Infective endocarditis

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Infective endocarditis

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Infective endocarditis

  1. 1. INFECTIVE ENDOCARDITISan updateDr.T.V.Rao MD6/21/2013 Dr.T.V.Rao MD 1
  2. 2. Beginning of Knowledge onEndocarditis• Knowledge about theorigins of endocarditisstems from the work ofFernel in the early1500s, and yet thisinfection still presentsphysicians with majordiagnostic andmanagementdilemmas.6/21/2013 Dr.T.V.Rao MD 2
  3. 3. Definition of Infective Endocarditis• Infective endocarditis, a serious infection ofthe endocardium of the heart, particularly theheart valves, is associated with a high degreeof illness and death. It generally occurs inpatients with altered and abnormal heartarchitecture, in combination with exposure tobacteria through trauma and other potentiallyhigh-risk activities involving transientbacteraemia.6/21/2013 Dr.T.V.Rao MD 3
  4. 4. DefinitionInfective Endocarditis (IE): an infection of theheart’s endocardial surfaceMain Classification:– Native Valve IE– Prosthetic Valve IEAdditional Consideration– Intravenous drug abuse (IVDA) IE– Nosocomial IE6/21/2013 Dr.T.V.Rao MD 4
  5. 5. Infective Endocarditis• Febrile illness• Persistent bacteremia• Characteristic lesion of microbial infection ofthe endothelial surface of the heart– Variable in size– Amorphous mass of fibrin & platelets– Abundant organisms– Few inflammatory cellsThe vegetation6/21/2013 Dr.T.V.Rao MD 5
  6. 6. Bacterial EndocarditisPredisposing Factors1. Dental manipulation2. Dental disease (caries, abscess)3. Extra cardiac infection (lung, urinary tract,4. skin, bone, abscess)4. Instrumentation (urinary tract, GI tract, IVinfusions)5. Cardiac surgery6. Injection drug use7. None apparent6/21/2013 Dr.T.V.Rao MD 6
  7. 7. Infective Endocarditis• Acute– Toxic presentation– Progressive valve destruction & metastatic infection developing indays 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 enterococcus6/21/2013 Dr.T.V.Rao MD 7
  8. 8. Infective Endocarditis• Adult population–Rheumatic Heart Disease• 20 – 25% of cases of IE in 1970’s & 80’s• 7 – 18% of cases in recent reported series• Mitral site more common in women• Aortic site more common in men–Congenital Heart Disease• 10 – 20% of cases in young adults• 8% of cases in older adults• PDA, VSD, bicuspid aortic valve (esp. in men>60)6/21/2013 Dr.T.V.Rao MD 8
  9. 9. Infective Endocarditis• Intravenous Drug Abuse– Risk is 2 – 5% per pt./year– Tendency to involve right-sided valves• Distribution in clinical series– 46 – 78% tricuspid– 24 – 32% mitral– 8 – 19% aortic– Underlying valve normal in 75 – 93%– S. aureus predominant organism (>50%, 60-70%of tricuspid cases)6/21/2013 Dr.T.V.Rao MD 9
  10. 10. Causes of BacteraemiaBrushing teethEating/chewingDental workIV lines (colonised/infected)IV drug useInfected site/abscessalpha-haemolyticstreptococci fromoral floraStaphylococcusaureus fromskin/noseStrep.pneumoniae, S.aureus6/21/2013 Dr.T.V.Rao MD 10
  11. 11. Infecting OrganismsCommon bacteria– Alpha haem streptococci (viridans – S. mitis, S. sanguis) SUBACUTE– Enterococci (E. faecalis) SUBACUTE– Coagulase Negative Staphylococci – PROSTHETIC VALVES, SUBACUTELess common bacteria– S. aureus ACUTE– B-Haemolytic streptococci ACUTE– Streptococcus pneumoniaNot so common– Fungi– Pseudomonas / Coliforms– HACEK group organisms6/21/2013 Dr.T.V.Rao MD 11
  12. 12. Bacterial PathogensHACEK Group• Haemophilus spp.• Actinobacillusactinomycetemcomitans• Cardiobacterium hominis• Eikenella corrodens• Kingella kingae6/21/2013 Dr.T.V.Rao MD 12
  13. 13. Infecting OrganismsStreptococci 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 – rareGram-negative bacteria – rareCulture-negative endocarditis HACEK, Q-fever – cases do occur, subacute6/21/2013 Dr.T.V.Rao MD 13
