Infective endocarditis-1


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  • IE often occurs when there is an underlying cardiac abnormality that creates a high-low pressure gradient.
    The resultant turbulent blood flow disrupts the endocardial surface by peeling away the endothelium.
    The body’s natural response to endothelial damage is to repair it by laying down a sticky platelet-fibrin meshwork, which is a nidus for infection.
    Temporary bacteremia delivers the offending organism to the endocardial surface where is sticks to the platelet-fibrin meshwork. This festers into an infection that eventually invades the cardiac valves.
    The pathophysiology is slightly different with IVDA. It has been postulated that repeated injections of drugs and particulate material causes microtrauma to the cardiac valves, thereby starting the infection cascade.
  • There is an estimated 10-15,000 new cases of IE diagnosed in the U.S. each year, although the exact incidence of IE is difficult to ascertain. IE is a relatively uncommon disease, is not a reportable disease, and different case definitions have existed throughout the years. Furthermore, the incidence varies greatly depending on geographic regions.
    IE is more common among males. The male:female ratio varies from 2:1 to 9:1 depending on the source.
    In the past, IE was a disease of children and young adults. It predominantly affected children with congenital heart disease and adults with rheumatic heart disease. Today, IE commonly affects the elderly, with almost 50% of cases in the U.S. occurring in patients over the age of 60. This may be due to the decreasing incidence of rheumatic heart disease and the increasing proportion of elderly in the U.S.
    Mortality from IE remains high, and ranges from 20-30% despite newer antibiotics and surgical options.
  • The top three risk factors for IE include, IVDA, prosthetic heart valves, and structural heart disease.
    IVDA – one large study of IVDAs found that the use of cocaine was associated with a higher risk of IE than other injectable drugs. The most significant risk factor for right-sided IE is IVDA, although left sided disease is quite common among IVDAs. The most common infecting organism is clearly S. aureus, particularly in right-sided infection.
    Prosthetic valve IE comprises a small proportion of all cases of IE and occurs in only 1% of all patients with artificial heart valves. The greatest risk is in the first year following valve replacement.
    Structural heart disease – approximately ¾ of all cases of IE occur in patients with preexisting structural heart abnormalities. The most common underlying heart abnormalities include mitral valve prolapse with mitral regurgitation and aortic stenosis.
    The most common congenital heart defects include Tetralogy of Fallot, bicuspid aortic valves, coarctation of the aorta, VSDs, and patent ductus arteriosus. In general, the higher the gradient of the valvular insufficiency, the higher the risk of IE.
    One of the greatest risk factors of all is a prior episode of IE. Some studies have documented recurrence as high as 9%.
  • Staphlococcal and Streptococcal organisms comprise over 80% of all infecting organisms.
  • Subungal hemorrhages that extend the entire length of the nail or are primarily located at the proximal end of the nail (near the cuticle) are like due to trauma.
  • If you suspect the pt has subacute IE or is not critically ill, then the three samples can be collected over 24-72 hours and antibiotics can be held until all three samples have been drawn.
    However, if the pt is acutely ill, critical, or unstable, the three cultures should be obtained over a 1 hour time span before beginning empiric therapy.
    There is no need to collect anaerobic blood cultures since virtually all cases of IE are caused by aerobic organisms.
    There is little additional diagnostic yield to collecting more than three blood cultures unless the pt was previously on antibiotics. In one study of 206 cases of IE, the initial blood culture was positive in 96% of streptococcal IE and one of the first two cultures were positive 98% of the time. For pt’s with IE cause by organisms other than strep, one of the first two blood culture was positive in 100% of the cases.
    The estimated diagnostic yield of a blood culture increases by about 3% per mL of blood cultured. One study found that the detection rate for bacteremia increased from 69% to 92% when at least 5mL of blood were used for culture.
    The most common cause of negative cultures in patients with IE is prior antibiotic use.
  • CBC – Look for a normochromic normocytic anemia and/or a leukocytosis.
    ESR and CRP - Look for an elevated erythrocyte sedimentation rate and/or an elevated C-reactive protein which are present 90-100% of the time.
    RF - Occasionally there will be an elevated levels of Rheumetoid Factor, particularly in patients who have been infected for six weeks or more. (Minor Duke’s Criteria)
    UA - Urinalysis may reveal microscopic or gross hematuria, proteinuria, and pyuria. These findings along with a low serum complement level indicate a glomerulonephritis or “immunologic phenomena”. (Minor Duke’s Criteria)
  • CXR – A chest xray can contain multiple diagnostic clues such as calcification of heart valves, which should raise suspicion in a febrile patient without an obvious source. More commonly, the chest xray may reveal septic pulmonary emboli in a patient with right-sided IE (Minor Duke’s Criteria).
    EKG – An EKG alone cannot diagnose IE but it may show evidence of some of the disease’s complications. For example, EKG with ST changes may indicate ischemia or infarction from septic emboli. Arrhythmias such as heart block may indicated extension of the infection from the valves into the septum and surrounding cardiac tissue.
