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  1. 2. <ul><li>Endocarditis is an inflammation of the inner layer of the heart, the endocardium. It usually involves the heart valves (native or prosthetic valves). Other structures which may be involved include the interventricular septum, the chordae tendinae, the mural endocardium, or even on intracardiac devices. </li></ul><ul><li>Endocarditis is characterized by a prototypic lesion, the vegetation , which is a mass of platelets, fibrin, microcolonies of microorganisms, and scant inflammatory cells. </li></ul>
  3. 4. <ul><li>Infectious endocarditis involves the heart valves and is most commonly found in people who have underlying heart disease. Sources of the infection may be transient bacteremia, which is common during dental, upper respiratory, urologic, and lower gastrointestinal diagnostic and surgical procedures. </li></ul><ul><li>The infection can cause growths on the heart valves, the lining of the heart, or the lining of the blood vessels. These growths may be dislodged and send clots to the brain, lungs, kidneys, or spleen. </li></ul><ul><li>Classified in to two types on the basis of etiology </li></ul><ul><li>Infective endocarditis </li></ul><ul><li>Non-infective endocarditis </li></ul>
  4. 5. INFECTIVE ENDOCARDITIS <ul><li>Infective endocarditis (IE): is due to microbial infection of heart valve(native or Prosthetic) . The lining of cardiac chamber or blood vessel, or congenital anomaly. The causative agent is usually bacterium, but may be arickettsia, chlamydia or fungus. </li></ul><ul><li>Pathophysiology. Is occur typically at sites of prexisting endocardial damage. However ,infection in prviously normal heart occur by S aureus. </li></ul><ul><li>Infection tend to occur at site of endothelial damage bcz these area attract deposit of platelets and fibrin, which are vulnerable to colonisation by blood born organisms. Adjecent tissue are destroyed and abscess may form, valve regurgitation may develop or increased. </li></ul>
  5. 6. <ul><li>If the affected valve is damage by tissue distortion. </li></ul><ul><li>Extra cardiac manifestations e.g. vacuities ,infarcts of skin, spleen ,kidney and brain due to emboli or immune complex deposits. </li></ul><ul><li>CLASSIFICATION </li></ul><ul><li>Sub-acute bacterial endocarditis </li></ul><ul><li>Acute bacterial endocarditis </li></ul><ul><li>Post operative endocarditis </li></ul>
  6. 7. <ul><li>CLASSIFICATION </li></ul><ul><li>Infective endocarditis may have an indolent, subacute course or a more acute, fulminant course with greater potential for rapid decompensation. </li></ul><ul><li>Subacute bacterial endocarditis (SBE), although aggressive, usually develops insidiously and progresses slowly (i.e, over weeks to months). Often, no source of infection or portal of entry is evident. SBE is caused most commonly by streptococci (especially viridans, microaerophilic, anaerobic, and nonenterococcal group D streptococci and enterococci) and less commonly by S. aureus, Staphylococcus epidermidis, Gemella morbillorum, Abiotrophia defectiva, Granulicatella sp, and fastidious Haemophilus sp. SBE often develops on abnormal valves after asymptomatic bacteremia due to periodontal, GI, or GU infections. </li></ul><ul><li>Acute bacterial endocarditis (ABE) usually develops abruptly and progresses rapidly (ie, over days). A source of infection or portal of entry is often evident. When bacteria are virulent or bacterial exposure is massive, ABE can affect normal valves. It is usually caused by S. aureus, group A hemolytic streptococci, pneumococci, or gonococci. </li></ul>