  14. 14. Infective Endocarditis• Prosthetic Valve Endocarditis (PVE)– 10 – 30% of all cases in developed nations– Cumulative incidence• 1.4 – 3.1% at 12 months• 3.2 – 5.7% at 5 years– Early PVE – within 60 days• Nosocomial (s. epi predominates)– Late PVE – after 60 days• Community (same organisms as NVE)6/21/2013 Dr.T.V.Rao MD 14
  15. 15. Infective Endocarditis• Pathology– NVE infection is largely confined to leaflets– PVE infection commonly extends beyond valvering into annulus/periannular tissue• Ring abscesses• Septal abscesses• Fistulae• Prosthetic dehiscence– Invasive infection more common in aortic positionand if onset is early6/21/2013 Dr.T.V.Rao MD 15
  16. 16. PathophysiologyTurbulent blood flow within the heart - most often(but not always) – patient has risk factors for thisTurbulent blood flow disrupts valve surface(endocardium) to produce suitable (sticky) site forbacterial attachmentPlatelet deposition + fibrin may lead to non-bacterialthrombus or vegetationBacteraemia – delivers organisms to the damaged(sticky) endocardial surface resulting in adherence &colonisationEventual invasion of valve leaflets results in infectedvegetation (sheath of fibrin & platelets, idealconditions for further bacterial multiplications,protection from polymorphs)6/21/2013 Dr.T.V.Rao MD 16
  17. 17. Infected vs Normal Valve6/21/2013 Dr.T.V.Rao MD 17
  18. 18. Local Spread of InfectionAcute S. aureus IE with perforation of theaortic valve and aortic valve vegetation.Acute S. aureus IE with mitral valve ringabscess extending into myocardium.6/21/2013 Dr.T.V.Rao MD 18
  19. 19. Turbulent Blood FlowRheumatic fever historyOld age – calcified valvesMitral valve prolapse with regurgitationProsthetic heart valvesCongenital defects / any structural defectCardiac surgeryCentral linesPacemakersIntravenous drug abuseVarying predisposing conditions exist, but in over 50% of cases, no identified valvular lesioncan be found.6/21/2013 Dr.T.V.Rao MD 19
  20. 20. Distinction between Acute andSubacute Bacterial EndocarditisFeature Acute SubacuteUnderlying HeartDiseaseHeart may be normal RHD,CHD, etc.Organism S. aureus, PneumococcusS. pyogenes,EnterococcusviridansStreptococci,EntercoccusTherapy Prompt, vigorous and initiatedon empirical groundCan often be delayeduntil culture reports andsusceptibilitiesavailable6/21/2013 Dr.T.V.Rao MD 20
  21. 21. Bacterial EndocarditisClinical Features1. Fever. Antibiotics, salicylates, steroids, severe CHF, uremia maymask temperature elevations.2. Murmurs3. Petechial and cutaneous manifestations. Roth spots Conjunctivaland mucosal petechiae, splinter hemorrhages, Osler nodes andJanway lesions.4. Splenomegaly5. Embolism. Septic or sterile. CNS, spleen, lung, retinalvessels, coronary artery, large vessels.6. Renal disease, infarction. Multiple abscesses.Glomerulonephritis and uremia7. CHF8. General. Weight loss, anorexia, debilitation, loss of libido.6/21/2013 Dr.T.V.Rao MD 21
  22. 22. SymptomsAcute– High grade fever andchills– SOB– Arthralgias/ myalgias– Abdominal pain– Pleuritic chest pain– Back painSub acute– Low grade fever– Anorexia– Weight loss– Fatigue– Arthralgias/ myalgias– Abdominal pain– N/VThe onset of symptoms is usually ~2 weeks or lessfrom the initiating bacteremia6/21/2013 Dr.T.V.Rao MD 22
  23. 23. SignsFeverHeart murmurNonspecific signs – petechiae,subungal or “splinter” hemorrhages,clubbing, splenomegaly, neurologicchangesMore specific signs - Osler’s Nodes,Janeway lesions, and Roth Spots6/21/2013 Dr.T.V.Rao MD 23
  24. 24. Janeway Lesions6/21/2013 Dr.T.V.Rao MD 24
  25. 25. Janeway Lesions1. More specific2. Erythematous, blanching macules3. Nonpainful4. Located on palms and soles6/21/2013 Dr.T.V.Rao MD 25
  26. 26. Splinter Hemorrhage6/21/2013 Dr.T.V.Rao MD 26
  27. 27. Splinter Hemorrhages1. Nonspecific2. Nonblanching3. Linear reddish-brown lesions found under the nail bed4. Usually do NOT extend the entire length of the nail6/21/2013 Dr.T.V.Rao MD 27
  28. 28. Subconjuctival Hemorrhages6/21/2013 Dr.T.V.Rao MD 28
  29. 29. Septic Retinal Embolus6/21/2013 Dr.T.V.Rao MD 29
  30. 30. Roth’s Spots6/21/2013 Dr.T.V.Rao MD 30