  • TTE and TEE are complementary for evaluating cardiac hemodynamics and anatomy, but TEE has superior sensitivity, especially in detecting native valve vegetations, prosthetic valve vegetations, and local extension of infection. However, it is significantly more expensive and invasive.
    If there is any suspicion of IE, get a TTE.
    If there is staph or fungal bacteremia, a TEE should probably be obtained.
    If there is a high clinical suspicion for IE and the TTE is negative, you should proceed to a TEE.
    If there is a concern for intracardiac complications, a TEE is warranted.
    It’s important to remember that the negative predictive value of a TEE is between 96-98%, meaning that a TEE cannot definitively rule out endocarditis. If the initial TEE is negative in a patient with a high clinical suspicion for IE, a repeat examiniation should be done if the pt does not improve.
  • Pelletier and Petersdorf criteria – 3 case categories:
    Definite – histologic evidence of endocardial vegetations on examination of tissue
    Probable - uniformly positive blood cultures with know underlying heart disease or embolic phenomena OR negative blood cultures in pts with fever, new regurgitant valvular heart murmur, and embolic phenomena
    Possible - uniformly positive blood cultures with know underlying heart disease or embolic phenomena OR negative blood cultures with fever and known underlying heart disease and embolic phenomena
    Von Reyn criteria – modified the above criteria to improve specificity and clinical utility.
    Duke Criteria – relies upon major and minor clinical and pathologic criteria to classify cases as definite, possible, and rejected
  • Multiple studies have validated the Duke criteria. When applied and reapplied over the entire evaluation, these criteria are sensitive and specific and very rarely erroneously reject a true endocarditis.
  • Systemic emboli are among the most common complications of IE, occurring in up to 40% of patients. Subclinical emboli are often found on autopsy.
  • Infective endocarditis-1

    1. 1. Infective Endocarditis DR MOHAMMAD ALI KHALID, Assistant professor of medicine, RMC and allied teaching hospitals.
    2. 2. Definition Infectious Endocarditis (IE): an infection of the heart’s endocardial surface Classified into four groups: – Native Valve IE – Prosthetic Valve IE – Intravenous drug abuse (IVDA) IE – Nosocomial IE
    3. 3. HIGHLIGHTS Fever. Murmer. Worsening of valve dysfunction. Heart failure? Vegetations seen on echocardiography. Systemic manifestations. Positive blood cultures.
    4. 4. Further Classification Acute – Affects normal heart valves – Rapidly destructive – Metastatic foci – Commonly Staph. – If not treated, usually fatal within 6 weeks Subacute – Often affects damaged heart valves – Indolent nature – If not treated, usually fatal by one year
    5. 5. Pathophysiology 1. Turbulent blood flow disrupts the endocardium making it “sticky” 2. Bacteremia delivers the organisms to the endocardial surface 3. Adherence of the organisms to the endocardial surface 4. Eventual invasion of the valvular leaflets
    6. 6. Epidemiology Incidence difficult to ascertain and varies according to location Much more common in males than in females May occur in persons of any age and increasingly common in elderly Mortality ranges from 20-30%
    7. 7. Risk Factors Intravenous drug abuse Artificial heart valves and pacemakers Acquired heart defects – Calcific aortic stenosis – Mitral valve prolapse with regurgitation Congenital heart defects Intravascular catheters
    8. 8. Infecting Organisms Common bacteria – S. aureus – Streptococci – Enterococci Not so common bacteria – Fungi – Pseudomonas – HACEK
    9. 9. HACEK Haemophilis parainfluenzae Actinobacillus Cardiobacterium Eikenella Kingella
    10. 10. Symptoms Acute – High grade fever and chills – SOB – Arthralgias/ myalgias – Abdominal pain – Pleuritic chest pain – Back pain Subacute – – – – – – – Low grade fever Anorexia Weight loss Fatigue Arthralgias/ myalgias Abdominal pain N/V The onset of symptoms is usually ~2 weeks or less from the initiating bacteremia
    11. 11. HISTORY Rhuematic fever Valve surgery or repair Fever SOB Arthralgias Embolic phenomenon Fatigue,dizziness,palpitations.
    12. 12. Signs Fever . Heart murmur. Nonspecific signs – petechiae, subungal or “splinter” hemorrhages, clubbing, splenomegaly, neurologic changes. More specific signs - Osler’s Nodes, Janeway lesions, and Roth Spots. Features particular to a specific valve.
