infective endocarditis olcay Özveren, m.d

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Infective endocarditis Olcay ÖZVEREN, M.D.

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Infective endocarditis Olcay ÖZVEREN, M.D. Definition. - PowerPoint PPT Presentation

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  • Infective endocarditis

    Olcay ZVEREN, M.D.

  • DefinitionInfective endocarditis is characterized by colonization or invasion of the heart valves orthe mural endocardium by a microbe, leading to the formation of bulky,friable vegetations composed of thrombotic debris and organisms, often associated with destruction of the underlying cardiac tissues

  • A changing epidemiology:

    Once a disease affecting young adults with previously well-identified (mostly rheumatic) valve disease, IE is now affecting older patients who more often develop IE as the result of health care-associated procedures, either in patients with no previously known valve disease or in patients with prosthetic valves.Trials showed an increasing incidence of IE associated with a prosthetic valve, an increase in cases with underlying mitral valve prolapse, and a decrease in those with underlying rheumatic heart disease.Newer predisposing factors have emergedvalve prostheses, degenerative valve sclerosis, intravenous drug abuseassociated with increased use of invasive procedures at risk for bacteraemia, resulting in health care-associated IE.

  • 310 episodes/100 000 person-years.increased dramatically with age.The male:female ratio is 2:1.Positive blood cultures representing 85% of all IE. Causative microorganisms are most often staphylococci, streptococci, and enterococci.S. Aureus is the most frequent cause not only of IE but also of prosthetic valve IE. Conversely, coagulase-negative staphylococci can also cause native valve IE. Especially S. lugdunensis, which frequently has an aggressive clinical course.Oral (formerly viridans) streptococci species such as S. sanguis, S. mitis, S. salivarius, S. mutans, and Gemella morbillorum. Microorganisms of this group are almost always susceptible to penicillin G.Infective endocarditis with negative blood cultures because of prior antibiotic treatment.

  • Infective endocarditis associated withnegative blood cultures

    They are usually due to fastidious organisms such as nutritionallyvariant streptococci fastidious Gram-negative bacilli of the HACEK group: (Haemophilus parainfluenzae, H. aphrophilus, H. paraphrophilus, H. influenzae, Actinobacillus actinomycetemcomitans,Cardiobacterium hominis, Eikenella corrodens, Kingella kingae, and K. denitrificans), Brucellafungi.Infective endocarditis associated with constantly negative blood cultures: Coxiella burnetii,Bartonella, Chlamydia Tropheryma whipplei,

  • Classification and definitions of infective endocarditis

  • Classification of infective endocarditis

  • Classification of infective endocarditis

  • PathophysiologyThe normal valve endothelium is resistant to colonization and infection by circulating bacteria.mechanical disruption of the endothelium (Endothelial damage may result from mechanical lesions provoked by turbulent blood flow, electrodes or catheters inflammation, as in rheumatic carditis, or degenerative changes in elderly individuals, which are associated with inflammation, microulcers, and microthrombi)exposure of underlying extracellular matrix proteinsthe production of tissue factorthe deposition of fibrin and platelets-Nonbacterial thrombotic endocarditis (NBTE)-

  • Microbial pathogens and host defencesClassical IE pathogens (S. aureus, Streptococcus spp., and Enterococcus spp.) share the ability to adhere to damaged valves, trigger local procoagulant activity, and nurture infected vegetations in which they can survive. surface determinants that mediate adherence to host matrix molecules present (e.g. fibrinogen, fibronectin, platelet proteins)trigger platelet activation. colonizationGram positive bacteria are resistant to complement. However, they may be the target of platelet microbicidal proteins (PMPs), which are produced by activated platelets and kill microbes by disturbing their plasma membrane. Bacteria resistant to PMP-induced killing, THS is a typical characteristic of IE-causing pathogens.

  • Janeway LesionsMore specificErythematous, blanching macules NonpainfulLocated on palms and solesMicroabscess of the dermis with marked necrosis and inflammatory infiltrate not involving the epidermis.

  • Oslers NodesMore specificPainful and erythematous nodulesLocated on pulp of fingers and toesimmuncomplex

  • Splinter HemorrhagesNonspecificNonblanchingLinear reddish-brown lesions found under the nail bedUsually 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).

  • PetechiaeNonspecificOften located on extremities or mucous membranes

  • Roth Spotsseptic embolization, leukemia, lupus erythematosus, or pernicious anemia.

  • ImagingChest x-ray Look for multiple focal infiltrates and calcification of heart valvesEKGRarely diagnosticLook for evidence of ischemia, conduction delay, and arrhythmiasEchocardiography

  • ComplicationsCongestive heart failureMost common complicationMain indication to surgical treatment~60% of IE patientsUncontrolled infectionPersisting infection Perivalvular extension in infective endocarditisSystemic embolismBrain, spleen and lungs30% of IE patientsMay be the first symptom

  • Complications Neurologic eventsAcute renal failureRheumatic problemsMyocarditis

  • Cardiac conditions at highest risk of infective endocarditis for which prophylaxis is recommended when a high risk procedure is performed

  • Recommendations for prophylaxis of infective endocarditis

  • Definition Current Diagnosis 07An acute systemic immune disease that may develop after an infection with Group A beta- hemolytic Streptococcal infection of the pharynx. This disease can affect the HEART, JOINTS, SKIN, SUBCUTANEOUS TISSUE, BRAIN, RESPIRATORY SYSTEM, VESSELS, SEROSAL MEMBRANES, TENDONS AND FASCIAL SHEATHS