  31. 31. 6/21/2013 Dr.T.V.Rao MD 31
  32. 32. Osler’s Nodes1. More specific2. Painful and erythematous nodules3. Located on pulp of fingers and toes4. More common in subacute IE6/21/2013 Dr.T.V.Rao MD 32
  33. 33. Bacterial EndocarditisLaboratory Features1. Anemia2. Most commonly elevated WBC3. ESR elevated, ↓ C′ in patients withglomerulonephritis4. Microscopic hematuria5. Bacteremia. Persistent.≥ 3, ≤ 5 blood cultures.Aerobic and anaerobic. Different sites.6/21/2013 Dr.T.V.Rao MD 33
  34. 34. Blood cultures• Recommendation: Blood cultures remain acornerstone of the diagnosis of IE cases andshould be taken prior to starting treatment inall case• Meticulous aseptic technique is requiredwhen taking blood cultures, to reduce the riskof contamination with skincommensals, which can lead to misdiagnosis.Guidelines for best practice should beconsulted6/21/2013 Dr.T.V.Rao MD 34
  35. 35. When to Collect the blood• In patients with a chronic or sub acutepresentation, three sets of optimallyfilled blood cultures should be takenfrom peripheral sites with ≥6 h betweenthem prior to commencing antimicrobialtherapy.• Taking blood cultures at different times iscritical to identifying a constantbacteraemia, a hallmark of endocarditis.6/21/2013 Dr.T.V.Rao MD 35
  36. 36. Timing of blood collection• In patients with suspected IE and severesepsis or septic shock at the time ofpresentation, two sets of optimally filledblood cultures should be taken atdifferent times within 1 h prior tocommencement of empirical therapy, toavoid undue delay in commencingempirical antimicrobial therapy.6/21/2013 Dr.T.V.Rao MD 36
  37. 37. Start with Empherical Treatment• It is not always appropriate to withholdantimicrobial therapy while three sets ofblood cultures are taken over a 12 hperiod. This recommendation is intendedto be pragmatic, allowing time to take atleast two sets of blood cultures (theminimum for a secure microbiologicaldiagnosis) prior to commencingantimicrobial therapy.6/21/2013 Dr.T.V.Rao MD 37
  38. 38. How to collect the Blood• Sampling ofintravascular linesshould beavoided, unless part ofpaired through-line andperipheral sampling todiagnose concurrentintravascular catheter-related bloodstreaminfection.6/21/2013 Dr.T.V.Rao MD 38
  39. 39. Longer Incubation is notNeeded• In the previous BSAC guideline,1 the traditionalrecommendation for extended incubation andterminal subculture was maintained to increase theyield of fastidious and slow-growing bacteria,although the evidence for this was tenuous in the eraof automated continuous-monitoring blood culturesystems. In the light of further data and the provenutility of complementary non-culture-basedtechnologies, the case for extended incubation andblind subculture is not justified and therefore it is notrecommended6/21/2013 Dr.T.V.Rao MD 39
  40. 40. Blood CulturesBlood Cultures– Minimum of three blood cultures (ideally spread over 24hrs)– Three separate venipuncture sites ideally– Obtain correct volume of blood for culture bottlesPositive Result– 1 set gives 90% sensitivity, remaining 2 sets add 8%– Multiple same cultures are important in confirmingsignificance, especially for less typical organismsNegative Result– Prior antibiotic therapy– ‘Culture negative endocarditis’ – fastidous orgs / non-culturable– May support a non-endocarditis patient diagnosis6/21/2013 Dr.T.V.Rao MD 40
  41. 41. Blood CulturesAlways need to get full identificationof bacteria from positive bloodcultures in suspected endocarditisFull sensitivity testingNeed full MIC (minimum inhibitoryconcentration) for PenicillinLiaison with Lab/microbiologist incases where endocarditissuspected/diagnosed6/21/2013 Dr.T.V.Rao MD 41
  42. 42. Be cautious when you sendmultiple samples• Bacteraemia iscontinuous in IErather thanintermittent, sopositive results fromonly one set out ofseveral bloodcultures should beregarded withcaution.6/21/2013 Dr.T.V.Rao MD 42
