Infective endocarditis@ghanem@


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A lecture on common problem infective endocarditis prepared by IslamGhanem Ahmed Ghanem assistant lecturer of cardiology Zagazig university 2013

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  • 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.
  • 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.
  • Sometimes its difficult to see your way!
    Too easy – the patients fault self inflicted – the just desert of a lifetime of gluttony and sloth; or too difficult time consuming unrewarding
    Gps the gate keeper
  • Infective endocarditis@ghanem@

    1. 1.  Infective Endocarditis (IE): an infection of the heart’s endocardial surface
    2. 2.  The valves involved › Mitral 28-45% › Aortic 5-36% › Both 0-35% › Tricuspid 0-6% › Pulmonary <1%
    3. 3.  Incidence - varies according to location  Males > females  May occur at any age and increasingly common in elderly  Mortality 20-30%  Decline in incidence of rheumatic fever  The commonest cause in adults is mitral valve prolapse with regurgitation  More prosthetic valves  More nosocomial cases, injected drug use  More staphylococcal infection
    4. 4.  Native IE:  Streptococcus viridnas  Streptococcus bovis  Staphylococcus aureus  Staphylococcus epidermidis  HACEK organisms  Prosthetic IE:  Early (>1year)  Staphylococcus epidermidis  Staphylococcus aureus  Streptococcus viridnas  Enerococci  Late(<1year)  As native IE
    5. 5.  Haemophilus aphrophilus, H. paraphrophilus, parainfluenzae  Actinobacillus actinomycetemcomitans  Cardiobacterium hominis  Eikenella corrodens  Kingella kingae
    6. 6.  High risk › MVP with regurgitaion › Prosthetic cardiac valve › Prior episodes of endocarditis › Degenerative valvular diseases › Complex congenital cardiac defect › Surgical systemic-pulmonary shunts – Intravenous drug abuse – Intravascular catheters
    7. 7.  Moderate risk › PDA, VSD, primum ASD › Co-Aorta › Bicuspid aortic valve › Hypertrophic cardiomyopathy
    8. 8.  Low risk › Isolated secundum atrial septal defect › ASD, VSD, or PDA > 6 months past repair
    9. 9. nfective Endocarditis: a changing disease new high-risk subgroups IVDA elderly intracardiac devices nosocomial diseases more difficult to prevent more difficult to treat
    10. 10. 1. Endocardium is resistant to infection 2. Turbulent blood flow disrupts the endocardium making it “sticky” 3. Bacteremia delivers the organisms to the endocardial surface 4. Adherence of the organisms to the endocardial surface 5. Eventual invasion of the valvular leaflets
    11. 11.  Alteration of the valvular endothelial surface leading to deposition of platelets and fibrin  Bacteremia with seeding of non- bacterial thrombotic vegetation (NBTE)  Adherence and growth, further platelet and fibrin deposition  Extension to adjacent structures › Papillary muscle, aortic valve ring abscess, conduction system
    12. 12.  Low pressure side of structural lesion › Atrial side of mitral valve (MR) › Ventricular side of aortic valve (AR, AS with R) › But, Non infective endocarditis vegetations occur at atrial side of mitral valve, aortic side of aortic valve › Congenital abnormality (MV prolapse, bicuspid AV) › Scarring from rheumatic heart disease or sclerosis as a consequence of aging › Prosthetic valves  Other turbulence, high-velocity jets › Ventricular septal defect › Stenotic valve  Direct mechanical damage from catheters, pacemaker leads
    13. 13. The clinical manifestation IE result from: 1. The local destructive effects of intracardial infection; 2. The embolization of septic fragments of vegetations to distant sites, resulting in infarction or infection; 3. The hematogenous seeding of remote sites during continuous bacteremia and 4. An antibody response to the infecting organism with subsequent tissue injury due to deposition of preformed immune complexes.
    14. 14.  Vegetations on valve closure lines  Destruction and perforation of valve leaflet  Rupture of chordae tendinae, intraventricular septum, papillary muscles  Valve ring abscess  Myocardial abscess  Conduction abnormalities
    15. 15.  Heart murmurs › It has been found that 15% don’t have murmurs at initial diagnosis, however most develop a murmur during the course of the disease › Changing murmurs – factors other than valvular integrity like change in cardiac output, temperature, hematocrit may play a role. However new onset regurgitant murmur in a setting of acute sepsis is virtually diagnostic.