  7. 8. <ul><li>Post oprative or PVE endocarditis: develops in 2 to 3% of patients within 1 yr after valve replacement and in 0.5%/yr thereafter. It is more common after aortic than after mitral valve replacement and affects mechanical and bioprosthetic valves equally. </li></ul><ul><li>Early-onset infections (< 2 mo after surgery) are caused mainly by contamination during surgery with antimicrobial-resistant bacteria (eg, S. epidermidis, diphtheroids, coliform bacilli, Candida sp, Aspergillus sp). </li></ul><ul><li>Late-onset infections are caused mainly by contamination with low-virulence organisms during surgery or by transient asymptomatic bacteremias, most often with streptococci; S. epidermidis; diphtheroids; and the fastidious gram-negative bacilli, Haemophilus sp, Actinobacillus actinomycetemcomitans, and Cardiobacterium hominis. </li></ul>
  8. 9. CAUSES OF INFECTIVE ENDOCARDITIS Causes by gram- ve, gram+ve bact & fungi. Most often caused by Staph and strep cocci an recently recognise bact S lugdensis affect previously normal valve Patient wd native valve endocarditis: 70% a-hemolytic strep 25% S aures and S epidermidis 5% othe bact and fungi Endocaditis in drug addicts : S aureus (55%),S viridans (15%),gram neg-ve bact 1 Prosthetic valvular endocarditis (PVE):
  9. 10. <ul><li>MORPHOLOGY </li></ul><ul><li>The hallmark of IE is presence of friable, bulky, potentially destructive vegetations containing fibrin, inflammatory cells and bacteria or other organisms. </li></ul><ul><li>Aortic and mitral valve most common sites, valves of right heart may be involved particularly in intravenous drug abusers. </li></ul><ul><li>Vegetations sometimes erode into the underlying myocardium and produce an abscess ( ring abscess ). </li></ul><ul><li>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 . </li></ul><ul><li>The vegetations of subacute endocarditis are associated with less valvular destruction than acute endocarditis. </li></ul><ul><li>Microscopically vegetations of typical subacute IE often have granulation tissue indicating healing at the bases. </li></ul><ul><li>With time fibrosis, calcification and a chronic inflammatory infiltrate can develop. </li></ul>
  10. 11. 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.
  11. 12. 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.
  12. 13. 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.
  13. 14. Acute bacterial endocarditis caused by Staphylococcus aureus with perforation of the aortic valve and aortic valve vegetations.
  14. 15. Acute bacterial endocarditis caused by Staphylococcus aureus with aortic valve ring abscess extending into myocardium.
  15. 17. The small pink vegetation on the rightmost cusp margin represents the typical finding with non-bacterial thrombotic endocarditis (or so-called &quot;marantic endocarditis&quot;). This is non-infective. It tends to occur in persons with a hypercoagulable state (Trousseau's syndrome, a paraneoplastic syndrome associated with malignancies) and in very ill persons
  16. 18. Bartonella henselae bacilli in cardiac valve of a patient with blood culture-negative endocarditis The bacilli appear as black granulations.
  17. 19. <ul><li>SYMPTOM AND SIGNS: </li></ul><ul><li>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. </li></ul><ul><li>Retinal emboli can cause round or oval hemorrhagic retinal lesions with small white centers (Roth's spots). </li></ul><ul><li>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. </li></ul>
  18. 20. Petechial rash. He was diagnosed with right-sided staphylococcal endocarditis. Osler nodes
  19. 21. 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.
  20. 22. Roth spots: red center with pale periphery; top and left (The one on right is the optic disc, as it has pale center and red periphery)
  21. 23. <ul><li>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. </li></ul><ul><li>Renal emboli may cause flank pain and, rarely, gross hematuria. </li></ul><ul><li>Splenic emboli may cause left upper quadrant pain. Prolonged infection may cause splenomegaly or clubbing of fingers and toes. </li></ul>
  22. 24. 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.
