Infective endocarditis


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Infective endocarditis

  1. 1. Infective Endocarditis
  2. 2. Definition: Infection of the endocardial surface of heart characterized by - Colonization or invasion of the heart valves (native or prosthetic) or the mural endocardium by a microbe, - leading to formation of bulky, friable vegetation composed of thrombotic debris and organisms - often associated with destruction of underlying cardiac tissue.
  3. 3. Sites involved: • Heart valves • Mural endocardium • Intracardiac devices • Ventricular septum defects
  4. 4. CLASSIFICATION : Infective endocarditis may have an indolent, subacute course or a more acute, fulminant course with greater potential for rapid decompensation.  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 B hemolytic streptococci, pneumococci, or gonococci.
  5. 5.  Subacute bacterial endocarditis (SBE): • usually develops insidiously • progresses slowly (i.e, over weeks to months). • Often, no source of infection or portal of entry is evident. • SBE often develops on abnormal valves after asymptomatic bacteremia due to periodontal, GI, or GU infections. • 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, and fastidious Haemophilus sp.
  6. 6.  Post oprative endocarditis or PVE • 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. I. 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). II. Late-onset infections 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.
  7. 7. Predisposing factors: CARDIAC AND VASCULAR ABNORMALITIES: • RHD • Myxomatous mitral valve • Degenerative calcific valvular stenosis HOST FACTORS: • Neutropenia • Immunodeficiency • Malignancy • Therapeutic immunosuppression • Bicuspid aortic valves • Diabetes mellitus • Prosthetic valves • Alcohol • IV drug abuse
  8. 8. Microbiology: • Staphylococcus aureus (35%) : Either healthy or deformed valves, IV drug abusers (polymicrobial), devices • Streptococcus viridans (32%) : Native but previously damaged/abnormal valves •Enterococci (8 %) •Coagulase negative staphylococcus - S. epidermidis (4%): Prosthetic valve endocarditis, devices •G –ve bacilli of HACEK group (4%) •Yeast and Fungi(1%) •Culture negative endocarditis (5 %)
  9. 9. Pathogenesis: Portal of entry: ◦ Dental / Surgical Procedures ◦ Contamination by IV drug use ◦ Obvious infections (RS/Skin) ◦ Occult source from gut, oral cavity ◦ Trivial injuries. ◦ Intravascular catheter infection ◦ Nosocomial wounds ◦ Chronic invasive procedures
  10. 10. Endothelial Injury Uninfected Platelet-Fibrin thrombus (NBTE) Transient bacteremia and attachment at NBTE Proliferation and pro-coagulant state Infected, friable, bulky vegetation
  11. 11. Morphology: •Friable, bulky vegetation containing fibrin, inflammatory cells, and microbes •Aortic and mitral valves involved most commonly. •Right side valve involvement in iv drug users.
  12. 12. Symptoms: Acute Subacute ◦ High grade fever and chills ◦ Low grade fever ◦ SOB ◦ Arthralgias/ myalgias ◦ Abdominal pain ◦ Pleuritic chest pain ◦ Back pain ◦ ◦ ◦ ◦ ◦ Anorexia Weight loss Fatigue Arthralgias/ myalgias Abdominal pain
  13. 13. Signs: • Fever • Heart murmur • More specific signs - Osler’s Nodes, Janeway lesions, and Roth Spots • Nonspecific signs – petechiae, “splinter” hemorrhages, clubbing, splenomegaly, neurologic changes
  14. 14. Petechiae 1. Nonspecific 2. Often located on palpebral conjunctiva, buccal and palatal mucosa and the extremities
  15. 15. Splinter Hemorrhages 1. 2. 3. 4. 5. Non-specific Non-blanching Linear reddish-brown lesions found under the nail bed Usually do NOT extend the entire length of the nail Vessel damage from swelling of the blood vessels (vasculitis) or tiny clots that damage the small capillaries (microemboli).
  16. 16. Osler’s Nodesimmune 1. 2. 3. 4. More specific Painful, erythematous and subcutaneous nodules Located on pulp of fingers and toes More common in subacute IE
  17. 17. Janeway Lesions 1. 2. 3. 4. 5. More specific Erythematous, blanching macules Nonpainful Located on palms and soles Microabscess of the dermis with marked necrosis and inflammatory infiltrate not involving the epidermis.
  18. 18. Roth Spots Oval, retinal hemorrhages with pale centers.
  19. 19. Modified Dukes Criteria for diagnosis of Infective Endocarditis
  20. 20. Major Criteria: Positive blood culture ◦Typical organism from two cultures ◦Persistent positive blood cultures taken > 12 hours apart ◦Three or more positive cultures taken over more than 1 hour. Endocardial involvement ◦Positive echocardiographic findings of vegetations ◦New valvular regurgitation
  21. 21. Minor Criteria: • Predisposition: Predisposing valvular or cardiac abnormality • Intravenous drug misuse • Pyrexia ≥38°C (≥100.4°F) • Embolic phenomenon • Vasculitic/ immunologic phenomenon • Blood cultures suggestive: -organism grown but not achieving major criteria • Suggestive echocardiographic findings
  22. 22. Definitive Endocarditis if, - Two major or, - One major and three minor or, - five minor Possible Endocarditis if, - One major and one minor or, - Three minor
  23. 23. Complications of Endocarditis: Cardiac Neurologic Emboli Metastatic Abscesses 33-50% 25-35% 15-35% <5%
  24. 24. Cardiac complications Congestive heart failure Valvular damage leads to valvular regurgitation Valvular stenosis Coronary embolism Prosthetic dehiscence Abscess extending to myocardium causing conduction disturbances extending to pericardium causing purulent pericarditis.