    16. 16. MORPHOLOGY  The hallmark of IE is presence of friable, bulky, potentially destructive vegetations containing fibrin, inflammatory cells and bacteria or other organisms.  Aortic and mitral valve most common sites, valves of right heart may be involved particularly in intravenous drug abusers.  Vegetations sometimes erode into the underlying myocardium and produce an abscess (ring abscess).  Emboli may shed from the vegetation leading to abscesses formation at the site where emboli lodged, this may lead to sequelae such as septic infracts or mycotic aneurysms.  The vegetations of subacute endocarditis are associated with less valvular destruction than acute endocarditis.  Microscopically vegetations of typical subacute IE often have granulation tissue indicating healing at the bases.  With time fibrosis, calcification and a chronic inflammatory infiltrate can develop.
    17. 17. The aortic valve with a large, irregular, reddish tan vegetation Here, infective endocarditis on the mitral valve has spread into the septum all the way to the tricuspid valve, producing a fistula.
    18. 18. Microscopically, the valve in infective endocarditis demonstrates friable vegetations of fibrin and platelets (pink) mixed with inflammatory cells and bacterial colonies (blue). The friability explains how portions of the vegetation can break off and embolize.
    19. 19. Here is a valve with infective endocarditis. The blue bacterial colonies on the lower left are extending into the pink connective tissue of the valve. Valves are relatively avascular, so high dose antibiotic therapy is needed to eradicate the infection.
    20. 20. Acute bacterial endocarditis caused by Staphylococcus aureus with perforation of the aortic valve and aortic valve vegetations.
    21. 21. Acute bacterial endocarditis caused by Staphylococcus aureus with aortic valve ring abscess extending into myocardium.
    22. 22. Bartonella henselae bacilli in cardiac valve of a patient with blood culture- negative endocarditis The bacilli appear as black granulations.
    23. 23. S. Aureus mitral valve vegetation, anterior leaflet
    24. 24.  Systemic embolism is reported to occur in over 50% cases in autopsy studies.  Most common sites are brain, kidneys, skin, spleen, eye and CNS (coronary embolization is rare).  There is increasing evidence to show that embolic phenomena actually represent “immune complex” deposition in small systemic arteries.
    25. 25.  Cutaneous manifestations › Petichiae (20-40%) › Subcunjunctival and subungual splinter hemorrhages due to lipid microembolism. › Osler nodes  Tender, purplish erythematous papules in pulp of distal fingers  Due to hypersensitive angitis – cultures are negative › Janeway lesions  Erythematous, non-tender nodules on palms or soles. › Clubbing found only in 10-20%.  Ocular manifestations › Roth spot- flame shaped hemorrhage occasionally takes the form of cotton wool spot(rounded red with pale center).
    26. 26. Janeway lesions Splinter hemorrhages Osler node
    27. 27. Petechial rash. He was diagnosed with right- sided staphylococcal endocarditis. Osler nodes
    28. 28. Osler's nodes on a finger and foot. Janeway lesions are Flat, painless, erythematous lesions seen on the palm of this patient's hand. Frequently associated with bacterial endocarditis.
    29. 29. Seen here in the finger at the right are small splinter hemorrhages in a patient with infective endocarditis. These hemorrhages are subungual, linear, dark red streaks. Similar hemorrhages can also appear with trauma.
    30. 30. Roth spots: it has pale center and red periphery
    31. 31.  Renal › Immune complex mediated glomerulonephritis (improve with effective antibiotics) › Focal glomerulonephritis and embolic renal infarct manifest with hematuria but rarely leading to renal failure › Renal failure is mostly due to impaired hemodynamics, antibiotics toxicity  Splenic enlargement, infarction  Septic or bland pulmonary embolism
    32. 32.  Neurological (mostly Staph.aureus) › Embolic stroke is the commonest (Antibiotic is the anticoagulant in this case, Thrombolytics and anticoagulants are relatively contraindicated) › Intracranial hemorrhage (rupture of mycotic aneurysm, septic arteritis, hemorrhage into an infarct)  Mycotic aneurysm: Focal dilatations of arteries occuring at points in the arterial wall that have been weakened by infection in the vasa vasorum or where septic emboli have lodged. › Encephalopathy,cerebritis, brain abcesses, meninigitis
    33. 33.  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
    34. 34.  The terms acute and subacute are used to define duration of infection, however are older terms and should not be used
    35. 35.  Symptoms › Fever, sweats, chills › Anorexia, malaise, weight loss  Signs › Anemia (normochromic, normocytic) › Splenomegaly › Microscopic hematuria, proteinuria › New or changing heart murmur, CHF › Embolic or immunologic dermatologic signs › Hypergammaglobulinemia, elevated ESR, CRP, RF
    36. 36. SYMPTOM AND SIGNS SBE: Initially, symptoms are vague: low-grade fever (< 39° C), night sweats, fatigability, malaise, and weight loss. Chills and arthralgias may occur. Symptoms and signs of valvular insufficiency may be a first clue. Initially, ≤ 15% of patients have fever or a murmur, but eventually almost all develop both. Physical examination may be normal or include pallor, fever, change in a preexisting murmur or development of a new regurgitant murmur, and tachycardia.  Retinal emboli can cause round or oval hemorrhagic retinal lesions with small white centers (Roth's 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's nodes), nontender hemorrhagic macules on the palms or soles (Janeway lesions), and splinter hemorrhages under the nails.
