Presentation on theme: "Infecctive Endocarditis (IE) Dr mirdamadi Cardiologist, fellowship of echocardiography."— Presentation transcript:
Infecctive Endocarditis (IE) Dr mirdamadi Cardiologist, fellowship of echocardiography
Reference : Braunwalds heart disease Harrisons principles of internal medicine
Acute IE is cused typically by staphylococcus aureus, with marked toxicity and progresses over days to weeks to valvular destruction and metastic infection. Subacute IE usally caused by viridans streptococci,enterococci,cougulase negative staphlococci or gram-negative coccoba cilli, evolves over weeks to months with only modest toxicity and rarely causes metastatic.
#Prototypic lesion of IE,the vegetation is mass of platlets,fibrin,microorganisms and inflammatory cells. # Site of infection :heart valves (native or prosthetic), site of VSD, mural endocardium at site of aberrent jets of blood or freign bodies,on intracardiac devices,arteriovenousshunt, arterioarterial shunt (PDA)or coarctation of aorta.
Neonate : often TV involved as a consequencec of infected intravascular catheters or cardiac surgery Childern and adults : RHD,CHD,MVP,DHD
IV drug abuser: Mostly involved TV,then MV and AOV Multiple site involvement may occure Recurrent IE may occure Although S.aureus is characteristic but unusual organisms and polymicrobial IE may occure. Infection with HIV is not a significant risk factor for IE unless associated with IV drug abuse.
Prosthetic valve endocarditic (PVE):great frequency during first 6 months Early:within 60 days, as a complication of surgery and s.epidermidis is prominent. Late :after 60 days,as a common microorganism.
Transvenous pacemaker lead and/or implanted defibrillator :is usually nosocomial and is moe within weeks of implantation or generator change,mostly s.aureus or s.aureus or s.epidermidis Healthcare –associated :after hospitaliazation or as a cnsequence of indwelling devices, or hemodialysis catheter, s.aureus is the most common cause.
Normal endothelium is resistant to infection and thrombus formation. Endothelial injury allows direct infection by virulent organisms or development of an uninfected platelet-fibrin thrombus (nonbacterial thrombotic endocarditis,NBTE). Thrombus is a site of bacterial attachment during transient bacteremin NBTE: DIC,burn,SLE uremin,valvular heart disease and intracardiac catheters, marantic endocarditis (malignancy and ohronic disease).
Organisms enter the bloodstream from mucosal surfaces,skin or site of focal infection. Except for virulent bacteria (e.g.aureus) that can adhere to intact endothelium, other microorganisms adhere to NBTE. Organism proliferate and induce a procoagulant state at the site. Fibrin deposition with platelet aggregation,stimulated by tissue factor and proliferating microorganisms,generate vegetation.
Microorganisms can cause endocarditis have microbial surface components recognizing adhesin matrix molecules (MSCRAMMs) that mediate adherence to NBTE or injured endothelium Glucans or dextran is surface polysaccharides of streptococci Fibronectin is in lesion ofheart valves and produced by endothelial cells platlets and fibroblasts in response to vascular injury Fibronectine-binding proteins present on many gram-positive bacterin.
910 Bacteria in vegetations reach to organisms per pram and organisms deep in vegetation are metabolically inactive (non growing) and relatively resistant to killing by antimicrobial agents
Fever: is low –grade in subacute (<39.4c) but temperatures of 39.4° - 40 °c are often in acute if fever may be absent in elderly severely debilitated patient or who have marked cardiac or renal failure
Valvula regurgitation due to valvular damage or ruptured chordae CHF due to valvular regurgitation or myocarditis or intracardiac fistula Perivalvular abscesses (mostly AOV) Pericarditis due to extension through epicardium (mostly AOV) Heart block due to extension to conduction system (mostly AOV)
Non cardiac manifestation
Musculoskeletal symptom (arthralgin,myalgia,arthritis,back pain) Emboli to brain,coronary artery, extremities,mesenteric arteries Splenomegaly and clubbing Petechiae in conjunctiva,buccal &palatal mucosa and extremities Splinter or subungual hemorrhages Osler nodes Janeway lesion Roth spot (oval retinal hemorrhage with pale center) Neurological symptum: stroke,ICH,cerebritis and microabscesses headache(potentially due to mycotic aneurysm),seizure,encephalopathy Renal insufficiency due to glomerulonephritis,emboli, impaired hemodynamic andvantimicrobial toxicities.
%50 of patients associated with IV drug use,infection is limited to the tricupid valve. These patient present with fever,faint or no mumur,cough,pleuritic chest pain,pulmonary infiltration,pyopneumothorax.
Anemia (normochromic,normocytic),false positive serologic test for syphilis and rheumatoid factor. ESR elevation (average 55mm/hr),positive CRP. Urinalysis (proteinuria, hematuria).
Blood culture :3 blood culture sets(two bottles per set )with at least 1 h separation from different vien over 24 h should be obtained. If culture remain negative after h,two or three additional blood culture sets should be obtained. 5-10% of patiants with IE may have negative blood cultures.due to previous antibiotic therapy or fastidious organisms or fongal IE.
Echcardiography can confirmed IE, sizing of vegetation,detection of intracardiac complications assesment of cardiac function. TTE detects vegetation in 65% of patients and TEE in 99%
Definite diagnosis is when vegetation obtained at cardiac surgery, an autopsy or from an artery (embolus) and examined histologically & microbiologically. Duke criteria : Developed on the basis of clinical, laboratory &echocardiography.
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Definite diagnosis according to documentation of 2 major ocriteria,1 major &3 minor criteria or 5 minor criteria Rejection if an alternative dianosis is established if symptom resolve with
It is difficult to eradicate bacteria from the avascular vegetation with largely nongrowing,methabolically inactive bacteria Therapy must be bactericidal and prolonged, prenterally with high serum concentrations that will through passive diffusion lead to effective concenterations in the depths of vegetation.
Antibiotic toxicities,including allergic reactions occur in % of patients. blood test to detect renal,hepatic & hematologic toxicity should be performed periodically. In most patients,effective therapy results in resolution of fever in 5-7 days When fever persists for 7 days patients should be evaluated for paravaluvlar abscess and for extracardiac abscesses (spleen, kidney) or complications (embolic events) drug reactions or complications of hospitalization. Vegetation become smaller with treatment,but at 3 months after cure half are unchanged and 25%are slightly larger.
Moderate to severe CHF due to value dysfunction Unstable prothesis, prosthesis orifice obstructed Uncontrolled infection Unavailable effective antimicrobial therapy (fungi,brucellae,pseudomonas aeruginosa) Relapse after optimal therapy Perivalvular extension Culture negative IE with persistent fever( >10d) Large (>10 mm) hypermobile vegetation
Oral hygiene and dental health should be addressed before prosthetic valves are placed electively Oral irrigating devices are not recommended Use irrigating devices are not recommended Transient bacteremia occure after dental manipnlation (daily or surgical)
Antibiotic prophylaxis recommended in dental procedures that involve gingival tissue or perforate oral mucosa tonsilectomy a denoidectomy or bronchoscopy, surgery of infected skin or musculoskeletal tissue
Cardiac condition that need prophlaxis : Prosthetic valus Previous IE Unrepaired cyanotic CHD Repaired CHD with residual defect Completely repaired during the first 6 months after procedure Cardiac transplantation with cardiac valvulopathy
Prophylaxy:30-60 min before procedure: Amoxicillin 2g po Cephalixin 2g po( azithromycin or clatrithromycin 500g or clindamycin 600g)