbacterial thrombotic endocarditis (NBTE). This thrombus serves as a site of bacterial attachment during transient bacteremia. The cardiac conditions most commonly resulting in NBTE are mitral regurgitation， aortic stenosis， aortic regurgitation， ventricular septal defects， and complex congenital heart disease. NBTE also arises as a result of a hypercoagulable state; this gives rise to marantic endocarditis (uninfected vegetations seen in patients with malignancy and chronic diseases) and to bland vegetations.