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Infective endocarditis
This document provides information on infective endocarditis. It begins by discussing the history and challenges of diagnosing and managing this infection. Key points include that infective endocarditis involves infection of the endothelial surface of the heart. Predisposing factors include dental procedures, infections elsewhere in the body, medical instrumentation, and intravenous drug use. Symptoms can range from acute toxicity and fever to more mild subacute presentations. Echocardiography, blood cultures, and applying the Duke criteria are important for diagnosis. Treatment involves intravenous antibiotics for a prolonged period, sometimes along with surgery for complications. Complications can include embolisms, local or metastatic spread of infection, and immune complex disease. Prevention focuses on prophylactic antibiotics
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Infective endocarditis
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- 2. CARDIAC LAYERS &VALVES 7/29/2019 2
- 3. 7/29/2019 3 Carditis Rubor, Calor,Tumor, Dolor, Functio Laesa Endo Involves endocardium Only Spares other layers Infective Infective Non Infective Acute Fulminating Life Threatening Sub Milder Variant
- 4. Old Hard Disease •Knowledge about the origins of endocarditis stems from the work of Fernel in the early 1500s, and yet this infection still presents physicians with major diagnostic and management dilemmas. 7/29/2019 4
- 5. 7/29/2019 5 Infective Endocarditis •Febrile illness • Persistent bacteremia • Characteristic lesion of microbial infection of the endothelial surface of the heart The vegetation – Variable in size – Amorphous mass of fibrin & platelets – Abundant organisms – Few inflammatory cells
- 6. Predisposing Factors 7/29/2019 6 1.Dental manipulation 2. Extra cardiac infection (lung, urinary tract, skin, bone, abscess) 3. Instrumentation (urinary tract, GI tract, IV infusions) 4. Cardiac surgery 5. Injection drug use 6. Intravenous catheters
- 7. Infective Endocarditis • Acute –Toxic presentation – Progressive valve destruction & metastatic infection developing in days to weeks – Most commonly caused by S. aureus • Sub acute – Mild toxicity – Presentation over weeks to months – Rarely leads to metastatic infection – Most commonly S. viridans or enterococcus 7/29/2019 7
- 8. Infecting Organisms Common bacteria –Alpha haem streptococci (viridans – S. mitis, S. sanguis) SUBACUTE – Enterococci (E. faecalis) SUBACUTE – Coagulase Negative Staphylococci – PROSTHETIC VALVES, SUBACUTE Less common bacteria – S. aureus ACUTE – B-Haemolytic streptococci ACUTE – Streptococcus pneumonia Not so common – Fungi – Pseudomonas / Coliforms – HACEK group organisms 7/29/2019 8
- 9. Bacterial Pathogens HACEK Group •Haemophilus spp. • Actinobacillus actinomycetemcomitans • Cardiobacterium hominis • Eikenella corrodens • Kingella kingae 7/29/2019 9
- 10. Infecting Organisms Streptococci 60-80% –Alpha-haemolytic Streptococci (viridans – S. mitis, S. oralis) 30-40% (subacute) – Enterococci (E. faecalis) 5-18% (subacute) – Beta-haemolytic streptococci (e.g. Gp A Strep) – rare (acute) Staphylococci 20-35% – S. aureus 10-27% (acute) – Coagulase negative staphylococci (Staph epidermidis) 1-3 % (mainly prosthetic valve risk, subacute) Fungi – Candida – IVDU at risk (usually indolent) – Aspergillus – rare Gram-negative bacteria – rare Culture-negative endocarditis HACEK, Q-fever – cases do occur, subacute 7/29/2019 10
- 11. Infective Endocarditis 7/29/2019 11 •Pathology – NVE infection is largely confined to leaflets – PVE infection commonly extends beyond valve ring into annulus/periannular tissue • Ring abscesses • Septal abscesses • Fistulae • Prosthetic dehiscence – Invasive infection more common in aortic position and if onset is early