  43. 43. Prior administration of Antibiotics giveNegative Culture Results• Failure to culture a causative microorganism inIE is often due to the administration ofantimicrobials prior to blood culture, but mayalso be due to infection caused by fastidiousor slow-growing microorganisms. Diagnosticmethods should include serologicalinvestigations where they are available and asystematic approach is advised, based on theclinical history of the patient and theirexposure to possible risk factors.6/21/2013 Dr.T.V.Rao MD 43
  44. 44. Culture Negative Results may yield..less known microbes• Microorganismsthat should beconsidered firstinclude Coxiellaburnetii (Qfever) andBartonella spp.6/21/2013 Dr.T.V.Rao MD 44
  45. 45. Additional TestsCBCESR and CRPComplement levels (C3, C4, CH50)RFUrinalysisBaseline chemistries6/21/2013 Dr.T.V.Rao MD 45
  46. 46. ImagingChest x-ray– Look for multiple focal infiltrates and calcificationof heart valvesECG– Rarely diagnostic– Look for evidence of ischemia, conduction delay,and arrhythmiasEchocardiography6/21/2013 Dr.T.V.Rao MD 46
  47. 47. Indications for EchocardiographyTransthoracic echocardiography (TTE)–First line if suspected IE–Native valvesTrans esophageal echocardiography (TEE)–Prosthetic valves–Intracardiac complications–Inadequate TTE–Fungal or S. aureus or bacteremia6/21/2013 Dr.T.V.Rao MD 47
  48. 48. Making the DiagnosisPelletier and Petersdorf criteria (1977)– Classification scheme of definite, probable, and possible IE– Reasonably specific but lacked sensitivityVon Reyn criteria (1981)– Added “rejected” as a category– Added more clinical criteria– Improved specificity and clinical utilityDuke criteria (1994)– Included the role of echocardiography in diagnosis– Added IVDA as a “predisposing heart condition”6/21/2013 Dr.T.V.Rao MD 48
  49. 49. Modified Duke CriteriaDefinite IE– Microorganism (via culture or histology) in a valvularvegetation, embolized vegetation, or intracardiac abscess– Histologic evidence of vegetation or intracardiac abscessPossible IE– 2 major– 1 major and 3 minor– 5 minorRejected IE– Resolution of illness with four days or less of antibiotics6/21/2013 Dr.T.V.Rao MD 49
  50. 50. Bacterial EndocarditisTherapy and Prophylaxis1. Prolonged; high dosages; use of bactericidaldrugs2. Serum antibiotic levels and MBC of theorganism3. Viridans streptococci, Enterococcus, S.aureus, S. pneumoniae, S. pyogenes4. Institution of therapy on empirical grounds5. Proven negative blood cultures on Abx6. Prophylaxis: dental extraction, GU.6/21/2013 Dr.T.V.Rao MD 50
  51. 51. TreatmentParenteral (IV) antibiotics–High serum concentrations to penetratevegetations–Prolonged treatment to kill dormantbacteria clustered in vegetationsSurgery–Intracardiac complications/paravalveabscessSurveillance blood cultures6/21/2013 Dr.T.V.Rao MD 51
  52. 52. Treatment - SpecificModify empiric therapy oncecultures/sensitivities knownLong duration 4-6 weeks Rx is requiredRefer to Trust Guidelines / BSAC Working PartyGuidelines (2004)Liaise with MicrobiologistLiaise with Cardiac Surgeon if neededMonitor response to treatment(clinical, CRP, ECHO) & look for complications6/21/2013 Dr.T.V.Rao MD 52
  53. 53. ComplicationsFour etiologies–Embolic–Local spread of infection–Metastatic spread of infection–Formation of immune complexes –glomerulonephritis and arthritis6/21/2013 Dr.T.V.Rao MD 53
  54. 54. Embolic ComplicationsOccur in up to 40% of patients with IEPredictors of embolization–Size of vegetation–Left-sided vegetations–Fungal pathogens, S. aureus, and Strep.BovisIncidence decreases significantly afterinitiation of effective antibiotics6/21/2013 Dr.T.V.Rao MD 54
  55. 55. Embolic ComplicationsStrokeMyocardial Infarction– Fragments of valvular vegetation or vegetation-induced stenosis of coronary ostiaIschemic limbsHypoxia from pulmonary emboliAbdominal pain (splenic or renal infarction)6/21/2013 Dr.T.V.Rao MD 55
  56. 56. Metastatic Spread of InfectionMeningitis and/or encephalitisVertebral osteomyelitisMetastatic abscess–Kidneys, spleen, brain, softtissuesSeptic arthritis6/21/2013 Dr.T.V.Rao MD 56