    13. 13. Petechiae 1. Nonspecific 2. Often located on extremities or mucous membranes blpetechiaephoto.htm Photo credit, Josh Fierer, M.D. Eye-Petechiae.html Harden Library for the Health Sciences hardin/ md/cdc/3184.html
    14. 14. 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
    15. 15. Osler’s Nodes American College of Rheumatology default/pages/3b5.htm Hand10/Hand10dx.html 1. More specific 2. Painful and erythematous nodules 3. Located on pulp of fingers and toes 4. More common in subacute IE
    16. 16. Janeway Lesions 1. More specific 2. Erythematous, blanching macules 3. Nonpainful 4. Located on palms and soles
    17. 17. The Essential Blood Test Blood Cultures – – – Minimum of three blood cultures1 Three separate venipuncture sites Obtain 10-20mL in adults and 0.5-5mL in children2 Positive Result – Typical organisms present in at least 2 separate samples – Persistently positive blood culture (atypical organisms) Two positive blood cultures obtained at least 12 hours apart Three or a more positive blood cultures in which the first and last samples were collected at least one hour apart
    18. 18. Additional Labs CBC ESR and CRP Complement levels (C3, C4,) RF Urinalysis Baseline chemistry
    19. 19. Imaging Chest x-ray – Look for multiple focal infiltrates and calcification of heart valves EKG – Rarely diagnostic – Look for evidence of ischemia, conduction delay, and arrhythmias Echocardiography
    20. 20. Indications for Echocardiography Transthoracic echocardiography (TTE) – First line if suspected IE – Native valves Transesophageal echocardiography (TEE) – Prosthetic valves – Intracardiac complications – Inadequate TTE – Fungal or S. aureus or bacteremia
    21. 21. Making the Diagnosis Pelletier and 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”
    22. 22. DUKE CRITERIA MAJOR Positve cultures Positive echo New valvular regurgitation MINOR IV drug abuser Heart disease Fever>38 C Minor echo findings(eg deformed valve but no vegetation)
    23. 23. MAJOR MINOR Vascular embolic events like janeway lesions septic pul infarcts arterial emboli. Immunological events osler nodes Roth spots GN Enlarged spleen
    24. 24. Modified Duke Criteria Definite IE – 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
    25. 25. Treatment Parenteral antibiotics – High serum concentrations to penetrate vegetations – Prolonged treatment to kill dormant bacteria clustered in vegetations Surgery – Intracardiac complications Surveillance blood cultures
    26. 26. ANTIBIOTICS Recommended Benzyl penicillin 2-4 mu QID for 2-6 wks Gentamycin 1-2mg/kg TDS for 2-6 wks. Alternatively Ceftriaxone 1 -2 gm BD Vancomycin 15mg/kg BD Piperacillin 2-4 gmQID Imepeum 250 mg QID Cefotaxime 2gm BD
    27. 27. FUNGAL Amphoterecin B 1mg/kg QID 2 wks max upto 4 wks. Donot exceed 50mg/day Flucytocine 150mg/kg oral for four days
    28. 28. Caution Highly toxic Liver and kidneys Valve replacement mandatory after 2wks therapy with amphoterecin therapy. Monitor drug levels according to manufacturers guidelines.
    29. 29. Complications Four etiologies – Embolic – Local spread of infection – Metastatic spread of infection – Formation of immune complexes – glomerulonephritis and arthritis
    30. 30. Embolic Complications Occur in up to 40% of patients with IE Predictors of embolization – Size of vegetation – Left-sided vegetations – Fungal pathogens, S. aureus, and Strep. Bovis Incidence decreases significantly after initiation of effective antibiotics
    31. 31. 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)
    32. 32. Septic Pulmonary Emboli
    33. 33. Septic Retinal Embolus
    34. 34. Local Spread of Infection Heart failure – Extensive valvular damage Paravalvular abscess (30-40%) – Most common in aortic valve, IVDA, and S. aureus – May extend into adjacent conduction tissue causing arrythmias – Higher rates of embolization and mortality Pericarditis Fistulous intracardiac connections
    35. 35. Local Spread of Infection Acute S. aureus IE with perforation of the aortic valve and aortic valve vegetations. Acute S. aureus IE with mitral valve ring abscess extending into myocardium.
    36. 36. Metastatic Spread of Infection Metastatic abscess – Kidneys, spleen, brain, soft tissues Meningitis and/or encephalitis Vertebral osteomyelitis Septic arthritis
    37. 37. Poor Prognostic Factors Female S. aureus Vegetation size Aortic valve Prosthetic valve Older age Diabetes mellitus Low serum albumen Apache II score Heart failure Paravalvular abscess Embolic events
    38. 38. PROPHYLAXIS Dental/oral/Respira tory/esophageal procedures. Genitourinary/GE procedures Amoxicillin 2gm oral 1 hr before.Clindamycin 600mg or clarithromycin500mg if allergic to penicillin. – . Ampicillin 2gm +Gentamycin 1mg/kg within ½ hr of starting IV followed byAmpicillin 1gm IV 6 hrs later.
    40. 40. REQUIRED Prosthetic valves Previous IE CCHD MVP with regurgitation HOCM/IHSS
    41. 41. NOT REQUIRED MVP Isolated ASD CAD or CABG PPM’S or ICD’S
    42. 42. THANK YOU.