- 13. Turbulent Blood Flow Rheumaticfever history Old age – calcified valves Mitral valve prolapse with regurgitation Prosthetic heart valves Congenital defects / any structural defect Cardiac surgery Central lines Pacemakers Intravenous drug abuse 7/29/2019 13
- 14. Sub-Acute Vs Acute 7/29/201914 Feature Acute Subacute Underlying Heart Heart may be normal RHD,CHD, etc. Disease Organism S. aureus, Pneumococcus S. pyogenes, Enterococcus viridans Streptococci, Entercoccus Therapy Prompt, vigorous and initiated on empirical ground Can often be delayed until culture reports and susceptibilities available
- 15. Bacterial Endocarditis Clinical Features 7/29/201915 1. Fever. Antibiotics, salicylates, steroids, severe CHF, uremia may mask temperature elevations. 2. Murmurs 3. Petechial and cutaneous manifestations. Roth spots Conjunctival and mucosal petechiae, splinter hemorrhages, Osler nodes and Janway lesions. 4. Splenomegaly 5. Embolism. Septic or sterile. CNS, spleen, lung, retinal vessels, coronary artery, large vessels. 6. Renal disease, infarction. Multiple abscesses. Glomerulonephritis and uremia 7. CHF 8. General. Weight loss, anorexia, debilitation, loss of libido.
- 16. Symptoms Acute – High gradefever and chills – SOB – Arthralgias/ myalgias – Abdominal pain – Pleuritic chest pain – Back pain Sub acute 7/29/2019 16 – Low grade fever – Anorexia – Weight loss – Fatigue – Arthralgia's/ myalgia's – Abdominal pain – N/V The onset of symptoms is usually ~2 weeks or less from the initiating bacteremia
- 17. Signs • Fever • Heartmurmur • Nonspecific signs – petechiae, subungal or “splinter” hemorrhages, clubbing, splenomegaly, neurologic changes • More specific signs - Osler’s Nodes, • Janeway lesions • Roth Spots 6/21/ 237/29/2019 17
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- 19. Janeway Lesions 1. Morespecific 2. Erythematous, blanching macules 3. Nonpainful 4. Located on palms and soles 7/29/2019 19
- 20. Splinter Hemorrhages 1. Nonspecific 2.Nonblanching 3. Linear reddish-brown lesions found under the nail bed 4. Usually do NOT extend the entire length of the nail 7/29/2019 20
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- 23. Osler’s Nodes 6/21/2013 1. Morespecific 2. Painful and erythematous nodules 3. Located on pulp of fingers and toes 4. More common on in Sub-Acute 3223
- 24. 7/29/2019 24 Bacterial Endocarditis LaboratoryFeatures 1. Anemia 2. Most commonly elevated WBC 3. ESR elevated 4. Microscopic hematuria 5. Bacteremia.
- 25. 7/29/2019 25 Blood cultures •Recommendation: Blood cultures remain a cornerstone of the diagnosis of IE cases and should be taken prior to starting treatment in all case • Meticulous aseptic technique is required when taking blood cultures, to reduce the risk of contamination with skin commensals, which can lead to misdiagnosis. Guidelines for best practice should be consulted
- 26. 7/29/2019 26 When toCollect the blood • In patients with a chronic or sub acute presentation, three sets of optimally filled blood cultures should be taken from peripheral sites with ≥6 h between them prior to commencing antimicrobial therapy. • Taking blood cultures at different times is critical to identifying a constant bacteraemia, a hallmark of endocarditis.
- 27. 7/29/2019 27 Timing ofblood collection • In patients with suspected IE and severe sepsis or septic shock at the time of presentation, two sets of optimally filled blood cultures should be taken at different times within 1 h prior to commencement of empirical therapy, to avoid undue delay in commencing empirical antimicrobial therapy.
- 28. 7/29/2019 28 Start withEmpherical Treatment • It is not always appropriate to withhold antimicrobial therapy while three sets of blood cultures are taken over a 12 h period. This recommendation is intended to be pragmatic, allowing time to take at least two sets of blood cultures (the minimum for a secure microbiological diagnosis) prior to commencing antimicrobial therapy.