  57. 57. Prevention – the procedure• Dental proceduresknown to producebleeding• Tonsillectomy• Surgery involving GI,respiratory mucosa• Esophageal dilation• ERCP for obstruction• Gallbladder surgery• Cystoscopy, urethraldilation• Urethral catheter ifinfection present• Urinary tractsurgery, includingprostate• I&D of infected tissue6/21/2013 Dr.T.V.Rao MD 57
  58. 58. Antibiotic Therapy• Treatment tailored to etiologic agent–Important to note MIC/MBCrelationship for each causativeorganism and the antibiotic used–High serum concentration necessary topenetrate avascular vegetation–ID CONSULT EVERY TIME6/21/2013 Dr.T.V.Rao MD 58
  59. 59. Antibiotic Therapy• Effective antimicrobial treatment shouldlead to defervescence within 7 – 10 days–Persistent fever in:• IE due to staph, pseudomonas, culture negative• IE with micro vascular complications/majoremboli• Intracardiac/extra cardiac septic complications• Drug reaction6/21/2013 Dr.T.V.Rao MD 59
  60. 60. Prevention• Prophylactic regimen targeted againstlikely organism–Strep. viridans – oral, respiratory,esophageal–Enterococcus – genitourinary,gastrointestinal–S. aureus – infected skin, mucosal surfaces6/21/2013 Dr.T.V.Rao MD 60
  61. 61. Prevention – the underlying lesion• High risk lesions– Prosthetic valves– Prior IE– Cyanotic congenital heart disease– PDA– AR, AS, MR,MS with MR– VSD– Coarctation– Surgical systemic-pulmonaryshunts• Intermediate risk– MVP with murmur– Pure MS– Tricuspid disease– Pulmonary stenosis– ASH– Bicuspid Ao valve with nohemodynamic significanceLesions at highest risk6/21/2013 Dr.T.V.Rao MD 61
  62. 62. Current TrendsUncommon bacteria a concern• Endocarditis has been documented forapproximately 450 years, the diagnostic challengesand treatment dilemmas are as real today as theywere in the time of Fernel . Major advances havebeen made in the diagnosis of endocarditis, in bothlaboratory and clinical (imaging) parameters, but weare witnessing the emergence of several newlydescribed causal bacterial species, such asTropheryma whippelii and Bartonella spp., as well assporadic case reports of unusual and uncommoncausal organisms, including Finegoldia sp., Gemellaspp., and Abiotrophia defective.6/21/2013 Dr.T.V.Rao MD 62
  63. 63. Molecular Methods• In addition, since diagnostic methods, mainly16S rDNA polymerase chain reaction (PCR) andsequencing, are now beginning to identify suchinfections, no evidence base exists to help determineeffective antimicrobial drug regimens to successfullytreat endocarditis caused by such organisms.Furthermore, as specimens from many of theseinfections are culture-negative, conventionalantibiotic susceptibility testing does not help thecardiologist decide on the most suitableantimicrobial drug regimens.6/21/2013 Dr.T.V.Rao MD 63
  64. 64. New challenges in Endocarditis• 1) the emergence of antimicrobial resistance in classicinfective endocarditis microflora, namely, the gram-positive cocci; 2) the existence of antimicrobialresistance in complex ecologic biofilms; 3) the changingpattern of causal agents now regarded as importantpathogens of infective endocarditis, e.g., Bartonellaspp., T. whippelii, and fungi; and 4) changingepidemiologic trends of persons who acquire infectiveendocarditis, including injection drug users, personswith HIV/AIDS, children with congenital heartdefects, and persons undergoing body piercing.6/21/2013 Dr.T.V.Rao MD 64
  65. 65. References• Emerging Issues in Infective EndocarditisBeverley C. Millar* and John E. Moore• Guidelines for the diagnosis andantibiotic treatment of endocarditis inadults: a report of the Working Party ofthe British Society for AntimicrobialChemotherapy F. Kate Gould etal6/21/2013 Dr.T.V.Rao MD 65
  66. 66. • The Programme created byDr.T.V.Rao MD for MedicalProfessionals in the DevelopingWorld• Email• doctortvrao@gmail.com6/21/2013 Dr.T.V.Rao MD 66

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