  23. 25. <ul><li>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. </li></ul><ul><li>Right-sided endocarditis: Septic pulmonary emboli may cause cough, pleuritic chest pain, and sometimes hemoptysis. A murmur of tricuspid regurgitation is typical. </li></ul>
  24. 26. Duke Criteria for Infective Endocarditis <ul><li>Major criteria: </li></ul><ul><li>A. Positive blood culture for Infective Endocarditis </li></ul><ul><li>1- Typical microorganism consistent with IE from 2 separate blood cultures, as noted below: </li></ul><ul><li>viridans streptococci, Streptococcus bovis, or HACEK* group, or </li></ul><ul><li>community-acquired Staphylococcus aureus or enterococci, in the absence of a primary focus </li></ul><ul><li>or </li></ul><ul><li>2- Microorganisms consistent with IE from persistently positive blood cultures defined as: </li></ul><ul><li>2 positive cultures of blood samples drawn >12 hours apart, or </li></ul><ul><li>all of 3 or a majority of 4 separate cultures of blood (with first and last sample drawn 1 hour apart) </li></ul><ul><li>B. Evidence of endocardial involvement </li></ul><ul><li>1- Positive echocardiogram for IE defined as : </li></ul><ul><li>·        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 </li></ul><ul><li>         ab  new partial dehiscence of prosthetic valveor </li></ul><ul><li>2- New valvular regurgitation (worsening or changing of preexisting murmur not sufficient) </li></ul>
  25. 27. <ul><li>Minor criteria: </li></ul><ul><li>Predisposition: predisposing heart condition or intravenous drug use </li></ul><ul><li>Fever: temperature > 38.0° C (100.4° F) </li></ul><ul><li>Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, and Janeway lesions </li></ul><ul><li>Immunologic phenomena: glomerulonephritis, Osler's nodes, Roth spots, and rheumatoid factor </li></ul><ul><li>Microbiological evidence: positive blood culture but does not meet a major criterion as noted above¹ or serological evidence of active infection with organism consistent with IE </li></ul><ul><li>Echocardiographic findings: consistent with IE but do not meet a major criterion as noted above </li></ul>
  26. 28. <ul><li>Clinical criteria for infective endocarditis requires: </li></ul><ul><li>• Two major criteria, or </li></ul><ul><li>• One major and three minor criteria, or </li></ul><ul><li>• Five minor criteria </li></ul><ul><li>*HACEK group:  Haemophilus sp, Actinobacilius actinomycetemcomitans, Cardiobacterium hominis, Eikenella rodens y Kingella sp </li></ul><ul><li>  </li></ul>
  27. 29. Non Infective Endocarditis <ul><li>Noninfected (sterile) vegetation are caused by non bacterial thrombotic endocarditis </li></ul><ul><li>The endocarditis of SLE called Libman-sacks endocarditis. </li></ul><ul><li>NBTE is characterized by deposition of small sterilte thrombi on the leaflet of cardiac valve </li></ul><ul><li>Grossly the lesions are 1mm-5mm in size occur singly on the line of closure of leaflets. </li></ul><ul><li>Histologically : they composed of bland thrombi that are loosely attached. </li></ul>
  28. 30. <ul><li>They are source of systemic emboli that produce infarcts in brain,heart or elsewhere. </li></ul><ul><li>NBTE or marantic endocarditis also occur in debilitated patient. </li></ul><ul><li>NBTE occur in DVT, mucinousadenocarcinoma, is part of Trousseau syndrome of migratory thrombophelebitis. </li></ul><ul><li>Endocarditis of SLE ( Libman-Sacks Disease). Mitral and tricuspid valvulitis with small sterile vegetations. </li></ul>
  29. 31. 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.
  30. 32. 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.
  31. 33. <ul><li>Grossly the lesion are small(1-4mm) single or pink vegetation with warty appearance may located on under surface of AV valve , valvular endocardium, on the cords or on mural endocardium. </li></ul><ul><li>Histologically consist finally granular eosinophilicmaterial that may contain hematoxilin bodies. </li></ul>
  32. 34. Libman-sacks endocarditis. Here are flat, pale tan, spreading vegetations over the mitral valve surface and even on the chordae tendineae.
  33. 35. <ul><li>INVESTIGATIONS: </li></ul><ul><li>Blood Examination. </li></ul><ul><li>Blood culture </li></ul><ul><li>ECG </li></ul><ul><li>Echocardiography: esp transesophageal echocardiography. </li></ul><ul><li>Immunoglobulins and compliment. </li></ul><ul><li>Urine exam: protein urea and microscopic hemeturia is common </li></ul>