- 29. Blood Cultures Blood Cultures –Minimum of three blood cultures (ideally spread over 24 hrs) – Three separate venipuncture sites ideally –Obtain correct volume of blood for culture bottles Positive Result – 1 set gives 90% sensitivity, remaining 2 sets add 8% – Multiple same cultures are important in confirming significance, especially for less typical organisms Negative Result – Prior antibiotic therapy – ‘Culture negative endocarditis’ – fastidous orgs / non- culturable – May support a non-endocarditis patient diagnosis 7/29/2019 29
- 30. Culture Negative Resultsmay yield ..less known microbes • Microorganisms that should be considered first include Coxiella burnetii (Q fever) and Bartonella spp. 7/29/2019 30
- 31. Additional Tests CBC ESR andCRP Complement levels (C3, C4, CH50) RF Urinalysis Baseline chemistries 7/29/2019 31
- 32. Imaging Chest x-ray – Lookfor multiple focal infiltrates and calcification of heart valves ECG – Rarely diagnostic – Look for evidence of ischemia, conduction delay, and arrhythmias Echocardiography 7/29/2019 32
- 33. Echocardiography Transthoracic echocardiography (TTE) –First line if suspected IE – Native valves Trans esophageal echocardiography (TEE) – Prosthetic valves – Intracardiac complications – Inadequate TTE – Fungal or S. aureus or bacteremia 7/29/2019 33
- 34. Making the Diagnosis Pelletierand Petersdorf criteria (1977) – Classification scheme of definite, probable, and possible IE – Reasonably specific but lacked sensitivity Von Reyn criteria (1981) – Added “rejected” as a category – Added more clinical criteria – Improved specificity and clinical utility Duke criteria (1994) – Included the role of echocardiography in diagnosis – Added IVDA as a “predisposing heart condition” 7/29/2019 34
- 35. Modified Duke Criteria DefiniteIE – Microorganism (via culture or histology) in a valvular vegetation, embolized vegetation, or intracardiac abscess – Histologic evidence of vegetation or intracardiac abscess Possible IE – 2 major – 1 major and 3 minor – 5 minor Rejected IE – Resolution of illness with four days or less of antibiotics 7/29/2019 35
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- 37. Treatment Parenteral (IV) antibiotics –High serum concentrations to penetrate vegetation's – Prolonged treatment to kill dormant bacteria clustered in vegetation’s – Empirical in Acute Condition Surgery – Intracardiac complications/paravalve abscess 517/29/2019 37
- 38. Treatment - Specific •Modify empiric therapy once cultures/sensitivities known • Long duration 4-6 weeks Rx is required • Liaise with Microbiologist • Liaise with Cardiac Surgeon if needed Monitor response to treatment • (clinical, CRP, ECHO) & look for complications 7/29/2019 38
- 39. Complications Four etiologies –Embolic –Local spreadof infection –Metastatic spread of infection –Formation of immune complexes – glomerulonephritis and arthritis 7/29/2019 39
- 40. Embolic Complications Occur inup to 40% of patients with IE Predictors of embolization –Size of vegetation –Left-sided vegetation's –Fungal pathogens, S. aureus, and Strep. Bovis Incidence decreases significantly after initiation of effective antibiotics 7/29/2019 40
- 41. Embolic Complications Stroke Myocardial Infarction –Fragments of valvular vegetation or vegetation- induced stenosis of coronary ostia Ischemic limbs Hypoxia from pulmonary emboli Abdominal pain (splenic or renal infarction) 7/29/2019 41
- 42. Metastatic Spread ofInfection Meningitis and/or encephalitis Vertebral osteomyelitis Metastatic abscess –Kidneys, spleen, brain, soft tissues Septic arthritis 7/29/2019 42
- 43. 7/29/2019 43 Prevention • Prophylacticregimen targeted against likely organism – Strep. viridans – oral, respiratory, esophageal – Enterococcus – genitourinary, gastrointestinal – S. aureus – infected skin, mucosal surfaces
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