Infective endocarditis


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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.
  • 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.
  • 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.
  • 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.
  • Infective endocarditis

    1. 1. Infective Endocarditis Dr.Khalid Hama salih, MD Pediatrics specialist M.B.Ch. D. C.H B.F.I.B.M.S.ped
    2. 2. DefinitionInfectious Endocarditis (IE): an infection ofthe heart’s endocardial surfaceClassified into four groups:– Native Valve IE– Prosthetic Valve IE– Intravenous drug abuse (IVDA) IE– Nosocomial IE
    3. 3. EpidemiologyIncidence difficult to ascertain and variesaccording to locationMuch more common in males than infemalesMay occur in persons of any age andincreasingly common in elderlyMortality ranges from 20-30%
    4. 4. Risk FactorsArtificial heart valves and pacemakersAcquired heart defects– Calcific aortic stenosis– Mitral valve prolapse with regurgitationCongenital heart defectsIntravascular catheters
    5. 5. Infecting OrganismsCommon bacteria– S. aureus– Streptococci– EnterococciNot so common:– Fungi– Pseudomonas– HACEK group - Haemophilus spp,. Actinobacillus actinomycete comitants, Cardiobacterium hominis, Eikenella spp, and Kingella kingae.
    6. 6. Pathophysiology Turbulent blood flow disrupts the endocardium making it “sticky”n Bacteremia delivers the organisms to the endocardial surface– Adherence of the organisms to the endocardial surface– Eventual invasion of the valvular leaflets
    7. 7. SIGNS:SYMPTOMS: Elevated temperature Fever, Chills Tachycardia Night Embolic phenomena (Roth sweats spots, petechiae, splinter Weight loss, Malaise hemorrhages, Osler nodes, CNS or ocular lesions) CNS:manifestations(strok Janeway lesions e,seizures,headache) Splenomegaly Dyspnea Arthritis Heart failure Chest and abdominal Arrhythmias pain Metastatic infection Arthralgia, myalgia (arthritis, meningitis, mycotic arterial aneurysm, pericarditis, abscesses) Clubbing
    8. 8. Petechiae 1. Nonspecific 2. Often located on extremities or mucous membranes blpetechiaephoto.htm Harden Library for the Health SciencesPhoto credit, Josh Fierer, M.D. hardin/ Eye-Petechiae.html md/cdc/3184.html
    9. 9. Splinter Hemorrhages1. Nonspecific2. Nonblanching3. Linear reddish-brown lesions found under the nail bed4. Usually do NOT extend the entire length of the nail
    10. 10. Osler’s NodesAmerican College of 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
    11. 11. Janeway Lesions1. More specific2. Erythematous, blanching macules3. Nonpainful4. Located on palms and soles
    12. 12. Investigation: Renal failure: azotemia, Positive blood culture highcreatinine(glomerulon ephritis) Elevated erythrocyte sedimentation rate. Chest radiograph: bilateral infiltrates,,pleural Elevated C-reactive protein effusions. Anemia Echocardiographic Leukocytosis evidence of valve Hypergammaglobulinemia vegetations, prosthetic Hypocomplementemia valve dysfunction or leak, Hematuria myocardial abscess, new- onset valve insufficiency
    13. 13. Duke criteria :-Major criteria include (1) positive blood cultures (twoseparate cultures for a usual pathogen) and (2) evidence of endocarditis on echocardiographyMinor criteria include:predisposing conditions fever embolic-vascular signs immune complex phenomena a single positive blood culture or serologic evidence ofinfection, and echocardiographic signs not meeting themajor criteria.NB/ Two major criteria, one major and three minor, orfive minor criteria suggest definite endocarditis
    14. 14. TreatmentParenteral antibiotics– High serum concentrations to penetrate vegetations– Prolonged treatment to kill dormant bacteria clustered in vegetations 4–6 wk .Surgery– Intracardiac complicationsSurveillance blood cultures
    15. 15. Poor Prognostic FactorsFemale Diabetes mellitusS. aureus Low serum albumenVegetation size Heart failureAortic valve Paravalvular abscessProsthetic valve Embolic eventsOlder age
    16. 16. PREVENTIONAntimicrobial prophylaxis before variousprocedures and other forms of dentalmanipulation may reduce the incidence ofinfective endocarditis in susceptiblepatients