  25. 25. Neurologic Complications • Acute encephalopathy • Meningitis • Embolic stroke • Cerebral hemorrhage • Brain abscess
  26. 26. Embolic Phenomena • Stroke • Ischemic extremities • Pulmonary emboli • Paralysis due to embolic infarction of either the brain or spinal cord • Hypoxia from pulmonary emboli • Abdominal pain (splenic or renal infarction
  27. 27. Metastatic Spread of Infection Metastatic abscess ◦ Kidneys, spleen, brain, soft tissues Meningitis and/or encephalitis Vertebral osteomyelitis Septic arthritis
  29. 29. Microbiology:  Blood cultures: Key diagnostic investigation in infective endocarditis. Isolation of microorganism from culture is important for diagnosis and also for treatment. At least 3 sets of samples should be taken from different venepuncture sites over 24 hours. Serology:  Can be sent when the diagnosis is suspected and the cultures are negative. They aid in cases where the organisms will not grow in blood cultures(Coxiella,Legionella,Bartonella
  30. 30. 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
  31. 31. Septic Pulmonary Emboli:
  32. 32. Echocardiography It can identify the presence and size of vegetations,detect intracardiac complications and assess cardiac function. Transthoracic echocardiography is noninvasive and has high specificity for visualising vegetations. Transoesophageal echocardiography is more sensitive than TTE.It can detect small vegetations,prosthetic endocarditis and intra cardiac complications.
  33. 33. Complete blood counts may show anemia and increased WBC counts. Urea and Creatinine: may be elevated due to glomerulonephritis Liver biochemistry: Serum alkaline phosphatase may be increased Inflammatory markers CRP,ESR are increased in infection .CRP also helps in monotoring response to therapy. Urine proteinuria and hematuria occur frequently.
  34. 34. TREATMENT: Antimicrobial Therapy • Therapy requires identification of specific pathogen and its susceptibility to antimicrobials. • Empirical therapy should be started as soon as possible targeting most likely pathogens. • Bactericidal drugs should be used.
  35. 35. • Resolution of fever occurs in 5 to 7 days.if fever persists patient should be evaluated for complications like paravalvular abscess and extracardiac abscess. • Serologic abnormalities resolve slowly and do not reflect response to treatment.
  36. 36. Antibotic regimen for infective endocarditis:  Viridians Streptococci and Strep.bovis Benzyl penicillin (1.2g 4 hourly) 4-6 weeks Gentamicin (1mg/kg 8-12 hourly) 2 weeks Alternative Cefriaxone (2g once daily, iv) Vancomycin (15mg/kg 12 hourly) duration 4 weeks
  37. 37. Enterococci Ampicillin sensitive Ampicillin (2 g 4 hourly) 4-6 weeks, and Gentamicin (1mg/kg 8-12 hourly) o Ampicillin resistant Vancomycin(1g 12hourly) 4-6 weeks, and Gentamicin (1mg/kg 8-12 hourly) Alternative Cefriaxone (2g once daily, iv) Vancomycin (15mg/kg 12 hourly) duration 4 weeks o
  38. 38.  Staphycocci oPenicillin sensitive Benzyl penicillin I.V(1.2 g 4 hourly) oPenicillin resistant but methicillin sensitive Flucloxacillin I.V (2g 4 hourly ) oBoth penicillin and methicillin resistant Vancomycin I.V (1g 12 hourly) and Gentamicin (1mg/kg 8 hourly) duration 4-6 weeks
  39. 39. Surgery: Indications: Failure of antibiotic therapy  patients with direct extension of infection to myocardial structuires. Prosthetic valve dysfunction. Congestive heart failure. Badly damaged valves. IE caused by fungi or gram-ve or resistant organisms. Large vegetations on echocardiography Recurrent embolic attacks. Abscess formation.
  40. 40. . Prophylaxis: High risk category:  Prosthetic cardiac valves Previous bacterial endocarditis,even in absense of heart disease. Complex cyanotic congenital heart disease (TOF)  Surgically constructed systemic pulmonary shunts.
  41. 41. Moderate risk category: Rheumatic and other valvular dysfunction Congenital cardiac malformations Hypertrophic cardiomyopathy Mitral valve prolapse with valvular regurgitation
  42. 42. Regimen for IE prophylaxis:  Standard oral regime Amoxicillin 2 g 1hr before procedure  Inability to take oral medication Ampicillin 2g IV or IM 1hr before procedure  Penicillin allergy Clindamycin 600 mg Clarithromycin 500 mg Cephalexin 2 g.
  43. 43. Poor Prognostic Factors: • Female • Diabetes mellitus • S. aureus • Low serum albumen • Vegetation size • Apache II score • Aortic valve • Heart failure • Prosthetic valve • Paravalvular abscess • Older age • Embolic events
  44. 44. Prevention – the procedure • Dental procedures known to produce bleeding • Tonsillectomy • Surgery involving GI, respiratory mucosa • Esophageal dilation • ERCP for obstruction 2/23/2014 • Gallbladder surgery • Cystoscopy, urethral dilation • Urethral catheter if infection present • Urinary tract surgery, including prostate • I&D of infected tissue 49