    37. 37.  About 35% of patients have CNS effects, including transient ischemic attacks, stroke, toxic encephalopathy, and, if a mycotic CNS aneurysm ruptures, brain abscess and subarachnoid hemorrhage.  Renal emboli may cause flank pain and, rarely, gross hematuria.  Splenic emboli may cause left upper quadrant pain. Prolonged infection may cause splenomegaly or clubbing of fingers and toes.
    38. 38.  ABE and PVE: Symptoms and signs are similar to those of SBE, but the 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.  Right-sided endocarditis: Septic pulmonary emboli may cause cough, pleuritic chest pain, and sometimes hemoptysis. A murmur of tricuspid regurgitation is typical.
    39. 39.  Congestive heart failure  Extravalvular cardiac manifestations ( myocarditis, conduction disturbances)  Systemic and pulmonary embolism  Mycotic aneurysm  Neurologic – stroke, neuropsychiatric syndromes  Renal – glomerulonephritis, renal infarcts  Hematological – anemia, TTP
    40. 40.  Most patients with infective endocarditis should respond within 48 hours of initiation of appropriate antibiotic therapy. If persistent fever consider:  perivalvular extension of infection and possible abscess formation.  Extracardiac embolic complications  Pulmonary embolism (secondary right-sided endocarditis or prolonged hospitalization).  Drug reaction (the fever should promptly resolve after drug withdrawal)  Nosocomial infection (i.e. venous access site, urinary tract infection)
    41. 41.  Echocardiography: esp transesophageal echocardiography.  Blood culture.  Serology(Immunoglobulins and compliment).  ECG: Conduction abnormalities.  CBC: Normocytic normochromic anemia, leukocytosis.  ESR.  Urine exam: proteinurea and microscopic hemeturia is common
    42. 42.  Transthoracic › Relatively low sensitivity › Good specificity  Transesophageal › Detection of valve ring abscess (87% vs. 28% sensitivity for TTE) › Detection of prosthetic valve IE especially in mitral position › Detection of small vegetations (less than 2mm) › Echocardiography cannot distinguish • between infective and non infective vegetations • Between vegetation, thrombus and pannus • Between active and healed endocarditis
    43. 43.  Limited thoracic windows = TTE low sensitivity  Prosthetic valves  Prior valvular abnormality  S. aureus bacteremia and suspected IE  Bacteremia with organisms likely to cause IE = high prior probability of IE
    44. 44. mitral valve vegetation
    45. 45.  MULTIPLE BLOOD CULTURES BEFORE EMPIRIC THERAPY  If not critically ill › 3 blood cultures over 12-24 hour period › ? Delay therapy until diagnosis confirmed  If critically ill › 3 blood cultures over one hour  20 cm each sample from 3 different puncture sites  Not mandatory during the fever
    46. 46.  Less common with improved blood culture methods  Causes:  Prior antibiotic therapy(40%)  Fastidious(slowly growing organisms): HACEK, Brucella, Bartonella, TropherymaWhipplei  Non bacterial organisms: Marantic, fungal endocarditis  Special media required › Brucella, Mycoplasma, Chlamydia, Histoplasma, Legionella, Bartonella  Longer incubation may be required › HACEK  Coxiella burnetii (Q Fever), Trophyrema whipplei will not grow in cell-free media(Serology)
    47. 47.  Electrocardiogram › Conduction delays › Ischemia or infarction (coronary embolism)  Chest X-ray › Septic emboli in right-sided IE › Valve calcification (degenerative heart disease) › CHF
    48. 48.  PCR › Coxiella burnetii › Tropheryma whipplei › Bartonella henselae  Serology › Coxiella burnetii › Bartonella › Brucella › Legionella › Chlamydophila psittaci
    49. 49.  1977 Pelletier and Petersdorf criteria  1981 von Reyn criteria  1994 Duke criteria  2000 Modified Duke criteria: It is of limited value in PVE, CDRIE, BCNIE and should not replace the clinical judgment
    50. 50.  Major criteria:  A. Positive blood culture for Infective Endocarditis 1- Typical microorganism consistent with IE from 2 separate blood cultures, as noted below: viridans streptococci, Streptococcus bovis, or HACEK group, or community-acquired Staphylococcus aureus or enterococci, in the absence of a primary focus  or 2- Microorganisms consistent with IE from persistently positive blood cultures defined as:  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 1 hour apart)(Persistntly +ve blood cultures The best)  Single positive blood culture for Coxeilla burnetti or phase IgG antibody titer < 1 : 800