  • General Consideration

  • Pathology

  • PATHOLOGYThe Aschoff bodies comprises a localised area of inflammation having a central deposit of amorphous fibrinoid material surrounded by an inflammatory infiltrate of mesenchymal cells known as Anitschkow giant cells or caterpillar cells (because the chromatin is distributed in the centre of the nucleus in the forrm of a slender wavy ribbon that resemles the attenuated body with innumerable fine leg like projections ) and an occasional multinucleated Aschoff giant cell withowl eyed nucleoliFully developed Aschoff bodies are pathognomonic of RFAschoff bodies proceed thru 3 phases- exudative, proliferative and healed

  • The heart has been sectioned to reveal the mitral valve as seen from above in the left atrium. The mitral valve demonstrates the typical "fish mouth" shape with chronic rheumatic scarring. Mitral valve is most often affected with rheumatic heart disease, followed by mitral and aortic together, then aortic alone, then mitral, aortic, and tricuspid together.

  • Microscopically, acute rheumatic carditis is marked by a peculiar form of granulomatous inflammation with so-called "Aschoff nodules" seen best in myocardium. These are centered in interstitium around vessels as shown here. The myocarditis may be severe enough to cause congestive heart failure.

  • Here is an Aschoff nodule at high magnification. The most characteristic component is the Aschoff giant cell. Several appear here as large cells with two or more nuclei that have prominent nucleoli. Scattered inflammatory cells accompany them and can be mononuclears or occasionally neutrophils.

  • Another peculiar cell seen with acute rheumatic carditis is the Anitschkow myocyte. This is a long, thin cell with an elongated nucleus.

  • MODIFIED JONES CRITERIAMAJOR:PolyarthritisCarditisChoreaSubcutaneous nodulesErythema marginatum

  • MINOR CRITERIA

    ClinicalFeverPolyarthralgiah/o previous ARF or Rheum. heart diseaseLabReversible prolongation of PR intervalInc ESRInc C Reactive Protein+ throat culture Or rapid streptococcal antigen testInc ASO titre

  • Laboratory Findings

  • Supporting evidence of Streptecoccal infection

  • Rapid antigen detecting test

  • REQUIRED FOR DIAGNOSISTwo major criteria OROne major and two minor criteria

  • Exceptions to Jones Criteria

  • POLYARTHRITISMigratory flitting and fleetingInvolves large joints sequentiallyPolyarthritis- in adults only a single joint may be affectedLasts 1-5 weeks Occurs in 75% or patientsSubsides without residual deformityDramatic response of arthritis to therapeutic doses of aspirin or NSAIDs

  • CARDITISMost likely in children and adolescentsOccurs in 1/3 of casesAny of the following signs suggest the presence of carditisEndocardial- - MR or AR murmurs indicative of dilatation of valve ring with or without associated valvulitis -Short mid-diastolic murmur (Carey-Coombs) may be present - Changing quality of heart sounds2. Myocardial - Tachycardia even at rest. Arrhythmias or ectopic beats - Cardiomegaly- on physical exam, CXR or ECHO - Congestive cardiac failure right or left sided3. Pericardial - Pericarditis - Pericardial effusionECG Changes - Changing contour of P waves - Inversion of T waves - Prolongation of PR interval

    Maybe self limiting or may lead to slowly progressive valvular deformityMitral valve attacked in 75% cases, aortic in 30% ( but rarely as the sole valve), tricuspid and pulmonary in < 5% cases

  • SYDENHAMS CHOREAInvoluntary choreo- athetoid movements primarily of the face, tongue, and upper extremities,detoriation of hand writing,emotional lability ,grimacing of face Maybe sole manifestation- in 50% of cases no other signs of RFGirls more frequenty affectedRare in adultsLease common(
  • Erythema Marginatum.

  • Subcutaneous Nodule

  • Imaging

  • DIFFERENTIAL DIAGNOSISRheumatoid arthritisOsteomyelitisEndocarditisChronic meningiococcemiaSLELyme diseaseSickle cell diseaseSurgical abdomen

  • TREATMENTPHARYNGITISBenzathene penicillin 1.2 million units ( 50,000 units/kg to a max of 1.2 million units) is injected IM once orInj Procaine penicillin 600,000 units once daily for 10 daysErythromycin can be substituted ( 40mg/kg/day)CARDITISBed rest until temp, ESR, resting pulse rate and ECG have all returned to normalPrednisone if there is CCF or cardiomegalyPOLYARTHRITISAnti inflammatory agent - Aspirin markedly reduces fever, joint pain and swellingNo effect on the natural course of the disease100mg / kg/day in 4-6 divided doses. Can be reduced to 75mg/Kg/day once there is a response . Given for 4-6 weeksToxicity includes- tinnitus, vomiting and GI bleeding.When response to aspirin is inadequate a short course of prednisone (1 mg/kg/day) orally daily usually causes rapid improvement of joint symptoms. It is tapered over 2 weeks. Add aspirin when tapering begins.

  • Treatment Strategy

  • Other alternative drugs used

  • Anti inflamatory treatment

  • Rheumatic carditis without failure

  • Rheumatic carditis without failure

  • Management of complications

  • *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.*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 Dukes Criteria).

    EKG An EKG alone cannot diagnose IE but it may show evidence of some of the diseases 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.