    51. 51.  B. Evidence of endocardial involvement 1- Positive echocardiogram for IE defined as :  (vegetation) 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, or  (abcess) , or    new partial dehiscence of prosthetic valve 2- New valvular regurgitation (New or changing of preexisting murmur)
    52. 52.  Minor criteria: 1- Predisposition: predisposing heart condition or intravenous drug use 2- Fever: temperature > 38.0° C (100.4° F) 3- Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, and Janeway lesions 4- Immunologic phenomena: glomerulonephritis, Osler's nodes, Roth spots, and rheumatoid factor 5- Microbiological evidence: positive blood culture but does not meet a major criterion as noted above or serological evidence of active infection with organism consistent with IE
    53. 53.  Diagnosis  Definite:  Pathological criteria: Microorganisms demonstrated by histological examination of a vegeation or intracardiac abcess or peripheral embolus showing active endocarditis  Clinical criteria :  Definite: • Two major criteria, or • One major and three minor criteria, or • Five minor criteria  Possible: •   One major and one minor criteria, or • Three minor criteria  Rejected: • Firm alternative diagnosis, or • Resolution of IE syndrome (fever) ≥ 4 days of antibiotics, or • No pathological evidence of IE at surgery or autopsy with
    54. 54.  Noninfected (sterile) vegetation are caused by non bacterial thrombotic endocarditis  The endocarditis of SLE called Libman-sacks endocarditis.  NBTE is characterized by deposition of small sterile thrombi on the leaflet of cardiac valve  Grossly the lesions are 1mm-5mm in size occur singly on the line of closure of leaflets (at atrial side of mitral valve, aortic side of aortic valve).  Histologically :they composed of bland thrombi(Platelets+Fibrin, No bacteria or inflammatory cells) that are loosely attached.
    55. 55.  They are source of systemic emboli that produce infarcts in brain,heart or elsewhere.  NBTE or marantic endocarditis also occur in debilitated patient.  NBTE occur in DVT, mucinous adenocarcinoma, is part of Trousseau syndrome of migratory thrombophelebitis.  Endocarditis of SLE ( Libman-Sacks Disease). Mitral and tricuspid valvulitis with small sterile vegetations.
    56. 56. Here is another marantic vegetation on the leftmost cusp. These vegetations are rarely over 0.5 cm in size. However, they are very prone to embolize.
    57. 57. The valve is seen on the left, and a bland vegetation is seen on the right. It appears pink because it is composed of fibrin and platelets. It displays about as much morphologic variation as a brown paper bag. Such bland vegetations are typical of the non- infective forms of endocarditis.
    58. 58. Libman-sacks endocarditis. Here are flat, pale tan, spreading vegetations over the mitral valve surface and even on the chordae tendineae.
    59. 59.  Non infective Endocarditis (as in SLE, Antiphospholipid Syndrome)  Cardiac Neoplasms, Primary  Vegetations from pannus, thrombus
    60. 60.  Resolution of fever within 5-7 days  Blood culture become sterile within 2 days (Except in Staph. up to 9 days)  Blood culture should be repeated daily until sterile, rechecked if recrudescent fever , performed again 4-6 weeks after therapy to document cure  Blood tests to detect renal, hepatic, hematological toxicity should be done periodically (especially in 3rd w. of therapy)
    61. 61.  Emergent: Within 24h.  Urgent: Within few days.  Elective: After 1-2w.of antibiotics.  If there is indication for surgery&  Cerebral hemorrhage: Postpone for 4w.  Cerebral infarction: Postpone for 2w.
    62. 62.  Use ampho B and flucytosine ( toxic to B. marrow and kidneys)  Almost always needs surgery .  Long term oral prophylaxis is often given to prevent relapse
    63. 63. 513 patients with complicated IE , 230 (40%) surgical therapy513 patients with complicated IE , 230 (40%) surgical therapy 6 month mortality6 month mortality Impact of surgery on mortalityImpact of surgery on mortality